Introduction: An increased demand for monitoring aspirin treatment by platelet function tests has been observed, but data on the biological variation of these tests are insufficient. The aim of this study was to assess the biological variation of optical platelet aggregometry and closure time in healthy subjects without aspirin and after aspirin ingestion. Subjects and Methods: In 20 healthy subjects, blood was sampled 4 times: on 2 consecutive mornings a day after aspirin ingestion (100 mg/daily) and on 2 consecutive days of no treatment. In all samples, arachidonic acid-, ADP- and collagen-induced optical platelet aggregation was measured, and closure times were determined by collagen/epinephrine (CEPI) and collagen/ADP (CADP) cartridges in a platelet function analyzer-100. Results: Aspirin significantly reduced arachidonic acid- and ADP-induced platelet aggregation and significantly prolonged CEPI closure time, but had no significant effect on collagen-induced platelet aggregation and CADP closure time. Aspirin increased both within- and between-subject coefficients of variation. Arachidonic acid-induced platelet aggregation was the most sensitive to aspirin and no aspirin-resistant subjects were detected on either day after aspirin. According to ADP-induced platelet aggregation or CEPI closure time, 25 and 30% of healthy subjects, respectively, changed from aspirin resistant to aspirin responsive or vice versa from one day to another. There was no agreement between platelet function tests in determining aspirin resistance. Conclusions: A significant variation in optical platelet aggregometry and closure time exists and is presumed to have a major effect on determination of aspirin resistance.

PCOS was not associated with increased OHP compared with BMI and age-matched controls. However, increase in OHP was positively associated with BMI in PCOS and healthy women.

Background: Endocrine disorders in patients after heart transplantation (HT) remain understudied. We aimed to assess endocrine profiles and management of HT recipients in the early post-transplant period. Methods: We conducted a retrospective cohort study on 123 consecutive HT recipients in the Advanced Heart Failure and Transplantation Programme between 2009 and 2018. All recipients had per-protocol endocrine followup within the first postoperative year. The median time to first post-transplant endocrine follow-up was 3 months (IQR 2-4). We assessed the incidence of vitamin D deficiency, bone mineral density, history of low energy fractures, hypogonadism in male recipients, posttransplant diabetes mellitus, and thyroid and parathyroid function. Results: We enrolled 22 women and 101 men of median age 57 years (IQR 50-63). Post-transplant diabetes mellitus developed in 14 patients (11.4%). 18 of 25 patients (14.6%) with preexisting type 2 diabetes mellitus required intensification of antidiabetic therapy. 38 male patients (40.4%) had hypogonadism. 5 patients (4.6%) were hypothyroid and 10 (9.3%) latent hyperthyroid. Secondary hyperparathyroidism was present in 19 (17.3%), 25hydroxyvitamin D deficiency in 64 (54.7%) of patients. Osteoporosis was present in 26 (21.1%), osteopenia in 59 (48.0%) patients. 47 vertebral fractures, 3 hip and 1 humerus fractures occurred in 21 patients. Most of the patients had coincidence of two or three disorders, while less than 5% did not have any endocrine irregularities. All patients received calcium and vitamin D supplements. Forty-six patients (37.4%) were treated with zoledronic acid, 12 (9.8%) with oral bisphosphonates. Two patients were treated with teriparatide. Conclusions: The prevalence of multiple endocrine disorders early after heart transplantation is high. Assessment and management of increased fracture risk and all other potentially affected endocrine axes should be considered as a standard of care in this early period.

Most data on natural history of nonfunctioning adrenal incidentalomas (NFAI) are provided by follow-ups up to 5 years. We conducted a 10.5 (9.1-11.9)-year follow-up study of NFAI in 67 participants (20 (29.9%) males, 47 (70.1%) females) of mean age 57.9 (52.3-63.9) years and BMI 27.42 (24.07-30.56) kg/m2). We also evaluated the associations between baseline body mass index (BMI) and changes of NFAIs’ characteristics at follow-up. Progression to mild autonomous cortisol excess (MACE) was observed in 15 (22 %) patients, with 14 of them having post overnight dexamethasone suppression test (ODST) cortisol between 50-138 nmol/L and only one >138 nmol/L. The progression rate was significantly higher in overweight and obese than in normal weighted subjects. Patients that developed MACE had significantly higher baseline mean cortisol after 1 mg ODST. Tumor enlargement ≥10 mm occurred in 8.9% of patients. All tumors had persistent radiological characteristics typical for adrenal adenoma. In comparison with reports of shorter observational periods, we observed higher growth rate ≥10 mm and higher progression rate from NFAI to MACE, particularly in overweight and obese subjects. We concluded that duration of the follow-up period is an important factor in characterizing the natural history of NFAI. Higher baseline BMI and higher baseline cortisol after ODST might predict the long-term likelihood of progression in hormonal activity. The magnitudes of observed progressions in growth or hormonal activity were clinical insignificant. Our long-term follow-up therefore clearly supports the general view that long term monitoring of patients with NFAI is not necessary.

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Trabecular bone score (TBS) is a textural index that provides indirect evaluation of trabecular microarchitecture. It improves fracture risk assessment in several high‐risk populations. We aimed to evaluate the role of TBS assessment in heart transplant recipients (HTR). In a cross‐sectional study with 87 HTR (69 males and 18 females), we assessed TBS and evaluated potential associations between TBS and factors related to increased fracture risk. We also evaluated the correlations between the presence of vertebral fractures (VF) and degraded TBS. We confirmed degraded TBS in the majority of HTR. 27.6% of HTR had partially degraded, 27.6% had degraded TBS. HTR with degraded TBS were older, had higher body mass index, lower bone mineral density (BMD), and T‐score. As opposed to stable BMD over different time points, TBS significantly differed among different post‐transplant time periods. TBS did not correlate with current methylprednisolone or past zoledronic acid treatment, presence of hypogonadism or diabetes. TBS did not have additional value over BMD in predicting the presence of VF. Most fractures occurred in patients with osteopenia and in patients with partly degraded TBS. Studies with longitudinal designs and larger sample sizes are warranted to further assess the potential role of TBS in HRT.

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