m+Medelevator.RU
← Поиск публикаций
Cureus · 2026

Necrotizing Myopathy Presenting With Guillain-Barré-Like Areflexic Paraparesis, Severe Rhabdomyolysis, and Dialysis-Requiring Acute Kidney Injury.

Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

История · было → стало

Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.

Baghdasaryan Eric J, Soltani Hasti, Lada Sari, Simpson Chelsea, Nathan Ramesh

Аннотация

Necrotizing myopathy typically presents with subacute symmetric proximal weakness and marked creatine kinase elevation. Acute areflexic paraparesis with sensory abnormalities may instead suggest Guillain-Barré syndrome and create uncertainty regarding neuromuscular localization. A man in his 50s presented after collapse with abrupt bilateral lower-extremity paralysis. Examination demonstrated 0/5 strength across proximal and distal lower-extremity muscle groups, marked rigidity and hypercontracture, areflexia, and sensory impairment, with preserved upper-extremity function. Early laboratory abnormalities included serum sodium 164 mmol/L, potassium peaking at 6.5 mmol/L, creatinine 4.96 mg/dL, blood urea nitrogen 194 mg/dL, creatine kinase greater than 60,000 IU/L, and marked aminotransferase elevations. Lumbar puncture on hospital day (HD) 3 showed cerebrospinal fluid protein 70 mg/dL, glucose 66 mg/dL, and fewer than one nucleated cell/mm3. Guillain-Barré syndrome remained an early consideration; intravenous immunoglobulin was administered, and hemodialysis was initiated for severe hyperkalemia in the setting of acute renal failure. Inpatient electromyography and nerve conduction studies were unavailable; therefore, a concurrent neuropathic process could neither be confirmed nor excluded. Bilateral thigh magnetic resonance imaging demonstrated diffuse intramuscular edema, and right-thigh biopsy subsequently established a necrotizing myopathic pattern with frequent necrotic and regenerating myofibers and sparse inflammation. The biopsy pattern was etiologically nonspecific, and the underlying cause remained unresolved. This case illustrates that areflexia and cerebrospinal fluid albuminocytologic dissociation should not override substantial biochemical, radiographic, and histopathologic evidence of muscle injury. In patients with acute paralysis and massive creatine kinase elevation, neuropathic and myopathic processes should be evaluated in parallel.

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

Реквизиты и контакты