Medium-Term Cardiovascular Effects of High-Dose Growth Hormone Treatment in Growth Hormone-Deficient Children

Radetti, Giorgio; Crepaz, R; Paganini, Chiara; Gentili, Lino; W, Pitscheider

doi:10.1159/000023469

Cited by 15 publications

(16 citation statements)

References 19 publications

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“…The results of the present study are different from those obtained in our recent survey where the cardiac morphology and function were investigated, with the same modalities, in a group of GHD children treated with the same dosage of GH (1 U/kg/ week) and for a comparable period of time [6]. In that study we showed that the patients had an increase in mass and mass/volume ratio, reduced systolic performance and initial alterations of the diastolic function of the left ventricle after long-term therapy.…”

Section: Discussioncontrasting

confidence: 99%

“…Left ventricular (LV) hypertrophy, together with increased morbidity and mortality from cardiovascular diseases, are well-known complications of GH excess in acromegalic patients [4, 5]. Furthermore, we also found that GHD children treated for many years with high doses of GH show subclinical morphofunctional alterations of the left ventricle [6]. Since previous studies in TS patients were more focused on the effects of GH treatment on cardiac morphology [7, 8, 9], we decided to further explore this field by evaluating heart function, as well as morphology, in TS patients treated with high-dose GH for a mean period of 4.9 years.…”

Section: Introductionmentioning

confidence: 99%

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Cardiac Performance in Turner’s Syndrome Patients on Growth Hormone Therapy

et al. 2001

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Objectives: To investigate possible cardiac morphofunctional alterations observed in 26 Turner’s syndrome (TS) patients on prolonged high-dose growth hormone (GH) therapy. Study Design: We examined 26 TS subjects treated with rhGH (1 U/kg/week) for a mean period of 4.9 years (range 1–7.8) and 37 age-, weight- and height-matched healthy girls. Left ventricular volume, mass, systolic function, cardiac index, systemic vascular resistance and diastolic function were evaluated by two-dimensional and Doppler echocardiography. Results: Heart rate and systolic blood pressure (BP) were higher in TS patients than in controls, while diastolic BP was lower. Left ventricular volumes, ejection fraction, mass index, M/V ratio and cardiac index did not differ significantly; systemic vascular resistance was slightly decreased. Left ventricular fractional shortening and mean velocity of circumferential shortening were slightly increased while end-systolic meridional stress was decreased in TS. Contractile state was normal in TS. Diastolic function assessment showed a shortening of isovolumetric relaxation and diastolic filling times with an increased atrial contribution and a normal pulmonary venous flow. Conclusion: Cardiac morphology in TS patients on GH therapy is similar to controls. The observed changes in left ventricular systolic and diastolic function should be interpreted as an adaptation to the higher heart rate and reduced peripheral vascular resistance induced by GH therapy.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cardiac Performance in Turner’s Syndrome Patients on Growth Hormone Therapy

et al. 2001

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“…We did not find, however, any signs of glucose intolerance in our patients. Moreover, the potential side-effects of highdose GH treatment on the cardiovascular system have not as yet been fully clarified (19). The theoretical risk of an increased incidence of adulthood cancer associated with an elevated serum insulin-like growth factor (IGF)-I level in a GH recipient, is, however, lowered by the fact that GH also increases the level of IGF-binding protein-3, which would inhibit IGF-I action (20).…”

Section: Discussionmentioning

confidence: 99%

Treatment of GH-deficient children with two different GH doses: effect on final height and cost-benefit implications

Radetti

Buzi²,

Paganini³

et al. 2003

Eur J Endocrinol

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Objective: Treatment of GH-deficient (GHD) children with higher doses of recombinant human GH (rhGH) than conventional ones has been reported to result in higher growth velocity and increased final height. These findings, however, were observed by comparing large but heterogeneous groups of children. We wanted to verify whether the same results could be obtained in two groups of appropriately well-matched children with isolated GHD treated with high vs conventional doses of rhGH. Methods: Out of two cohorts of GHD children, cohort A (on a weekly rhGH dose of 0.3 mg/kg body weight) and cohort B (on a weekly rhGH dose of 0.15 mg/kg body weight), we selected two groups, each including 13 patients, who before treatment were matched for age, sex and height standard deviation score (SDS). They were followed up until final height. Results: Final height SDS was significantly higher in group A ð20:45^0:36 (S.D.) vs 21:07^0:7; P ¼ 0:008Þ; as well as height gain SDS ð1:81^0:58 vs 1:23^0:62; P ¼ 0:002Þ: The difference between final height SDS and target height SDS was positive only in group A and significantly higher in group A than in group B ð0:33^0:51 vs 20:46^0:7; P ¼ 0:01Þ: Glucose tolerance was always normal in the group treated with higher doses. Conclusion: The final height of children treated with higher doses of rhGH is increased, also in relation to their genetic target. The economical burden of this choice of treatment, however, has to be taken into account when evaluating the results.

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“…Treatment of normal volunteers with GH doses similar to those used in TS (0.06 mg/kg/d) increased cardiac output and left ventricular mass in just 4 weeks (16). Finally, treatment of GH-deficient children with exogenous GH has been associated with disproportionate left ventricular growth (17,18). Given the cardiac involvement in TS there has been concern over potential adverse cardiovascular effects of GH treatment.…”

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confidence: 99%

“…Thus we confirm the earlier studies that lacked control groups with TS, and extended our own previous study showing no apparent effect of GH on aortic diameter in TS (26). It is curious that there seems to be no cardio-selective effect by GH in girls with TS, although GH treatment of GH-deficient children has been associated with disproportionate left ventricular growth (17,18). Perhaps this is because in GH deficiency there is a relative cardiac hypoplasia and associated catch-up growth with GH treatment.…”

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Growth Hormone Treatment and Left Ventricular Dimensions in Turner Syndrome

Matura

Sachdev

Bakalov

et al. 2007

The Journal of Pediatrics

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Objective-To determine if cardiac dimensions were different in girls with Turner syndrome (TS) that did receive growth hormone (GH) vs. those who did not receive GH.Study design-This was a retrospective, cross sectional study analyzing echocardiograms in 86 females with TS divided into GH-treated (n=67) vs. untreated (n=19) groups. These were subjects with TS participating in the National Institutes of Health protocol between 2001 and 2006.Results-The average age was 16.2 years (range 10-25 yrs) and duration of GH treatment was 4.4 (range 1-14 yrs). The GH-treated group was taller by ∼6 cm (P=0.004) but, cardiac dimensions normalized to body surface area (BSA), including septal and posterior wall thicknesses, left ventricular (LV) mass and LV internal diameters, were not significantly different in the two groups. The fractional shortening index was similar in the two groups. Multiple regression analyses indicated that BSA, but not duration of GH treatment predicted LV dimensions in girls with TS.Conclusions-GH treatment of girls with TS increases stature but does not disproportionately affect cardiac dimensions. Keywords echocardiography; growth hormone; cardiac dimensions; Turner Syndrome All correspondence to: Lea Ann Matura, CRC 10 Center Dr, NIH,, Bethesda, MD 20892, maturale@mail.nih.gov Disclosures: The authors have nothing to disclose and there are no conflict of interests. There is no potential conflict of interest, real or perceived, by the authors. The study was supported by a NIH grant. Lea Ann Matura wrote the first draft of the manuscript no honorarium, grant, or other form of payment was given to anyone to produce the manuscript.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Turner syndrome (45,X, TS) is the most common chromosomal disorder in females, occurring in ∼1/2500 live female births (1). Short stature and ovarian failure are the most prevalent findings, but the most medically significant feature is congenital heart disease with a high risk for aortic dilatation and dissection(2-4). In addition to anatomical defects, recent studies have demonstrated electrocardiographic abnormalities and evidence of autonomic and diastolic dysfunction in individuals with TS suggesting a more extensive involvement of the cardiovascular system than previously appreciated (5-8). Although girls with short stature in the context of TS are not usually growth hormone (GH) deficient, the FDA has approved treatment of these girls with recombinant human GH to augment adult height (9-12). Girls with TS are typically treated with GH for ∼5 years using pharmacological d...

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Medium-Term Cardiovascular Effects of High-Dose Growth Hormone Treatment in Growth Hormone-Deficient Children

Cited by 15 publications

References 19 publications

Cardiac Performance in Turner’s Syndrome Patients on Growth Hormone Therapy

Cardiac Performance in Turner’s Syndrome Patients on Growth Hormone Therapy

Treatment of GH-deficient children with two different GH doses: effect on final height and cost-benefit implications

Growth Hormone Treatment and Left Ventricular Dimensions in Turner Syndrome

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