No abstract

Drugs have often been implicated as the cause of pemphigus. Lisinopril is a drug of the angiotensin-converting enzyme inhibitor class primarily used in the treatment of hypertension, congestive heart failure, heart attacks, and also in preventing renal and retinal complications of diabetes mellitus. Various side-effects have been described in the English medical literature related to lisinopril, but only one case with pemphigus foliaceus as an adverse reaction to lisinopril. To the best of our knowledge, we present the second case of lisinopril-induced pemphigus foliaceus complicated with Kaposi-Juliusberg varicelliform eruption in a patient diabetes mellitus type II. A 60-year-old man presented with diffuse erythema on the face, trunk and extremities. Disseminated erosions, 2-5 mm in diameter, and umbilicated vesicles were present. Erosions with remnants of the blister roof were partially found on the trunk. Semiannular erosions were present. On the posterior part of the trunk (paravertebral and vertebral) there were inifiltrated, partially grouped, sharply delineated yellowish-reddish plaques, up to 2 cm in diameter. Direct and indirect immunofluorescence test as well as histological analysis revealed a drug-induced pemphigus foliaceus. After treatment of Kaposi-Juliusberg eruption and impetiginization, lisinopril was discontinued. Rapid involution of the skin lesions, was observed. Since, only minor skin lesions still persisted after 6 months of follow-up and treatment, the diagnosis of druginduced pemphigus foliaceus was established. It usually takes 1 - 6 months for angiotensin-converting enzyme inhibitors to induce pemphigus. All drugs taken by the patient, including homeopathic agents, over-the-counter drugs, and even medications that were discontinued should be taken into consideration. Medical history taking should be repeated in cases where there is no response to therapy.

In cases of dermatomyositis with the serious dysphagia, percutaneous endoscopic gastrostomy should be performed as soon as possible. Overall survival rate is low, even with an adequate therapy administration. Inflammatory myopathies should be considered in any patient with oropharyngeal dysphagia.

There is a correlation with lung pathologic physical findings, lower values of FEV1 (in a range of normal values) and the degree of nonspecific bronchial sensitivity as objective indices of activity of bronchial asthma. There is no correlation of these parameters with patient's symptoms as subjective indices of bronchial asthma.