Purpose The standard treatment of hypothyroidism is levothyroxine (LT4), which is available as tablets or soft-gel capsules in Denmark. This study aimed to investigate Danish endocrinologists’ use of thyroid hormones in hypothyroid and euthyroid patients. Methods An e-mail with an invitation to participate in an online survey investigating practices about substitution with thyroid hormones was sent to all members of the Danish Endocrine Society (DES). Results Out of 488 eligible DES members, a total of 152 (31.2%) respondents were included in the analysis. The majority (94.1%) of responding DES members use LT4 as the treatment of choice. Other treatment options for hypothyroidism are also used, as 58.6% prescribe combination therapy with liothyronine (LT3) + LT4 in their clinical practice. LT4 + LT3 combination is preferred in patients with persistent symptoms of hypothyroidism despite biochemical euthyroidism on LT4 treatment. Over half of the respondents answered that thyroid hormone therapy is never indicated for euthyroid patients, but 42.1% will consider it for euthyroid infertile women with high antibody levels. In various conditions that could interfere with the absorption of LT4, most responding Danish endocrinologists prefer tablets and do not expect a significant difference when switching from one type of tablet formulation to another. Conclusion The treatment of choice for hypothyroidism is LT4. Combination therapy with LT4 + LT3 is considered for patients with persistent symptoms. Even in the presence of conditions affecting bioavailability, responding Danish endocrinologists prefer LT4 tablets rather than newer LT4 formulations, such as soft-gel capsules. Supplementary Information The online version contains supplementary material available at 10.1007/s40618-021-01555-y.

Fat percentage and body mass index were positive predictors of the resumption of menses, however, body composition measured by dual energy X-ray absorptiometry was not superior to body mass index in predicting menstrual recovery, which is of great clinical relevance as body mass index is easier and cheaper to obtain. Body composition measures only account for one of numerous factors involved in the resumption of menses. Regression models based on our data had a R value of 0.14, indicating that only 14% of the variation in menstrual recovery could be explained by the variables included. © 2016 Wiley Periodicals, Inc.(Int J Eat Disord 2017; 50:370-377).

ObjectiveMalnutrition and low weight in eating disorders (EDs) are associated with increased fracture risk compared to the general population. In a cohort study we aimed to determine fracture rates compared to age and gender matched controls (ratio 5:1), assess the impact of disease remission on fracture risk and establish predictive factors for fractures.Method 803 ED patients referred to specialized ED treatment between 1994 and 2004 were included. In 2016, data on fractures were obtained through the Danish National Registry of Patients. ResultsFracture risk was increased in anorexia nervosa (AN) (IRR 2.2 (CI 99%: 1.6-3.0)) but not in bulimia nervosa (BN) (IRR 1.3, ns) or other specified feeding or eating disorders (OSFED) (IRR 1.8, ns). IRR in the AN group were increased for vertebral fractures (IRR 3.8 (CI 99%: 1.4-10.3)), upper arm (IRR 3.0 (CI 99% 1.6-5.5) and hip (IRR 6.6 (CI 99 %: 2.6-18.0)). Disease remission in AN is associated to lower fracture risk compared to active disease, but higher fracture risk compared to controls (IRR 1.7 (CI 99 %: 1.1-2.7)).In regression analysis, age at debut of disease, nadir BMI and duration of disease before referral to treatment, independently predicted fracture.

Anorexia nervosa (AN) is associated with decreased bone mineral density and increased risk of fracture. The aim of this study was to assess bone geometry, volumetric bone mineral density (vBMD), trabecular microarchitecture and estimated failure load in weight-bearing vs. non-weight-bearing bones in AN. We included twenty-five females with AN, and twenty-five female controls matched on age and height. Bone geometry, vBMD and trabecular microarchitecture were assessed using high-resolution peripheral quantitative computed tomography of the distal radius and tibia. At both sites, cortical perimeter and total bone area were similar in patients and controls. Total vBMD was lower in the AN group in the tibia (p < 0.0005) but not in the radius. In the tibia, cortical thickness was approximately 25% lower (p < 0.0005) in the AN group, whereas there was no significant difference in the radius. In terms of trabecular microarchitecture, all indices [bone volume/tissue volume (BV/TV); trabecular thickness (Tb.Th.), trabecular number (Tb.N) and trabecular spacing (Tb.Sp.)] were impaired in AN in the tibia (p values range < 0.01–0.0001). In the radius, BV/TV and Tb.N were lower (p < 0.05 and p < 0.001, respectively); Tb.Sp. was higher (p < 0.001), whereas Tb.Th. did not differ, compared to controls. Estimated failure load was lower in patients in both the radius and the tibia (p < 0.0005 and p < 0.0001, respectively), most pronounced in the tibia. In conclusion, the impairment of cortical thickness and estimated failure load were significantly more pronounced in the weight-bearing tibia, compared to the non-weight-bearing radius, implying a direct effect of low body weight on bone loss in AN.Electronic supplementary materialThe online version of this article (doi:10.1007/s00223-017-0254-7) contains supplementary material, which is available to authorized users.

Abstract:The relationship between gut and skeleton is increasingly recognized as part of the integrated physiology of the whole organism. The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are secreted from the intestine in response to nutrient intake and exhibit several physiological functions including regulation of islet hormone secretion and glucose levels. A number of GLP-1 receptor agonists (GLP-1RAs) are currently used in treatment of type 2 diabetes and obesity. However, GIP and GLP-1 cognate receptors are widely expressed suggesting that incretin hormones mediate effects beyond control of glucose homeostasis, and reports on associations between incretin hormones and bone metabolism have emerged. The aim of this MiniReview was to provide an overview of current knowledge regarding the in vivo and in vitro effects of GIP and GLP-1 on bone metabolism. We identified a total of 30 pre-clinical and clinical investigations of the effects of GIP, GLP-1 and GLP-1RAs on bone turnover markers, bone mineral density (BMD), bone microarchitecture and fracture risk. Studies conducted in cell cultures and rodents demonstrated that GIP and GLP-1 play a role in regulating skeletal homeostasis, with preclinical data suggesting that GIP inhibits bone resorption whereas GLP-1 may promote bone formation and enhance bone material properties. These effects are not corroborated by clinical studies. While there is evidence of effects of GIP and GLP-1 on bone metabolism in pre-clinical investigations, clinical trials are needed to clarify whether similar effects are present and clinically relevant in humans.Bone remodelling is the regenerative mechanism that maintains the skeletal health and biomechanical competence through resorption of bone by osteoclasts and formation of new bone by osteoblasts. These processes are highly co-ordinated and under the influence of several hormonal factors [1].Incretin hormones encompass a group of hormones characterized by their ability to enhance insulin secretion in response to intake of nutrients, such as glucose and fat. The most important incretin hormones are gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) [2]. Both of these hormones interact with cognate receptors, which are widely expressed in human tissues: the GIP receptor (GIPR) is expressed in pancreas, central nervous system, thyroid as well as adipose tissue [3], and the GLP-1 receptor (GLP-1R) is expressed in the kidney, stomach, duodenum, central nervous system and pancreas [4]. Both the GIP and the GLP-1 receptors are 7-transmembrane proteins, and activation of these receptors by binding of either GIP or GLP-1 increases intracellular levels of cyclic adenosine monophosphate (cAMP) and Ca 2+ [5].Gastric inhibitory polypeptide and GLP-1 are secreted from enteroendocrine cells of the small intestine. Once secreted, GLP-1 binds to the GLP-1 receptors expressed on pancreatic b-cells, leading to a glucose-dependent insulin secretion but the effect is short-lived as GLP...

To our knowledge, this is the first study to include all the aspects of MetS in a sample of drug-naive adolescents followed over the first 12 months after starting SGA treatment. A significant shift in all parameters (except BP) toward MetS was found, presumably due to SGA use. Therefore, these adolescents will need proper follow-up, consisting of not only monitoring but also preventive measures to diminish these effects of SGA use.

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