A 38-year-old man was admitted to an outside hospital intensive care unit because of fever associated to gastrointestinal symptoms and progressive centripetal muscle weakness, rapidly evolving into flaccid tetraplegia, absent reflexes response, and paresthesias combined with dysphagia and dysphonia. Electroneuromyography showed a pattern diagnostic for demyelinating motor polyneuropathy with proximal and distal conduction blocks, consistent with GBS. Cerebral spinal fluid exam and tests for anti-gangliosides antibodies were not performed. Corticosteroids and intravenous human immunoglobulins at the dose of 2 g/kg were administered, followed by physiotherapy for the next 2 months.

During rehabilitation, a mild aspartate aminotransferase (AST) and alanine aminotransferase (ALT) elevation was observed; AST and ALT levels progressively and constantly increased (13.8 × upper normal limit (UNL) and 16.2 × UNL, respectively) while HBsAg and anti-HCV antibodies were negative.

Within the next 6 days, liver enzymes almost doubled (AST 23.8 × UNL, ALT 34.3 × UNL, γ-glutamyl transferase 3.6 × UNL), ferritin peaked at 3024 mg/dl, while C-reactive protein, procalcitonin, white blood cells, red blood cells, platelets, and kidney function tests remained normal.

The patient was referred to our unit for further investigation. He complained of severe weakness, difficulty to stand up, and a slowed gait. He denied assumption of foods, drugs, or teas known to be hepatotoxic. Clinical examination showed mild hepatomegaly, a residual lower limb weakness, and finger tips dysesthesia, while there was a complete recovery of dysphagia, dysphonia, and reflexes response. Reported comorbidities included a treated Hashimoto’s thyroiditis and Gilbert’s disease.

Because of the possible accidental job-related exposure to materials contaminated with biologic samples, we analyzed all available tests the patient did in the previous years: HBsAg and anti-HCV antibodies resulted absent until 7 weeks before GBS onset.

A detailed work-up for diagnosis of acute and chronic hepatitis was performed: tests for hepatis viruses type A, B, C, D, E; HAV, HCV, HBV, HEV, cytomegalovirus, Epstein-Barr virus, herpes simplex virus 1 and 2; autoimmune liver markers (anti-mitochondrial antibodies, antinucleous antibodies, liver-kidney microsomal antibodies type 1, anti-smooth muscle antibodies, anti-neutrophil cytoplasma antibodies, cryoglobulins), α-ceruloplasmin, α-1-antitripsin, iron status assessment. Among these, only HAV IgG and anti-HCV antibodies were positive.

HCV-RNA level was 1.06 × 107 IU/ml, HCV genotype 3a, while ALT peaked at 46.8 × UNL and AST at 28.8 × UNL, remaining persistently elevated. Bilirubin, mainly indirect, was slightly elevated and other liver function tests were normal.

Liver ultrasound was normal and liver elastography reported a stiffness of 6.9 kPa (fibrosis stage 1).

Antiviral therapy with sofosbuvir/velpatasvir (400/100 mg/day for 12 weeks) was started, with rapid drop of ALT and AST; after 1 month of treatment, AST and ALT were normal and serum HCV RNA became undetectable. HCV RNA remained undetectable during the 24 weeks following the end of treatment, showing a sustained viral response (SVR 24) (Fig. 1).

Clinical course of HCV infection over time

Patient gave his written informed consent to the processing and publication of his clinical data.