a 20-year - old female with extensive terminal ileal and colonic crohn 's disease was initially successfully managed on a drug regimen of prednisolone and mesalazine which helped to induce remission .
this maintained her disease remission but was associated with neutropenic sepsis , necessitating the withdrawal of the thiopurine therapy with subsequent clinical and endoscopic disease flare .
this required an infusion dose and frequency escalation to maintain clinical response . after 58 weeks of infliximab therapy , the patient was requiring 10 mg / kg 6 times weekly and hence was transferred to the fully human anti - tnf- injection adalimumab for loss of response to infliximab .
initially this strategy regained disease control , but due to relapse at 40 mg every other week , the dose was increased step - wise to 80 mg weekly which fortunately maintained remission . during her treatment with adalimumab the presence of purple - coloured plaque - like lesions primarily on her abdomen
figure 1 demonstrates the presence of psoriasis which is presumed to be a result of treatment with adalimumab .
tnf- has been identified as a key cytokine in the pro - inflammatory pathways that drive diseases such as inflammatory bowel disease and rheumatoid arthritis .
anti - tnf- agents such as infliximab and adalimumab are widely used in the treatment of these conditions and have been shown to have an impact on pro - inflammatory and apoptotic pathways .
they are also effective in the treatment of the dermatological and rheumatological manifestations of psoriasis .
however , there have been a number of cases reported where such agents may be responsible for new onset or worsening of psoriasis .
a study of 126 patients who underwent treatment with anti - tnf- inhibitors demonstrated evidence of psoriasis in 76 individuals , palmoplantar pustular psoriasis in 37 cases and psoriasis of the nails in 6 cases .
there is mounting evidence that a key innate immune pathway for triggering common human autoimmune diseases , including psoriasis , involves plasmacytoid dendritic cell precursors and type 1 interferon ( ifn ) production . a recent study involving immunohistochemical staining of skin biopsy specimens for myxovirus - resistance protein a ( mxa , a surrogate marker for lesional type 1 ifn activity ) demonstrated increased staining in tnf- inhibitor - induced psoriasis compared with psoriasis vulgaris .
research suggests that a psoriasiform eruption during anti - tnf- treatment seems to be a class effect without any confirmed predisposing factors and does not specifically require treatment discontinuation .
further studies are however needed to determine the exact mechanism of and appropriate treatment for anti - tnf--induced psoriasis .
 anti - tnf- agents are currently utilised for the treatment of a vast array of autoimmune conditions including inflammatory bowel disease , rheumatoid arthritis , ankylosing spondylitis and psoriasis . 
 it is however noted that such therapeutic strategies have been linked to the specific induction of cutaneous - based reactions such as dermatitis , erythema multiforme and psoriasis . 
 here we present the case of a young female patient with crohn 's disease who developed psoriasis following treatment with the anti - tnf- drug adalimumab and highlight the possible pathogenetic mechanisms involved in such an occurrence . 
Case Presentation
What Is the Diagnosis?