Growth Hormone Replacement in Adults with Growth Hormone Deficiency: Assessment of Current Knowledge

Carroll, Paul; Christ, Emanuel; Sönksen, Peter H.

doi:10.1016/s1043-2760(00)00268-x

Cited by 41 publications

(45 citation statements)

References 74 publications

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“…The technique used for assessing LDL size is crucial; while, in fact, there is a general agreement on sizing based on electrophoretic mobility, the conclusions are far less clear for other techniques, such as those based on ultracentrifugation or, more so, on nuclear magnetic resonance (37). GHRT resulted in a decrease in total and LDL cholesterol concentrations but did not significantly influence triglycerides or HDL cholesterol concentrations, in keeping with previous results (23,24). Since no effect was found on HDL cholesterol and triglyceride levels, it is no surprise that GHRT had no significant impact on LDL size or subclasses, since these variables are strongly metabolically related (16,18).…”

Section: Ghd Versus Controls (Pz)supporting

confidence: 88%

“…It has been reported that GHRT tends to correct the dyslipidaemia found in hypopituitary patients with GHD, mainly by reducing total and LDL cholesterol concentrations, whereas the effect on HDL cholesterol and triglycerides is less clear (23,24). Thus, so far no studies have directly investigated: (1) whether hypopituitary patients with GHD have increased small dense LDL; (2) whether GHRT reduces levels of small dense LDL and (3) the prevalence of ALP in GHD and GHRT patients.…”

Section: Introductionmentioning

confidence: 99%

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Atherogenic lipoprotein phenotype and low-density lipoprotein size and subclasses in patients with growth hormone deficiency before and after short-term replacement therapy

Rizzo

Trepp²,

Berneis³

et al. 2007

eur j endocrinol

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Objective: Patients with growth hormone deficiency (GHD) have increased cardiovascular risk and may show elevated triglyceride and reduced high density lipoprotein (HDL) cholesterol concentrations, two lipid abnormalities usually accompanied by increased small dense LDL in the 'atherogenic lipoprotein phenotype' (ALP). In the present study, we directly investigated (1) whether hypopituitary patients with GHD have increased small dense LDL; (2) whether growth hormone replacement therapy (GHRT) beneficially impact on such particles; (3) the prevalence of ALP in GHD and GHRT patients. Design and methods: In 14 hypopituitary patients with GHD (44G13 years, body mass index (BMI) 27G3) before and after 4 months of GHRT, and in 11 healthy age-and BMI-matched controls we measured plasma lipids and LDL size and subclasses by gradient gel electrophoresis. Results: Compared with controls, GHD showed increased triglycerides (PZ0.0024), similar total and LDL cholesterol levels and a tendency towards reduced HDL cholesterol concentrations (PZ0.0894). GHRT reduced total and LDL cholesterol levels (PZ0.0303 and 0.0120 respectively), but no effect was found on triglycerides and HDL cholesterol levels. LDL size was unchanged in GHD versus controls (269G9 vs 274G6 Å , PZns), but LDL subclass analysis revealed a shift towards more dense particles (PZ0.0046). GHRT had no significant impact on LDL size and subclasses. The prevalence of ALP was 14% in GHD and 7% in GHRT. Conclusions: In GHD patients, individual features of ALP (including increased small dense LDL) may be common, but complete ALP is relatively uncommon. Short-term replacement therapy seems to be ineffective on such lipid alterations, but the effect of a longer GHRT remains to be assessed.

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Section: Ghd Versus Controls (Pz)supporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Atherogenic lipoprotein phenotype and low-density lipoprotein size and subclasses in patients with growth hormone deficiency before and after short-term replacement therapy

Rizzo

Trepp²,

Berneis³

et al. 2007

eur j endocrinol

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“…Indeed, debates were held about this issue at recent meetings of the Society for Endocrinology (London 2001) and the 5th International hGH Symposium on GH Deficiency in Adults (Copenhagen 1998), and many recent reviews are unabashedly partisan in favoring (Deijen & van der Veen 1999, Carroll et al 2000, Simpson et al 2002 or condemning (Barkan et al 2000) its use in adults. Economic reasons must also be considered, since GH therapy remains expensive despite the widespread availability of recombinant GH.…”

Section: Gh Deficiencymentioning

confidence: 99%

Growth hormone therapy and Quality of Life: possibilities, pitfalls and mechanisms

Hull

Harvey²

2003

Journal of Endocrinology

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The actions of growth hormone (GH) are not restricted to growth: GH modulates metabolic pathways as well as neural, reproductive, immune, cardiovascular, and pulmonary physiology. The importance of GH in most physiological systems suggests that GH deficiency at any age would be associated with significant morbidity. However, prior to the advent of recombinant GH, cadaverderived GH was only used therapeutically to correct the height deficit, and thereby hypothetically improve quality of life (QoL), in GH-deficient children. Physicians now have access to unlimited, albeit expensive, supplies of recombinant GH, and are considering the advisability of GH replacement or supplementation in other patient populations. This paper analyses studies investigating the relationship between GH and QoL in GH-deficient children or adults, in GH-replete short children suffering from idiopathic short stature, Turner syndrome, or intrauterine growth retardation and in GH-deficient or replete elderly adults. Possible mechanisms by which GH might improve QoL at neural and somatic sites are also proposed.

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“…GH has important physiological functions in adult humans and several studies have shown that GHD in adult patients is associated with abnormalities in body composition, visceral obesity, metabolic derangements and impaired physical performance (2 -7). These impairments improve with recombinant human GHreplacement therapy (rhGH) (2,4,6,(8)(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

The cut-off limits of the GH response to GH-releasing hormone-arginine test related to body mass index

et al. 2005

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Objective: The diagnosis of growth hormone (GH) deficiency (GHD) in adults is based on a reduced peak GH response to provocative tests, such as the insulin tolerance test (ITT) and the GH-releasing hormone-arginine (GHRH-ARG) test. However, the cut-off limits of peak GH response in lean subjects are not reliable in obese patients; this is noteworthy since adult GHD is often associated with obesity. Aim of this study was to evaluate the diagnostic cut-off limits of peak GH response to the GHRH-ARG test in overweight and obese as well as in lean population. Design and methods: The GH responses to the GHRH-ARG test were studied in 322 patients with organic hypothalamic-pituitary disease and in 318 control subjects. Patients were subdivided into two groups on the basis of the number of pituitary hormone deficits, except for GH deficiency: (a) patients with total pituitary hormone deficit (TPHD) and (b) patients without or with no more than two pituitary hormone deficits (PHD). Both patients and control subjects were divided into three subgroups according to body mass index (BMI): lean (BMI , 25 kg/m 2 ), overweight (BMI $ 25 and , 30 kg/m 2 ) and obese (BMI $30 kg/m 2 ). TPHD patients were assumed to be GH deficient, whereas PHD patients may include subjects with either normal or impaired GH secretion. The statistical analysis was carried out by the Receiver-Operating Characteristic curve analysis (Medcalc 7.2). The diagnostic cut-off points were calculated for lean, overweight and obese subjects to provide optimal separation of GH-deficient patients and control subjects according to two criteria: (1) a balance between high sensitivity and high specificity; (2) to provide the highest pair of sensitivity/specificity values for GH deficiency. Results: In the lean population the best pair of values, with highest sensitivity as 98.7% and highest specificity as 83.7%, was found using a peak GH cut-off point of 11.5 mg/l. In the overweight population the best pair of values, 96.7 and 75.5%, respectively, was found using a peak GH cut-off point of 8.0 mg/l. In the obese population the best pair of values, 93.5 and 78.3%, respectively, was found using a peak GH cut-off point of 4.2 mg/l. Applying the above mentioned cut-off points, among PHD patients we found that 80 subjects (72%) were GHD whereas 31 (28%) had normal GH secretion. Conclusions: In conclusion the GHRH-ARG test is a reliable tool for the diagnosis of adult GH deficiency in lean, overweight and obese patients, provided that specific BMI-related cut-off limits are assumed.European Journal of Endocrinology 153 257-264

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Growth Hormone Replacement in Adults with Growth Hormone Deficiency: Assessment of Current Knowledge

Cited by 41 publications

References 74 publications

Atherogenic lipoprotein phenotype and low-density lipoprotein size and subclasses in patients with growth hormone deficiency before and after short-term replacement therapy

Atherogenic lipoprotein phenotype and low-density lipoprotein size and subclasses in patients with growth hormone deficiency before and after short-term replacement therapy

Growth hormone therapy and Quality of Life: possibilities, pitfalls and mechanisms

The cut-off limits of the GH response to GH-releasing hormone-arginine test related to body mass index

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