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Catherine E de Keyser, Filipe Valerio de Lima, Frank H de Jong, Albert Hofman, Yolanda B de Rijke, André G Uitterlinden, Loes E Visser, and Bruno H Stricker

Objective

Statins, or HMG-CoA reductase inhibitors, decrease cholesterol production. Because cholesterol is a precursor of the testosterone biosynthesis pathway, there is some concern that statins might lower serum testosterone levels. The objective of the present study was to investigate the association between the use of statins and serum testosterone levels in men.

Design

Cross-sectional study within the prospective population-based Rotterdam Study.

Subjects and methods

We included 4166 men with available data on total testosterone, non-sex hormone-binding globulin (SHBG)-bound testosterone, and medication use. Multivariable linear regression analysis was used to compare the differences in serum testosterone levels (nmol/l) between current, past, and never statin users. We considered dose and duration of use. Analyses were adjusted for age, BMI, cardiovascular disease, diabetes mellitus, hypertension, and estradiol levels.

Results

We identified 577 current (mean age 64.1 years), 148 past (mean age 64.6 years), and 3441 never (mean age 64.6 years) statin users. Adjusted for all covariables, current statin use of 1–≤6 months or >6 months was significantly associated with lower total testosterone levels as compared to non-users (β −1.24, 95% CI −2.17, −0.31, and β −1.14, 95% CI −2.07, −0.20 respectively). Current use of 1–≤6 months was also associated with significantly lower non-SHBG-bound testosterone levels (β −0.42, 95% CI −0.82, −0.02). There was a trend toward lower testosterone levels at higher statin doses both for total (P trend 2.9×10−5) and non-SHBG-bound (P trend 2.0×10−4) testosterone. No association between past statin use and testosterone levels was found.

Conclusion

We showed that current use of statins was associated with significantly lower serum total and non-SHBG-bound testosterone levels. The clinical relevance of this association should be further investigated.

Free access

Yvette Roke, Peter N van Harten, Jan K Buitelaar, Diederik E Tenback, Lorentz G B A Quekel, Yolanda B de Rijke, and Annemieke M Boot

Objective

To investigate the long-term effects of antipsychotic (AP) treatment and AP-induced hyperprolactinemia on bone mineral density (BMD) and body composition in male adolescents with autism spectrum disorders (ASDs) and/or disruptive behavior disorder (DBD).

Design

Physically healthy 10- to 20-year-old boys with ASD and/or DBD, chronically treated (n=56; mean 52 months, range 16–126 months) or not treated (n=47) with an AP, were recruited to this observational study. Prolactin levels and biochemical bone parameters were measured and BMD of the lumbar spine and total body, and body composition were assessed by dual-energy X-ray absorptiometry, and volumetric BMD of the lumbar spine calculated. Group differences were tested with Student's t-test, χ 2 test, Fisher exact test, and logistic regression analysis.

Results

Forty-nine percent of the boys treated with an AP had hyperprolactinemia. The mean volumetric lumbar spine BMD z-score was lower (P=0.043), the total percentage of body fat z-score was higher (P=0.042), and biochemical bone marker carboxyterminal cross-linking telopeptide of bone collagen was lower in the AP-treated boys with hyperprolactinemia than in the AP-treated boys without hyperprolactinemia. Seven to 11% of the hyperprolactinemic boys had low BMD. The mean lumbar spine and total body BMD z-scores and body composition were similar in the boys who were or were not treated with an AP. The total study population had a lower mean lean tissue mass (mean z-score −0.37, P=0.004) and a higher percentage of total body fat (mean z-score 1.16, P<0.001) than healthy controls (normative data); biochemical bone parameters were within normal limits.

Conclusion

AP-induced hyperprolactinemia in boys with ASD or DBD may have a negative effect on lumbar spine BMD. Longitudinal studies are needed to confirm this finding and further disentangle the effects of the disorder, lifestyle, treatment, and hyperprolactinemia.

Free access

Mirjana Barjaktarovic, Tim I M Korevaar, Romy Gaillard, Yolanda B de Rijke, Theo J Visser, Vincent W V Jaddoe, and Robin P Peeters

Objective

The cardiovascular system is a known target for thyroid hormone. Early-life cardiovascular alterations may lead to a higher risk of cardiovascular disease in adulthood. Little is known about the effects of thyroid hormone on cardiovascular function during childhood, including the role of body composition in this association.

Design

Population-based prospective cohort of children (n = 4251, median age 6 years, 95% range: 5.7–8.0 years).

Methods

Thyroid-stimulating hormone (TSH) and free thyroxine (FT4) concentrations were measured to assess thyroid function. Left ventricular (LV) mass was assessed with echocardiography. Arterial stiffness was assessed with carotid-femoral pulse wave velocity (CFPWV). Systolic and diastolic blood pressure (BP) was measured. Body composition was assessed by dual-energy X-ray absorptiometry scan.

Results

FT4 was inversely associated with LV mass (P = 0.002), and with lean body mass (P < 0.0001). The association of FT4 with LV mass was partially mediated through variability in lean body mass (55% mediated effect). TSH was inversely associated with LV mass (P = 0.010), predominantly in boys. TSH was positively associated with systolic and diastolic BP (both P < 0.001). FT4 was positively associated with CFPWV and diastolic BP (P < 0.0001, P = 0.008, respectively), and the latter association attenuated after adjustment for CFPWV.

Conclusions

At the age of 6 years, higher FT4 is associated with lower LV mass (partially through effects on lean body mass) and with higher arterial stiffness, which may lead to higher BP. Our data also suggest different mechanisms via which TSH and FT4 are associated with cardiovascular function during early childhood.

Free access

Rosalie M Kiewiet, Maarten O van Aken, Kim van der Weerd, Piet Uitterlinden, Axel P N Themmen, Leo J Hofland, Yolanda B de Rijke, Patric J D Delhanty, Ezio Ghigo, Thierry Abribat, and Aart Jan van der Lely

Objective

To investigate the effects of unacylated ghrelin (UAG) and co-administration of acylated ghrelin (AG) and UAG in morbid obesity, a condition characterized by insulin resistance and low GH levels.

Design and method

Eight morbidly obese non-diabetic subjects were treated with either UAG 200 μg, UAG 100 μg in combination with AG 100 μg (Comb) or placebo in three episodes of 4 consecutive days in a double-blind randomized crossover design. Study medication was administered as daily single i.v. bolus injections at 0900 h after an overnight fast. At 1000 h, a standardized meal was served. Glucose, insulin, GH, free fatty acids (FFA) and ghrelin were measured up to 4 h after administration.

Results

Insulin concentrations significantly decreased after acute administration of Comb only, reaching a minimum at 20 min: 58.2±3.9% of baseline versus 88.7±7.2 and 92.7±2.6% after administration of placebo and UAG respectively (P<0.01). After 1 h, insulin concentration had returned to baseline. Glucose concentrations did not change after Comb. However, UAG administration alone did not change glucose, insulin, FFA or GH levels.

Conclusion

Co-administration of AG and UAG as a single i.v. bolus injection causes a significant decrease in insulin concentration in non-diabetic subjects suffering from morbid obesity. Since glucose concentration did not change in the first hour after Comb administration, our data suggest a strong improvement in insulin sensitivity. These findings warrant studies in which UAG with or without AG is administered for a longer period of time. Administration of a single bolus injection of UAG did not influence glucose and insulin metabolism.

Free access

Vincent L Wester, Martin Reincke, Jan W Koper, Erica L T van den Akker, Laura Manenschijn, Christina M Berr, Julia Fazel, Yolanda B de Rijke, Richard A Feelders, and Elisabeth F C van Rossum

Objective

Current first-line screening tests for Cushing’s syndrome (CS) only measure time-point or short-term cortisol. Hair cortisol content (HCC) offers a non-invasive way to measure long-term cortisol exposure over several months of time. We aimed to evaluate HCC as a screening tool for CS.

Design

Case-control study in two academic referral centers for CS.

Methods

Between 2009 and 2016, we collected scalp hair from patients suspected of CS and healthy controls. HCC was measured using ELISA. HCC was available in 43 confirmed CS patients, 35 patients in whom the diagnosis CS was rejected during diagnostic work-up and follow-up (patient controls), and 174 healthy controls. Additionally, we created HCC timelines in two patients with ectopic CS.

Results

CS patients had higher HCC than patient controls and healthy controls (geometric mean 106.9 vs 12.7 and 8.4 pg/mg respectively, P < 0.001). At a cut-off of 31.1 pg/mg, HCC could differentiate between CS patients and healthy controls with a sensitivity of 93% and a specificity of 90%. With patient controls as a reference, specificity remained the same (91%). Within CS patients, HCC correlated significantly with urinary free cortisol (r = 0.691, P < 0.001). In two ectopic CS patients, HCC timelines indicated that cortisol was increased 3 and 6 months before CS became clinically apparent.

Conclusions

Analysis of cortisol in a single scalp hair sample offers diagnostic accuracy for CS similar to currently used first-line tests, and can be used to investigate cortisol exposure in CS patients months to years back in time, enabling the estimation of disease onset.

Restricted access

Eline Sofia van der Valk, Bibian van der Voorn, Anand M. Iyer, Sjoerd van den Berg, Mesut Savas, Yolanda B de Rijke, Erica van den Akker, Olle Melander, and Elisabeth F.C. van Rossum

Context. Obesity and cardiometabolic diseases are associated with higher long-term glucocorticoid levels, measured as scalp hair cortisol (hairF) and cortisone (hairE). Cardiometabolic diseases have also been associated with copeptin, a stable surrogate marker for the arginine-vasopressin (AVP) system. Since AVP is, together with corticotropin-releasing hormone (CRH) an important regulator of the hypothalamic- pituitary adrenal axis (HPA-axis), we hypothesize that AVP contributes to chronic hypercortisolism in obesity.

Objective. To investigate whether copeptin levels are associated with higher hairF and hairE levels in obesity.

Design. A cross-sectional study in 51 adults with obesity (body mass index ≥30 kg/m2).

Methods. Associations and interactions between copeptin, hairF, hairE, and cardiometabolic parameters were cross-sectionally analyzed.

Results. Copeptin was strongly associated with body mass index (BMI) and waist circumference (WC), (rho=0.364 and 0.530, p=0.008 and <0.001 respectively), also after correction for confounders. There were no associations between copeptin and hairF or hairE on a continuous or dichotomized scale, despite correction for confounders.

Conclusion. In patients with obesity, AVP seems not a major contributor to the frequently observed high cortisol levels. Other factors which stimulate the HPA-axis or affect cortisol synthesis or breakdown may be more important than the influence of AVP on long-term glucocorticoid levels in obesity.

Restricted access

Ivona Lončar, Roderick R Dulfer, Elske T Massolt, Reinier Timman, Yolanda B de Rijke, Gaston J H Franssen, Pim J W A Burger, Casper Smit, Frans A L van der Horst, Robin P Peeters, Casper H J van Eijck, and Tessa M van Ginhoven

Objective

Hypoparathyroidism is a common complication after thyroidectomy. It is not yet possible to predict in which patients hypoparathyroidism will persist. We aim to determine whether a decrease in PTH levels, measured at the first postoperative day, can identify patients with a high risk for persistent hypoparathyroidism one year after thyroidectomy.

Design

Prospective multi-center cohort study.

Methods

Patients undergoing total or completion thyroidectomy were included. We measured PTH levels preoperatively and on the first postoperative day. Primary outcome is the proportion of patients with persistent hypoparathyroidism, defined as the need for calcium supplementation one year after surgery.

Results

We included 110 patients of which 81 were used for analysis of the primary outcome. At discharge 72.8% of patients were treated with calcium supplementation. Persistent hypoparathyroidism was present in 14 patients (17.3%) at one-year follow-up, all of them had a decrease in PTH >70% at the first postoperative day. These 14 were 43.8% of the 32 patients who had such a decrease. In the group of 49 patients (59.8%) without a PTH >70% decrease, none had persistent hypoparathyroidism one year after surgery (P-value <0.001). A decrease of >70% in PTH levels had a sensitivity of 100.0% (95% CI: 85.8–100.0%), a specificity of 73.1% (95% CI: 62.5–83.7%) and an area under the curve of 0.87 (95% CI: 0.79–0.94) to predict the risk for persistent hypoparathyroidism.

Conclusion

In our study a decrease in PTH levels of >70% after total or completion thyroidectomy is a reliable predictor for persistent hypoparathyroidism, and this should be confirmed in larger cohorts.