RESUMO
Mycobacterium leprae (ML) infection causes nerve damage that often leads to permanent loss of cutaneous sensitivity and limb deformities, but understanding of the pathogenesis of leprous neuropathy that would lead to more effective treatments is incomplete. We studied reactional leprosy patients with (n = 9) and without (n = 8) acute neuritis. Nerve conduction studies over the course of the reactional episode showed the findings of demyelination in all patients with neuritis. Evaluation of patient sera revealed no correlation of the presence of antibodies against gangliosides and the clinical demyelination. In nerve biopsies of 3 patients with neuritis, we identified tumor necrosis factor (TNF), TNF receptors, and TNF-converting enzyme in Schwann cells (SCs) using immunofluorescence. To elucidate immunopathogenetic mechanisms, we performed experiments using a human SC line. ML induced transmembrane TNF and TNF receptor 1 expression in the SCs; TNF also induced interleukin (IL)- 6 and IL-8 production by the SCs; and ML induced IL-23 secretion, indicating involvement of this previously unrecognized factor in leprosy nerve damage. These data suggest that ML may contribute to TNF-mediated inflammation and focal demyelination by rendering SCs more sensitive to TNF within the nerves of patients with leprous neuropathy.
Assuntos
Citocinas/metabolismo , Doenças Desmielinizantes/complicações , Doenças Desmielinizantes/metabolismo , Hanseníase/complicações , Neurite (Inflamação)/complicações , Adulto , Idoso , Linhagem Celular Transformada , Citocinas/genética , Doenças Desmielinizantes/patologia , Estimulação Elétrica , Feminino , Expressão Gênica/efeitos dos fármacos , Expressão Gênica/fisiologia , Humanos , Masculino , Pessoa de Meia-Idade , Mycobacterium leprae/fisiologia , Proteínas do Tecido Nervoso/metabolismo , Condução Nervosa/fisiologia , Exame Neurológico , Tempo de Reação , Células de Schwann/efeitos dos fármacos , Células de Schwann/metabolismo , Fator de Necrose Tumoral alfa/farmacologia , Adulto JovemAssuntos
Humanos , Masculino , Adulto , Hanseníase/complicações , Neuritos/diagnóstico , Condução Nervosa , EletromiografiaAssuntos
Humanos , Adulto , Pessoa de Meia-Idade , Neuropatias Amiloides/diagnóstico , Eletromiografia , PolineuropatiasAssuntos
Humanos , Masculino , Feminino , Adulto , Eletromiografia , Neuropatias Amiloides , PolineuropatiasRESUMO
A 50 years old male with previous history of dilated cardiomyopathy was admitted to cardio-intensive unit with dyspnea, cough, ascites and lower limb edema ascending to the inguinal region. 2D-Ecocardiogram revealed large pericardial effusion, without signs of diastolic restriction. The patient underwent pericardial drainage, which rapidly recollected in the following day. Abdominal ultrasound showed fibrotic and reduced size liver and subsequent radionuclide scan demonstrated direct communication between peritoneal and pericardial spaces. With the resolution of ascites, pericardial effusion did not recur. Embryologic explanation of this rare condition is still elusive, but incomplete closure of diaphragmatic muscle and thoracic-abdominal communication may represent the model of this anatomic functional anomaly.
