A 15-year-old male was admitted with a two-week history of hypoxia and vomiting. During the last week, the patient developed jaundiced skin, mucous membranes, and urine collection.
She reported no pruritus or other symptoms.
Two months prior to admission, she had undergone aortic coarctation, with reactive hypertension after surgery, and was treated with labetalol (400 mg/day).
This intervention transfused four tapered units.
She did not take other drugs or consume toxic substances, nor did she mention other epidemiological risk factors.
On physical examination, only cutaneomucosa was highlighted.
On admission labetalol was suspended, an abdominal ultrasound showed no abnormalities and blood tests were performed with complete liver battery with the following results: total Bb: 12.9 mg / dl (0-1.37 BTT; 0-1.14 BPT).
Serology for HAV, HBV, HCV, EBV, CMV and ESR was negative, including HCV viral load.
Autoimmunity, ceruloplasmin, α1-antitrypsin and ferrokinetic studies were negative.
In the absence of another cause and considering the temporal correlation, the definitive diagnosis was acute drug-induced hepatitis secondary to labetalol.
During admission, the patient showed progressive improvement in liver analytical, with no data of coagulopathy or encephalopathy, and was asymptomatic at discharge.
Subsequently, she was followed up in the clinic, with complete normalization of liver tests at two months and repeatedly negative etiological study.
