Chronic hepatitis B (HBV) and C (HCV) coinfection are frequently observed in clinical practice. The interaction between HCV and HBV is complex and not completely understood, and usually results in the suppression of hepatitis B replication by HCV superinfection or coinfection. Cases of hepatitis B reactivation during and after HCV treatment with direct acting antivirals (DDA) have been described, and it is recommended to screen all patients starting DAA therapy for HBV infection markers and to monitor those that have positive markers of HBV infection. HBs antigen (HBsAg) positivity is the main risk factor for HBV reactivation, and this phenomenon is rarer in those with "resolved" HBV infection (negative HBsAg, positive antiHBc antibody (HBcAb) and anti-HBs antibody (HBsAb) positive or negative). The authors present a case of HBV reactivation after HCV treatment with sofosbuvir/ ledipasvir that occurred in a 54-year-old male that was HIV-coinfected and had "resolved" hepatitis B infection (negative HBsAg, positive HBcAb and positive HBsAb). Our case reinforces the need to screen all patients who will start DAA therapy for hepatitis C infection, and alerts clinicians to the need to closely monitor patients with evidence of previous HBV infection no only during treatment but also after HCV treatment with DAAs.

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IntroductionConcomitant use of ledipasvir and boosted protease inhibitors (PIs) may increase the risk of tenofovir (TDF) nephrotoxicity, since both these drugs increase TDF levels. Our aim was to evaluate glomerular filtration rate (eGFR) evolution during HCV treatment with sofosbuvir/ledipasvir (SOF/LDV) in HCV/HIV coinfected patients, according to their antiretroviral treatment (ARV).MethodsObservational prospective study of HCV/HIV coinfected patients treated with SOF/LDV. eGFR evolution was evaluated during and 12 weeks after HCV treatment. Patients were categorized in three groups based on ARV regimen: non TDF, non-boosted TDF and TDF + boosted PI.ResultsWe included 273 patients: 145 were receiving a non-TDF regimen, 78 a non-boosted TDF scheme and 50 were receiving TDF + boosted PI. We observed a statistically significant decrease in eGFR during treatment in all groups (non TDF p = 0.03, 95%CI [0.23–3.86], non-boosted TDF p < 0.01, 95%CI [3.36–7.44], TDF + PI p = 0.01, 95%CI [1.09–7.53]). The decrease was more pronounced in those receiving unboosted TDF (− 5.40 ml/min/1.73m2), but differences in eGFR decrease between the three groups were small and not statistically different (p = 0.06). eGFR decrease was greater in patients treated for 24 weeks (p = 0.009) and in cirrhotic patients (p = 0.036). At the end of follow up a recovery of eGFR was observed in all groups.ConclusionWe observed a significant decrease in eGFR during treatment in all study groups, that was small and reversible after SOF/LDV discontinuation. TDF was not associated with an increase in renal toxicity.

39% (29/74) were under antirretroviral therapy (ART), and only 6 patients had HIV viral load < 40 copies/ml. 69% (51/74) presented opportunistics infections, being tuberculosis the most prevalent one (52%). 58% (43/74) had presented a recent hospitalization, and 55% (41/74) had received some antibiotic in the same period.The most commonly used antibiotics during hospitalization were piperaziline-tazobactam and/or carbapenems (59%), and firstline antituberculous drugs (49%).The relapse rate was 30% (22/74), with a median of CD4 + LT in this group of 28 cells/mm3 (non different from the one without relapse; p = 0.5).The overall mortality was 50% (37/74), being 73% (16/22) in the cases of relapse (p < 0.01). Conclusion:Severe immunosuppression and lack of effective ART predisposes to frequent hospitalizations and use of multiple antibiotic treatments, increasing subsequently the risk of CDAD.A high association of CDAD with antituberculous drugs was observed.The relapse rate in HIV patients was similar to that reported in the literature for general population, but highlighting a high mortality in this group of patients.