Clinical expression of 'silent' hepatitis B virus infection in a patient with visceral leishmaniasis

A 69-year-old male was hospitalized in January 1999 because of visceral Lei shmaniasis, He had also suffered from anti-hepatitis C virus (HCV)-positive chronic hepatitis for years. ALL serum hepatitis B virus (HBV) antigens an d antibodies were negative except for anti-HBc, The patient was treated wit h amphotericin B cholesteryl sulfate (2 mg/kg twice a day for 7 days, iv). Fever disappeared on the 3rd day of treatment, the clinical condition impro ved rapidly and the patient recovered, In May 1999 the patient developed icteric HBsAg-negative acute hepatitis (a spartate aminotransferase 722 U/l; alanine aminotransferase 988 U/l), Anti- HBc IgM was positive and HBV-DNA was detected in serum by PCR, Anti-HAV IgM was negative. A serum sample obtained on presentation and stored at -80 de greesC was retrospectively tested and found positive for HBV-DNA. In July 1 999, complete remission of acute hepatitis and seroconversion to anti-HBs w as observed, We suppose that a moderate depression of the immune system, probably associ ated with Leishmaniasis, may have enhanced HBV replication in the patient w ho had an HBsAg-negative 'silent' HBV infection, Restoration of the immune system after successful antiprotozoan therapy might have induced cell-media ted necrosis of the HBV-infected hepatocytes and seroconversion to anti-HBs .