Hormone researchPub Date : 2009-01-01Epub Date: 2009-08-18DOI: 10.1159/000232161
J N Boeloni, N M Ocarino, A B Melo, J F Silva, P Castanheira, A M Goes, R Serakides
{"title":"Dose-dependent effects of triiodothyronine on the osteogenic differentiation of rat bone marrow mesenchymal stem cells.","authors":"J N Boeloni, N M Ocarino, A B Melo, J F Silva, P Castanheira, A M Goes, R Serakides","doi":"10.1159/000232161","DOIUrl":"https://doi.org/10.1159/000232161","url":null,"abstract":"<p><strong>Background/aims: </strong>The aim of this study was to investigate the dose-dependent effects of triiodothyronine (T3) on the osteogenic differentiation of mesenchymal stem cells(MSCs).</p><p><strong>Methods: </strong>MSCs that express CD73, CD54 (intercellular adhesion molecule-1) and CD90 were cultured in triplicate (1 x 10(5)/well) in osteogenic medium with T3 (1, 10, 10(3) or 10(5) pM) or without T3 (control) for 7, 14 and 21 days. Alkaline phosphatase activity, conversion of MTT into formazan crystals, collagen synthesis, collagen maturation, the number of mineralized nodules and their diameters were all determined, and the means were compared by the Student-Newman-Keuls test.</p><p><strong>Results: </strong>A dose of 10(5) pM T3 resulted in a negative effect on MSC osteogenic differentiation, with less collagen synthesis. The 1 pM T3 dose resulted in greater collagen synthesis and alkaline phosphatase activity and more mineralized nodules than in the control group, similar to the 10 pM dose. Nevertheless, the 10 pM dose demonstrated better results than the 1 pM dose with regard to MSC osteogenic differentiation, with greater MTT reduction, better collagen maturation and a larger mean diameter of mineralized nodules.</p><p><strong>Conclusions: </strong>The effect of T3 on MSC differentiation is dose-dependent, with the 10 pM dose promoting better bone marrow MSC osteogenic differentiation.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"72 2","pages":"88-97"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000232161","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28347844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hormone researchPub Date : 2009-01-01Epub Date: 2009-08-18DOI: 10.1159/000232166
R Capanna, M L Marcovecchio, A Verrotti, D Trotta, F Chiarelli, A Mohn
{"title":"Episodic spontaneous hypothermia potentially triggered by hyperinsulinemia.","authors":"R Capanna, M L Marcovecchio, A Verrotti, D Trotta, F Chiarelli, A Mohn","doi":"10.1159/000232166","DOIUrl":"https://doi.org/10.1159/000232166","url":null,"abstract":"<p><p>Episodic spontaneous hypothermia is an infrequent disorder, the pathogenic mechanisms of which have not been completely clarified, although alterations in the serotoninergic system have been suggested. We report the history of a girl with episodes of dizziness and shivering associated with a body temperature lower than 35 degrees C since the age of 10 months. At the age of 11 years, she was admitted to a local hospital and an oral glucose tolerance test showed high total insulin levels. Hypoglycemia secondary to hyperinsulinemia was suspected, and a low-carbohydrate (simple) diet was proposed without results. Due to the recurrence of the episodes, episodic spontaneous hypothermia triggered by hyperinsulinemia was suspected, and treatment with flunarizine, a drug considered the first line in the treatment of migraine-related disorders, was started with a resulting reduction in the episodes. A new endocrinological evaluation showed decreased insulin secretion. In our patient, the success of the therapy might be due to the well-known effect of calcium antagonists in inhibiting serotonin uptake and thereby regulating serotonin levels after hyperinsulinism. This case suggests hyperinsulinemia as a potential mechanism for episodic spontaneous hypothermia, probably mediated by an interaction between insulin and the serotoninergic system.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"72 2","pages":"124-8"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000232166","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28349369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hormone researchPub Date : 2009-01-01Epub Date: 2008-11-27DOI: 10.1159/000173737
Ethel Codner, Fernando Cassorla
{"title":"Puberty and ovarian function in girls with type 1 diabetes mellitus.","authors":"Ethel Codner, Fernando Cassorla","doi":"10.1159/000173737","DOIUrl":"https://doi.org/10.1159/000173737","url":null,"abstract":"<p><p>Insulin is well known for its effects on carbohydrate metabolism, but this hormone also plays an important role in regulating ovarian function. Granulosa, theca and stromal ovarian cells may be affected by insulin deficiency or excess, which may be present in women with type 1 diabetes mellitus (T1D). Recent publications have shown that in spite of intensive insulin therapy, some delay in the age of thelarche, pubarche and menarche is still observed in girls with T1D. In addition, ovarian hyperandrogenism may be observed during late adolescence and an increased prevalence of hirsutism and polycystic ovarian syndrome (PCOS) has been described in adult women with T1D. These endocrine abnormalities may be related to nonphysiologic insulin replacement therapy and to hyperglycemia. This paper reviews the pubertal development and the clinical reproductive abnormalities observed in girls with type 1 diabetes mellitus, and shows that several significant clinical problems, such as pubertal delay, menstrual disturbances and hyperandrogenism which may ultimately lead to the development of PCOS in adulthood, may be observed in some of these patients.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 1","pages":"12-21"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173737","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27863977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hormone researchPub Date : 2009-01-01Epub Date: 2008-11-27DOI: 10.1159/000173740
M Alharbi, G Pinto, G Finidori, J C Souberbielle, F Guillou, S Gaubicher, M Le Merrer, M Polak
{"title":"Pamidronate treatment of children with moderate-to-severe osteogenesis imperfecta: a note of caution.","authors":"M Alharbi, G Pinto, G Finidori, J C Souberbielle, F Guillou, S Gaubicher, M Le Merrer, M Polak","doi":"10.1159/000173740","DOIUrl":"https://doi.org/10.1159/000173740","url":null,"abstract":"<p><strong>Background/aims: </strong>Bisphosphonates have been reported to decrease fractures related to osteogenesis imperfecta (OI). We assessed the efficacy and long-term safety of pamidronate therapy in patients with moderate-to-severe OI.</p><p><strong>Methods: </strong>We conducted an open-label uncontrolled study in 14 boys and 13 girls whose mean age was 6.8 years at baseline. Intravenous pamidronate, 1 mg/kg/day, was given for 3 consecutive days every 4 months for 2-6 years, with physical therapy and orthopedic surgery as appropriate. Mobility score, fracture rate, height, bone mineral density (BMD) and bone healing were evaluated throughout follow-up.</p><p><strong>Results: </strong>In 24 (89%) patients, the fracture rate decreased to <or=2/year and/or the mobility score improved. The remaining 3 (11%) patients continued to experience more than 2 fractures per year with mobility scores <2 despite significant BMD gains. Delayed radiographic fracture healing (>6 months) occurred in 8 (29.6%) patients; their BMD gains, baseline age and treatment duration were not significantly different from those in the other patients. Tolerance was good.</p><p><strong>Conclusion: </strong>Pamidronate with physiotherapy and orthopedic management improved outcomes without delaying fracture healing in 19 (70%) of 27 patients. Delayed fracture healing occurred in 8/27 patients. Pamidronate should be reserved for severe OI with multiple fractures and/or flattened vertebras.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 1","pages":"38-44"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173740","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27863980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hormone researchPub Date : 2009-01-01Epub Date: 2008-11-27DOI: 10.1159/000173742
Moshe Phillip, Yael Lebenthal, Jan Lebl, Nehama Zuckerman-Levin, Maria Korpal-Szczyrska, Jorge Sales Marques, Adam Steensberg, Kirsten Jons, Anne-Marie Kappelgaard, Lourdes Ibanez
{"title":"European multicentre study in children born small for gestational age with persistent short stature: comparison of continuous and discontinuous growth hormone treatment regimens.","authors":"Moshe Phillip, Yael Lebenthal, Jan Lebl, Nehama Zuckerman-Levin, Maria Korpal-Szczyrska, Jorge Sales Marques, Adam Steensberg, Kirsten Jons, Anne-Marie Kappelgaard, Lourdes Ibanez","doi":"10.1159/000173742","DOIUrl":"https://doi.org/10.1159/000173742","url":null,"abstract":"<p><strong>Background: </strong>The most effective growth hormone (GH) treatment regimen for increasing height in short children born small for gestational age (SGA) has not been well defined.</p><p><strong>Methods: </strong>Short SGA children (n = 151, age 3-8 years, height less than -2.5 standard deviation scores) were randomised to receive low-dose GH for 2 years (0.033/0.033 mg/kg/day, n = 51), high-dose GH for 1 year and then no treatment for 1 year (0.100/0 mg/kg/day, n = 51) or were untreated for 1 year then received mid-dose GH for 1 year (0/0.067 mg/kg/day, n = 47). Height, bone age and adverse events were determined at check-ups every 3 months.</p><p><strong>Results: </strong>The mean +/- SD additional height gain with GH after 1 year, relative to untreated controls, was higher with discontinuous high-dose than with continuous low-dose GH (6.5 +/- 0.2 vs. 3.3 +/- 0.2 cm). After 2 years, the additional height gain was similar between high- and low-dose GH groups (between-group treatment difference = 0.2, 95% CI = -0.8 to 1.2 cm, p = 0.702). Patients treated exclusively in the last year had a similar height gain to those in the other treatment groups (p = 0.604).</p><p><strong>Conclusions: </strong>In short SGA children, continuous low-dose and discontinuous high-dose GH regimens were associated with similar height gain. Treatment with mid-dose GH for 1 year also led to a similar improvement in growth.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 1","pages":"52-9"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173742","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27864992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hormone researchPub Date : 2009-01-01Epub Date: 2009-01-21DOI: 10.1159/000178029
Robert M Carey
{"title":"Primary aldosteronism.","authors":"Robert M Carey","doi":"10.1159/000178029","DOIUrl":"https://doi.org/10.1159/000178029","url":null,"abstract":"Background: Hypertension is one of the world’s leading risk factors for morbidity and mortality. Most affected individuals have primary hypertension, while the most common cause of secondary hypertension is primary aldosteronism (6–10%). Primary Aldosteronism: Clinical manifestations include hypertension, hypokalemic alkalosis, renal dysfunction, nephrogenic diabetes insipidus, muscle weakness, paresthesias, tetany and, in severe cases, paralysis. The cardiovascular risks for patients with primary aldosteronism are greater than those for patients with primary hypertension. Compared with normotensive subjects, patients with primary aldosteronism have a 4.2-fold greater risk of stroke, a 6.5-fold greater risk of myocardial infarction and a 12.1-fold greater risk of atrial fibrillation. Diagnosis: Patients with hypertension are screened for primary aldosteronism based on the plasma aldosterone to plasma renin activity ratio. A value >30 constitutes a positive result. The diagnosis must be confirmed using one of four available aldosterone suppression tests. Lateralization of aldosterone hypersecretion is documented by adrenal venous sampling. Management: The foundation of primary aldosteronism management is normalization of circulating aldosterone and/or mineralocorticoid blockade. Optimal treatment of unilateral disease is adrenalectomy; spironolactone is the treatment of choice for bilateral disease.","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 Suppl 1 ","pages":"8 - 12"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000178029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27932278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hormone researchPub Date : 2009-01-01Epub Date: 2009-01-21DOI: 10.1159/000178030
Robert A Waterland
{"title":"Is epigenetics an important link between early life events and adult disease?","authors":"Robert A Waterland","doi":"10.1159/000178030","DOIUrl":"https://doi.org/10.1159/000178030","url":null,"abstract":"<p><strong>Background: </strong>Epigenetic mechanisms provide one potential explanation for how environmental influences in early life cause long-term changes in chronic disease susceptibility. Whereas epigenetic dysregulation is increasingly implicated in various rare developmental syndromes and cancer, the role of epigenetics in complex chronic diseases, such as cardiovascular disease, type 2 diabetes and obesity, remains largely uncharacterized. Extensive work in animal models is required to develop specific hypotheses that can be practicably tested in humans.</p><p><strong>Animal models: </strong>We have developed a mouse model showing that methyl donor supplementation prevents transgenerational amplification of obesity, suggesting a role for DNA methylation in the developmental establishment of body weight regulation.</p><p><strong>Conclusions: </strong>Coupling such models with recently developed epigenomic technologies should ultimately enable us to determine if epigenetics is an important link between early life events and adult disease.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 Suppl 1 ","pages":"13-6"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000178030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27932279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hormone researchPub Date : 2009-01-01Epub Date: 2009-01-21DOI: 10.1159/000178052
Gudmundur Johannsson
{"title":"Treatment of growth hormone deficiency in adults.","authors":"Gudmundur Johannsson","doi":"10.1159/000178052","DOIUrl":"https://doi.org/10.1159/000178052","url":null,"abstract":"<p><strong>Background: </strong>The Growth Hormone Research Society held a Consensus Workshop in Sydney, Australia, in March 2007 to review advances in the management of growth hormone (GH) deficiency in adults and to update consensus recommendations.</p><p><strong>Objective: </strong>This short review summarizes key background information presented at the workshop and the consensus recommendations that followed.</p><p><strong>Conclusions: </strong>The benefits of GH replacement in GH-deficient adults are evident throughout life. Clinical response to treatment should be assessed by monitoring biochemistry values, body composition and quality of life. There is no evidence that GH replacement increases the risk of tumour recurrence or de novo malignancy.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 Suppl 1 ","pages":"116-22"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000178052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27933132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hormone researchPub Date : 2009-01-01Epub Date: 2009-01-21DOI: 10.1159/000178053
Francesca Pecori Giraldi
{"title":"Recent challenges in the diagnosis of Cushing's syndrome.","authors":"Francesca Pecori Giraldi","doi":"10.1159/000178053","DOIUrl":"https://doi.org/10.1159/000178053","url":null,"abstract":"<p><strong>Background: </strong>The diagnosis of Cushing's syndrome still represents a challenge for the endocrinologist. Correct implementation and interpretation of diagnostic procedures require expertise and a high degree of clinical knowledge. The diagnosis should be established based on results of two or more concordant first-line tests (e.g., urinary free cortisol, midnight serum cortisol and low-dose dexamethasone testing); otherwise, second-line tests such as the dexamethasone-suppressed corticotrophin-releasing hormone (CRH) test, desmopressin stimulation or later reevaluation can confirm/exclude the diagnosis. Aetiological diagnosis requires measurement of plasma corticotrophin (ACTH) to distinguish between ACTH-dependent (pituitary or extrapituitary ACTH-secreting tumors) and ACTH-independent Cushing's syndrome (adrenal cortisol-secreting lesions), and the possible detection of normal ACTH levels in patients with adrenal Cushing's syndrome must be kept in mind. Lastly, the differential diagnosis between pituitary and ectopic ACTH secretion can be performed using CRH testing, high-dose dexamethasone suppression and inferior petrosal sinus sampling.</p><p><strong>Conclusions: </strong>The different epidemiology of the two entities and the incomplete diagnostic accuracy of diagnostic procedures mandate careful evaluation of test results.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 Suppl 1 ","pages":"123-7"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000178053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27933133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hormone researchPub Date : 2009-01-01Epub Date: 2008-11-27DOI: 10.1159/000173739
B Ezquieta, M Oyarzabal, R Barrio, C Luzuriaga, F Hermoso, J L Lechuga, S Quinteiro, A Rodríguez, J I Labarta, A Gutierrez Macias, M Gallego, J M Bellón
{"title":"Monogenic and polygenic models detected in steroid 21-hydroxylase deficiency-related paediatric hyperandrogenism.","authors":"B Ezquieta, M Oyarzabal, R Barrio, C Luzuriaga, F Hermoso, J L Lechuga, S Quinteiro, A Rodríguez, J I Labarta, A Gutierrez Macias, M Gallego, J M Bellón","doi":"10.1159/000173739","DOIUrl":"https://doi.org/10.1159/000173739","url":null,"abstract":"<p><strong>Aims: </strong>Hyperandrogenism, although mostly due to polygenic interactions, is monogenic for some enzymatic adrenal deficiencies. This study evaluates mono- and biallelic 21-hydroxylase deficiency (21OHD)-related hyperandrogenism in pediatric patients. Sensitizing and protective polymorphisms were investigated in carriers and cryptic forms of 21OHD.</p><p><strong>Methods: </strong>The study involved a monogenic analysis of CYP21A2 in patients (375 nonclassical 21OHD [NC21OHD] children; 306 hyperandrogenic 21OHD carriers, n = 306) and a polygenic association study (CAPN10-UCSNP44, PON1-108, TNFR2-M196R, IGF2-ApaI and IRS1-G972R polymorphisms) of 170 hyperandrogenic carriers plus 277 family members (control groups). The metabolic marker 17OH progesterone defined the degree of deficiency; clinical expressivity was determined by pediatric endocrinologists.</p><p><strong>Results: </strong>The group of 21OHD carriers manifesting hyperandrogenism was enriched in the CAPN-UCSNP44 rare variant in homozygosity (4.9 vs. 0.4%, NCBI data for the general population; p = 0.004). In our patients and controls, contrasting distributions were observed for this and another polymorphism, TNFR2-196R. In a recessive model, their rare variants were more frequently detected among the forms with high (p = 0.048) and low (p = 0.034) expressivity respectively.</p><p><strong>Conclusions: </strong>21OHD-related pediatric hyperandrogenism follows monogenic and polygenic models. The opposite behaviors in terms of clinical expressivity detected for CAPN-UCSNP44 and TNFR2-M196R rare variants suggest these variants to be sensitizing and protective factors respectively in adrenal hyperandrogenism.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 1","pages":"28-37"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173739","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27863979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}