Yazar "Akinci A." seçeneğine göre listele
Listeleniyor 1 - 5 / 5
Sayfa Başına Sonuç
Sıralama seçenekleri
Öğe Cerebrospinal fluid and serum levels of growth hormone, insulinlike growth factor 1, insulinlike growth factor binding protein 3, and ghrelin in patients with bacterial and tuberculous meningitis(2012) Akinci A.; Gungor S.; Yucel G.; Gungor S.; Ozerol H.I.BACKGROUND: The somatotropic hormone levels change in acute and prolonged critical illnesses such as tuberculous meningitis (TbM). This study aimed to determine the cerebrospinal fluid (CSF) and serum levels of growth hormone (GH), insulinlike growth factor 1 (IGF-1), insulinlike growth factor-binding protein 3 (IGFBP-3), and ghrelin in patients with TbM and to compare the results with those of the patients with bacterial meningitis (BM) and of healthy controls. METHODS: Nine patients with TbM and 14 patients with BM between the ages of 7 and 12 years were enrolled in this study. The control group was composed of 14 patients with no central nervous system infections. Growth hormone, IGF-1, and IGFBP-3 levels in serum and CSF were measured by enzyme-linked immunosorbent assay, and ghrelin levels were measured by radioimmunoassay. RESULTS: Growth hormone and IGF-1 levels in serum and CSF were significantly lower in the TbM group than in the BM and control groups (P < 0.05). Insulinlike growth factor-binding protein 3 levels were lower in the TbM and BM groups than in the control group (P < 0.05). Ghrelin level in the TbM group was significantly higher than in the BM and control groups (P < 0.05). CONCLUSIONS: Levels of growth factors such as GH and IGF-1 were lower in TbM than in other central nervous system infections. These data suggest that IGF-1, which is known to have a neuroprotective effect, may be the cause of neuronal loss and cerebral atrophy in TbM. Copyright © 2012 by Lippincott Williams & Wilkins.Öğe The Effects of Hypothyroidism Due to Iodine Deficiency in Neonatal Brain: The Changes in Brain Metabolites Detected by Magnetic Resonance Spectroscopy(Elsevier, 2009) Akinci A.; KarakaŞ H.M.Most studies show that iodine deficiency and maternal-fetal hypothyroxinemia have negative effects on fetal neural maturation, dendritic arborization and synaptic formation. They delay the myelinization process and gliogenesis, which start in the second half of gestation and continue in postnatal life. Altered levels of iodine are correlated with defective brain development and neuronal maturation. Various degrees of irreversible neurocognitive defects that are caused by severe iodine deficiency, and subsequent maternal and fetal hypothyroxinemia are wellknown. Recent studies further showed that, even in cases without clinical hypothyroidism, maternal hypothyroxinemia due to mild-to-moderate iodine deficiency would lead to fetal brain damage that could be reversed with early thyroxine therapy. Magnetic resonance spectroscopy (MRS) is a sensitive technique that detects alterations in brain metabolite levels in various neurodevelopmental disorders. The most prominent MRS change in congenital hypothyrodism due to iodine deficiency is decreased NAA level. Decreased NAA level that is caused by maternal and fetal hypothyroxinemia due to iodine deficiency implies the adverse effect of intrauterine hypothyroxinemia on fetal neuronal development. Iodine deficiency at any degree of severity causes maternal and fetal hypothyroxinemia. As thyroid hormones of the mother and the fetus must be kept at optimal levels, iodine prophylaxis should be provided, especially in iodine deficient areas. To establish normal fetal brain development, iodine supplementation must be started before pregnancy and should be continued during the gestational period. © 2009 Elsevier Inc. All rights reserved.Öğe Eosinophilic fasciitis - Progression to linear scleroderma. A Case Report(1999) Balat A.; Akinci A.; Turgut M.; Mizrak B.; Aydin A.Eoslnophilic fasciitis is a rare disease in children. Although changes similar to linear scleroderma have been reported, the outcome is usually good. In this report, a 10-year-old boy who developed eosinophilic fasciitis without a good response to steroids is presented. He progressed to linear scleroderma within months. Our case reinforces the hypothesis that eosinophilic fasciitis may be an early manifestation or a variant of localized scleroderma similar to the other cases in the literature.Öğe Glucagon-like peptide-1 and-2 levels in children with diabetic ketoacidosis.(2009) Akinci A.; Aydin O.; Özerol H.I.The aim of this study was to investigate whether insulin deficiency and increased catabolism may have a role in the regulation of plasma glucagon-like peptide (GLP)-1 and GLP-2 levels in children with diabetic ketoacidosis (DKA) and whether insulin treatment may affect the levels of these polypeptides. Plasma GLP-1 and -2 levels were measured in 24 patients with DKA aged 8 to 14 years before insulin infusion (time 0), when ketonemia and acidosis disappeared (time 1), and when weight gain started (time 2). Eighteen healthy children aged 8 to 14 years constituted the control group. At time 0, mean plasma GLP-1 and GLP-2 levels were significantly elevated in the patients compared with the control group (p<0.05 and p<0.01, respectively). At time 1 when ketonemia and acidosis disappeared, GLP-1 and GLP-2 levels decreased significantly from the initial levels (p<0.05 and p<0.01, respectively). At this time, while GLP-1 level was not different from that of the controls, GLP-2 level was higher than that of the controls (p<0.05). GLP-1 and-2 levels did not show any significant differences between the patients and controls when weight gain started (time 2). Our results show that DKA is associated with increased plasma GLP-1 and -2 concentrations. Effective fluid and insulin treatment resulted in a significant decrease in plasma GLP-1 and -2 levels. This may be due to the negative feedback effect of insulin on the production of these polypeptides.Öğe Helicobacter pylori infection in children with poorly controlled type I diabetes mellitus(2005) Gülcan H.; Akinci A.; Yolo?lu S.An increased prevalence of Helicobacter pylori (Hp) infection in children with type I diabetes mellitus have been reported in a few studies. Helicobacter pylori infection may be one of the causes of gastrointestinal symptoms and chronic atrophic gastritis frequently seen in diabetes of long duration. This study aimed to assess the prevalence of Hp infection and its relationship with glycemic control and duration of diabetes in children with poorly controlled type I diabetes mellitus. Helicobacter pylori was investigated using the C13-urea breath test in 19 diabetics and 26 healthy controls. C13-urea breath test was positive in 68.6% (13/19) of diabetics and 38.4% (10/26) of controls (p<0.05). Diabetic children were divided into two groups according to Hp status: Hp (+) and Hp (-). The two groups were compared for age, gender, body for weight and height, duration of diabetes and glycemic control (HbA1c). Duration of diabetes was significantly longer in the Hp (+) group than in the Hp (-) group (p<0.05). There was no significant difference between the two groups for glycemic control (p>0.05). In our study, prevalence of Hp infection was significantly higher in poorly controlled diabetic children than in healthy controls. Poor glycemic control and duration of diabetes are the important causes of increased rate of Hp infection in diabetic children.
