Vitamin D, calcium or a combination of vitamin D and calcium for the treatment of nutritional rickets in children.
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ABSTRACT:
SUBMITTER: Chibuzor MT
PROVIDER: S-EPMC7164979 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:To determine whether children with calcium-deficiency rickets have a better response to treatment with vitamin D and calcium than with calcium alone.Randomised controlled trial.Jos University Teaching Hospital, Jos, Nigeria.Nigerian children with active rickets treated with calcium carbonate as limestone (approximately 938 mg elemental calcium twice daily) were, in addition, randomised to receive either oral vitamin D2 50,000?IU (Ca+D, n=44) or placebo (Ca, n=28) monthly for 24?weeks.Achievement of a 10-point radiographic severity score ?1.5 and serum alkaline phosphatase ?350?U/L.The median (range) age of enrolled children was 46 (15-102) months, and baseline characteristics were similar in the two groups. Mean (±SD) 25-hydroxyvitamin D (25(OH)D) was 30.2±13.2?nmol/L at baseline, and 29 (43%) had values <30?nmol/L. Baseline alkaline phosphatase and radiographic scores were unrelated to vitamin D status. Of the 68 children (94% of original cohort) who completed 24?weeks of treatment, 29 (67%) in the Ca+D group and 11 (44%) in the Ca group achieved the primary outcome (p=0.06). Baseline 25(OH)D did not alter treatment group effects (p=0.99 for interaction). At the end of 24?weeks, 25(OH)D values were 55.4±17.0?nmol/L and 37.9±20.0?nmol/L in the Ca+D and Ca groups, respectively, (p<0.001). In the Ca+D and Ca groups, the final 25(OH)D concentration was greater in those who achieved the primary outcome (56.4±17.2?nmol/L) than in those who did not (37.7±18.5?nmol/L, p<0.001).In children with calcium-deficiency rickets, there is a trend for vitamin D to improve the response to treatment with calcium carbonate as limestone, independent of baseline 25(OH)D concentrations.ClinicalTrials.gov NCT00949832.
| S-EPMC4145444 | biostudies-literature
Project description:This review describes the pathogenesis, clinical presentation and biochemical perturbations found in privational (nutritional) rickets and pseudo-vitamin D deficiency rickets (PDDR), an autosomal recessive condition with loss of function mutations in CYP27B1. It may seem strange to combine a discussion on privational rickets and PDDR as a single topic, but privational rickets and PDDR present with similar clinical signs and symptoms and with similar perturbations in bone and mineral metabolism. Of interest is the characteristic lack of features of rickets at birth in infants with PDDR, a finding which has also been reported in infants born to vitamin D-deficient mothers. This highlights the independence of the fetus and neonate from the need for vitamin D to maintain calcium homeostasis during this period. The variable roles of vitamin D deficiency and dietary calcium deficiency in the pathogenesis of privational rickets are discussed and the associated alterations in vitamin D metabolism highlighted. Although PDDR is a rare autosomal recessive disorder, results of long-term follow-up are now available on the effect of treatment with calcitriol, and these are discussed. Areas of uncertainty, such as should affected mothers breastfeed their infants, are emphasized.
| S-EPMC4015456 | biostudies-other
Project description:OBJECTIVES:A high prevalence of rickets of unknown aetiology has been reported in Chakaria, Bangladesh. Classically, rickets is caused by vitamin D deficiency but increasing evidence from Africa and Asia points towards other nutritional deficiencies or excessive exposure to some metals. The aim of this study was to investigate the aetiology of rickets in rural Bangladeshi children. METHODS:64 cases with rickets-like deformities were recruited at first presentation together with age-sex-village matched controls. Data and sample acquisition included anthropometry, radiographs, fasted plasma and urinary samples, 24 h weighed dietary intake together with a 24 h urine collection, and 13C-breath tests to detect Helicobacter (H.) pylori infection. RESULTS:One child had active rickets and frank hypovitaminosis D (F, n = 1) and one had deformities with radiological features of Blount disease (M, n = 1). The remaining cases were grouped into those with active rickets, defined as a radiographic Thacher score ?1.5 (Group A, n = 24, 12M, 12F) and rickets-like bone deformities but not active rickets (Group B, n = 38, 28M, 10F). All children had a low dietary calcium intake, but this was lower in Group A than their controls (mean (SD): 156 (80) versus 323 (249) mg/day, p = 0.005). Plasma 25-hydroxyvitamin D (25OHD) was lower in Group A compared to controls; 63% of Group A and 8% of controls had a concentration <25 nmol/L (p ? 0.0001). There was, however, no evidence of differences in skin sunshine exposure. Group A had lower plasma calcium and phosphate and higher 1,25-dihydroxyvitamin D (1,25(OH)2D) and parathyroid hormone (PTH). 88% of Group A and 0% of controls had undetectable plasma intact fibroblast growth factor (iFGF23), with c-terminal FGF23 (cFGF23) concentrations in the normal range. Urinary phosphate and daily outputs of environmental metals relative to creatinine were higher and tubular maximal phosphate reabsorption per unit glomerular filtration rate (TmP/GFR) was lower in Group A compared to controls. Although less pronounced than Group A, Group B had higher alkaline phosphatase, 1,25(OH)2D and PTH concentrations than controls but similar calcium intake, TmP/GFR, iFGF23 and cFGF23 concentrations. Mean 25OHD concentrations were also similar to controls and there was no significant difference in the percentage <25 nmol/L (Group B: 13%, controls: 5%, p = 0.2) No group differences were seen in prevalence of anaemia, iron deficiency or H. pylori infection. CONCLUSION:Nutritional rickets in this region is likely to be predominantly due to low calcium intake in the context of poor vitamin D status and exposure to environmental metals, but not H. pylori infection, anaemia or iron deficiency.
| S-EPMC7262584 | biostudies-literature
Project description:Introduction. Rickets is softening of bones caused by defective mineralization of the cartilage in the epiphyseal growth plate, causing widening of the ends of long bones, growth retardation, and skeletal deformities in children. It can be classified into calciopenic and phosphopenic, each type with various subclasses. Case Presentations. We presented 2 cases, first of a 1 year and 4-month-old male, with a history of recurrent episodes of cough for 8 months and bowing of the legs 6 months prior to admission. Clinical and laboratory investigation was suggestive of vitamin D-dependent rickets, and he started vitamin D treatment with minimal response. The second case is of a 4 years and 7-month-old male who presented with developmental delay, poor weight gain, and recurrent chest infection and worsening of bone pain since 9 months of age. Laboratory investigation was suggestive of phosphopenic rickets, and he was started on treatment at 9 months of age with little improvement and at 4 years, he sustained multiple fractures and succumbed to severe respiratory tract infection and died at 4 years and 7 months of age. Conclusion:Rickets pose a diagnostic and treatment challenge in resource-limited countries, and clinical judgment and early initiation of treatment are important.
| S-EPMC7008276 | biostudies-literature
Project description:The story of rickets leading to the discovery of vitamin D is an extraordinary tale, spread over many centuries and involving some remarkable characters with much speculation and a few mysteries, before reaching an exciting climax. It would be wrong to credit a single person as discovering rickets or being the first to describe its features, for reasons that will be set out here. Yet the emergence of the term 'rickets' is as important as the discovery of vitamin D itself and the possible causes of its deficiency. It permitted identification of a hitherto ill-defined disease entity, typically occurring in infants and children. It also provided a way for deciding if features of diseases that had been described earlier in the history of medicine could be seen as the symptoms and signs of related conditions.
| S-EPMC3899557 | biostudies-other
Project description:The term "vitamin D dependent rickets" describes a group of genetic disorders that are characterized by early-onset rickets due to the inability to maintain adequate concentrations of active forms of vitamin D or a failure to respond fully to activated vitamin D. Although the term is now admittedly a pathophysiological misnomer, there remains clinical relevance for its continued use, as patients have a lifelong "dependency" on administration of specialized regimens of vitamin D replacement. This review provides an update on the molecular bases for the three forms of vitamin D dependent rickets, and summarizes current protocols for management of affected subjects.
| S-EPMC7303887 | biostudies-literature
Project description:Heterogeneous loss of function mutations in the vitamin D receptor (VDR) interfere with vitamin D signaling and cause hereditary vitamin D-resistant rickets (HVDRR). HVDRR is characterized by hypocalcemia, secondary hyperparathyroidism and severe early-onset rickets in infancy and is often associated with consanguinity. Affected children may also exhibit alopecia of the scalp and total body. The children usually fail to respond to treatment with calcitriol; in fact, their endogenous levels are often very elevated. Successful treatment requires reversal of hypocalcemia and secondary hyperparathyroidism and is usually accomplished by administration of high doses of calcium given either intravenously or sometimes orally to bypass the intestinal defect in VDR signaling.
| S-EPMC4015455 | biostudies-literature
Project description:ObjectivesPoor vitamin D status has been reported to be highly prevalent in many non-western immigrant groups living in Norway and other western countries. However, data on rickets are scarce, and the aim of the current study was to identify new cases of nutritional rickets in Norway in the period 2008-2012 among children under the age of 5 years.DesignRegister-based cohort study.SettingThe Norwegian population from 2008 to 2012.ParticipantsChildren with nutritional rickets under the age of 5 years.Main outcome measureNutritional rickets. Patients with ICD10 (International Statistical Classification of Diseases and Related Health Problems, 10th revision) diagnosis code E55.0 (active rickets) treated at all Norwegian hospitals were identified in the Norwegian Patient Registry. We were able to review 85% of the medical records for diagnosis confirmation. In addition, we identified patients with the diagnoses E55.9, E64.3 and E83.3 to identify individuals with rickets who had been given other diagnoses.ResultsNutritional rickets was confirmed in 39 children aged 0-4 years with the diagnosis of E55.0. In addition, three patients with the diagnosis of unspecified vitamin D deficiency (E55.9) were classified as having nutritional rickets, giving a total of 42 patients. Mean age at diagnosis was 1.40 years (range 0.1-3.5 years), and 93% had a non-western immigrant background. The incidence rate of rickets was estimated to be 0.3 per 10 000 person-years in the total Norwegian child population under the age of 5 years and 3.1 per 10 000 person-years in those with an immigrant background from Asia or Africa.ConclusionThe number of children with nutritional rickets in Norway remained low in the period 2008-2012. Nearly all children had a non-western immigrant background.
| S-EPMC5729986 | biostudies-literature
Project description:Calcium is an important nutrient for child development. The main objective of this study was to assess calcium intake and its adequacy with dietary reference intake (DRI) in Spanish children. The ANIVA (Antropometría y Nutrición Infantil de Valencia) study is a descriptive cross-sectional study. During two academic years 2013-2014 and 2014-2015, 1176 schoolchildren aged 6-9 years were selected from 14 primary schools in Valencia (Spain). Three-day food records were used to assess dietary intake, completed by parents/guardian. Anthropometric data (weight and height) were evaluated in all subjects. Nutritional intake was compared to estimated average requirements (EARs) and adequate intake (AI) values to determine nutritional adequacy. A percentage of 25.77% had inadequate calcium intake, and a significantly higher prevalence was observed in girls (p = 0.006). Adequate calcium intake showed a positive association with the height z-score (p = 0.032). When assessing dietary patterns, schoolchildren with adequate calcium intakes had better nutritional adequacy in all nutrients, except cholesterol (p = 0.086) and fluorine (p = 0.503). These results suggest a public health problem that must be addressed through nutrition education programs to increase intake of calcium-rich food and to correct the associated dietary pattern.
| S-EPMC5331601 | biostudies-literature
Project description:Hereditary hypophosphatemic rickets represented by X-linked hypophosphatemic rickets (XLH) is a rare disorder characterized by hypophosphatemia, elevated alkaline phosphatase (ALP) and undermineralization of bone. Active vitamin D and phosphate are administered to correct hypophosphatemia and elevation of ALP. Overtreatment with phosphate leads to secondary hyperparathyroidism, and a large dose of active vitamin D has a risk of hypercalciuria. To understand the situation concerning treatment of patients with hereditary hypophosphatemic rickets in Japan, we conducted a questionnaire survey of pediatric endocrinologists. Answers were obtained from 53 out of 68 hospitals where the pediatric endocrinologists worked. One hundred and thirty-five patients were treated in 28 hospitals during November 2009 and May 2010; 126 patients suffered from hereditary hypophosphatemic rickets, and 9 had hypophosphatemia caused by other miscellaneous reasons. The distribution of patient age was as follows: 27 (21%) were between 6 mo and 6 yr of age, 39 (31%) were between 6 and 12 yr of age, and 60 (48%) were more than 12 yr of age. Active vitamin D was given to 123 patients, and phosphate was given to 106 patients. As for the dose of phosphorus, 37.2-58.1 mg/kg/d was given divided into 2 to 6 aliquots. There were various control targets of treatment, including serum phosphate, serum ALP, rachitic change, urinary Ca/Cr, parathyroid hormone and growth. It is very important to avoid side effects of these treatments. No evidence is available about the optimal dose of phosphate or number of administrations in the treatment of patients with hypophosphatemic rickets. Although there is a recommendation for clinical management of patients with hypophosphatemic rickets, we should set a clinical guideline for it in Japan.
| S-EPMC3748281 | biostudies-literature