Renal effects of growth hormone. II. Electrolyte homeostasis and body composition

Rosenberg, Andrew R.; Kainer, Gad

doi:10.1007/bf00874021

Cited by 30 publications

(30 citation statements)

References 74 publications

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“…Recently there has been interest in the use of GH in children with XLH and short stature [4,14,15,31]. In addition to its growth-promoting effect, there is the theoretical advantage that GH, by increasing the tubular reabsorption of phosphate, may lead to a reduction in phosphate supplement requirements, which have been linked to the development of nephrocalcinosis [13,15]. XLH patients are reported to have normal GH concentrations and normal or near-normal responses to provocative pharmacological stimuli, thus definite GH deficiency is not part of the XLH sequence [6,32].…”

Section: Discussionmentioning

confidence: 98%

“…Because of its positive effect on phosphate retention, rhGH could have a doubly positive impact on growth in XLH. Firstly by increasing serum phosphate levels and (at least in part) correcting hypophosphatemia, secondly by its classical hormonal effect on growth [13]. There are few data on the application of GH in XLH patients [4,[14][15][16].…”

Section: Introductionmentioning

confidence: 99%

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X-linked hypophosphatemia: effects of treatment with recombinant human growth hormone

Reusz

Miltényi

Stubnya

et al. 1997

Pediatric Nephrology

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The impact of recombinant human growth hormone (rhGH) treatment on growth, bone mineral metabolism, and bone mineral density (BMD) was evaluated in six children (3 girls, 3 boys) with familial hypophosphatemic rickets (XLH). Five were prepubertal (aged 6-8.8 years), one 15.3-year-old boy had combined XLH and GH deficiency, but had not been treated with rhGH previously. rhGH was administered daily for 1 year, at a dose of 1 IU/kg per week, combined with 1,25-dihydroxyvitamin D3 and oral phosphate therapy. Z scores for growth velocity and height improved significantly (-2.9 vs. 2.5, P < 0.01, and -2.2 vs. -1.5, P < 0.01, respectively). However, the ratio of Z score for height to that of subischial leg length decreased significantly (0.65 vs. 0.43, P < 0.01), indicating disproportionate growth in favor of the trunk. The height-corrected BMD Z increased slightly (-0.99 vs. -0.94, P < 0.05). A slight increase in serum phosphate occurred (0.78 vs. 0.88 mmol/l, P < 0.02). Tubular reabsorption of phosphate/glomerular filtration rate increased from 0.45 mmol/l to 0.55 mmol at 6 months (P < 0.02), but returned to the initial level at 12 months. These results indicate that children with XLH can benefit from the positive effect of rhGH on growth, however treatment could aggravate the already existing tendency to disproportionate growth. GH production should be evaluated in poorly growing patients with XLH, because it can mask GH deficiency. rhGH can be safely combined with conventional treatment in XLH. Further studies are needed to determine the effect of treatment on final height and maximal BMD.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

X-linked hypophosphatemia: effects of treatment with recombinant human growth hormone

Reusz

Miltényi

Stubnya

et al. 1997

Pediatric Nephrology

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“…Recent studies suggest that GH could further improve calcium phosphate metabolism (16,19,20) and linear growth in XLH (14,19). Therefore, GH therapy in XLH has been investigated in a few small cohorts regardless of a GH secretion defect.…”

Section: Discussionmentioning

confidence: 99%

Effect of GH replacement therapy in two male siblings with combined X-linked hypophosphatemia and partial GH deficiency

Schütt

Schumacher²,

Holterhus³

et al. 2003

European Journal of Endocrinology

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Objective: X-linked hypophosphatemia (XLH) is characterized by low serum phosphorus, relative 1,25-dihydroxyvitamin D 3 deficiency and rickets. It is caused by mutations in the phosphate-regulating gene with homologies to endopeptidases on the X chromosome (PHEX). The conventional treatment of XLH includes the administration of phosphate and calcitriol; however, treated patients usually present with a short stature. Therefore, additional coexistent defects, such as GH deficiency, are under debate. Patients and methods: Two male siblings presented with a disproportionate growth failure and rickets. Investigation of calcium and phosphate metabolism, molecular genetic analysis of the PHEX gene and GH function tests were initiated. Results: Both patients showed typical clinical and biochemical signs of XLH. Molecular genetic analysis revealed a 747 CGA (Arg)-TGA (End) mutation in exon 22 of the PHEX gene, confirming XLH. Since treatment with phosphate and calcitriol alone failed to improve growth in both patients, the GH axis was examined and a partial GH deficiency was diagnosed in both cases. Almost 3 years of additional therapy with recombinant human GH (rhGH) led to a significant improvement of height standard deviation scores (HtSDS). Conclusions: Poor growth in XLH may, in at least some patients, be aggravated by GH deficiency. Hence, GH deficiency should be considered in extremely poorly growing patients with XLH, because these patients are likely to benefit from rhGH therapy.

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“…The marked decrease and increase in serum phosphate after hypo-and hypercalcemic stimuli, observed in this study, would in part be due to the increase and decrease in serum PTH concentration observed during the period of the infusion. The significant difference in the percent change in serum phosphate in response to hypoand hypercalcemic stimuli after 12 mo on GHR may in part be due to the GH antiphosphaturic effect (28,32), negating some of the PTH-induced renal loss. The decrease in serum phosphate concentration observed after 10 -12 h of PTH-(1-34) infusion in AGHD patients before and after GHR may also, in part, be explained by the PTH effects on renal tubules.…”

Section: Discussionmentioning

confidence: 99%

Parathyroid responsiveness to hypocalcemic and hypercalcemic stimuli in adult growth hormone deficiency after growth hormone replacement

Ahmad

Hopkins²,

Thomas³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

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. Parathyroid responsiveness to hypocalcemic and hypercalcemic stimuli in adult growth hormone deficiency after growth hormone replacement. Am J Physiol Endocrinol Metab 286: E986 -E993, 2004; 10.1152/ajpendo. 00325.2003.-Adult growth hormone deficiency (AGHD) is associated with osteoporosis. Previous reports have suggested that alterations in parathyroid gland responsiveness to changes in calcium concentration may play a role in the genesis of osteoporosis in untreated AGHD patients. We investigated the endogenous parathyroid hormone ] response to hypocalcemic and hypercalcemic stimuli induced by sodium EDTA and calcium gluconate infusion, respectively, and to PTH-(1-34) infusion in AGHD patients before and during GH replacement (GHR). We have demonstrated that the maximum PTH-(1-84) stimulation and suppression occurred at significantly higher calcium concentrations and in response to smaller changes in calcium concentrations after GHR. The calcemic response to the effects of PTH-(1-34) infusion significantly increased after GHR. The calcium set point (the calcium concentration at which the rate of PTH secretion is one-half of its maximal value) significantly increased in all groups after 3 mo on GHR, and it increased further at 12 mo. Our results suggest increased parathyroid gland sensitivity to smaller changes in serum calcium and increased endorgan sensitivity to the effects of PTH in AGHD patients after GHR. These findings may help us to understand the mechanisms underlying the genesis of osteoporosis in AGHD patients. sodium ethylenediaminetetraacetic acid; calcium gluconate; parathyroid hormone-(1-84); parathyroid hormone-(1-34); calcium set point EXTRACELLULAR IONIZED CALCIUM concentration is maintained near constancy via a complex homeostatic mechanism, which includes the calcium-sensing receptors found in the parathyroid glands (15), and by an effector system with specialized cells in the kidneys, bone, and intestines that responds to calciotropic hormones with changes in the transport of mineral ions so as to restore calcium and phosphate concentrations toward normal (13). The parathyroid gland calcium-sensing receptor cell is remarkably sensitive to alterations in extracellular calcium concentration, and an inverse sigmoidal relationship has been shown between parathyroid hormone (PTH) release and extracellular calcium concentration in normal and abnormal parathyroid tissue (12).Extracellular ionized calcium concentration is generally regarded as the principal regulator of PTH secretion in vivo (34). However, it has been suggested that changes in maximal PTH secretion, slope of the PTH secretory curve at the calcium set point (the calcium concentration at which the rate of PTH secretion is one-half of its maximal value) (17), and the calcium set point and maximum suppressibility of PTH release might all contribute to PTH secretion (12). On a quantitative basis, changes in calcium set point have been shown to produce the largest alteration in PTH secretory rate for a given change in the value of a p...

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Renal effects of growth hormone. II. Electrolyte homeostasis and body composition

Cited by 30 publications

References 74 publications

X-linked hypophosphatemia: effects of treatment with recombinant human growth hormone

X-linked hypophosphatemia: effects of treatment with recombinant human growth hormone

Effect of GH replacement therapy in two male siblings with combined X-linked hypophosphatemia and partial GH deficiency

Parathyroid responsiveness to hypocalcemic and hypercalcemic stimuli in adult growth hormone deficiency after growth hormone replacement

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