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article-31240_29 | Unilateral Vocal Fold Paralysis -- Treatment / Management | UVFP management should focus on removing the identified cause, preventing aspiration, and improving dysphonia. Treatment decisions must be tailored to each clinical scenario. | Unilateral Vocal Fold Paralysis -- Treatment / Management. UVFP management should focus on removing the identified cause, preventing aspiration, and improving dysphonia. Treatment decisions must be tailored to each clinical scenario. |
article-31240_30 | Unilateral Vocal Fold Paralysis -- Treatment / Management | Idiopathic UVFP and its prognosis deserve special mention. Although not well-defined in the literature, this condition is believed to be secondary to a postviral or postinfectious insult, as happens in postviral facial paralysis and sensorineural hearing loss. | Unilateral Vocal Fold Paralysis -- Treatment / Management. Idiopathic UVFP and its prognosis deserve special mention. Although not well-defined in the literature, this condition is believed to be secondary to a postviral or postinfectious insult, as happens in postviral facial paralysis and sensorineural hearing loss. |
article-31240_31 | Unilateral Vocal Fold Paralysis -- Treatment / Management | Sulica reported in 2008 that individuals who develop idiopathic UVFP do not completely recover vocal cord mobility at the same time, though vocal therapy can promote dysphonia resolution before full recovery. Most of these patients should recover fully a year after symptom onset. [56] | Unilateral Vocal Fold Paralysis -- Treatment / Management. Sulica reported in 2008 that individuals who develop idiopathic UVFP do not completely recover vocal cord mobility at the same time, though vocal therapy can promote dysphonia resolution before full recovery. Most of these patients should recover fully a year after symptom onset. [56] |
article-31240_32 | Unilateral Vocal Fold Paralysis -- Treatment / Management | If the diagnostic workup does not find aspiration or any ominous pathology, a 12-month observation period and a speech therapy referral are recommended to see if the patient can regain vocal fold motion without aggressive intervention. Speech therapy can help patients recover vocal and swallowing functions and may negate the need for surgery even if complete vocal fold motion recovery does not occur [57] . | Unilateral Vocal Fold Paralysis -- Treatment / Management. If the diagnostic workup does not find aspiration or any ominous pathology, a 12-month observation period and a speech therapy referral are recommended to see if the patient can regain vocal fold motion without aggressive intervention. Speech therapy can help patients recover vocal and swallowing functions and may negate the need for surgery even if complete vocal fold motion recovery does not occur [57] . |
article-31240_33 | Unilateral Vocal Fold Paralysis -- Treatment / Management | Surgical interventions include temporary or permanent vocal fold augmentation, formal thyroplasty (medialization laryngoplasty), and arytenoid adduction. Vocal fold augmentation repositions the paralyzed vocal fold closer to the midline. Thus, the contralateral, fully functional true vocal fold can close the glottis during deglutition and phonation, helping prevent aspiration and improve dysphonia. | Unilateral Vocal Fold Paralysis -- Treatment / Management. Surgical interventions include temporary or permanent vocal fold augmentation, formal thyroplasty (medialization laryngoplasty), and arytenoid adduction. Vocal fold augmentation repositions the paralyzed vocal fold closer to the midline. Thus, the contralateral, fully functional true vocal fold can close the glottis during deglutition and phonation, helping prevent aspiration and improve dysphonia. |
article-31240_34 | Unilateral Vocal Fold Paralysis -- Treatment / Management | On the other hand, patients with UVFP and aspiration require a more aggressive approach, such as immediate injection augmentation, to protect the airway and prevent pneumonia. This procedure may still help patients without aspiration but are symptomatically dysphonic, as temporary injection augmentation can improve the voice. Hyaluronic acid is the preferred injectable agent if spontaneous recovery is expected. [58] | Unilateral Vocal Fold Paralysis -- Treatment / Management. On the other hand, patients with UVFP and aspiration require a more aggressive approach, such as immediate injection augmentation, to protect the airway and prevent pneumonia. This procedure may still help patients without aspiration but are symptomatically dysphonic, as temporary injection augmentation can improve the voice. Hyaluronic acid is the preferred injectable agent if spontaneous recovery is expected. [58] |
article-31240_35 | Unilateral Vocal Fold Paralysis -- Treatment / Management | Permanent augmentation is indicated for patients with UVFP longer than 12 months. Permanent vocal-fold-augmentation options include formal thyroplasty and serial injections with longer-acting injectable materials, such as autologous fat. [59] | Unilateral Vocal Fold Paralysis -- Treatment / Management. Permanent augmentation is indicated for patients with UVFP longer than 12 months. Permanent vocal-fold-augmentation options include formal thyroplasty and serial injections with longer-acting injectable materials, such as autologous fat. [59] |
article-31240_36 | Unilateral Vocal Fold Paralysis -- Treatment / Management | Teflon was a widely used injectable vocal-fold-augmenting agent in the past. However, this material is rarely used today, given the potential for morbidity from Teflon granuloma. [60] Historically, gel foam has also been used, though it lasts only 4 to 6 weeks. [61] By comparison, acellular dermal matrix (AlloDerm, Cymetra) can last 2 to 4 months. However, potential risks include intralaryngeal abscess and, if injected into Rienke's space, micronodule formation. [61] Calcium hydroxyapatite can last 18 months and has comparable safety and efficacy to hyaluronic acid. | Unilateral Vocal Fold Paralysis -- Treatment / Management. Teflon was a widely used injectable vocal-fold-augmenting agent in the past. However, this material is rarely used today, given the potential for morbidity from Teflon granuloma. [60] Historically, gel foam has also been used, though it lasts only 4 to 6 weeks. [61] By comparison, acellular dermal matrix (AlloDerm, Cymetra) can last 2 to 4 months. However, potential risks include intralaryngeal abscess and, if injected into Rienke's space, micronodule formation. [61] Calcium hydroxyapatite can last 18 months and has comparable safety and efficacy to hyaluronic acid. |
article-31240_37 | Unilateral Vocal Fold Paralysis -- Treatment / Management | Hyaluronic acid is the most widely studied injectable vocal-fold-augmenting material available in various brands. This material's viscosity is similar to that of natural mucosa and thus interferes less with the mucosal wave. Low-viscosity preparations are injected submucosally or into Rienke's space, while high-viscosity preparations can be injected intramuscularly. [62] Reported duration is variable but averages 4 to 12 months, depending on the brand or formulation used. [63] | Unilateral Vocal Fold Paralysis -- Treatment / Management. Hyaluronic acid is the most widely studied injectable vocal-fold-augmenting material available in various brands. This material's viscosity is similar to that of natural mucosa and thus interferes less with the mucosal wave. Low-viscosity preparations are injected submucosally or into Rienke's space, while high-viscosity preparations can be injected intramuscularly. [62] Reported duration is variable but averages 4 to 12 months, depending on the brand or formulation used. [63] |
article-31240_38 | Unilateral Vocal Fold Paralysis -- Treatment / Management | Potentially permanent injectable materials include autologous fat and fascia. Both are advantageous in that they are completely autologous, living material. The long-term outcomes, however, have been extremely variable in terms of duration and phonatory results. For example, autologous fat has nearly the same viscoelastic properties as the native mucosa. However, fat's survival and duration of benefit are extremely variable. Thus, this option has fallen from favor in many centers. [64] Meanwhile, fascia can last years but is less widely used. Donor site morbidity remains a concern, and fascia has been described as less suitable for correcting wide glottic gaps. [65] | Unilateral Vocal Fold Paralysis -- Treatment / Management. Potentially permanent injectable materials include autologous fat and fascia. Both are advantageous in that they are completely autologous, living material. The long-term outcomes, however, have been extremely variable in terms of duration and phonatory results. For example, autologous fat has nearly the same viscoelastic properties as the native mucosa. However, fat's survival and duration of benefit are extremely variable. Thus, this option has fallen from favor in many centers. [64] Meanwhile, fascia can last years but is less widely used. Donor site morbidity remains a concern, and fascia has been described as less suitable for correcting wide glottic gaps. [65] |
article-31240_39 | Unilateral Vocal Fold Paralysis -- Treatment / Management | Injection augmentation can be performed under general anesthesia in a hospital setting with direct vocal cord visualization via microsuspension laryngoscopy. Alternatively, the procedure can be done percutaneously via nasolaryngoscopy in an office setting and with the patient awake. | Unilateral Vocal Fold Paralysis -- Treatment / Management. Injection augmentation can be performed under general anesthesia in a hospital setting with direct vocal cord visualization via microsuspension laryngoscopy. Alternatively, the procedure can be done percutaneously via nasolaryngoscopy in an office setting and with the patient awake. |
article-31240_40 | Unilateral Vocal Fold Paralysis -- Treatment / Management | Awake procedures in these cases may be indicated if multiple comorbidities can make general anesthesia risky. [66] Additionally, office-based injection has the benefit of immediate feedback regarding dysphonia resolution. However, one limitation of this approach is that injection might not be as accurately placed or as easy as compared to augmentation in an anesthetized patient. [67] | Unilateral Vocal Fold Paralysis -- Treatment / Management. Awake procedures in these cases may be indicated if multiple comorbidities can make general anesthesia risky. [66] Additionally, office-based injection has the benefit of immediate feedback regarding dysphonia resolution. However, one limitation of this approach is that injection might not be as accurately placed or as easy as compared to augmentation in an anesthetized patient. [67] |
article-31240_41 | Unilateral Vocal Fold Paralysis -- Treatment / Management | A more permanent surgical option is laryngeal framework surgery (medialization laryngoplasty or thyroplasty), commonly used in longstanding UVFP. The surgical detail of this procedure is beyond the scope of this article, but in brief, a window is made in the thyroid cartilage, and an implant is placed to medialize the true vocal fold. Various materials have been used, including Gore-Tex, Silastic implants, and Silicone blocks. [68] | Unilateral Vocal Fold Paralysis -- Treatment / Management. A more permanent surgical option is laryngeal framework surgery (medialization laryngoplasty or thyroplasty), commonly used in longstanding UVFP. The surgical detail of this procedure is beyond the scope of this article, but in brief, a window is made in the thyroid cartilage, and an implant is placed to medialize the true vocal fold. Various materials have been used, including Gore-Tex, Silastic implants, and Silicone blocks. [68] |
article-31240_42 | Unilateral Vocal Fold Paralysis -- Treatment / Management | Laryngeal reinnervation utilizes functioning nerves in the RLN's vicinity to reestablish laryngeal tone and movement. The ansa cervicalis, phrenic, and hypoglossal nerves have all been used as nerve pedicles with good voice outcomes [69] . | Unilateral Vocal Fold Paralysis -- Treatment / Management. Laryngeal reinnervation utilizes functioning nerves in the RLN's vicinity to reestablish laryngeal tone and movement. The ansa cervicalis, phrenic, and hypoglossal nerves have all been used as nerve pedicles with good voice outcomes [69] . |
article-31240_43 | Unilateral Vocal Fold Paralysis -- Treatment / Management | Arytenoid adduction is specifically used to treat persistent or severe posterior glottic gaps. [54] A suture is suspended from the arytenoid muscular process anterior to the thyroid cartilage. Thus, the muscle can mimic the lateral cricoarytenoid's vocal-fold adducting effect. Although rarely used alone, this procedure may be a useful adjunct in treating UVFP in select cases. | Unilateral Vocal Fold Paralysis -- Treatment / Management. Arytenoid adduction is specifically used to treat persistent or severe posterior glottic gaps. [54] A suture is suspended from the arytenoid muscular process anterior to the thyroid cartilage. Thus, the muscle can mimic the lateral cricoarytenoid's vocal-fold adducting effect. Although rarely used alone, this procedure may be a useful adjunct in treating UVFP in select cases. |
article-31240_44 | Unilateral Vocal Fold Paralysis -- Differential Diagnosis | The differential diagnosis of UVFP includes the conditions listed below. A thorough clinical evaluation and judicious use of diagnostic tests can help differentiate UVFP from these conditions. Allergy and environmental asthma Anaphylaxis Asthma Bilateral vocal fold paralysis Epiglottitis Exercise-induced asthma Foreign body obstruction Laryngeal abnormalities Laryngeal edema from C1 inhibitor deficiency or ACE inhibitor use Laryngeal spasm Upper respiratory tract infection Vocal polyps and nodules | Unilateral Vocal Fold Paralysis -- Differential Diagnosis. The differential diagnosis of UVFP includes the conditions listed below. A thorough clinical evaluation and judicious use of diagnostic tests can help differentiate UVFP from these conditions. Allergy and environmental asthma Anaphylaxis Asthma Bilateral vocal fold paralysis Epiglottitis Exercise-induced asthma Foreign body obstruction Laryngeal abnormalities Laryngeal edema from C1 inhibitor deficiency or ACE inhibitor use Laryngeal spasm Upper respiratory tract infection Vocal polyps and nodules |
article-31240_45 | Unilateral Vocal Fold Paralysis -- Pertinent Studies and Ongoing Trials | Siu et al's systematic review revealed that injection thyroplasty, type 1 thyroplasty, laryngeal reinnervation, and arytenoid adduction do not exhibit significant differences in voice outcome or quality of life. [70] Type 1 Isshiki thyroplasty is often highly favored due to its greater long-term benefit over injection techniques. However, a growing body of evidence supports long-acting injectable materials' comparable longitudinal outcomes. [71] Thus, surgical intervention for UVFP should be reserved after a lack of response to a trial of conservative management has been demonstrated. The choice of surgical technique must be based on the surgeon's experience and patient preference. | Unilateral Vocal Fold Paralysis -- Pertinent Studies and Ongoing Trials. Siu et al's systematic review revealed that injection thyroplasty, type 1 thyroplasty, laryngeal reinnervation, and arytenoid adduction do not exhibit significant differences in voice outcome or quality of life. [70] Type 1 Isshiki thyroplasty is often highly favored due to its greater long-term benefit over injection techniques. However, a growing body of evidence supports long-acting injectable materials' comparable longitudinal outcomes. [71] Thus, surgical intervention for UVFP should be reserved after a lack of response to a trial of conservative management has been demonstrated. The choice of surgical technique must be based on the surgeon's experience and patient preference. |
article-31240_46 | Unilateral Vocal Fold Paralysis -- Prognosis | The outlook for most patients with UVFP depends on the underlying pathology. Spontaneous recovery is expected in most individuals with idiopathic UVFP. However, cases with malignant and CNS etiologies have variable outcomes. [72] | Unilateral Vocal Fold Paralysis -- Prognosis. The outlook for most patients with UVFP depends on the underlying pathology. Spontaneous recovery is expected in most individuals with idiopathic UVFP. However, cases with malignant and CNS etiologies have variable outcomes. [72] |
article-31240_47 | Unilateral Vocal Fold Paralysis -- Complications | The potential complications of UVFP include the following: Aspiration pneumonia Respiratory distress Dysphagia Decreased exercise tolerance Psychosocial effects of vocal changes Underlying conditions like malignancies, thoracic injuries, and neurologic disease also bring unique sets of complications, such as debility, paraneoplastic syndromes, and death. | Unilateral Vocal Fold Paralysis -- Complications. The potential complications of UVFP include the following: Aspiration pneumonia Respiratory distress Dysphagia Decreased exercise tolerance Psychosocial effects of vocal changes Underlying conditions like malignancies, thoracic injuries, and neurologic disease also bring unique sets of complications, such as debility, paraneoplastic syndromes, and death. |
article-31240_48 | Unilateral Vocal Fold Paralysis -- Deterrence and Patient Education | Preventing UVFP involves addressing its potential underlying causes and minimizing the risk of RLN damage. Measures that can help patients include taking precautions to avoid neck and throat trauma, treating infections promptly, and going to regular health checkups. Some UVFP risk factors are beyond an individual's control, but maintaining overall health can minimize the risk of complications that might lead to this condition. | Unilateral Vocal Fold Paralysis -- Deterrence and Patient Education. Preventing UVFP involves addressing its potential underlying causes and minimizing the risk of RLN damage. Measures that can help patients include taking precautions to avoid neck and throat trauma, treating infections promptly, and going to regular health checkups. Some UVFP risk factors are beyond an individual's control, but maintaining overall health can minimize the risk of complications that might lead to this condition. |
article-31240_49 | Unilateral Vocal Fold Paralysis -- Deterrence and Patient Education | For clinicians, head and neck surgical and instrumentation procedures must be performed carefully. Providers should seek to improve competence in performing common procedures like ETT insertion by continuous training and simulation. | Unilateral Vocal Fold Paralysis -- Deterrence and Patient Education. For clinicians, head and neck surgical and instrumentation procedures must be performed carefully. Providers should seek to improve competence in performing common procedures like ETT insertion by continuous training and simulation. |
article-31240_50 | Unilateral Vocal Fold Paralysis -- Enhancing Healthcare Team Outcomes | In summary, UVFP is a relatively common disorder presenting to otolaryngologists and other medical practitioners. The condition can arise from RLN and laryngeal lesions from sources like malignancy and iatrogenic injuries. Some common symptoms are hoarseness, coughing, choking, aspiration, dyspnea, dysphagia, and globus sensation. | Unilateral Vocal Fold Paralysis -- Enhancing Healthcare Team Outcomes. In summary, UVFP is a relatively common disorder presenting to otolaryngologists and other medical practitioners. The condition can arise from RLN and laryngeal lesions from sources like malignancy and iatrogenic injuries. Some common symptoms are hoarseness, coughing, choking, aspiration, dyspnea, dysphagia, and globus sensation. |
article-31240_51 | Unilateral Vocal Fold Paralysis -- Enhancing Healthcare Team Outcomes | Once identified, imaging from the skull base superiorly to the aortic arch inferiorly is necessary to evaluate the RLN for any lesions. Treatment plans vary depending on the patient and etiology, but options are generally focused on airway protection and improving dysphonia. In idiopathic UVFP, spontaneous recovery can be expected in most patients after a year. Interval speech therapy may improve long-term outcomes. Early injection medialization has also been shown to improve final voice outcomes. | Unilateral Vocal Fold Paralysis -- Enhancing Healthcare Team Outcomes. Once identified, imaging from the skull base superiorly to the aortic arch inferiorly is necessary to evaluate the RLN for any lesions. Treatment plans vary depending on the patient and etiology, but options are generally focused on airway protection and improving dysphonia. In idiopathic UVFP, spontaneous recovery can be expected in most patients after a year. Interval speech therapy may improve long-term outcomes. Early injection medialization has also been shown to improve final voice outcomes. |
article-31240_52 | Unilateral Vocal Fold Paralysis -- Enhancing Healthcare Team Outcomes | UVFP is best managed with an interprofessional approach. Both primary care providers and specialists in clinical practice encounter this disorder often. Referral to an otolaryngologist is highly recommended for formal laryngoscopic evaluation, emphasizing the need for comprehensive care in UVFP cases. Early referral for speech therapy is beneficial in nearly all patients. The anesthesiologist may be involved if the vocal-fold-augmentation procedure is performed under general anesthesia. Surgical nurses' services are crucial in caring for patients with UVFP admitted for surgical augmentation or respiratory distress. | Unilateral Vocal Fold Paralysis -- Enhancing Healthcare Team Outcomes. UVFP is best managed with an interprofessional approach. Both primary care providers and specialists in clinical practice encounter this disorder often. Referral to an otolaryngologist is highly recommended for formal laryngoscopic evaluation, emphasizing the need for comprehensive care in UVFP cases. Early referral for speech therapy is beneficial in nearly all patients. The anesthesiologist may be involved if the vocal-fold-augmentation procedure is performed under general anesthesia. Surgical nurses' services are crucial in caring for patients with UVFP admitted for surgical augmentation or respiratory distress. |
article-31240_53 | Unilateral Vocal Fold Paralysis -- Review Questions | Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. | Unilateral Vocal Fold Paralysis -- Review Questions. Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. |
article-26886_0 | IgA Pemphigus -- Continuing Education Activity | IgA pemphigus, an uncommon autoimmune blistering skin disorder, manifests as painful, itchy blisters that fill with neutrophils and evolve into pustules. This condition encompasses 2 clinically similar subtypes: subcorneal pustular dermatosis and intraepidermal neutrophilic dermatosis. Both subtypes exhibit distinct immunologic mechanisms targeting keratinocyte cell surface components. Diagnosis and subtype determination rely on histopathology and immunofluorescence findings. Despite typically presenting a less severe course than IgG-driven pemphigus, precise diagnosis and aggressive treatment with steroids and dapsone are imperative to avert relapses. Given the potential association with underlying malignancies or rheumatological and gastrointestinal disorders, a thorough physical examination and pertinent testing are essential for comprehensive patient evaluation. | IgA Pemphigus -- Continuing Education Activity. IgA pemphigus, an uncommon autoimmune blistering skin disorder, manifests as painful, itchy blisters that fill with neutrophils and evolve into pustules. This condition encompasses 2 clinically similar subtypes: subcorneal pustular dermatosis and intraepidermal neutrophilic dermatosis. Both subtypes exhibit distinct immunologic mechanisms targeting keratinocyte cell surface components. Diagnosis and subtype determination rely on histopathology and immunofluorescence findings. Despite typically presenting a less severe course than IgG-driven pemphigus, precise diagnosis and aggressive treatment with steroids and dapsone are imperative to avert relapses. Given the potential association with underlying malignancies or rheumatological and gastrointestinal disorders, a thorough physical examination and pertinent testing are essential for comprehensive patient evaluation. |
article-26886_1 | IgA Pemphigus -- Continuing Education Activity | This activity reviews a better understanding of IgA pemphigus, its clinical nuances, and the latest evidence-based management strategies. In addition, the interplay between circulating IgA antibodies and specific keratinocyte cell surface autoantigens is discussed. By empowering healthcare professionals with valuable insights and tools, this activity aims to optimize patient care for this complex and rare condition, thereby enhancing their competence in managing IgA pemphigus effectively. | IgA Pemphigus -- Continuing Education Activity. This activity reviews a better understanding of IgA pemphigus, its clinical nuances, and the latest evidence-based management strategies. In addition, the interplay between circulating IgA antibodies and specific keratinocyte cell surface autoantigens is discussed. By empowering healthcare professionals with valuable insights and tools, this activity aims to optimize patient care for this complex and rare condition, thereby enhancing their competence in managing IgA pemphigus effectively. |
article-26886_2 | IgA Pemphigus -- Continuing Education Activity | Objectives: Identify the clinical presentation and characteristic features of IgA pemphigus, including painful and pruritic vesiculopustular eruptions and associated intraepidermal blistering. Differentiate IgA pemphigus from other blistering skin diseases based on clinical manifestations, histopathology, and immunofluorescence findings. Apply evidence-based treatment strategies for IgA pemphigus, including aggressive treatment with steroids and dapsone, to prevent recurrence and promote healing. Coordinate multidisciplinary care seamlessly, facilitating transitions between healthcare professionals and specialties to provide continuous and integrated management of IgA pemphigus throughout the patient's journey. Access free multiple choice questions on this topic. | IgA Pemphigus -- Continuing Education Activity. Objectives: Identify the clinical presentation and characteristic features of IgA pemphigus, including painful and pruritic vesiculopustular eruptions and associated intraepidermal blistering. Differentiate IgA pemphigus from other blistering skin diseases based on clinical manifestations, histopathology, and immunofluorescence findings. Apply evidence-based treatment strategies for IgA pemphigus, including aggressive treatment with steroids and dapsone, to prevent recurrence and promote healing. Coordinate multidisciplinary care seamlessly, facilitating transitions between healthcare professionals and specialties to provide continuous and integrated management of IgA pemphigus throughout the patient's journey. Access free multiple choice questions on this topic. |
article-26886_3 | IgA Pemphigus -- Introduction | Immunoglobulin A (IgA) pemphigus, a rare autoimmune blistering disease, manifests as painful and pruritic vesiculopustular eruptions. These eruptions occur due to circulating IgA antibodies targeting keratinocyte cell surface components involved in cell-to-cell adherence. Although associated with various malignancies and chronic conditions, its precise etiology remains unclear. IgA pemphigus comprises 2 distinct subtypes: subcorneal pustular dermatosis and intraepidermal neutrophilic dermatosis. The subcorneal pustular dermatosis subtype presents with intercellular IgA deposition against desmocollin-1 glycoprotein, primarily in the upper epidermis, whereas the intraepidermal neutrophilic dermatosis subtype exhibits autoantibodies targeting desmoglein members in the cadherin superfamily, predominantly in the lower epidermis. [1] [2] Although IgA pemphigus typically has a milder disease course compared to IgG-driven pemphigus, it necessitates careful diagnosis and aggressive treatment with steroids and dapsone to prevent recurrence. | IgA Pemphigus -- Introduction. Immunoglobulin A (IgA) pemphigus, a rare autoimmune blistering disease, manifests as painful and pruritic vesiculopustular eruptions. These eruptions occur due to circulating IgA antibodies targeting keratinocyte cell surface components involved in cell-to-cell adherence. Although associated with various malignancies and chronic conditions, its precise etiology remains unclear. IgA pemphigus comprises 2 distinct subtypes: subcorneal pustular dermatosis and intraepidermal neutrophilic dermatosis. The subcorneal pustular dermatosis subtype presents with intercellular IgA deposition against desmocollin-1 glycoprotein, primarily in the upper epidermis, whereas the intraepidermal neutrophilic dermatosis subtype exhibits autoantibodies targeting desmoglein members in the cadherin superfamily, predominantly in the lower epidermis. [1] [2] Although IgA pemphigus typically has a milder disease course compared to IgG-driven pemphigus, it necessitates careful diagnosis and aggressive treatment with steroids and dapsone to prevent recurrence. |
article-26886_4 | IgA Pemphigus -- Etiology | Antikeratinocyte cell surface autoantibodies are responsible for the disease process associated with IgA pemphigus, but the inciting mechanism is unknown. Research suggests the potential involvement of interleukin 5 (IL-5), a type 2 T-helper cytokine associated with stimulating IgA class antibody and γδ T-cell receptor–containing T cells, crucial for mucosal IgA production. Moreover, the IgA autoantibodies possess specific binding sites for the monocyte/granulocyte IgA-Fc receptor (CD89), which may allow neutrophils to accumulate intraepidermally, causing the blistering process to occur. | IgA Pemphigus -- Etiology. Antikeratinocyte cell surface autoantibodies are responsible for the disease process associated with IgA pemphigus, but the inciting mechanism is unknown. Research suggests the potential involvement of interleukin 5 (IL-5), a type 2 T-helper cytokine associated with stimulating IgA class antibody and γδ T-cell receptor–containing T cells, crucial for mucosal IgA production. Moreover, the IgA autoantibodies possess specific binding sites for the monocyte/granulocyte IgA-Fc receptor (CD89), which may allow neutrophils to accumulate intraepidermally, causing the blistering process to occur. |
article-26886_5 | IgA Pemphigus -- Etiology | IgA pemphigus is associated with monoclonal IgA gammopathy and multiple myeloma. [3] Experts are uncertain if monoclonal gammopathy precedes or follows IgA pemphigus, but most cases are present at the time of diagnosis. Other associated diseases include HIV infection, Sjögren syndrome, rheumatoid arthritis, lung cancer, ulcerative colitis, peripheral T-cell lymphoma, chronic myeloid leukemia, and diffuse large B-cell lymphoma. Although the direct relationship between the various diseases and IgA pemphigus is still unclear, healthcare professionals should thoroughly diagnose patients presenting with IgA pemphigus for hematologic, gastrointestinal, rheumatological, and infectious disorders. [4] [5] | IgA Pemphigus -- Etiology. IgA pemphigus is associated with monoclonal IgA gammopathy and multiple myeloma. [3] Experts are uncertain if monoclonal gammopathy precedes or follows IgA pemphigus, but most cases are present at the time of diagnosis. Other associated diseases include HIV infection, Sjögren syndrome, rheumatoid arthritis, lung cancer, ulcerative colitis, peripheral T-cell lymphoma, chronic myeloid leukemia, and diffuse large B-cell lymphoma. Although the direct relationship between the various diseases and IgA pemphigus is still unclear, healthcare professionals should thoroughly diagnose patients presenting with IgA pemphigus for hematologic, gastrointestinal, rheumatological, and infectious disorders. [4] [5] |
article-26886_6 | IgA Pemphigus -- Epidemiology | IgA pemphigus stands out as one of the most uncommon types of autoimmune blistering diseases, with a limited understanding of its epidemiology, including age and race demographics. Although it can manifest at any age, the reported range is 1 month to 94 years, predominantly emerging in adulthood, with the average onset occurring between the fourth and sixth decades. [6] Notably, no distinct gender predilection is apparent in reported cases. [7] | IgA Pemphigus -- Epidemiology. IgA pemphigus stands out as one of the most uncommon types of autoimmune blistering diseases, with a limited understanding of its epidemiology, including age and race demographics. Although it can manifest at any age, the reported range is 1 month to 94 years, predominantly emerging in adulthood, with the average onset occurring between the fourth and sixth decades. [6] Notably, no distinct gender predilection is apparent in reported cases. [7] |
article-26886_7 | IgA Pemphigus -- Pathophysiology | The pathogenesis of IgA pemphigus involves IgA autoantibodies that specifically target desmosomal and nondesmosomal keratinocyte cell surface components, notably desmoglein-1, desmoglein-3, and desmocollin-1. These molecules are integral to cell-to-cell adherence and belong to the cadherin superfamily of glycoproteins. In the subcorneal pustular dermatosis subtype, desmocollin-1 serves as the antigen. In contrast, in the intraepidermal neutrophilic dermatosis subtype, interactions occur with both desmoglein-1 and desmoglein-3. [8] [9] The binding of IgA antibodies to the IgA-Fc receptor triggers an intense inflammatory response, leading to epidermal neutrophilic infiltration followed by the formation of blisters and pustules. Despite identifying IgA antibody targets, the precise mechanistic cascade underlying the clinical presentation of IgA pemphigus remains elusive and necessitates further research. [1] | IgA Pemphigus -- Pathophysiology. The pathogenesis of IgA pemphigus involves IgA autoantibodies that specifically target desmosomal and nondesmosomal keratinocyte cell surface components, notably desmoglein-1, desmoglein-3, and desmocollin-1. These molecules are integral to cell-to-cell adherence and belong to the cadherin superfamily of glycoproteins. In the subcorneal pustular dermatosis subtype, desmocollin-1 serves as the antigen. In contrast, in the intraepidermal neutrophilic dermatosis subtype, interactions occur with both desmoglein-1 and desmoglein-3. [8] [9] The binding of IgA antibodies to the IgA-Fc receptor triggers an intense inflammatory response, leading to epidermal neutrophilic infiltration followed by the formation of blisters and pustules. Despite identifying IgA antibody targets, the precise mechanistic cascade underlying the clinical presentation of IgA pemphigus remains elusive and necessitates further research. [1] |
article-26886_8 | IgA Pemphigus -- Histopathology | Histological examination of IgA pemphigus reveals subcorneal blisters with massive neutrophilic infiltration and a mild loss of cohesion between keratinocytes. This histopathological analysis aids in distinguishing the 2 major subtypes of IgA pemphigus. The subcorneal pustular dermatosis subtype may reveal minimal subcorneal acantholysis and pustules with increased IgA autoantibody intensity on the epidermis's upper surface. In contrast, the characteristic features of the intraepidermal neutrophilic dermatosis subtype are pustules deeper in the epidermis and inflammatory infiltrates, primarily in the entire or lower part of the dermis (see Image. Intraepidermal Neutrophilic IgA Pemphigus). [10] [11] Although IgA is predominately detected on direct immunofluorescence, occasionally, IgG and complement component C3 may be detected to a much lesser extent. Unlike IgG pemphigus, acantholysis may be minimal or absent in IgA pemphigus. | IgA Pemphigus -- Histopathology. Histological examination of IgA pemphigus reveals subcorneal blisters with massive neutrophilic infiltration and a mild loss of cohesion between keratinocytes. This histopathological analysis aids in distinguishing the 2 major subtypes of IgA pemphigus. The subcorneal pustular dermatosis subtype may reveal minimal subcorneal acantholysis and pustules with increased IgA autoantibody intensity on the epidermis's upper surface. In contrast, the characteristic features of the intraepidermal neutrophilic dermatosis subtype are pustules deeper in the epidermis and inflammatory infiltrates, primarily in the entire or lower part of the dermis (see Image. Intraepidermal Neutrophilic IgA Pemphigus). [10] [11] Although IgA is predominately detected on direct immunofluorescence, occasionally, IgG and complement component C3 may be detected to a much lesser extent. Unlike IgG pemphigus, acantholysis may be minimal or absent in IgA pemphigus. |
article-26886_9 | IgA Pemphigus -- History and Physical | When obtaining a patient’s medical history, clinicians should ascertain the presence of mucosal involvement, as the presence of mucosal lesions can help distinguish between different subtypes of pemphigus disease. IgA pemphigus lacks mucosal involvement. The initial manifestation of IgA pemphigus involves a subacute onset of flaccid blisters on an erythematous base filled with clear fluid. These evolve into pustules that rapidly rupture, forming annular crusts. Patients often describe these plaques as both painful and pruritic. Although commonly observed in flexural areas such as the axilla and groin, the trunk and extremities are the most commonly affected areas. [12] Patients typically experience symptoms limited to skin manifestations, with no systemic symptoms such as fever, malaise, headache, or weight loss. [13] [14] | IgA Pemphigus -- History and Physical. When obtaining a patient’s medical history, clinicians should ascertain the presence of mucosal involvement, as the presence of mucosal lesions can help distinguish between different subtypes of pemphigus disease. IgA pemphigus lacks mucosal involvement. The initial manifestation of IgA pemphigus involves a subacute onset of flaccid blisters on an erythematous base filled with clear fluid. These evolve into pustules that rapidly rupture, forming annular crusts. Patients often describe these plaques as both painful and pruritic. Although commonly observed in flexural areas such as the axilla and groin, the trunk and extremities are the most commonly affected areas. [12] Patients typically experience symptoms limited to skin manifestations, with no systemic symptoms such as fever, malaise, headache, or weight loss. [13] [14] |
article-26886_10 | IgA Pemphigus -- Evaluation | The evaluation of suspected IgA pemphigus begins with a skin biopsy. Clinicians use histopathology and direct and indirect immunofluorescence techniques to establish the diagnosis. Clinicians should obtain a 4-mm lesional biopsy from the edge of an early lesion or erosion for hematoxylin and eosin staining and routine histopathological examination. For direct immunofluorescence, an additional perilesional skin biopsy should be taken from unaffected skin, situated 4 mm away from a vesicle or erosion. Lesional skin biopsies for direct immunofluorescence are more likely to give a false negative result due to the inflammatory response potentially destroying the immunoreactants. | IgA Pemphigus -- Evaluation. The evaluation of suspected IgA pemphigus begins with a skin biopsy. Clinicians use histopathology and direct and indirect immunofluorescence techniques to establish the diagnosis. Clinicians should obtain a 4-mm lesional biopsy from the edge of an early lesion or erosion for hematoxylin and eosin staining and routine histopathological examination. For direct immunofluorescence, an additional perilesional skin biopsy should be taken from unaffected skin, situated 4 mm away from a vesicle or erosion. Lesional skin biopsies for direct immunofluorescence are more likely to give a false negative result due to the inflammatory response potentially destroying the immunoreactants. |
article-26886_11 | IgA Pemphigus -- Evaluation | Histological examination reveals the hallmark of intraepidermal neutrophilic infiltration and the additional classic histopathological changes (refer to the Histology section for more information on the histopathology of IgA pemphigus). [15] [16] As acantholysis is minimal in IgA pemphigus, direct immunofluorescence may be considered an early screening tool for diagnosing IgA pemphigus in patients with diffuse pustular eruptions. Direct immunofluorescence allows clinicians to detect the absence or presence of IgA autoantibodies on epidermal cell surfaces. Indirect immunofluorescence detects the presence of IgA circulating autoantibodies in patient serum using patient serum on monkey esophagus or other epithelial substrates. Indirect immunofluorescence detects circulating IgA autoantibodies in approximately 50% of affected patients. [1] | IgA Pemphigus -- Evaluation. Histological examination reveals the hallmark of intraepidermal neutrophilic infiltration and the additional classic histopathological changes (refer to the Histology section for more information on the histopathology of IgA pemphigus). [15] [16] As acantholysis is minimal in IgA pemphigus, direct immunofluorescence may be considered an early screening tool for diagnosing IgA pemphigus in patients with diffuse pustular eruptions. Direct immunofluorescence allows clinicians to detect the absence or presence of IgA autoantibodies on epidermal cell surfaces. Indirect immunofluorescence detects the presence of IgA circulating autoantibodies in patient serum using patient serum on monkey esophagus or other epithelial substrates. Indirect immunofluorescence detects circulating IgA autoantibodies in approximately 50% of affected patients. [1] |
article-26886_12 | IgA Pemphigus -- Evaluation | Immunoblotting allows clinicians to document the specific skin antigen recognized by the patient's IgA autoantibodies. The sensitivity of immunoblotting is approximately 40% in revealing IgA reactivity to any autoantigen. Enzyme-linked immunosorbent assay can detect specific desmosomal antigens in patients with IgA pemphigus but is associated with a low sensitivity of approximately 55%. | IgA Pemphigus -- Evaluation. Immunoblotting allows clinicians to document the specific skin antigen recognized by the patient's IgA autoantibodies. The sensitivity of immunoblotting is approximately 40% in revealing IgA reactivity to any autoantigen. Enzyme-linked immunosorbent assay can detect specific desmosomal antigens in patients with IgA pemphigus but is associated with a low sensitivity of approximately 55%. |
article-26886_13 | IgA Pemphigus -- Treatment / Management | Due to the inflammatory nature of the disease, the primary treatment approach for IgA pemphigus involves the use of oral and topical corticosteroids with a suggested daily dose of 0.5 to 1 mg/kg. [17] However, patients should be aware of the potential adverse effects associated with the long-term use of steroids, including osteoporosis, diabetes, cataracts, adrenal suppression, and infection. In contrast to IgG pemphigus, IgA pemphigus typically does not respond adequately to steroid therapy alone. [18] Numerous studies demonstrate that combining dapsone with corticosteroids yields significantly better outcomes. Dapsone primarily works by suppressing neutrophilic infiltration. Healthcare professionals should carefully monitor patients receiving dapsone for potential adverse effects, such as hemolysis and methemoglobinemia. | IgA Pemphigus -- Treatment / Management. Due to the inflammatory nature of the disease, the primary treatment approach for IgA pemphigus involves the use of oral and topical corticosteroids with a suggested daily dose of 0.5 to 1 mg/kg. [17] However, patients should be aware of the potential adverse effects associated with the long-term use of steroids, including osteoporosis, diabetes, cataracts, adrenal suppression, and infection. In contrast to IgG pemphigus, IgA pemphigus typically does not respond adequately to steroid therapy alone. [18] Numerous studies demonstrate that combining dapsone with corticosteroids yields significantly better outcomes. Dapsone primarily works by suppressing neutrophilic infiltration. Healthcare professionals should carefully monitor patients receiving dapsone for potential adverse effects, such as hemolysis and methemoglobinemia. |
article-26886_14 | IgA Pemphigus -- Treatment / Management | Other medications reported to effectively treat IgA pemphigus include colchicine, retinoids, mycophenolate mofetil, and adalimumab. [19] [20] Many of these medications were tested based on their successful treatment of other forms of neutrophilic dermatoses and classic pemphigus. For example, adalimumab, a recombinant human immunoglobulin antibody, is believed to be therapeutic due to its tumor necrosis factor-α (TNF-α) inhibition. TNF-α activates neutrophilic infiltration in the epidermis; thus, its inhibition may hinder the further progression of IgA pemphigus. [21] Rituximab, a monoclonal antibody targeting the B-lymphocyte antigen CD20 (CD-20) protein on cells, has also been safely used to treat patients with IgA pemphigus. [22] | IgA Pemphigus -- Treatment / Management. Other medications reported to effectively treat IgA pemphigus include colchicine, retinoids, mycophenolate mofetil, and adalimumab. [19] [20] Many of these medications were tested based on their successful treatment of other forms of neutrophilic dermatoses and classic pemphigus. For example, adalimumab, a recombinant human immunoglobulin antibody, is believed to be therapeutic due to its tumor necrosis factor-α (TNF-α) inhibition. TNF-α activates neutrophilic infiltration in the epidermis; thus, its inhibition may hinder the further progression of IgA pemphigus. [21] Rituximab, a monoclonal antibody targeting the B-lymphocyte antigen CD20 (CD-20) protein on cells, has also been safely used to treat patients with IgA pemphigus. [22] |
article-26886_15 | IgA Pemphigus -- Treatment / Management | Clinicians should also consider providing proton-pump inhibitors and bisphosphonate therapy to prevent peptic ulceration and osteoporosis. Patients should receive counseling regarding weight-bearing exercise and adequate calcium and vitamin D intake. Patients should undergo a thorough physical examination and, when clinically indicated, appropriate testing for concurrent malignancies, inflammatory bowel disease, rheumatological diseases, and infectious diseases. | IgA Pemphigus -- Treatment / Management. Clinicians should also consider providing proton-pump inhibitors and bisphosphonate therapy to prevent peptic ulceration and osteoporosis. Patients should receive counseling regarding weight-bearing exercise and adequate calcium and vitamin D intake. Patients should undergo a thorough physical examination and, when clinically indicated, appropriate testing for concurrent malignancies, inflammatory bowel disease, rheumatological diseases, and infectious diseases. |
article-26886_16 | IgA Pemphigus -- Differential Diagnosis | Due to the rarity of IgA pemphigus, clinicians should consider various differential diagnoses when managing and treating the condition. The clinical presentation of these conditions is remarkably similar, and careful investigation using histology and immunofluorescence may be necessary to differentiate the conditions. [13] The following are potential differential diagnoses for IgA pemphigus. Bullous impetigo Pustular psoriasis Linear IgA bullous dermatosis Dermatitis herpetiformis Subcorneal pustular dermatosis or Sneddon-Wilkinson disease Pemphigus foliaceus | IgA Pemphigus -- Differential Diagnosis. Due to the rarity of IgA pemphigus, clinicians should consider various differential diagnoses when managing and treating the condition. The clinical presentation of these conditions is remarkably similar, and careful investigation using histology and immunofluorescence may be necessary to differentiate the conditions. [13] The following are potential differential diagnoses for IgA pemphigus. Bullous impetigo Pustular psoriasis Linear IgA bullous dermatosis Dermatitis herpetiformis Subcorneal pustular dermatosis or Sneddon-Wilkinson disease Pemphigus foliaceus |
article-26886_17 | IgA Pemphigus -- Differential Diagnosis | Classic subcorneal pustular dermatosis, also known as Sneddon-Wilkinson disease, is a chronic dermatosis characterized by sterile pustular lesions that erupt in cyclical patterns. Similar to the subcorneal pustular dermatosis subtype of IgA pemphigus, the pustular lesions observed in Sneddon-Wilkinson disease coalesce in an annular pattern and eventually burst to form crusted plaques. The 2 conditions have the same distribution area, favoring the groin, trunk, and axillae while avoiding mucosal surfaces. Histological examination of Sneddon-Wilkinson disease demonstrates perivascular infiltration of neutrophils and mild spongiosis. However, in contrast to IgA pemphigus, direct immunofluorescence of Sneddon-Wilkinson disease reveals a negative result for IgA deposits against adhesion molecules such as desmocollin-1. [23] | IgA Pemphigus -- Differential Diagnosis. Classic subcorneal pustular dermatosis, also known as Sneddon-Wilkinson disease, is a chronic dermatosis characterized by sterile pustular lesions that erupt in cyclical patterns. Similar to the subcorneal pustular dermatosis subtype of IgA pemphigus, the pustular lesions observed in Sneddon-Wilkinson disease coalesce in an annular pattern and eventually burst to form crusted plaques. The 2 conditions have the same distribution area, favoring the groin, trunk, and axillae while avoiding mucosal surfaces. Histological examination of Sneddon-Wilkinson disease demonstrates perivascular infiltration of neutrophils and mild spongiosis. However, in contrast to IgA pemphigus, direct immunofluorescence of Sneddon-Wilkinson disease reveals a negative result for IgA deposits against adhesion molecules such as desmocollin-1. [23] |
article-26886_18 | IgA Pemphigus -- Differential Diagnosis | Pemphigus foliaceus is characterized by flaccid bullae typically found on the trunk that eventually crust over, much like the lesions in IgA pemphigus. Generally considered a benign disease, pemphigus foliaceus responds well to topical and oral corticosteroids. A clinical differentiation between IgA pemphigus and pemphigus foliaceus is nearly impossible. Thus, immunofluorescence is critical in diagnosis. Direct immunofluorescence of pemphigus foliaceus demonstrates IgG autoantibodies against desmoglein-1 in contrast to the IgA deposits against desmocollin-1 found in IgA pemphigus. Therefore, proper histology and immunofluorescence diagnosis are essential in differentiating the 2 conditions. [24] | IgA Pemphigus -- Differential Diagnosis. Pemphigus foliaceus is characterized by flaccid bullae typically found on the trunk that eventually crust over, much like the lesions in IgA pemphigus. Generally considered a benign disease, pemphigus foliaceus responds well to topical and oral corticosteroids. A clinical differentiation between IgA pemphigus and pemphigus foliaceus is nearly impossible. Thus, immunofluorescence is critical in diagnosis. Direct immunofluorescence of pemphigus foliaceus demonstrates IgG autoantibodies against desmoglein-1 in contrast to the IgA deposits against desmocollin-1 found in IgA pemphigus. Therefore, proper histology and immunofluorescence diagnosis are essential in differentiating the 2 conditions. [24] |
article-26886_19 | IgA Pemphigus -- Prognosis | In contrast to classic pemphigus, IgA pemphigus typically manifests as a less severe and more localized condition. With appropriate treatment and regular monitoring, IgA pemphigus commonly resolves without scarring. Studies indicate that abruptly discontinuing oral steroids may lead to lesion recurrence; therefore, clinicians should gradually reduce and taper the dosage. Prognosis in cases of IgA pemphigus associated with other conditions such as malignancies, gastrointestinal diseases, or monoclonal gammopathy depends on the progression of the underlying conditions. [1] [25] | IgA Pemphigus -- Prognosis. In contrast to classic pemphigus, IgA pemphigus typically manifests as a less severe and more localized condition. With appropriate treatment and regular monitoring, IgA pemphigus commonly resolves without scarring. Studies indicate that abruptly discontinuing oral steroids may lead to lesion recurrence; therefore, clinicians should gradually reduce and taper the dosage. Prognosis in cases of IgA pemphigus associated with other conditions such as malignancies, gastrointestinal diseases, or monoclonal gammopathy depends on the progression of the underlying conditions. [1] [25] |
article-26886_20 | IgA Pemphigus -- Complications | Many potential complications associated with IgA pemphigus are due to the effects of long-term treatment. Secondary infection of the lesions and scarring are the primary complications associated with IgA pemphigus. The following are potential complications related to corticosteroid use. Osteoporosis Peptic ulcer disease Adrenal insufficiency Infection Growth restriction in children Weight gain Anemia Hypertension Diabetes [1] Potential complications related to dapsone use include: Methemoglobinemia Hemolytic anemia Neutropenia Agranulocytosis Hepatic failure Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome | IgA Pemphigus -- Complications. Many potential complications associated with IgA pemphigus are due to the effects of long-term treatment. Secondary infection of the lesions and scarring are the primary complications associated with IgA pemphigus. The following are potential complications related to corticosteroid use. Osteoporosis Peptic ulcer disease Adrenal insufficiency Infection Growth restriction in children Weight gain Anemia Hypertension Diabetes [1] Potential complications related to dapsone use include: Methemoglobinemia Hemolytic anemia Neutropenia Agranulocytosis Hepatic failure Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome |
article-26886_21 | IgA Pemphigus -- Deterrence and Patient Education | IgA pemphigus is a rare autoimmune blistering disease that can cause painful and pruritic skin eruptions. These eruptions result from the body's immune system mistakenly attacking certain skin proteins. Unlike some other forms of pemphigus, IgA pemphigus usually presents as a milder condition with limited skin involvement. [26] Affected patients are at risk of secondary infection of open wounds and scarring. Pruritus is a prominent symptom; patients may scratch the lesions, increasing the risk of secondary infection. Patients should be aware that they must seek medical attention if they notice increased erythema, fevers, or purulent drainage. | IgA Pemphigus -- Deterrence and Patient Education. IgA pemphigus is a rare autoimmune blistering disease that can cause painful and pruritic skin eruptions. These eruptions result from the body's immune system mistakenly attacking certain skin proteins. Unlike some other forms of pemphigus, IgA pemphigus usually presents as a milder condition with limited skin involvement. [26] Affected patients are at risk of secondary infection of open wounds and scarring. Pruritus is a prominent symptom; patients may scratch the lesions, increasing the risk of secondary infection. Patients should be aware that they must seek medical attention if they notice increased erythema, fevers, or purulent drainage. |
article-26886_22 | IgA Pemphigus -- Deterrence and Patient Education | Although IgA pemphigus typically heals without scarring, patients must understand the medications used for treatment, including any potential adverse effects. Clinicians should stress the importance of continuing treatment and regularly attending scheduled follow-up appointments. Abruptly stopping medications, especially oral steroids, can lead to a recurrence of skin lesions and adrenal insufficiency. Patients must understand the need for a gradual reduction in medication dosage. In addition, if concurrent medical conditions are present, such as malignancies or gastrointestinal diseases, effectively diagnosing and managing these conditions are essential for overall health and may impact the prognosis of IgA pemphigus. | IgA Pemphigus -- Deterrence and Patient Education. Although IgA pemphigus typically heals without scarring, patients must understand the medications used for treatment, including any potential adverse effects. Clinicians should stress the importance of continuing treatment and regularly attending scheduled follow-up appointments. Abruptly stopping medications, especially oral steroids, can lead to a recurrence of skin lesions and adrenal insufficiency. Patients must understand the need for a gradual reduction in medication dosage. In addition, if concurrent medical conditions are present, such as malignancies or gastrointestinal diseases, effectively diagnosing and managing these conditions are essential for overall health and may impact the prognosis of IgA pemphigus. |
article-26886_23 | IgA Pemphigus -- Pearls and Other Issues | A newer classification of IgA pemphigus exists, describing 5 subtypes as follows: Subcorneal pustular dermatosis type IgA pemphigus Intraepidermal neutrophilic type IgA pemphigus IgA-pemphigus vegetans IgA-pemphigus vulgaris Unclassified IgA pemphigus | IgA Pemphigus -- Pearls and Other Issues. A newer classification of IgA pemphigus exists, describing 5 subtypes as follows: Subcorneal pustular dermatosis type IgA pemphigus Intraepidermal neutrophilic type IgA pemphigus IgA-pemphigus vegetans IgA-pemphigus vulgaris Unclassified IgA pemphigus |
article-26886_24 | IgA Pemphigus -- Pearls and Other Issues | Pemphigus vegetans is a rare variant of pemphigus vulgaris. Clinicians classify patients with vegetating lesions and histology similar to pemphigus vegetans but with IgA antibodies as IgA pemphigus vegetans (IgA-PVeg). Those with desmoglein-1 or desmoglein-3 target antigens are diagnosed with having IgA pemphigus foliaceus (IgA-PF) or IgA pemphigus vulgaris (IgA-PV), respectively. The remainder that do not meet these criteria are diagnosed as unclassified or atypical IgA dermatosis. | IgA Pemphigus -- Pearls and Other Issues. Pemphigus vegetans is a rare variant of pemphigus vulgaris. Clinicians classify patients with vegetating lesions and histology similar to pemphigus vegetans but with IgA antibodies as IgA pemphigus vegetans (IgA-PVeg). Those with desmoglein-1 or desmoglein-3 target antigens are diagnosed with having IgA pemphigus foliaceus (IgA-PF) or IgA pemphigus vulgaris (IgA-PV), respectively. The remainder that do not meet these criteria are diagnosed as unclassified or atypical IgA dermatosis. |
article-26886_25 | IgA Pemphigus -- Enhancing Healthcare Team Outcomes | IgA pemphigus is a rare autoimmune blistering disease characterized by painful and pruritic vesiculopustular eruptions resulting from IgA antibodies targeting keratinocyte cell surface components involved in cell-to-cell adherence. Two distinct forms of IgA pemphigus exist, both clinically similar but with distinct autoantibody target proteins. Although associated with various malignancies and chronic conditions, its exact cause remains unclear. Although typically milder than IgG-driven pemphigus, IgA pemphigus requires aggressive treatment with steroids and dapsone to prevent a recurrence. Collaborative healthcare teams should monitor patients for adverse effects and assess for concurrent conditions, ensuring tailored management. | IgA Pemphigus -- Enhancing Healthcare Team Outcomes. IgA pemphigus is a rare autoimmune blistering disease characterized by painful and pruritic vesiculopustular eruptions resulting from IgA antibodies targeting keratinocyte cell surface components involved in cell-to-cell adherence. Two distinct forms of IgA pemphigus exist, both clinically similar but with distinct autoantibody target proteins. Although associated with various malignancies and chronic conditions, its exact cause remains unclear. Although typically milder than IgG-driven pemphigus, IgA pemphigus requires aggressive treatment with steroids and dapsone to prevent a recurrence. Collaborative healthcare teams should monitor patients for adverse effects and assess for concurrent conditions, ensuring tailored management. |
article-26886_26 | IgA Pemphigus -- Enhancing Healthcare Team Outcomes | Physicians, advanced care practitioners, nurses, pharmacists, and all other healthcare professionals caring for patients with IgA pemphigus must work collaboratively, each contributing their unique expertise. Seamless interprofessional communication is crucial for prompt information sharing and care coordination, optimizing patient outcomes and quality of life. [18] This coordination minimizes errors, reduces delays, and enhances patient safety, leading to improved team performance and patient-centered care that prioritizes improving immediate and long-term outcomes. | IgA Pemphigus -- Enhancing Healthcare Team Outcomes. Physicians, advanced care practitioners, nurses, pharmacists, and all other healthcare professionals caring for patients with IgA pemphigus must work collaboratively, each contributing their unique expertise. Seamless interprofessional communication is crucial for prompt information sharing and care coordination, optimizing patient outcomes and quality of life. [18] This coordination minimizes errors, reduces delays, and enhances patient safety, leading to improved team performance and patient-centered care that prioritizes improving immediate and long-term outcomes. |
article-26886_27 | IgA Pemphigus -- Review Questions | Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. | IgA Pemphigus -- Review Questions. Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. |
article-130737_0 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Continuing Education Activity | Healthcare professionals face challenges when addressing mental health issues among American Indian and Alaska Native individuals. Disproportionate rates of posttraumatic stress disorder, substance use disorders, and suicide risks are prevalent within these communities. Cultural sensitivities, historical contexts, and tailored care approaches significantly elevate treatment and care strategies. | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Continuing Education Activity. Healthcare professionals face challenges when addressing mental health issues among American Indian and Alaska Native individuals. Disproportionate rates of posttraumatic stress disorder, substance use disorders, and suicide risks are prevalent within these communities. Cultural sensitivities, historical contexts, and tailored care approaches significantly elevate treatment and care strategies. |
article-130737_1 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Continuing Education Activity | This course explores the impact of trauma, societal factors, and the interplay between mental health and substance use within these populations. Clinicians learn to recognize early signs, conduct appropriate screenings, and implement culturally competent interventions. The healthcare team must coordinate efforts to foster understanding, improve care outcomes, and bridge the gap in addressing mental health disparities among American Indian and Alaska Native individuals. | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Continuing Education Activity. This course explores the impact of trauma, societal factors, and the interplay between mental health and substance use within these populations. Clinicians learn to recognize early signs, conduct appropriate screenings, and implement culturally competent interventions. The healthcare team must coordinate efforts to foster understanding, improve care outcomes, and bridge the gap in addressing mental health disparities among American Indian and Alaska Native individuals. |
article-130737_2 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Continuing Education Activity | Objectives: Screen for mental health concerns while respecting cultural variations in symptom expression and help-seeking behaviors. Implement culturally competent interventions tailored to the specific needs and beliefs of Native communities. Identify specific risk factors for increased suicidality in American Indians and Alaskan Natives. Coordinate with the interprofessional team across settings to ensure continuity and cultural relevance in mental health services for Native populations. Access free multiple choice questions on this topic. | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Continuing Education Activity. Objectives: Screen for mental health concerns while respecting cultural variations in symptom expression and help-seeking behaviors. Implement culturally competent interventions tailored to the specific needs and beliefs of Native communities. Identify specific risk factors for increased suicidality in American Indians and Alaskan Natives. Coordinate with the interprofessional team across settings to ensure continuity and cultural relevance in mental health services for Native populations. Access free multiple choice questions on this topic. |
article-130737_3 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Introduction | Native Americans, encompassing both American Indian and Alaska Native individuals, are descendants of the original inhabitants of the United States and represent an increasingly diverse and expanding demographic. Research indicates that these populations experience reduced life expectancy and a diminished quality of life compared to the broader US population. [1] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Introduction. Native Americans, encompassing both American Indian and Alaska Native individuals, are descendants of the original inhabitants of the United States and represent an increasingly diverse and expanding demographic. Research indicates that these populations experience reduced life expectancy and a diminished quality of life compared to the broader US population. [1] |
article-130737_4 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Introduction | In addition to experiencing elevated rates of prevalent medical conditions, including diabetes, obesity, and hypertension, American Indian and Alaska Native individuals also face a significant prevalence of mental health conditions. [2] [3] A national study comparing the prevalence of mental health disorders and associated treatment-seeking results showed higher rates of psychiatric disorders in American Indians and Alaska Natives than non–Hispanic White individuals. [4] [5] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Introduction. In addition to experiencing elevated rates of prevalent medical conditions, including diabetes, obesity, and hypertension, American Indian and Alaska Native individuals also face a significant prevalence of mental health conditions. [2] [3] A national study comparing the prevalence of mental health disorders and associated treatment-seeking results showed higher rates of psychiatric disorders in American Indians and Alaska Natives than non–Hispanic White individuals. [4] [5] |
article-130737_5 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Introduction | Post-traumatic stress disorder (PTSD), violence, suicide, and substance abuse have been identified as some of the more prevalent mental health issues among American Indian and Alaska Native individuals when compared with the general population in the US. [6] Sociodemographic characteristics, including age, education, and income, are likely contributing factors for the number of psychiatric disorders seen in American Indian and Alaska Native individuals compared to other racial groups. [4] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Introduction. Post-traumatic stress disorder (PTSD), violence, suicide, and substance abuse have been identified as some of the more prevalent mental health issues among American Indian and Alaska Native individuals when compared with the general population in the US. [6] Sociodemographic characteristics, including age, education, and income, are likely contributing factors for the number of psychiatric disorders seen in American Indian and Alaska Native individuals compared to other racial groups. [4] |
article-130737_6 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Introduction | The cumulative emotional and psychological impact of colonization, forced relocation, and cultural disruption contributes to the intergenerational trauma faced by many in various American Indian and Alaska Native communities. This trauma can manifest as depression, anxiety, substance abuse, and other mental health disorders. [7] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Introduction. The cumulative emotional and psychological impact of colonization, forced relocation, and cultural disruption contributes to the intergenerational trauma faced by many in various American Indian and Alaska Native communities. This trauma can manifest as depression, anxiety, substance abuse, and other mental health disorders. [7] |
article-130737_7 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Introduction | Efforts should be intensified to address mental health care disparities among American Indian and Alaska Native populations through culturally sensitive clinical interventions. Pinpointing the existing gaps in mental health care provision and outcomes within these communities is crucial. Identifying mental health disparities directs essential actions for enhancing outcomes and reducing health inequalities. | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Introduction. Efforts should be intensified to address mental health care disparities among American Indian and Alaska Native populations through culturally sensitive clinical interventions. Pinpointing the existing gaps in mental health care provision and outcomes within these communities is crucial. Identifying mental health disparities directs essential actions for enhancing outcomes and reducing health inequalities. |
article-130737_8 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern | American Indian and Alaska Native individuals experience disproportionately high rates of mental disorders and psychiatric diagnoses such as PTSD, substance use disorder, and suicide compared to other racial and ethnic groups. [4] [6] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern. American Indian and Alaska Native individuals experience disproportionately high rates of mental disorders and psychiatric diagnoses such as PTSD, substance use disorder, and suicide compared to other racial and ethnic groups. [4] [6] |
article-130737_9 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Posttraumatic Stress Disorder | Research has found a high rate of American Indian and Alaska Native individuals with PTSD and PTSD-related symptoms compared to other races and ethnicities. In the general US population, the prevalence of lifetime PTSD is 4.8% to 6.4%. [8] Among American Indian and Alaskan Native populations, the prevalence of PTSD is estimated somewhere between 16% to 24%. [9] [10] [11] PTSD is a clinical diagnosis that is often the result of exposure to a severe stressor or a traumatic event. [12] Several risk factors have been identified for PTSD among American Indian and Alaska Native groups, including high exposure to violence, substance use disorders, history of sexual or physical abuse, pre-existing psychiatric disorders, and combat experience. [13] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Posttraumatic Stress Disorder. Research has found a high rate of American Indian and Alaska Native individuals with PTSD and PTSD-related symptoms compared to other races and ethnicities. In the general US population, the prevalence of lifetime PTSD is 4.8% to 6.4%. [8] Among American Indian and Alaskan Native populations, the prevalence of PTSD is estimated somewhere between 16% to 24%. [9] [10] [11] PTSD is a clinical diagnosis that is often the result of exposure to a severe stressor or a traumatic event. [12] Several risk factors have been identified for PTSD among American Indian and Alaska Native groups, including high exposure to violence, substance use disorders, history of sexual or physical abuse, pre-existing psychiatric disorders, and combat experience. [13] |
article-130737_10 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Posttraumatic Stress Disorder | PTSD manifests through various signs and symptoms, which may include intrusive memories, negative changes in mood and cognition, avoidance of reminders of the traumatic event, and alterations in arousal and reactivity. These symptoms can lead to significant distress or impair daily functioning and need to be present for four or more weeks. [12] Healthcare providers must recognize the signs and symptoms of PTSD to facilitate early intervention and treatment. | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Posttraumatic Stress Disorder. PTSD manifests through various signs and symptoms, which may include intrusive memories, negative changes in mood and cognition, avoidance of reminders of the traumatic event, and alterations in arousal and reactivity. These symptoms can lead to significant distress or impair daily functioning and need to be present for four or more weeks. [12] Healthcare providers must recognize the signs and symptoms of PTSD to facilitate early intervention and treatment. |
article-130737_11 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Posttraumatic Stress Disorder | A study focusing on American Indian veterans who served in the Vietnam War revealed a remarkably high prevalence of PTSD, with lifetime rates between 40% and 60%. This rate was higher than that of any other racial or ethnic group of Vietnam veterans studied, further emphasizing the significant impact of PTSD on the American Indian and Alaska Native communities. [14] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Posttraumatic Stress Disorder. A study focusing on American Indian veterans who served in the Vietnam War revealed a remarkably high prevalence of PTSD, with lifetime rates between 40% and 60%. This rate was higher than that of any other racial or ethnic group of Vietnam veterans studied, further emphasizing the significant impact of PTSD on the American Indian and Alaska Native communities. [14] |
article-130737_12 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Substance Use Disorder | Substance use, encompassing both illicit drugs and alcohol, is a critical issue to address when considering the unique mental health care needs of American Indian and Alaska Native individuals. One study involving 489 American Indian females at an Indian Health Service (IHS) institution revealed a lifetime prevalence of over 60% for any substance use disorder. [15] Another study conducted on a group of 89 adolescent American Indians found that an alarming 94% met the criteria for substance use disorder, with a high percentage also meeting the criteria for alcohol use disorder. [16] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Substance Use Disorder. Substance use, encompassing both illicit drugs and alcohol, is a critical issue to address when considering the unique mental health care needs of American Indian and Alaska Native individuals. One study involving 489 American Indian females at an Indian Health Service (IHS) institution revealed a lifetime prevalence of over 60% for any substance use disorder. [15] Another study conducted on a group of 89 adolescent American Indians found that an alarming 94% met the criteria for substance use disorder, with a high percentage also meeting the criteria for alcohol use disorder. [16] |
article-130737_13 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Substance Use Disorder | Given the high prevalence of substance use disorders among American Indian and Alaska Native individuals, it is essential to routinely screen for alcohol and substance use. There is a known association between substance use disorder and PTSD, with a considerable number of individuals meeting the criteria for both conditions. [17] Alcohol use significantly contributes to the higher rate of premature deaths in American Indian and Alaska Native individuals compared to other races in the US, especially given its legality and ubiquity. [18] The U.S. Preventive Services Task Force has put forth 3 techniques to detect heavy alcohol consumption. These methods include using the Alcohol Use Disorders Identification Test (AUDIT), the AUDIT-C, or a single-question approach which involves asking individuals how frequently they consumed 5 or more drinks in a day (for men) or 4 or more drinks in a day (for women) in the past year. [19] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Substance Use Disorder. Given the high prevalence of substance use disorders among American Indian and Alaska Native individuals, it is essential to routinely screen for alcohol and substance use. There is a known association between substance use disorder and PTSD, with a considerable number of individuals meeting the criteria for both conditions. [17] Alcohol use significantly contributes to the higher rate of premature deaths in American Indian and Alaska Native individuals compared to other races in the US, especially given its legality and ubiquity. [18] The U.S. Preventive Services Task Force has put forth 3 techniques to detect heavy alcohol consumption. These methods include using the Alcohol Use Disorders Identification Test (AUDIT), the AUDIT-C, or a single-question approach which involves asking individuals how frequently they consumed 5 or more drinks in a day (for men) or 4 or more drinks in a day (for women) in the past year. [19] |
article-130737_14 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Substance Use Disorder | Heavy alcohol consumption can lead to several conditions, including fatty liver disease or steatosis, alcoholic hepatitis, and, ultimately, cirrhosis. Alcoholic hepatitis, a serious form of alcoholic liver disease, is marked by a sudden onset of jaundice, malaise, tender hepatomegaly, and a systemic inflammatory response. The condition can be identified when jaundice appears within 60 days of heavy alcohol consumption, defined as more than 50 grams per day for at least 6 months. In addition, diagnostic criteria include serum bilirubin levels exceeding 3 mg/dL, aspartate aminotransferase (AST) levels ranging from 50 U/L to 400 U/L, and an AST to ALT (alanine aminotransferase) ratio greater than 1.5. [20] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Substance Use Disorder. Heavy alcohol consumption can lead to several conditions, including fatty liver disease or steatosis, alcoholic hepatitis, and, ultimately, cirrhosis. Alcoholic hepatitis, a serious form of alcoholic liver disease, is marked by a sudden onset of jaundice, malaise, tender hepatomegaly, and a systemic inflammatory response. The condition can be identified when jaundice appears within 60 days of heavy alcohol consumption, defined as more than 50 grams per day for at least 6 months. In addition, diagnostic criteria include serum bilirubin levels exceeding 3 mg/dL, aspartate aminotransferase (AST) levels ranging from 50 U/L to 400 U/L, and an AST to ALT (alanine aminotransferase) ratio greater than 1.5. [20] |
article-130737_15 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Suicide | Historically, suicide rates among the American Indian and Alaska Native populations have been higher than those of the overall US population. In 2015, the National Violent Death Reporting System (NVDRS) discovered that in 18 participating states, suicide rates were over 3.5 times higher among American Indian and Alaska Native individuals compared to ethnic groups with the lowest rates. [21] Another study reported rates of completed suicides, attempts, and suicidal ideation were 50% higher for American Indian and Alaska Native individuals than for the non–Hispanic White population. While suicidality is a significant concern across all ethnic and age groups, previous research has identified a disproportionately high risk for suicide among American Indian adolescents. [22] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Suicide. Historically, suicide rates among the American Indian and Alaska Native populations have been higher than those of the overall US population. In 2015, the National Violent Death Reporting System (NVDRS) discovered that in 18 participating states, suicide rates were over 3.5 times higher among American Indian and Alaska Native individuals compared to ethnic groups with the lowest rates. [21] Another study reported rates of completed suicides, attempts, and suicidal ideation were 50% higher for American Indian and Alaska Native individuals than for the non–Hispanic White population. While suicidality is a significant concern across all ethnic and age groups, previous research has identified a disproportionately high risk for suicide among American Indian adolescents. [22] |
article-130737_16 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Suicide | Compared to other ethnic groups, American Indian and Alaska Native adolescents have been found to experience more severe experiences, such as victimization, substance abuse, and depression, which may contribute to increased suicidality. [23] [24] Specifically, American Indian and Alaska Native adolescent males are at the highest risk of completing suicide. [25] In particular, American Indian and Alaska Native adolescent males who are unemployed, uneducated, or have a history of trauma face an even greater risk of suicide. [26] [27] In terms of suicide prevention among American Indian and Alaska Native individuals, several factors have been identified as contributing to building resilience against suicide risk. These include fostering meaningful social connections, being mindful of the negative impact one's suicide may have on loved ones, and utilizing available health resources and services. [28] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Suicide. Compared to other ethnic groups, American Indian and Alaska Native adolescents have been found to experience more severe experiences, such as victimization, substance abuse, and depression, which may contribute to increased suicidality. [23] [24] Specifically, American Indian and Alaska Native adolescent males are at the highest risk of completing suicide. [25] In particular, American Indian and Alaska Native adolescent males who are unemployed, uneducated, or have a history of trauma face an even greater risk of suicide. [26] [27] In terms of suicide prevention among American Indian and Alaska Native individuals, several factors have been identified as contributing to building resilience against suicide risk. These include fostering meaningful social connections, being mindful of the negative impact one's suicide may have on loved ones, and utilizing available health resources and services. [28] |
article-130737_17 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Suicide | Early identification and intervention may be useful for American Indian and Alaska Native individuals experiencing suicidality. Suicidal behaviors have also been found to co-occur with substance use, including alcohol and drug use, in many American Indian and Alaska Native communities. Prior research on this topic has pinpointed potential targets for intervention, such as enhancing coping skills, reducing the stigma surrounding mental health services, and establishing a well-organized community infrastructure of healthcare for American Indian and Alaska Native individuals. [28] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Issues of Concern -- Suicide. Early identification and intervention may be useful for American Indian and Alaska Native individuals experiencing suicidality. Suicidal behaviors have also been found to co-occur with substance use, including alcohol and drug use, in many American Indian and Alaska Native communities. Prior research on this topic has pinpointed potential targets for intervention, such as enhancing coping skills, reducing the stigma surrounding mental health services, and establishing a well-organized community infrastructure of healthcare for American Indian and Alaska Native individuals. [28] |
article-130737_18 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Clinical Significance | It is well-established that American Indian and Alaska Native individuals experience a disproportionate burden of various health conditions, including numerous mental health disorders, compared to other ethnic and racial groups. These health disparities among American Indian and Alaska Native individuals can be partially attributed to significant sociodemographic and socioeconomic differences, such as lower levels of educational achievement, income, and overall health status. [5] Improved mental health care can lead to better health outcomes and reduced health disparities. Moreover, early identification and intervention can prevent the worsening of mental health conditions and reduce the risk of suicide and substance use disorder-related complications. | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Clinical Significance. It is well-established that American Indian and Alaska Native individuals experience a disproportionate burden of various health conditions, including numerous mental health disorders, compared to other ethnic and racial groups. These health disparities among American Indian and Alaska Native individuals can be partially attributed to significant sociodemographic and socioeconomic differences, such as lower levels of educational achievement, income, and overall health status. [5] Improved mental health care can lead to better health outcomes and reduced health disparities. Moreover, early identification and intervention can prevent the worsening of mental health conditions and reduce the risk of suicide and substance use disorder-related complications. |
article-130737_19 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Clinical Significance | Clinicians and public health officials must acknowledge the demographic and socioeconomic factors contributing to these health inequalities and prioritize further research and efforts to address these disparities. Moreover, it is crucial to understand the role of cultural issues and other risk factors in the high prevalence of mental health disorders among American Indian and Alaska Native individuals. The National Institutes of Health (NIH) has taken the initiative to allocate funding for promoting health and disease prevention in Native American communities, including American Indian and Alaska Native communities. This funding opportunity has led to the launch of multiple projects aimed at improving health outcomes for this population group. [29] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Clinical Significance. Clinicians and public health officials must acknowledge the demographic and socioeconomic factors contributing to these health inequalities and prioritize further research and efforts to address these disparities. Moreover, it is crucial to understand the role of cultural issues and other risk factors in the high prevalence of mental health disorders among American Indian and Alaska Native individuals. The National Institutes of Health (NIH) has taken the initiative to allocate funding for promoting health and disease prevention in Native American communities, including American Indian and Alaska Native communities. This funding opportunity has led to the launch of multiple projects aimed at improving health outcomes for this population group. [29] |
article-130737_20 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes | Health disparities for American Indian and Alaska Native individuals have been linked to limited access to healthcare services, education, and poverty. [30] To provide more equitable health care for this population, enhancing the cultural competence of health services and providers is crucial. | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes. Health disparities for American Indian and Alaska Native individuals have been linked to limited access to healthcare services, education, and poverty. [30] To provide more equitable health care for this population, enhancing the cultural competence of health services and providers is crucial. |
article-130737_21 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes -- Access to Health Services | Improving mental health outcomes among American Indian and Alaska Native individuals requires increased access to healthcare services and facilities. Established in 1955, the Indian Health Service (IHS) is a federal agency serving many Native Americans. [6] IHS offers healthcare services, including behavioral health, to federally recognized American Indian and Alaska Native tribes. Mental health services are among the leading causes of hospitalization and ambulatory visits through IHS. [5] However, there are limitations to this healthcare system. Despite improvements in the overall health status of American Indian and Alaska Native individuals following the introduction of IHS, significant health disparities persist. [30] [31] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes -- Access to Health Services. Improving mental health outcomes among American Indian and Alaska Native individuals requires increased access to healthcare services and facilities. Established in 1955, the Indian Health Service (IHS) is a federal agency serving many Native Americans. [6] IHS offers healthcare services, including behavioral health, to federally recognized American Indian and Alaska Native tribes. Mental health services are among the leading causes of hospitalization and ambulatory visits through IHS. [5] However, there are limitations to this healthcare system. Despite improvements in the overall health status of American Indian and Alaska Native individuals following the introduction of IHS, significant health disparities persist. [30] [31] |
article-130737_22 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes -- Access to Health Services | IHS-funded federal hospitals are the only facilities that can provide coverage for health services. Most of these hospitals are geographically isolated, making it challenging for American Indian and Alaska Native individuals seeking care in urban areas and larger cities with limited IHS-associated facilities. [30] [3] Telepsychiatry and teletherapy are important and effective tools to reach rural American Indian and Alaska Native communities, especially when combining evidence-based Western treatment and traditional Native healing. [32] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes -- Access to Health Services. IHS-funded federal hospitals are the only facilities that can provide coverage for health services. Most of these hospitals are geographically isolated, making it challenging for American Indian and Alaska Native individuals seeking care in urban areas and larger cities with limited IHS-associated facilities. [30] [3] Telepsychiatry and teletherapy are important and effective tools to reach rural American Indian and Alaska Native communities, especially when combining evidence-based Western treatment and traditional Native healing. [32] |
article-130737_23 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes -- Cultural Differences | Recognizing cultural differences in health-related values and beliefs is crucial. While various evidence-based treatments and Western models of intervention are widely used to treat mental health disorders, some American Indian and Alaska Native individuals prefer traditional healing and tribal traditions for addressing substance use and other mental health issues. Overcoming the distrust of formal services in Indigenous communities is a significant challenge. [26] Even with a broader range of evidence-based therapies, American Indian and Alaska Native individuals may prefer traditional and informal services over clinic-based interventions. [6] Therefore, it is essential to continue exploring methods for integrating American Indian and Alaska Native cultural values and traditions into clinical practice. [33] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes -- Cultural Differences. Recognizing cultural differences in health-related values and beliefs is crucial. While various evidence-based treatments and Western models of intervention are widely used to treat mental health disorders, some American Indian and Alaska Native individuals prefer traditional healing and tribal traditions for addressing substance use and other mental health issues. Overcoming the distrust of formal services in Indigenous communities is a significant challenge. [26] Even with a broader range of evidence-based therapies, American Indian and Alaska Native individuals may prefer traditional and informal services over clinic-based interventions. [6] Therefore, it is essential to continue exploring methods for integrating American Indian and Alaska Native cultural values and traditions into clinical practice. [33] |
article-130737_24 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes -- Cultural Differences | Cultural competence in healthcare means understanding and respecting the diverse cultures of different patient groups and using this knowledge to provide more culturally and linguistically appropriate interventions. [34] Several culturally congruent intervention strategies have been proposed for American Indian and Alaska Native individuals. For instance, historical trauma interventions address the psychological trauma and unresolved grief resulting from generations of discrimination, oppression, genocide, and colonization. [35] Another intervention fosters positive ethnic identity by encouraging culture-specific stress-coping strategies, enabling American Indian and Alaska Native individuals to engage in cultural healing practices and connect with their rich history and traditions. [36] [37] | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes -- Cultural Differences. Cultural competence in healthcare means understanding and respecting the diverse cultures of different patient groups and using this knowledge to provide more culturally and linguistically appropriate interventions. [34] Several culturally congruent intervention strategies have been proposed for American Indian and Alaska Native individuals. For instance, historical trauma interventions address the psychological trauma and unresolved grief resulting from generations of discrimination, oppression, genocide, and colonization. [35] Another intervention fosters positive ethnic identity by encouraging culture-specific stress-coping strategies, enabling American Indian and Alaska Native individuals to engage in cultural healing practices and connect with their rich history and traditions. [36] [37] |
article-130737_25 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes -- Research | Limited literature is available on mental health disorders and appropriate treatment for American Indian and Alaska Native individuals. Although knowledge about American Indian and Alaska Native mental health problems is growing, little research has been published on treatment efficacy and outcomes. For example, between 1986 and 2005, none of the 10,000 participants in randomized control trials on major mental health disorders were identified as American Indian and Alaska Native. [38] A recent literature search for mental health treatments for American Indian and Alaska Native individuals yielded 3,500 initial citations, but only 2 were controlled clinical trials. [39] Collecting more data and objective evidence on mental health and psychiatric disorders in the American Indian and Alaska Native populations may help reduce mental health disparities. | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes -- Research. Limited literature is available on mental health disorders and appropriate treatment for American Indian and Alaska Native individuals. Although knowledge about American Indian and Alaska Native mental health problems is growing, little research has been published on treatment efficacy and outcomes. For example, between 1986 and 2005, none of the 10,000 participants in randomized control trials on major mental health disorders were identified as American Indian and Alaska Native. [38] A recent literature search for mental health treatments for American Indian and Alaska Native individuals yielded 3,500 initial citations, but only 2 were controlled clinical trials. [39] Collecting more data and objective evidence on mental health and psychiatric disorders in the American Indian and Alaska Native populations may help reduce mental health disparities. |
article-130737_26 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes -- Summary | Mental health disparities for American Indian and Alaskan Native individuals are linked to limited access to healthcare services, intergenerational trauma, and cultural differences. Enhancing the cultural competence of health services and providers is crucial for equitable healthcare. Telepsychiatry and teletherapy can help reach rural communities, but recognizing and integrating cultural values and beliefs is essential. More research on mental health disorders and appropriate treatments for American Indian and Alaska Native individuals is needed to reduce health disparities. A multidisciplinary team includes clinicians, mid-level practitioners, nurses, pharmacists, lab technicians, medical technicians, physical and occupational therapists, and ancillary staff. Enhancing healthcare standards for the American Indian and Alaska Native populations requires fostering open communication, engaging in collaborative efforts, and demonstrating empathy toward the challenges faced by these patients. By doing so, optimal care can be ensured and overall well-being improved. | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Enhancing Healthcare Team Outcomes -- Summary. Mental health disparities for American Indian and Alaskan Native individuals are linked to limited access to healthcare services, intergenerational trauma, and cultural differences. Enhancing the cultural competence of health services and providers is crucial for equitable healthcare. Telepsychiatry and teletherapy can help reach rural communities, but recognizing and integrating cultural values and beliefs is essential. More research on mental health disorders and appropriate treatments for American Indian and Alaska Native individuals is needed to reduce health disparities. A multidisciplinary team includes clinicians, mid-level practitioners, nurses, pharmacists, lab technicians, medical technicians, physical and occupational therapists, and ancillary staff. Enhancing healthcare standards for the American Indian and Alaska Native populations requires fostering open communication, engaging in collaborative efforts, and demonstrating empathy toward the challenges faced by these patients. By doing so, optimal care can be ensured and overall well-being improved. |
article-130737_27 | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Review Questions | Access free multiple choice questions on this topic. Comment on this article. | Mental Health Challenges in Caring for American Indians and Alaska Natives -- Review Questions. Access free multiple choice questions on this topic. Comment on this article. |
article-17166_0 | Physiology, Acute Phase Reactants -- Introduction | Acute phase reactants (APR) are inflammation markers that exhibit significant changes in serum concentration during inflammation. These are also important mediators produced in the liver during acute and chronic inflammatory states. Interleukin-6 (IL-6) is the primary cytokine responsible for inducing the production in the liver. IL-1, tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma) can also induce the production of acute-phase reactants. Acute phase reactants cause several adverse effects. These include fever, anemia of chronic disease, anorexia, somnolence, lethargy, amyloidosis, and cachexia (fat and muscle loss, anorexia, weakness). | Physiology, Acute Phase Reactants -- Introduction. Acute phase reactants (APR) are inflammation markers that exhibit significant changes in serum concentration during inflammation. These are also important mediators produced in the liver during acute and chronic inflammatory states. Interleukin-6 (IL-6) is the primary cytokine responsible for inducing the production in the liver. IL-1, tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma) can also induce the production of acute-phase reactants. Acute phase reactants cause several adverse effects. These include fever, anemia of chronic disease, anorexia, somnolence, lethargy, amyloidosis, and cachexia (fat and muscle loss, anorexia, weakness). |
article-17166_1 | Physiology, Acute Phase Reactants -- Introduction | Acute phase reactants can be classified as positive or negative, depending on their serum concentrations during inflammation. Positive acute phase reactants are upregulated, and their concentrations increase during inflammation. Negative acute phase reactants are downregulated, and their concentrations decrease during inflammation. Positive acute phase reactants include procalcitonin, C-reactive protein, ferritin, fibrinogen, hepcidin, and serum amyloid A. Negative acute phase reactants include albumin, prealbumin, transferrin, retinol-binding protein, and antithrombin. [1] | Physiology, Acute Phase Reactants -- Introduction. Acute phase reactants can be classified as positive or negative, depending on their serum concentrations during inflammation. Positive acute phase reactants are upregulated, and their concentrations increase during inflammation. Negative acute phase reactants are downregulated, and their concentrations decrease during inflammation. Positive acute phase reactants include procalcitonin, C-reactive protein, ferritin, fibrinogen, hepcidin, and serum amyloid A. Negative acute phase reactants include albumin, prealbumin, transferrin, retinol-binding protein, and antithrombin. [1] |
article-17166_2 | Physiology, Acute Phase Reactants -- Cellular Level | Macrophages sense bacterial products through Toll-like receptors (TLR) and regulate the inflammatory response. TLR4 senses the gram-negative bacterial lipopolysaccharide (LPS). Downstream signaling leads to the activation of the transcription factor, nuclear factor kappa beta (NF-kB), and increased production of IL-6. IL-6 activates liver production of other acute-phase proteins. Tissue injury and trauma can also activate the acute-phase reaction (APR). The purpose of acute-phase proteins released during APR is to participate in blood coagulation, defense against infection, transport metabolites, nutrients and hormones, and maintenance of homeostasis. IL-6, IL-1beta, TNF-alpha, glucocorticoids, and growth factors are the primary mediators of acute-phase proteins (APP) gene expression. [2] [3] | Physiology, Acute Phase Reactants -- Cellular Level. Macrophages sense bacterial products through Toll-like receptors (TLR) and regulate the inflammatory response. TLR4 senses the gram-negative bacterial lipopolysaccharide (LPS). Downstream signaling leads to the activation of the transcription factor, nuclear factor kappa beta (NF-kB), and increased production of IL-6. IL-6 activates liver production of other acute-phase proteins. Tissue injury and trauma can also activate the acute-phase reaction (APR). The purpose of acute-phase proteins released during APR is to participate in blood coagulation, defense against infection, transport metabolites, nutrients and hormones, and maintenance of homeostasis. IL-6, IL-1beta, TNF-alpha, glucocorticoids, and growth factors are the primary mediators of acute-phase proteins (APP) gene expression. [2] [3] |
article-17166_3 | Physiology, Acute Phase Reactants -- Cellular Level | APPs are divided into positive and negative APPs. The concentrations of positive APPs increase during inflammation, and the concentration of negative APPs decrease. Positive APPs include C-reactive protein, haptoglobin, angiotensinogen, alpha1-acid glycoprotein, serum amyloid A, lipopolysaccharide-binding protein (LBP), ferritin, alpha1-antitrypsin, hepcidin, fibrinogen, serum amyloid A, vitronectin, procalcitonin, among others. Negative APPs include albumin, transthyretin (prealbumin), antithrombin, and transferrin. | Physiology, Acute Phase Reactants -- Cellular Level. APPs are divided into positive and negative APPs. The concentrations of positive APPs increase during inflammation, and the concentration of negative APPs decrease. Positive APPs include C-reactive protein, haptoglobin, angiotensinogen, alpha1-acid glycoprotein, serum amyloid A, lipopolysaccharide-binding protein (LBP), ferritin, alpha1-antitrypsin, hepcidin, fibrinogen, serum amyloid A, vitronectin, procalcitonin, among others. Negative APPs include albumin, transthyretin (prealbumin), antithrombin, and transferrin. |
article-17166_4 | Physiology, Acute Phase Reactants -- Cellular Level | Erythrocyte sedimentation rate (ESR) : ESR measures the distance that red blood cells in the anticoagulated blood fall in a vertical tube after one hour. Fibrinogen reduces the charge on the red blood cell surface, which causes them to aggregate rapidly. As a result, ESR increases. ESR is used to indirectly measure the amount of fibrinogen by determining the rate at which erythrocytes settle inside a vertical tube in one hour. The ESR level starts to rise within 24 to 48 hours of inflammation. An increase in ESR can be indicative of inflammation. [4] | Physiology, Acute Phase Reactants -- Cellular Level. Erythrocyte sedimentation rate (ESR) : ESR measures the distance that red blood cells in the anticoagulated blood fall in a vertical tube after one hour. Fibrinogen reduces the charge on the red blood cell surface, which causes them to aggregate rapidly. As a result, ESR increases. ESR is used to indirectly measure the amount of fibrinogen by determining the rate at which erythrocytes settle inside a vertical tube in one hour. The ESR level starts to rise within 24 to 48 hours of inflammation. An increase in ESR can be indicative of inflammation. [4] |
article-17166_5 | Physiology, Acute Phase Reactants -- Cellular Level | C-reactive protein: CRP is a marker of bacterial inflammation and has a higher sensitivity than ESR, and is a direct measure of the inflammatory response. It was first discovered by Tillet and Francis in 1930 when they showed it reacted to the C-polysaccharide of Streptococcus pneumoniae in patients with pneumococcal pneumonia. It belongs to a highly conserved family of proteins referred to as pentraxins, which are typified by five protomers around a central pore, and its half-life does not change between health and disease, making the production rate the sole determinant of plasma concentrations. [2] [3] The normal range for CRP is between 2 to 10 mg/L. The CRP levels start to rise after 4 to 6 hours and peaks by 36 to 50 hours. Levels of CRP can increase 100- to 1000-fold during acute inflammation. The main functions of CRP are to help promote phagocytosis and the innate immune response against foreign infectious pathogens. [4] | Physiology, Acute Phase Reactants -- Cellular Level. C-reactive protein: CRP is a marker of bacterial inflammation and has a higher sensitivity than ESR, and is a direct measure of the inflammatory response. It was first discovered by Tillet and Francis in 1930 when they showed it reacted to the C-polysaccharide of Streptococcus pneumoniae in patients with pneumococcal pneumonia. It belongs to a highly conserved family of proteins referred to as pentraxins, which are typified by five protomers around a central pore, and its half-life does not change between health and disease, making the production rate the sole determinant of plasma concentrations. [2] [3] The normal range for CRP is between 2 to 10 mg/L. The CRP levels start to rise after 4 to 6 hours and peaks by 36 to 50 hours. Levels of CRP can increase 100- to 1000-fold during acute inflammation. The main functions of CRP are to help promote phagocytosis and the innate immune response against foreign infectious pathogens. [4] |
article-17166_6 | Physiology, Acute Phase Reactants -- Cellular Level | Procalcitonin: PCT is a 14.5 kDa peptide. IL-6, IL-1, and TNF-alpha stimulate its secretion. However, it appears that secretion is not activated by IFN-gamma (produced mainly in response to viral infections), making it a sensitive marker of bacterial infections. [5] | Physiology, Acute Phase Reactants -- Cellular Level. Procalcitonin: PCT is a 14.5 kDa peptide. IL-6, IL-1, and TNF-alpha stimulate its secretion. However, it appears that secretion is not activated by IFN-gamma (produced mainly in response to viral infections), making it a sensitive marker of bacterial infections. [5] |
article-17166_7 | Physiology, Acute Phase Reactants -- Function | Procalcitonin : Under normal conditions, procalcitonin is produced by the parafollicular (C cells) of the thyroid gland. It is then converted to calcitonin and released from C cells. However, during inflammation, LPS, microbial toxins, or inflammatory mediators can activate the procalcitonin gene in other tissues, including the liver, kidney, adipocytes, pancreas, colon, and brain. Unlike the procalcitonin produced by the thyroid gland, procalcitonin produced in response to inflammation is directly released into blood circulation. Procalcitonin is a sensitive marker for following the progression of infections, especially for pneumonia and sepsis. Levels of procalcitonin can be used to guide antibiotic therapy. | Physiology, Acute Phase Reactants -- Function. Procalcitonin : Under normal conditions, procalcitonin is produced by the parafollicular (C cells) of the thyroid gland. It is then converted to calcitonin and released from C cells. However, during inflammation, LPS, microbial toxins, or inflammatory mediators can activate the procalcitonin gene in other tissues, including the liver, kidney, adipocytes, pancreas, colon, and brain. Unlike the procalcitonin produced by the thyroid gland, procalcitonin produced in response to inflammation is directly released into blood circulation. Procalcitonin is a sensitive marker for following the progression of infections, especially for pneumonia and sepsis. Levels of procalcitonin can be used to guide antibiotic therapy. |
article-17166_8 | Physiology, Acute Phase Reactants -- Function | C-reactive protein : CRP binds to several pathogens acting as an opsonin. It can also bind to degenerating cells and cell remnants. CRP also activates complement by the classical C1q pathway. CRP is used as a clinical measurement of ongoing inflammation. [3] | Physiology, Acute Phase Reactants -- Function. C-reactive protein : CRP binds to several pathogens acting as an opsonin. It can also bind to degenerating cells and cell remnants. CRP also activates complement by the classical C1q pathway. CRP is used as a clinical measurement of ongoing inflammation. [3] |
article-17166_9 | Physiology, Acute Phase Reactants -- Function | Serum amyloid A : The role of SAA is to function as an inhibitor of many biological processes, including fever, platelet activation, mobilization of monocytes, and chemotactic effect on various immune cells. In tissues, SAA attracts and modulates inflammatory cells and inhibits respiratory burst. As an APP, SAA influences HDL cholesterol transport. SAA can bind to the LPS comparable to LPS binding protein (LBP). The prolonged elevation of SAA can lead to secondary amyloidosis. [6] | Physiology, Acute Phase Reactants -- Function. Serum amyloid A : The role of SAA is to function as an inhibitor of many biological processes, including fever, platelet activation, mobilization of monocytes, and chemotactic effect on various immune cells. In tissues, SAA attracts and modulates inflammatory cells and inhibits respiratory burst. As an APP, SAA influences HDL cholesterol transport. SAA can bind to the LPS comparable to LPS binding protein (LBP). The prolonged elevation of SAA can lead to secondary amyloidosis. [6] |
article-17166_10 | Physiology, Acute Phase Reactants -- Function | Hepcidin : Hepcidin inhibits iron absorption in the intestinal mucosal cells by binding to the ferroportin and inhibits iron transport by binding to ferroportin in macrophages. Increased hepcidin during inflammation causes anemia of chronic disease. [2] [3] | Physiology, Acute Phase Reactants -- Function. Hepcidin : Hepcidin inhibits iron absorption in the intestinal mucosal cells by binding to the ferroportin and inhibits iron transport by binding to ferroportin in macrophages. Increased hepcidin during inflammation causes anemia of chronic disease. [2] [3] |
article-17166_11 | Physiology, Acute Phase Reactants -- Function | Haptoglobin : Intravascular hemolysis releases free hemoglobin in the circulation. Free hemoglobin is an oxidizing agent and can cause tissue damage. Bacteria can utilize heme for the iron requirement. Haptoglobin is a scavenger protein that has antioxidant, antimicrobial, and anti-inflammatory properties. It is an antioxidant because it removes free hemoglobin from the blood, and it is antimicrobial because it reduces iron availability to the pathogens. Its anti-inflammatory properties are due to its binding to CD11b/CD18 integrins on neutrophils. [7] Because haptoglobin binds to hemoglobin, levels of haptoglobin decrease during intravascular hemolysis. As a positive APP, its levels increase during inflammation. Therefore, haptoglobin levels can appear within normal limits in patients with intravascular hemolysis and inflammation. | Physiology, Acute Phase Reactants -- Function. Haptoglobin : Intravascular hemolysis releases free hemoglobin in the circulation. Free hemoglobin is an oxidizing agent and can cause tissue damage. Bacteria can utilize heme for the iron requirement. Haptoglobin is a scavenger protein that has antioxidant, antimicrobial, and anti-inflammatory properties. It is an antioxidant because it removes free hemoglobin from the blood, and it is antimicrobial because it reduces iron availability to the pathogens. Its anti-inflammatory properties are due to its binding to CD11b/CD18 integrins on neutrophils. [7] Because haptoglobin binds to hemoglobin, levels of haptoglobin decrease during intravascular hemolysis. As a positive APP, its levels increase during inflammation. Therefore, haptoglobin levels can appear within normal limits in patients with intravascular hemolysis and inflammation. |
article-17166_12 | Physiology, Acute Phase Reactants -- Function | Ferritin : The role of ferritin is to sequesters iron to inhibit microbial iron scavenging. During malignancy and infection, ferritin concentrations are elevated to reduce free iron available to tumor cells or pathogens, respectively. It is upregulated by proinflammatory cytokines. Some organisms like pseudomonas cause ferritin levels to drop because they have virulence factor siderophores (pyoverdine and pyocyanin) that chelate and import iron. Fibrinogen : The role of fibrinogen as a coagulation factor is to promote endothelial repair. Fibrinogen also has a C3 complement function. Fibrinogen correlates with ESR. | Physiology, Acute Phase Reactants -- Function. Ferritin : The role of ferritin is to sequesters iron to inhibit microbial iron scavenging. During malignancy and infection, ferritin concentrations are elevated to reduce free iron available to tumor cells or pathogens, respectively. It is upregulated by proinflammatory cytokines. Some organisms like pseudomonas cause ferritin levels to drop because they have virulence factor siderophores (pyoverdine and pyocyanin) that chelate and import iron. Fibrinogen : The role of fibrinogen as a coagulation factor is to promote endothelial repair. Fibrinogen also has a C3 complement function. Fibrinogen correlates with ESR. |
article-17166_13 | Physiology, Acute Phase Reactants -- Function | Alpha-1 antitrypsin (AAT): AAT is a serine protease inhibitor (serpin) that breaks down neutrophil elastase. It protects the cells against neutrophil elastase activity. AAT deficiency can cause hepatitis, liver cirrhosis, and panacinar emphysema. | Physiology, Acute Phase Reactants -- Function. Alpha-1 antitrypsin (AAT): AAT is a serine protease inhibitor (serpin) that breaks down neutrophil elastase. It protects the cells against neutrophil elastase activity. AAT deficiency can cause hepatitis, liver cirrhosis, and panacinar emphysema. |
article-17166_14 | Physiology, Acute Phase Reactants -- Function | Others: Ceruloplasmin (Cp) contains copper, and it has histaminase-and ferroxidase-activity. Cp also scavenges Fe2+ and free radicals. Alpha2-macroglobulin (a2MG) binds to the proteolytic enzymes. Alpha1-glycoprotein (a1AGP) influences T-cell function and binds to the steroids such as progesterone. Alpha1-antichymotrypsins inhibit leukocytes and lysosomal proteolytic enzymes. Transferrin : Transferrin is a negative APP. Macrophages internalize transferrin to sequester iron and inhibit microbial iron scavenging. Albumin : Albumin is a negative APP, and its production is decreased to conserve amino acids for positive APPs. [1] | Physiology, Acute Phase Reactants -- Function. Others: Ceruloplasmin (Cp) contains copper, and it has histaminase-and ferroxidase-activity. Cp also scavenges Fe2+ and free radicals. Alpha2-macroglobulin (a2MG) binds to the proteolytic enzymes. Alpha1-glycoprotein (a1AGP) influences T-cell function and binds to the steroids such as progesterone. Alpha1-antichymotrypsins inhibit leukocytes and lysosomal proteolytic enzymes. Transferrin : Transferrin is a negative APP. Macrophages internalize transferrin to sequester iron and inhibit microbial iron scavenging. Albumin : Albumin is a negative APP, and its production is decreased to conserve amino acids for positive APPs. [1] |
article-17166_15 | Physiology, Acute Phase Reactants -- Related Testing | The best accepted clinical measures of acute inflammation are CRP and ESR. CRP has the advantage of being more sensitive and easily measured on automated platforms by nephelometry and turbidimetry in the majority of clinical laboratories and is a direct readout of the APR. ESR is an indirect measure of APR proteins, mainly fibrinogen. Both can provide results within hours. However, the quantification of some APPs such as alpha-1antitrypsin (AAT), alpha-1-acid glycoprotein, alpha-2 macroglobulin is not as well validated and standardized as CRP. Fibrinogen rises much later than CRP, and its concentration only increased around two folds. [2] | Physiology, Acute Phase Reactants -- Related Testing. The best accepted clinical measures of acute inflammation are CRP and ESR. CRP has the advantage of being more sensitive and easily measured on automated platforms by nephelometry and turbidimetry in the majority of clinical laboratories and is a direct readout of the APR. ESR is an indirect measure of APR proteins, mainly fibrinogen. Both can provide results within hours. However, the quantification of some APPs such as alpha-1antitrypsin (AAT), alpha-1-acid glycoprotein, alpha-2 macroglobulin is not as well validated and standardized as CRP. Fibrinogen rises much later than CRP, and its concentration only increased around two folds. [2] |
article-17166_16 | Physiology, Acute Phase Reactants -- Related Testing | Assessing intravascular hemolysis with haptoglobin can be inaccurate without tests such as bilirubin, lactate dehydrogenase, and hemoglobin. Haptoglobin levels increase during inflammation and decrease during hemolysis. In patients with hemolysis and inflammation, levels can appear normal. | Physiology, Acute Phase Reactants -- Related Testing. Assessing intravascular hemolysis with haptoglobin can be inaccurate without tests such as bilirubin, lactate dehydrogenase, and hemoglobin. Haptoglobin levels increase during inflammation and decrease during hemolysis. In patients with hemolysis and inflammation, levels can appear normal. |
article-17166_17 | Physiology, Acute Phase Reactants -- Related Testing | Procalcitonin is a sensitive marker for sepsis and can be used to guide treatment. Procalcitonin has replaced CRP as a diagnostic parameter in sepsis because PCT has higher sensitivity than CRP in sepsis. CRP is no longer used as a diagnostic parameter in sepsis, but it can be useful in the follow-up. | Physiology, Acute Phase Reactants -- Related Testing. Procalcitonin is a sensitive marker for sepsis and can be used to guide treatment. Procalcitonin has replaced CRP as a diagnostic parameter in sepsis because PCT has higher sensitivity than CRP in sepsis. CRP is no longer used as a diagnostic parameter in sepsis, but it can be useful in the follow-up. |
article-17166_18 | Physiology, Acute Phase Reactants -- Related Testing | Ferritin levels are increased in inflammatory conditions, and levels of transferrin, a negative APP that transports iron, decrease. Ferritin sequesters iron. Prolonged inflammation or malignancy can lead to anemia of chronic disease. Ferritin, transferrin, and serum iron are part of the iron panel laboratory studies. Iron deficiency anemia and anemia of chronic disease can both present as microcytic anemia. They can be distinguished by assessing ferritin and transferrin levels. Anemia of chronic disease patients will have elevated ferritin and low transferrin. Iron deficiency anemia patients will have lower ferritin and elevated transferrin. Serum iron will be low in both patients for different reasons. In iron deficiency, low serum iron could be due to malnutrition, increased demand, or hemorrhage. In anemia of chronic disease, low serum iron is from impaired distribution of iron mainly due to hepcidin-mediated reduced absorption from enterocytes and macrophages. [8] | Physiology, Acute Phase Reactants -- Related Testing. Ferritin levels are increased in inflammatory conditions, and levels of transferrin, a negative APP that transports iron, decrease. Ferritin sequesters iron. Prolonged inflammation or malignancy can lead to anemia of chronic disease. Ferritin, transferrin, and serum iron are part of the iron panel laboratory studies. Iron deficiency anemia and anemia of chronic disease can both present as microcytic anemia. They can be distinguished by assessing ferritin and transferrin levels. Anemia of chronic disease patients will have elevated ferritin and low transferrin. Iron deficiency anemia patients will have lower ferritin and elevated transferrin. Serum iron will be low in both patients for different reasons. In iron deficiency, low serum iron could be due to malnutrition, increased demand, or hemorrhage. In anemia of chronic disease, low serum iron is from impaired distribution of iron mainly due to hepcidin-mediated reduced absorption from enterocytes and macrophages. [8] |
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