Patients with immunosuppression are at increased risk for occurrence, delayed diagnosis, and progression of AE.

This review gives a critical update of the situation regarding alveolar echinococcosis (AE) in Europe in humans, based on existing publications and on findings of national and European surveillance systems. All sources point to an increase in human cases of AE in the "historic endemic areas" of Europe, namely Germany, Switzerland, Austria and France and to the emergence of human cases in countries where the disease had never been recognised until the end of the 20th century, especially in central-eastern and Baltic countries. Both increase and emergence could be only due to methodological biases; this point is discussed in the review. One explanation may be given by changes in the animal reservoir of the parasite, Echinococcus multilocularis (increase in the global population of foxes in Europe and its urbanisation, as well as a possible increased involvement of pet animals as definitive infectious hosts). The review also focuses onto 2 more original approaches: (1) how changes in therapeutic attitudes toward malignant and chronic inflammatory diseases may affect the epidemiology of AE in the future in Europe, since a recent survey of such cases in France showed the emergence of AE in patients with immune suppression since the beginning of the 21st century; (2) how setting a network of referral centres in Europe based on common studies on the care management of patients might contribute to a better knowledge of AE epidemiology in the future.

No abstract

Response-guided pegylated interferon (peg-IFN) plus ribavirin (P/R) therapy trials on genotype (G)1 and G2/G3 hepatitis C virus-infected patients provide contradictory results. We conducted meta-analyses of randomized, controlled trials to address (1) the benefit of a 72-week extended-duration therapy in G1-slow responders and (2) adequate shortened duration therapy in G1 and G2/G3-rapid responders. Seventeen trials were selected, including 624 G1 rapid responders, 570 G1 slow responders, and 2,062 G2/G3 rapid responders. Virologic outcomes and treatment discontinuation data were collected from published articles and by asking investigators. Pooled estimates of sustained virologic response (SVR), relapse, and dropouts were calculated using the random effects model, considering the variability of shortened duration, ribavirin dose, genotype, and baseline viral load. In G1 slow responders, a 72-week extended duration increased SVR (110.7%; 95% CI [confidence interval]: 14.4% to 1 17.1%), decreased relapse (212.3%; 95% CI: 225.4% to 0%), and did not significantly increase drop-out rates (14.5%; 95% CI: 20.6% to 1 9.6%). The benefit of extended duration was lower when using a weight-based ribavirin regimen (18.7%; 95% CI: 11.7% to 1 15.8%). In G1 rapid responders, a 24-week shortened duration decreased SVR (212.5%; 95% CI: 219.2% to 25.8%) and increased relapse rates (18.8%; 95% CI: 12.9% to 1 14.8%). Such differences were not significant in patients with baseline viral load <400,000 UL/mL (24.4%; 95% CI: 29.8% to 1 1%). In G2/G3 rapid responders, SVR was more common for standard 24-week duration than for shortened durations (14.1%; 95% CI: 10.1% to 1 8.5), but this benefit was not significant when ribavirin was weight-adjusted and the short duration was 16 weeks (21.7%; 95% CI: 26.1% to 1 2.7%) and for G2 patients (11.6%; 95% CI: 20.2% to 1 5.5%). Conclusion: Long durations of P/R therapy improve SVR, regardless of genotype. This effect is nonetheless negligible in rapid responders, with the most favorable conditions for SVR (G2, G1 with low viral load, and G3 with weight-adjusted ribavirin regimen). (HEPATOLOGY 2011;54:789-800) T he standard of care for chronic hepatitis C is the combination of peg-interferon plus ribavirin that leads to hepatitis C virus (HCV) eradication in 60% of cases, with variations depending on the characteristics of host and virus and, in particular, viral genotype. 1,2 Patients infected with genotype 1Abbreviations: 95% CI, 95% confidence interval; cEVR, complete early virologic response; G1, genotype 1; G2/G3, genotype 2 and 3; HCV, hepatitis C virus; IFN, Interferon; IL-28B, interleukin-28B; ITT, intention-to-treat method LVL, low viral load; PCR, polymerase chain reaction; peg-IFN, pegylated interferon; P/ R, peg-interferon plus ribavirin; RCTs, randomized, controlled clinical trials; RVR, rapid virologic response; SRs, slow responders; SVR, sustained virologic response.From the

Serum total cortisol levels overestimated the prevalence of adrenal dysfunction in cirrhotics with end-stage liver disease. Since serum-free cortisol cannot be measured routinely, salivary cortisol testing could represent a useful approach but needs to be standardized.