The Role of Supportive Treatment in the Management of Hyperammonemia in Neonates and Infants.

BACKGROUND: The objective of this study is to investigate the efficacy of continuous renal replacement therapy (CRRT), mainly continuous venovenous hemodiafiltration (CVVHDF), and evaluate vasoactive requirements in hyperammonemic neonates and infants. METHODS: Patients who underwent CRRT for hyperammonemia were retrospectively analyzed. MEASUREMENTS AND MAIN RESULTS: Patients in 7 of the encounters were treated solely by CVVHDF. During 3 encounters, patients who received continuous venovenous hemodialysis (CVVHD) were transitioned to CVVHDF. CVVHD was used in 3 encounters. The median 50% reduction time for ammonia was 8 h (range 3-15 h). The median duration of CRRT treatment was 40 h (range 24-89 h). Survival to hospital discharge occurred in 12 encounters (92.3%). Eleven encounters (84.6%) were treated with different vasoactive agents. In those encounters, the median vasoactive medications' start time was the 6th hours (range 2-60 h) of CRRT. There was no association between the vasoactive index score and pre-dialysis ammonia concentration. CONCLUSIONS: CRRT achieves timely control of hypeammonemic states. Hemodynamic instability necessitating intervention with vasoactive medications is a common finding in patients with hyperammonemia.

Omentin-1 level in adolescents with polycystic ovarian syndrome.

BACKGROUND: Adipokines have been suggested to play an important role in the pathogenesis of polycystic ovarian syndrome (PCOS). Omentin is an adipokine secreted essentially by visceral adipose tissue with an insulin-sensitizing effect. Insulin resistance (IR) is a common feature of PCOS, therefore the aim of this study was to investigate omentin-1 level in adolescent girls with PCOS and its relationship with IR and androgens. METHOD: A total of 41 obese girls with PCOS, and 30 age- and body mass index (BMI)-matched obese girls without PCOS were enrolled in the study. The demographic, clinic and laboratory characteristics of the groups were compared. Additionally, bivariate correlation analysis of omentin-1 with BMI standard deviation score (BMI-SDS), insulin, glucose, homeostatic model assessment of IR (HOMA-IR), total and free testosterone was performed. RESULTS: In the PCOS group HOMA-IR, free and total testosterone were higher than in the control group. Omentin-1 was lower in the PCOS group compared with the controls (55.01 ± 7.99 ng/mL vs 59.10 ± 7.02 ng/mL, respectively; P = 0.027). Omentin-1 was inversely correlated with free testosterone (r = -0.527, P = 0.030) and BMI-SDS (r = -0.241, P = 0.046) but it was not correlated with total testosterone, HOMA-IR, glucose, insulin or serum lipids. CONCLUSION: Omentin-1 was lower in obese girls with PCOS and hyperandrogenism was associated with this condition.

Normosmic idiopathic hypogonadotropic hypogonadism due to a novel homozygous nonsense c.C969A (p.Y323X) mutation in the KISS1R gene in three unrelated families.

OBJECTIVE: The spectrum of genetic alterations in cases of hypogonadotropic hypogonadism continue to expand. However, KISS1R mutations remain rare. The aim of this study was to understand the molecular basis of normosmic idiopathic hypogonadotropic hypogonadism. METHODS: Clinical characteristics, hormonal studies and genetic analyses of seven cases with idiopathic normosmic hypogonadotropic hypogonadism (nIHH) from three unrelated consanguineous families are presented. RESULTS: One male presented with absence of pubertal onset and required surgery for severe penoscrotal hypospadias and cryptorchidism, while other two males had absence of pubertal onset. Two of four female cases required replacement therapy for pubertal onset and maintenance, whereas the other two had spontaneous pubertal onset but incomplete maturation. In sequence analysis, we identified a novel homozygous nonsense (p.Y323X) mutation (c.C969A) in the last exon of the KISS1R gene in all clinically affected cases. CONCLUSIONS: We identified a homozygous nonsense mutation in the KISS1R gene in three unrelated families with nIHH, which enabled us to observe the phenotypic consequences of this rare condition. Escape from nonsense-mediated decay, and thus production of abnormal proteins, may account for the variable severity of the phenotype. Although KISS1R mutations are extremely rare and can cause a heterogeneous phenotype, analysis of the KISS1R gene should be a part of genetic analysis of patients with nIHH, to allow better understanding of phenotype-genotype relationship of KISS1R mutations and the underlying genetic basis of patients with nIHH.

Determination of early urinary renal injury markers in obese children.

BACKGROUND: Obesity is an important health issue, the prevalence of which is increasing in childhood. The aim of this study was to examine urinary renal injury markers in order to determine the renal effect of obesity and its comorbidities in a pediatric population. METHODS: Eighty-four obese children and 64 healthy control subjects were enrolled in the study. We checked their urine using N-acetyl-beta-D-glucosaminidase (NAG), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and microalbumin as renal injury markers. Associations of renal damage markers with hypertension, an impaired glucose tolerance test, and insulin resistance were assessed. RESULTS: Obese individuals had higher urinary NAG and KIM-1 values compared to those of healthy controls (p = 0.027, p = 0.026). There was no difference in urinary NGAL between obese and lean subjects (p = 0.885). Urinary renal injury markers were not statistically different in the obese group when checked for impaired glucose tolerance, insulin resistance, and hypertension (p > 0.05). CONCLUSIONS: This study shows that urinary NAG and KIM-1 could be used as a screening method for detection of early renal damage in obese children.

Investigation of irisin's role in pubertal onset physiology in female rats.

OBJECTIVE: The timing of pubertal development is closely related to metabolic status and energy reserves. It is thought that irisin, which is involved in the regulation of energy metabolism and is shown to be present in the hypothalamo-pituitary-gonadal (HPG) axis, may play a role in this process. In our study, we aimed to investigate the effect of irisin administration on pubertal development and HPG axis in rats. DESIGN-METHODS: 36 female rats were included in the study were divided into 3 groups: 100 ng/kg/day irisin treatment group (irisin-100), 50 ng/kg/day irisin treatment group (irisin-50), and control group. On the 38th day, serum samples were taken to determine levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH), estradiol and irisin. Brain hypothalamus samples were taken to determine levels of pulsatile gonadotropin-releasing hormone (GnRH), kisspeptin, neurokinin-B, dynorphin (Dyn), and makorin ring finger protein-3 (MKRN3). RESULTS: Vaginal opening and estrus were seen firstly in the irisin-100 group. At the end of the study, the highest rate of vaginal patency was found in the irisin-100 group. Hypothalamic protein expression levels of GnRH, NKB and Kiss1 in homogenates; serum FSH, LH, and estradiol levels were the highest in the irisin-100 group, followed by the irisin-50 and control groups, respectively. Ovarian sizes were significantly greater in the irisin-100 group compared to the other groups. The hypothalamic protein expression levels of MKRN3 and Dyn were the lowest in the irisin-100 group. CONCLUSIONS: In this experimental study, irisin triggered the onset of puberty in a dose-dependent manner. Irisin administration caused the excitatory system to dominate in the hypothalamic GnRH pulse generator.

Oxidant/antioxidant system markers and trace element levels in children with nutritional rickets.

OBJECTIVE: To determine the oxidative stress and trace element levels in vivo in patients with nutritional rachitism associated with vitamin D deficiency. MATERIALS AND METHOD: A total of 30 patients, 18 males and 12 females, were included in the study. Age, sex, medical history, vital, and physical examination findings of each patient documented at presentation were recorded. Serum calcium, phosphorus, alkaline phosphatase, parathormone, and 25-OH vitamin D levels, as well as oxidant and antioxidant system parameters and trace element levels were studied. After being diagnosed with rachitism, the patients were administered a single dose of 300,000 IU vitamin D by intramuscular injection. The same analyses were repeated post-treatment. Thirty children with normal anthropometric measurements were included as the control group. The analyses described above were performed only once for the control group. RESULTS: Serum calcium, phosphorus, alkaline phosphatase, parathormone, and 25-OH vitamin D levels were different between the controls and children in the patient group (p<0.001). Analysis of trace element levels demonstrated markedly lower pretreatment zinc levels for the patient group compared to the controls, with a statistically significant difference (p=0.001). Comparison of pretreatment oxidant and antioxidant system markers between the patient and control groups demonstrated higher values for vitamin C, ß-carotene, reduced glutathione, and superoxide dismutase in the control group, whereas MDA was higher in the patient group. CONCLUSION: The present study demonstrated increased oxidative stress, reduced antioxidant defence system in patients with nutritional rachitism, with reduced oxidative stress and a pronounced improvement in the antioxidant system with vitamin D treatment.

TSHR is the main causative locus in autosomal recessively inherited thyroid dysgenesis.

Congenital hypothyroidism (CH) is the most common neonatal endocrine disorder and results in mental retardation if untreated. Eighty-five percent of CH cases are due to disruptions in thyroid organogenesis and are mostly sporadic, but about 2% of thyroid dysgenesis is familial, indicating the involvement of genetic factors in the aetiology of the disease. In this study, we aimed to investigate the Mendelian (single-gene) causes of non-syndromic and non-goitrous congenital hypothyroidism (CHNG) in consanguineous or multi-case families. Here we report the results of the second part (n=105) of our large cohort (n=244), representing the largest such cohort in the literature, and interpret the overall results of the whole cohort. Additionally, 50 sporadic cases with thyroid dysgenesis and 400 unaffected control subjects were included in the study. In familial cases, first, we performed potential linkage analysis of four known genes causing CHNG (TSHR, PAX8, TSHB, and NKX2-5) using microsatellite markers and then examined the presence of mutations in these genes by direct sequencing. In addition, in silico analyses of the predicted structural effects of TSHR mutations were performed and related to the mutation specific disease phenotype. We detected eight new TSHR mutations and a PAX8 mutation but no mutations in TSHB and NKX2-5. None of the biallelic TSHR mutations detected in familial cases were present in the cohort of 50 sporadic cases. Genotype/phenotype relationships were established between TSHR mutations and resulting clinical presentations. Here we conclude that TSHR mutations are the main detectable cause of autosomal recessively inherited thyroid dysgenesis. We also outline a new genetic testing strategy for the investigation of suspected autosomal recessive non-goitrous CH.

The frequency of Hashimoto thyroiditis in children and the relationship between urinary iodine level and Hashimoto thyroiditis.

The aim of this study was to determine the frequency of thyroid autoimmunity in second grade primary school students and to examine the relationship between iodine and Hashimoto thyroiditis (HT). This was a cohort study performed with 1000 students. Urinary iodine levels, antithyroid peroxidase (anti-TPO) and antithyroglobulin (anti-Tg) antibodies were determined in all children. Children with anti-TPO or anti-Tg antibody positivity or with goiter were summoned for detailed examinations. In total, 36 cases (3.6%) were diagnosed as HT. The goiter frequency was found in 17.5% of the whole cohort. Additionally, iodine deficiency was found in 64.2% of all children. The median urinary iodine excretion was determined as 132 microg/L (range 382 microg/L) in the HT group, whereas it was 73 microg/L (range 390 microg/L) in children with goiter but without HT and 81 microg/L (range 394 microg/L) in normal children. The urinary iodine level of HT cases was significantly higher than the other two groups (p < 0.001). HT was also determined in 2% of patients with low urinary iodine levels, in 6.2% of patients with normal urinary iodine levels, and in 7.5% of patients with high urinary iodine levels. Our data demonstrates the close relationship between excessive iodine levels and autoimmunity.

Evaluation of children with nutritional rickets.

AIM: To evaluate the clinical findings, risk factors, therapy and outcome in 946 children with nutritional rickets. PATIENTS AND METHODS: This retrospective study included a review of medical records of patients with nutritional rickets between March 2004 and 2009. Patients who displayed both the biochemical inclusion criteria and the clinical signs/symptoms or radiological signs of rickets were included in the study. RESULTS: The present study included 946 patients aged between 4 months and 15 years. Distribution of the cases showed a density between December and May. The age at diagnosis, showed two peaks and most of the patients were in the age range 0-23 months and 12.0-15 years. In infants and young children, most of the patients had been admitted to the hospital due to infectious diseases. In older children, short stature and obesity were the most common complaints. CONCLUSION: Children aged between 0-23 months and 12.0-15 years were under most risk for nutritional rickets, especially in winter and spring and vitamin D should be given to them as supplementation dose.

Serum Irisin Levels in Central Precocious Puberty and Its Variants.

AIM: The exact mechanisms that trigger the onset of puberty are not well known. Adipomyokines are postulated to stimulate the central neural network. In the present study, we investigated irisin levels in girls with central precocious puberty (CPP), slowly progressing precocious puberty (SPPP), or premature thelarche (PT); we also studied prepubertal girls and to determine if this adipomyokine could be used as a marker in this context. METHODS: A total of 94 girls including 33 with CPP, 31 with precocious puberty (PP) variants (SPPP or PT), and 30 healthy controls were enrolled to the study. The mean irisin levels were compared between groups. The bivariate correlations of irisin levels with clinical and laboratory parameters were assessed. Multivariate linear regression analysis was performed to determine independent predictive factors of irisin levels. RESULTS: Irisin levels were higher in the CPP group compared with the other groups (CPP group: 723.25 ±â€…62.35 ng/mL; PP variants group: 529.60 ±â€…39.66 ng/mL; and control group: 325.03 ±â€…27.53 ng/mL) (P < 0.001). Irisin levels were positively correlated with body mass index standard deviation scores (BMI-SDS), height-SDS, weight-SDS, bone age, uterus long axis, ovary size, baseline FSH and LH, and peak LH levels. Multivariate linear regression analysis revealed that irisin levels had the strongest correlation with peak LH. The other independent predictive factor of irisin levels was BMI-SDS. CONCLUSIONS: The mean irisin levels were higher in patients with CPP compared with other groups. The results of this study imply that increased irisin levels may be used as a marker of CPP provided that these findings are confirmed in larger prospective studies.

Novel TSHR mutations in consanguineous families with congenital nongoitrous hypothyroidism.

OBJECTIVE: Nonsyndromic autosomal recessively inherited nongoitrous congenital hypothyroidism (CHNG) can be caused by mutations in TSHR, PAX8, TSHB and NKX2-5. We aimed to investigate mutational frequencies of these genes and genotype/phenotype correlations in consanguineous families with CHNG. DESIGN: Because consanguinity in individuals with a presumptive genetic condition is often an indicator of an autosomal recessive inheritance and allows firmer correlations to be established between genotype and phenotype, we planned to execute our study in consanguineous families. PATIENTS: Hundred and thirty-nine children with CHNG phenotype born to consanguineous families. MEASUREMENTS: First, we investigated cases for evidence of linkage to the four known CHNG genes by microsatellite marker analysis. Mutation analysis by direct sequencing was then performed in those cases in whom linkage to the relevant candidate gene could not be excluded. In addition, in silico analysis of the predicted structural effects of TSHR mutations was performed and related to the mutation-specific disease phenotype. RESULTS: Homozygous germline TSHR mutations were detected in six families (5%), but no mutations were detected in PAX8, TSHB and NKX2-5. Four of TSHR mutations had not previously been described. Genotype-phenotype correlations were established and found to be related to the predicted structural effects of the mutations. CONCLUSIONS: Known causative genes account for the development of CHNG only in a minority of cases, and our cohort should provide a powerful resource to identify novel causative genes and to delineate the extent of locus heterogeneity in autosomal recessively inherited CHNG.

Avian influenza A (H5N1) infection in eastern Turkey in 2006.

BACKGROUND: An outbreak of highly pathogenic avian influenza A (H5N1) that had previously been detected throughout Asia, with major economic and health repercussions, extended to eastern Turkey in late December 2005 and early January 2006. METHODS: We documented the epidemiologic, clinical, and radiologic features of all cases of confirmed H5N1 virus infection in patients who were admitted to Yuzuncu Yil University Hospital in Van, Turkey, between December 31, 2005, and January 10, 2006. RESULTS: H5N1 virus infection was diagnosed in eight patients. The patients were 5 to 15 years of age, and all eight had a history of close contact with diseased or dead chickens. The mean (+/-SD) time between exposure and the onset of illness was 5.0+/-1.3 days. All the patients had fever, and seven had clinical and radiologic evidence of pneumonia at presentation; four patients died. Results of enzyme-linked immunosorbent assay and rapid influenza tests were negative in all patients, and the diagnosis was made by means of a polymerase-chain-reaction assay. CONCLUSIONS: H5N1, which causes a spectrum of illnesses in humans, including severe and fatal respiratory disease, can be difficult to diagnose.

Serum insulin-like growth factor-I and insulin-like growth factor binding protein-3 levels in children with zinc deficiency and the effect of zinc supplementation on these parameters.

AIM: To determine the effect of zinc (Zn) therapy on serum insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3) levels in children with Zn deficiency and growth retardation, but without systemic disease, and to investigate the effect of Zn supplementation on these parameters. METHODS: Twenty-nine children (11 girls and 18 boys) were included. Blood samples were obtained for serum IGF-I and IGFBP-3 determination before and after 50 mg/day Zn supplementation for two months. RESULTS: The mean age of the children was 11.0 +/- 3.1 years (range 3.7-16.2 years). Serum IGF-I and IGFBP-3 levels were below the mean values in 28 (96.6%) and all children, respectively. After Zn therapy, serum IGF-I levels were increased in 62% of the children; this increase was statistically significant in 48.3% of the children. Serum IGFBP-3 levels were significantly increased in 10 children. There was a positive correlation between serum Zn level and bone age, and serum IGF-I and IGFBP-3 levels. A positive correlation was present between BMI (r = 0.485, p < 0.001) and serum IGF-I levels before therapy. CONCLUSION: Serum IGF-I and IGFBP-3 levels were decreased in children with Zn deficiency, and were increased after Zn supplementation. In addition, after Zn supplementation, increment of serum IGF-I levels was found to be higher in children with low BMI than those with normal BMI; therefore, the nutritional status of children may also be important, as well as Zn supplementation. Additionally, the determination of higher variation percentile of serum IGF-I level in prepubertal children compared to pubertal children was an interesting finding and necessitates further investigation.

The effect of 25-hydroxyvitamin D3 on the immune system.

AIM: To examine the effect of 25-OH vitamin D3 on the immune system in patients with nutritional rickets. METHODS: Fifty-three patients were included in our study between April 2002 and March 2004. Diagnosis of rickets was based on clinical, biochemical and radiological examinations. Cell surface markers (CD), complement factors (C), and immunoglobulin (Ig) levels were determined to find out any relationship between rickets and immune system deficiency. RESULTS: Among the causes of admission to hospital, fever (66%) and coughing (62.2%) were the most frequent. Pneumonia was accompanied by rickets in 47.1% of the cases. Plasma CD4 levels before the treatment were higher than those in the post-treatment period, whereas CD20 and CD56 levels were lower. CONCLUSION: B cell and natural killer cell reduction which occur because of vitamin D deficiency may contribute to the development of pneumonia and other infections in patients with nutritional rickets.

Psychotic disorder and extrapyramidal symptoms associated with vitamin B12 and folate deficiency.

Vitamin B12 and folate deficiency causing neuropsychiatric and thrombotic manifestations, such as peripheral neuropathy, subacute combined degeneration of cord, dementia, ataxia, optic atrophy, catatonia, psychosis, mood disturbances, myocardial infarction and portal vein thrombosis are well known. This present report highlights an unusual presentation of vitamin B12 deficiency-psychotic disorder, extrapyramidal symptoms in a 12-year-old boy. His symptoms responded to parenteral vitamin B12 therapy. So with this report we emphasized that serum vitamin B12 and folate levels should be measured, especially in those patients who present with other known neuropsychiatric features of vitamin B12 and folate deficiency.

Rickets in the Middle East: role of environment and genetic predisposition.

CONTEXT: The Middle East has a high incidence of rickets, and it is also common in Europe-dwelling children of Middle Eastern origin. OBJECTIVE: The objective of the study was to explore the mechanisms leading to rickets in children of the Middle East. DESIGN AND SETTING: We conducted a prospective study in 98 rachitic and 50 controls (aged 6 months to 4 yr) from university and community outpatient hospitals in Egypt and Turkey. MAIN OUTCOME MEASURES: We collected epidemiological, maternal, nutritional, radiographic, and biochemical parameters; markers of bone turnover; and vitamin D receptor (VDR) gene polymorphisms. RESULTS: Epidemiological factors had a key role in pursuit of rickets; Egyptian and Turkish patients had lower (P < 0.01) dietary calcium intake than controls and the recommended dietary intakes, and serum 25-hydroxyvitamin D levels were reduced in patients, the difference with controls being significant (P < 0.001) only in Turkey, although rickets was more severe in Egypt as determined by the x-ray score (P < 0.05). In Turkey, the F VDR allele frequency was significantly (P < 0.05) increased in patients. The BB VDR genotype was associated with lower serum 25-hydroxyvitamin D levels in both patients and controls and with severity of rickets. CONCLUSIONS: In Turkey most patients had vitamin D deficiency, whereas in Egypt they had mostly calcium insufficiency combined with vitamin D deficiency. In this environ, VDR genotypes may predispose to rickets by increased frequency of the F allele. The unique environs and genetic predisposition have to be accounted for in the design of preventive measures, rather than using European or American recommended dietary intake for calcium and vitamin D.

Incidence of Type 1 Diabetes in Children Aged Below 18 Years during 2013-2015 in Northwest Turkey

Objective: To assess the incidence of type 1 diabetes mellitus (T1DM) in children under 18 years of age in the northwest region of Turkey during 2013-2015. Methods: All newly diagnosed T1DM cases were recorded prospectively during 2013-2015. Total, as well as gender and age group specific (0-4, 5-9, 10-14 and 15-17 age) mean incidences per 100,000 per year were calculated. Results: There were 1,773 patients diagnosed during 2013-2015 (588 cases in 2013, 592 cases in 2014, 593 cases in 2015). Of these, 862 (48.6%) were girls and 911 (51.4%) were boys. The mean age at diagnosis was 9.2±4.2 years and it was not significantly different between girls (9.0±4.1 years) and boys (9.4±4.4 years) (p=0.052). The crude mean incidence was 8.99/100.000 confidence interval (CI) (95% CI: 8.58-9.42). Although mean incidence was similar between boys [8.98/100.000 (CI: 8.40 to 9.58)] and girls [9.01/100.000 (CI: 8.42 to 9.63)], there was male predominance in all groups except for 5-9 year age group. The standardized mean incidence was 9.02/100.000 according to the World Health Organization standard population. The mean incidence for the 0-4, 5-9, 10-14 and 15-17 age groups was 6.13, 11.68, 11.7 and 5.04/100.000 respectively. The incidence of T1DM was similar over the course of three years (p=0.95). A significant increase in the proportion of cases diagnosed was observed in the autumn-winter seasons. Conclusion: The northwest region of Turkey experienced an intermediate incidence of T1DM over the period of the study.

Cystinosis in Eastern Turkey.

BACKGROUND: This study was conducted to investigate CTNS (cystinosin, lysosomal cystine transporter) gene mutations and the clinical spectrum of nephropathic cystinosis among patients diagnosed with the disease in a single center in Turkey. METHODS: Patients' clinical and laboratory data were extracted from an electronic health registry. Molecular CTNS gene analysis was performed using either next-generation sequencing or Sanger sequencing. RESULTS: Eleven patients (age range: 1.5-12 years) from nine families were identified. The presenting complaint was growth retardation in seven patients; polydipsia and polyuria in three patients; and vomiting in two patients. At presentation, electrolyte loss was noted in all patients, of which eight patients presented with metabolic acidosis, and three patients presented with metabolic alkalosis. All patients also presented with proteinuria and glucosuria, and four patients developed varying degrees of renal insufficiency, for which peritoneal dialysis was initiated in one patient. Cystine crystals were detected via ocular examination in one patient at presentation. No cystine crystals were detected among patients who underwent bone marrow aspiration. In the CTNS gene, a p.T7FX7 (c.18-21del4bp) mutation was detected in three patients, whereas a p.E227E (c.681 G>A) (homozygous) mutation was detected in eight patients. CONCLUSIONS: We detected two distinct mutations, p.T7FX7 (c.18-21del4bp) and p.E227E (c.681 G>A) (homozygous), in the CTNS gene in 11 patients with cystinosis from the East Anatolian region of Turkey. Patients with a homozygous c.681 G>A (p.E227E) mutation are more likely to develop chronic renal failure and should be monitored closely, whereas patients with a p.T7FX7 (c.18-21del4bp) mutation have a milder phenotype. Additionally, metabolic alkalosis does not exclude cystinosis, although cystinosis is a cause of proximal renal tubular acidosis.

Prevalence, Demographic Characteristics and Associated Risk Factors of Malnutrition Among 0-5 Aged Children: A Cross-Sectional Study From Van, Eastern Turkey.

Malnutrition in childhood is a dramatic indicator of poor socio-economical status worldwide. To recognize and reveal the socio-demographic features is crucial, especially for developing countries. Our aim was to investigate the prevalence and association with sociodemographic variables of malnutrition in 0-5 years old children in Van, Turkey. A total of 702 children are included in this cross-sectional study. Demographic features of subject including age, gender, family characteristics and other data were obtained. Nutritional assessment was done using anthropometric indices including weight-for-age, height-for-age, weight-for-height, head circumference and body mass index-for-age. Multivariate logistic regressions were carried out to assess malnutrition-associated factors. Prevalence of underweight, stunting and wasting were 19.7, 17.7 and 16.2%, respectively. Socio-demographic variables that statistical significantly in association with malnutrition were low monthly family income, educational level and employment status of father, parental consanguinity, number of pregnancies, regular intake of vitamin D and history of prematurity. The prevalence of children with head circumference-z score ≤2SD and body mass index-for-age ≤2SD were 9.8 and 16.3%, respectively. Multivariate analysis detected following risk factors for these indices; low monthly family income, history of prematurity, unemployed father and the period between pregnancies (1-2 years). We found that prevalence of malnutrition in the city of Van, was still higher than more developed regions of Turkey. The associated risk factors of malnutrition should be specifically interpreted by health professionals and also by government authorities that are responsible for making practical politics of public health.

The relation of urinary bisphenol A with kisspeptin in girls diagnosed with central precocious puberty and premature thelarche.

BACKGROUND: Bisphenol A (BPA) is known as an endocrine disruptor and it is supposed to have a role on the development of central precocious puberty (CPP). Kisspeptin, a hypothalamic peptide, is a neuromodulator of gonadotropin releasing hormone and it has an important role on regulation of the onset of puberty. The BPA levels in girls with CPP and premature thelarche (PT) and its relation with kisspeptin levels were investigated. METHODS: Twenty-eight girls with CPP, 28 girls with PT and 22 prepubertal girls as a control group were enrolled to the study. Urinary BPA and serum kisspeptin levels were compared in the groups. Bivariate correlations were performed to evaluate the relations of BPA with kisspeptin and estradiol. RESULTS: There was no statistical difference between groups regarding BPA levels. Serum kisspeptin levels were higher in CPP group than controls [306.56 (interquartile range (IQR), 175.63-504.66) vs. 157.62 (IQR, 55.61-285.00) p: 0.008]. There were no correlations between BPA and kisspeptin levels (r: 0.088, p: 0.391) and between BPA and estradiol (r: -0.171, p: 0.144). CONCLUSIONS: The BPA levels did not differentiate between groups and it seems that the exposed amount of BPA in daily life did not affect kisspeptin levels in girls with CPP and PT.