Nutritional Rickets in Turkey

Özkan, Behzat

doi:10.5152/eajm.2010.24

Cited by 15 publications

(18 citation statements)

References 14 publications

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“…Vitamin D deficiency is the most common cause of nutritional rickets; a vitamin D level <20 ng/mL is defined as vitamin D deficiency (VDD). Until recently, rickets posed an important health problem in Turkey; however, its incidence decreased with the use of vitamin D prophylaxis (2,3).…”

Section: Introductionmentioning

confidence: 99%

Ghrelin Levels in Patients with Rickets

Şen

Demirol

et al. 2013

ELECTRON J GEN MED

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Section: Introductionmentioning

confidence: 99%

Ghrelin Levels in Patients with Rickets

Şen

Demirol

et al. 2013

ELECTRON J GEN MED

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“…The hypertrophic chondrocytes are subjected to calcification of the surrounding matrix, followed by vascularisation of the calcified tissue and accumulation of osteoclasts and osteoblasts. 2 In rickets, the resting and proliferative zones are unaffected. 25 Failure of apoptosis of the hypertrophic chondrocytes results in irregular and deformative expansion of the cartilage tissue formed by hypertrophic chondrocytes.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4] Nutritional rickets has been widely studied in terms of aetiologies, 3,4 variants, [5][6][7] clinical presentations, 8,9 and drug treatments [10][11][12] and responses. 13,14 The growth plates of the proximal femur develop rapidly during infancy and childhood.…”

Section: Introductionmentioning

confidence: 99%

Radiographic Changes in Nutritional Ricket Hips in Children in Response to Treatment

Agarwal

Talwar

2014

J Orthop Surg (Hong Kong)

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Purpose. To review radiographic changes in the proximal femurs of children of different ages during the course of treatment for nutritional rickets. Methods. Pelvic radiographs of 161 children aged ≤13 years with nutritional rickets were retrospectively reviewed. Patients were treated with dietary counselling and vitamin D and calcium supplementation. Patients were followed up at week 3 and thereafter at a 2-month interval until ulnar convexity was achieved. Sequential radiographs of the hips in children of different ages were reviewed for each growth plate in terms of (1) the direction of growth, (2) active areas, (3) contribution of growth, and (4) the structure of the epiphysis. Radiographs were superimposed for comparison by matching the triradiate cartilage and the ischial portion of the obturator foramen. Results. The direction of growth of the growth plates was from the physeal plate that is the longitudinal growth plate of the neck (LGP), the femoral neck isthmus (FNI), and the trochanteric growth plate (TGP) to the diaphyseal region, and from the perichondrium to the ossification centre in the proximal femoral epiphysis. Before the age Orthopaedic Surgery 2014;22(3):368-73 of one year, the growth zone of the proximal femur was homogenous, with no differentiation between the LGP, FNI, and TGP. By the age of 2 years, the differentiation was more clearly established; the FNI was usually smaller than the TGP and LGP. By the age of 3 years, the FNI became prominent and the TGP remained small. By the age of 4 years, the ossification centre of the greater trochanter appeared, and the LGP extended medially as a medial overhang (MOH). During the children's growth, the LGP, FNI, or TGP remained active to a variable extent and were distinct until the age of 6 years. Gradually, the periphery of the LGP became less active than the centre of the LGP and gave rise to the 'eye sign'. The MOH generally ceased to be active beyond the age 9 years. By the age of 12 years, the TGP and FNI were minimally active and only the centre of the LGP remained active. Conclusion. The mineralisation process of healing rickets provides a useful biological marker for patterns of growth. Knowledge of the quantitative contribution of various growth plates of the proximal femur in childhood may increase the understanding of the pathomechanism of hip deformations. Journal of

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“…Em um terceiro estágio, a deformidade óssea se acentua, ocorrendo alterações raquíticas graves; nesste estágio, a hipocalcemia e a hipofosfatemia tornamse evidentes. Além disso, acentuam-se a elevação das concentrações de FA e PTH e a diminuição das de 25(OH)D; as concentrações de 1,25(OH)D podem estar normais, aumentadas ou diminuídas 17,46 .…”

Section: Diagnósticounclassified

“…A baixa ingestão de alimentos ricos em VD pela população se soma como fator de risco para a deficiência desta vitamina 17,18,37,46 .…”

Section: A Prevalência De Dvd No Brasil E No Mundounclassified

Vitamina D em pediatria

Almeida¹,

Nogueira‐de‐Almeida²,

Ferraz³

2018

Int J Nutrol

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A vitamina D (VD) é uma das vitaminas lipossolúveis. Suas principais fontes na natureza são a dieta e a produção endógena mediada pela exposição à luz solar. Descobertas recentes mostraram que outros órgãos, que não o rim e o fígado, são também capazes de sintetizar a VD metabolicamente ativa (calcitriol). A deficiência de vitamina D (DVD) foi descrita há quase 2.000 anos e é classicamente relacionada às doenças do sistema ósteo-muscular (em especial, raquitismo e osteomalácia). Adicionalmente nos últimos anos, a DVD tem sido associada à desordens que acometem outros sistemas do organismo, como, por exemplo, asma e diabetes. Além disso, tem sido observada uma elevação da prevalência da DVD em todo o mundo, mesmo em países com boas condições de insolação. A forma mais adequada de prevenção da DVD se dá pela suplementação vitamínica já que não há limites seguros para a exposição solar. O tratamento da DVD baseia-se, principalmente, na reposição da vitamina e está indicado nas formas sintomáticas (sintomas ósteo-musculares) da carência. A intoxicação pela VD é rara e observada em lactentes e crianças jovens que ingerem doses elevadas de VD de forma aguda. Este artigo de revisão aborda estas e outras questões a respeito da VD, com ênfase especial às particularidades relacionadas às crianças e aos adolescentes. Palavras-chave:Colecalciferol. Lactente. Vitamina D. ABSTRACTVitamin D (VD) is one of the fat-soluble vitamins. Its main sources in nature are diet and exposure to sunlight. Recent findings have shown that organs other than the kidney and liver are also able to synthesize VD metabolically active (calcitriol). Vitamin D deficiency (VDD) has been described almost 2.000 years ago and is classically related to diseases of the musculoskeletal system (especially rickets and osteomalacia). However, in recent years, VDD has been linked to disorders that affect other systems in the body, such as asthma and diabetes. In addition, an increase in the prevalence of VDD worldwide has been observed, even in countries with good insolation conditions. The most appropriate way to prevent VDD is by vitamin supplementation since there are no safe limits to sun exposure.

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Nutritional Rickets in Turkey

Cited by 15 publications

References 14 publications

Ghrelin Levels in Patients with Rickets

Ghrelin Levels in Patients with Rickets

Radiographic Changes in Nutritional Ricket Hips in Children in Response to Treatment

Vitamina D em pediatria

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