Myasthenia gravis and amyotrophic lateral sclerosis: A pathogenic overlap.
The aim was to examine potential joint disease mechanisms for myasthenia gravis (MG) and amyotrophic lateral sclerosis (ALS) through the examination of long-term patient cohorts for comorbidity. Recent studies support early involvement of the neuromuscular junction in ALS patients with subsequent degeneration of motor neurons. Medical records at Haukeland University Hospital from 1987 to 2012 were examined for International Classification of Diseases diagnostic codes for MG and ALS. Sera were re-tested for antibodies to acetylcholine receptor, titin, MuSK and GM1. We report one patient with both MG and ALS, and another 3 patients with suggestive evidence of both conditions. This is far more than expected from prevalence and incidence figures in this area if the disorders were unrelated. Our data suggest that immunological mechanisms in the neuromuscular junction are relevant in ALS pathogenesis. Attention should be given to possible therapeutic targets in the neuromuscular junction and muscle in ALS patients.
Department of Clinical Medicine, University of Bergen, Bergen, Norway; Department of Oncology, Oslo University Hospital, Oslo, Norway.
Håvard Torvik
HT
Gotaas
Department of Clinical Medicine, University of Bergen, Bergen, Norway; Department of Neurology, Haukeland University Hospital, Bergen, Norway.
Geir Olve
GO
Skeie
Department of Clinical Medicine, University of Bergen, Bergen, Norway; Department of Neurology, Haukeland University Hospital, Bergen, Norway. Electronic address: nils.erik.gilhus@helse-bergen.no.
Nils Erik
NE
Gilhus
D000328:Adult; D000368:Aged; D000690:Amyotrophic Lateral Sclerosis / Q000097:blood / Q000150:complications* / Q000276:immunology* / Q000628:therapy; D015897:Comorbidity; D017809:Fatal Outcome; D005260:Female; D006801:Humans; D008297:Male; D009157:Myasthenia Gravis / Q000097:blood / Q000150:complications* / Q000276:immunology* / Q000628:therapy
Acetylcholine receptor antibodies; Amyotrophic lateral sclerosis; Immunological mechanisms; Myasthenia gravis; Neuromuscular junction