Male patient with a history of type 2 diabetes mellitus and chronic alcohol consumption.
Diagnosis of cirrhosis in 2002 at 48 years.
In 2004, PCR for HCV was positive, with a viral load of 280,998 IU/ml (Log 5.45) and genotype 3a.
She was not treated.
She was admitted to our hospital in 2005 due to the presence of two lesions compatible with hepatocellular carcinoma.
Chemoembolization was performed in October 2005, with multiple chemoembolizations and alcohol until July 2006, when episodes were resolved.
After transplantation immunosuppression with prednisone and cyclosporine was started.
At 5 months post-transplantation, transaminase levels increased to 12 times the normal value, rejection vs HCV reactivation was proposed.
Sirolimus was added.
Liver biopsy showed steatosis and mild acute hepatitis, with no elements of specificity.
Viral load 3,000,694 IU/ml (Log 6,48).
Transaminases remained 1.5 to 3 times the normal value.
Due to pancit was discontinued sirolimus.
At 3 and a half years post-transplantation, HCV treatment is proposed again with a new liver biopsy showing chronic hepatitis with mild portal inflammation of the lobular and interphase, focal perisinusoidal fibrosis, and cholangitis.
At this time, the patient develops cholestasis, which is secondary to stenosis of the biliary anastomosis.
A new viral load was controlled with 355,882 IU/ml (Log 5.55) in October 2010.
With the intention of initiating treatment in March 2011, a new viral load was requested which was negative; in addition, PCR for HCV was performed, also negative, which was confirmed with a new sample.
At this time, the liver profile was normal, receiving immunosuppression with cyclosporine 100 mg daily.
It was interpreted as spontaneous elimination of HCV.
