Aikaterini Theodoraki

Testosterone therapy in men.

Androgens exert effects on virtually all bodily tissues, and have a multitude of physiological roles in health. Testosterone, the predominant androgen in men, when deficient (hypogonadism), leads to a multiplicity of symptoms and signs that are corrected with physiological substitution. The impact of hypogonadism depends on the age at which it occurs. In any case, when testosterone replacement is initiated close monitoring for efficacy and safety is advised. The relation of ageing, the metabolic syndrome, type 2 diabetes, obesity and survival with plasma testosterone has been closely examined in recent studies. However, the effect of testosterone replacement therapy on the above clinical states needs to be clarified in large long-term duration/outcome studies. Recent research has shed light on possible molecular testosterone targets. Based on those research outcomes, drugs targeting the androgen receptor, which spare androgenic effects and preserve anabolic tissue effects, called selective androgen receptor modulators (SARMS), are under clinical trials. The role of testosterone in regulating erectile function has been studied in animal models and critical tissue testosterone targets have been elucidated.

Performance of a third-generation TSH-receptor antibody in a UK clinic.

Background  UK national guidelines recommend the measurement of TSH receptor antibodies (TRAb) in certain clinical scenarios. A commercial third‐generation TRAb autoantibody M22‐biotin ELISA assay was introduced in May 2008 in our centre.

An objective scoring tool in the management of patients with pituitary apoplexy

1 Bilezikian, J.P., Khan, A.A. & Potts, J.T. (2009) Guidelines for the management of asymptomatic primary hyperparathyroidism: summary statement from the third international workshop. Journal of Clinical Endocrinology and Metabolism, 94, 335–339. 2 Sakaran, S., Damble, G., Bolland, M. et al. (2010) Skeletal effects of intervention of mild primary hyperparathyroidism: a meta analysis. Journal of Clinical Endocrinology and Metabolism, 95, 1653–1662.

Running on empty

A patient presented with spells of light-headedness, confusion and collapses, improving on eating. During a supervised fast, plasma glucose dropped to 1.7 mmol/l, with inappropriately high insulin, raised C-peptide and no sulphonylurea detectable, diagnostic of an insulinoma [1]. CT, MRI and abdominal ultrasound scanning failed to find any evidence of a lesion in the pancreas and all showed a liver lesion (a: black arrow). Somatostatin subtype 2 (sst2) receptor imaging with Ga-DOTATATE PET/CT was normal (b). The white arrow shows the body of the pancreas in each panel. Glucagon-like peptide-1 (GLP-1) receptor SPECT/CT was performed. This showed strong focal uptake posteriorly within the pancreatic body (c: white arrow). Notably, the liver lesion

Radiology reporting of adrenal incidentalomas - who requires further testing?

Adrenal incidentalomas (AIs) are common and guidelines recommend testing to exclude functioning lesions and malignancy. Their increasing prevalence results in several investigations that are usually conducted in the endocrinology clinic. In 2011, we audited the prevalence and management of AIs identified on computed tomography (CT) imaging of abdomen over 1 calendar month. Consequently, a decision pathway for adrenal lesions was introduced in the radiology department of the Royal Free London Hospital. One year later, we re-audited the local practice. In total, 690 CT scans were reviewed in 2011 compared with 1,264 in 2012. In 2011, 17 (2.46%) patients with AIs were identified, and 26 (2.01%) in 2012. Of those, 1.01% in 2011 and 0.95% in 2012 had newly identified AIs. Only a few patients had been tested to exclude a functional lesion and there was inconsistent terminology in reporting adrenal lesions. Therefore, we support comprehensive reporting of AIs and a selective testing strategy.

Low sex hormones in heart failure

Chronic heart failure (CHF) represents a debilitating condition with morbidity and mortality comparable to other end-stage disease states.1 Non-oedematous weight loss in the context of chronic heart failure is associated with adverse prognosis, as it is a strong independent risk factor for mortality in patients with CHF and cachexia: patients with CHF with wasting have a mortality at 18 months as high as 50% compared to 17% in those without cachexia.2 A number of different mediators have been implicated in the wasting process, including activation of pro-inflammatory cytokines, secretion of neurohormones and peptides, including PYY, ghrelin, leptin, growth hormone and insulin, and a relative deficiency of micronutrients and macronutrients.3 It has been suggested that a low testosterone level may represent one of the factors contributing to the anabolic/catabolic imbalance characteristically present in many patients with advanced CHF.4 In the study by Guder et al ( see page 504 ) total (TT) and free serum testosterone (FT), dehydroepiandrosterone sulfate (DHEAS), and sex hormone binding globulin (SHBG) were studied in a cohort of 191 patients with heart failure (mean age 64 years; NYHA class I–IV 24/35/35/6%).5 Free testosterone (0.5–3% of the total testosterone) represents the biologically active unbound testosterone fraction. The current gold-standard method of determining free testosterone is equilibrium dialysis, but this is technically demanding and laborious, and in clinical practice, a derived method for free testosterone is employed, calculated from the total testosterone, serum albumin and SHBG. There is good correlation between the two methods. The bioavailable testosterone represents the fraction of testosterone that is unbound (free) plus the albumin bound testosterone, which is readily dissociable and thus ‘bioavailable’. A reduction in free testosterone …

Nonfunctioning Pituitary Tumour Apoplexy

Nonfunctioning pituitary tumours account for one-third of all pituitary neoplasms, with an incidence of 7–9 new cases/106 every year. They are slow-growing benign monoclonal adenomas that do not cause any hormone hypersecretion syndromes. Symptoms arise from local compression of normal pituitary tissue and surrounding structures. The aim of treatment is the preservation of residual pituitary function and alleviation of local compressive mass effects. The available published series show that nonfunctioning adenomas constitute the underlying diagnosis in 45 % of patients with pituitary apoplexy. Apoplexy occurs more often in macroadenomas, men and with antithrombotic use. Headache, ophthalmoplegia, reduced visual acuity and visual filed defects are common presenting features. ACTH, TSH and gonadotropin deficiencies are frequently present and need to be assessed biochemically in patients with suspected pituitary apoplexy. A low serum prolactin at presentation has been linked with the severity of hypopituitarism postsurgical decompression. Patients with nonfunctioning pituitary adenomas who present with apoplexy have reduced 5-year rates of tumour regrowth (11 %) compared to non-apoplectic surgically treated nonirradiated nonfunctioning pituitary adenomas (18–34 % in different series). In those patients operated for pituitary apoplexy, tumour recurrence seems to be more common in patients with residual post-operative tumour.