[Chloroquine-induced myopathy and neuropathy: progressive tetraparesis with areflexia that simulates a polyradiculoneuropathy. Two case reports]. / Miopatía y neuropatía inducida por cloroquina: tetraparesia progresiva con arreflexia que simula una polirradiculoneuropatía. A propósito de dos casos.

INTRODUCTION: Chloroquine is a drug that is widely used in rheumatology and occasionally prescribed in dermatology. From a neurotoxicological point of view, chloroquine can have effects on the peripheral nerves, muscles, neuromuscular junctions and the central nervous system. In this study we analyse the clinical, neurophysiological and anatomopathological findings in two patients with chloroquine induced neuromyopathy, which took the form of a polyradiculoneuropathy. CASE REPORTS: Case 1: a 75 year old female with rheumatoid arthritis treated with daily doses of 250 mg of chloroquine for four years. The patient visited because of several months history of predominantly proximal progressive tetraparesis with areflexia. Analytical tests and lumbar puncture were normal. Electromyogram (EMG): proximal myopathic and distal neuropathic patterns. Muscular biopsy: vacuolar myopathy with accumulations of phagolysosomes, lipids, lipofuscin, myelinic curvilinear bodies. Case 2: a 74 year old female with arthropathy treated with daily doses of 250 mg of chloroquine for nine months. The patient presented a progressive proximal paraparesis with generalised areflexia. Analytical tests and lumbar puncture were normal. EMG: mixed sensory motor polyneuropathy, myogenic pattern with high frequency discharges in the iliac psoas and a neurogenic pattern in the distal muscles. Muscular biopsy: vacuolar myopathy suggesting a myopathy due to chloroquine. After stopping treatment with this drug the patients progressed favourably. CONCLUSION: Chloroquine can induce a clinical pattern that suggests a polyradiculoneuropathy. It is important to establish a history of having taken this drug. If this is indeed the case, then an electromyographic study of the most proximal muscles should be performed in order to detect a myogenic pattern and the same exploration should be applied to the distal muscles to reveal a neurogenic pattern. The final diagnosis will be established by muscular biopsy.

Miopatía y neuropatía inducida por cloroquina: tetraparesia progresiva con arreflexia que simula una polirradiculoneuropatía. A propósito de dos casos / Chloroquine-induced myopathy and neuropathy: progressive tetraparesis with areflexia that simulates a polyradiculoneuropathy. Two case reports

Introducción. La cloroquina es un fármaco ampliamente utilizado en reumatología y, ocasionalmente, en dermatología. Desde el punto de vista neurotoxicológico, la cloroquina puede afectar a los nervios periféricos, a los músculos, a la unión neuromuscular y al sistema nervioso central. En el presente trabajo se analizan los hallazgos clínicos, neurofisiológicos y anatomopatológicos de dos pacientes con una neuromiopatía inducida por cloroquina, que se manifestaron como una polirradiculoneuropatía. Casos clínicos. Caso 1. Mujer de 75 años con artritis reumatoide tratada con cloroquina 250 mg/día durante cuatro años. Consultó por tetraparesia progresiva de predominio proximal de meses de evolución con arreflexia. Las pruebas analíticas y la punción lumbar fueron normales. Electromiograma (EMG): patrones miopáticos proximales y neuropáticos distales. Biopsia muscular: miopatía vacuolar con acúmulo de fagolisosomas, lípidos, lipofucsina, cuerpos mielínicos y curvilíneos. Caso 2. Mujer de 74 años con artropatía tratada con cloroquina 250 mg/día durante nueve meses. Presentó una paraparesia proximal progresiva con arreflexia universal. Las pruebas analíticas y la punción lumbar fueron normales. EMG: polineuropatia mixta sensitivomotora, patrón miógeno con descargas de alta frecuencia en psoas ilíaco y patrón neurógeno en los músculos distales. Biopsia muscular: miopatía vacuolar sugestiva de miopatía por cloroquina. Tras la retirada de la medicación presentaron una evolución favorable de la clínica. Conclusión. La cloroquina puede inducir un cuadro clínico sugestivo de polirradiculoneuropatía. Es importante interrogar sobre el antecedente de ingesta del fármaco. En caso positivo tiene interés el estudio electromiográfico de los músculos más proximales para detectar patrón miógeno y de los músculos distales para evidenciar patrón neurógeno. La biopsia muscular establecerá el diagnóstico definitivo (AU)

Chloroquine is a drug that is widely used in rheumatology and occasionally prescribed in dermatology. From a neurotoxicological point of view, chloroquine can have effects on the peripheral nerves, muscles, neuromuscular junctions and the central nervous system. In this study we analyse the clinical, neurophysiological and anatomopathological findings in two patients with chloroquine-induced neuromyopathy, which took the form of a polyradiculoneuropathy. Case reports. Case 1: a 75-year-old female with rheumatoid arthritis treated with daily doses of 250 mg of chloroquine for four years. The patient visited because of several months’ history of predominantly proximal progressive tetraparesis with areflexia. Analytical tests and lumbar puncture were normal. Electromyogram (EMG): proximal myopathic and distal neuropathic patterns. Muscular biopsy: vacuolar myopathy with accumulations of phagolysosomes, lipids, lipofuscin, myelinic curvilinear bodies. Case 2: a 74-year-old female with arthropathy treated with daily doses of 250 mg of chloroquine for nine months. The patient presented a progressive proximal paraparesis with generalised areflexia. Analytical tests and lumbar puncture were normal. EMG: mixed sensory-motor polyneuropathy, myogenic pattern with high frequency discharges in the iliac psoas and a neurogenic pattern in the distal muscles. Muscular biopsy: vacuolar myopathy suggesting a myopathy due to chloroquine. After stopping treatment with this drug the patients progressed favourably. Conclusion. Chloroquine can induce a clinical pattern that suggests a polyradiculoneuropathy. It is important to establish a history of having taken this drug. If this is indeed the case, then an electromyographic study of the most proximal muscles should be performed in order to detect a myogenic pattern and the same exploration should be applied to the distal muscles to reveal a neurogenic pattern. The final diagnosis will be established by muscular biopsy (AU)