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Open access

Mark R Postma, Pia Burman, and André P van Beek

Introduction:

Adult-onset growth hormone deficiency (AGHD) is usually the last deficiency to be substituted in hypopituitarism. In children with documented GH deficiency, treatment without delay is crucial for achieving optimal effects on growth and development. In adults, it is not known whether a delay in treatment initiation influences biochemical response and the favourable physiological effects resulting from GH replacement therapy (GHRT).

Methods:

A total of 1085 GH-deficient adults from KIMS (Pfizer International Metabolic Database) were included, adequately replaced with all pituitary hormones except for GH at baseline. Patients were stratified by sex and age (20–50 years and ≥50 years) and subsequently divided into two groups below and above the median duration of unsubstituted AGHD for that subgroup. The median time of unsubstituted GHD for the total cohort was 2.53 years (P5 = 0.35, P95 = 24.42).

Results:

Beneficial effects of 4 years of GHRT were observed on lipids and quality of life in all subgroups. A decrease in waist circumference was observed only in older (>50 years) patients. There was no difference in IGF-I SDS and in GH dose required to normalize IGF-I in patients with a duration of unsubstituted AGHD above or below the median. No relevant differences were found between the groups for anthropometric measures, cardiovascular risk factors and quality of life scores.

Conclusion:

In contrast to GHD in children and adolescents, no difference could be established in treatment response between early or late initiation of GHRT in AGHD in terms of required GH dose, IGF-I, metabolic health and quality of life.

Open access

Sweta Budyal, Swati Sachin Jadhav, Rajeev Kasaliwal, Hiren Patt, Shruti Khare, Vyankatesh Shivane, Anurag R Lila, Tushar Bandgar, and Nalini S Shah

Variable prevalence of subclinical Cushing's syndrome (SCS) has been reported in patients with type 2 diabetes mellitus (T2DM), making the need for screening in this population uncertain. It is unknown if this variability is solely due to study-related methodological differences or a reflection of true differences in ethnic predisposition. The objective of this study is to explore the prevalence of SCS in Asian Indian patients with T2DM. In this prospective single center study conducted in a tertiary care referral center, 993 T2DM outpatients without any discriminatory clinical features (easy bruising, facial plethora, proximal muscle weakness, and/or striae) of hypercortisolism underwent an overnight 1 mg dexamethasone suppression test (ODST). ODST serum cortisol ≥1.8 μg/dl was considered positive, and those with positive results were subjected to 48 h, 2 mg/day low dose DST (LDDST). A stepwise evaluation for endogenous hypercortisolism was planned for patients with LDDST serum cortisol ≥1.8 μg/dl. Patients with positive ODST and negative LDDST were followed up clinically and re-evaluated a year later for the development of clinically evident Cushing's syndrome (CS). In this largest single center study reported to date, we found 37 out of 993 (3.72%) patients had ODST serum cortisol ≥1.8 μg/dl. None of them had LDDST cortisol ≥1.8 μg/dl, nor did they develop clinically evident CS over a follow-up period of 1 year. Specificity of ODST for screening of CS was 96.3% in our cohort. None of the T2DM outpatients in our cohort had SCS, hence cautioning against routine biochemical screening for SCS in this cohort. We suggest screening be based on clinical suspicion only.

Open access

Qinglei Yin, Zhou Jin, Yulin Zhou, Dalong Song, Chenyang Fu, Fengjiao Huang, and Shu Wang

Graves’ disease (GD) is a common autoimmune disease that affects the thyroid gland. As a new class of modulators of gene expression, long non-coding RNAs (lncRNAs) have been reported to play a vital role in immune functions and in the development of autoimmunity and autoimmune disease. The aim of this study is to identify lncRNAs in CD4+ T cells as potential biomarkers of GD. lncRNA and mRNA microarrays were performed to identify differentially expressed lncRNAs and mRNAs in GD CD4+ T cells compared with healthy control CD4+ T cells. Quantitative polymerase chain reaction (qPCR) was used to validate the results, and correlation analysis was used to analyze the relationship between these aberrantly expressed lncRNAs and clinical parameters. The microarray identified 164 lncRNAs and 93 mRNAs in GD CD4+ T cells differentially expressed compared to healthy control CD4+ T cells (fold change >2.0 and a P<0.05). Further analysis consistently showed that the expression of HMlincRNA1474 (P<0.01) and TCONS 00012608 (P<0.01) was suppressed, while the expression of AK021954 (P<0.01) and AB075506 (P<0.01) was upregulated from initial GD patients. In addition, their expression levels were recovered in euthyroid GD patients and GD patients in remission. Moreover, these four aberrantly expressed lncRNAs were correlated with GD clinical parameters. Moreover, the areas under the ROC curve were 0.8046, 0.7579, 0.8115 for AK021954, AB075506, HMlincRNA1474, respectively. The present work revealed that differentially expressed lncRNAs were associated with GD, which might serve as novel biomarkers of GD and potential targets for GD treatment.

Open access

Rosalie Cabry, Philippe Merviel, Aicha Madkour, Elodie Lefranc, Florence Scheffler, Rachel Desailloud, Véronique Bach, and Moncef Benkhalifa

gavaging the pregnant dams) was associated with changes in puberty onset, spermatogenesis, and the development of ovarian follicles up to the F3 generation. The direct, toxic endocrine-disrupting effect (i.e. a dose-response relationship) has rarely been

Open access

I Savchuk, M L Morvan, J P Antignac, K Gemzell-Danielsson, B Le Bizec, O Söder, and K Svechnikov

development of and hormonal production by the HFA are critical for normal fetal maturation and survival. The HFA develop from the intermediate mesoderm and by GW7 have acquired two distinct zones, the inner fetal (FZ) and outer definitive zone (DZ) ( 2 ). In

Open access

Anna-Pauliina Iivonen, Johanna Känsäkoski, Kirsi Vaaralahti, and Taneli Raivio

Introduction Congenital hypogonadotropic hypogonadism (cHH) is a rare genetic disease that prevents pubertal development and causes infertility due to deficient secretion or action of gonadotropin-releasing hormone (GnRH) ( 1 ). Congenital

Open access

Fan Zhang, Jian Chen, Xinyue Lin, Shiqiao Peng, Xiaohui Yu, Zhongyan Shan, and Weiping Teng

levels of 62 children aged 7–9 years who were born to mothers with thyroid dysfunction during early pregnancy. They found that even mild and asymptomatic hypothyroidism in pregnant women, including SCH, could affect the development of intelligence in

Open access

Mette H Viuff and Claus H Gravholt

drug for a certain period of time. When the child with TS has finished treatment in the pediatric department, usually consisting of growth hormone treatment for promoting linear growth and induction of puberty to ensure appropriate development of

Open access

Monia Cito, Silvia Pellegrini, Lorenzo Piemonti, and Valeria Sordi

expressed in combination with NKX6.1 and PTF1α, key transcription factors in pancreas development, and it was demonstrated that hPSC-derived GP2 + cells, differentiated in pancreatic progenitors expressing high levels of NKX6.1, generate β-like cells more

Open access

Andrew R Dismukes, Vanessa J Meyer, Elizabeth A Shirtcliff, Katherine P Theall, Kyle C Esteves, and Stacy S Drury

aging spectrum, DHEA is positively associated with pubertal development. A steady increase in DHEA production is observed with adrenarche, the maturation of the adrenal gland ( 1 ) and the hallmark of pubertal initiation. The adrenal glands continue to