A 52-year-old woman with hepatitis C virus infection, genotype 1b, with a high viral load (> 5 E5 IU/ml) came to the clinic complaining of asthenia and the appearance of skin lesions on the chest and face that bled, which spontaneously disappeared after compression. Physical examination revealed slight splenomegaly and the presence of spiders in the nasal region and chest. Laboratory tests showed GOT 108 U/l, GPT 113 U/l, GGT 131 U/l, alkaline phosphatase 116 U/l, total bilirubin 2.3 mg/dl, albumin 3.5 g/dl, prothrombin activity 75%, leukocytes 6,890, haemoglobin 10 g/dl, platelets 132,000, Ig G 1970, Ig M 162, ANA 1/40. Abdominal ultrasound: heteroechoic liver, irregular surface with hypertrophy of the caudate lobe. Permeable portal 10 mm. Spleen 14 cm. Upper gastrointestinal endoscopy: no oesophageal or gastric varices; no signs of portal hypertension gastropathy.
Treatment was started with combination therapy with PegINF alfa 2a 180 mg/weekly sc. and ribavirin 1,000 mg/day, discontinued after 12 weeks due to lack of response.
During follow-up, the patient reported worsening asthenia and dyspnoea on moderate exertion. Suspicion of hepatopulmonary syndrome led to arterial blood gases and spirometry: FEV1 105.9%, FVC 101.8%, FEV1/FVC 87.52 and a sonicated contrast echocardiogram which showed the passage of serum from the right atrium to the left suggesting cardiac shunt. These findings established the diagnosis of hepatopulmonary syndrome (4).
The patient presented with new episodes of bleeding from spider veins located in the thorax that did not respond to cauterisation, requiring surgical excision on two occasions. Treatment was started with tamoxifen, which reduced the bleeding episodes, and three weeks after starting treatment there were no new bleeding episodes and the number of lesions had stabilised.