Vitamin K, a cofactor for the γ-glutamyl carboxylase enzyme, is required for the post-translational activation of osteocalcin and matrix Gla protein, which play a key role in bone and muscle homeostasis. In vivo and in vitro models for osteoporosis and sarcopenia suggest the vitamin K could exert a positive effect in both conditions. In bone, it increases osteoblastogenesis, whilst decreases osteoclast formation and function. In muscle, it is associated with increased satellite cell proliferation and migration and might play a role in energy metabolism. Observational trials suggest that high levels of vitamin K are associated with increased bone mineral density and reduced fracture risk. However, interventional studies for vitamin K supplementation yielded conflicting results. Clinical trials in sarcopenia suggest that vitamin K supplementation could improve muscle mass and function. One of the main limitations on the vitamin K studies are the technical challenges to measure its levels in serum. Thus, they are obtained from indirect sources like food questionnaires, or levels of undercarboxylated proteins, which can be affected by other environmental or biological processes. Although current research appoints to a beneficial effect of vitamin K in bone and muscle, further studies overcoming the current limitations are required in order to incorporate this supplementation in the clinical management of patients with osteosarcopenia.

Background: Posttraumatic stress disorder (PTSD) is a frequently observed stress-related disorder after acute myocardial infarction (AMI) and it is characterized by numerous symptoms, such as flashbacks, intrusions and anxiety, as well as uncontrollable thoughts and feelings related to the trauma. Biological correlates of severe stress might contribute to identifying PTSD-vulnerable patients at an early stage. Objective: Aims of the study were (1) to determine whether blood levels of trimethylamine N-oxide (TMAO) vary immediately after AMI in patients with/without AMI-induced PTSD symptomatology, (2) to investigate whether TMAO is a potential biomarker that might be useful in the prediction of PTSD and the PTSD symptom subclusters re-experiencing, avoidance and hyperarousal, and (3) to investigate whether TMAO varies immediately after AMI in patients with/without depression 6 months after AMI. Method: A total of 114 AMI patients were assessed with the Hamilton-Depression Scale after admission to the hospital and 6 months later. The Clinician Administered PTSD Scale for DSM-5 was used to explore PTSD-symptoms at the time of AMI and 6 months after AMI. To assess patients' TMAO status, serum samples were collected at hospitalization and 6 months after AMI. Results: Participants with PTSD-symptomatology had significantly higher TMAO levels immediately after AMI than patients without PTSD-symptoms (ANCOVA: TMAO(PTSD x time), F = 4.544, df = 1, p = 0.035). With the inclusion of additional clinical predictors in a hierarchical logistic regression model, TMAO became a significant predictor of PTSD-symptomatology. No significant differences in TMAO levels immediately after AMI were detected between individuals with/without depression 6 months after AMI. Conclusions: An elevated TMAO level immediately after AMI might reflect severe stress in PTSD-vulnerable patients, which might also lead to a short-term increase in gut permeability to trimethylamine, the precursor of TMAO. Thus, an elevated TMAO level might be a biological correlate for severe stress that is associated with vulnerability to PTSD.

Acute myocardial infarction is not only a somatic disease but potentially triggers psychological effects, too. Post-traumatic stress disorder (PTSD) is a common stress-related disorder. It is characterized by numerous symptoms, such as flashbacks, intrusions, nightmares and severe anxiety, as well as uncontrollable, intense and disturbing thoughts and feelings related to the traumatic experience. However, with regard to the development of PTSD, individual stress perception might be crucial since not every serious traumatic experience leads to PTSD. To date, almost no biological correlates of an individual's perception of stress have been identified as being associated with the long-term development of PTSD. The aim of the study was to determine whether blood levels of TMAO vary immediately after AMI (1) in patients with or without depression, and (2) in patients with AMI induced PTSD symptomatology (subsyndromal PTSD and full PTSD). Furthermore, we investigated whether TMAO is a potential biomarker that might be useful in the prediction of PTSD symptomatology in the long term. A total of 114 AMI patients were assessed with standardized clinical psychiatric interviews based on the Hamilton Depression Scale (HAMD-17) after admission to the hospital and 6 months later. In addition, the CAPS-5 was used to explore PTSD symptoms (subsyndromal PTSD and full PTSD) 6 months after AMI. To assess patients' TMAO status, serum samples were collected at hospitalization and 6 months after AMI. Study participants with post-myocardial infarction PTSD symptomatology (subsyndromal PTSD and full PTSD) had significantly higher TMAO levels immediately after AMI than patients without PTSD symptoms (ANCOVA: TMAO (PTSD x time), F = 4.544, df = 1, p=0.035). In contrast, depressive symptomatology 6 months after AMI had no influence on TMAO levels (TMAO (depression x time), F = 0.083, df = 1, p=0.774). With the inclusion of additional clinical predictors in a hierarchical logistic regression model, TMAO becomes a significant predictor of PTSD symptomatology. An elevated TMAO level immediately after AMI might reflect severe stress in PTSD-vulnerable patients, which might also lead to a short-term increased gut permeability to trimethylamine (TMA), the precursor of TMAO. Thus, elevated TMAO might be a biological correlate for stress that is associated with vulnerability to PTSD and might help to identify patients at increased risk. Type of funding sources: None.

Background: Blood transfusions make significant contribution to iron overload in patients with myelodysplastic syndrome. However, the excess iron accumulation is observed even on the early stage of disease, before repeated blood transfusions. During this compensatory response, the excess production of GDF 15 suppresses the hepcidin synthesis and provides an increasing iron availability for erythropoiesis by rising an iron absorption and iron releasing from macrophages. Such effect becomes more significant in non-effective erythropoiesis, in which erythroid precursors undergo apoptosis, not maturation. As a result, the hepcidin deficiency leads to iron overload in absence of transfusion dependence. Aims: To analyze the ferritin and hepcidin serum levels in patients with myelodysplastic syndrome in accordance with transfusion burden. Methods: 22 patients with myelodysplastic syndrome were enrolled in the study. According to IPSS criteria, there were four patients (18,2%) with low risk MDS, two patients (9,1%) with intermediate-2 risk and 16 patients (72,2%) with intermediate-1 risk. In accordance with WPSS, 14 (63,6%) patients were RBC transfusion-dependent and 8 (36,4%) patients were transfusion-independent. The ferritin and hepcidin serum levels were measured by ELISA method. The findings from healthy controls (n = 18) were used to evaluate the hepcidin level. Results: The average level of ferritin in the group of MDS patients was 624,5 ± 194,89 ng/ml, that was 8-fold higher the controls group (70,39 ± 65,7ng/ml; p < 0,001). The positive correlation between the annual transfusion burden and ferritin serum level demonstrated the important role of multiple blood transfusion in the development of iron overload syndrome (r = 0,4, p < 0,05, n = 22). The average hepcidin serum level in patients group was 51,12 ± 26,46 ng/ml, that was 2,4-fold higher the controls group (22,8 ± 20,97 ng/ml). Thus, in presence of the excess iron accumulation the hepcidin serum level is increasing together with the ferritin level as attempt to suppress to cell iron export in the excess iron accumulation. To evaluate the relationship between ferritin and hepcidin serum level, we estimated the correlation between these markers in patients, divided on three subgroups according to annual transfusion burden (similarly to the work done by Niraj Shenoy, 2014). There was a strong positive correlation between hepcidin and ferritin serum level (r = 0,96 (n = 6,p < 0,001)) in the subgroup of patients who received less than 9 RBC units. There was no correlation (r = 0,009 (n = 9, p>0,05) in those patients who received from 9 to 24 RBC units per year and the negative correlation between these markers was observed in subgroup of patients who received more than 24 RBC units per year (r = −0,55 (n = 7, p>0,05). Therefore, the hepcidin serum level remains sensitive to the iron serum level in patients with relatively low transfusion dependence. Multiple RBC transfusions lead to activation of circulating hepcidin, but its level is inadequate in relation to the level of excess iron accumulation. Summary/Conclusion: The patients with low- and intermediate risk of myelodysplastic syndrome and with relatively low degree of transfusion dependence probably are more susceptible to excess iron accumulation not due to the repeated blood transfusions, but because of the development non-transfusional iron overload and inappropriate hepcidin synthesis.

Background Standardized commercially available control material for internal quality control (IQC) of light transmission aggregometry (LTA) is still lacking. Moreover, the availability of normal blood donors to provide fresh platelets is difficult in small laboratories, where volunteers' may be in short supply. Objectives To evaluate the implementation of buffy-coat-derived pooled platelet concentrates (PCs) for IQC material for LTA. Methods We used buffy-coat-derived pooled PCs from the blood bank as IQC material for LTA. On each weekend one PC was prepared (>200mL) and aliquoted from the original storage bag on a daily basis in four baby bags (40-50mL), which were delivered from Monday to Friday to our laboratory. The IQC measurements of at least 85 work-weeks (from Monday to Friday) were evaluated with this new IQC material. LTA was performed on a four-channel Chronolog 700 Aggregometer (Chronolog Corporation, Havertown, PA, USA) (agonists: collagen, adenosine diphosphate [ADP], arachidonic acid [AA] and thrombin receptor activator peptide-6 [TRAP-6]). Results The medians of platelet aggregation from IQC measurements with collagen, ADP and AA from Monday to Friday were 68.0-59.5, 3.0-2.0 and 51.0-50.0%, respectively, and the mean of platelet aggregation with TRAP-6 was 71.2-66.4%. Conclusions Buffy-coat-derived pooled PCs serve as a reliable and robust IQC material for LTA measurements and would be beneficial for the whole laboratory procedure and employees' safety.

In the gastrointestinal (GI) tract the non-absorbable carbohydrates are known to build complexes with tryptophan (TRP), which is the precursor for the synthesis of serotonin in the brain. This study aimed to investigate the relationship between primary adult-type lactose malabsorption (PALM), fructose malabsorption (FM), TRP metabolism and the presence of depressive signs.

Introduction: H. pylori is a remarkable bacterium, because it has one of the highest urease activities of all known bacteria. Since H. pylori infection may increase the intra-gastric pH due to the production of ammonia, this bacterium may be a causative agent of small intestinal bacterial overgrowth (SIBO). The purpose of the present study was to investigate the presence of small intestinal bacterial overgrowth (SIBO) in patients with active H. pylori infection assessed by functional breath testing.

Primary adult-type lactose malabsorption (PALM) is a widespread inherited autosomal recessive condition, which is considered to be associated with osteoporosis. This prospective study aimed at assessing the 25-hydroxy-vitamin D (25(OH)D) status and serum CrossLaps levels in individuals with PALM and normal controls. All participants (n=210) underwent genotyping for the LCT C/T-13910 polymorphism, 25(OH)D and CrossLaps measurements and clinical examinations. In addition, the anthropometric data (that is, height, weight and body mass index) were determined. Fifty-five individuals with PALM (that is, LCT C/C-13910 homozygotes) showed lower 25(OH)D (mean: 24.95±10.04 vs 28.59±9.56 ng/ml, P=0.018) and higher CrossLaps serum levels (mean: 0.46±0.31 vs 0.43±0.49 ng/ml, P=0.251) compared with 155 normal controls (that is, LCT C/T-13910 hetero- or T/T-13910 homozygotes). Anthropometric data were similar between PALM probands and controls. Individuals with PALM were found to have lower 25(OH)D and higher CrossLaps serum levels compared with normal controls. In order to preserve life-long bone health, routine 25(OH)D and CrossLaps serum measurements should be performed in individuals with PALM.

Objectives: Cardiovascular risk is increased in obese subjects. Nevertheless, some overweight and obese individuals are cardio-metabolically healthy. Conversely, cardio metabolic abnormalities are found among normal-weight individuals. Hence, there is a need to identify persons at risk for cardio metabolic disease independent of BMI. Herein, we investigate the potential of branched-chain amino acids (BCAAs) to identify such individuals.

Background: Carbohydrate malabsorption is a considerable problem in patients with non-specific abdominal complaints. While lactose malabsorption is well investigated, few epidemiologic data are available for fructose and sorbitol malabsorption or combined carbohydrate malabsorption syndromes. The purpose of this study was to assess the prevalence rates for primary lactose malabsorption, fructose and sorbitol malabsorption, and carbohydrate-specific small intestinal bacterial overgrowth (cs-SIBO) in an Austrian outpatient center. Additionally the diagnostic value of methane (CH4) measurements in carbohydrate malabsorption breath testing was evaluated.