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Aim: To estimate the proportion of persons with type 2 diabetes (T2DM) receiving intensive insulin treatment in the secondary healthcare who could be candidates for continuous glucose monitoring (CGM), based on different HbA1c criteria. For comparison, the results are also presented as proportion of persons with type 1 diabetes (T1DM) in the same region. Patients and Methods: In the Central Denmark Region, we identified all persons with T1DM (n = 6179) and T2DM (n = 4315) who had a minimum of one contact to a diabetes outpatient clinic from September 2021 to September 2022. Insulin regimen and HbA1c measured after a minimum of 2 months with a stable insulin regimen were retrieved from the healthcare administrative electronic platform used in the region. Results: The numbers of persons with T1DM and T2DM with HbA1c meeting the criteria were 5145 and 3090, respectively. The fraction of T2DM with basal‐bolus insulin was 35.3%, and the fraction with basal‐bolus insulin and HbA1c >53 (7%) mmol/mol or >58 (7.5%) mmol/mol was 20.5% and 16.6%, respectively. These proportions correspond to 19.4%, 14.4% and 11.7% of the persons with T1DM in the same geographical area. Conclusion: The proportion of persons with T2DM in secondary healthcare undergoing intensive insulin treatment who could be candidates for CGM corresponded to only a minor fraction of persons with T1DM in the same region, irrespective of any HbA1c criteria applied. [ABSTRACT FROM AUTHOR]

Key Clinical Message Low-dose QT-prolonging drugs may have detrimental effects on women with Turner's syndrome. Preventive measures would be to use potential QT-prolonging drugs with precaution and ensure that both before and during treatment, ECGs are evaluated and drug treatment stopped if the QT interval increases. [ABSTRACT FROM AUTHOR]

Background An unfavourable cardiovascular and metabolic phenotype causes threefold excess mortality in Turner syndrome ( TS), and perturbed cardiac substrate metabolism is increasingly recognized as a common component of cardiovascular and metabolic diseases. We therefore hypothesized that myocardial glucose uptake ( MGU) is reduced in TS and that growth hormone ( GH) treatment improves MGU. To this end, this controlled trial elucidates MGU in TS and the impact of 6 months of growth hormone treatment on MGU. Methods and Results Women with TS ( n = 9) were examined at baseline, sequentially treated with either Norditropin® SimpleXx or placebo and re-examined after 6 months. MGU and myocardial blood flow ( MBF) were measured using 2-deoxy-2-[18F]fluoro-D-glucose positron emission tomography ( FDG- PET) during a hyperinsulinaemic euglycaemic clamp (at baseline and 6 months). Blood pressure measurement, blood sampling, echocardiography and dual energy X-ray absorptiometry scan were also performed. Age-matched female controls ( n = 9) were examined once. Baseline MGU was reduced in TS (0·24 ± 0·08 vs. 0·36 ± 0·13 μmol/g/min in controls; P = 0·036) despite similar insulin sensitivity (whole body glucose uptake (M-value): 9·69 ± 1·86 vs. 9·86 ± 2·58 mg/(min*kg) in controls; P = 0·9). Six months of GH carried no impact on MGU (0·25 ± 0·08 vs. 0·26 ± 0·12 μmol/g/min in the placebo group; P = 0·8). Plasma glucose, low-density cholesterol and triglycerides increased, while M-value and exercise capacity decreased during 6 months of GH treatment. Conclusion MGU is reduced in TS despite normal insulin sensitivity. GH treatment does not alter MGU despite decreased whole body insulin sensitivity. A perturbed cardiac glucose uptake appears to be a feature of TS. [ABSTRACT FROM AUTHOR]

Background Klinefelter syndrome (KS) is a sex chromosomal aneuploidy (47,XXY) affecting 1/660 males. Based on findings in Turner syndrome, we hypothesized that electrocardiogram (ECG) abnormalities would be present in males with KS. Objective To investigate ECGs in males with KS and compare with controls. Methods Case control study of 62 males with KS and 62 healthy males matched on age. The primary outcome parameter was a difference in the ECG presentation between the two groups. The ECGs were analyzed by one blinded examiner (intraobserver variability 0.2-2.1%). The QT-interval was measured using 'teach-the-tangent' method excluding the U-wave. QTc was calculated using Bazett's equation, Hodges' equation, and a linear regression model. Body mass index, abdominal fat, and muscle mass as well as sex hormone levels were secondary parameters. The prevalence of mutations in genes related to short QT syndrome was determined in participants with a QTc < 330 ms. Results Compared to controls, the QTc-interval was shorter (P = 0.02-0.06) in males with KS depending on the applied correction method. QTc was shortest among testosterone (T)-treated males with KS, while untreated and thus hypogonadal KS had QTc interval comparable to controls. No mutations in genes related to short QT syndrome were found. Conclusion We found short QTc interval in males with KS, with further shortening of the QTc interval by T. These results suggest that genes on the X chromosome could be involved in regulation of the QTc interval and that T treatment may aggravate this mechanism. [ABSTRACT FROM AUTHOR]

Background Cardiovascular disease is a cardinal trait of Turner syndrome ( TS), causing half of the threefold excess mortality. As osteoprotegerin ( OPG) is a potential biomarker of cardiovascular disease, this cross-sectional and prospective study aimed at elucidating OPG levels in TS and its relationship to aortic diameter as well as validated cardiovascular risk markers. Methods Adult women with TS ( n = 99) were examined thrice (mean follow-up 4·7 ± 0·5 years), and 68 age-matched healthy female controls were examined once. Aortic diameter was assessed by cardiovascular magnetic resonance. Twenty-four-hours blood pressure monitoring and biochemical assessments were also performed. Results Osteoprotegerin levels (median with range) were lower in TS (777 [326-10 569] ng/l) compared with controls (979 [398-1987] ng/l; P < 0·05) and did not change during follow-up. The OPG concentration was higher among women with TS older than 50 years of age (996 [542-4996] vs 756 [326-10 569] ng/l; P < 0·05) with a trend towards a higher OPG in TS who were on antihypertensive medication (938 [490-2638] vs 752 [326-10 569] ng/l; P = 0·09). Contrary to controls, OPG levels correlated with BSA-indexed aortic diameter ( r = 0·31-0·45; P < 0·05), age ( r = 0·29; P < 0·05) and high-sensitivity C-reactive protein ( r = 0·23; P = 0·02) and inversely with BSA ( r = −0·20; P < 0·05), weight ( r = −0·23; P < 0·05) and plasma oestradiol levels ( r = −0·34; P < 0·05). Conclusion Levels of OPG are lower in TS and correlate with aortic diameter, age, BSA, weight and oestradiol in TS, but not controls. Future studies are needed to assess whether OPG may serve as a biomarker of aortic or cardiovascular disease in TS. [ABSTRACT FROM AUTHOR]

A response from the authors of the article "Short QTc interval in males with Klinefelter syndrome-influence of CAG repeat length, body composition, and testosterone replacement therapy" is presented.