Clinical endocrinology
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Clinical endocrinology · Apr 1998
Serum leptin and insulin in paediatric end-stage liver disease and following successful orthotopic liver transplantation.
Leptin, the product of the ob gene, is a postulated feedback regulator of adiposity with appetite suppressant and catabolic effects. Catabolic states are associated with decreased body fat mass as a result of both nutritional and metabolic perturbation. Low serum leptin has been described previously in a number of catabolic states. It has been unclear whether the observed changes in leptin are a cause or consequence of changes in adiposity. Paediatric end-stage liver disease (ESLD) is characterized by decreased body fat mass and poor linear growth. Successful treatment by orthotopic liver transplantation (OLT) is accompanied by increase in fat mass. We investigated the hypothesis that serum leptin would be low in paediatric ESLD and that increase in body fat mass post-OLT would result in increased serum leptin. ⋯ Serum leptin is low in children with end-stage liver disease but does not show the expected correlation with measures of body fat mass. Surprisingly, following orthotopic liver transplantation serum leptin falls significantly despite significant increases in measures of body fat mass (triceps skinfold thickness standard deviation scores, mid-arm circumference standard deviation scores). Orthotopic liver transplantation restores the expected correlation of serum leptin with measures of body fat mass within the treatment group. The elevation of serum leptin above predicted levels in paediatric end-stage liver disease offers a mechanism for the anorexia and cachexia characteristic of this disease.
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Following apparent subacute thyroiditis, a 16-year-old girl developed a left thyroid abscess thought to be secondary to steroids and haematogenous spread from a pilonidal abscess. The thyroid suppuration became recurrent and required partial thyroidectomy. ⋯ All patients with a tender thyroid should have ultrasound-guided fine needle aspiration to establish the diagnosis. If suppuration is confirmed, a barium swallow is advised to exclude a sinus tract from the piriform fossa.
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Clinical endocrinology · Feb 1998
Case ReportsAcromegaly and Cushing's syndrome due to ectopic production of GHRH and ACTH by a thymic carcinoid tumour: in vitro responses to GHRH and GHRP-6.
A 50-year-old male presented with diabetes mellitus and Cushing's syndrome associated with a large mediastinal mass. The levels of serum cortisol were high (1500-1800 nmol/l) without diurnal variation. Plasma ACTH levels (200-250 ng/l) and urinary excretion of cortisol were also increased. ⋯ Immunoreactive GHRH, ACTH and NPY, but not immunoreactive GH, were detected in 80-90% of the tumour cells and the three peptides appeared to be co-localized. In primary culture, cells from this tumour displayed calcium influx in response to GHRH or GH releasing peptide-6 (GHRP-6), while there were not such responses by cells from another carcinoid not producing GHRH, ACTH or NPY. These results demonstrate a rare case of ectopic production of GHRH, ACTH and NPY, and indicate that the tumour cells were responsive to GHRH and GHRP-6 as well as octreotide.
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Clinical endocrinology · Jan 1998
Randomized Controlled Trial Clinical TrialBright light exposure and pituitary hormone secretion.
Exposure to bright light inhibits melatonin secretion in man. As the relationship between melatonin and pituitary function remains controversial, we investigated the effect of altering the melatonin rhythm by bright light during the early hours of darkness on pituitary hormone secretion in man. ⋯ Exposure to bright light during the early hours of darkness delays the nocturnal melatonin peak and alters cortisol, GH, PRL and nocturnal vasopressin secretion, while modification of the sleep pattern decreases vasopressin concentrations and alters its nocturnal peak.
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Clinical endocrinology · Jan 1998
A very high dose dexamethasone suppression test for differential diagnosis of Cushing's syndrome.
The high-dose dexamethasone (dex) suppression test of cortisol secretion (8 x 2 mg dex over two days or 8 mg overnight) is a mainstay in the differential diagnosis of Cushing's syndrome (CS). In some patients with pituitary Cushing's disease (CD), however, plasma cortisol is not suppressed to < 50% of control by 8 mg of dex. We therefore hypothesized that a higher dose of dex might produce more effective suppression of cortisol secretion in CD. ⋯ In this series, the hCRH test was the most reliable test for the differential diagnosis of Cushing's syndrome. The 32 mg dexamethasone test with measurement of urinary free cortisol was clearly superior to the 8 mg test and to other aspects of the very high dose dexamethasone test. It can be recommended for 'non-suppressible' patients with ACTH-dependent Cushing's syndrome and can be performed on outpatients.