In addition to ANA many other

In addition to ANA, many other serologic similarities exist between leprosy and autoimmune disease. Rheumatoid factor, antineutrophil cytoplasmic antibody, anticyclic citrullinated peptide, and antiphospholipid pak 4 have been reported with varying incidences in different forms of leprosy. These serology findings in conjunction with the rheumatic manifestations described above may lead to misdiagnosis as rheumatic disorders. Misdiagnosis often leads to years of corticosteroid or immunosuppressant administration, which probably modifies the clinical presentation of leprosy towards lepromatous forms. Between 12% and 55% of new cases of leprosy have clinical signs and symptoms of neuropathy at diagnosis. In the tuberculoid pole, isolated damage of nerve trunks or more superficial dermal nerves occurs, while in the lepromatous pole, glove and stocking sensory loss often take place. Granulomatous inflammation of peripheral nerves in leprosy causes nerve enlargement and impairs sensory, motor, and autonomic function. Among them, numbness and sensory loss occur earliest. As for sensory loss, temperature and pain sensations generally decreased earlier than position and vibration sense, and warmth perception is affected earlier than cold perception. Motor function impairment, presenting later in the disease course, results in muscle weakness and atrophy in the distribution of involved peripheral nerves. As in our patient, enlarged ulnar and median nerves are vulnerable to entrapment and irritation behind the olecranon process and flexor retinaculum, respectively. They are usually the first nerves to be compromised. Sensory nerve conduction parameters, in particular amplitude, and warm perception thresholds were by far the most sensitive measures for detecting neuropathy.
Introduction
Case report A 74-year-old man presented with a blistering pruriginous eruption evolving for 3 months. Skin lesions were mainly localized on palms and soles with erythematous plaques and vesicles or tense blisters (Figure 1A). Oral and genital mucosae were involved with large painful erosions (Figure 1B). The trunk and limbs showed polymorphic erythematous plaques (Figure 1C). The patient was treated for several years with nebivolol and amlodipine for hypertension. There was no new medication introduced. A personal history for cutaneous disease was negative. Standard blood analysis showed no specificity and particularly no hypereosinophilia. Histopathological analysis of the lesional skin revealed a slight dermal–epidermal separation and a neutrophilic and eosinophilic infiltrate in the dermal papillae (Figure 2A). Direct immunofluorescence (IF) showed the presence of linear immunoglobulin G (IgG) and complement 3 (C3) at the DEJ (Figure 2B). Diagnosis of bullous pemphigoid (BP) was established and the patient was successfully treated by clobetasol propionate 0.05% cream 40 g daily. However, skin lesions reappeared when the treatment was tapered. Because of this steroid resistance, new analyses were realized. Secondary histopathological analysis and direct IF confirmed the diagnosis of BP. Indirect IF disclosed circulating antibodies at a titer of 1:10, which is not significant. Those antibodies reacted with the floor of an artificial blister created by the salt-split skin technique (Figure 3). Enzyme-linked immunosorbent assay (ELISA) with basal membrane zone proteins of 230 kDa (BP230) and 180 kDa (BP180) were negative. Western immunoblot analysis using a dermal extract showed the reactivity of circulating IgG4 antibodies with the 200-kDa antigen, suggesting the diagnosis of anti-p200 pemphigoid (Figure 4). The patient was successfully treated by combining clobetasol propionate 0.05% cream 30 g daily and dapsone 100 mg daily, with a progressive healing of erosions without scarring and milia formation (Figure 1D). His disease is currently controlled with dapsone 100 mg daily and without the use of corticosteroids.