Left ventricular mass and function in children with GH deficiency before and during 12 months GH replacement therapy

Salerno, Mariacarolina; Esposito, V.; Spinelli, Letizia; Somma, Carolina Di; Farina, Vincenzo; Muzzica, Stefania; Horatio, Laura Tanturri de; Lombardi, Gaetano; Colao, Annamaria

doi:10.1111/j.1365-2265.2004.02026.x

Cited by 54 publications

(40 citation statements)

References 60 publications

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“…In the prospective, uncontrolled study of Shulman et al, [24] , 10 prepubertal children (mean age 5.7 ± 2.7 years; 5 IGHD/5 MPHD (7 with abnormal pituitary gland on MRI and 3 idiopathic) had reduced left ventricular mass that significantly increased after 1 year of GH treatment without any changes in cardiac function, findings similar to those reported by Metwalley et al [25] and Salerno et al [26,27] . In the followup by Salerno's group, a 2-year prospective case-control study involving 30 prepubertal children with GHD (27 IGHD and 3 MPHD) compared to healthy children matched by age, sex, BSA, and BMI, reduced left ventricular mass normalized after the first year of GH treatment and improvement in left ventricular mass positively correlated with the increase in IGF-I levels [26] .…”

Section: Guiding Principlessupporting

confidence: 76%

Guidelines for Growth Hormone and Insulin-Like Growth Factor-I Treatment in Children and Adolescents: Growth Hormone Deficiency, Idiopathic Short Stature, and Primary Insulin-Like Growth Factor-I Deficiency

DiVall²,

et al. 2016

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Background/Aims: On behalf of the Drug and Therapeutics, and Ethics Committees of the Pediatric Endocrine Society, we sought to update the guidelines published in 2003 on the use of growth hormone (GH). Because idiopathic short stature (ISS) remains a controversial indication, and diagnostic challenges often blur the distinction between ISS, GH deficiency (GHD), and primary IGF-I deficiency (PIGFD), we focused on these three diagnoses, thereby adding recombinant IGF-I therapy to the GH guidelines for the first time. Methods: This guideline was developed following the GRADE approach (Grading of Recommendations, Assessment, Development, and Evaluation). Results: This guideline provides recommendations for the clinical management of children and adolescents with growth failure from GHD, ISS, or PIGFD using the best available evidence. Conclusion: The taskforce suggests that the recommendations be applied in clinical practice with consideration of the evolving literature and the risks and benefits to each individual patient. In many instances, careful review highlights areas that need further research.

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Section: Guiding Principlessupporting

confidence: 76%

Guidelines for Growth Hormone and Insulin-Like Growth Factor-I Treatment in Children and Adolescents: Growth Hormone Deficiency, Idiopathic Short Stature, and Primary Insulin-Like Growth Factor-I Deficiency

DiVall²,

et al. 2016

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“…Whereas GH therapy may be associated with neurodevelopmental and cardiovascular improvements, more research is needed to elucidate these benefits in the CRI population [60,61]. Several studies have already documented the important role of GH in maintaining cardiovascular health in children and adolescents with GHD [62][63][64].…”

Section: Efficacy Of Gh Therapy In Children With Ckdmentioning

confidence: 96%

Assessment and treatment of short stature in pediatric patients with chronic kidney disease: a consensus statement

Mahan

Warady

Fielder³

et al. 2006

Pediatr Nephrol

176

140

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Growth failure is a clinically important issue in children with chronic kidney disease (CKD) and is associated with significant morbidity and mortality. Many factors contribute to impaired growth in these children, including abnormalities in the growth hormone (GH)-insulin-like growth factor-I (IGF-I) axis, malnutrition, acidosis, and renal bone disease. The management of growth failure in children with CKD is complicated by the presence of other disease-related complications requiring medical intervention. Despite evidence of GH efficacy and safety in this population, some practitioners and families have been reluctant to institute GH therapy, citing an unwillingness to comply with daily injections, reimbursement difficulties, or impending renal transplantation. Suboptimal attention to growth failure management may be further compounded by a lack of clinical guidelines for the appropriate assessment and treatment of growth failure in these children. This review of growth failure in children with CKD concludes with an algorithm developed by members of the consensus committee, outlining their recommendations for appropriate steps to improve growth and overall health outcomes in children with CKD.

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“…St€ ollberger and Finsterer [this issue] also raised the question of previous growth hormone therapy (GHT) as a possible causative agent for the LVNC. Although growth hormone may cause myocardial cell hypertrophy [Salerno et al, 2004], we are not aware of any documented occurrence of LVNC from such hormone therapy. In our patient, GHT was instituted over a decade ago, and therefore the possible linkage seems quite remote since myocardial hypertrophy during GHT is reportedly reversed after cessation of the therapy [Lipshultz et al, 2005].…”

Section: To the Editormentioning

confidence: 99%

Response to Drs. Stöllberger and Finsterer “Noncompaction Is Already Known in DiGeorge Anomaly From 22q11.2 Deletion Syndrome”

Madan

Madan‐Khetarpal

Park

et al. 2010

American J of Med Genetics Pt A

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We appreciate the insightful and relevant comments of Drs. Claudia St€ ollberger and Josef Finsterer [2011] on our report ''Left ventricular non-compaction on MRI in a patient with 22q11.2 distal deletion'' [Madan et al., 2010].Our patient had dysmorphic features, cardiac manifestations including left ventricular non-compaction (LVNC), and a 22q11.2 distal deletion encompassing the BCR gene. He does not have the well-known velocardiofacial (VCF)/DiGeorge syndrome, which presents as a 22q11.2 deletion in the proximal region and encompasses the TBRX gene. The TBRX region was not deleted in our patient. The literature describes deletions similar to those found in our patient and they are now recognized as the 22q11.2 distal deletion syndrome. Thus the VCF/DiGeorge syndrome and 22q11.2 distal deletion syndromes are clinically and genetically distinct syndromes [Ben-Shachar et al., 2008].As indicated in our report, the patient was followed at our institution for bicuspid aortic valve with both dilated aortic root and ascending aorta. The serial echocardiograms performed over the years showed no apparent diagnostic features of LVNC, and even retrospective reviews were still inconclusive. As the patient matured, the aortic arch could not be visualized well by echocardiography, and therefore cardiac magnetic resonance imaging (CMRI) was performed. For this reason, we stated that the CMRI was superior to echocardiography in this particular case, as reported in the past [Alhabshan et al., 2005]. However, most of our other LVNC patients have shown compatible findings between CMRI and echocardiography, as previously noted by St€ ollberger et al. [2008].The ratio of non-compacted to compacted myocardium (NC/C ratio) in diastole was calculated in the segment with the most pronounced trabeculations on the steady-state free precession (SSFP) cine images in each of the three long-axis views (horizontal, vertical long-axis, and LV outflow tract) as described by Petersen et al. [2005]. A NC/C ratio of >2.3 distinguished pathological non-compaction. The patient's echocardiograms showed reasonable left ventricular myocardial function with ejection fraction of 54% and shortening fraction of 28-29%. Serial electrocardiograms (ECG) were unremarkable and showed no evidence of chamber enlargement, ST-T changes, or conduction abnormality. A recent Holter monitor showed rare isolated premature atrial contractions, but no other abnormal findings.The patient has an active lifestyle and has had no significant cardiac symptoms such as exercise intolerance, dizziness, or syncope. Despite mild mental retardation, he is quite independent and

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Left ventricular mass and function in children with GH deficiency before and during 12 months GH replacement therapy

Abstract: GH deficiency in children affects heart morphology, by inducing a significant decrease in cardiac size, but does not modify cardiac function and lipid profile. Twelve months of GH replacement treatment normalizes cardiac mass, and reduces the atherogenic index.

Cited by 54 publications

References 60 publications

Guidelines for Growth Hormone and Insulin-Like Growth Factor-I Treatment in Children and Adolescents: Growth Hormone Deficiency, Idiopathic Short Stature, and Primary Insulin-Like Growth Factor-I Deficiency

Guidelines for Growth Hormone and Insulin-Like Growth Factor-I Treatment in Children and Adolescents: Growth Hormone Deficiency, Idiopathic Short Stature, and Primary Insulin-Like Growth Factor-I Deficiency

Assessment and treatment of short stature in pediatric patients with chronic kidney disease: a consensus statement

Response to Drs. Stöllberger and Finsterer “Noncompaction Is Already Known in DiGeorge Anomaly From 22q11.2 Deletion Syndrome”

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