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At least 451 records · Page 25Linked to original sources
PubMed2000

Bone turnover in children with vitamin D deficiency rickets before and during treatment.

UNLABELLED: Biochemical markers of bone formation [alkaline phosphatase, osteocalcin, and carboxyterminal propeptide of type I procollagen (PICP)] and bone resorption [cross-linked carboxyterminal telopeptide of type I collagen (ICTP) and cross-linked N-telopeptides of type I collagen (NTX)] were measured in 14 children aged 8.5-10.5 mo with vitamin D deficiency rickets before and longitudinally during vitamin D treatment (3000-4000 IU/daily). Forty-four healthy children aged 8-10.5 mo were enrolled as sex- and age-matched controls. Before treatment, serum levels of alkaline phosphatase, PICP, and ICTP, and urinary excretion values of NTX were significantly higher, and serum osteocalcin levels significantly lower than controls (31.4 +/- 3.5 microkat/L and 9.8 +/- 2.9 microkat/L, p < 0.001; 1025 +/- 89 microg/L and 952 +/- 97.4 microg/L, p < 0.02; 15.6 +/- 2.6 microg/L and 14.2 +/- 1.3 microg/L, p < 0.01; 370.7 +/- 109.4 nmol BCE and 201.8 +/- 69.2 nmol BCE, p < 0.001: 17.6 +/- 9.1 microg/L and 22.5 +/- 7.6 microg/L, p < 0.05, respectively). During treatment, serum alkaline phosphatase levels progressively declined in association with the radiographic healing of the skeletal lesions. Serum levels of osteocalcin, PICP, and ICTP, and urinary excretion values of NTX showed a transient but significant (p < 0.05 to p < 0.001) increase in comparison with baseline values during the first 2-4 wk of treatment, and decreased slowly thereafter. They were within the mean +/- 2 SD of controls before the recovery of the skeletal lesions. CONCLUSIONS: These findings suggest that children with vitamin D deficiency rickets have increased bone turnover before and during the first weeks of treatment. Alkaline phosphatase is a more reliable marker than osteocalcin, PICP, ICTP and NTX for diagnosing and monitoring these patients.

Alkaline Phosphatase↗
PubMed2003

Congenital rickets.

Although rickets in premature newborns is known to occur, term babies presenting at birth is uncommon. We report a term baby born to a mother with osteomalacia, and presented at birth with signs of florid rickets which was confirmed biochemically. After 4 weeks of treatment, radiological signs of healing were seen.

Female↗
PubMedDate not supplied

Knee angles and rickets in nigerian children.

Knee angles of 2,036 normal Nigerian children up to 12 years old were measured directly or from photographs. The knees were bowed (varus) in the first 6 months. At 21 to 23 months, the distribution of angles became strongly bimodal: about half were varus and half were valgus (knock-kneed), with few in between. After this they were all valgus, with few exceptions. Hence, the change from varus to valgus in individual infants must be sudden (a few weeks), although the changeover of the whole population appears smooth and gradual. They became maximally and uniformly knock-kneed (-7.1 degrees +/- 1.4 degrees) between 3 and 3.5 years, with little change thereafter. On the other hand, 120 patients with rickets discovered during screening had large knee angles, in either sense, with a bimodal distribution and frequency maxima at +10 degrees (varus) and -12 degrees (valgus). Varus knee is uncommon after 2 years. Large knee angles between 2 and 5 years suggest rickets.

Age Factors↗
PubMedDate not supplied

Arginine-induced insulin and growth hormone secretion in children with nutritional rickets.

We evaluated arginine-induced insulin and growth hormone (GH) secretion in ten children with vitamin D deficiency rickets and compared these values with those of eight age-matched control children. All rachitic children had biochemical (increased serum alkaline phosphatase activity and decreased calcium x phosphate product) and clinical evidence for rickets. After an intravenous infusion of arginine-HCl (10% solution, 0.5 g/kg), blood samples were obtained for the measurement of serum insulin and GH concentrations. The mean insulin level 30 min after the start of the infusion was 22.2 +/- 17.1 microU/ml for the rachitic children. This value is significantly below that for the normal children, 63.4 +/- 38.7 microU/ml (p = 0.004). Neither the fasting insulin level nor any others after the arginine infusion differed significantly from those for the control children. There were no significant differences in the fasting or the arginine-stimulated GH levels between the rachitic and control children. The concentrations of insulin-like growth factors did not differ between the two groups.

Alkaline Phosphatase↗
PubMedDate not supplied

Rickets.

Nutritional (vitamin D deficiency) rickets is now a rarity in the industrial world because of food fortification. Most cases result from hereditary inborn errors of vitamin D metabolism or end-organ unresponsiveness as is exemplified in this case of hypophosphatemic rickets.

Child, Preschool↗
PubMed1998

The importance of 25-hydroxyvitamin D3 1 alpha-hydroxylase gene in vitamin D-dependent rickets.

Vitamin D plays a role in a wide variety of biological events such as calcium homeostasis, bone formation and cellular differentiation. An active form of vitamin D acting as a ligand specific vitamin D receptor (VDR), 1 alpha,25(OH)2D3, is biosynthesized from cholesterol, and during this biosynthesis a renal 25-hydroxylation at the final stage by 25-hydroxyvitamin D3 1 alpha-hydroxylase is critical. Recent studies isolated the cDNA encoding 1 alpha-hydroxylase from several species, and revealed that this enzyme belongs to a member of the cytochrome p450 enzyme superfamily, with highest homologies to the p450 hydroxylases for vitamin D derivatives. One of three kinds of hereditary rickets (vitamin D-dependent rickets type I) displays an autosomal recessive trait and clinical features consistent with a defect of 1 alpha-hydroxylase activity, and the genetic analysis of the type I patients identified missense mutations of the 1 alpha(OH)ase gene that results in a loss of this enzymatic activity.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed2003

Anemia and hepatosplenomegaly as presenting features in a child with rickets and secondary myelofibrosis.

Anemia and hepatosplenomegaly are common reasons for referring a child to a pediatric hematologist or oncologist. Among the many causes for these findings is severe rickets, which has been shown to be associated with secondary myelofibrosis and myeloid metaplasia. The authors present the case of an infant with severe rickets and secondary myelofibrosis and review the differential diagnosis of hepatosplenomegaly from the viewpoint of the pediatric hematologist/oncologist.

Anemia↗
PubMed2006

Rickets in an adolescent girl.

The authors present a case of rickets in an adolescent girl who presented to the emergency department with bone pain. Emergency department staff should be aware that rickets is not just a disease of early childhood.

Adolescent↗
PubMed2006

Nutritional rickets: beyond the chief complaint.

In the emergency department, opportunities exist for the emergency physician to make a diagnosis beyond the chief complaint. For example, an astute reader of pediatric radiographs may detect signs of rickets on plain films that are obtained for other reasons. Risk factors that should suggest nutritional rickets in an infant include a history of exclusive breast-feeding, time of presentation in late winter or early spring, and a physical examination that reveals pigmented skin.

Humans↗
PubMed1981

Vitamin D deficiency rickets simulating child abuse.

This paper describes a 2 1/2-year-old Bengali child who presented with failure to thrive and was found to have several fractures of the extremities. The skull radiographs showed widening of the sutures and fracture-like appearances. However, there was no evidence of a subdural haematoma. Minor rachitic changes were at first disregarded, and he was assumed to have been neglected and to have sustained nonaccidental injury. He was discharged to foster parents. It was eventually recognised that the skeletal changes were all appearances of rickets and that some of the fractures were in fact pseudofractures. The child returned to his own parents at the age of 4. Malnutrition, a well known consequences of rickets, may make interpretation of radiographs of the epiphyses difficult.

Battered Child Syndrome↗
PubMedDate not supplied

Nutritional rickets.

Over a 2-year period, the Orthopaedic Service at the Cincinnati (OH) Children's Hospital Medical Center noted eight patients to present with unusual fractures and musculoskeletal problems due to nutritional rickets. All were black, had been breast-fed until 6-12 months of age, and were vegetarians. Four were Black Hebrews who did not include any dairy products or vitamin D supplements in their diet. The diagnosis of nutritional rickets must still be considered when patients present with bone problems and the history reveals a dairy product-free diet.

Black or African American↗
PubMed1995

Lymphocyte subpopulations in children with vitamin D deficient rickets.

Recent studies have shown 1,25(OH)2D3-mediated modulation of the immune system. We examined lymphocyte subpopulations of 16 children with nutritional rickets. Most of the patients suffered more frequent infection episodes than the control group of 15 healthy children and low serum levels of 25OHD and 1,25(OH)2D, such as 38.2 +/- 8.6 ng/mL and 15.7 +/- 2.6 pg/mL respectively. This decrease correlated with a significant decrease in total T lymphocytes and an increase in B lymphocytes expressing surface IgA, IgM, IgG molecules. These results suggest that vitamin D plays an important role in the impaired functions of T lymphocytes which may lead to frequent infection episodes in nutritional rickets.

Child, Preschool↗
PubMed1983

Plasma concentrations of vitamin D metabolites in a case of rickets of prematurity.

Rickets was diagnosed in an extremely low-birthweight infant 16 weeks after birth. She had a normal plasma concentration of 25-hydroxyvitamin D, a relatively low level of 24,25-dihydroxyvitamin D, and a markedly elevated 1,25-dihydroxyvitamin D level compared with adult standards. The plasma concentrations of the vitamin D metabolites were, however, indistinguishable from those of healthy preterm infants who received a similar diet of human milk and vitamins. The results indicate that rickets was not caused by vitamin D deficiency or by abnormal vitamin D metabolism, but by calcium and/or phosphate deficiency, and that the calcium and phosphorous content of human milk may be inappropriately low for very low-birthweight infants.

24,25-Dihydroxyvitamin D 3↗
PubMed1985

Vitamin D deficiency rickets and vitamin B12 deficiency in vegetarian children.

During the years 1978-83 four vegetarian children have been admitted to the pediatric departments of Ullevaal and Aker Hospitals in Oslo and Haukeland Hospital, Bergen, with the diagnosis of vitamin D deficiency rickets. One had vitamin B12 deficiency as well. All had been fed a vegetarian diet with some cows' milk, but without vitamin supplementation. All had marked hypocalcemia, and three had tetany or convulsions. All responded well to conventional doses of vitamin D therapy. Two of the mothers had vitamin D deficiency, and one of them also had vitamin B12 deficiency. This report describes the case histories of these children, and also discusses predisposing factors of vegetarian diets for the development of nutritional rickets.

Child Nutritional Physiological Phenomena↗
PubMed1995

Vitamin D deficiency rickets in breast-fed infants presenting with hypocalcaemic seizures.

At the Aga Khan Hospital (AKUH), 65 infants presented with hypocalcaemic seizures, subsequently found to have rickets. Forty-six infants less than 6 months were totally or predominantly breast fed. In a subgroup of 15 mothers and their infants, we found very low plasma levels of 25(OH) vitamin D of < 5 micrograms/l and 7.5 +/- 3.3 micrograms/l, respectively. Neither mothers nor infants received vitamin D supplementation. Maternal vitamin D deficiency and non-supplementation in the infants were the likely causes of rickets in our patients. Prophylactic vitamin D 400 i.u. administered to infants up to 2 years and 800 i.u. to women in pregnancy and during lactation is recommended to prevent vitamin D deficiency.

Breast Feeding↗
PubMed2000

Vitamin D-deficient rickets: a multifactorial disease.

We present a case of an African-American child with vitamin D-deficient rickets. In addition to being solely breast-fed for the period of 1 year, he resided in New England, where exposure to ultraviolet light is limited owing to its northern latitude and long cold winters. He presented with classical signs of nutritional rickets and was immediately responsive to treatment with vitamin D supplementation.

Cholecalciferol↗
PubMed2005

The re-emerging burden of rickets: a decade of experience from Sydney.

AIM: To define the demographics and clinical characteristics of cases presenting with nutritional rickets to paediatric centres in Sydney, Australia. METHODS: Retrospective descriptive study of 126 cases seen from 1993 to 2003 with a diagnosis of vitamin D deficiency and/or confirmed rickets defined by long bone x ray changes. RESULTS: A steady increase was seen in the number of cases per year, with a doubling of cases from 2002 to 2003. Median age of presentation was 15.1 months, with 25% presenting at less than 6 months of age. The most common presenting features were hypocalcaemic seizures (33%) and bowed legs (22%). Males presented at a younger age, with a lower weight SDS, and more often with seizures. The caseload was almost exclusively from recently immigrated children or first generation offspring of immigrant parents, with the region of origin predominantly the Indian subcontinent (37%), Africa (33%), and the Middle East (11%). Seventy nine per cent of the cases were born in Australia. Eleven cases (all aged <7 months) presented atypically with hyperphosphataemia. CONCLUSIONS: This large case series shows that a significant and increasing caseload of vitamin D deficiency remains, even in a developed country with high sunlight hours. Cases mirror recent immigration trends. Since birth or residence in Australia does not appear to be protective, screening of at risk immigrant families should be implemented through public health policies.

Child, Preschool↗
PubMed1976

Genetic aspects of nutritional rickets.

Amino acid excretion was investigated in 21 rachitic infants and in 22 of their parents. There was (a) increased alpha-amino acid excretion in one-third of the infants a long time after the rickets had healed, (b) an abnormally high excretion of alpha-amino nitrogen and of phosphorus in many of the parents (c) an abnormal pattern of amino acid excretion in all 9 infants tested, and (d) a good correlation between the excretion of individual amino acids by an infant and by its parents. Our findings suggest that in at least some cases of nutritional rickets there is a genetic element which may manifest itself only under adverse environmental conditions.

Adult↗