Ahmet Muzaffer Demir

The effects of fat distribution and some adipokines on insulin resistance.

INTRODUCTION The risk of developing insulin resistance and metabolic syndrome is particularly high in central obesity. In this study we evaluated the effects of fat distribution and some adipokines on insulin resistance in prediabetic patients. MATERIAL AND METHODS Eighty-seven age- and sex-matched patients were divided into three groups according to their 75-gram oral glucose tolerance test results as follows: impaired fasting glucose group, impaired glucose tolerance group, and normal glucose tolerance group. Fasting insulin levels were measured. Homeostatic model assessment of insulin resistance was calculated. Body fat mass measurements were assessed by bioelectric impedance analyser and abdominal fat thicknesses (subcutaneous, visceral, and preperitoneal) by ultrasonography. The fasting serum levels of several adipokines [adiponectin, leptin, resistin, vaspin, visfatin, retinol-binding protein-4 (RBP-4), tumour necrosis factor-alpha (TNF-alpha)] were measured by ELISA method. RESULTS The mean body mass index, fat mass measurements, and abdominal fat thicknesses of the groups were similar. There were no differences between groups in terms of the mean fasting insulin, vaspin, RBP-4, leptin, resistin, and TNF-alpha. In comparison of the prediabetic and normal groups, the levels of adiponectin (p < 0.001) and visfatin (p < 0.001) were lower in the prediabetic group. Furthermore, we found that high body mass index (p < 0.01) and fat mass (p < 0.01) and low adiponectin (p < 0.05) levels have roles in the development of insulin resistance in the prediabetic group. CONCLUSIONS We suggested that in the prediabetic period not only obesity but also decreased adiponectin levels play some role in the pathogenesis of insulin resistance. (Endokrynol Pol 2016; 67 (3): 277-282).

High-intensity interval training acutely alters plasma adipokine levels in young overweight/obese women

Abstract The aim of this study was to investigate the plasma adipokine responses to high-intensity interval training (HIT) in overweight/obese women. Twelve women (age 21.7 ± 3.8 years) completed a 19 days of HIT comprising six session of 4–6 repeats of a Wingate test (0.065 kg load/kg). Plasma adipokine levels were measured before exercise, and at 5 and 90 min after exercise on the first and the last training days. Adiponectin was higher at 5 min than 90 min post-exercise (11.7 ± 7.3 and 10.5 ± 5.8 ng/ml; p = .01) in the first exercise day. Leptin decreased 5 min after exercise (23.6 ± 13.2 vs. baseline 27.8 ± 14.4 ng/ml; p < .01) and remained depressed following 90 min (p < .01). The changes in adiponectin and leptin concentrations were similar on the first and last exercise days. No consistent effect was found on resistin concentration. Future studies are required to disclose the functional consequences of these alterations in plasma adipokine levels.

Multiple Liver and Muscle Abscesses and Sepsis with Bacillus pantothenticus in a Leukemia Patient.

Received/Geliş tarihi : September 14, 2013 Accepted/Kabul tarihi : December 16, 2013 To the Editor, Bacilli infections in patients with hematological disorders have been reported, although rare, and subtypes such as Bacillus pantothenticus have been reported in immunocompetent patients with liver abscess [1]. Here we present a case of acute myeloid leukemia and multiple liver and muscle abscesses and sepsis with B. pantothenticus during the neutropenic period, treated successfully with meropenem. Informed consent was obtained. A 49-year-old male patient diagnosed with acute myeloid leukemia was started on remission induction chemotherapy with cytosine arabinoside and idarubicin (7+3). On day 8 of treatment, he had severe neutropenia (40/mm3) and fever (40.0 °C). His physical examination was normal, without organomegaly or tenderness, revealing no hints regarding the source of infection. According to the American Society of Clinical Oncology guidelines for febrile neutropenia, cefepime was started empirically at 2 g 3 times daily after blood and urine samples for culture had been obtained. After 48 h, the patient still had fever (38.3 to 39.4 °C) as tested 6 times a day. The antibiotherapy was switched to meropenem at 1 g 3 times daily following a second set of samples for culture. Fever persisted despite 48 h of meropenem treatment. Serum galactomannan antigen was negative. Thorax computerized tomography revealed no lung infection but multiple masses were seen in the liver (the largest being 3 cm). Magnetic resonance imaging indicated multiple liver abscesses with central necrosis and peripheral contrast enhancement with a single focus of abscess localized in the right paravertebral muscle groups with similar properties (Figure 1).

Thalidomide for the Management of Bleeding Episodes in Patients with Hereditary Hemorrhagic Telangiectasia, Effects on Epistaxis Severity Score and Quality of Life

Address for Correspondence/Yazışma Adresi: Mehmet BAYSAL, M.D., Trakya University Faculty of Medicine, Department of Hematology, Edirne, Turkey Phone : +90 284 235 76 41/2687 E-mail : drmehmetbaysal@gmail.com ORCID-ID: orcid.org/0000-0001-7681-4623 Received/Geliş tarihi: June 02, 2018 Accepted/Kabul tarihi: June 08, 2018 ©Copyright 2019 by Turkish Society of Hematology Turkish Journal of Hematology, Published by Galenos Publishing House Introduction Hereditary hemorrhagic telangiectasia (HHT) is a rare autosomal dominant disorder characterized by telangiectasia and arteriovenous malformations of the skin, mucosal tissues, and internal organs including the gastrointestinal tract, liver, and lungs. Its prevalence is estimated to be between 1/5000 and 1/10,000 worldwide. Recurrent epistaxis due to nasal telangiectasia is the most common finding [1,2]. There are several mutations linked with the disease and the most frequent mutations are reported as the ENG gene encoding endoglin and the ACVRL1 gene encoding activin A receptor type II-like kinase 1 [3]. Anemia is a very common symptom in HHT patients, not only due to bleeding from telangiectases located in the nasal mucosa but also to telangiectases located in the gastrointestinal tract, especially active in older ages. The diagnostic criteria for HHT were defined in 2000 and updated in 2011, including epistaxis, telangiectases, vascular malformations, and family history. The presence of 3 of these criteria is suggested to be sufficient for diagnosis [4]. Since epistaxis is the most common

Drug Induced Thrombotic Microangiopathy with Certolizumab Pegol

Background: Certolizumab pegol is used to treat ankylosing spondylitis, Crohn’s disease, psoriatic arthritis, and rheumatoid arthritis. Unlike other monoclonal antibodies such as infliximab and adalimumab, certolizumab does not contain an Fc fraction and hence does not induce complement activation. In this report, we describe the case of a patient with thrombotic microangiopathy caused due to certolizumab pegol, with a brief description about the pathophysiological approach to thrombotic microangiopathy. Case Report: A-39-year-old man suffering from ankylosing spondylitis for the past 10 years presented with fatigue. He had been on certolizumab pegol treatment for 6 months, starting with 400 and 200 mg every 2 weeks. He had significant nonimmune hemolytic anemia and thrombocytopenia without a disseminated intravascular coagulopathy. Schistocytes were observed in more than 10% of the erythrocytes per field. Plasma exchange along with corticosteroid treatment was started. There was a dramatic improvement within a week, and after 10 sessions of plasma exchange, the patient was discharged on corticosteroids with a tapering plan. ADAMTS13 enzyme activity was determined to be normal. Conclusion: The development of drug-induced thrombotic microangiopathy may be either immune-mediated or dose-dependent toxicity-mediated Anti-drug antibodies and their immunological aspects are still unclear and yet to be elucidated.

Hypogammaglobulinemia and Poor Performance Status are Predisposing Factors for Vancomycin Resistant Enterococcus Colonization in patients with Hematological Malignancies.

Objective: Vancomycin-resistant enterococci (VRE) are common pathogens of hospital-acquired infection. Long hospitalization periods, use of broad-spectrum antibiotics, and immunosuppression are major risks for VRE colonization. We aimed to evaluate patients’ characteristics and factors that may contribute to VRE colonization. Materials and Methods: Data of 66 patients with colonization and 112 patients without colonization who were hospitalized in the hematology clinic were collected. Hematological malignancies, preexisting gastrointestinal complaints, the presence of hypogammaglobulinemia at the time of diagnosis, complications like neutropenic enterocolitis (NEC), and Eastern Cooperative Oncology Group (ECOG) and Karnofsky performance statuses were recorded. Results: Ages of the patients ranged between 19 and 95 years (mean: 55.99). Karnofsky and ECOG scores were statistically related to VRE colonization (p<0.000 and p<0.000), though only the Karnofsky score was significant based on logistic regression analysis. Almost all patients with acute leukemia (45 patients) had been on antibiotics (piperacillin-tazobactam, ceftazidime, and meropenem), while no patients with myelodysplastic syndrome, myeloma, or benign diseases and 2 patients with lymphoma and 1 with chronic myeloid leukemia were on antibiotics. Median time for colonization regardless of antibiotic use and diagnosis was 4.5 days (range: 3-11 days). In the VRE-colonized group, 40.9% of patients had NEC development, while in the non-colonized group, only 1.7% had NEC development. In the VRE-colonized group 46 patients (69.7%) and in the non-colonized group 27 patients (24.1%) had hypogammaglobulinemia at diagnosis; among these patients, 23 patients in the VRE-colonized group (50%) had a B-cell malignancy (lymphoma, myeloma, or chronic lymphocytic leukemia). Conclusion: Besides already anticipated diseases like leukemia, B-cell malignancies are also at high risk for colonization. This proclivity may be attributed to lack of gastrointestinal IgA due to hypogammaglobulinemia. Prolonged hospitalization (>7 days) may also be accepted as a risk factor, independent of diagnosis or antibiotic use. Performance status is also an important factor for colonization, which may be related to poorer hygiene and increased external help.

CD11c expression in chronic lymphocytic leukemia revisited, related with complications and survival

Chronic lymphocytic leukemia (CLL) is a disorder of mature but dysfunctional monoclonal B cells. Microenvironment, antigenic stimulation and genetical mutations are demonstrated in etiopathogenesis. We aimed to evaluate the expression of CD11c in patients with CLL and its possible clinical significance.

Could the mosaic pattern of chromosomal abnormality predict overall survival of patients with myelodysplastic syndrome

OBJECTIVE/BACKGROUND Myelodysplastic syndromes (MDSs) are a group of monoclonal hematopoietic diseases consisting of a number of various entities. The presence of differences in chromosomal content of cells within the same individual is known as chromosomal mosaicism. The impact of mosaic pattern on the prognosis of MDS has been unclear. In this study, we aimed to determine the impact of mosaic pattern on the survival of patients with MDS. METHODS We retrospectively evaluated 119 patients diagnosed with MDS at the Trakya University Faculty of Medicine, Department of Hematology. Giemsa-Trypsin-Giemsa banding was used to evaluate chromosomal abnormality. The effect of chromosomal abnormality mosaicism on overall survival and transformation to acute leukemia was evaluated by Kaplan-Meier survival analysis. RESULTS The mean age at diagnosis was 66.3years, and the mean disease duration was 24.2months. Chromosomal abnormality was observed in 32.5% of patients. Patients with chromosomal abnormalities comprising at least 50% metaphases had significantly lower overall survival than patients with abnormality comprising up to 50% of all abnormal metaphases (p=.003). There were no differences in transformation to acute leukemia among patients with higher and lower chromosomal mosaicism (p=.056). CONCLUSION The most important outcome of this study was to demonstrate worse overall survival rates in MDS patients with higher abnormal chromosomal mosaicism than patients with lesser abnormal chromosomal mosaicism. Higher levels of abnormal chromosomal mosaicism did not predict transformation to acute leukemia. The cause of worse outcomes of patients with higher abnormal chromosomal mosaicism may be related to clonal mass.

Effect of obesity on TAFI in postmenopausal period

SUMMARY AIM The aim of the study was to evaluate how obesity effects the coagulation and fibrinolytic system in the postmenopausal period. METHOD Forty-eight obese (body mass index (BMI) ≥30 kg/m(2)) and 38 nonobese (BMI < 30 kg/m(2)) postmenopausal women were enrolled in the study. Fat mass and insulin resistance were calculated. Plasma levels of plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA), d-dimer, thrombomodulin, and thrombin activatable fibrinolysis inhibitor (TAFI) antigen were determined by ELISA method. TAFI activity was measured using the chromogenic assay. RESULTS Obese subjects had higher PAI-1 (73.5 ± 35.7 ng/mL vs. 57.1 ± 34.2 ng/mL, p < 0.05) levels but lower tPA/PAI-1 ratio (0.59 ± 0.50 vs. 38 ± 0.21, p < 0.05) than their nonobese counterparts. Obesity was not statistically significant for other haemostatic variables. BMI and fat mass were positively correlated with PAI-1 (r = 0.312, p = 0.003; r = 0.381, p = 0.005, respectively) and negatively correlated with tPA/PAI-1 ratio (r = -0.273, p = 0.01; r = -0.545, p = 0.01, respectively). HOMA scores were also positively correlated with PAI-1 levels (r = 0.236, p = 0.04). CONCLUSION We found that tendency to hypercoagulability in the postmenopausal women was due to increased PAI-1 rather than TAFI levels, which may contribute to adverse cardiovascular outcomes in this cohort. Further studies should be undertaken to evaluate effects of weight loss on the coagulation and fibrinolytic system.