Vol. 10 Issue 2 April - June / 2012
Published on website | Date : 2016-04-04 21:29:45
ANTIPHOSPHOLIPID ANTIBODY IN SERUM OF GUILLAIN-BARRE SYNDROME PATIENTS
Temeem M Al-Temeemi, Ahmed S Al-Naaimi, Hasan A Al-Hamadani, Estabraq A Al-Wasiti
Background:Studies have provided convincing evidence that Guillain-Barre syndrome [GBS] is caused by an infection-induced aberrant immune response that damages peripheral nerves. Despite intensive research over the past two decades, the immune target is still unknown in patients with acute inflammatory demyelinating polyradiculoneuropathy [AIDP], the most frequent variant of GBS.
Objective:Measuring of immunoglobulin G [IgG] and immunoglobulin M [IgM] antiphospholipid antibodies [aPL] of incidental untreated GBS patients and comparing them with that of normal population.
Methods:This is an age and gender matched paired case-control study at Al-Kadhimiya Teaching Hospital between 1-Dec-2008 and 31-Jan-2010. Each patient was paired with the age and sex matched control which was useful in controlling the confounding effect of age and gender on possible case-control differences. The aPL were measured by Immunometric Enzyme Immunoassay.
Results:Eleven patients with GBS (cases) and eleven age and gender matched controls included in current study. The GBS cases have higher IgM and IgGaPL titers than healthy controls [P=0.026, P=0.13 respectively]. The GBS cases IgMaPL titers have negative correlation with duration of illness [r=-0.494, P=0.12], while the cases IgGaPL titer have positive correlation with duration of illness [r=0.243, P=0.47]. The GBS cases that need mechanical ventilation have lower IgM and IgGaPL titers than cases that do not need mechanical ventilation [P=0.1, P=0.06 respectively].
Conclusion: GBS cases have statistically significant higher IgMaPL titers during the first week [p=0.028] and the first two weeks [p=0.026]of illness than healthy controls, and aPL may have a protective effect in GBS.
Keywords: Guillain-Barre syndrome, Demyelination, Antiphospholipid antibodies and autoantibodies.
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