Acute hepatitis associated with use of paroxetine

Abstract

Paroxetine belongs to the family of selective serotonin reuptake inhibitors; these antidepressant drugs are becoming widely used because of their favourable side effects and safety profile. Hepatotoxicity due to paroxetine is very rare, and, to the best of our knowledge, only a few cases of severe liver injury following paroxetine administration have been reported in the medical literature. All of these cases showed a favourable prognosis after drug discontinuation [1-3]. We report here a new case of severe liver injury associated with paroxetine intake.An 84-year-old woman was admitted to our department because of mental confusion, hyporexia, nausea and vomiting. The symptoms had begun 3 days before hospitalization and after the first administration of paroxetine 10 mg/day prescribed for chronic mild depression. The patient was affected by chronic atrial fibrillation, arterial hypertension and brain atherosclerosis with two previous episodes of transitory ischemic attacks, and was treated with verapamil 80 mg/day, ticlopidine 500 mg/day, spironolactone 25 mg/day and nimodipine 60 mg/day. One week before the hospitalization, the patiente was submitted to clinical evaluation and laboratory tests during a routine periodic medical check-up. Apart from cardiac arrhythmia related to atrial fibrillation, the physical examination was normal and the mental status was good. The serum level of common biochemical markers was normal (aspartate aminotransferase (ALT) 13 IU/L, alanine aminotransferase (ALT) 17 IU/L, total bilirubin 1.03 mg/dL, alkaline phosphatase (AP) 180 IU/L, urea nitrogen 31.4 mg/dL, creatinine 1.13 mg/dL, sodium 139 mEq/L, potassium 4.8 mEq/L, hemoglobin (Hb) 14.5 g/dL, white blood cell count (WBC) 8.80 9 10 9 /L, platelet count 176 9 10 9 /L). On admission, laboratory blood tests revealed abnormal serum transaminase levels (AST 186 IU/L, ALT 245 IU/L, normal values 7-45 IU/L) associated with mild hyperbilirubinemia (1.5 mg/dL) and mild renal failure (urea nitrogen 34 mg/dL, creatinine 1.2 mg/dL, sodium 132 mEq/L, potassium 5.0 mEq/L). The hematologic parameters were in the normal range apart from a mild increase of WBC (12.30 9 10 9 /L) without eosinophilia (eosinophils 0.1%). The paroxetine intake was immediately discontinued, while the remaining therapy was confirmed. One day after, a marked increase of serum transaminase level was found (AST 2,208 IU/L, ALT 2,110 IU/L) along with normal levels of alkaline phosphatase (277 IU/L, normal values 98-279 IU/L), and mild increase of gamma-glutamyltransferase (175 IU/l, normal values 5-36 IU/L) and total bilirubin (2.5 mg/dL, normal values 0.3-1.2 mg/dL) and was associated with hematochemical signs of liver function failure [increased prothrombin time with international normalized ratio (INR) of 2.13 and hyperammonia (335 gamma/dL, normal values 31-123 gamma/dL)] and clinical signs of hepatic encephalopathy stage I (bilateral asterixis, confusion, lethargy). A Doppler ultrasound study of the abdomen was performed and showed normal findings at the level of the...

Paroxetine Induced Toxic Hepatitis: Case Report

“…Clinical and laboratory improvement was observed in all of cases after the cessation of the drug. [3][4][5][6][7][8][9][10] Here we report a case who was treated with paroxetine because of depressive symptoms and developed a severe hepatocellular toxic hepatitis, which completely recovered after the cessation of the drug.…”