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1 januari 2010, Contains fulltext : 89243.pdf (publisher's version ) (Open Access), CONTEXT: A wide range (15-56%) of prevalences of anterior pituitary insufficiency are reported in patients after traumatic brain injury (TBI). However, different study populations, study designs, and diagnostic procedures were used. No data are available on emergency-department-based cohorts of TBI patients. OBJECTIVE: To assess the prevalence of pituitary dysfunction in an emergency-department-based cohort of TBI patients using strict endocrinological diagnostic criteria. METHODS: Of all the patients presenting in the emergency department with TBI over a 2-year period, 516 matched the inclusion criteria. One hundred and seven patients (77 with mild TBI and 30 with moderate/severe TBI) agreed to participate. They were screened for anterior pituitary insufficiency by GHRH-arginine testing, evaluation of fasting morning hormone levels (cortisol, TSH, free thyroxine, FSH, LH, and 17beta-estradiol or testosterone), and menstrual history 3-30 months after TBI. Abnormal screening results were defined as low peak GH to GHRH-arginine, or low levels of any of the end-organ hormones with low or normal pituitary hormone levels. Patients with abnormal screening results were extensively evaluated, including additional hormone provocation tests (insulin tolerance test, ACTH stimulation test, and repeated GHRH-arginine test) and assessment of free testosterone levels. RESULTS: Screening results were abnormal in 15 of 107 patients. In a subsequent extensive endocrine evaluation, anterior pituitary dysfunction was diagnosed in only one patient (partial hypocortisolism). CONCLUSION: By applying strict diagnostic criteria to an emergency-department-based cohort of TBI patients, it was shown that anterior pituitary dysfunction is rare (<1%). Routine pituitary screening in unselected patients after TBI is unlikely to be cost-effective.

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Item does not contain fulltext, OBJECTIVE: Untreated GH-deficient adults are predisposed to insulin resistance and excess cardiovascular mortality. We showed previously that short-term treatment with a very low GH dose (LGH) enhanced insulin sensitivity in young healthy adults. The present study was therefore designed to explore the hypothesis that LGH, in contrast to the standard GH dose titrated to normalize serum IGF-I levels (SGH), may have differing effects on insulin sensitivity, body composition, and cardiovascular risk markers [lipid profile, C-reactive protein (CRP), interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and adiponectin] in adults with severe GH deficiency. PATIENTS AND METHODS: In this 12-month open, prospective study, 25 GH-deficient adults were randomized to receive either a fixed LGH (0.10 mg/day, n = 13) or SGH (mean dose 0.48 mg/day, n = 12), and eight age- and body mass index (BMI)-matched GH-deficient adults acted as untreated controls. Fasting blood samples were collected at baseline and at months 1, 3, 6, 9 and 12. Assessments of insulin sensitivity, using the hyperinsulinaemic euglycaemic clamp technique, and body composition, using dual-energy X-ray absorptiometry, were performed at baseline and at month 12. RESULTS: The LGH decreased fasting glucose levels (P < 0.01) and enhanced insulin sensitivity (P < 0.02), but body composition, nonesterified fatty acid (NEFA) levels and cardiovascular risk markers were unchanged. The SGH did not modify insulin sensitivity, decreased truncal fat mass (P < 0.05), CRP (P < 0.05) and IL-6 (P < 0.05) levels, and increased NEFA levels (P < 0.05). No changes were observed with the untreated controls. CONCLUSION: Our data indicate that, in contrast to the SGH, fixed administration of the LGH enhances insulin sensitivity with no apparent effects on body composition, lipolysis and other surrogate cardiovascular risk markers in adults with severe GH deficiency. Thus, the LGH may potentially be a beneficial replacement dose

Item does not contain fulltext, A recently developed assay for quantification of remnant-like particle cholesterol has provided considerable evidence that reinforces the concept that elevated levels of plasma remnants are associated with increased cardiovascular disease in different populations and distinct patient groups. In this review, we provide a brief summary of the most recently published studies, emphasizing the clinical relevance of remnant analysis. We discuss recent evidence that sheds light on the mechanisms that may underlie the atherogenicity of remnant lipoproteins. Taken together, these data provide new insight into the significance of remnant lipoproteins in the onset and development of premature atherosclerosis.

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Item does not contain fulltext, Cardiomyopathy is a major cause of death in overt acromegaly. Recent progress in research has increasingly revealed the molecular mechanisms concerning growth hormone and insulin-like growth factor in the development of heart failure. In this article, we propose mechanisms according to which heart failure occurs, and we aim to extrapolate this knowledge to more general processes involved in heart failure.

Item does not contain fulltext, The occurrence of insulin resistance syndrome (IRS), which is also called the metabolic syndrome, has rapidly increased over the last decade. IRS involves such major clinical features as premature atherosclerosis and its related complications. The major proatherogenic phenotype includes elevated plasma levels of apolipoprotein B-containing lipid particles. Another lipid particle of high-density lipoprotein (HDL) plays a key role in the prevention of atherosclerotic disease. Decreased levels of HDL cholesterol are found in IRS; however, little is known about metabolic pathways related to HDL antiatherogenic properties in this pathological condition. Hitherto, in other dyslipidemic populations, the antiatherogenic properties of HDL have been most frequently characterized in vitro. Recently, knowledge about antiatherogenic pathways in which HDL particles are involved in vivo has been accumulating. Consistent with these developments, new therapeutic strategies can be envisaged for IRS, including treatment with recombinant HDL particles and inhibitors of cholesteryl ester transfer protein.

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Item does not contain fulltext, In addition to cholecystokinin, other hormones have been suggested to be involved in regulation of postprandial gallbladder contraction. We aimed to evaluate effects of growth hormone (GH) on gallbladder contractility and cholecystokinin release. Gallbladder and gastric emptying (by ultrasound) and cholecystokinin release were determined before and after 6 months of recombinant human GH (rhGH) therapy in 12 patients with GH deficiency, after either a mixed (n = 5) or a liquid (n = 7) meal. Basal postprandial gallbladder contraction was severely impaired (19 +/- 2 and 26 +/- 3% of fasting volume after mixed and liquid meal, respectively). Histology and cholecystokinin sulfation patterns in duodenal biopsies from two patients were normal. After 6 months of rhGH therapy, fasting gallbladder volumes increased (from 20.8 +/- 0.9 to 25.9 +/- 1.1 mL, P < 0.05) and postprandial gallbladder emptying was restored (70 +/- 6 and 70 +/- 7% of fasting volume after mixed and liquid meal, respectively), without change of gastric emptying. Cholecystokinin secretion after a mixed meal and gallbladder sensitivity to cholecystokinin were significantly enhanced during rhGH replacement compared to the basal state. Postprandial cholecystokinin release, gallbladder responsiveness to cholecystokinin, and gallbladder emptying are severely impaired in the absence of GH. Reversibility during GH suppletion suggests its involvement in regulation of gallbladder contractility.

Item does not contain fulltext, Insulin-like growth factors (IGFs) have been implicated in normal growth, and especially foetal pancreas beta-cell development. As low birth weight has been implicated in the development of obesity and type 2 diabetes, much research has evolved into the importance of IGF and their signalling pathways for pancreas beta-cell development, and for type 2 diabetes. Insulin-like growth factor-I signalling has a lot in common with insulin signalling, and is involved in diverse cellular effects such as antiapoptosis, protein synthesis, cell growth and mitogenesis. Insulin-like growth factor-II can be bound by the insulin receptor A subtype and the IGF-1 receptor, which may explain its antiapoptotic effect. Various knock-out model studies indicate that absence of IGF-I or the IGF-1 receptor is critical for foetal and postnatal growth. Similarly, knock-out models of post-receptor molecules (such as IRS-2) point to the physiological role of IGFs for pancreas beta-cell development. A beta-cell-specific IGF-1 receptor knock out model indicates the importance of IGF-I for beta-cell function. The Goto-Kakizaki (GK) rat, a model for diabetes, has insufficient beta-cell development, which may be related to its defective IGF-II synthesis. As normal pancreas beta cells adapt to the prevailing insulin resistance with increasing beta-cell function, it is possible that insulin resistance interacts with IGF signalling in pancreas beta cells. van Haeften, T W

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