Is late-night salivary cortisol a better screening test for possible cortisol excess than standard screening tests in obese patients with Type 2 diabetes?

Aim: To compare the performance, in terms of specificity for cortisol excess, of late-night salivary cortisol with 24-hour urine-free cortisol (24hr UFC) and overnight 1mg dexamethasone suppression test (1mg DST) in a group of obese T2DM patients.

Methods: Forty obese patients with T2DM without clinical features of Cushing's syndrome were recruited. Plasma, urinary and salivary cortisol were measured directly by an enzyme-linked immunosorbent assay using monoclonal antibodies.

Four cases of autosomal dominant hypocalcaemia with hypercalciuria including two with novel mutations in the calcium-sensing receptor gene.

We present four cases with clinical and biochemical hypocalcaemia and evidence supportive of hypoparathyroidism. One case had been previously ascribed a diagnosis of idiopathic hypoparathyroidism. Following the detection of relative hypercalciuria, all cases were found to have autosomal dominant hypocalcaemia with hypercalciuria and mutations of the calcium-sensing receptor gene, of which two were novel.

FGF23 elevation and hypophosphatemia after intravenous iron polymaltose: a prospective study.

Context: Parenteral iron administration has been associated with hypophosphatemia. Fibroblast growth factor 23 (FGF23) has a physiological role in phosphate homeostasis via suppression of 25-hydroxyvitamin D [25(OH)D] activation and promotion of phosphaturia. We recently reported a case of iron-induced hypophosphatemic osteomalacia associated with marked FGF23 elevation.

Iron polymaltose-induced FGF23 elevation complicated by hypophosphataemic osteomalacia.

Iron-induced renal phosphate wasting, hypophosphataemia and osteomalacia have previously been reported in a small number of Japanese patients receiving parenteral iron sucrose. We report the case history of a European male who, as a result of regular intravenous iron polymaltose, developed prolonged hypophosphataemia complicated by widespread insufficiency fractures. The pathogenesis of this complication remains unknown however our novel finding of a marked elevation in fibroblast growth factor 23 (FGF23), which normalized after ceasing parenteral iron, suggests an important and previously unreported effect of iron on FGF23 homeostasis.

Corticotropin tests for hypothalamic-pituitary- adrenal insufficiency: a metaanalysis.

Context: The diagnostic value of tests for detecting hypothalamic-pituitary adrenal insufficiency (HPAI) is controversial.

Objective: Our objective was to compare standard-dose and low-dose corticotropin tests for diagnosing HPAI.

Data Sources: We searched the PubMed database from 1966-2006 for studies reporting diagnostic value of standard-dose or low-dose corticotropin tests, with patient-level data obtained from original investigators.

Characterisation of proghrelin peptides in mammalian tissue and plasma.

Ghrelin is a 28 amino acid stomach peptide, derived from proghrelin(1-94), that stimulates GH release, appetite and adipose deposition. Recently, a peptide derived from proghrelin(53-75) -- also known as obestatin -- has been reported to be a physiological antagonist of ghrelin in the rat. Using four specific RIAs, we provide the first characterisation of proghrelin(1-94) peptides in human plasma, their modulation by metabolic manipulation and their distribution in mammalian tissues.

Macroprolactin, big-prolactin and potential effects on the misdiagnosis of hyperprolactinemia using the Beckman Coulter Access Prolactin assay.

Objective: To examine whether use of the Beckman Coulter Access Prolactin (PRL) assay, which has low reactivity with macro-PRL, obviates the need for screening hyperprolactinemic samples.

Design And Methods: Samples from 1020 hyperprolactinemic individuals and 401 healthy volunteers were treated with polyethylene glycol (PEG). Macro-PRL was assessed from (1) percent PRL recovery, using cut-off values derived by gel filtration chromatography (GFC) and (2) significant (p<0.

A new mutation, R563Q, of the beta subunit of the epithelial sodium channel associated with low-renin, low-aldosterone hypertension.

Objective: To determine the relationship between R563Q, a mutation of the renal epithelial sodium channel, and hypertension.

Methods: Hypertensive patients with low renin and aldosterone, hypokalemia or resistant hypertension were selected for DNA analysis. Genomic DNA encoding the C-terminal domain of the epithelial sodium channel beta subunit from hypertensives and controls was amplified by polymerase chain reaction and screened for the R563Q mutation by digestion with Sfc1 restriction enzyme, or sequenced.