Guillain-Barre Syndrome Linked to Hepatitis C Virus Infection

The development of Guillain-Barre syndrome (GBS) has demonstrated an association with existing hepatitis C virus (HCV) infection and mixed cryoglobulinemia, according to a case study published in BMC Infectious Diseases. The subtype severe acute motor sensory axonal neuropathy was classified as a subtype of GBS through electromyography, associated with severe clinical presentation. Researchers noted that only 7 other cases of GBS associated hepatitis C have previously been reported.

This case study focused on a 56-year-old man with a 28 year history of intravenous drug addiction, and chronic respiratory failure as a result of chronic obstructive pulmonary disease, who was admitted to the emergency department with complaints of areflexia and muscle weakness of all limbs. The patient also had an estimated 36 pack-year history of tobacco consumption, and at the time of admission to the hospital, he was receiving buprenorphine to treat his substance addiction. One year previous to admission, the patient was found to have positive immunoassay results for anti-HCV antibodies, HCV RNA viral load of 87 IU/mL, and significantly elevated liver enzymes. Four months prior to admission, chronicity of HCV infection was confirmed via a persistent, and further elevated viral load (25,200 U/mL).

On admission the patient had quadriplegia, decreased muscle tension and tendon areflexia in all limbs. Four days after admission, the patient was transferred to the intensive care unit because of acute respiratory failure, and was subsequently intubated. Blood gases showed severe hypoxemia and respiratory acidosis, chest x-ray did not demonstrate pneumonia, and cerebrospinal fluid samples did not indicate albuminocytologic dissociation. The physicians suspected GBS, and thus started treatment with intravenous immunoglobulins for 5 days, and a total of 5 plasma exchanges over 2 weeks. Eight days after admission, HCV RNA viral load increased to 1,710,000 IU/mL, and liver functions tests also demonstrated new increases. A cryoglobulin screening demonstrated type 3 mixed cryoglobulinemia. Electromyography demonstrated severe acute motor sensory axonal neuropathy with demyelinated lesions, consistent with GBS. The patient received 2 months of treatment with direct-acting antiviral agents. At day 27 of treatment, electromyography showed significant improvements, suggesting the patient’s recovery from GBS; 1 month after treatment, HCV viral load was undetectable and liver enzymes were normal. Three months after admission, the patient was discharged to a rehabilitation center and did not experience relapse.

One limitation to this study was a lack of a second cerebrospinal fluid sample, which would have aided the study researchers in demonstrating albuminocytologic dissociation.

Study researchers concluded that GBS warrants addition to the list of extrahepatic manifestations of hepatitis C. In addition, they purport hepatitis C virus as an additional cause of GBS. Moreover, researchers highlighted their successful classification of  the subtype of GBS (severe acute motor sensory axonal neuropathy) based on the characteristics of electromyography testing and correlated these to the clinical presentation. The study authors “thus observed that chronic active hepatitis C is a general disorder, which can lead to severe peripheral neuropathy requiring admission in [an intensive care unit] in absence of treatment.”

Reference

Chlilek A, Roger C, Muller L, et al. Severe Guillain-Barré syndrome associated with chronic active hepatitis C and mixed cryoglobulinemia: a case report. BMC Infect Dis. 2019;19:636.