A Rare Cause of Neuropathy and Failure to Thrive in a Chronic Hepatitis C Patient

Abstract

Purpose: A 51-year-old African American gentleman with a history of Type 2 Diabetes and treatment naïve Hepatitis C presented with worsening thrombocytopenia, an involuntary weight loss, numbness and progressive weakness in both the upper and lower extremities. He also had difficulty ambulating with a recent onset of recurrent falls for the past 3 months and a failure to thrive. Pertinent laboratory evaluation revealed a platelet count of 80,000/mm3, a normal CPK, normal Vitamin D, B12, Folate, as well as cryoglobulin level. The patient was thought to have AIDS, but antibodies and viral loads were negative on multiple occasions. Malignancy was considered likely, but an MRI of the brain and spine, CT scan of the chest, abdomen and pelvis, and an upper and lower GI series were all negative. Urine evaluation revealed a protein of 29.0 mg/dl, but a Serum Protein Electrophoresis showed no M spike or light chains. CSF evaluation to rule out Guillian Barre revealed 190 mg/dL protein without evidence of cytoalbuminic dissociation. The patient's Hepatitis C levels was found to be over 100 million, and the patient did not have evidence of cirrhosis. EMG to evaluate the patient's numbness and weakness were consistent with diabetic peripheral neuropathy, but surprisingly revealed demyelination. The demyelination pattern on EMG revealed that the patient had Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) explaining his numbness and weakness. The patient's numbness and weakness responded well to corticosteroid and IV IgG treatment. Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) is a highly treatable, yet underdiagnosed acquired, immune mediated group of related polyneuropathies affecting the peripheral nerve myelin and spinal nerve roots. It runs a chronic course (usually >8 weeks) and is associated with inflammation with demyelination as a consistent feature. CIDP is also under-recognized in association with Hepatitis C and there are only a few cases reported in the literature. The majority of reported cases in the literature of CIDP occurred after PEG Interferon treatment of Hepatitis C. However, there is a paucity in the literature regarding Hepatitis C induced CIDP. Our case is one of the first to report CIDP development from Hepatitic C viremia. We also stress the importance of early recognition and treatment of CIDP. It is also essential to differentiate CIDP from sensory motor diabetic polyneuropathy, Hepatitis C induced neuropathy, and cryoglobulinema. Providers should have a higher suspicion for CIDP in Hepatitis C patients with disabling neuropathy and profound weakness.