Improved understanding of risk factors associated with carbapenem-resistant-Klebsiella pneumoniae (CR-KP) infection after liver transplantation (LT) can aid development of effective preventive strategies. We performed a prospective cohort study of all adult patients undergoing LT at our hospital during 30-month period to define risk factors associated with CR-KP infection. All patients were screened for CR-KP carriage by rectal swabs before and after LT. No therapy was administered to decolonize or treat asymptomatic CR-KP carriers. All patients were monitored up to 180 days after LT. Of 237 transplant patients screened, 41 were identified as CR-KP carriers (11 at LT, 30 after LT), and 20 developed CR-KP infection (18 bloodstream-infection, 2 pneumonia) a median of 41.5 days after LT. CR-KP infection rates among patients non-colonized, colonized at LT, and colonized after LT were 2%, 18.2% and 46.7% (p < 0.001). Independent risk factors for CR-KP infection identified by multivariate analysis, included: renal-replacement-therapy; mechanical ventilation > 48 h; HCV recurrence, and colonization at any time with CR-KP. Based on these four variables, we developed a risk score that effectively discriminated patients at low versus higher risk for CR-KP infection (AUC 0.93, 95% CI 0.86-1.00, p < 0.001). Our results may help to design preventive strategies for LT recipients in CR-KP endemic areas.

Recent studies have shown that rosuvastatin significantly decreases serum levels of inflammatory biomarkers and slows progression of carotid atherosclerosis in the general population. However, there are no data about its effect on progression of atherosclerosis in HIV-infected patients. Adult patients with HIV infection, on stable antiretroviral therapy, with asymptomatic carotid atherosclerosis and hypercholesterolemia, who started a rosuvastatin treatment at 10 mg daily during the period 2007-2009 were enrolled and followed-up for 24 months. Thirty-six patients (30 males) were enrolled, with a mean age of 49 years, a mean duration of current antiretroviral therapy of 38 months, and a mean 10-year risk of myocardial infarction of 18.5%. Rosuvastatin led to a significant decrease in mean values of intima-media thickness in all extracranial carotid arteries, with the greatest magnitude observed in carotid bifurcations (a mean decrease of 18.7% in the right artery and of 21.4% in the left artery) and in internal carotid arteries (a mean decrease of 23.7% in the right artery and of 25.6% in the left artery). Moreover, there was a significant reduction in mean levels of total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides versus respective baseline values associated with a significantly decreased mean cardiovascular risk. The treatment with rosuvastatin was well tolerated, and serious adverse events were not reported. A 24-month treatment with rosuvastatin in HIV-infected patients on highly active antiretroviral therapy (HAART) with subclinical atherosclerosis and a moderate cardiovascular risk seems to promote significantly favorable changes in carotid atherosclerosis, associated with a favorable effect on serum lipid levels and a good tolerability profile.

In our study, simplification to a dual therapy containing raltegravir plus darunavir/ritonavir after 48 weeks maintained viral suppression in more than 90% of patients and showed a good tolerability with a favourable effect on proteinuria, ipophosphoremia, and lipid metabolism.

To evaluate the frequency of myopathy and serum creatine kinase (CK) elevation associated with the use of the integrase inhibitor raltegravir we conducted a retrospective, cohort analysis assessing the incidence of skeletal muscle toxicity among HIV-infected patients treated with raltegravir. Adult HIV-infected patients who started a raltegravir-containing therapy were enrolled into the study. The skeletal muscle toxicity was defined by the presence of one or more of the following parameters: (1) isolated and significant CK elevation without signs or symptoms; (2) diffuse myalgia without weakness; (3) proximal muscle weakness; (4) rhabdomyolysis. On the whole, 155 patients were included in the study, with a mean age of 49.2 years; the median duration of the raltegravir treatment was 30.7 months. The overall frequency of skeletal muscle toxicity was 23.9%, with an incidence of 4.7/100 person-years. An isolated CK elevation was reported in 21.3% of cases, while less than 3% of patients complained of myalgia or muscle weakness. The CK elevation was usually of grade 1 or 2 and self-limiting, and laboratory or clinical abnormalities did not require discontinuation of raltegravir in any patient. Factors significantly associated with skeletal muscle toxicity were previous use of zidovudine, higher baseline CK levels, previous increase of the CK levels, and a higher body mass index. Skeletal muscle toxicity is not an unusual adverse event in subjects receiving raltegravir, but it is usually represented by a mild-to-moderate increase in CK concentration, while clinical symptoms of myopathy are very uncommon.

The mean plasma concentration of efavirenz was significantly higher in HCV-positive than in HCV-negative patients without liver cirrhosis, while the mean plasma levels of darunavir/ritonavir and raltegravir were comparable in both groups.