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Onder A.,Pediatrics Research and Training Hospital | Aycan Z.,Pediatrics Research and Training Hospital | Cetinkaya S.,Pediatrics Research and Training Hospital | Kendirci H.N.P.,Pediatrics Research and Training Hospital | And 2 more authors.
Journal of Pediatric Endocrinology and Metabolism | Year: 2012

There are few reports of an association between Turner syndrome (TS) and 21-hydroxylase deficiency. However, this association is more frequent in some populations. The aim of this study was to evaluate the incidence of 21-hydroxylase deficiency in patients with TS in our population. 21-hydroxylase deficiency was evaluated in 44 TS cases with 45X (n = 20) and 24 mosaic cases. A standard dose adrenocorticotropic (ACTH) stimulation test (Synacthen, Novartis, Basel, Switzerland) was performed, and 17 hydroxyprogesterone (17OHP), dehydroepiandrosterone sulfate (DHEAS) and cortisol responses were evaluated. Patients with increased 17OHP responses in the stimulation test also underwent 21-hydroxylase gene analysis. The mean age was 14.6 ± 4 (2.6-22.4); 37 patients were on growth hormone (GH) treatment. Nine patients were at prepubertal stage, whereas 35 were pubertal (24 on gonadal steroids and 11 spontaneously). Six patients were obese. Only one of our patients had a level of 7.5 ng/mL of 17OHP, and there was no mutation found in congenital adrenal hyperplasia (CAH) genetic analysis. In other cases, peak 17OHP levels were ≤ 6 ng/mL. The mean peak 17OHP was 2.62 ± 1.48 (1.19-7.5) ng/mL, the cortisol level was 37.6 ± 8.43 (23.9-56.2) μ g/dL and the DHEAS was 135.2 ± 87.3 (15-413) μ g/dL. The increased mean basal and peak cortisol levels (20.5 ± 10.2 and 37.6 ± 8.4 μ g/dL) were remarkable findings. Whereas basal cortisol was above 20 μ g/dL in 38.7 % of patients, exaggerated results up to 56.2 μ g/dL were obtained in peak cortisol levels. The basal and peak 17OHP cortisol levels were not correlated with the presence of puberty, chromosome structure, gonadal steroid use, obesity or growth hormone use. This trial suggested that 21-hydroxylase deficiency was not common among patients with TS in our population. Adrenal function should be assessed, at least in the presence of clitoral enlargement in patients with TS, particularly if their karyotype does not contain a Y chromosome.


Bicer S.,Pediatrics Research and Training Hospital | Sahin G.T.,Pediatrics Research and Training Hospital | Koncay B.,Pediatrics Research and Training Hospital | Gemici H.,Pediatrics Research and Training Hospital | And 3 more authors.
Infezioni in Medicina | Year: 2011

This study was undertaken to give an insight into the incidence of acute gastroenteritis cases of rotaviral/adenoviral aetiology in patients presenting to the emergency room of an inner-city government teaching hospital. Group A rotavirus and adenovirus serotype 40-41 antigen results were obtained via immunochromatography. In 2007, there were 1543 patients with gastroenteritis between 0-5 years of age whose stool samples were tested for rota and adenovirus, of whom 386 (25%) had positive stool samples for rotavirus, and 133 (8.6%) for adenovirus serotype 40-41. The majority of rotavirus (74.6%) and adenovirus (73%) cases were between 0-2 years of age. The peak season for rotavirus gastroenteritis was January (44%) and February (50.6%), whereas July (9.7%) and August (9%) were months of low incidence. For enteric adenoviral infections summer was the peak season, with August (20.9%) and July (17.3%) being the foremost months. Among the viral gastroenteritis cases, rotavirus infections were in the majority. A seasonal trend emerges for viral gastroenteritis: Rota virus infections are most frequently seen in winter whereas adenoviral infections prefer summer months. Both viruses mostly affect children up to 2 years.


PubMed | Pediatrics Research and Training Hospital
Type: Controlled Clinical Trial | Journal: Journal of pediatric endocrinology & metabolism : JPEM | Year: 2012

There are few reports of an association between Turner syndrome (TS) and 21-hydroxylase deficiency. However, this association is more frequent in some populations. The aim of this study was to evaluate the incidence of 21-hydroxylase deficiency in patients with TS in our population. 21-hydroxylase deficiency was evaluated in 44 TS cases with 45X (n=20) and 24 mosaic cases. A standard dose adrenocorticotropic (ACTH) stimulation test (Synacthen, Novartis, Basel, Switzerland) was performed, and 17 hydroxyprogesterone (17OHP), dehydroepiandrosterone sulfate (DHEAS) and cortisol responses were evaluated. Patients with increased 17OHP responses in the stimulation test also underwent 21-hydroxylase gene analysis. The mean age was 14.6 +/- 4 (2.6-22.4); 37 patients were on growth hormone (GH) treatment. Nine patients were at prepubertal stage, whereas 35 were pubertal (24 on gonadal steroids and 11 spontaneously). Six patients were obese. Only one of our patients had a level of 7.5 ng/mL of 17OHP, and there was no mutation found in congenital adrenal hyperplasia (CAH) genetic analysis. In other cases, peak 17OHP levels were < or = 6 ng/mL. The mean peak 17OHP was 2.62 +/- 1.48 (1.19-7.5) ng/mL, the cortisol level was 37.6 +/- 8.43 (23.9-56.2) microg/dL and the DHEAS was 135.2+/- 87.3 (15-413) microg/dL. The increased mean basal and peak cortisol levels (20.5 +/- 10.2 and 37.6 +/- 8.4 microg/dL) were remarkable findings. Whereas basal cortisol was above 20 microg/dL in 38.7% of patients, exaggerated results up to 56.2 microg/dL were obtained in peak cortisol levels. The basal and peak 17OHP cortisol levels were not correlated with the presence of puberty, chromosome structure, gonadal steroid use, obesity or growth hormone use. This trial suggested that 21-hydroxylase deficiency was not common among patients with TS in our population. Adrenal function should be assessed, at least in the presence of clitoral enlargement in patients with TS, particularly if their karyotype does not contain a Y chromosome.

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