Endocrine Abstracts

Background: Bone turnover markers (BTM) are potential measures for understanding the effect of antiresorptive medications upon osteoclast activity. As a dynamic marker of therapy effect, they could complement or replace DXA-BMD. The translation of population data on BTM changes with therapy to the individual patient is less established. Post-hoc trial data suggests a reduction in BTM of 40% may represent a target for defining appropriate response to therapy.<p class="abste...

Background: Primary aldosteronism is identified in approximately 10% of hypertensive all-comers. Adrenal vein sampling (AVS) allows localization of aldosterone production, identifying cases where unilateral adrenalectomy can be curative. Unfortunately, AVS is technically challenging.Methods: Data from AVS procedures performed in BC were extracted from the SunQuest laboratory information system in Vancouver Coastal Health. Cortisol and aldosterone levels ...

Glucocorticoids have profound effects on the brain, particularly during development and during the ageing process. The glucocorticoid metabolising enzymes, 11beta-hydroxysteroid dehydrogenases (11β-HSDs) type 1 and 2, interconvert active corticosterone (or cortisol) and inactive 11keto-derivatives to modify intracellular glucocorticoid levels. Hence, these enzymes add another layer of complexity to glucoocorticoid action in addition to circulating hormone and receptor (MR...

A 53-year-old caucasian female presented with tremor, palpitations, sweating, breathlessness and chest discomfort. Examination revealed a non-tender, large diffuse goitre and TFT showed an elevated T4 and undetectable TSH. Thyroid antibodies were elevated; 115 IU/ml (NR <35) and thyroid ultrasound confirmed diffuse vascular goitre. Patient was diagnosed with thyrotoxicosis with a likely aetiology of Grave’s disease.Carbimazole was com...

Introduction: Testosterone replacement therapy is the standard treatment for hypogonadism. However, there are also serious side effects which clinicians should be aware of. Here we present a case of unusual side effect related to testosterone therapy.Case history: A 90 year-old gentleman attended A&E with gradually worsening confusion and dyspnoea. His breathing had deteriorated in the last week with marked decrease in exercise tolerance. Investigati...

Prenatal exposure to excess glucocorticoids may be causal in programming mood disorders in later life. In support of this hypothesis, maternal stress, treatment during pregnancy with dexamethasone (which crosses the placenta) or inhibitors of feto-placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), the physiological ‘barrier’ to maternal glucocorticoids, reduces birth weight and programmes offspring cardio-metabolic and affective behaviours. The e...

Placental 11β-hydroxysteroid dehydrogenase-2 (11β-HSD2) rapidly converts glucocorticoids to inactive metabolites, thus protecting the developing fetus from high maternal glucocorticoids. Genetic deficiency or inhibition of 11β-HSD2 associates with fetal growth restriction, low birth weight, and cardiometabolic disease in adulthood. Similar ‘programming’ effects are seen with maternal malnutrition or stress; these challenges associate with reduced place...

Prenatal glucocorticoid overexposure is a key risk factor for susceptibility to neuropsychiatric disorders in adult life. Fetal exposure to glucocorticoids is regulated by 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) an enzyme which inactivates glucocorticoids and is highly expressed in the placenta and fetus. Previous work has established that 11β-HSD2−/− offspring generated by heterozygous matings exhibit altered placental developm...

An 83-year-old gentleman was referred to the endocrine clinic with incidentally found abnormal thyroid function tests (TFT): TSH <0.02 (0.2–4.0 mU/l), free T4 20.4 (9–19 pmol/l), and free T3 7.6 (2.5–5.7 pmol/l). His TFT done 6 months previously were normal with TSH 1.21 mU/l and FT4 11.8 pmol/l. His past medical history included BPH, peripheral vascular disease and chronic kidney disease (CKD), and medications were tamsulosi...

Fetal glucocorticoid exposure is a key mechanism involved in adverse programming outcomes in the adult, including hypertension, anxiety and insulin resistance. While glucocorticoids may exert their effects directly on the fetus, they may also affect fetal growth through indirect effects on placental function. Regulation of fetal glucococorticoid exposure is achieved by the placental glucocorticoid barrier, which involves glucocorticoid inactivation within the labyrinth zone of...