Rutkove S B, De Girolami U, Preston D C, Freeman R, Nardin R A, Gouras G K, Johns D R, Raynor E M
Department of Neurology, Beth Israel Hospital, Boston, MA 02215, USA.
Muscle Nerve. 1996 Jul;19(7):870-5. doi: 10.1002/(SICI)1097-4598(199607)19:7<870::AID-MUS9>3.0.CO;2-6.
Colchicine may induce a myoneuropathy in patients with renal insufficiency. To date, myotonia has not been described in this disorder. We recently studied 4 patients treated with routine doses of colchicine who, in the setting of renal insufficiency, developed a severe myoneuropathy characterized by prominent myotonic discharges on electromyography. In addition, 1 of the 4 patients had profound clinical myotonia. In the 3 patients in whom biopsies were performed, marked myopathic change with intracytoplasmic vacuolization was identified. All 4 patients improved rapidly with discontinuation of the medication. The patient in whom electrophysiologic studies were repeated had a complete resolution of the myotonic discharges. Colchicine myoneuropathy can present with prominent clinical and electrophysiologic myotonia that resolves completely with discontinuation of the medication.
秋水仙碱可能会在肾功能不全患者中诱发肌神经病变。迄今为止，尚未在这种病症中描述过肌强直。我们最近研究了4例接受常规剂量秋水仙碱治疗的患者，这些患者在肾功能不全的情况下出现了严重的肌神经病变，其特征是肌电图上有明显的肌强直放电。此外，4例患者中有1例有严重的临床肌强直。在进行活检的3例患者中，发现有明显的肌病性改变及胞浆内空泡形成。所有4例患者在停药后均迅速好转。重复进行电生理研究的患者，其肌强直放电完全消失。秋水仙碱肌神经病变可表现为明显的临床和电生理肌强直，停药后可完全缓解。
