Book picture of Primary Biliary Cirrhosis, one of those that do not occur in real life. The diagnosis would be practically made with the AMA (1). With 2 we would rule out hemochromatosis, with 3 we would rule out Wilson's disease. With 4 we could rule out rare diseases such as biliary tract malformations or Caroli's disease and with 5 we could rule out viral hepatitis.

A 52-year-old woman consulted because she had noticed during the previous week a yellowish discoloration of the conjunctivae. She does not refer to risky sexual behaviors or epidemiological history of risk of viral hepatitis. She does not consume alcohol or hepatotoxic drugs. She reports a one-year history of generalized pruritus, asthenia, dry mouth and absence of lacrimation with no known cause. Rest of the anamnesis without pathological data. Physical examination showed scratching lesions, conjunctival jaundice and non-painful hepatomegaly. The patient brings a blood test carried out in his company with the following pathological results: Bilirubin 3 mg/dl, FA 400 UI/ VSG 40mm 1 hour. Indicate which would be the best recommendation to establish the etiological diagnosis of the patient's condition:

Epstein-Barr Virus Hepatitis Masquerading as Painless Jaundice.

Epstein-Barr virus (EBV) infection typically presents with pharyngeal symptoms and subclinical transaminitis. We present a case of a 27-year-old woman with no known past medical history who presented with painless jaundice and dark-colored urine for three days. Her review of systems was negative for fever, sore throat, nausea, vomiting, pruritus, or rash. Her last sexual contact was six months ago with a male partner, and she only drank alcohol socially. Family and surgical history were non-significant. Physical examination revealed 3+ bilateral conjunctival icterus without abdominal tenderness or organomegaly. She had elevated transaminases: alanine transaminase (ALT) of 1287U/L and aspartate aminotransferase of (AST) 1057U/L but her alkaline phosphatase (ALP) was only slightly above normal at 109U/L (normal range 35-104U/L), with a direct hyperbilirubinemia - total bilirubin 9.5mg/dl, direct bilirubin 6.8mg/dl; the abdominal ultrasound revealed non-dilated bile ducts. Hepatitis A, B, and C serology was negative, but her EBV serology showed an infection. She had incidental thalassemia minor without splenomegaly or asterixis. She was managed conservatively, and her liver enzymes trended down with supportive management. Although EBV is an uncommon cause of painless jaundice, this diagnosis should be considered, especially when other more common causes of jaundice have been ruled out. A high index of suspicion should be maintained to detect EBV hepatitis as it can easily be diagnosed through serological testing.

Anita Roddick

Roddick explained that her hepatitis C was unexpectedly diagnosed in 2004, following a blood test that was part of a medical examination needed for a life insurance policy. The blood test indicated abnormal liver function and subsequent blood tests diagnosed hepatitis C. Roddick explained that she had a large blood transfusion in 1971, after the birth of her younger daughter, and that she was convinced that the transfusion had infected her with hepatitis C. This was about twenty years before blood donors in the United Kingdom were screened for hepatitis C. She reported that she had developed cirrhosis of the liver, and that her main symptoms were itching and poor concentration. She briefly mentioned that medical treatment with interferon did not suit her. Roddick explained that she kept fit and active, and that she attended biannual out-patient hospital appointments in Southampton, as well as being under review by the liver transplant team at the Addenbrooke's Hospital in Cambridge.

Social history of viruses

Hepatitis is a disease of the liver that has been recognised since antiquity. Symptoms include jaundice, a yellowing of the skin, eyes and body fluids. There are numerous causes, including viruses – particularly hepatitis A virus, hepatitis B virus and hepatitis C virus. Throughout history epidemics of jaundice have been reported, mainly affecting soldiers at war. This "campaign jaundice" was common in the Middle Ages. It occurred among Napoleon's armies and during most of the major conflicts of the 19th and 20th centuries, including the American Civil War, where over 40,000 cases and around 150 deaths were reported. The viruses that cause epidemic jaundice were not discovered until the middle of the 20th century. The names for epidemic jaundice, hepatitis A, and for blood-borne infectious jaundice, hepatitis B, were first used in 1947, following a publication in 1946 giving evidence that the two diseases were distinct. In the 1960s, the first virus that could cause hepatitis was

InternalMed_Harrison

Approach to the Patient with Liver Disease Suspected Liver Disease Abnormal liver tests Acute < 6 months Chronic > 6 months Diagnostic evaluation 1. IgM Anti-HAV 2. HBsAg 3. IgM Anti-HBc 4. Anti-HCV 5. ANA, SMA 6. Monospot, heterophile 7. Ceruloplasmin 8. Alcohol history 9. Drug history Diagnostic evaluation 1. AMA 2. Drug history 3. Ultrasound/MRI 4. MRCP/ERCP Liver biopsy in acute liver disease: Reserved for patients in whom the diagnosis remains unclear despite medical evaluation Liver biopsy in chronic liver disease: Often valuable for diagnosis as well as staging and grading liver disease Diagnostic evaluation 1. HBsAg 2. Anti-HCV 3. Fe saturation, ferritin 4. Ceruloplasmin 5. ˜1AT 6. ANA, SMA 7. Ultrasound 8. Alcohol history Diagnostic evaluation 1. Drug history 2. AMA 3. P-ANCA 4. Ultrasound 5. MRCP/ERCP Hepatitic: °°ALT Mixed: ˛ALT, ˛AlkP Cholestatic: °°AlkP, °°gGT, ˛ALT Hepatitic: °°ALT Mixed: ˛ALT, ˛AlkP Cholestatic: °°AlkP, °°gGT, ˛ALT

Pharmacology_Katzung

Her social history is significant for alcohol use (three to four glasses of wine/night). Her vital signs include the following: temperature 99.8°F, blood pressure 132/64 mm Hg, pulse 78 bpm, and respiratory rate 15/min. On physical examination, she had left upper abdominal tenderness with evidence of hepatomegaly and mild scleral icterus. Laboratory data revealed the following: alanine aminotransferase, 527 IU/L (normal 10–35 IU/L); aspartate aminotransferase, 425 IU/L (normal < 35 IU/L); and bilirubin, 2.9 mg/dL (normal 0.1–0.3 mg/dL). What medications do OTC cold and flu preparations typically contain? Which of the OTC medications might have contrib-uted to the patient’s current symptoms? KH, a 55-year-old woman, presents to the emergency department with nausea, vomiting, and complaints of new-onset flu symptoms over the past several days. Her past medical history is significant for allergic rhinitis and chronic lower back pain secondary to a work-related fall 2 years ago. Her

Jaundice -- History and Physical -- History

Patients usually present with varying symptoms apart from yellowish discoloration of skin along with pruritus, thus providing clues to narrow down the etiology or can also be asymptomatic. A thorough questioning regarding the use of drugs, alcohol or other toxic substances, risk factors for hepatitis (travel, unsafe sexual practices), HIV status, personal or family history of any inherited disorders or hemolytic disorders is vital. Other important points include the duration of jaundice; and the presence of any coexisting signs and symptoms, like a joint ache, rash, myalgia, changes in urine and stool. [22] A history of arthralgias and myalgias before yellowing indicates hepatitis, either due to drugs or viral infections.

Hepatitis -- History and Physical -- Viral Hepatitis

Phase 2 (prodromal phase) - Patients in this phase usually present with anorexia, nausea, vomiting, malaise, pruritus, urticaria, arthralgias, and fatigue. Many times these patients are misdiagnosed as having gastroenteritis or viral infection. Phase 3 (icteric phase) - Patients in this phase present with dark-colored urine and pale-colored stool. Some patients develop jaundice and right upper quadrant pain with liver enlargement. Phase 4 (convalescent phase) - Patients typically start noticing the resolution of symptoms, and laboratory studies show liver enzymes returning to normal levels. [32]

Fatal hepatitis E viral infection in pregnant women in Ghana: a case series.

Viral infections during pregnancy can pose serious threats to mother and fetus from the time of conception to the time of delivery. These lead to congenital defects, spontaneous abortion and even death. The definitive diagnosis and management of pregnancy-related viral infections may be challenging especially in less resourced countries. We present clinical and laboratory responses to the diagnosis and management of three cases of fulminant hepatitis secondary to Hepatitis E viral infection in pregnancy.Case 1 was a 31-year-old Ghanaian woman who presented with a week's history of passing dark urine as well as yellowish discoloration of the eyes. She subsequently developed fulminant hepatitis secondary to Hepatitis E viral infection, spontaneously aborted at 24 weeks of gestation and later died.Case 2 was also a 31-year-old Ghanaian woman who was admitted with a four-day history of jaundice. She had low grade fever, but no history of abdominal pain, haematuria, pale stool or pruritus. She next developed fulminant hepatitis secondary to Hepatitis E viral infection. However, she did not miscarry but died at 28 weeks of gestation.Case 3 was a 17-year-old Ghanaian woman who was referred to the tertiary health facility on account of jaundice and anaemia. She had delivered a live male infant at maturity of 32 weeks but noticed she was jaundiced and had a presentation of active disease 3 days prior to delivery. The baby was icteric at birth and on evaluation, had elevated bilirubin (mixed type) with normal liver enzymes. Hepatitis E virus infection was confirmed in both mother and baby. However, the jaundice and the hepatomegaly resolved in mother and baby after 5 and 12 days respectively. To the best of our knowledge, these are the first documented cases of fatal fulminant hepatic failures resulting from HEV infection in Ghana.

[Dynamics of serum copper level in patients in the acute phase of hepatitis B and in early convalescence].

Analysis of serum copper (Cu) level dynamics during the acute phase of hepatitis acute B and the early convalescence in compliance with gravity of the acute disease course. The study included 39 patients (12 men and 27 women), aged 18 to 76 years. They were hospitalised in the Department of Infectious Diseases of Medical Academy in Lublin because of the hepatitis acute B, without coexisting diseases. The diagnosis was based on the epidemiologic anamnesis, clinical symptoms, biochemical and serological examinations. The studied group was divided in respect to sex and the course of the disease as: light, medium-weighty and weighty. In all examined patients, the serum Cu level was determined according to the following scheme: at the first, tenth, twentieth and the last day of the hospitalisation and additionally one time at four weeks after discharging from the clinic. The serum Cu level was made by atomic absorption spectrometry (AAS) at the wave length of 324.8 nm. The received data were subjected to statistical analysis according to t-Student's test and in cases of significant differences according to the variants of c-Cochran and Cox's tests. According to the SI Unit Conversion Guide, the values 11.22 to 23.58 mumol/l were taken as the normal range. The values derived from the control group of 24 healthy persons (13 men and 11 women) aged 22 to 69 years. The significant increase of serum Cu level in comparison with the control values was found both in the acute phase of hepatitis B and the early convalescence. It could be observed a correlation between serum Cu level and the course of hepatitis viralis acuta B.

Spontaneous Cure of Acute Hepatitis C.

The statistics proved that approximately 25% of the patients with acute HCV present with jaundice, and only 10-20% develop gastrointestinal symptoms. We present the case of a 58 year-old woman, with prior antecedents of arterial hypertension and diabetes mellitus since 25 years old, hypercholesterolemia and hypertriglyceridemia, psoriasis, epilepsy and depressive syndrome. She clinically presents asthenia, anorexia, itching, jaundice and choluria. The objective examination showed an orientated patient, without flapping, hemorrhagic dyscrasia or signs of chronic hepatic disease, with icteric mucosa and skin, abdominal pain, with hepatomegaly and splenomegaly. The laboratory tests have been compatible with acute hepatitis with colestatic pattern: AST/ALT 969/798 UI/ml, FA 796 UI/ml, GGT 2476 UI/ml, BT/BD 7.39/6.10, INR 0.9. The abdominal echography showed: hepatomegaly, regular borders, hepatic steatosis, splenomegaly without ascitic fluid. The viral serological tests revealed protection for hepatitis A ( IgM neg/IgG pos), negative for HVB infection (AgHBs neg, anti-HBc neg), negative for HVE and other viruses (CMV Herpes virus, Epstein Barr, HIV), positive antibodies for HCV and positive RNA VHC (164200 UI/ml), HCV genotype 3a, IL-28B CT, negative autoimmunity. The previous HCV tests were negative, sustaining the recent infection. We assumed an acute hepatitis C. The patient was symptomatically treated with hydroxyzine for the skin itch, with vitamin K for INR correction and she was closely monitored. She had good clinical and laboratorial evolution and she was discharged after one week, maintaining hepatology consultation. She spontaneously cleared HCV infection after 3 months, maintaining negative RNA VHC 6 months after infection. The patient has cured the HCV infection with no need for antiviral treatment.

[Finding and significance of copper protein complexes in liver cirrhoses (author's transl)].

302 liver cirrhoses obtained from the post-mortem material 1970 to 1979 have been examined for the occurrence of the cuprous protein complexes by means of the orcein-staining according to Shikata. The part of the B-posthepatic cirrhoses (89%) could be simultaneously determined with the help of this method. Cuprous protein complexes have been found in bilious (100%), alcoholic (43.9%), etiologically uncertain (34.4%), and B-posthepatic (25,9%) liver cirrhoses. They prove an existing or experienced chronic cholestasis. The demonstration of copper has no principal significance for the etiologic classification of cirrhoses. In the bioptic diagnostics the demonstration of copper has a certain significance for the differentiation of the primary destructive cholangitis from chronically active hepatites of other genesis. The investigations incidentally revealed that HBsAg-containing hepatocytes could be identified by means of orcein in sections performed on archive material after destaining independent of the age of the sections and their primary staining.

Tenpō Tsūhō

History The Tenpō Tsūhō came around a century after the introduction of the Hōei Tsūhō (Kyūjitai: 寳永通寳 ; Shinjitai: 宝永通宝) during the 5th year of the Hōei era (1708), which had a face value of 10 mon (while only containing 3 times as much copper as a 1 mon Kan'ei Tsūhō coin), but was discontinued shortly after it started circulating as it wasn't accepted for its nominal value.

Cases from the Osler Medical Service at Johns Hopkins University.

A 37-year-old woman presented with increasing abdominal pain and jaundice. Six weeks before admission, she developed persistent diarrhea and jaundice of the skin. She also bruised easily, and her gums bled. In the subsequent weeks, her appetite decreased, she was fatigued, and she had nausea, vomiting, and abdominal distension. She had a history of drinking 1 quart of vodka every day for 20 years, with brief periods of abstinence; she stopped consuming alcohol 11 days before admission because it no longer provided symptomatic relief. Her past medical history was also notable for depression, including a suicide attempt 4 years earlier. She did not smoke, use illicit drugs, or have unprotected sexual intercourse. She had received no blood transfusions and had not traveled recently. She took no medications, except for occasional ibuprofen. On physical examination, she was thin and deeply jaundiced, and she trembled and responded slowly to questions. She was afebrile but tachypneic, and she had orthostatic hypotension. Her HEENT examination was notable for scleral and sublingual icterus, as well as crusted blood on her gums and teeth. The jugular veins were flat. The cardiac examination revealed tachycardia (heart rate, 103 beats per minute) without murmurs, rubs, or gallops. The abdomen was nontender and protuberant, with hypoactive bowel sounds; the spleen was not palpable, and there was no fluid wave or caput medusae. The liver percussed to 18 cm, with a smooth edge extending 10 cm below the costal margin. She had cutaneous telangiectases on her chest and bilateral palmar erythema. There was no peripheral edema. The neurologic examination was notable for asterixis. Her stool was guaiac positive. Laboratory studies revealed the following values: hematocrit, 21.2%; white blood cells, 17,310/mm(3); ammonia, 42 micromol/L; serum creatinine, 3.9 mg/dL; serum urea nitrogen, 70 mg/dL; albumin, 2.1 g/dL; total bilirubin, 26.8 mg/dL; alanine aminotransferase, 14 U/L; aspartate aminotransferase, 77 U/L; alkaline phosphatase, 138 U/L; prothrombin time, 103 seconds (international normalized ratio, 10.6); and urinary sodium, <5 mg/dL. Urinalysis revealed an elevated specific gravity and numerous muddy granular casts. Hepatitis A, B, and C serologies were negative. On abdominal ultrasound examination, there was no ascites, and the liver was echogenic. The portal and hepatic veins were patent, and the hepatic arteries were normal. The spleen measured 14 cm. What is the diagnosis?

Hepatitis B -- Differential Diagnosis

Wilson disease is a disease of excessive copper accumulation. It is associated with psychiatric disturbances due to copper accumulation in the basal ganglia. Kayser-Fleischer rings are pathognomonic for Wilson disease but are not completely sensitive (requires an expert ophthalmologist to confirm this finding). Laboratory evaluation that favors a diagnosis of Wilson disease includes low serum ceruloplasmin levels and elevated urinary copper, and if abnormal, requires further evaluation by a hepatologist. Alcoholic hepatitis Autoimmune hepatitis Cirrhosis Drug-induced liver injury Hemochromatosis Hepatitis A Hepatitis C Hepatitis D Hepatitis E Hepatocellular carcinoma Human immunodeficiency virus Wilson disease

Acute Cholestatic Liver Injury From Hydralazine Intake.

Hydralazine is a commonly used oral antihypertensive agent. We report a rare case of hydralazine-induced hepatotoxicity in the form of subacute hepatic necrosis. A 75-year-old African American woman presented with jaundice of 7-day duration. She was started on hydralazine 100 mg 3 times a day 10 weeks before presentation. On physical examination, scleral icterus was noted. Workup revealed elevated liver transaminases, alkaline phosphatase, and conjugated bilirubin. She had no history of liver disease, and liver function tests had been normal before starting hydralazine. Other etiologies, including viruses, common toxins, drugs, autoimmune, and copper-induced hepatitis, were excluded. Abdominal imaging studies did not show any evidence of intrahepatic or extrahepatic biliary ductal dilatation, and no pathologies were seen in the liver and pancreas. The patient's liver biopsy revealed extensive lobular hepatitis, significant necrosis, mixed inflammatory infiltrate, and no significant fibrosis, supporting a diagnosis of drug-induced liver injury. Hydralazine was immediately discontinued. She showed improvement of clinical and laboratory abnormalities within 5 days after discontinuation of hydralazine. To establish the diagnosis of hydralazine-induced liver injury, we used assessment tool outlined by the Council for International Organization of Medical Sciences (CIOMS) scale that led to "high probable" relationship. Although rare, clinically significant, and potentially life-threatening liver injury can result from use of hydralazine. Both clinical and histological presentations in our patient suggest acute liver injury. The hydralazine-induced hepatitis seems to be reversible as discontinuation of the drug improves clinical outcomes. We highly recommend monitoring of the liver function during hydralazine treatment.

[Clinical and morphological correlations in occult hepatitis B].

Occult hepatitis B (ОHB) characterized by the absence of blood HBsAg attracts the attention of specialists of different profiles; however, its clinical morphological aspects have not been practically studied. to estimate the proportion of OHB in the structure of fatal outcomes in chronic viral hepatitis (CVH) and to characterize its clinical course and structural changes on autopsy materials. A total of 455 autopsy cases of CVH were examined for its etiology in the S.P. Botkin Clinical Hospital of Infectious Diseases in 2014-2016. An in-depth prospective clinical analysis was made to investigate 28 cases of OHB in the stage of decompensated liver cirrhosis, which had subsequently culminated in death. The criteria of inclusion were history data and clinical symptoms of CVH in the detection of markers for hepatitis A, C, and D and HIV in serum HBcAb in the absence of HBsAg. HBsAbs were also determined. Along with the traditional morphological examination, immunohistochemistry (IHC) for HBsAg and HBcAg was carried out. There were 108 CVHB cases (23.7% of the total cases of CVH), including 77 OHB cases (71.3% of those of CVHB) while HBsAg was not determined. HBsAb-negative patients were more often observed to have clinical signs of jaundice (p<0.05) and skin itching (p<0.05). Dyspepsia and hemorrhagic manifestations prevailed in patients with HBsAb (more than 10 IU/l) (p<0.05). All the cases were found to have characteristic morphological signs of CVH, including intranuclear inclusions and nuclear polymorphism in 10.7% of deaths. There was an IHC-positive reaction to VHB antigens in 28.6% of the patients and a doubtful reaction in 25.0%. Serum НВсAb may serve as a diagnostic marker for HBV infection. Clinical and morphological correlations enabled the authors to state that CVHB was present in all cases in the absence of serum HBsAg in the patients.

InternalMed_Harrison

Diagnosing NAFLD requires demonstration of increased liver fat in the absence of hazardous levels of alcohol consumption. Thresholds for potentially dangerous alcohol ingestion have been set at more than one drink per day in women and two drinks per day in men based on epidemiologic evidence that the prevalence of serum aminotransferase elevations increases when alcohol consumption habitually exceeds these levels. In those studies, one drink was defined as having 10 g of ethanol and, thus, is equivalent to one can of beer, 4 ounces of wine, or 1.5 ounces (one shot) of distilled spirits. Other causes of liver fat accumulation (particularly exposure to certain drugs; Table 364-2) and liver injury (e.g., viral hepatitis, autoimmune liver disease, iron or copper overload, α1 antitrypsin deficiency) must also be excluded. Thus, establishing the diagnosis of NAFLD does not require invasive testing: it can be accomplished by history and physical examination, liver imaging (ultrasound is an

Ginseng-Related Drug-Induced Liver Injury.

Ginseng is commonly used as a medicinal herb for memory and concentration and general well-being. Drug-induced liver injury (DILI) is one of the most challenging disorders and trending events in the United States which are related to body building and weight loss supplements. Currently, herbal and dietary supplementation is the second most common cause of DILI. Here, we report on a 45-year-old healthy Chinese woman who presented with dull intermittent left upper quadrant abdomen pain for a month. Upon thorough history taking, she had been taking ginseng tea and supplementation for her menopausal symptoms for almost 3 months. Physical examination was unremarkable except mild tenderness in left upper quadrant of the abdomen. Liver function test showed aspartate transaminase (AST) 717 U/L, alanine transaminase (ALT) 343 U/L, total bilirubin 5 mg/dL, direct bilirubin 3.3 mg/dL, alkaline phosphatase 182 U/L, with international normalized ratio (INR) 1.2. Prior liver enzymes (6 months earlier) showed AST 21 U/L, ALT 18 U/L, total bilirubin 0.8 mg/dL, direct bilirubin 0.3 mg/dL, alkaline phosphatase 34 U/L, with INR 0.7. Viral serology for acute hepatitis B, C, E, cytomegalovirus, Epstein-Barr virus, and varicella zoster virus was negative. She was immune to hepatitis A. Her antinuclear antibody was positive. Her anti-Smith antibody, anti-smooth muscle antibody, HFE gene mutation, ceruloplasmin, alpha-1 antitrypsin serologies were within normal references. An abdomen sonogram showed fatty infiltration. Liver biopsy showed moderate to severe portal inflammation and marked lobular disarray. Portal and lobular inflammatory infiltrates consisted of a mixture of histiocytes, lymphocytes, plasma cells, eosinophils, and neutrophils with centrilobular necrosis and focal bridging necrosis, and necro-inflammation. After 6 weeks of follow-up, the patient improved physically, and the abdomen pain resolved. Ginseng has been widely used in the Chinese community as medicinal herb for a variety of conditions for decades. However, proper research has never been done regarding its pharmacokinetics, efficacy, and safety issues. In our case report, the idiosyncratic DILI resulted from ingestion of ginseng as herbal supplementation for premenopausal symptoms. Physicians should be aware of and suspect DILI in any patient with acute liver injury, and patients should be reminded that all medications and supplements have a potential to cause DILI.

Jaundice -- Evaluation

The results of the bilirubin, enzymes, and liver function tests will direct the diagnosis towards a hepatocellular or cholestatic cause and offer some idea of the duration and severity of the disease. Further evaluation can be conducted based on the initial assessment. Hepatocellular workup: viral serologies, autoimmune antibodies, serum ceruloplasmin, ferritin.

Cerebral Venous Sinus Thrombosis in Systemic Lupus Erythematosus.

A 38-year-old woman presented with general weakness and vaginal bleeding. One month prior, she had been diagnosed with Evans syndrome (haemolytic anemia with positive Coombs test and thrombocytopenia) and was given oral steroid as maintenance therapy. Her serology examination was negative for hepatitis B, hepatitis C, and human immunodeficiency virus (HIV). Her obstetrical history was marked by miscarriage in second pregnancy and preeclampsia in third pregnancy. She used hormonal contraceptives until 5 months prior to admission. On physical examination, she had anemic conjunctiva and no organomegaly. Blood tests were significant for anemia (3.4 g/dl) and thrombocytopenia (28,000/µl). Her vaginal bleeding had ceased, however her platelet continued decreasing to 12,000/µl during first several days of hospitalization despite receiving platelet transfusion. On the tenth hospital day, she suddenly complained of severe headache and blurred vision. She had bilateral edema and erythema of palpebral, chemosis, decreased in visual acuity, and reduced ocular motility. Ear and nose examination were normal. Peripheral blood smear showed no blast. Prothrombine time (PT), INR, APTT tests were normal and D Dimer was slightly increased (3.3 mg/l; NV ≤0.5 mg/l). Urine examination revealed proteinuria with 24 hour urine protein was 1,863 mg (NV <150 mg/day). We assessed her as cavernous sinus thrombosis and treated her empirically with intravenous broad-spectrum antibiotics, morphine drip. Either digital subtraction angiography or anticoagulant was deferred due to low platelet. Further examination revealed positive for ANA, anti-SSA, and diagnosis of SLE was established. Anticardiolipin antibodies of IgG and IgM and anti-beta2 glycoprotein antibodies of IgM and IgG tests were non reactive. Methylprednisolone pulse therapy (1g/day) was given for 3 consecutive days, and then tapered to oral methylprednisolone. She additionally received azathioprine 50 mg tab BID. Meanwhile her clinical symptoms alleviated and platelet count was increased, brain MRI and MR venography finally performed suggesting cerebral venous sinus thrombosis. She got additional oral anticoagulant rivaroxaban 15 mg tab BID and eventually discharged. Cerebral venous sinus thrombosis may be the presenting symptoms or occur concomitantly within the onset of SLE. Our patient had SLE, meeting 4 of the Systemic Lupus International Collaborating Clinic classification criteria (hemolytic anemia, thrombocytopenia, renal involvement, and positive for ANA test). Vasculitis due to endothelial cell injury mediated by immune-complex deposition is proposed to be the pathogenesis of CVST in SLE. Hypercoagulable state could be other etiology factor. Antiphospholipid antibodies were absent in our case as reported in some cases, emphasizing vasculitis as the underlying mechanism. Treatment of CVST in SLE consisting of anticoagulant, steroid, and immunosuppressant. This case elicits intriguing problem: CVST and thrombocytopenia. Anticoagulant treatment is proposed as the cornerstone treatment for CVST, however it was deferred due to risk of bleeding in thrombocytopenia. Steroid plays role in treatment of CVST in SLE, owing to its anti-inflammatory property. As shown in previous cases, the patient had remarkable response to high dose steroid treatment and eventually got anticoagulant after her platelet had increased. In summary, prompt diagnosis and treatment of CVST are important for a favorable prognosis.

[Rare, but important chronic liver diseases].

The presence of steatosis and inflammatory infiltrate in liver biopsies is essential for the diagnosis of non-alcoholic steatohepatitis (NASH). These findings are similar to those with alcoholic liver disease. However, in the NASH-situation alcohol doesn't play an important role. Risk factors for the development of NASH are obesity and diabetes. Most of the patients are clinically asymptomatic. This means, that a diagnosis of NASH is a diagnosis of exclusion: Viral induced, autoimmune, metabolic and toxic liver disease have to be excluded. The disease has a benign clinical course. The risk of cirrhosis is low. So far, there is no established treatment. Preliminary reports suggest a positive effect of weight-loss and ursodeoxycholic acid. Wilson's disease, a copper storage disorder, in which biliary copper excretion is reduced, is inherited as an autosomal recessive trait. Most patients with Wilson disease become symptomatic between the ages of 6 and 15. In about 90% of patients serum ceruloplasmin levels and serum copper concentrations are reduced. Copper excreation is increased. Histologic examination of liver biopsy specimens reveals fatty infiltration, Mallory bodies and ballooned glycogen nuclei, abnormalities which are also found in alcoholic liver disease. The definitive diagnostic parameter is the quantitative determination of liver copper content (> 250 micrograms/g dryweight). Untreated Wilson disease is always fatal. Lifelong treatment with anti-copper drugs are essential, D-penicillamine being the firstline therapy. Hereditary hemochromatosis (HH) is an iron overload disease inherited as an autosomal recessive trait. The frequency of the disease is high. The first symptoms usually can be found at the age of 20-50 years. Arthralgia develops in up to 50% of the patients. Many organs are involved, most often the liver. The organ is usually enlarged, transaminases are always moderately elevated. Laboratory findings disclose a marked elevation in serum ferritin and transferrin saturation. More than 80% of HH-patients are homozygous for the C282Y-mutation in the HFE-gene. The firstline treatment of HH is phlebotomy. Treatment is lifelong. When serum ferritin drops below 50 micrograms/l, the frequency of phlebotomy should be reduced (4-12 per year). If the patient already has cirrhosis, the risk of HCC is very high.

Paraneoplastic Encephalopathy in a Patient With Metastatic Lung Cancer: A Case Study.

<bCASE STUDY</b RS, a 36-year-old female, presented to the emergency department (ED) of a large academic medical center upon the advice of her primary care provider because of 3 weeks of progressive mental status changes, weakness, and decreased oral intake. According to her husband, RS was diagnosed with stage IIIA large cell lung cancer 8 months earlier and was treated with concurrent chemotherapy (carboplatin, pemetrexed, and bevacizumab) and radiation therapy that was completed 4 months prior to admission. No other specific information about her treatment or outside health records was available. According to her husband, RS had been in her usual state of health until approximately 3 weeks prior, when she began having significant mental status changes. She first exhibited some difficulty finding words and later was noted to be putting food in a coffee maker. This spontaneously resolved after approximately 1 week; however, she rapidly developed slurred speech and began to make nonsensical statements. These manifestations also slowly improved but were followed by worsening speech deficit, difficulty walking, and impaired balance. During one of these episodes, she had an occurrence of incontinence. Her husband also noted an incident where her "eyes were beating back and forth and the left side of her face was twitching." RS also had periods (according to her husband) where she "did not seem to be interacting with her environment." These progressively worsened during the last week, and she completely stopped walking and talking 2 days prior to coming to the ED. According to her husband, RS had rheumatoid arthritis and no surgical history. Her family history was unknown except that RS's mother had "seizures." RS had reportedly not used tobacco, alcohol, or drugs, and she was sexually active with her husband. Home medications included transdermal fentanyl 12 μg/hr patch changed every 72 hours; oxycodone-acetaminophen tablets 5-325 mg, two every 4 hours as needed for pain; prednisone 10 mg, one tablet daily; and megestrol 40 mg/mL suspension, 20 mL once daily for appetite stimulation. RS was admitted to an inpatient medical oncology service and evaluated by the oncology advanced practitioner (AP) on her second inpatient day. Upon exam, RS was nonverbal except for moaning in response to painful stimuli and to her sister's voice. Her vital signs were normal. She appeared ill but well-nourished, and she was mildly diaphoretic. Neurologic examination revealed that her pupils were slightly sluggish but equal, round, and reactive to light. Extraocular muscle movements were intact, but she did not move her eyes in response to commands. She tracked the AP and family members around the room with her eyes. Cranial nerve examination was intact with the exception of cranial nerves IX, X, and XI, which were difficult to examine given her inability to cooperate and open her mouth. Motor examination revealed increased tone throughout and intermittent, inconsistent resistance to passive movement. She was seen to move all four extremities spontaneously although not in response to commands. Deep tendon reflexes were intact and equal in all extremities. Examination of other body systems was as follows: there was dry, peeling skin on her lips, but her mucous membranes were moist and free of erythema or lesions. Her lungs were clear to auscultation bilaterally. Her heart rate and rhythm were regular, there were no murmurs, rubs, or gallops, and distal pulses were intact. Her abdomen was nondistended with normally active bowel sounds in all four quadrants. Her abdomen was soft, nontender to palpation, and without palpable masses. There was no peripheral discoloration, temperature changes, or edema, and examination of her skin was benign. <bWorkup</b On admission to the emergency department, serum laboratory studies were unrevealing for any potential causes of encephalopathy. Kidney and liver function were normal, making diagnoses of uremic and hepatic encephalopathies less likely. Cultures of the urine and blood were negative. Samples of cerebrospinal fluid (CSF) were obtained via lumbar puncture and were unrevealing for any abnormalities. Computed tomography (CT) of the head without contrast was negative for any acute intracranial process. Ultrasound of the right upper quadrant revealed a single, nonspecific, hypoechoic hepatic lesion. Computed tomography scans of the chest, abdomen, and pelvis demonstrated the primary malignancy in the upper lobe of the left lung, as well as possible metastatic disease within the left lung, right lung, and liver, and widespread osseous metastatic disease. Magnetic resonance imaging (MRI) of the brain performed 1 day after admission demonstrated numerous scattered punctate foci of enhancement throughout the supratentorial and infratentorial brain parenchyma, measuring at most 3 to 4 millimeters in diameter. There was no significant mass effect or midline shift. A paraneoplastic panel was sent to an outside laboratory and returned positive for antivoltage-gated potassium channel (VGKC) autoantibodies. <bDifferential Diagnosis</b Clinically, RS was exhibiting signs of encephalopathy, a broad term that indicates general brain dysfunction, the hallmark of which is altered mental status. Diagnosing encephalopathy is challenging, as many differential diagnoses must be considered. The clinician must consider metabolic derangements, toxic and infectious etiologies, psychiatric disorders, and less commonly, prion disorders and progressive dementia. Cultures of RS's blood and urine as well as other specialized endocrine tests were negative, decreasing the likelihood of a metabolic or infectious cause for her presentation. The abnormalities on her brain MRI were reviewed by a neuro-oncology team, who felt that the faint, nondescript nature of the visualized lesions was not suspicious for metastatic disease. Sequelae of seizures was also considered by neuro-oncology but dismissed given a grossly normal prolonged electroencephalogram. Some encephalopathies are caused by autoimmune or inflammatory mechanisms, which are confirmed by the presence of autoantibody markers and/or clear response to immunomodulatory treatment (Vernino, Geschwind, & Boeve, 2007). These types of encephalopathies have been seen in patients with cancer and have thus been termed paraneoplastic. The presence of anti-VGKC antibodies on RS's paraneoplastic panel directed the inpatient medical oncology team toward a paraneoplastic neurologic disorder (PND) as the most likely diagnosis.

[Severe hemolytic anemia with tear drop red cells as initial manifestation of Wilson's disease].

A 16-year-old girl was admitted for a detailed examination of hemolytic anemia in November 1995. Initial laboratory findings included a total bilirubin concentration of 1.46 mg/dl, hemoglobin of 9.1 g/dl, and a reticulocyte count of 89/1000 percent. The plasma haptoglobin concentration was below 10 mg/dl. A blood smear showed many dacryocytes and a few echinocytes and codocytes. GOT was 71 IU/l; GPT, 44 IU/l; and LDH, 812 IU/l; the results of a hepaplastin test were 45% of normal. On further investigation, the level of serum ceruloplasmin was found to be 4 mg/dl, and of serum copper, 43 micrograms/dl. Urinary copper excretion was markedly increased, at 345 micrograms per day. Slit-lamp examination of both corneas revealed obvious Kayser-Fleischer rings. A liver biopsy sample showed fibrosis histologically and an elevated copper concentration of 535 micrograms/g dry weight and 183 micrograms/g wet weight. In family studies, the patient's asymptomatic 5-year-old sister was observed to have metabolic abnormalities consistent with Wilson's disease. These findings suggested that the patient's hemolytic anemia with red cell deformities was due to abnormal copper metabolism associated with Wilson's disease.

Subcutaneous panniculitis-like T-cell lymphoma with hemophagocytic syndrome successfully treated with cyclosporin A.

A 17-year-old girl previously in good health presented with a 2-month history of recurrent, high-grade fever; general fatigue; anorexia; a 10-kg weight loss; and multiple, painful, reddish skin lesions on the lower abdomen. Some lesions were ulcerated, with an oily yellowish brown discharge. A systemic review was unremarkable other than bleeding from the nose. Her medical and family histories were unremarkable. On examination, the patient was pale, jaundiced, and febrile (temperature of 39 degrees C). She had enlarged lymph nodes in the axillary and inguinal areas. There was moderate hepatosplenomegaly. Local skin examination revealed multiple erythematous, tender, and firm subcutaneous nodules of variable size (1-2 cm) on the lower abdomen. Some nodules were ulcerated, with oily yellowish brown discharge and overlying ecchymosis (Figures 1 and 2). Mucous membranes were free of lesions. Laboratory investigations showed pancytopenia, an elevated erythrocyte sedimentation rate (>80 mm/h), normal renal function tests, abnormal hepatic function tests (alanine aminotransferase 172 U/L, aspartate aminotransferase 229 U/L, alkaline phosphatase 725 U/L, and total bilirubin 100 mmol/L [normal range 0-18 mmol/L]), conjugated bilirubin 45 mmol/L (normal range 0-5 mmol/L), and high triglycerides 855 mg/dL (normal range 20-200 mg/dL). Prolonged prothrombin time, 26 seconds (normal range 13-16 seconds); prolonged activated partial thromboplastin time, 61 seconds (normal range 26-38 seconds); positive disseminated intravascular coagulation studies evidenced by low fibrinogen, 74 mg/dL (normal range 160-350 mg/dL); and positive fibrinogen degradation products were also noted. Throat, midstream urine, and blood culture results were negative. Serologic tests for syphilis, HIV, and hepatitis B and C viruses were negative. Epstein-Barr virus and cytomegalovirus serologic values revealed evidence of past infection. Tuberculin and Coombs tests were negative. The alpha1-antitrypsin level was normal. Antinuclear and anti-smith antibodies, rheumatoid factor, and cryoglobulins were negative. CT showed enlarged lymph nodes in the axillary and inguinal areas, bilateral small pleural effusion, moderate hepatosplenomegaly, severe fatty infiltration of the liver, and thickening of lower abdominal subcutaneous tissue. A liver biopsy showed steatohepatitis. Bone marrow aspirate and trephine were normal. A deep punch biopsy of a nodule from the right lower abdomen revealed lobular panniculitis with atypical lymphocytes and large macrophages with cytophagocytosis ("beanbag" cells) (Figures 3 and 4). Immunohistochemistry showed that these atypical cells were positive for CD3, CD8, granzyme B, and perforin, and negative for CD56. T-cell gene rearrangement studies on skin lesions revealed a monoclonal T-cell receptor (gamma-chain) gene rearrangement, supporting the diagnosis of subcutaneous panniculitis-like T-cell lymphoma. On presentation, the initial treatment included 6 U of fresh frozen plasma, 2 U of packed red blood cells, and 2 g IV fibrinogen for 3 consecutive days. The patient was started on prednisolone 60 mg orally once daily and cyclosporine A 5 mg/kg/d orally in two divided doses. The fever and other systemic symptoms and skin lesions resolved within 2 weeks after the treatment. The prednisolone dose was tapered gradually, and a maintenance dose of cyclosporine A was continued. The patient's condition remained in remission at 12-month follow-up; there was no evidence of clinical relapse.

Gastric Antral Vascular Ectasia as the First Presentation of Primary Biliary Cholangitis.

Primary biliary cholangitis (PBC), a chronic, autoimmune, cholestatic disease, typically occurs in elderly women and commonly presents with pruritus, fatigue, and cholestasis and its complications. Gastric antral vascular ectasia (GAVE), an uncommon cause of upper gastrointestinal bleeding, leading to transfusion-dependent chronic iron deficiency anemia, as the first presentation of PBC is unusual. We present the case of an elderly female with recurrent melena and transfusion-dependent anemia for a year without any history of jaundice, ascites, or hepatic encephalopathy. Investigations revealed iron-deficiency anemia, elevated transaminases, alkaline phosphatase (ALP), coarse liver, splenomegaly, and portal vein dilatation on ultrasound. An endoscopic evaluation revealed erythematous linear stripes in the antrum suggestive of GAVE, without esophageal or gastric varices. FibroScan (Echosens, Paris, France) revealed advanced F3 fibrosis. Further etiological workup showed positive antinuclear and antimitochondrial antibodies, elevated IgM levels, and negative viral markers (hepatitis B, C, A, and E). Clinically significant portal hypertension was revealed by the hepatic venous pressure gradient (HVPG), while transjugular liver biopsy (TJLB) revealed lymphocytic infiltration of bile duct epithelium with the destruction of small and medium-sized bile ductules. Iron supplementation, low-dose ursodeoxycholic acid, and argon plasma coagulation were used to treat the patient. At the three-month follow-up, no melena was reported and her hemoglobin and liver function tests remained normal. Patients with PBC presenting with GAVE and recurrent melena as a presenting symptom are rarely reported. An awareness of this presentation is important for its early diagnosis and effective treatment.

Pharmacogenomics of drug-induced liver injury (DILI): Molecular biology to clinical applications.

A 21-year old woman was admitted to hospital with a two-week history of painless jaundice, fatigue and anorexia having previously been fit and well. One month prior to presentation, the patient had taken a five-day course of amoxicillin-clavulanic acid for an infected skin cyst. Otherwise, she was only on the oral contraceptive pill and reported minimal alcohol intake. On examination, she was deeply jaundiced, but alert and oriented with no asterixis. She had no stigmata of chronic liver disease, but hepatomegaly extending 3 cm from below the right subcostal margin was evident. Investigations showed: white cell count 13.4 × 10<sup9</sup/L (normal 3.6-9.3), haemoglobin 11.8 g/dl (normal 11-15), platelet count 356 × 10<sup9</sup/L (normal 170-420), sodium 138 mmol/L (normal 134-144), potassium 3.5 mmol/L (normal 3.5-5.0), creatinine 32 µmol/L (normal 40-75), albumin 30 g/L (normal 35-48), alanine aminotransferase 707 IU/L (normal 15-54), alkaline phosphatase 151 IU/L (normal 30-130), bilirubin 384 µmol/L (normal 7-31) and prothrombin time 27.2 s (normal 11.7-14). Screening for hepatitis A, B, C, E, Epstein-Barr virus, cytomegalovirus and autoimmune hepatitis was negative. Tests for anti-smooth muscle, antinuclear, and anti-liver-kidney microsomal-1 antibodies were negative; immunoglobulin levels and ceruloplasmin levels were normal. Liver ultrasonography demonstrated a liver of normal contour with no biliary dilatation, a normal spleen size and patent vessels. Liver biopsy revealed severe portal interface hepatitis with lobular inflammation and scant plasma cells. Her clinical condition deteriorated in the following days with prothrombin time and bilirubin rising to 56.6 s and 470 µmol/L, respectively. At follow-up after 11 days, her alanine aminotransferase level was 1,931 IU/L. She developed grade 2 hepatic encephalopathy 14 days after presentation, and was listed for a super-urgent liver transplant. Human leucocyte antigen (HLA) typing was performed as a part of preparatory investigations and showed the patient carried the HLA haplotype HLA-DRB1∗15:02-DQB1∗06:01. Following orthotopic transplantation of a deceased donor graft her explant histology revealed severe ongoing hepatitis with multi-acinar necrosis (Fig. 1A and B). This case raised a number of important questions about the diagnosis of drug-induced liver injury and tools available for clinicians to make the best decisions for patient care: In this Grand Rounds article, we will explore these questions, describing the pathophysiology, diagnostic and prognostic biomarkers, and clinical management of drug-induced liver injury. We will also discuss ongoing areas of uncertainty.

InternalMed_Harrison

TAblE 428-2 REPRESEnTATivE iRon vAluES in noRmAl SubJECTS, PATiEnTS wiTH HEmoCHRomAToSiS, AnD PATiEnTS wiTH AlCoHoliC livER DiSEASE Adult first-degree relative of patient with HH Subjects with unexplained liver disease Individual with suggestive symptoms (see text) Transferrin saturation and serum ferritin* TS <45% SF <300 TS ˜45% and/or SF >300 °gL Reassure, possibly retest later HFE Genotype PhlebotomyNormal Counsel and consider non-HFE hemochromatosis Serum ferritin – 300–1000 °g/L LFT normal Serum ferritin > 1000 °g/L and/or LFT abnormal Serum ferritin <300 °g/L LFT normal Observe retest in 1–2 years C282Y Homozygote C282Y/H63D (Compound Heterozygote) Confirmed iron overload *For convenience both genotype and phenotype (iron tests) can be performed together at a single visit in first-degree relatives. Liver biopsy No iron overload Investigate and treat as appropriate

Acute cytomegalovirus hepatitis in an immunocompetent host.

A 52-year-old woman presented with a 1-week history of recurrent fevers and joint pains accompanied by abdominal and low back discomfort. She has a history of hypoparathyroidism and is on calcium supplements. Physical examination revealed fever and tachycardia. The rest of the examination was normal. Laboratory tests showed newly increased transaminase activity. Serum bilirubin and prothrombin time were normal. She was admitted for evaluation of acute hepatitis. Serology for hepatitis A, B, C and HIV were negative. Her serum acetaminophen and alcohol were undetected. Abdominal imaging was normal. Cultures were sterile. Additional tests for uncommon viral hepatitis included herpes simplex virus, cytomegalovirus and Epstein-Barr virus. Liver biopsy revealed non-specific inflammation. Subsequently, cytomegalovirus serology showed an IgM positive and negative IgG titre. Cytomegalovirus DNA qualitative PCR was also positive. No antiviral medication was given. She continued to have intermittent daily fever but reported no associated symptoms. She was discharged 9 days after admission in stable condition per her request with the advice to follow-up in the clinic in 1 week. Her serum hepatic profile returned to normal and she reported no more episodes of fever. Repeated titres of cytomegalovirus serology showed seroconversion.

[Primary biliary cirrhosis--analysis of clinical material].

The analysis is presented of 67 patients with primary biliary cirrhosis treated in the years 1971-1988. The group consisted of 60 women (89.5%) and seven men (10.5%). Presenting symptoms were mostly itching (66%) and jaundice (12%). The time between the onset of the first symptoms and the diagnosis was three years, on the average. Autoantibodies to mitochondria were present in 86% of patients. In 27% of cases markers of HB virus infection were found. Cholelithiasis was present in 19 patients (28%). Primary biliary cirrhosis was diagnosed with delay. Third degree of histological changes was observed in 38.8% of cases and in 18% of patients it was already fourth degree. Eighteen patients (27%) died after six years, on the average, from the onset of symptoms. The direct causes of death were, most frequently, liver failure and haemorrhage from oesophageal varices.

[Manganese superoxide dismutase-inhibiting autoantibodies in cholestatic Epstein-Barr viral hepatitis].

A 21-year-old woman reported no serious previous illness. For 3 days before admission she had a fever, headache and joint pains. She had become progressively more jaundiced. Physical examination was normal except for enlarged liver and spleen, swollen lymph nodes and facial oedema. GOT (30 U/l), GPT (33 U/l) and alkaline phosphatase (172 U/l) were slightly elevated. Serum bilirubin was raised to 12.4 mg/dl. The total white blood cell count was normal, but there were 45% atypical lymphocytes (activated T lymphocytes). Abdominal sonography and endoscopic retrograde cholangiopancreatography were unremarkable. Serology for hepatitis A, B and C as well as for antimitochondrial antibodies was negative, but there were specific IgM (1:640) and IgG antibodies (1:80) against Epstein-Barr virus (EBV) capsid antigen in the immunofluorescence test. The EBV infection (infectious mononucleosis) was complicated by cholestatic hepatitis. High concentrations (1832 Göttingen units/ml) of enzyme-inhibiting autoantibodies against the antioxidative enzyme manganese-superoxide dismutase (MSD) were demonstrated. The autoantibodies reduced the antioxidative action of the enzyme by more than 70% and favoured the oxidative cell damage in vitro. After bed-rest for one week without further treatment the symptoms improved and the abnormal laboratory values, including the autoantibodies against MSD, regressed. Autoantibodies against MSD are formed during an acute infection with EBV. Their enzyme-inhibiting action promotes abnormalities of oxidative cell function and may thus be the cause of cholestatic hepatitis in this infection.

[The characteristics of the course of viral hepatitis C].

Time-related course and results of examination were studied in patients with viral hepatitis C, having gotten infected through blood. Based on the comparison of similar indicators in patients with viral hepatitis B particular features were revealed of the clinical course of viral hepatitis C. These are as follows: short-in-duration prejaundice period, in other instances there is no prejaundice period at all, subfebrile states set in quite often; among other features are dyspepsia-like events together with signs of a damage to pancreas. There has been noted a slow dynamics of the icteric period reversibility, with biochemical indicators showing the same tendency.

Idiopathic autoimmune hemolytic anemia due to lecithin overdose: a case report.

Idiopathic Autoimmune Hemolytic Anemia is a potentially fatal condition which requires prompt and potent treatment. Diagnosis of idiopathic autoimmune hemolytic anemia requires both serologic evidence of autoantibody presence and hemolysis. Although most of the times it is considered idiopathic, several underlying causes have been identified, like autoimmune and connective tissue diseases, viral infections, drugs or hyper function of the immune system. To our knowledge, this is the first case in the international literature describing lecithin-induced autoimmune hemolytic anemia. This case report is to highlight a rare but dangerous adverse reaction to overdose of lecithin. A 38 year old white female from Greece, presented to our emergency room with progressive fatigue over a period of ten days and icteric discoloration of her skin and conjunctiva. The patient had been taking lecithin supplements (1200 mg, 3 capsules a day) over a period of ten days for weight loss. She reports that the last 3 days, prior to the examination, she took 5 capsules/day, so that the supplement would take effect more rapidly. Her past medical, social and family history showed no disturbance. Relatives of the patient were requested to submit any blood-tests taken over a period of 20 days prior to the onset of symptoms caused by Lecithin. All tests proved that all functions were within normal scale. Her physical examination revealed pallor and jaundice without palpable hepatosplenomegaly. Blood biochemistry tests showed total bilirubin 7.5 mg/dl, with indirect bilirubin 6.4 mg/dl and complete blood count showed hemoglobin 7.6 g/dl with blood levels 21.4%. In every case of idiopathic autoimmune hemolytic anemia the administration of pharmaceutical substances should always be examined, except for the standard reasons that cause it. In this case the cause of hemolysis was attributed to the excessive intake of lecithin capsules for the loss of body weight. It is important that clinicians and immunologists are aware of this adverse effect.