Prevalence, comorbidities and mediators of childhood anxiety disorders in urban Turkey: a national representative epidemiological study.

PURPOSE: The aim of this study is to evaluate the prevalence of anxiety disorders, its correlation with sociodemographic characteristics, its comorbidities with other psychiatric disorders and its predictors in school-aged children. METHODS: This study is part of a representative, multi-centered national study that is planned by the Turkish Association of Child and Adolescent Mental Health to evaluate the prevalence of psychopathology among elementary school students in Turkey between the years 2014-2015. Children are screened via Kiddie Schedule for Affective Disorders and Schizophrenia for School Age Children Present and Lifetime Version. Impairment is assessed by a 3-point Likert type scale independently by the parent and the teacher. The final sample included 5842 children with the mean age of 8.7 years. RESULTS: The prevalence of any anxiety disorder without considering impairment is 16.7% and considering impairment is 5.2% in children according to our study. We found significant differences for comorbid Attention Deficit Hyperactivity Disorder, Disruptive Behavior Disorder, Mood Disorders, Tic Disorders, Obsessive Compulsive Disorder, Enuresis Nocturna, Encopresis, and Intellectual Disability. Having a history of paternal physical disorder, living in the regions of Marmara, Mediterranean and Black Sea were found to be the main predictors of having childhood anxiety disorders according to the logistic regression analysis. CONCLUSION: Better understanding of childhood anxiety disorders, comorbid conditions and predictors will result in earlier diagnosis and more appropriate treatment.

The combination of tumour necrosis factor-α -308A and interleukin-10 -1082G gene polymorphisms and increased serum levels of related cytokines: susceptibility to vitiligo.

BACKGROUND: The aetiopathogenesis of vitiligo is still under investigation. AIM: To assess the role of single nucleotide polymorphisms (SNPs) of the genes for tumour necrosis factor (TNF)-α, interleukin (IL)-6 and IL-10, as well as the serum levels of these three cytokines in the pathogenesis of vitiligo. METHODS: The study enrolled 105 patients with vitiligo, and 211 age- and sex-matched controls. TNF-α (-308), IL-6 (-174) and IL-10 (-1082) promoter polymorphisms were investigated by LightSNiP assay and analysed by χ(2) test. Subsequently, the serum cytokine levels were assessed by ELISA and evaluated by Mann-Whitney U-test and Kruskal-Wallis test. RESULTS: The frequency of the GG genotype of the IL-10 -1082 polymorphism was significantly higher in the vitiligo group compared with the healthy control group (P = 0.02). Further investigations using combinations of these variant alleles detected a significant risk for vitiligo for individuals carrying both the IL-10 -1082G and TNF-α -308A alleles (OR = 12.57, 95% CI 1.44-110.0, P < 0.01). Serum IL-10 and TNF-α levels were higher in the vitiligo group (P = 0.001). In addition, TNF-α levels in patients with active disease were significantly higher than in patients with stable disease (P < 0.02). CONCLUSIONS: The concomitant presence of IL-10 -1082G and TNF-α -308A alleles significantly raises the risk for vitiligo. Furthermore, in accordance with these findings, serum IL-10 and TNF-α were also increased in this study, confirming the role of these cytokines in the pathogenesis of vitiligo.

Vascular endothelial growth factor +405 G/C,-460 T/C and -2578 A/C polymorphisms are not associated with insulin resistance in polycystic ovary syndrome.

Insulin resistance (IR) and pancreatic beta-cell dysfunction are usual comorbidities in polycystic ovary syndrome (PCOS). Vascular endothelial growth factor (VEGF) is known to play an important role in the pathogenesis of PCOS. This study examined firstly the possible association of common +405 G/C,-460 T/C and -2578 A/C polymorphisms of VEGF gene with fasting glucose, fasting insulin and the indices of IR [glucose/insulin ratio (GIR), homoeostasis model assessment (HOMA) and quantitative insulin sensitivity check index (QUICKI)] in 137 patients with PCOS. None of the studied polymorphisms were found to affect IR indices significantly. However, there was a trend towards higher HOMA in +405 G and -460 T allele carriers in comparison with homozygotes +405 CC and -460 CC, respectively. With regard to -2578 A/C polymorphism, although not significant, in -2578 C carriers HOMA was lower, and GIR was higher in comparison with -2578 AA genotype. Alteration of QUICKI between genotypes was minimal and varied from 4% to 7%. Because of the relatively small sample size, more studies with greater number of cases are necessary to confirm our observations before any statement can be made about the relationship between VEGF gene polymorphism and IR parameters in PCOS.

The combinations of TNFalpha-308 and IL-6 -174 or IL-10 -1082 genes polymorphisms suggest an association with susceptibility to sporadic late-onset Alzheimer's disease.

OBJECTIVE: Single nucleotide polymorphisms in the regulatory regions of the cytokine genes for tumor necrosis factor alpha (TNFalpha), interleukin (IL)-6 and IL-10 have been suggested to influence the risk of Alzheimer's disease (AD) with conflicting results. AIM: To investigate the TNFalpha-308, IL-6 -174 and IL-10 -1082 gene polymorphisms as susceptibility factors for AD. METHODS: We analyzed genotype and allele distributions of these polymorphisms in 101 sporadic AD patients and 138 healthy controls. RESULTS: Heterozygotes (AG) or combined genotype (AG+AA) for IL-10 -1082 were associated with approximately two-fold increase in the risk of AD. Carriers of A alleles of both TNFalpha-308 and IL-10 -1082 had 6.5 times higher risk for AD in comparison with non-carriers. Concomitant presence of both mutant TNFalpha-308 A and IL-6 -174 C alleles raised three-fold the AD risk, whereas there was no notable risk for AD afflicted by IL-6 -174 polymorphism alone. CONCLUSION: Our results suggest that TNFalpha and IL-10 promoter polymorphism might be a risk factor for AD. The combined effects of TNFalpha-308, IL-6 -174 and IL-10 -1082 variant alleles may be more decisive to induce functional differences and modify the risk for AD.

Gastrocystoplasty in pigs and effect of selective antral vagotomy on acid secretion of the reconstructed bladder.

INTRODUCTION: The aim of this study was to investigate the outcome of gastrocystoplasty and the effects of selective antral vagotomy (SAV) on the postprandial gastrin secretion from the antrum as well as on the acid secretion from the augmented bladder. MATERIALS AND METHODS: In this study on 12 male pigs, we applied subtotal cystectomy plus gastric augmentation plus SAV to the study group and the same procedure without SAV to the control group. The animals were followed up for 3 months with respect to feeding, weight, and urine output. The urine pH levels and the gastrin levels of the pigs in the two groups were then followed up and compared. RESULTS: The use of gastric segments in bladder reconstruction was found to be appropriate in terms of both gastric function and urinary system function. Nevertheless, regarding the effect of SAV, the differences between either the urinary pH levels or the gastrin levels of the pigs in the two groups were statistically significant. CONCLUSIONS: Although gastric segments in the bladder reconstruction were found to be appropriate in terms of both gastric function and urinary system function, SAV did not prevent postprandial gastrin secretion and the resulting increase of the urine acidity.

Nitric oxide and endothelin-1,2 in actinic keratosis and basal cell carcinoma: changes in nitric oxide/endothelin ratio.

BACKGROUND: Nitric oxide (NO) is an inorganic free radical gas which has cytostatic/cytotoxic actions in tumoral tissues, including gynecologic, breast, and colon cancer. Nitric oxide is also a multifunctional signaling molecule active in many cells of the body, including endothelial cells, macrophages, monocytes, hepatocytes, mast cells, osteoblasts, and astrocytes. Endothelin-1 (ET-1) is a 21-amino acid peptide that stimulates the proliferation of vascular smooth muscle cells, fibroblasts, and keratinocytes, and plays a role in the expression of proto-oncogenes (c-myc, c-fos), which precedes cell proliferation. Similar to NO, ET is secreted by different cell types, including macrophages, monocytes, hepatocytes, endothelial cells, vascular smooth muscle cells, and various tumor cells. Elevated ET-1 levels are observed in pulmonary, hepatocellular, and prostate cancers. Actinic keratosis (AK) and basal cell carcinoma (BCC) are common skin tumors with accentuated hyperkeratinization, hyperpigmentation, and keratinocyte proliferation. AIM: To investigate plasma NOx (nitrite/nitrate -- the end products of NO metabolism), ET, and the NOx/ET ratio in patients with AK and BCC in comparison with healthy controls. METHODS: NOx, ET, and the NOx/ET ratio were measured in 13 patients with AK, 12 patients with BCC, and in 16 healthy controls. RESULTS: Data analysis indicated a significant increase in plasma NOx, ET, and NOx/ET values in BCC patients in comparison with controls (P < 0.001, P < 0.05 and P < 0.001, respectively). Plasma ET levels in AK were also increased in comparison with controls (P < 0.001). When the two study groups (AK and BCC) were compared, a significant increase (P < 0.001) in the NOx/ET ratio in BCC was found. CONCLUSIONS: The increased plasma ET and NOx levels in AK and, especially, BCC are probably the result of and/or reason for the accentuated hyperkeratinization, hyperpigmentation, and keratinocyte proliferation. The increased production of ET and NO by keratinocytes may function as growth and cytotoxic factors and potential mitogens, and may accelerate further proliferation of these skin tumors. In addition, the increased NOx/ET ratio probably reflects a disturbed equilibrium between these two substances, leading to cell damage and tumor promotion and proliferation.

Alterations of total and lipid-bound sialic acid levels in recurrent abortion.

OBJECTIVE: Sialic acid, a terminal component of glycoproteins and glycolipids, is found to be elevated in many pathologic conditions, including preterm deliveries and uterine dysfunction. Along with increased lipid peroxides, it is one of the indices of oxidative stress seen in recurrent abortion. This article investigates whether changes in plasma total sialic acid (TSA) and lipid-bound sialic acid (LSA) contribute to this condition. PATIENTS AND METHODS: Plasma samples of 25 nonpregnant (NP) healthy women, 25 normotensive pregnant women (NTP), and 120 women with recurrent abortion (RA) were assayed for TSA, LSA, total protein (TP), and TSA/TP. Recurrent aborters were divided into four subgroups according to etiology: 25 autoimmune (AUTO), 25 luteal phase defect (LPD), 20 anatomical defect (AD), and 50 with unexplained etiology (UNEx). RESULTS: Plasma TSA and LSA levels were significantly elevated in AUTO aborters in comparison with controls (NP and NTP) and other recurrent abortion subgroups. TSA/TP value was significantly increased in abortion with immunological and unexplained etiology (AUTO and UNEx). CONCLUSIONS: According to our results we can suggest that elevation of TSA and LSA is indeed a reflection of the immunologic abnormalities in the AUTO group, and that TSA and LSA increase is secondary to the underlying disease of AUTO aborters.

Antioxidant defence in recurrent abortion.

Increased free radical activity has been implicated in the pathogenesis of recurrent abortion. This investigation was conducted to determine if changes in some parameters of the antioxidant system contribute to this condition. Plasma ascorbic acid, alpha-tocopherol, total thiols, ceruloplasmin, uric acid, albumin, and erythrocyte glutathione (GSH) were assayed in 25 nonpregnant (NP) healthy women, 25 normotensive pregnants (NTP), and 120 women with recurrent abortion. Recurrent aborters were divided into four subgroups according to the etiology: autoimmune (AUTO, n=25), luteal phase defect (LPD, n=25), anatomical defect (AD, n=20) and unexplained (UNEx, n=50). Plasma levels of ascorbic acid, alpha-tocopherol, and erythrocyte GSH were significantly decreased in AUTO, UNEx and LPD subgroups than those in two control groups and the AD group (ANOVA). Plasma thiols of UNEx and AUTO aborters were diminished according to controls and other abortion subgroups (ANOVA). Ceruloplasmin levels showed a decline in AUTO and UNEx subgroups when compared to controls, AD and LPD aborters (ANOVA). When UNEx, AUTO and LPD recurrent abortion subgroups were compared with each other (Student's t-test) total thiols and erythrocyte GSH of UNEx and AUTO subgroups were diminished in comparison with LPD. We suggest that decreased concentrations of plasma ascorbic acid, alpha-tocopherol, total thiols and erythrocyte GSH in UNEx, AUTO and LPD reflect the increased oxidative stress, expressing a progress of the condition. Also, the imbalance between antioxidant defence and free radical activity is more evident in the AUTO subgroup. As a conclusion, although impaired antioxidant defence may be responsible for recurrent abortions, the recurrent abortions may also result in oxidative stress and depletion and weakness of antioxidant defence.

Plasma antioxidant defense in actinic keratosis and basal cell carcinoma.

BACKGROUND: Reactive oxygen species and lipid peroxides have been implicated in the pathogenesis of a variety of diseases, particularly cancer. There may be an inverse correlation between lipid peroxidation and antioxidant defense mechanisms. The aim of this study was to investigate whether certain plasma antioxidants (ascorbic acid, alpha-tocopherol, total thiol groups, ceruloplasmin, urate, albumin and erythrocyte glutathione) are altered in actinic keratosis (AK) and basal cell carcinoma (BCC). METHODS: Plasma samples and red blood cells (RBC) of 13 patients with AK, 12 with BCC and 16 healthy controls were investigated. RESULTS: Data analysis indicates significant decrease of ascorbic acid (P < 0.001), alpha-tocopherol (P < 0.05 and P < 0.001), total thiol groups (P < 0.001), ceruloplasmin (P < 0.001 and P < 0.05), and RBC glutathione (P < 0.05) values in both AK and BCC groups compared to controls. Comparison of AK and BCC groups evidenced a significant decrease of alpha-tocopherol and RBC glutathione (P < 0.05) in BCC patient. CONCLUSION: Plasma antioxidants are decreased in the AK and BCC, probably due to the long exposure to UV irradiation which is one of the most important factors in the etiology of AK and BCC and alpha-tocopherol and RBC glutathione (P < 0.05) are most altered in BCC.

Lipid profile in actinic keratosis and basal cell carcinoma.

BACKGROUND: The lipid content of the skin and its changes are important in the pathogenesis of many disorders affecting the skin, particularly actinic keratosis (AK) and basal cell carcinoma (BCC). METHODS: Cholesterol, phospholipid, triglyceride, and total lipid levels were studied in paired lesional (AK and BCC) and nonlesional intact skin of 13 patients with AK and 12 patients with BCC. Serum concentrations of the same lipid fractions studied in the skin were investigated in AK and BCC patients and in 11 healthy, age-matched controls. RESULTS: Levels of all lipid fractions were increased in both AK and BCC skin. When AK and BCC skin were compared with each other, a significant increase in phospholipids (p < 0.02) and total lipids (p < 0.01) was found in BCC. Serum cholesterol (p < 0.001), phospholipid (p < 0.001), triglyceride (p < 0.05), and total lipid (p < 0.001) concentrations of AK patients were significantly higher than those of the control group. When BCC and controls were compared, a significant increase in phospholipids and total lipids (p < 0.001) was seen. Serum cholesterol in BCC patients was significantly lower (p < 0.001) and serum phospholipid levels were significantly higher (p < 0.05) than those in the AK group. CONCLUSIONS: An increase in the metabolically active serum phospholipid fraction is reflected in elevated neoplastic tissue phospholipid. This produces altered proportions between lipid fractions in tumorous areas and may result in changes in the intact nature of the cellular membrane, spread, and malignant proliferation.

Hormone replacement therapy and urinary prostaglandins in postmenopausal women.

The objective of the study was to observe the effects of hormone replacement therapy upon urinary prostaglandin E2 and prostaglandin F2 alpha levels in postmenopausal patients. A total number of 55 women were enrolled in this study and 15 premenopausal (PreM) healthy subjects constitute the control group. A total of 40 patients at least 12 months after their natural menopause were divided into two groups: 15 of them was not medicated hormone replacement therapy (which composed NRHRT group) while 25 of the rest, received conjugated estrogen (Premarin) 0.625 mg/day orally plus medroxyprogesterone acetate (Farlutal) 10 mg/day orally built up the RHRT group. PGE2 and PGF2 alpha levels were measured with PGE2 [125I] and PGF2 alpha [3H] RIA kits. Statistical significance was analyzed by Student's t-test for impaired data. NRHRT and RHRT patients had had increased urinary PGE2 levels when compared with PreM (P < 0.001). HRT caused a significant decrease in PGE2 levels in menopausal women (P < 0.001). Urinary PGF2 alpha values of NRHRT and RHRT were significantly lower (P < 0.001) in comparison with PreM group. There was no difference in PGF2 alpha values between two postmenopausal groups. HRT given to postmenopausal patients might have a positive impact on prostaglandins and therefore on bone turnover in a series of various mechanisms.

Impact of calcitonin on urinary excretion of prostaglandins during menopause.

The aim of this study was to investigate the effects of calcitonin as an antiresorptive agent in postmenopausal osteoporosis in prostaglandin metabolism. Urinary prostaglandin E2 (PGE2) concentrations were determined by PGE2 (125I) RIA kit in a total number of 37 patients in postmenopause; 27 in study group with established osteoporosis (WEO) and 10 in another group without osteoporosis (WO). An additional group of 12 patients in the premenopausal period were selected as controls (PreM). Data were given as mean +/- SD and statistical analysis was performed by Student's t test for paired and unpaired values. A significant decrease in urinary PGE2 concentrations was observed in WEO (7.91 +/- 3.08 vs. 3.79 +/- 3.01 ng/l) (p < 0.001), WO (9.06 +/- 6.76 vs. 6.06 +/- 3.90 ng/l) (p < 0.05) and PreM (7.14 +/- 1.68 vs. 5.16 +/- 1.91 ng/l) (p < 0.01). As a conclusion, calcitonin seems to exert a negative effect on prostaglandin metabolism resulting in reduced new prostaglandin formation.

Urinary PGE2 and PGF2alpha levels and renal functions in preeclampsia.

The role of prostaglandin E2 (PGE2) and prostaglandin F2alpha (PGF2alpha) in the pathogenesis of hypertension and altered renal functions, which are the main symptoms of preeclampsia, has gained importance. Serum and urine samples of 59 women (24 preeclamptic pregnant (PEP), 20 normotensive pregnant (NTP) and 15 nonpregnant) were investigated by means of prostaglandin levels and urea, creatinine and creatinine clearance values. PEP patients, when compared with NTP patients, show a significant decrease in PGE2 and PGF2alpha levels (p < 0.01 and p < 0.05, respectively) accompanied by changes in some parameters of renal function such as serum urea, creatinine and creatinine clearance. Although disorders in prostaglandin levels may be responsible for some renal pathologic changes, renal functional and morphologic alterations may also result in abnormal prostaglandin activity.