Leukocytoclastic vasculitis and necrolytic acral erythema in patients with hepatitis C infection: do viral load and viral genotype play a role?

BACKGROUND: Leukocytoclastic vasculitis (LCV) and necrolytic acral erythema (NAE) are skin disorders associated with hepatitis C virus (HCV) infection. However, they have not been found to occur simultaneously in the same patient. OBJECTIVE: We sought to analyze the role of serum HCV-RNA levels and HCV genotype in the pathogenesis of both LCV and NAE in an attempt to assess whether these two parameters play a role in mutual exclusivity of LCV and NAE in the same patient. METHODS: The study included 11 patients with LCV and 13 with NAE, all of whom were infected with HCV. All 24 patients were evaluated for the quantitative levels of HCV-RNA, using real-time polymerase chain reaction. HCV genotyping was performed on 10 patients in each group (N = 20). RESULTS: Patients with LCV had a higher prevalence of moderate and high levels of HCV-RNA viremia (P = .038) than those with NAE. However, there was no significant difference in HCV genotype between LCV and NAE groups (P = .211). LIMITATIONS: Small number of cases is a limitation. CONCLUSION: Viral load seems to play a role in determining the response of the skin to HCV infection. High levels of HCV viremia were found to be significantly associated with LCV but not with NAE. HCV viremia may play a role in the development of LCV in HCV-infected patients.

Histopathological study of apparently normal skin of patients with leprosy.

BACKGROUND: Several clinical and laboratory observations point to the possible microscopical affection of normal-looking skin in leprosy. OBJECTIVE: This study was carried out to verify the microscopical affection of apparently normal-looking skin in different types of leprosy. PATIENTS AND METHODS: The study included 50 patients with different clinical types of leprosy. Biopsies from both skin lesions and normal-looking skin were obtained from each patient and examined for microscopical evidence of leprosy. RESULTS: Microscopical affection of normal-looking skin was detected in 52% of our cases, with higher incidence of affection towards the lepromatous end of the disease. CONCLUSION: Our findings underscore that the incidence of microscopical affection of normal-looking skin in leprosy is much higher on the lepromatous end of the spectrum of leprosy than on the tuberculoid end; during treatment, the leprosy granulomas may disappear from the normal skin before the clinical lesions. Moreover, the microscopic picture of indeterminate leprosy can be observed in the normal-looking skin of patients with tuberculoid leprosy or lepromatous leprosy, and this description appears not to be confined to the entity known as indeterminate leprosy.

Familial gigantic melanocytosis.

BACKGROUND: Familial gigantic melanocytosis (FGM) is a rare disorder first described in 1984 and termed "familial melanopathy with gigantic melanocytes". The cause of the disorder is still unknown. Melanocytes in both hyper- and hypopigmented skin seem to be unable to deliver melanin to the surrounding keratinocytes. OBJECTIVE: In this study, we report four new cases of FGM. Electron microscopic examination was performed in a trial to shed more light on the underlying defect in this disorder. PATIENTS AND METHODS: Patients were examined clinically and biopsies were taken from both hyperpigmented and hypopigmented areas, and divided into two parts; one part was processed for routine microscopic examination with hematoxylin and eosin and Masson Fontana stains. The other portion of the biopsy was fixed in glutraldhyde 3% and processed for electron microscopic (EM) examination. RESULTS: By light microscopy, the patients' skin showed areas of hyperpigmented basal cells alternating with poorly pigmented areas. Hair follicles in the scalp biopsies showed the same pathology. By EM, pigmented areas showed gigantic melanocytes and heavily pigmented keratinocytes. Nonpigmented areas showed poorly pigmented keratinocytes and fewer, but also gigantic melanocytes. CONCLUSIONS: The raindrop-like hypopigmentation in this disorder can be explained by a failure of melanocytes to deliver melanin to their surrounding keratinocytes. The cause of the presence of heavily pigmented keratinocytes in the hyperpigmented zones could not be determined. There is a strong possibility of a more widespread abnormality affecting not just the melanocytes.