Title : Association between tuberculosis and guillain-barre syndrome: A systematic review
Abstract:
Background: Guillain-Barré Syndrome (GBS) is an acute autoimmune polyneuropathy commonly preceded by infections. Although bacterial or viral infections are well-known contributors to GBS, little is known about TB as a potential trigger. In this systematic review, we seek to assess the association between TB and GBS, outgoing clinical patterns and recognise gaps in comprehension of the underlying mechanisms.
Methods: A systematic literature search was performed with PubMed, Google Scholar, Scopus, and Web of Science, Semantic Scholar databases, until December 2024, according to PRISMA guidelines. Studies were eligible if they were case reports, case series or review articles that included at least one patient diagnosed with TB and GBS, without limitations on age, sex, or geographic location. Demographics, TB characteristics, GBS subtype, time interval of TB to onset of GBS, treatment modality, and outcomes were extracted and analyzed. The Joanna Briggs Institute (JBI) Critical Appraisal Checklist was used to assess quality.
Results: A total of 29 TB-associated GBS cases were identified, with the highest prevalence in India (44.8%). The median age was 43.7 years with male predominance (72.4%). The common type of TB is pulmonary TB (62.1%), followed by meningeal TB (13.8%) and disseminated TB (10.3%). Acute motor axonal neuropathy (AMAN) and acute inflammatory demyelinating polyneuropathy (AIDP) both were the most frequent (20.7%) GBS subtypes, followed by acute motor-sensory axonal neuropathy (AMSAN) (17.2%) and Miller Fisher syndrome (3.4%). The temporal onset of GBS ranged within 2 weeks post-TB diagnosis was 60.7%. In the sub-analysis, AMAN was common in pulmonary TB (27.8%), and AIDP predominated in extra-pulmonary TB (36.4%). Neurological residual deficits were higher in extrapulmonary TB (27.3%) compared to pulmonary TB (22.2%). The majority were given anti tubercular treatment (100%), intravenous immunoglobulin (51.7%), steroids (31%), and plasmapheresis (10.3%). 58.6% attained complete recovery, and 24.1% had residual neurological deficits. Mortality was reported in 17.2% of cases, mostly attributable to sepsis and respiratory failure.
Conclusion: The first line of evidence was case reports and series indicating TB must be a possible trigger for GBS, with the majority of cases presented within 2 weeks of TB onset. There may be a potential immune-mediated link between tuberculosis and Guillain–Barré syndrome. Due to the heterogeneity in reported cases and increased mortality rates, timely identification and consistent management strategies are necessary.
