Pegylated interferon-α monotherapy leads to low response rates in HIV-infected patients with acute hepatitis C.

BACKGROUND: Despite a rising incidence of acute HCV in patients infected with HIV, the optimal therapeutic strategy (pegylated interferon-α [PEG-IFN-α] monotherapy or in combination with ribavirin) is still under debate. METHODS: A total of 23 HIV-infected patients were prospectively diagnosed with acute HCV and treated with PEG-IFN-α2a monotherapy (180 µg/week) for 24 or 48 weeks. Add-on ribavirin was allowed from week 4 of therapy onwards. There were three patients who were not included for different reasons. Blood samples were routinely drawn for viral load measurement and IL28B polymorphism analysis. RESULTS: Spontaneous viral clearance occurred in 1 (4%) patient. Nineteen patients (13 genotype 1 and 6 genotype 4) received treatment with PEG-IFN-α monotherapy (3 with add-on ribavirin) resulting in a rapid virological response (HCV RNA<50 IU/ml at week 4) in 7 (37%) patients. A sustained virological response (SVR) was reached in 7 (37%) patients, whereas 9 (47%) patients were null-responders to treatment (that is, <2 log10 drop in HCV RNA at week 12 of therapy). The unfavourable G allele of the IL28B polymorphism rs8099917 was detected in 66% of the non-responders. In case of re-emergence of HCV viraemia after treatment discontinuation, sequence analysis of quasispecies confirmed an HCV relapse in 3 patients while 2 patients were re-infected by their previously non-responding partner. CONCLUSIONS: PEG-IFN-α monotherapy resulted in a low SVR rate and a high percentage of null-response, whereas non-SVR was associated with a polymorphism in the IL28B gene (rs8099917).

Two donor-related infections in a heart transplant recipient: one common, the other a tropical surprise.

BACKGROUND: Infection is the most frequent complication after heart transplantation (HTx). In this report and brief literature review we present a recipient who some 6 weeks post-HTx had two donor-related infections: a "common" primary cytomegalovirus (CMV) infection and, simultaneously, a highly unusual donor-related Strongyloides stercoralis infection. METHODS: The parasite was discovered by chance in a skin biopsy. CMV was treated with ganciclovir and the strongyloidiasis was cured with two courses of anti-helminthic therapy--initially with ivermectine and albendazol and, in response to eosinophilia, with ivermectine monotherapy. The patient's recovery was further complicated by two successive rejection episodes, a relapse of the CMV syndrome and a novel influenza A/H1N1 infection. These episodes were treated with steroids, ganciclovir and oseltamivir, respectively. RESULTS: It took almost 9 months before a permanent IgG anti-CMV response was seen. At 13 months post-HTx, coronary angiography showed only slight vessel wall abnormalities. At present, the patient is back at home and in good condition. CONCLUSION: Until now, only 4 recipient-derived strongyloidiasis cases have been described in post-HTx patients, all diagnosed by autopsies. This is the first report of a donor-related Strongyloides infection in a patient after HTx.