ABSTRACT
A 63-year-old male experienced sudden diplopia after 9 weeks of administration of pegylated interferon (IFN) alpha-2b and ribavirin for chronic hepatitis C (CHC). Ophthalmologic examinations showed ptosis on the right upper lid and restricted right eye movement without any other neurological signs. A brain imaging study and repetitive nerve stimulation test indicated no abnormality. The acetylcholine receptor antibody titer and response to acetylcholinesterase inhibitors were negative, and the results of thyroid function tests were normal. The patient's ophthalmological symptoms improved rapidly 3 weeks after discontinuation of pegylated IFN alpha-2b and ribavirin. The ocular myasthenia associated with combination therapy of pegylated IFN alpha-2b and ribavirin for CHC is very rarely reported; therefore, we present this case with a review of the various eye complications of IFN therapy.
Subject(s)
Humans , Male , Middle Aged , Antiviral Agents/adverse effects , Drug Therapy, Combination , Hepatitis C, Chronic/complications , Interferon-alpha/adverse effects , Myasthenia Gravis/chemically induced , Polyethylene Glycols/adverse effects , Ribavirin/adverse effectsABSTRACT
Los inhibidores de 3-hidroxi-3 metil glutaril coenzima A reductasa (estatinas) son eficaces para el descenso de los nivelesde colesterol sérico y, consecuentemente, la prevención de la enfermedad isquémica cardíaca, cerebrovascular y vascularperiférica. Una de las principales limitaciones del uso de estas drogas es la aparición de sintomatología muscular como la elevación de la CK, mialgias, miositis o rabdomiolisis. La miastenia gravis (MG) es una enfermedad autoinmune caracterizada por la presencia de debilidad fluctuante de los músculos voluntarios. La enfermedad se desencadena por el ataque de anticuerpos dirigidos contra los receptores nicotínicosde acetilcolina (ACRA) localizados en la membrana del músculo a nivel de la unión neuromuscular. Existe un número interesante de fármacos que empeoran el curso de la enfermedad o que en algunos casos la "desenmascaran". Recientemente se publicaron casos de pacientes con MG que presentaron exacerbación de su enfermedad con laingesta de estatinas. Presentamos 11 pacientes que comenzaron con síntomas de MG luego de la toma de estas drogas. Seis recibieron atorvastatina (54.5%), tres simvastatina (27.3%) y dos rosuvastatina (18.2%).
3-hydroxi-3 metyl glutaryl coenzyme A reductase inhibitors, also known as statins, are effective in reducing plasmaticcholesterol and thus preventing cardiac, cerebral, and peripheral vascular ischemia. One of the main reasons that limit their use is the potential for muscular disorders, such as the increase of plasmatic CK, myalgia, myositis, and rhabdomyolysis. Myasthenia gravis (MG) is an autoimmune disease characterized by the presence of fluctuating voluntary muscle weakness. It is triggered by antibodies directed against nicotinic acetylcholine receptors (AChR) located at the neuromuscular junction, within the muscle membrane. A number of drugs may either unmask the disease or worsen it when installed. Recent publications have reported on cases of MG who aggravated their condition with the intake of statins. Here, we report on eleven patients who presented symptoms of MG after medication with statins. Six patients received atorvastatin (54.5%), three simvastatin (27.3%), and two rosuvastatin (18.2%).
Subject(s)
Male , Female , Acetylcholine/antagonists & inhibitors , Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Cholinesterase Inhibitors/therapeutic use , Myasthenia Gravis/etiology , Myasthenia Gravis/chemically induced , Recurrence , Neuromuscular DiseasesABSTRACT
Myasthenia gravis is one of the typical organ specific autoimmune disease and the CD5+ B-lymphocytes are known to be associated with the secretion of autoimmune antibodies. The authors performed the study to establish an animal model of experimental autoimmune myasthenia gravis (EAMG) by immunizing the nicotinic acetylcholine receptor (AChR) and to understand CD5+ B-lymphocyte changes in peripheral blood of EAMGs. Lewis rats weighing 150-200 g were injected subcutaneously three times with 50 microg AChR purified from the electric organ of Torpedo marmorata and Freund's adjuvant. The EAMG induction was assessed by evaluating clinical manifestations. The CD5+ B-lymphocyte was double stained using monoclonal PE conjugated anti-CD5+ and FITC conjugated anti-rat CD45R antibodies and calculated using a fluorescence-activated cell sorter (FACS). In three out of ten Lewis rats injected with purified AChR, the EAMG models were established. The animals showed definite clinical weakness responded to neostigmine; they had difficulty in climbing the slope, or easily fell down from a vertical cage. The range of CD5+ B-lymphocytes of peripheral blood in the EAMG models was 10.2%-17.5%, which was higher than in controls. In conclusion, the EAMG models were successfully established and the CD5+ B-lymphocyte expression in peripheral blood increased in EAMGs. This provided indirect evidence of the autoimmune pathomechanism of human myasthenia gravis.
Subject(s)
Rats , Animals , CD5 Antigens/immunology , B-Lymphocytes/immunology , Disease Models, Animal , Myasthenia Gravis/immunology , Myasthenia Gravis/chemically induced , Rats, Inbred LewABSTRACT
La asociación entre miastenia gravis y D-penicilamina ha sido reportada en pacientes que recibían esta droga por presentar artritis reumatoidea, enfermedad de Wilson, esclerodermia o cistinuria. El cuadro es indistingible, clínica y electrofisiológicamente, de la miastenia gravis de aparición espontánea; solo se puede diferenciar por la mejoría clínica y por la caída del título de anticuerpos antirreceptor colinérgico luego de la suspensión del tratamiento con D-penicilamina. El mecanismo de inducción de los anticuerpos antirreceptor colinérgico en esta enfermedad es desconocido. Reportamos una paciente de 55 años de edad que padece artritis reumatoidea, que a los doce meses de ser tratada con D-penicilamina, presentó un cuadro de ptosis palpabral bilateral, diplopía, disartría, disfagia y debilidad en los miembros superiores. Ante la sospecha de miastenia gravis se realizaron: prueba de tensilon (edrofonio), electromiograma con estimulación repetitiva y dosaje de anticuerpos antirreceptor colinérgico, que confirmaron este diagnóstico. Al poco tiempo de suspender la D-penicilamina, e iniciar el tratamiento con piridostigmina la paciente mejoró, no requiriendo más esta última medicación.
Subject(s)
Humans , Middle Aged , Female , Penicillamine/adverse effects , Myasthenia Gravis/chemically induced , Penicillamine/pharmacology , Arthritis, Rheumatoid/drug therapyABSTRACT
Trata-se de um relato de um caso onde a autora discute uma possível implicaçäo do carbonato de lítio como fator desencadeante de Miastenia Gravis. Foi realizado levantamento bibliográfico, encontrando relatos de caso e citaçöes que confirmam a associaçäo entre síndrome miastênica e carbonato de lítio. O lítio estaria envolvido no aumento da atividade dos linfócitos T, assim como na diminuiçäo da síntese e liberaçäo da acetilcolina na junçäo neuromuscular
Subject(s)
Middle Aged , Humans , Male , Lithium/adverse effects , Myasthenia Gravis/chemically inducedABSTRACT
Os autores relatam um caso de artrite reumatóide que desenvolveu miastenia gravis (MG) e polimiosite (PM) após uso de D-penicilamina. O diagnóstico de MG e PM associados foi baseado em achados eletroneurográficos, enzimas musculares elevadas e biópsia muscular. Os autores discutem a reduçäo dessas drogas pelo uso de diferentes drogas e a infreqüente associaçäo de duas entidades miopáticas numa mesma paciente