BACKGROUND:The need for minimally invasive biomarkers for the early diagnosis of type 2 diabetes (T2DM) prior to the clinical onset and monitoring of β-pancreatic cell loss is emerging. Here, we focused on studying circulating cell-free DNA (ccfDNA) as a liquid biopsy biomaterial for accurate diagnosis/monitoring of T2DM. METHODS:ccfDNA levels were directly quantified in sera from 96 T2DM patients and 71 healthy individuals via fluorometry, and then fragment DNA size profiling was performed by capillary electrophoresis. Following this, ccfDNA methylation levels of five β-cell-related genes were measured via qPCR. Data were analyzed by automated machine learning to build classifying predictive models. RESULTS:ccfDNA levels were found to be similar between groups but indicative of apoptosis in T2DM. INS (Insulin), IAPP (Islet Amyloid Polypeptide-Amylin), GCK (Glucokinase), and KCNJ11 (Potassium Inwardly Rectifying Channel Subfamily J member 11) levels differed significantly between groups. AutoML analysis delivered biosignatures including GCK, IAPP and KCNJ11 methylation, with the highest ever reported discriminating performance of T2DM from healthy individuals (AUC 0.927). CONCLUSIONS:Our data unravel the value of ccfDNA as a minimally invasive biomaterial carrying important clinical information for T2DM. Upon prospective clinical evaluation, the built biosignature can be disruptive for T2DM clinical management.

Our aim was to estimate the date of the origin and the transmission rates of the major local clusters of subtypes A1 and B in Greece. Phylodynamic analyses were conducted in 14 subtype A1 and 31 subtype B clusters. The earliest dates of origin for subtypes A1 and B were in 1982.6 and in 1985.5, respectively. The transmission rate for the subtype A1 clusters ranged between 7.54 and 39.61 infections/100 person years (IQR: 9.39, 15.88), and for subtype B clusters between 4.42 and 36.44 infections/100 person years (IQR: 7.38, 15.04). Statistical analysis revealed that the average difference in the transmission rate between the PWID and the MSM clusters was 6.73 (95% CI: 0.86 to 12.60; p = 0.026). Our study provides evidence that the date of introduction of subtype A1 in Greece was the earliest in Europe. Transmission rates were significantly higher for PWID than MSM clusters due to the conditions that gave rise to an extensive PWID HIV-1 outbreak ten years ago in Athens, Greece. Transmission rate can be considered as a valuable measure for public health since it provides a proxy of the rate of epidemic growth within a cluster and, therefore, it can be useful for targeted HIV prevention programs.

OBJECTIVES:Recent evidence has linked circadian rhythm dysregulation to an increased risk of metabolic disorders. This study explores a potential association between variation in genes regulating the endogenous circadian timing system (clock genes) and the risk of type 2 diabetes (T2D) in a sample of Greek elderly people.STUDY DESIGN:Variants within and upstream or downstream of PPARA, PPARD, CLOCK/TMEM165, PER1, PER2 and PER3 genes were genotyped in 716 individuals with T2D (A) and 569 normoglycemic controls (B), and allele frequencies were compared between the groups in a case control study design.MAIN OUTCOME MEASURES:Samples were genotyped on Illumina Human PsychArray. Permutation test analysis was implemented to determine statistical significance. To avoid the possibility of subjects with prediabetes being included in the control group, people with HbA1c <5.7% and fasting glucose <100 mg/dl comprised group C (n = 393), for whom a separate analysis was performed (secondary analysis).RESULTS:A protective role against T2D was identified for 14 variants in the PPARA gene. The rs7291444, rs36125344, rs6008384 in PKDREJ, located upstream of PPARA, and rs2859389 in UTS2, located upstream of PER3, demonstrated a protective role against T2D in both analyses. In contrast, rs6744132, located between HES6 and PER2, was positively correlated with T2D risk. Only in the secondary analysis, rs2278637 in VAMP2, located downstream of PER1, and rs11943456 in CLOCK/TMEM165 were found to confer protection against T2D. In a recessive model analysis of all groups, PPARD variants exhibited a protective role against disease.CONCLUSIONS:Our findings suggest a possible implication of clock genes in T2D susceptibility. Further studies are needed to clarify the mechanisms that connect circadian rhythm dysfunction and T2D pathogenesis.

Introduction: The aim of this study was to estimate the prevalence of Type 2 Diabetes and related metabolic disorders in the Evros region. Material-Methods: A random sample of 541 people was studied using the Finnish Type 2 Diabetes Risk Score, and measurement of weight, height, waist and hip circumference, blood pressure, as well as Fasting Glucose and Postprandial Glucose with a reflectometer. The participants with a score of 15-20, score ≥20, FG ≥100 mg/dl and / or PG 140 mg/dl (n = 206) were subjected to a oral glucose tolerance test, according to WHO. Lipid profile, metabolic syndrome and cardiovascular risk were also assessed. Results: Prevalence of DM T2 in the study population was: 29.6%, and that of prediabetes was 10.9%. Obese (Body Mass Index ≥ 30 kg/m2) were: 52.5%, overweight (BMI 25-30kg/m2) were 33.2% and normal/low weight (BMI <25 kg/m2) were 14.1% of the population. Central obesity with a waist circumference of ≥ 102cm had 58,6% of men and ≥ 88cm 86,8% of women. Hypertension was 66.9% of the sample and 58.8% were on antihypertensive treatment. In 206 subjects, CHOL 200-239 mg/dl had 32.5% and CHOL≥ 240 mg/ dl 13.6%. 10.2% of women had HDL – CHOL <45 and <35:3,4 % of men. 5,9 % of subjects had LDL – CHOL≥ 160 mg/dl. 18% of subjects had TG: 200 – 499 mg/dl and TG ≥ 500 mg/dl:1.5%. High index Apo-B / Apo-A1 had 19.4% and Lp (a) 33% of individuals. 92.2% of these people had metabolic syndrome. Conclusions: The upward trend of DM T2 and cardiometabolic risk parameters raises the need for targeted prevention and treatment policies.

BackgroundMyasthenia gravis (MG) is a rare autoimmune disorder affecting the neuromuscular junction (NMJ). Here, we investigate the genetic architecture of MG via a genome-wide association study (GWAS) of the largest MG data set analysed to date.MethodsWe performed GWAS meta-analysis integrating three different data sets (total of 1401 cases and 3508 controls). We carried out human leucocyte antigen (HLA) fine-mapping, gene-based and tissue enrichment analyses and investigated genetic correlation with 13 other autoimmune disorders as well as pleiotropy across MG and correlated disorders.ResultsWe confirmed the previously reported MG association with TNFRSF11A (rs4369774; p=1.09×10−13, OR=1.4). Furthermore, gene-based analysis revealed AGRN as a novel MG susceptibility gene. HLA fine-mapping pointed to two independent MG loci: HLA-DRB1 and HLA-B. MG onset-specific analysis reveals differences in the genetic architecture of early-onset MG (EOMG) versus late-onset MG (LOMG). Furthermore, we find MG to be genetically correlated with type 1 diabetes (T1D), rheumatoid arthritis (RA), late-onset vitiligo and autoimmune thyroid disease (ATD). Cross-disorder meta-analysis reveals multiple risk loci that appear pleiotropic across MG and correlated disorders.DiscussionOur gene-based analysis identifies AGRN as a novel MG susceptibility gene, implicating for the first time a locus encoding a protein (agrin) that is directly relevant to NMJ activation. Mutations in AGRN have been found to underlie congenital myasthenic syndrome. Our results are also consistent with previous studies highlighting the role of HLA and TNFRSF11A in MG aetiology and the different risk genes in EOMG versus LOMG. Finally, we uncover the genetic correlation of MG with T1D, RA, ATD and late-onset vitiligo, pointing to shared underlying genetic mechanisms.

ObjectiveThe clinical profile, management and outcome of infective endocarditis (IE) may be influenced by socioeconomic issues.MethodsA nationwide prospective study evaluated IE during the era of deep economic crisis in Greece. Epidemiological data and factors associated with 60-day mortality were analyzed through descriptive statistics, logistic and Cox-regression models.ResultsAmong 224 patients (male 72.3%, mean age 62.4 years), Staphylococcus aureus (n = 62; methicillin-resistant S. aureus (MRSA) 33.8%) predominated in the young without impact on mortality (p = 0.593), whilst Enterococci (n = 36) predominated in the elderly. Complications of IE were associated with mortality: heart failure [OR 2.415 (95% CI: 1.159–5.029), p = 0.019], stroke [OR 3.206 (95% CI: 1.190–8.632), p = 0.018] and acute kidney injury [OR 2.283 (95% CI: 1.085–4.805), p = 0.029]. A 60-day survival benefit was solely related to cardiac surgery for IE during hospitalization [HR 0.386 (95% CI: 0.165–0.903), p = 0.028] and compliance with antimicrobial treatment guidelines [HR 0.487 (95% CI: 0.259–0.916), p = 0.026]. Compared with a previous country cohort study, history of rheumatic fever and native valve predisposition had declined, whilst underlying renal disease and right-sided IE had increased (p < 0.0001); HIV infection had emerged (p = 0.002). No difference in rates of surgery and outcome was assessed.ConclusionsA country-wide survey of IE highlighted emergence of HIV, right-sided IE and predominance of MRSA in the youth during a severe socioeconomic crisis. Compliance with treatment guidelines promoted survival.

Background: Approximately one third of type 2 diabetes mellitus (T2DM) cases present with diabetic nephropathy (DN), the leading cause of end-stage renal disease. Inflammation plays an important role in T2DM disease and DN pathogenesis. NLRP3 inflammasomes are complexes that regulate interleukin-1B (IL-1B) and IL-18 secretion, both involved in inflammatory responses. Activation of NLRP3 is associated with DN onset and progression. Here, we explore whether DN is associated with variants in genes encoding key members of the NLRP3 inflammasome pathway. Methods: Using genome-wide association data, we performed a pilot case-control association study, between 101 DN-T2DM and 185 non-DN-T2DM cases from the Hellenic population across six NLRP3 inflammasome pathway genes. Results: Three common CARD8 variants confer decreased risk for DN, namely rs11665831 (OR = 0.62, p = 0.016), rs11083925 (OR = 0.65, p = 0.021), and rs2043211 (OR = 0.66, p = 0.026), independent of sex or co-inheritance with an IL-1B variant. Conclusion: CARD8 acts as an NLRP3, NF-κB and caspase-1 inhibitor; perhaps, alterations in the cross-talk between CARD8, NF-κB, and NLRP3, which could affect the pro-inflammatory environment in T2DM, render diabetic carriers of certain common CARD8 variants potentially less likely to develop T2DM-related pro-inflammatory responses followed by DN. These preliminary, yet novel, observations will require validation in larger cohorts from several ethnic groups.

Objectives Subtypes A1 and B are the most prevalent HIV-1 clades in Greece. Subtype A1 epidemic is highly monophyletic and corresponds to transmissions that occurred locally. Our aim in this molecular epidemiology analysis was to investigate the role of early treatment in preventing new HIV-1 transmissions. Methods Our analysis focused on 791 subtype A1 sequences from treatment-naïve individuals in Greece. Estimation of infection dates was performed by molecular clock calculations using Bayesian methods. We estimated the time interval between (1) the infection and sampling dates (linkage to care window), (2) the sampling dates and antiretroviral therapy (ART) initiation (treatment window), and (3) the infection dates and ART initiation (transmissibility window) for the study population. We also inferred the putative source of HIV infections between individuals of different groups divided according to the length of treatment, linkage to care or transmissibility window. Results A significant decline was detected for the treatment window during 2014–2015 versus the 2 previous years (p=0.0273), while the linkage to care interval remained unchanged during the study period. Inference of the putative source of HIV infections suggested that individuals with a recent diagnosis or narrow transmissibility window (time period between HIV infection and ART initiation) were not sources of HIV infections to other groups. Contrarily, a significant number of HIV infections originated from individuals with longer transmissibility window interval. Conclusions Our findings showed that the treatment window is decreasing over time, presumably due to the updated treatment guidelines. Our study also demonstrates that people treated earlier after infection do not transmit at high rates, thus documenting the benefits of early ART initiation in preventing ongoing HIV-1 transmission.

Background: Approximately one third of type 2 diabetes mellitus (T2DM) cases present with diabetic nephropathy (DN), the leading cause of end-stage renal disease. Inflammation plays an important role in T2DM disease and DN pathogenesis. NLRP3 inflammasomes are complexes that regulate interleukin-1B (IL-1B) and IL-18 secretion, both involved in inflammatory responses. Activation of NLRP3 is associated with DN onset and progression. Here, we explore whether DN is associated with variants in genes encoding key members of the NLRP3 inflammasome pathway. Methods: Using genome-wide association data, we performed a pilot case-control association study, between 101 DN-T2DM and 185 non-DN-T2DM cases from the Hellenic population across six NLRP3 inflammasome pathway genes. Results: Three common CARD8 variants confer decreased risk for DN, namely rs11665831 (OR = 0.62, p = 0.016), rs11083925 (OR = 0.65, p = 0.021), and rs2043211 (OR = 0.66, p = 0.026), independent of sex or co-inheritance with an IL-1B variant. Conclusion: CARD8 acts as an NLRP3, NF-κB and caspase-1 inhibitor; perhaps, alterations in the cross-talk between CARD8, NF-κB, and NLRP3, which could affect the pro-inflammatory environment in T2DM, render diabetic carriers of certain common CARD8 variants potentially less likely to develop T2DM-related pro-inflammatory responses followed by DN. These preliminary, yet novel, observations will require validation in larger cohorts from several ethnic groups.

Assessment for cardiovascular autonomic neuropathy (CAN) remains difficult in everyday clinical practice. We sought to examine the diagnostic utility of various simple tools for diabetic peripheral neuropathy (DPN) in the detection of CAN in type 2 diabetes mellitus. We examined 153 type 2 diabetes mellitus subjects by various DPN tools (vibration perception threshold, 10 g Semmes-Weinstein monofilament, Ipswich touch test, NC-stat®/DPNCheck, neuropathy disability score) for the detection of CAN. CAN was diagnosed by the standardised cardiovascular autonomic reflex function tests. For the diagnosis of CAN, assessment of small nerve fibre function (pinprick sensation, temperature perception) yielded a very high negative predictive value (97%), with high sensitivity (89%) and moderate specificity (73%). The vibration perception threshold was second in diagnostic utility (91% negative predictive value, 62% sensitivity and 75% specificity). Based on their high negative predictive value, simple tools for DPN may prove useful to exclude CAN in type 2 diabetes mellitus. These encouraging results merit further evaluation to enable wider screening for CAN.

AbstractBackgroundMyasthenia Gravis (MG) is a rare autoimmune disorder affecting the neuromuscular junction. Here, we investigate the genetic architecture of MG performing a genomewide association study (GWAS) of the largest MG dataset analyzed to date.MethodsWe integrated GWAS from three different datasets (1,401 cases, 3,508 controls) and performed MG GWAS and onset-specific analyses. We also carried out HLA fine-mapping, gene-based, gene ontology and tissue enrichment analyses and investigated genetic correlation to other autoimmune disorders.FindingsWe observed the strongest MG association toTNFRSF11A(rs4369774, p=1.09×10−13; OR=1.4). Gene-based analysis revealedAGRNas a novel MG susceptibility gene. HLA fine-mapping pointed to two independent loci significantly associated with MG:HLA-DRB1(with a protective role) andHLA-B. MG onset-specific analysis, reveals differences in the genetic architecture of Early-Onset vs Late-Onset MG. Furthermore, we find MG to be genetically correlated with Type 1 Diabetes, Rheumatoid Arthritis and late-onset Vitiligo.InterpretationOverall, our results are consistent with previous studies highlighting the role of the HLA andTNFRSF11Ain MG etiology and different risk genes in EOMG vs LOMG. Furthermore, our gene-based analysis implicates, for the first time,AGRNas a MG susceptibility locus.AGRNencodes agrin, which is involved in neuromuscular junction formation. Mutations inAGRNhave been found to underlie congenital myasthenic syndrome. Gene ontology analysis suggests an intriguing role for symbiotic processes in MG etiology. We also uncover genetic correlation of MG to Type 1 Diabetes, Rheumatoid Arthritis and late-onset Vitiligo, pointing to shared underlying genetic mechanisms.FundingThis work was supported by NSF award #1715202, the European Social Fund and Greek funds through the National Strategic Reference Framework (NSRF) THALES Programme 2012–2015 and the NSRF ARISTEIA II Programme 2007–2013 to PP, and grants from the Association Francaise contre les Myopathies (AFM, Grant No. 80077) to ST.Research in contextEvidence before this studyMyasthenia Gravis (MG) is a complex disease caused by the interaction of genetic and environmental factors that lead to autoimmune activation. Previous studies have shown that the human leukocyte antigen (HLA) displays the most robust genetic association signals to MG. Additional susceptibility genes that have emerged through genomewide association studies (GWAS), includeCTLA4andTNFRSF11A. Previous studies also support the hypothesis of distinct risk loci underlying Early-Onset versus Late-Onset MG subgroups (EOMG vs LOMG). For instance,PTPN22andTNIP1genes have been implicated in EOMG andZBTB10in LOMG. In the GWAS studies published so far,HLAandTNFRSF11Aassociations appear to be confirmed; however, the association of other implicated genes still requires replication.Added value of this studyWe present the largest GWAS for MG to date, integrating three different datasets. We identifyAGRNas a novel MG risk locus and replicate previously reported susceptibility loci, including HLA,TNFRSF11A, and CTLA4. Our analysis also supports the existence of a different genetic architecture in EOMG vs LOMG and identifies a region betweenSRCAPandFBRSas a novel EOMG risk locus. Additionally, through HLA fine-mapping, we observe different HLA genes implicated in EOMG vs LOMG (HLA-BandHLA-DRB1respectively). Finally, we detect positive genetic correlation of MG with other autoimmune disorders including Type 1 Diabetes, Rheumatoid Arthritis, and late-onset Vitiligo, suggesting a shared genetic basis across them.Implications of all the available evidenceOur study sheds light into the etiology of MG identifyingAGRNas a novel risk locus.AGRNencodes agrin, a protein with a significant role in the formation of the neuromuscular junction and mutations in this gene have been associated with congenital myasthenic syndrome. Our findings hint to an intriguing hypothesis of symbiotic processes underlying MG pathogenesis and points to muscle growth and development in EOMG and steroid hormones synthesis in LOMG. The observed genetic correlations between MG and certain other autoimmune disorders could possibly underlie comorbidity patterns across this group of disorders.

The aim of the study was to evaluate antifungal prescriptions among hospitalized adult patients in Greek hospitals. This multicenter two-times, 1-day, point-prevalence study was carried out in 2015 and 2017 in five and six hospitals, respectively. Among the 5812 patients screened in both periods, antifungals were prescribed in 129 patients (73 in 2015 and 56 in 2017); antifungals were used as prophylaxis in 31 patients (24%), pre-emptively in 32 (25%), empirically in 38 (30%), and as targeted therapy in 28 (22%). Triazoles were the class most commonly used (65 patients; 50%), followed by echinocandins (59; 46%) and liposomal amphotericin B (12; 9%). The use of echinocandins was higher (P 0.009) in the ICU (16 out of 22 patients), as compared with those in other departments (40%). Antifungal treatment was deemed inappropriate in 32/129 patients (25%) (16% in 2015 versus 36% in 2017; P 0.014). Inappropriate antifungal administration was more common if indicated by the primary physician, as compared with an infectious disease specialist (35% versus 5%; P < 0.001). Candidemia represented the majority of microbiologically documented infections (12 out of 28). Only two cases of proven pulmonary aspergillosis were diagnosed. Fluconazole and echinocandins were most frequently prescribed for identified or presumptive fungal infections, while fluconazole or posaconazole was given most frequently as prophylaxis. Antifungal treatment has been, ultimately, proven unnecessary in one-fourth of cases, underlining the need of a nationwide antifungal stewardship program.

Abstract Background The effect of neuraminidase inhibitor (NAI) treatment on length of stay (LoS) in patients hospitalized with influenza is unclear. Methods We conducted a one-stage individual participant data (IPD) meta-analysis exploring the association between NAI treatment and LoS in patients hospitalized with 2009 influenza A(H1N1) virus (A[H1N1]pdm09) infection. Using mixed-effects negative binomial regression and adjusting for the propensity to receive NAI, antibiotic, and corticosteroid treatment, we calculated incidence rate ratios (IRRs) and 95% confidence intervals (CIs). Patients with a LoS of <1 day and those who died while hospitalized were excluded. Results We analyzed data on 18 309 patients from 70 clinical centers. After adjustment, NAI treatment initiated at hospitalization was associated with a 19% reduction in the LoS among patients with clinically suspected or laboratory-confirmed influenza A(H1N1)pdm09 infection (IRR, 0.81; 95% CI, .78–.85), compared with later or no initiation of NAI treatment. Similar statistically significant associations were seen in all clinical subgroups. NAI treatment (at any time), compared with no NAI treatment, and NAI treatment initiated <2 days after symptom onset, compared with later or no initiation of NAI treatment, showed mixed patterns of association with the LoS. Conclusions When patients hospitalized with influenza are treated with NAIs, treatment initiated on admission, regardless of time since symptom onset, is associated with a reduced LoS, compared with later or no initiation of treatment.

A significant progress has been made over the years in the prognosis and treatment of patients with early diagnosis of HIV infection. However, late presentation of a large number of patients remains a serious public health problem. The aim of our study is to highlight the dimensions of the problem by evaluating the data from the HIV Unit of Alexandroupolis, a rural region with population heterogeneity and a strategic position between West and East, Europe, and Asia. This was a retrospective study, including 107 patients diagnosed with HIV infection in our unit from 2010 to 2018. Late presenters (LP) were defined as patients diagnosed with a CD4 cell count <350/mm3 or an AIDS-defining condition regardless of CD4 cell count. The proportion of patients diagnosed late was 49.5%. The majority were males in the age group 31-40 years (41.5%). Men who had sex with men were 37.8%. Among LP, 34% were at Center for Disease Prevention and Control stage C3. The most common AIDS-defining condition observed was Pneumocystis jirovecii Pneumonia (15.1%), followed by esophageal candidiasis (7.5%) and cryptococcal meningitis (3.8%). In addition, immune reconstitution inflammatory syndrome was documented (3.8%). A high percentage of patients were also coinfected with hepatitis B (22.6%) virus. The notably high percentage of LP in our unit demonstrates that late presentation remains a challenge for public health. Further efforts must be made to ensure an early diagnosis of HIV infection. The early initiation of antiretroviral therapy is vital to reduce viral load to undetectable levels and the risk of HIV transmission.

BACKGROUND AND PURPOSE Evidence suggests that cardioembolism represents the underlying mechanism in the minority of embolic strokes of undetermined source (ESUS). In this population-based study, we sought to compare the clinical and imaging characteristics as well as outcomes in patients with ESUS and cardioembolic stroke (CE). METHODS We included consecutive patients with first-ever ischemic stroke (IS) from the previously published population-based Evros-Stroke-Registry identified as ESUS or CE according to standardized criteria. Baseline characteristics, admission NIHSS scores, cerebral edema, hemorrhagic transformation, stroke recurrence, functional outcomes (determined by modified Rankin Scale [mRS] scores), and mortality rates were recorded during the 1-year follow-up period. RESULTS We identified 21 ESUS (3.7% of IS) and 211 CE (37.1% of IS) cases. Patients with ESUS were younger (median age: 68 years [interquartile range [IQR]: 61-75] vs 80 years [IQR: 75-84]; P < .001), had lower median admission NIHSS scores (4 points [IQR: 2-8] vs 10 points [IQR: 5-17]; P < .001), and lower prevalence of cerebral edema on neuroimaging studies (0 vs. 33.3%, P = .002). Functional outcomes were more favorable in ESUS at 28 (median mRS score: 2 [IQR: 1-3] vs 4 [IQR: 4-5]; P < .001), 90 (median mRS score: 1 [IQR: 0-2] vs 4 [IQR: 3-5]; P < .001), and 365 days (median mRS score: 1 [IQR: 0-2] vs 4 [IQR: 2-4]; P < 0.001). At 1-year, the mortality rate was lower in ESUS (0% [95% confidence interval [CI]: 0-13.5%] vs 34.6% [95% CI: 28.2-41.0%]; P < .001); the 1-year recurrent rate was also lower numerically (0% [95% CI: 0-13.5%] vs 9.5% [95% CI: 5.5-13.4%]; P = .140) but this difference failed to reach statistical significance due to the small study population. CONCLUSIONS The clinical and neuroimaging profiles as well as clinical outcomes vary substantially between ESUS and CE indicating different underlying mechanisms.

Introduction: Embolic stroke of undetermined source (ESUS) represents a subgroup of cryptogenic ischemic stroke (CS) distinguished by high probability of an underlying embolic mechanism. There are scarce population-based data regarding the incidence, characteristics and outcomes of ESUS. Methods: Consecutive patients included with first-ever ischemic stroke of undetermined cause in the previously published population-based Evros Stroke Registry were further subdivided into ESUS and non-ESUS CS. Crude and adjusted [according to the European Standard Population (ESP), WHO and Segi population] incidence rates (IR) for ESUS and non-ESUS CS were calculated. Baseline characteristics, admission stroke severity (assessed using NIHSS-score), stroke recurrence and functional outcomes [determined by modified Rankin Scale (mRS) scores], were recorded during the 1-year follow-up period. Results: We identified 21 and 242 cases with ESUS (8% of CS) and non-ESUS CS. The crude and ESP-adjusted IR for ESUS were 17.5 (95%CI: 10-25) and 16.6 (95%CI: 10-24) per 100,000 person-years. Patients with ESUS were younger [median age 68 years (IQR:61-75) vs. 79 years (IQR:73-83); p<0.001] and had lower median admission NIHSS-scores [4 points (IQR:2-8) vs. 8 points (IQR:5-16); p<0.001]. Functional outcomes were more favorable in ESUS at 28 [median mRS-score: 2 (IQR:1-3) vs. 4 (IQR:3-6)], 90 [median mRS-score: 1 (IQR:0-2) vs. 4 (IQR:2-6)] and 365 days [median mRS-score: 1 (IQR:0-2) vs. 5 (IQR:2-6)]. ESUS was independently (p=0.033) associated with lower admission NIHSS-scores (unstandardized linear regression coefficient: -13.34;95%CI: -23.34, -3.35) on multiple linear regression models. ESUS was not related to 1-year stroke recurrence (HR: 0.22, 95%CI: 0.01-4.06), mortality (HR: 0.25, 95%CI: 0.02-4.36) and functional improvement (1-point shift in mRS-scores; cOR: 1.47, 95%CI: 0.59-3.70) on multivariable analyses. Conclusions: ESUS cases represented 8% of CS patients in this population-based study. Despite the fact that ESUS was independently related to lower admission stroke severity, there was no association of ESUS with long-term outcomes.

The aim of this study was to assess the performance of VibraTip, a device used to test a person’s vibration perception during routine checks for peripheral neuropathy, against two thresholds of the Neuropathy Disability Score (NDS) for diagnosing distal symmetrical polyneuropathy (DSPN) in patients with type 2 diabetes mellitus (T2DM). One hundred consecutive subjects with T2DM were enrolled in the study, of whom 54 were men. The mean age was 62.3 years, and the mean T2DM duration was 12.6 years. VibraTip was used at one foot site (on the pulp of the hallux; protocol A) and at three foot sites (pulp of the hallux and first and third metatarsal head; protocol B). NDS thresholds of  ≥ 3 and ≥ 6 were used to establish the diagnosis of DSPN. Against the NDS ≥ 3 threshold, VibraTip showed a very high sensitivity (91.3%) and negative predictive value (NPV) (92%) and a high specificity (85.2%) with protocol A, and a very high sensitivity (95.6%) and NPV (96.1%) and a very high specificity (90.7%) with protocol B. Against the NDS ≥ 6 threshold, VibraTip showed a very high sensitivity (100%) and NPV (100%) and a very high specificity (95.2%) with protocol A, and very high sensitivity (100%) and NPV (100%) and very high specificity (96.8%) with protocol B. The diagnostic performance of VibraTip is very high in patients with T2DM, rendering it a very useful device as a screening tool, particularly for the exclusion of DSPN. VibraTip performs very well at both NDS thresholds, but particularly well at the NDS ≥ 6 threshold. There appears to be no need to examine sites other than the hallux site with Vibratip.

BACKGROUND & OBJECTIVES:Visceral leishmaniasis is endemic in Greece, with sporadic cases reported annually both in the mainland and in coastal areas. Seroepidemiological studies across Greece report seropositivity rates from 0.5 to 15%, in different parts of the country. The aim of the present study was to evaluate the Leishmania seropositivity rate of the general population of Drama prefecture, a rich in water supply region, in northern Greece.METHODS:Serum samples collected from 347 healthy individuals were tested for IgG Leishmania infantum antibodies. Furthermore, 132 domestic dogs, clinically suspected to suffer from canine leishmaniasis, from all across the prefecture, were also evaluated.RESULTS:Among 347 healthy individuals tested, 24 (6.9%) were positive for IgG L. infantum antibodies. Age, gender, occupational and leisure time activities didn't show significant relation to IgG seropositivity, whereas low altitude of place of residency and residency at places with surface water were significantly related to IgG seropositivity. All seropositive individuals follow a geographic pattern, gathering themselves in Drama basin (rich in surface and underground water bodies), whereas canine leishmaniasis cases show a wide distribution across the prefecture.INTERPRETATION & CONCLUSION:Evaluation of both human seroprevalence and high incidence of canine leishmaniasis, as well as favorable landscape and climatic conditions of the study area, indicates that high level of clinical awareness need to be employed by physicians, as human and canine visceral leishmaniasis constitutes a serious public health concern.

Posters are an established mode of disseminating scientific research. They require careful preparation and presentation. During the former, the authors need to pay attention to the following features: choice of text, fonts and colors, illustrations and graphics, adequate presentation of methods and results, as well as to-the-point discussion of key messages. The latter is regrettably slightly neglected but very important. Indeed, poster presenters need to give a brief talk highlighting the research question and communicating the findings of the study, their novelty, and the anticipated clinical implications. In conclusion, practice is needed to create successful posters, but the result may be useful and pleasing.

Background: Nosocomial transmission is a major mode of infection of Crimean-Congo haemorrhagic fever (CCHF). In May 2018, a patient with CCHF was hospitalised in Greece. Objective: Our aim was to present the management of healthcare workers (HCWs) to the CCHF case. Methods: Contact tracing, risk assessment and follow-up of exposed HCWs were performed. Testing (RT-PCR and/or serology) was offered to contacts. Post-exposure prophylaxis (PEP) with ribavirin was considered for high-risk exposures. Results: Ninety-one HCWs were exposed to the case. Sixty-six HCWs were grouped as high-risk exposures. Ribavirin PEP was offered to 29 HCWs; seven agreed to receive prophylaxis. Forty-one HCWs were tested for CCHF infection; none was found positive. Gaps in infection control occurred. Discussion: CCHF should be considered in patients with compatible travel history and clinical and laboratory findings. Early clinical suspicion and laboratory confirmation are imperative for the implementation of appropriate infection control measures. Ribavirin should be considered for high-risk exposures. Infection control capacity for highly pathogenic agents should increase.