Association of Peripheral Neuropathy in Hepatitis C Infection with and without Cryoglobulineamia

Abstract

Objective: The purpose of this study was to find out the association of peripheral neuropathy in hepatitis C infection with and without cryoglobulineamia. Study Design: Cross sectional study Place and Duration: Conducted in Liver Transplant Unit, Gambat Institute of Medical Sciences, Gambat Khairpur Mirs, Sindh for the duration of six months from November 2020 to April 2021. Methods: Total 50 patients who had hepatitis C infection and peripheral neuropathy were included in this study. Patients were aged between 18- 60 years. Detailed demographics of patients including age, sex and body mass index were recorded after taking informed written consent. When symptoms and evidence of peripheral sensory or motor involvement were evident, clinical neuropathy was diagnosed. Sural nerve biopsy was done on patients and the biopsy specimen was evaluated morphologically and morphometrically. Multiple neuropathy, cranial neuropathy, and polyneuropathy are all terms used to describe peripheral nerve involvement. Our research focused on the motor conduction of the median, ulnar, and common peroneal nerves, measuring MCV, CMAP amplitude, and distal latency (DL) in both patients with and without cryoglobulinaemia for each nerve. The SPSS 20.0 version was used to analyze the data. Results: Mean age of the patients was 46.23±9.87 years with mean BMI 29.16±11.27 kg/m2. There were 30 (60%) females and 20 (40%) were males. We found that 35 (70%) patients had CG involvement with peripheral neuropathy and 15 (30%) cases were without CG. Prevalence of polyneuropathy was higher 19 (54.3%) in CG patients as compared to non CG 2 (13.3%). Mononeuropathy or multiple neuropathy was higher in HCV CG patients 13 (37.1%) as compared to HCV non CG patients 4 (26.7%). 25 patients underwent nerve biopsy (20 CG patients and 5 non CG). Prevalence of epineurial vasculitis and fascicular loss of axons was higher in non CG patients while demyelination + axonal degeneration were prevalent in CG patients. MCV of the deep peroneal nerve in patients with CG+ was low as compared to CG. Even though no statistically significant differences were detected, the other neurophysiological measures pointed to a more extensive and severe involvement of peripheral nerve in CG+ patients. Conclusion: We concluded in this study that the association of peripheral neuropathy in HCV patients with cryoglobulinaemia was greater as compared to non-CG HCV patients. It appears that both CG+ and CG patients suffer from peripheral nerve injury via a vasculitic mechanism, as evidenced by clinical and morphological observations. Serum CG levels indicate a more severe and broad neuropathic involvement, however research suggests that cryoglobulins are not the only element in the vasculitic process. Keywords: Cryoglobulinemia, Peripheral Neuropathy, HCV