Citrate-Induced impairment of neuromuscular transmission in human and experimental autoimmune myasthenia gravis

✍ Scribed by I. Wirguin; T. Brenner; E. Shinar; Z. Argov

• Publisher: John Wiley and Sons
• Year: 1990
• Tongue: English
• Weight: 302 KB
• Volume: 27
• Category: Article
• ISSN: 0364-5134
• DOI: 10.1002/ana.410270316

✦ Synopsis

Two patients who underwent plamsapheresis for severe myasthenia gravis showed marked exacerbation of myasthenic weakness at the end of exchange sessions, in which citrate was used for anticoagulation. In one pa- tient, improvement occurred after the administration of calcium but not after edrophonium. In rabbits and in rats with experimental autoimmune myasthenia gravis, decremental muscle response to 3 Hz repetitive nerve stimulation worsened significantly after injection of the citrate anticoagulant. T h e worsened neuromuscular transmission defect was reversed by the administration of calcium. When used for anticoagulation, citrate reduces serum ionized calcium levels and thus may aggravate myasthenic weakness and endanger patients during or immediately after plasmapheresis.

Wirguin I, Brenner T, Shinar E, Argov Z.

Citrate

-induced impairment of neuromuscular transmission in human and experimental autoimmune myasthenia gravis. Ann Neurol 1990;27:328-3 30 ~ Plasmapheresis in myasthenia gravis (MG) is usually reserved for severely affected patients during disease relapses, during initiation of immunosuppressive therapy, and following thymectomy and other major surgical procedures 111. In 8 to 15% of treatment sessions, citrate-induced reduction in serum ionized calcium [Ca2+] occurs 12-41. This mild side effect usually causes only nausea and paresthesias. We encountered two patients with MG who showed severe transient exacerbation of muscle weakness during plasmapheresis. T h e features of these episodes suggested that the worsening was caused by reduced CCa2+1. We evalu-From the Departments of