A 57-year-old male with no interest history of smoking 10-20 cigarettes/day.
The patient had chronic hepatitis C genotype 1a/1c, viral load 1,662,178 Ul/ml and a grade of fibrosis F2-F3 (Fibroscan 9.9 Kilopascales) with a polymorphism
It was decided to start her first treatment for hepatitis C with RBV 400mg/12h, P-INF alpha 2a 180mcg/week and Telaprevir 750mg/8h (in meals).
At the beginning of treatment the patient had a hemoglobin (Hb) of 157 g/L, neutrophil count 4.2x109 no/L and 1 58x109 no/L platelets.
Liver enzymes were slightly increased, GPT 114 IU/L, ALAT 115 IU/L and ASAT 80 IU/L.
At week 4, the patient had an undetectable viral load, Hb of 136 g/L, neutrophil count 2.0 x 109 no/L and platelets 110 x 109 no/L. She reported mild anal pruritus anorectal hemoazepam, specifically improved
At week 8 of treatment, the patient was admitted to the hospital due to epigastric pain, which became more intense and resolved to both hypochondria during the last 36h.
He had no fever, chills, nausea, vomiting or choluria.
Laboratory tests showed an amylase of 1888 IU/L, Hb 107 g/L, neutrophil count 2.7 x 109 no/L and platelets 97x109 no/L. Analgesic diet was administered.
The patient was discharged home after 1 week with an amylase of 173 IU/L.
The next day she was admitted again due to severe epigastric pain radiating to both hypochondria and an amylase of 3406UI/L. Acute pancreatitis was diagnosed.
Given the relapsing course (two admissions), Telaprevir was discontinued (week 9 of treatment) due to the possibility that it was the cause and continued with RBV and P-INF.
The patient was discharged five days later with an amylase of 365 IU/L.
At week 12 after initiation of treatment, viral load was undetectable, Hb 109 g/L, neutrophil count 1.1 x109 no/L and platelet count 1 58x109 no/L.
