Browsing by Author "Tarim, Omer"

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Clinical and Laboratory Characteristics of Hyperprolactinemia in Children and Adolescents: National Survey
(Galenos Yayincilik, 2019) Eren, Erdal; Ergur, Ayca Torel; Isguven, Sukriye Pinar; Bitkin, Eda Celebi; Berberoglu, Merih; Siklar, Zeynep; Tarim, Omer
Objective: We aimed to report the characteristics at admission, diagnosis, treatment, and follow-up of cases of pediatric hyperprolactinemia in a large multicenter study. Methods: We reviewed the records of 233 hyperprolactinemic patients, under 18 years of age, who were followed by different centers. The patients were divided as having microadenomas, macroadenomas, drug-induced hyperprolactinemia and idiopathic hyperprolactinemia. Complaints of the patients, their mode of treatment (medication and/or surgery) and outcomes were evaluated in detail. Results: The mean age of the patients with hyperprolactinemia was 14.5 years, and 88.4% were females. In terms of etiology, microadenomas were observed in 32.6 %, macroadenomas in 27 %, idiopathic hyperprolactinemia in 22.7% and drug-induced hyperprolactinemia in 6.4 %. Other causes of hyperprolactinemia were defined in 11.3%. Common complaints in females (n = 206) were sorted into menstrual irregularities, headaches, galactorrhea, primary or secondary amenorrhea and weight gain, whereas headache, gynecomastia, short stature and blurred vision were common in males (n = 27). Median prolactin levels were 93.15 ng/mL, 241.8 ng/ml, 74.5 ng/mL, 93.2 ng/mL, and 69 ng/mL for microadenomas, macroadenomas, idiopathic hyperprolactinemia, drug-induced hyperprolactinemia, and other causes of hyperprolactinemia, respectively. Of 172 patients with hyperprolactinemia, 77.3 % were treated with cabergoline and 13.4 % with bromocriptine. 20.1 % of the patients with pituitary adenomas underwent pituitary surgery. Conclusion: We present the largest cohort of children and adolescents with hyperprolactinemia in the literature to date. Hyperprolactinemia is more common in females and cabergoline is highly effective and practical to use in adolescents, due to its biweekly dosing. Indications for surgery in pediatric cases need to be revised.
Clinical and Laboratory Characteristics of Hyperprolactinemic Children and Adolescents: National Survey
(Karger, 2017) Eren, Erdal; Ergur, Ayca Torel; Isguven, Sukriye Pinar; Bitkin, Eda Celebi; Berberoglu, Merih; Siklar, Zeynep; Tarim, Omer
Neonatal Adrenal Insufficiency: Turkish Neonatal and Pediatric Endocrinology and Diabetes Societies Consensus Report
(Turkish Pediatrics Assoc, 2018) Yigit, Sule; Turkmen, Munevver; Tuncer, Oguz; Taskin, Erdal; Guran, Tulay; Abaci, Ayhan; Tarim, Omer
It is difficult to make a diagnosis of adrenal insufficiency in the newborn, because the clinical findings are not specific and the normal serum cortisol level is far lower compared to children and adults. However, dehydratation, hyperpigmentation, hypoglycemia, hyponatremia, hyperkalemia and metabolic acidosis should suggest the diagnosis of adrenal insufficiency. Hypotension which does not respond to vasopressors should especially be considered a warning. if the adrenocorticotropin hormone level measured simultaneously with a low serum cortisol level is 2-fold higher than the upper normal limit of the reference range, a diagnosis of primary adrenal insufficiency is definite. Even if the serum cortisol level is normal, a diagnosis of relative adrenal insufficiency can be made with clinical findings, if the patient is under heavy stress. The serum cortisol level should be measured using the method of 'high pressure liquid chromatography' or 'LC mass spectrometry'. Adrenal steroid biosynthesis can be evaluated more specifically and sensitively with 'steroid profiling: Rennin and aldosterone levels may be measured in addition to serum electrolytes for the diagnosis of mineralocorticoid insufficiency. Adrenocorticotropic hormone stimulation test may be used to confirm the diagnosis and elucidate the etiology. In suspicious cases, treatment can be initiated without waiting for the adrenocorticotropic hormone stimulation test In schock which does not respond to vasopressors, intravenous hydrocortisone at a dose of 50-100 mg/m(2)or a glucocorticoid drug at an equivalent dose should be initiated In maintanence treatment the physiological secretion rate of hydrocortisone is 6 mg/m(2)/day (15 mg/m(2)/day in the newborn). The replacement dose should be adjusted with clinical follow-up and by monitoring growth rate, weight gain and blood pressure. Fludrocortisone (0,1 mg tablet) is given for mineralocorticoid treatment (2x0,5-1 tablets). A higher dose may be needed in the neonatal period and in patients with aldosterone resistance. If hyponatremia persists, oral NACl may be added to treatment In the long-term follow-up, patients should carry an identification card and the glucocorticoid dose should be increased 3-10-fold in cases of stress.
Tshr Is the Main Causative Locus in Autosomal Recessively Inherited Thyroid Dysgenesis
(Walter de Gruyter Gmbh, 2012) Cangul, Hakan; Aycan, Zehra; Saglam, Halil; Forman, Julia R.; Cetinkaya, Semra; Tarim, Omer; Maher, Eamonn R.
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 multicase 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.