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Autor:
Kie Yasuda, Shinsuke Onuma, Yoko Miyoshi, Miho Fukui, Yoshinori Satomura, Kazuhiko Bessho, Makiko Tachibana, Takeshi Kimura, Tomoya Fukuoka, Keiichi Ozono
Publikováno v:
Journal of Pediatric Endocrinology and Metabolism. 34:1411-1418
Objectives Iodine deficiency and excess both cause thyroid dysfunction. Few data describe the relationship between iodine status and outcomes of congenital hypothyroidism (CH) in iodine-sufficient areas. We investigated urinary iodine (UI) concentrat
Publikováno v:
Journal of Pediatric Endocrinology and Metabolism. 34:1023-1030
Objectives Medium-chain (MCA) and long-chain acylcarnitine (LCA) blood concentrations play a significant role in the fatty acid (FA) oxidation process, especially during the first days of life. Identification of their abnormal concentrations, via exp
Publikováno v:
Journal of Pediatric Endocrinology and Metabolism. 32:1259-1264
Background Fibroblast growth factor 23 (FGF23) is a recently discovered bone-derived regulator of vitamin D metabolism and phosphate homeostasis. It inhibits phosphate reabsorption and calcitriol production by the kidney. Myelomeningocele (MMC) remai
Publikováno v:
Journal of Pediatric Endocrinology and Metabolism. 31:1061-1064
Background Excessive iodine exposure is an often overlooked cause of neonatal hypothyroidism. Case presentation We present an infant with iodine-induced hypothyroidism, which was detected at age 15 days by newborn screening. The infant’s iodine exc
Autor:
Petar D Simić, Svetlana Perovic, George Mastorakos, Djuro Macut, Tatjana Simic, Marija Pljesa-Ercegovac, Ilijana Mažibrada, Dragana Bojanin, Ljiljana Plavsic, Ana Savic-Radojevic, Jelica Bjekic-Macut, Tatjana Djukic
Publikováno v:
Journal of Pediatric Endocrinology and Metabolism.
BackgroundThe aim of the study was to evaluate high-sensitivity C-reactive protein (hs-CRP) and fibrinogen in non-obese normoinsulinemic adolescent girls with polycystic ovary syndrome (PCOS) and their relationship with anthropometric and lipid param
Autor:
Susann Empting, Friedrich-Wilhelm Roehl, Klaus Mohnike, Isabelle Wieacker, Michael Peter, Katrin Borucki
Publikováno v:
Journal of Pediatric Endocrinology and Metabolism. 28:867-871
Careful monitoring of the therapy is crucial for patients with congenital adrenal hyperplasia (CAH) in order to prevent the effects of increased androgen production as well as life-threatening salt-wasting crisis. The key metabolite, 17α-hydroxyprog
Autor:
Magdy El-Ziny, Amany El-Hawary, Abelhady El-Gilany, Nanees Salem, Nehad Chalaby, Abdelhameed Metwali, Megahed Abo-Elmagd, Ashraf A. Elsharkawy, Alaa Wafa
Publikováno v:
Journal of Pediatric Endocrinology and Metabolism. 29
Annually, many children and adolescents with type 1 diabetes mellitus (T1DM) insist on fasting for Ramadan despite being exempted and despite knowing all the risks. We aimed to assess the safety and metabolic impact of Ramadan fasting in children wit
Autor:
Helena Kobe, Urh Groselj, Matic Kelvisar, Barbka Repic Lampret, Mojca Zerjav Tansek, Tadej Battelino
Publikováno v:
Journal of Pediatric Endocrinology and Metabolism. 29
Phenylalanine hydroxylase deficiency causes various degrees of hyperphenylalaninemia (HPA). Tetrahydrobiopterin (BH4; sapropterin) reduces phenylalanine (Phe) levels in responders, enabling relaxation of dietary therapy. We aimed to assess long-term
Autor:
Vincenzo Salpietro, Ashok Adams, Carlo Attilio Squeri, Valeria Chirico, Gaetano Tortorella, Maria Kinali, Martino Ruggieri, Kshitij Mankad, Conrad E. Johanson, Teresa Arrigo, Eloisa Gitto, Anna Claudia Romeo, Agata Polizzi, Salvatore Savasta, Emanuele David, Gian Luigi Marseglia, Mariella Valenzise, Francesco Nicita
Publikováno v:
Journal of Pediatric Endocrinology and Metabolism. 27
Aim To unravel the potential idiopathic intracranial hypertension (IIH) endocrine-metabolic comorbidities by studying the natural (and targeted drug-modified) history of disease in children. IIH is a disorder of unclear pathophysiology, characterized
Autor:
Adnan Al-Shaikh, Taiba Al-Harbi
Publikováno v:
Journal of Pediatric Endocrinology and Metabolism. 25
The syndrome of apparent mineralocorticoid excess (AME) is an autosomal recessive disorder characterized by hypertension, hypokalemia, low renin, and hypoaldosteronism. It is caused by deficiency of 11β-hydroxysteroid dehydrogenase, which results in