Guillain Barré syndrome precipitated by the use of antilymphocyte globulin in the treatment of severe aplastic anaemia

• Published in: Journal of clinical pathology Vol. 58; no. 9; pp. 994 - 995
• Main Authors: Kaya, B, Davies, C E, Oakervee, H E, Silver, N C, Gawler, J, Cavenagh, J D
• Format: Journal Article
• Language: English
• Published: London BMJ Publishing Group Ltd and Association of Clinical Pathologists 01-09-2005; BMJ; BMJ Publishing Group LTD; Copyright 2005 Journal of Clinical Pathology
• Subjects: ALG; Anemia, Aplastic - therapy; antilymphocyte globulin; Antilymphocyte Serum - adverse effects; aplastic anaemia; Autoimmune Diseases - chemically induced; Biological and medical sciences; Case Reports; Female; GBS; Guillain Barré syndrome; Guillain-Barre Syndrome - chemically induced; haemoglobin; Humans; Immunosuppressive Agents - adverse effects; intravenous immunoglobulin; Investigative techniques, diagnostic techniques (general aspects); IVIg; Medical sciences; Middle Aged; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis; Neurology; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques; WCC; white cell count; Nervous system diseases; Anatomic pathology; Treatment; Antilymphocyte globulin; Bone marrow failure; Use; Aplastic anemia; Hemopathy; Peripheral nerve disease; Severe; Guillain Barré syndrome; Inflammatory disease
• ISSN: 0021-9746; 1472-4146
• DOI: 10.1136/jcp.2004.020354

This report describes the case of a 54 year old woman with very severe aplastic anaemia who was treated with antilymphocyte globulin (ALG) and developed Guillain Barré syndrome (GBS). No antecedent infective aetiology was identified. Although there are numerous reports of autoimmune disease after treatment with ALG in aplastic anaemia, and GBS after immunosuppressive treatment, there are none reporting GBS after the use of ALG for severe aplastic anaemia. The occurrence of autoimmune disease after immunosuppressive treatment, in particular ALG, is discussed, together with the possible mechanisms that result from T cell depression.