Background: Recent studies that have examined the association between Helicobacter pylori infection and risk of nonalcoholic fatty liver disease (NAFLD) have produced conflicting data. We have performed a systematic review and meta-analysis to assess the association between H. pylori infection and risk of NAFLD. Methods: We searched PubMed, Web of Science and Scopus databases using predefined keywords to identify observational studies (published up to November 2018), in which NAFLD was diagnosed by histology, imaging or biochemistry. Data from selected studies were extracted and meta-analysis was performed using random-effects modeling. The statistical heterogeneity among studies (I 2-index), subgroup analyses and the possibility of publication bias were assessed. Results: Thirteen observational (11 cross-sectional/case-control and 2 longitudinal) studies involving a total of 81,162 middle-aged individuals of predominantly Asian ethnicity (47.5% of whom had H. pylori infection diagnosed by urea breath test, faecal or serological tests) were included in the final analysis. Meta-analysis of data from crosssectional and case-control studies showed that H. pylori infection was associated with increased risk of prevalent NAFLD (n=11 studies; random-effects odds ratio [OR] 1.20, 95%CI 1.07-1.35; I 2 =59.6%); this risk remained significant in those studies where analysis was fully adjusted for age, sex, smoking, adiposity measures, diabetes or dyslipidemia (random-effects OR 1.19, 95% CI 1.07-1.32, I 2 = 0%). Meta-analysis of data from longitudinal studies showed that H. pylori infection was also associated with increased NAFLD incidence (n=2 studies; random-effects hazard ratio 1.14, 95%CI 1.05-1.23; I 2 =0%). Sensitivity analyses did not alter these findings. Funnel plot did not reveal significant publication bias. Conclusions: H. pylori infection is associated with mildly increased risk of both prevalent and incident NAFLD in middle-aged individuals. More prospective studies, particularly in non-Asian populations, and mechanistic studies are required to better elucidate the link between chronic H. pylori infection and NAFLD.

In this observational study, we compared the effect of lipoprotein apheresis and evolocumab or alirocumab on levels of lipoprotein cholesterol, triglycerides and inflammatory markers (C reactive protein and interleukin 6) in cardiovascular patients ( n = 9). Patients were monitored during the last year of lipoprotein apheresis followed by six months of treatment with proprotein convertase subtilisin/kexin type 9 inhibitors. The biochemical parameters were determined pre- and post- every apheresis procedure for 12 months and then after one, three and six months of treatment with evolocumab (140 mg every two weeks [Q2W]) or alirocumab (75 mg or 150 mg every two weeks [Q2W]). Lipoprotein apheresis significantly reduced low-density lipoprotein cholesterol levels from 138 ± 32 mg/dl to 46 ± 16 mg/dl ( p < 0.001), with an inter-apheresis level of 114 ± 26 mg/dl. Lipoprotein(a) was also reduced from a median of 42 mg/dl to 17 mg/dl ( p < 0.01). Upon anti-proprotein convertase subtilisin/kexin type 9 therapy, low-density lipoprotein cholesterol levels were similar to post-apheresis (59 ± 25, 41 ± 22 and 42 ± 21mg/dl at one, three and six months, respectively) as well as those of lipoprotein(a) (18 mg/dl). However, an opposite effect was observed on high-density lipoprotein cholesterol levels: -16.0% from pre- to post-apheresis and +34.0% between pre-apheresis and proprotein convertase subtilisin/kexin type 9 inhibitors. Apheresis significantly reduced high-sensitivity C-reactive protein levels (1.5 ± 1.2 mg/l pre-apheresis to 0.6 ± 0.6 mg/l post-apheresis), while no changes were found upon proprotein convertase subtilisin/kexin type 9 mAbs administration. In conclusion, our study demonstrated that, by switching from lipoprotein apheresis to anti-proprotein convertase subtilisin/kexin type 9 therapies, patients reached similar low-density lipoprotein cholesterol and lipoprotein(a) levels, increased those of high-density lipoprotein cholesterol, and showed no changes on high-sensitivity C-reactive protein.

Aim.-Plasma levels of certain ceramides are increased in patients with ischemic heart disease (IHD). Many risk factors for IHD are also risk factors for chronic kidney disease (CKD), but it is currently uncertain whether plasma ceramide levels are increased in patients with CKD. Methods.-We measured six previously identified high-risk plasma ceramide concentrations

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A 49 years old woman (weight 68 kg, BMI 27.3 kg/m ) with heterozygous familial hypercholesterolemia (HeFH) and multiple statin intolerance with muscle aches and creatine kinase elevation, presented at the Outpatient Lipid Clinic of Verona University Hospital in May 2015. Hypercholesterolemia was firstly diagnosed during adolescence, followed in adulthood by a diagnosis of Cogan's syndrome, a rheumatologic disorder characterized by corneal and inner ear inflammation. No xanthomas, corneal arcus, or vascular bruits were detectable at physical examination. Screening for macrovascular complications did not reveal relevant damages. Ongoing medical therapy included salicylic acid, methylprednisolone, methotrexate, and protonic-pump inhibitor. In the absence of specific lipid-lowering therapy, plasma lipid levels at first visit were: total-cholesterol = 522 mg/dL, LDL-cholesterol = 434 mg/dL, HDL-cholesterol = 84 mg/dL, triglycerides = 120 mg/dL, Lp(a) = 13 mg/dL. On December 2015, evolocumab 140 mg sc every 2 weeks was initiated. After a 24-week treatment, the LDL-cholesterol levels decreased by an average of 21.2% to 342 ± 22 mg/dL (mean ± SD). On May 2016, LDL-apheresis (H.E.L.P.system) was started as add-on therapy. Compared to the average levels obtained during the evolocumab monotherapy period, the LDL-cholesterol was reduced by 49.4%, thus reaching an inter-apheresis level (mean ± SD) of 173 ± 37 mg/dL. This report suggests that a combination therapy with evolocumab and lipoprotein-apheresis may have synergic effects on circulating lipid levels. Its relevance as a highly effective treatment option for hyperlipidemia in HeFH patients warrants further investigation in larger datasets.

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Prevalence of diabetes is increasing worldwide and outcomes after ACS are thought to improve. We assessed the prevalence of DM, previously known (known-DM) or newly-diagnosed (new-DM), in all patients (n=1,017, males 66.6%) admitted for ACS at the Intensive Coronary Care Unit of the Verona University Hospital from 1/1/2015 to 12/31/2016. DM was ascertained according to previous diagnosis, glucose-lowering therapy at admission/discharge or random plasma glucose ≥11.1 mmol/L. The association of DM with in-hospital death, infectious/cardiorespiratory complications, duration and costs of hospitalization was tested in all patients and separately in known-DM and new-DM. The prevalence of DM was 27.2% (74.1% known-DM; 25.9% new-DM). In-hospital death rate was 4.72%. Compared to nondiabetic patients, those with DM showed an increased risk of death (7.6 vs. 3.6%; OR 2.17 95% CI, 1.20-3.90) and complications (34.4 vs. 23.9%; OR 1.67, 1.23-2.28), a longer hospital stay (median[IQR], 11 [7-17] vs. 8 [6-13] days), higher hospitalization costs (mean±SD, € 10,033±7,626 vs. 8,513±6,363) and more need of rehabilitation at discharge (10.8 vs. 5.9%); P&lt;0.for all comparisons. After multivariable adjustment (age, sex, BMI, e-GFR, LVEF, previous MI, lipid-lowering and anti-hypertensive drugs), DM remained an independent predictor of in-hospital death (OR 5.81, 1.31-25.7) but not complications (OR 1.14, 0.78-1.69). All study outcomes resulted significantly worse in new-DM vs. known-DM. In the former, ORs for in-hospital death and complications vs. nondiabetic controls were 2.40 (0.96-6.02) and 1.71 (0.99-2.96), respectively, while in known-DM figures were 2.09 (1.09-3.99) and 1.66 (1.18-2.33), respectively. These data highlight the extremely high frequency of DM in ACS and underscore the urgent need of strategies to anticipate DM diagnosis in patients at high cardiovascular risk. Disclosure M. Dauriz: None. L. Drezza: None. L. Santi: None. A. Altomari: None. E. Rinaldi: None. S. Tardivo: None. C. Bovo: None. F. Ribichini: None. E. Bonora: None.

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