Clinical presentation of tuberculoid leprosy in an epidermodysplasia verruciformis patient

Abstract

Epidermodysplasia verruciformis (EV) is triggered by a variety of mechanisms that at least partly include genetic background. We present a Brazilian man with a 30-year history of flat, wart-like lesions with clinical, histopathological, and evolutive aspects consistent with papillomavirus (HPV)-associated EV. Histological analysis of the wart lesions showed epidermis with hyperkeratosis, regular acanthosis, hypergranulosis, and cells with abundant basophilic cytoplasm. Moreover, a perivascular lymphocytic infiltrate was found in the superficial dermis, consistent with a viral wart. Type-2-HPV DNA was detected in various fragments of skin-wart lesions using the polymerase chain reaction (PCR). Two years after the EV diagnosis, the patient presented with an anesthetic well-demarcated, erythematous and mildly scaly plaque on his right forearm. A histopathological analysis of this lesion demonstrated the presence of a compact tuberculoid granuloma. ZiehlNeelsen staining demonstrated the presence of rare acid-fast bacilli and confirmed the tuberculoid leprosy diagnosis. The patient's Mitsuda Intradermal Reaction was positive. To elucidate the possible mechanism involved in this case of EV, we genotyped the HLA genes of this patient. DQB genotyping showed the polymorphic HLA alleles DQB1*0301 and 0501. The patient was treated with a paucibacillary multidrug therapy scheme, and the disease was cured in six months. This report describes an EV patient with an M. leprae infection, confirming that tuberculoid leprosy patients possess a relatively specific and efficient cell-mediated immunity against the bacillus and, therefore, localized forms of the disease. Moreover, we show the possible involvement of the polymorphic HLA alleles DQB1*0301 and 0501 in EV induction mechanisms.

Diagnosis of epidermodysplasia verruciformis: Two cases highlighting the role of direct HPV L1 gene sequencing

“…Acquired EV (aEV) is due to an immunodeficiency secondary to immunosuppressant medications following transplant, infection with HIV, or other diseases such as systemic lupus erythematous, tuberculoid leprosy and Hodgkin lymphoma . The underlying mechanism is believed to be similar to gEV: infected cells are not cleared by the immune system because of defective cell‐mediate immunity, leading first to disseminated hyperkeratotic lesions, and then transformation to SCC and other non‐melanoma skin cancer (NMSC).…”

“…The underlying mechanism is believed to be similar to gEV: infected cells are not cleared by the immune system because of defective cell‐mediate immunity, leading first to disseminated hyperkeratotic lesions, and then transformation to SCC and other non‐melanoma skin cancer (NMSC). Although the timing of infection and disease onset in acquired EV is variable after the onset of immunosuppression, approximately 92% of acquired EV patients develop lesions within 5 years . One study has suggested that immunosuppression regimens using azathioprine are potentially higher‐risk for EV‐development than other drug combinations .…”

Clinical, demographic, and epidemiologic characteristics of hepatitis B virus-infected patients at a tertiary public hospital in Presidente Prudente, State of São Paulo, Brazil

“…Few studies address the epidemiologic future of HBV infection in the general population, especially those living in small-and medium-sized cities. In these places, tertiary public hospitals have a crucial role in the Unifi ed Public Health System (SUS) for the diagnosis and treatment of infectious diseases including HIV, HBV, and HCV (5) . Our aim was to the determine the clinical, demographic, and epidemiologic characteristics of a cohort of patients diagnosed with HBV and followed up at an infectious diseases clinic of a public tertiary university hospital in the western region of State of São Paulo, Brazil.…”