Cytomegalovirus seronegativity rate in pregnant women and primary cytomegalovirus infection during pregnancy in rural Germany.

BACKGROUND: Congenital cytomegalovirus (CMV) infection is the most common congenital infection worldwide and one of the leading causes of congenital hearing loss in newborns. The aim of this study was to determine the seroprevalence rate for cytomegalovirus in pregnant women and the rate of CMV serological testing utilised during pregnancy in a rural region in Germany. METHODS: Retrospective data on the prevalence of CMV IgG and IgM antibodies were obtained from 3,800 women, identified in the study group of 19,511 pregnant women from outpatient settings whose samples were collected between 1 and 2014 and 30 April 2018. In addition, the serological CMV status in regards to various billing methods was further analyzed. RESULTS: Serological CMV tests were performed in 3,800 (19.5%) out of 19,511 pregnant women. 2,081 (54.8%) of these women were CMV seronegative. Among those, seroconversion rate of 0.37-1.42% was identified. A proportion of 2,710 (14.7%) of all 18,460 women with statutory health insurance made use of the CMV testing as an individual health service. CONCLUSIONS: The low uptake of CMV serological testing in the study population covered indicates low risk awareness among pregnant women and their healthcare professionals. Presented seronegativity rates and routine seroconversion rate, demonstrate importance to improve intervention strategy to prevent feto-maternal CMV transmission.

CKD prevalence based on real-world data: continuous age-dependent lower reference limits of eGFR with CKD-EPI, FAS and EKFC algorithms.

PURPOSE: Several recent articles discuss the need for a definition of chronic kidney disease (CKD) that embarks age-dependency and its impact on the prevalence of CKD. The relevance is derived from the common knowledge that renal function declines with age. The aim of this study was to calculate age-dependent eGFR lower reference limits and to consider their impact on the prevalence of CKD. METHODS: A real-world data set from patients with inconspicuous urinalysis was used to establish two quantile regression models which were used to calculate continuous age-dependent lower reference limits of CKD-EPI, FAS and EKFC-eGFR based on either single eGFR determinations or eGFR values that are stable over a period of at least 3 months (± 10% eGFR). The derived lower reference limits were used to calculate the prevalence of CKD in a validation data set. Prevalence calculation was done once without and once with application of the chronicity criterion. RESULTS: Both models yielded age-dependent lower reference limits of eGFR that are comparable to previously published data. The model using patients with stable eGFR resulted in higher eGFR reference limits. By applying the chronicity criterion, a lower prevalence of CKD was calculated when compared to one-time eGFR measurements (CKD-EPI: 9.8% vs. 8.3%, FAS: 8.0% vs. 7.2%, EKFC: 9.0% vs. 7.1%). CONCLUSION: The application of age-dependent lower reference intervals of eGFR together with the chronicity criterion result in a lower prevalence of CKD which supports the estimates of recently published work and the idea of introducing age-dependency into the definition of CKD.

Gene variants of the SLC2A5 gene encoding GLUT5, the major fructose transporter, do not contribute to clinical presentation of acquired fructose malabsorption.

BACKGROUND: While role of ALDOB-related gene variants for hereditary fructose intolerance is well established, contribution of gene variants for acquired fructose malabsorption (e.g. SLC2A5, GLUT5) is not well understood. METHODS: Patients referred to fructose breath test were further selected to identify those having acquired fructose malabsorption. Molecular analysis of genomic DNA included (I) exclusion of 3 main ALDOB gene variants causing hereditary fructose intolerance and (II) sequencing analysis of SLC2A5 gene comprising complete coding region, at least 20 bp of adjacent intronic regions and 700 bp of proximal promoter. RESULTS: Among 494 patients, 35 individuals with acquired fructose malabsorption were identified based on pathological fructose-breath test and normal lactose-breath test. Thirty four of them (97%) had negative tissue anti-transglutaminase and/or deamidated gliadin antibodies in their medical records. Molecular analysis of SLC2A5 gene of all 35 subjects identified 5 frequent and 5 singular gene variants mostly in noncoding regions (promoter and intron). Allele frequencies of gene variants were similar to those reported in public databases strongly implying that none of them was associated with acquired fructose malabsorption. CONCLUSIONS: Gene variants of coding exons, adjacent intronic regions and proximal promoter region of SLC2A5 gene are unlikely to contribute to genetic predisposition of acquired fructose malabsorption.

Estimated Prevalence of Harmful Alcohol Consumption in Pregnant and Nonpregnant Women in Saxony-Anhalt (NorthEast Germany) Using Biomarkers.

BACKGROUND: Alcohol consumption is commonly accepted in Western societies and is a known risk factor in pregnancy, which could lead to fetal alcohol spectrum disorders (FASDs). Prevalence of alcohol consumption during pregnancy is mostly unknown. Prevalence estimates in publications based on questionnaires are limited by possible underreporting due to social stigmatization. The aim of this study was to estimate the prevalence of harmful alcohol consumption in a large cohort of pregnant women using different biomarkers related to alcohol consumption and compare the findings with those of non-pregnant women METHODS: Routine parameters known to be influenced by alcohol consumption (γ-glutamyltransferase, GGT; carbohydrate-deficient transferrin, CDT/%CDT; mean corpuscular/cell volume, MCV; combined parameter of GGT and %CDT, GGT-CDT) were analyzed in serum samples of 2,182 pregnant women and 743 non-pregnant, age-matched females. Data were tested for (i) differences between pregnant and non-pregnant women and (ii) changes across the 3 trimesters of pregnancy. RESULTS: Prevalence rates differ greatly according to the parameter and cutoff, which reflects the limitations of assessing alcohol consumption with biomarkers. The prevalence of harmful alcohol consumption on the basis of a single or several elevated parameters was 13.8% (95% CI: 12.4 to 15.2) in pregnant women and 18.6% (95% CI: 15.8 to 21.4) in non-pregnant women, though 85.0% of the elevated measurements were attributable to an isolated elevation in %CDT only. Using GGT-CDT as the parameter with the highest specificity according to the literature, the estimated prevalence of harmful alcohol consumption in pregnancy is 0.5% (95% CI: 0.2 to 0.7). CONCLUSION: Estimated prevalence rates differ greatly with respect to the biomarkers and cutoffs used. The use of CDT/%CDT alone appears to overestimate harmful alcohol consumption during pregnancy.

Early effects on endothelial function of atorvastatin 40 mg twice daily and its withdrawal.

Combined hyperlipidemia is associated with endothelial dysfunction. Atorvastatin has lipid-lowering and pleiotropic properties, including a protective effect on endothelial function. This study investigated the short- and medium-term effects of therapy with atorvastatin and of its discontinuation on lipid lowering and endothelial function. In 33 patients with combined hyperlipidemia who had been randomized and treated for 6 weeks with 40 mg of atorvastatin twice daily (n = 23) or placebo (n = 10), fasting lipid levels and flow-mediated dilation (FMD) of the brachial artery were measured at baseline, after 12 hours, 1 week, and 6 weeks during therapy, and 36 hours after discontinuation of therapy. Thereafter, all patients received 20 mg/day of atorvastatin for another 6 weeks. In the atorvastatin group, low-density lipoprotein cholesterol was decreased by 30% and 46% after 1 and 6 weeks, respectively (p <0.0001 for the 2 comparisons). In patients who already showed an impaired FMD at the beginning of the study (n = 15), atorvastatin caused a significant improvement in FMD, from 2.6% at baseline to 4.0% and 6.3% after 1 and 6 weeks, respectively (p <0.05 and <0.001). Thirty-six hours after withdrawal of atorvastatin, the FMD in this group decreased again to 2.8% (p <0.05), whereas low-density lipoprotein cholesterol level remained unchanged. The 6 patients with normal FMD at baseline showed no improvement in FMD during therapy or any decrease after withdrawal of the drug. In conclusion, only patients with endothelial dysfunction profit from high-dose atorvastatin treatment. When the treatment is abruptly discontinued, the effect on FMD disappears in 36 hours.

Endothelial dysfunction induced by postprandial lipemia is neutralized by addition of proteins to the fatty meal.

BACKGROUND: Postprandial lipemia is known to reduce endothelium-dependent flow-mediated vasodilation (FMD). Because postprandial lipemia can be acutely mitigated when proteins are added to the fatty meal, we investigated whether this mitigation could neutralize the lipemia-induced endothelial dysfunction. DESIGN: Sixteen healthy students (aged 19-23, eight males and eight females) received three different test meals at intervals of 1 week between successive tests. Each meal contained whipping cream alone or whipping cream together with either caseinate or soy protein. The whipping cream contained 33% fat, and 3 ml (= 1 g fat) was given per kg body weight. The proteins added were either 50 g sodium caseinate or 50 g soy protein. FMD was assessed by two-dimensional ultrasonography of the brachial artery in the fasting state and 1, 2, 3, 4, 5, 6, 7, and 8h after the fatty meal. Blood was withdrawn at the same time-points from the other arm. Triglycerides, free fatty acids, and insulin were determined using routine methods, and both L-arginine and asymmetric dimethylarginine (ADMA) were determined by LC-MS. RESULTS: Postprandial lipemia reduced FMD, the reduction reaching a maximum of 58% after 3 h. This impairment of endothelial function was not observed when either of the test proteins had been added to the fatty meal (p < 0.01 for caseinate and p < 0.001 for soy protein). The effects of the protein addition were decreases in triglycerides and free fatty acids, increased insulin concentrations at all time-points, and an increased arginine/ADMA ratio between 1 and 5h after the meal, particularly in the case of the soy protein. CONCLUSION: We suggest that the neutralization of the lipemia-induced endothelial dysfunction is caused by direct and indirect effects of the proteins insulinotropy and, secondly, by an increased supply of L-arginine.

Postprandial lipid and carbohydrate responses after the ingestion of a casein-enriched mixed meal.

BACKGROUND: Postprandial lipemia is markedly modulated when carbohydrates are added to a fatty meal. The effect of added protein is less known, however, and the data are controversial. OBJECTIVE: We investigated the effects of casein added to various fat-rich meals in the absence and presence of oligosaccharides. DESIGN: Four different test meals were given to 24 healthy volunteers: 1) fat alone, consisting of 3 g cream/kg body wt; 2) fat plus 75 g oligosaccharides; 3) fat plus 50 g sodium caseinate; and 4) a combination of all 3 components. Blood samples were taken before the meals and 1, 2, 3, 4, 5, 6, 7, and 8 h thereafter. The variables measured were serum free fatty acids, arginine, glucose, insulin, and C-peptide as well as triacylglycerol in serum, in chylomicrons, and in VLDL. Gastric emptying was monitored with the use of a (13)C breath test. RESULTS: Addition of oligosaccharides resulted in the known delay and reduction in postprandial lipemia. Casein caused additional effects: chylomicrons were further reduced and delayed, independently of gastric emptying. C-peptide and insulin, as expressed by their areas under the curves, were raised not only during the early response to the glucose load but also in the postabsorptive state. Concentrations of free fatty acids, which were markedly suppressed by 24% after oligosaccharides alone, were lowered a further 20% after the addition of casein. CONCLUSIONS: Casein added to a fatty meal lowers free fatty acids markedly in the postprandial and postabsorption phases, probably via its insulinotropic activity. Postprandial lipemia is also moderately reduced.