Letter to the Editor
Seborrhoeic dermatitis and a herpes zoster infection developed during treatment with adalimumab due to Crohn’s disease

One indication for adalimumab therapy is severe, active Crohn’s disease when the response to treatment with a corticosteroid and/or an immunosuppressive agent is insufficient, the treatment is poorly tolerated or there are medical contraindications for this form of therapy [1]. Adverse reactions affecting the skin and mucous membranes during treatment with tumor necrosis factor (TNF) inhibitors are commonly described.
We present the case of a patient in whom severe seborrhoeic dermatitis and a herpes zoster infection developed while using of a TNF inhibitor due to Crohn’s disease.
A female patient aged 22. The first skin lesions in the form of erythematous and scaly foci located in the armpits, the groin and the scalp, had appeared 10 months earlier, 5 months after the beginning of treatment with adalimumab due to Crohn’s disease. The patient had been under the constant care of a gastroenterologist for 5 years. Azathioprine, prednisone and sulfasalazine had also been used without achieving any significant improvement. During the TNF inhibitor therapy, the skin lesions gradually increased. In addition, in the 12th month of adalimumab use, severe lesions in the form of blisters on an erythematous base with a segmental distribution appeared on the right thigh. The patient was diagnosed with zoster and started on aciclovir at a dose of 5 × 800 mg/day for 12 days; in addition, adalimumab was discontinued. The lesions caused by herpes zoster disappeared completely, but the eruptions within the scalp, armpits and groin exacerbated further (Figures 1, 2). Laboratory tests showed only slightly increased leucocytosis. Other laboratory tests with arthus-type reactions, general urine test, glucose levels and imaging studies (chest X-ray, abdominal ultrasound) were normal. Colonoscopy revealed signs of Crohn’s disease. Mycological tests (direct preparation and culture; axillary and inguinal fossae, external acoustic ducts, scalp) were negative. Bacteriological tests (the axillary and inguinal fossae, external acoustic ducts, scalp) – Pseudomonas aeruginosa, Staphylococcus aureus. Histopathological examination (axillary fossa) – thickening of the cornified layer of the epidermis, parakeratosis, spongiosis and slight signs of acanthosis, spinous layer oedema. Perivascular inflammatory infiltrates and dermal oedema. All the findings, which are consistent with the clinical picture, indicate seborrhoeic dermatitis. The patient was administered...


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