Hatice Yorulmaz

Metabolic syndrome frequency in inflammatory bowel diseases.

Background/Aim: Metabolic syndrome (MetS) is a clinical condition characterized by central obesity, elevated triglycerides, low–high density lipoproteins, impaired fasting glucose, and hypertension. There is insufficient data on the prevalence of MetS in patients with inflammatory bowel disease (IBD). This study sought to determine the prevalence of MetS in a Turkish cohort of patients with IBD and the association between insulin resistance (IR) and the MetS parameters, in this population. Patients and Methods: A total of 177 patients over 18 years of age (62 with Crohns disease (CD) and 115 with ulcerative colitis (UC)) were enrolled in the study. The presence of at least three criteria of the International Diabetes Federation (IDF) was accepted for the diagnosis of MetS. The Homeostasis Model Assessment (HOMA) was used to determine IR. HOMA values < 1 were considered normal and values > 2.5 indicated a high probability of IR. Results: MetS frequency was higher in patients n=34 (29.5%) with UC than in patients n=11 (17.7%) with CD (P < 0.01). MetS was detected in 12 of the 117 patients (10.3%) with IBD, under 45 years of age, and in 33 of 60 patients (55%) over 45 years of age. HOMA value in n=31 patients (27%) with UC was > 2.5. Body mass index, insulin (P < 0.001), waist circumference, fasting plasma glucose, leukocyte count (P < 0.01), triglycerides, C-reactive protein, and uric acid values (P < 0.05) were significantly higher in UC patients with IR than those without IR. Conclusion: Frequent occurrence of MS with increasing age in IBD, particularly in UC, showed the importance of early diagnosis and treatment of cardiovascular disease risk factors in the long-term follow-up of these diseases.

Prolonged QT dispersion in inflammatory bowel disease

AIM To investigate the frequency and factors of prolonged QT dispersion that may lead to severe ventricular arrhythmias in patients with inflammatory bowel disease (IBD). METHODS This study included 63 ulcerative colitis (UC) and 41 Crohns disease (CD) patients. Forty-seven healthy patients were included as the control group. Heart rate was calculated using electrocardiography, corrected QT dispersion (QTcd) and the Bazetts formula. Homeostasis model assessment (HOMA) was used to determine insulin resistance (IR). HOMA values < 1 were considered normal and values > 2.5 indicated a high probability of IR. RESULTS Prolonged QTcd was found in 12.2% of UC patients, and in 14.5% of CD patients compared with the control group (P < 0.05). A significant difference was found between the insulin values (CD: 10.95 ± 6.10 vs 6.44 ± 3.28, P < 0.05; UC: 10.88 ± 7.19 vs 7.20 ± 4.54, P < 0.05) and HOMA (CD: 2.56 ± 1.43 vs 1.42 ± 0.75, P < 0.05; UC: 2.94 ± 1.88 vs 1.90 ± 1.09, P < 0.05) in UC and CD patients with and without prolonged QTcd. Disease behavior types were determined in CD patients with prolonged QTcd. Increased systolic arterial pressure (125 ± 13.81 vs 114.09 ± 8.73, P < 0.01) and age (48.67 ± 13.93 vs 39.57 ± 11.58, P < 0.05) in UC patients were significantly associated with prolonged QTcd. CONCLUSION Our data show that IBD patients have prolonged QTcd in relation to controls. The routine follow-up of IBD patients should include determination of HOMA, insulin values and electrocardiogram examination.

Effect of Vitamin E on Blood-Brain Barrier Permeability in Aged Rats with PTZ-Induced Convulsions

The effect of vitamin E on blood-brain barrier (BBB) permeability was studied under conditions of pentylenetetrazole (PTZ)-induced convulsions in aged (23- to 24-month-old) male albino rats; Evans Blue was used as a tracer. The BBB permeability was found to increase considerably in rats with PTZ-evoked seizures; the Evans Blue contents in the left and right hemispheres and cerebellum + brainstem region were significantly higher than those in the control. Vitamin E at a dose of 70 mg/kg exerted practically no beneficial effect on the increased BBB permeability in rats with seizures, while a greater dose of vitamin E (700 mg/kg) exerted a significant protective effect, especially with respect to the cerebellum + brainstem regions (P < 0.01). The seizure-related rise in the arterial blood pressure was also smaller in the latter experimental group. Thus, our observations confirm the importance of the vitamin E dose as a protective factor for BBB permeability and demonstrate that the dose dependence of this antioxidant in aged animals differs from that in younger organisms.

Gestational treatment of folic acid attenuates blood–brain barrier leakage in pregnant- and prepubertal rats after pentylenetetrazole-induced seizure

Objectives: Folic acid (FA) is physiologically important in mammals and is a common vitamin supplement used during pregnancy and lactation. Numerous studies have reported that FA significantly improves endothelial function. The blood–brain barrier (BBB) plays an important role in maintaining the microenvironment required for neuronal function, but its unique structure is damaged by epileptic seizures. The aim of this study was to evaluate the potential protective role of FA on BBB leakage, as well as on the reactive astrogliosis in pregnant rats and their prepubertal offspring during pentylenetetrazole (PTZ)-induced epileptic seizure. Methods: Pregnant rats were treated with FA (5 mg/kg) and PTZ on gestational days 0–19 and 19, respectively. The pups were treated with PTZ at puberty. Evans blue was used to evaluate BBB integrity. Reactive astrogliosis was defined using immunohistochemical analysis for glial fibrillary acidic protein (GFAP). Mean arterial blood pressure (MABP) was measured at the femoral artery. Results: A moderate decrease in BBB leakage was observed in FA-treated pregnant and prepubertal animals (P < 0.05). MABP was decreased significantly in pregnant rats (P < 0.05). The epilepsy-induced increase in MABP was less prominent in pregnant animals (P < 0.05). GFAP intensity decreased in PTZ-treated pregnant animals (P < 0.01) and FA-treated prepubertal rats. Discussion: Our findings suggest that FA, which is used as a maternal vitamin to promote normal fetus development, may be beneficial against seizure-induced neuronal damage by decreasing BBB leakage and reactive astrogliosis in pregnant and prepubertal rats.

Type 1 diabetes exacerbates blood–brain barrier alterations during experimental epileptic seizures in an animal model

The aim of this study was to perform the effects of diabetes on the permeability of the blood–brain barrier (BBB) during pentylenetetrazole (PTZ)‐induced epileptic attacks. For this propose, the animals were divided into four groups. These groups contained were intact, PTZ‐treated, diabetic and PTZ‐treated diabetic individuals, respectively. To evaluate the functioning of the BBB, Evans blue was used as a BBB permeability indicator, and the expressions of zonula occludens‐1 and glial fibrillary acidic protein involving the functioning of the BBB were determined immunohistochemically. Also, the changes in the release of serum tumour necrosis factor‐alpha and interleukin‐10 and interleukin‐12 were studied by using enzyme‐linked immunosorbent assay method. BBB permeability in the seizures under diabetic conditions showed a considerable increase (p < 0·01) in all of the brain we studied. The immunoreactive staining intensity of zonula occludens‐1 and glial fibrillary acidic protein was found reduced in the brain regions of diabetic rats (p < 0·01). However, the serum level of tumour necrosis factor‐alpha increased in diabetes and diabetes + PTZ groups, and the serum level of interleukin‐12 increased significantly in all experimental groups (p < 0·05). In conclusion, diabetes dramatically increases BBB damage during epileptic seizures, and it may be derived from an elevation of paracellular passage. Copyright

Therapeutic Effects of Simvastatin on Galectin-3, and Oxidative Stress parameters in Lung Tissue in Endotoxemia

Galectins constitute of a soluble mammalian β-galactoside binding lectin family, which play homeostatic roles in the regulation of the cell cycle, and apoptosis, in addition to their inflammatory conditions. Galectin-3 has an important role in the regulation of various inflammatory conditions including endotoxemia, and airway inflammation. Statins, the key precursor inhibitors of 3-hydroxyl-3-methyl coenzyme A (HMG-CoA) reductase, may prevent the progression of inflammation in sepsis after prior statin treatment. Endotoxemia leads to the formation of oxidative stress parameters in proteins, carbohydrates, and DNA. In the present study, we aimed to show the effects of simvastatin on Galectin-3, and glutathione reductase (GR), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and thiobarbituric acid reactive substances (TBARS) levels in lung tissue of rats which were treated with lipopolysaccharides (LPS) during the early phase of sepsis. Rats were divided into four groups as the control, LPS (20 mg/kg), simvastatin (20 mg/kg), and simvastatin+LPS group. Galectin-3 expression in formalin-fixed paraffin-embedded lung tissue sections was demonstrated by using the immunohistochemistry methods. There were reduced densities, and the decreased number of Galectin-3 immunoreactivities in the simvastatin+LPS group compared with the LPS group in the pneumocytes, and in the bronchial epithelium of lung tissue. In the LPS group, GR, GSH-Px, and SOD were found lower than the levels in simvastatin-treated LPS group (P<0.05, P<0.01, P<0.01 respectively) in the lung tissue. However, TBARS decreased in the simvastatin+LPS group compared with the levels in LPS group (P<0.001). Simvastatin attenuates LPS-induced oxidative acute lung inflammation, oxidative stress, and suppresses LPS-induced Galectin-3 expression in the lung tissue.