Mustafa Ozbek

The Association Between Severity of Vitamin D Deficiency and Hashimoto's Thyroiditis

OBJECTIVE The relation between vitamin D and autoimmune disorders has long been investigated regarding the important roles of this hormone in immune regulation. We evaluated 25-hydroxyvitamin D (25OHD) status in subjects with Hashimotos thyroiditis (HT) and healthy controls. METHODS Group-1 included 180 euthyroid patients (123 females/57 males) with HT who were on a stable dose of L-thyroxine (LT). A total of 180 sex-, age-, and body mass index (BMI)-matched euthyroid subjects with newly diagnosed HT were considered as Group-2, and 180 healthy volunteers were enrolled as controls (Group-3). All 540 subjects underwent thyroid ultrasound and were evaluated for serum 25OHD, anti-thyroid peroxidase (anti-TPO), and anti-thyroglobulin (anti-TG) levels. RESULTS Group-1 had the lowest 25OHD levels (11.4 ± 5.2 ng/mL) compared to newly diagnosed HT subjects (Group-2) (13.1 ± 5.9 ng/mL, P = .002) and to control subjects (15.4 ± 6.8 ng/mL, P<.001). Serum 25OHD levels directly correlated with thyroid volume (r = 0.145, P<.001) and inversely correlated with anti-TPO (r = -0.361, P<.001) and anti-TG levels (r = -0.335, P<.001). We determined that 48.3% of Group-1, 35% of Group-2, and 20.5% of controls had severe 25OHD deficiency (<10 ng/mL). Female chronic HT patients had the lowest serum 25OHD levels (10.3 ± 4.58 ng/mL), and male control subjects had the highest (19.3 ± 5.9 ng/mL, P<.001). CONCLUSIONS We demonstrated that serum 25OHD levels of HT patients were significantly lower than controls, and 25OHD deficiency severity correlated with duration of HT, thyroid volume, and antibody levels. These findings may suggest a potential role of 25OHD in development of HT and/or its progression to hypothyroidism.

Hypokalemic periodic paralysis in Sjogren’s syndrome secondary to distal renal tubular acidosis

We report a 53-year-old Turkish female presented with progressive weakness and mild dyspnea. Laboratory results demonstrated severe hypokalemia with hyperchloremic metabolic acidosis. The urinary anion gap was positive in the presence of acidemia, thus she was diagnosed with hypokalemic paralysis from a severe distal renal tubular acidosis (RTA). Immunologic work-up showed a strongly positive ANA of 1:3,200 and positive antibodies to SSA and SSB. Schirmer’s test was abnormal. Autoimmune and other tests revealed Sjögren syndrome as the underlying cause of the distal renal tubular acidosis. Renal involvement in Sjogren’s syndrome (SS) is not uncommon and may precede sicca complaints. The pathology in most cases is a tubulointerstitial nephritis causing among other things, distal RTA, and, rarely, hypokalemic paralysis. Treatment consists of potassium repletion, alkali therapy, and corticosteroids. Primary SS could be a differential in women with acute weakness and hypokalemia.

Increased thrombin-activatable fibrinolysis inhibitor antigen levels as a clue for prothrombotic state in polycystic ovary syndrome

Objectives. Our study was undertaken to evaluate the levels of thrombin-activatable fibrinolysis inhibitor (TAFI) antigen and also its relationship with other hemostasis markers in a group of patients affected with polycystic ovary syndrome (PCOS)–under Diane-35 (ethinyl estradiol 0.035 mg/cyproterone acetate 2 mg) treatment or not–as compared with a group of healthy controls. Methods. Forty-two women with PCOS and 30 age-matched healthy controls were involved in the study. Group A were on Diane-35 for at least 6 months; group B did not take any drug; group C served as a control group. Results. TAFI antigen levels of groups A and B were significantly higher than in controls, but no difference was observed between them. All of the other coagulation and fibrinolysis parameters (including prothrombin time, activated partial thromboplastin time, fibrinogen and D-dimer) were comparable between the three groups. Conclusion. The evidence presented herein suggests that women with PCOS have impaired fibrinolysis, as reflected by increased TAFI. This impairment can contribute to the risk of cardiovascular disease in PCOS. Elucidation of the modifiable mechanisms in PCOS can represent an opportunity for preventive therapy of the cardiovascular risks associated with PCOS.

Heart-Type Fatty Acid Binding Protein (H-FABP): Relationship with arterial ıntima-media thickness and role as diagnostic marker for atherosclerosis in patients with ımpaired glucose metabolism

BackgroundHeart type fatty acid binding protein (H-FABP) has been closely associated with acute coronary syndrome, cardiac abnormalities, stroke, and obstructive sleep disorder in previous studies. The aim of this study was to evaluate and compare the serum H-FABP levels and carotid artery intima-media thickness (CIMT) between patients with prediabetes and control subjects.Research design and methodsWe measured serum H-FABP levels in 58 prediabetic patients, 29 with impaired fasting glucose (IFG) and 29 with impaired glucose tolerance (IGT) and 28 age-, sex- and body mass index-matched control subjects using a sandwich enzyme-linked immunosorbent assay (ELISA), and in order to measure CIMT, all participants underwent high-resolution B-mode ultrasonography.ResultsSerum H-FABP levels were significantly elevated in pre-diabetic patients when compared with that of control subjects (IFG: 32.5 ± 34.2 ng/dL, IGT: 45.4 ± 45.8 ng/dL, control: 16.8 ± 14.9 ng/dL; p = 0.011). The difference in means of H-FABP levels between patients with IGT or IFG and control subjects was significant (p = 0.010 and p = 0.009, respectively). CIMT was higher in the pre-diabetic groups compared with the control group (IFG: 0.6 ± 0.1, IGT: 0.6 ± 0.1, control: 0.5 ± 0.1; p < 0.001), and H-FABP level was positively correlated with CIMT (p < 0.001, rho = 0.626).ConclusionOur results indicate that patients with pre-diabetes are at increased risk for cardiovascular disease. In addition, serum H-FABP levels could represent a useful marker for myocardial performance in patients with IFG and IGT.

Hyperprolactinaemia associated with increased thyroid volume and autoimmune thyroiditis in patients with prolactinoma.

The aim of this investigation was to evaluate the effects of hyperprolactinaemia on thyroid function, volume and nodularity in patients with prolactinoma.

Preclinical atherosclerosis in patients with prolactinoma.

OBJECTIVE The aim of this study was to evaluate the effect of hyperprolactinemia on body fat, insulin sensitivity, inflammatory markers, and cardiovascular risk in patients with prolactinoma. METHODS The study included 35 untreated hyperprolactinemic patients with pituitary adenomas, and 36 age-, gender-, and body mass index (BMI)-matched healthy controls without any known disease. Serum glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR, lipid profile, high-sensitivity C-reactive protein (hs-CRP), and heart-type fatty acid binding protein (H-FABP) levels were measured. Waist and hip circumference (WC and HC) were measured in all the participants. The body fat percentage was measured, and the visceral fat and abdominal fat percentages were measured via bioelectrical impedance (BIA). In addition, carotid intima media thickness (CIMT) was measured using high-resolution B-mode ultrasound. RESULTS The serum glucose level, HOMA-IR, triglyceride level, and SC were significantly higher in the patient group than in the control group. The hs-CRP level and CIMT were significantly higher in the hyperprolactinemic patients. Visceral and truncal fat percentages were significantly higher in the patients with prolactinoma. H-FABP levels were similar in the 2 groups, and there was a positive correlation between the prolactin (PRL) and H-FABP protein levels. CONCLUSIONS Based on the present findings, hyperprolactinemia is associated with preclinical atherosclerosis and metabolic abnormalities. Patients with hyperprolactinemia might experience cardiovascular disease in the long term. Metabolic control should be achieved in addition to the control of hyperprolactinemia in the clinical management of patients diagnosed with prolactinoma.

Three noninvasive methods in the evaluation of subclinical cardiovascular disease in patients with acromegaly: epicardial fat thickness, aortic stiffness and serum cell adhesion molecules

Several studies have reported increased risk of cardiovascular disease due to early development of endothelial dysfunction and structural vascular changes in patients with acromegaly.

Copeptin, a surrogate marker for arginine vasopressin, is associated with cardiovascular risk in patients with polycystic ovary syndrome.

BackgroundWomen with polycystic ovary syndrome (PCOS) have higher risk for cardiovascular disease (CVD). Copeptin has been found to be predictive for myocardial ischemia. We tested whether copeptin is the predictor for CVD in PCOS patients, who have an increased risk of cardiovascular disease.MethodsThis was a cross sectional controlled study conducted in a training and research hospital. The study population consisted of 40 reproductive-age PCOS women and 43 control subjects. We evaluated anthropometric and metabolic parameters, carotid intima media thickness and copeptin levels in both PCOS patients and control group.ResultsMean fasting insulin, homeostasis model assessment insulin resistance index (HOMA-IR), triglyceride, total cholesterol, low density lipoprotein cholesterol (LDL-C), free testosterone, 17-OH progesterone, Dehydroepiandrosterone sulfate (DHEAS), carotid intima media thickness (CIMT) levels were significantly higher in PCOS patients. Mean copeptin level was in 12.61 ± 3.05 pmol/L in PCOS patients while mean copeptin level was 9.60 ± 2.80 pmol/L in healthy control women (p < 0.001). After adjustment for age and BMI, copeptin level was positive correlated with fasting insulin, free testosterone levels, CIMT, and HOM A-IR.ConclusionsCopeptin appeared to have an important role in metabolic response and subsequent development of atherosclerosis in insulin resistant, hyperandrogenemic PCOS patients.

Severe Arterial Thrombophilia Associated With a Homozygous MTHFR Gene Mutation (A1298C) in a Young Man With Klinefelter Syndrome

Klinefelter syndrome (KS) is the most common sex chromosome disorder in men. It may be associated with an increased risk for venous thrombosis and thromboembolism, which is partially explained by hypofibrinolysis due to androgen deficiency. Additional genetic or acquired thrombophilic states have been shown in KS patients complicated with venous thrombosis as isolated case reports. Arterial thrombotic events had not been previously reported in KS. In this study, a young man with KS who developed acute arterial thrombosis during testosterone replacement therapy is presented. He was homozygous for the A1298C mutation of the methylenetetrahydrofolate reductase (MTHFR) gene.

Familial Mediterranean fever with chronic ascites: a case report and a review of literature.

Familial Mediterranean fever (FMF) is an autosomal recessive inflammatory disease especially seen in Turks, Sephardic Jews, Armenians, and Arabs. Peritoneal and pleural inflammation, arthritis, erysipelas-like erythema, and arthralgia are well-known features of FMF. A small amount of peritoneal fluid collection can be seen during peritoneal attacks in FMF patients, but chronic ascites is a rather rare complication. We herein report a female FMF patient who developed chronic ascites. She was compound heterozygote for M694V/M680I mutation of the MEFV gene. Aspiration of the ascites fluid revealed a small amount of erythrocytes and mesothelial cells. After dose adjustment of colchicine the amount of ascites decreased. In conclusion, FMF should be considered in the differential diagnosis of chronic ascites in populations where the disease is endemic.