Esen Akbay

Respiratory symptoms and pulmonary functional changes in patients with irritable bowel syndrome

OBJECTIVE:Scientific evidence of functional interface between the immune and sensory motor systems of the gut and respiratory systems has been reported. In recent studies excess prevalence of bronchial hyper-responsiveness has been shown among patients with irritable bowel syndrome (IBS). The purpose of our study was to investigate the possible relationship between IBS and asthma.METHODS:One hundred thirty-three patients with IBS (108 women, 25 men) and 137 control subjects (105 women, 32 men) were included in this study. Both for IBS and the control group, the mean ages were 41.64 ± 9.45 yr and 39.94 ± 10.62 yr, respectively. Patients more than 50 yr old, with any organic GI disease, acute respiratory system infection, current or ex-smokers, and patients using drugs affecting smooth muscle and autonomic nervous system were not included in the study. Respiratory symptoms were questioned and pulmonary function tests were performed for every subject.RESULTS:There were 45 (33.8%) and eight (5.8%) subjects with respiratory symptoms in IBS and control groups, respectively (p < 0.0001). Twenty-one (15.8%) patients from the IBS group and two (1.45%) patients from the control group had the diagnosis of asthma according to history, clinical, and PFT findings. There was no statistical difference between two groups with respect to percentage of forced vital capacity and forced expiratory volume in 1 s-to-forced vital capacity. The difference between the two groups in forced expiratory volume in 1 s, flow after 50% of the vital capacity has been exhaled, peak expiratory flow rate, and maximal mid-expiratory flow rate was statistically significant (p < 0.01).Conclusion:We found that the prevalence of asthma was more common in the IBS group than in controls. Our finding supports the speculation that asthma and IBS may share common pathophysiological processes

Plasma visfatin level in lean women with PCOS: relation to proinflammatory markers and insulin resistance

Objectives. The present study was undertaken to investigate the association between plasma visfatin concentrations and inflammatory markers such as interleukin-6 (IL-6) and high-sensitive C-reactive protein (hsCRP) in company with several metabolic parameters in lean women with polycystic ovary syndrome (PCOS). Methods. The study group consisted of 21 lean women with PCOS (BMI 20.74 ± 1.74 kg/m2) and 15 healthy, normally menstruating women (BMI 20.85 ± 2.08 kg/m2 control group). PCOS was defined according to the Rotterdam criteria. Visfatin, IL-6, hsCRP, hyperandrogenism markers and metabolic markers were examined in all PCOS and control women. Results. Plasma visfatin level in the PCOS group was higher than that in the control group. Plasma hsCRP and IL-6 levels in PCOS group were similar with the control group. Plasma visfatin levels were positively associated with total cholesterol, high density lipoprotein, hirsutism score, total testosterone and FAI. Plasma visfatin level was negatively associated with SHBG. However, there were no correlation between plasma visfatin level and IL-6 and hsCRP. In multivariate regression analyses, only FAI and high density lipoprotein-cholesterol (HDL-C) showed a significant association with serum visfatin. Conclusion.  Our data indicates that plasma visfatin levels are associated with HDL-C and markers of hyperandrogenism, but it is not associated with proinflammatory markers and insulin resistance in lean women with PCOS.

Serum IL-18 levels in patients with type 1 diabetes : Relations to metabolic control and microvascular complications

The study was designed to examine serum IL-18 level and its relation to metabolic control parameters and microvascular complications in type 1 diabetes mellitus (DM). Sixty two patients with type 1 DM and 30 healthy individuals were enrolled in the study. Serum IL-18 levels of patients with type 1 DM were significantly increased compared to controls (293.4+/-133.4 vs 211.2+/-63.9 pg/ml, P=0.003). Patients with poor glycemic control had higher levels of IL-18 than patients with well glycemic control (329.9+/-141.0 vs 226.3+/-89.6 pg/ml, P=0.02). There was no significant difference between the serum IL-18 levels of patients with microvascular complications and those of patients without microvascular complications (307.6+/-127.6 vs 293.2+/-145.6 pg/ml, P>0.05). IL-18 correlated positively with HbA(1c) (r=0.32, P=0.01) and postprandial blood glucose (PPBG) (r=0.26, P=0.02); and negatively with HDL-cholesterol (HDL-C) (r=-0.38, P=0.007). By linear regression analysis, PPBG was determined as the most explanatory parameter for the alterations in serum IL-18 levels (P=0.02). High levels of IL-18 in patients with type 1 DM is related to short and long term glycemic control and HDL-C levels but not to microvascular complications.

Serum retinol binding protein 4 level is related with renal functions in Type 2 diabetes

Aim: We aimed to evaluate the metabolic parameters and diabetes complications which would probably affect the serum retinol-binding protein 4 (RBP4) levels in Type 2 diabetic individuals. In addition to serum RBP4 concentration, the levels of its ligands, serum retinol and transthyretin (TTR) were also considered in this evaluation. Subjects and methods: Serum RBP4, retinol, and TTR levels were measured in 53 Type 2 diabetic subjects and 30 body mass index (BMI)-matched controls. The molar ratios of RBP4 to retinol and RBP4 to TTR were compared. Results: While the RBP4 values were similar to those in the control group in Type 2 diabetic patients, the molar ratio of RBP4 to TTR was found to be higher than that of the control group. The serum RBP4 levels in patients who had retinopathy and macrovascular disease were similar to those in patients who did not. However, the RBP4 levels, molar ratios of RBP4 to retinol and RBP4 to TTR in micro-macroalbuminuric patients were found to be significantly higher than in normoalbuminuric subjects and controls. There was no correlation between the RBP4 levels and the patients’ age, BMI, duration of diabetes, LDL, triglyceride, serum creatinine, and glycated hemoglobin values. Micro-macroalbuminuria and estimated glomerular filtration rate were independent determinants for increased serum RBP4 levels. Conclusion: According to the data obtained from this study, diabetic retinopathy and cardiovascular complications do not affect the serum RBP4 level in Type 2 diabetes. Renal functions rather than the metabolic factors of diabetes determine the RBP4 level and its relation with its ligands.

Plasma Visfatin Concentrations in Subjects with Type 1 Diabetes Mellitus

Background/Aims: Visfatin is a recently discovered adipokine, and its circulating concentrations have not been adequately studied in type 1 diabetes mellitus (DM). Therefore, this study was designed to examine plasma visfatin levels in type 1 diabetic patients and to determine the relationships between visfatin and duration of diabetes, body mass index, glycemic control, insulin dosage and lipid profile. Methods: Forty-eight patients with type 1 DM and 26 healthy controls were investigated. Results: Type 1 diabetic patients had significantly low visfatin levels compared with controls (18.8 ± 1.7 vs. 20.2 ± 0.3 ng/ml; p < 0.0001). Visfatin levels were comparable between patients with a short duration of diabetes (<10 years) and patients with a long duration of diabetes (≥10 years) (18.9 ± 1.7 vs. 18.2 ± 2.0 ng/ml; p > 0.05). There was a significant correlation between visfatin and hemoglobin A1c (HbA1c) even after the adjustment for age, sex, body mass index and duration of diabetes (r = –0.48, p = 0.005) in the patient group. Multivariate analysis showed that significant determinants of visfatin concentrations were HbA1c and duration of diabetes (r2 = 0.27). Conclusion: These data emphasize that plasma visfatin concentrations are lower in patients with type 1 DM and related to glycemic control reflected by HbA1c.

Association of polymorphisms in the IL-18 and IL-12 genes with susceptibility to Type 1 diabetes in Turkish patients

Background: Recent studies have indicated that polymorphisms of the interleukin-18 (IL-18) and interleukin-12 (IL-12) genes are associated with the development of Type 1 diabetes mellitus (T1 DM) in some populations, but not all. Aim: The present study was designed to examine the roles of polymorphisms in the IL-18 promoter and IL-12p40 with respect to susceptibility to T1 DM in Turkish patients. Subjects and Methods: Ninety-one patients with T1 DM and 87 unrelated healthy subjects were included in the study. The IL-18 polymorphisms at positions −607 and −137 were detected by a sequence-specific PCR method. The single nucleotide polymorphism in the IL-12p40 3′ untranslated region (3′-UTR) at position +1188 was analyzed by the PCR-restriction fragment length polymorphism (RFPL) method. Results: The allelic and genotypic frequencies of the IL-18 and IL-12p40 polymorphisms did not differ significantly between subjects with T1DM and the controls (p>0.05). However, diabetic patients with the −137 (CC) genotype showed a younger onset age compared to patients with the −137 (GG) genotype (p=0.02). In addition, patients with the −607 (CC) genotype had higher levels of glycated hemoglobin (HbA1 c) than patients with the −607 (AC) genotype (p=0.004). Furthermore, patients with the IL-12p40 (AC) genotype had higher HbA1c levels than patients with the IL-12p40 (AA) genotype (p=0.01). Conclusions: The results of the present study show that the IL-18 and IL-12p40 polymorphisms may have some effect on the onset age and deterioration of glycemic control in Turkish patients with T1 DM.

Valsartan-Induced Hepatotoxicity in a HBs-Ag-Positive Patient

TO THE EDITOR: Hepatotoxicity caused by angiotensin II receptor blockers is a very rare disorder. We report the first case with acute hepatic injury associated with valsartan, which is an antihypertensive agent. A 52-yr-old hypertensive woman was admitted to our hospital with complaints of weakness, nausea, jaundice, and right subcostal abdominal pain. Her past medical history was unremarkable except for primary hypertension and hepatitis B surface antigen (HBs-Ag) positivity. She had been followed as a HBs-Ag carrier for 4 yr without clinical and laboratory symptoms and signs of acute or chronic liver disease in our hospital. She had been treated for primary hypertension by valsartan for 1 month. There was no other medication. The patient had manifested pruritic erytematous skin changes 1 wk before this admission. After this complaint, moderate nausea, jaundice, and right subcostal abdominal pain developed. On admission, her physical examination revealed no abnormality except for painful mild hepatomegaly. Laboratory findings were as follows: complete blood count was normal and eosinophilia was present. Her total and direct bilirubin levels were 3.2 mg/dl and 2.8 mg/dl, respectively, on admission, and peaked 7.8 and 6.9, respectively on the 7th day of admission. Liver enzymes peaked at the 6th day as follows: ALT 780 U/L, AST 1292 U/L, -glutamyl transferase 945 U/L, and liver-specific ALP 1840 U/L. Serological tests for hepatitis virus were negative (anti-hepatitis A virus IgM, anti-hepatitis B core IgM and IgG, hepatitis B virus DNA by polymerase chain reaction, hepatitis C virus antibody hepatitis C virus RNA by polymerase chain reaction, anti-Epstein-Barr virus IgM, and anti-cytomegalovirus IgM and IgG), except for HBs-Ag positivity. Markers for toxoplasmosis, herpes simplex virus, and HIV were all negative. International Normalized Ratio (INR) and PT were mildly elevated. Hepatobiliary ultrasonography revealed mild hepatomegaly. Liver biopsy was considered, but the patient refused. Valsartan therapy was discontinued at once. Hepatic failure and related complications were not seen. The complaints of the patient were resolved within 2 wk under conservative management. Liver enzymes and bilirubin levels decreased rapidly within 2 wk and returned to normal limits within 3 months. She has been followed for 6 months asymptomatically. As far as we know, this is the first case of valsartanassociated hepatotoxicity in a patient with HBs-Ag positivity. There is just one case report of valsartan-associated hepatic injury from Spain (1). There are not a lot of cases of angiotensin II receptor antagonists associated hepatotoxicity, and in this case, presumably this association is a hypersensitivity reaction together with pruritic skin changes. Valsartan is eliminated mainly by hepatic clearance. Headache, dizziness, and fatigue were the most common adverse events in placebocontrolled studies; the incidence of these adverse events was not significantly different between placebo and valsartan recipients (2). Rash and angioedema have been reported with angiotensin II receptor antagonists very rarely (3). Drug-induced hepatic injury associated with losartan was reviewed by Tabak et al. (4). The importance of HBs-Ag positivity in this hepatotoxicity remains unknown, and the physicians who recommended these agents should be careful about this complication.

The correlation of thrombolysis in myocardial infarction frame count with insulin resistance in patients with slow coronary flow

BackgroundIt has been reported that coronary endothelial dysfunction plays an important pathogenetic role in patients with slow coronary flow (SCF). Insulin resistance is defined as impairment of insulin-stimulated glucose and/or lipid metabolism, while endothelial dysfunction is defined as paradoxical or inadequate endothelial-mediated vasodilation. In this study, we aimed to evaluate insulin resistance in patients with SCF. MethodsThe study population included 25 patients with SCF and 28 healthy controls. Insulin resistance was estimated via homeostasis model assessment insulin resistance index (HOMA-IR). ResultsPatients with SCF had higher high-sensitive C-reactive protein (hs-CRP) and HOMA-IR scores (P<0.05) than controls. Mean thrombolysis in myocardial infarction frame count had significant correlation with hs-CRP, fasting plasma insulin levels and HOMA-IR score (r=0.566, P<0.05; r=0.883, P<0.05; r=0.884, P<0.05, respectively). ConclusionIn patients with SCF, thrombolysis in myocardial infarction frame counts and hs-CRP are correlated with increased insulin resistance and thus, it can be suggested that insulin resistance and inflammation may, in part, have a role in the pathogenesis of SCF.

Mean Platelet Volume and Related Factors in Patients at Different Stages of Diabetic Nephropathy A Preliminary Study

Introduction: Mean platelet volume (MPV) is an independent cardiovascular disease predictor, and characteristics of MPV in patients with diabetic nephropathy (DN) are not well known. Aim: To determine the MPV levels in patients at different stages of DN. Patients and Methods: The MPV levels were investigated in healthy participants (group 1, n = 157), patients with type 2 diabetes mellitus without complication (group 2, n = 160), diabetic patients with clinical proteinuria (group 3, n = 144), and in patients with chronic kidney disease due to DN (group 4, n = 160). Findings: The MPV level was higher in all diabetic patients than that in normal participants (P < .05). The MPV values had a positive correlation with the serum creatinine and proteinuria, and a negative correlation with the glomerular filtration rate ([GFR] P < .001 for all, r values; .72, and .82, and −.92, respectively). Conclusion: The MPV values were higher in diabetic groups than that in normal participants. Both GFR and proteinuria were the most powerful determinants of MPV.

Cushing Syndrome Caused by Topical Corticosteroid: A Case Report

Development of iatrogenic Cushing syndrome from topical steroid therapy is very rare in adults. A 48-year-old woman with a diagnosis of Cushing syndrome caused by long-term topical clobetasol propionate application was presented. Laboratory studies were consistent with adrenal suppression that improved after discontinuation of the use of topical glucocorticoids. Patients who will take treatment with steroids, even with topical steroids, should be offered information about the dose, duration, and type of the treatment and its systemic side-effects.