Development of myasthenia gravis after interferon alpha therapy

Electromyogr Clin Neurophysiol. 1999 Mar;39(2):75-8.

Abstract

Interferon (IFN) alpha is now used in the treatment of some malignant diseases and chronic viral hepatitis. There have been several reports of development of autoantibodies and autoimmune diseases or the deterioration of preexisting disorders in patients under treatment. We enclose a case of myasthenia gravis (MG) which developed after six weeks of treatment as fluctuating bilateral ptosis, intermittent diplopia, and mild weakness of limb and neck muscles. A test dose of edrophonium chloride was administered, resulting in improved muscle strength. Elevated anti acetylcholine receptor (AChR) antibody titer was found. Single fiber electromyography showed an increased jitter from extensor digitorum communis, frequently accompanied by transmission blocking. Repetitive electric 3 Hz stimulation of the abductor pollicis brevis muscle, revealed an abnormal decrement of 28% in compound motor action potential. Myasthenia gravis was diagnosed and the patient was given pyridostigmine, immunoglobulines and prednisone with benefit. Six months latter he developed an acute myasthenic crisis with severe respiratory failure and high anti AChR antibody titer. IFN-alpha can induce MG or simply manifests a preexisting subclinical disease, but otherwise its therapeutic efficacy in MG has been shown in experimental and clinical studies. Autoimmune mechanisms, as the release of different cytokines as IFN, by immunocompetent cells, may be involved in the pathogenesis of both MG and chronic active hepatitis. Autoantibody production against postsynaptic membrane structures by IFN-alpha could be the underlying pathophysiology.

Publication types

  • Case Reports

MeSH terms

  • Aged
  • Electromyography
  • Hepatitis C / complications
  • Hepatitis C / therapy*
  • Humans
  • Interferon-alpha / adverse effects*
  • Interferon-alpha / therapeutic use
  • Male
  • Muscles / physiopathology
  • Myasthenia Gravis / etiology*
  • Myasthenia Gravis / physiopathology
  • Neural Conduction / physiology

Substances

  • Interferon-alpha