A few studies have assessed the observed fibrosis progression between serial liver biopsies (LB) in human immunodeficiency virus (HIV) / hepatitis C virus (HCV)-coinfected patients. Approximately half of the patients progressed at least one fibrosis stage over a short period of time. The risk factors for this fast progression need clarification. Because of this, we evaluated the observed fibrosis progression rates of HIV/HCV-coinfected patients and the risk factors for accelerated progression. Overall, 135 HIV-infected patients with positive serum HCV RNA, without other possible causes of liver disease, who underwent two LB, separated at least by 1 year, were included in this retrospective cohort study. The median (Q1-Q3) time between both LBs was 3.3 (2.0-5.2) years. Patients showed the following changes in fibrosis stage: regression ≥1 stage: 23 (17%), no change: 52 (39%), progression 1 stage: 38 (28%), and progression ≥2 stages: 22 (16%). Seventeen (13%) patients had cirrhosis in the second biopsy. Factors independently associated with progression ≥1 stage were undetectable plasma HIV RNA during the follow-up (relative risk [RR] [95% confidence interval, 95% CI] 0.61 [0.39-0.93], P = 0.03), moderate-to-severe lobular necroinflammation (1.77 [1.16-2.7], P = 0.009), time between biopsies (1.11 [1.08-1.2], P = 0.01), and end of treatment response to anti-HCV therapy (0.41 [0.19-0.88], P = 0.02). Conclusion: Fibrosis progresses with high frequency in HIV/HCV-coinfected patients over a period of time of 3 years. Absent-to-mild lobular necroinflammation at baseline, achievement of response with anti-HCV treatment, and effective antiretroviral therapy are associated with slower fibrosis progression. (Hepatology 2009.)

Background. Transient elastometry (TE) is accurate for detecting significant liver fibrosis and cirrhosis in hepatitis C virus (HCV)–monoinfected pat

MURINE TYPHUS (MT), a zoonosis that is caused by Rickettsia typhi, occurs all over the world, with endemic areas in North and South America, Southeast Asia, Africa, Australia, and some southern European countries.^1-10 The importance of this illness has been underestimated. It is more frequent than is commonly believed and represents a worldwide health problem.¹¹ Studies on its prevalence have shown that it also occurs in Spain.^12,13 Sporadic cases have been reported in Seville, Huelva, and Murcia,^7-9 but, to our knowledge, no extensive studies have been performed to investigate its clinical and epidemiological characteristics. Therefore, its real incidence is not known.

Background. The objective of this study was to determine the impact of sustained virologic response (SVR) to pegylated interferon (peg-IFN) plus ribavirin (RBV) on the incidence of liver-related complications and overall mortality in human immunodeficiency virus (HIV)–infected patients with compensated hepatitis C virus (HCV)–related cirrhosis. Methods. We included in this prospective cohort study 166 coinfected patients with compensated cirrhosis, who received peg-IFN plus RBV, to assess the time from the starting date of HCV therapy to the first hepatic decompensation and death due to any cause. Results. SVR was observed in 43 (25%) individuals. Two (4.6%) patients with SVR developed liver decompensation vs 33 (26.8%) individuals without SVR (P = .002). The incidence of liver-related complications was 0.89 cases per 100 person-years (95% confidence interval [CI], .11–3.1) in SVR patients and 6.4 cases per 100 person-years (95% CI, 4.5–8.9) in non-SVR patients. Factors independently associated with liver decompensation were non-SVR (hazard ratio [HR], 8.1; 95% CI, 1.08–61.5; P = .042) and MELD score ≥9 at baseline (HR, 2.9; 95% CI, 1.2–7.2; P = .016). Two (4.6%) patients with SVR died due to any cause compared with 22 (17.9%) individuals without SVR (P = .02). MELD score ≥9 (HR, 3.1; 95% CI, 1.3–7.7; P = .011) and non-SVR (HR, 8.0; 95% CI, 1.07–61; P = .043) were independently associated with overall mortality. Conclusions. The achievement of SVR following peg-IFN plus RBV markedly reduces the incidence of liver-related decompensation and the overall mortality in HIV/HCV-coinfected patients with compensated cirrhosis.