Cardiac Functions in Children with Vitamin D Deficiency Rickets

Uysal, Serap; Kalaycı, Ayhan Gazi; Baysal, Kemal

doi:10.1007/s002469900464

Cited by 98 publications

(66 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Several case reports highlight pediatric cardiomyopathies, which are associated with vitamin D deficiency or rickets [73][74][75][76][77][78][79][80][81]. Importantly, children with vitamin D deficiency associated heart failure showed in most cases a significant clinical improvement after vitamin D and calcium supplementation [73][74][75][76][77][78][79][80].…”

Section: Vitamin D and Myocardial Dysfunction In Humans 71 Vitamin Dmentioning

confidence: 99%

“…Importantly, children with vitamin D deficiency associated heart failure showed in most cases a significant clinical improvement after vitamin D and calcium supplementation [73][74][75][76][77][78][79][80]. A post mortem examination of a child who died due to vitamin D deficiency associated cardiomyopathy showed a large pericardial effusion and an enlarged heart with a dilated and concentric hypertrophic left ventricle [73].…”

Section: Vitamin D and Myocardial Dysfunction In Humans 71 Vitamin Dmentioning

confidence: 99%

See 1 more Smart Citation

Vitamin D deficiency and myocardial diseases

Pilz

Tomaschitz

Drechsler

et al. 2010

Molecular Nutrition Food Res

135

142

View full text Add to dashboard Cite

Vitamin D deficiency is common among patients with myocardial diseases because sun-induced vitamin D production in the skin and dietary intake of vitamin D is often insufficient. Knockout mice for the vitamin D receptor develop myocardial hypertrophy and dysfunction. It has also been shown that children with rickets who suffered from severe heart failure could be successfully treated with supplementation of vitamin D plus calcium. In adults, almost all patients with heart failure exhibit reduced 25-hydroxyvitamin D levels, which are used to classify the vitamin D status. In prospective studies, vitamin D deficiency was an independent risk factor for mortality, deaths due to heart failure and sudden cardiac death. Several vitamin D effects on the electrophysiology, contractility, and structure of the heart suggest that vitamin D deficiency might be a causal factor for myocardial diseases. Data from interventional trials, however, are rare and urgently needed to elucidate whether vitamin D supplementation is useful for the treatment of myocardial diseases. In our opinion, the current knowledge of the beneficial effects of vitamin D on myocardial and overall health strongly argue for vitamin D supplementation in all vitamin D-deficient patients with or at high risk for myocardial diseases.

show abstract

Section: Vitamin D and Myocardial Dysfunction In Humans 71 Vitamin Dmentioning

confidence: 99%

Section: Vitamin D and Myocardial Dysfunction In Humans 71 Vitamin Dmentioning

confidence: 99%

Vitamin D deficiency and myocardial diseases

Pilz

Tomaschitz

Drechsler

et al. 2010

Molecular Nutrition Food Res

135

142

View full text Add to dashboard Cite

show abstract

“…We of course also had to be completely open to potential harmful effects. The origins of a direct or indirect link between vitamin D and cardiac structure and function emanated from observations of heart failure in children with rickets and their recovery following therapy with vitamin D, 46,47 and early experiments examining the cardiovascular effects of vitamin D-deficient animals. 48 Since then, other investigators have examined the effects of vitamin D on the cardiovascular system, including on ventricular myocytes 49 and in vitamin D receptor null mice.…”

mentioning

confidence: 99%

Is Calcitriol Life-Protective for Patients with Chronic Kidney Disease?

Thadhani¹

2009

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

In nephrology we are frequently confronted with association studies reporting novel biomarkers or mediators. Which among the myriad of potential candidates are amenable to intervention and, thereafter, which do we carry forward into clinical trials? Our group and others have considered the potential of vitamin D. Before commenting on vitamin D in chronic kidney disease, lessons learned from Alfred Sommer's initial observational studies and subsequent clinical trials with vitamin A-a journey of humility and perseverance-are worthy of reminder.Alfred Sommer, Dean Emeritus of the Johns Hopkins Bloomberg School of Public Health, received the Lasker Award in 1997 for his seminal work showing vitamin A deficiency is linked to increased risk of mortality and for demonstrating that correcting this deficiency reduces mortality. His series of studies started as simple observations, which led to community-based randomized trials. When Sommer initiated his work, vitamin A deficiency was highly prevalent, yet the connection between vitamin A deficiency and mortality had not been established. With the intent of examining night-blindness and dry eyes, Sommer and his colleagues stumbled across the observation that death rates in children with these ophthalmic conditions were several-fold higher than children without these conditions. 1 When Sommer first published his prospective observational study linking vitamin A deficiency with a 16% increased risk in mortality, 2 the field hardly took notice. As he articulated in a commentary written at the time of winning the Lasker, "The initial report associating vitamin A deficiency with increased mortality was received with deafening silence." 1 This response, as we know all too well, is common.Treatment with activated vitamin D, or calcitriol [1,25(OH) 2 D 3 ], has been used for over three decades to manage the secondary hyperparathyroidism and hypocalcemia accompanying chronic renal disease. [3][4][5][6] This intervention markedly changed the management of renal osteodystrophy, historically a severe debilitating condition. 7,8 By the late 1990s our attention in nephrology turned to altered mineral metabolism and its relationship to adverse outcomes. 9 The classic role for 1,25(OH) 2 D 3 is to maintain calcium homeostasis. 10 As an expected "side effect," it also raises serum levels of phosphate. 11 We were keenly interested in understanding the contribution of 1,25(OH) 2 D 3 to alterations in serum minerals and whether these alterations associated with increased mortality. In this effort, we accidentally came across a rather strong and consistent association between activated vitamin D therapy and reduced mortality, a finding independent of alterations in serum minerals. 12,13 Linking vitamin D therapy with altered minerals, and the two with increased mortality, would have "fit the prevailing paradigm" 1 and would have been more easily accepted. Speculating that 1,25(OH) 2 D 3 compounds-such as retinoic acid that activates nuclear receptors and leads to changes in gene transcription...

show abstract

“…Vitamin D 3 could overcome these processes, promoting, for example, synthesis of anti-inflammatory cytokines [4]. Severe vitamin D 3 deficiency in humans is associated with cardiomyopathy [52], and in a number of large epidemiologic studies, the association of increased cardiovascular disease risk with low vitamin D 3 blood levels has been found [53]. Obesity, a condition associated with cardiovascular disease [54], is related with a low vitamin D 3 status due to a sequestration and volumetric dilution of the lipophilic vitamin D 3 in the fat tissue [3,55,56].…”

Section: Cardiovascular and Cerebral Riskmentioning

confidence: 99%

Vitamin D in Oxidative Stress and Diseases

Uberti¹,

Morsanuto²,

Molinari³

2017

A Critical Evaluation of Vitamin D - Basic Overview

View full text Add to dashboard Cite

The data described in this chapter consider some new information about the benefits of vitamin D 3 comparing the results obtained by the authors on the effects of vitamin D 3 during oxidative stress with other works available in the literature. In particular, vitamin D 3 can induce a concentration-dependent increase in endothelial NO production through eNOS activation consequential to the phosphorylation of p38, AKT, and ERK. Additional information obtained by the author is about the ability of vitamin D 3 to prevent the endothelial cell death through modulation of interplay between apoptosis and autophagy. This effect is obtained by inhibiting superoxide anion generation, maintaining mitochondria function and cell viability, activating survival kinases (ERK and Akt), and inducing NO production. The results also describe that vitamin D 3 causes human endothelial cell proliferation and migration in a 3-D matrix through NOdependent mechanisms. These findings support the role of vitamin D 3 in the human angiogenic process, suggesting new applications for vitamin D 3 in tissue repair and wound healing. Finally, that the authors have demonstrated the ability of vitamin D 3 to counteract negative effects of oxidative stress in brain cells. These data suggest the potential therapeutic use of vitamin D to treat or prevent degenerative brain diseases.

show abstract

Cardiac Functions in Children with Vitamin D Deficiency Rickets

Cited by 98 publications

References 14 publications

Vitamin D deficiency and myocardial diseases

Vitamin D deficiency and myocardial diseases

Is Calcitriol Life-Protective for Patients with Chronic Kidney Disease?

Vitamin D in Oxidative Stress and Diseases

Contact Info

Product

Resources

About