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PubMed1980

Aetiological factors in rickets of prematurity.

Six very preterm (< 32 weeks' gestation) infants who developed late-onset respiratory distress were each matched for sex and gestation with 2 control preterm infants. Radiologically and biochemically the diagnosis of rickets and rachitic respiratory distress seemed clear and the pattern conformed with other reports of the syndrome. The control infants were of similar gastational ages but there was a significantly higher incidence of pre-eclampsia in the pregnancies of index cases. Also significant was a prolonged illness of several weeks' duration in the index cases; this illness was either heart failure due to patent ductus arteriosus or prolonged ventilation in the early weeks of life for apnoeic attacks. Awareness of these 2 aetiological factors shows the necessity of monitoring such infants for evidence of rickets. The use of water-soluble antirachitic prophylaxis such as 1 alpha-hydroxy-vitamin D or 1,25-dihydroxy-vitamin D is sometimes indicated.

Humans↗
PubMed1981

Plasma active vitamin D concentration in low birthweight infants with rickets and its response to vitamin D treatment.

Impairment of 25-hydroxylation may be a cause of rickets in infants of low birthweight, weighing between 2000 and 2500 g. In addition there may be impairment of 1 alpha-hydroxylation in infants weighing less than 2000 g. Our data show that a supplementary dose of vitamin D2 of at least 500 IU daily is a reasonable regimen for infants who weighed between 2000 and 2500 g at birth. However for infants who weighed less than 2000 g with a gestation of under 38 weeks, administration of 1 alpha-OHD3 may be more effective in preventing rickets.

25-Hydroxyvitamin D 2↗
PubMed1973

Serum alkaline phosphatase and rickets in urban schoolchildren.

Among 569 schoolchildren (386 boys and 183 girls) aged 14-17 years, 233 had serum alkaline phosphatase values of 30 K.A. units or greater. There was no significant difference in the results in Asian, white, or West Indian children. The mean values were significantly greater in boys than girls and both showed a fall in mean values with increasing age. Radiological rickets occurred in at least 4% of the survey, and was more common in Asians. Low calcium and high hydroxyproline excretion in most of those investigated and the response to vitamin D therapy suggests that most children with alkaline phosphatase levels above 30 K.A. units have rickets.Since the decline of the widespread supplementation of the diet with vitamin D, the demands of the physiological growth spurt for extra vitamin D in adolescents already on a borderline intake may be responsible for the great increase in "biochemical" rickets. Once the growth spurt is over the condition subsides but the results of impaired growth or permanent pelvic deformity will not necessarily be eradicated.

Adolescent↗
PubMed1972

Biochemical response of late rickets and osteomalacia to a chupatty-free diet.

Eight Pakistani children with late rickets and two Pakistani women with osteomalacia were given a chupatty-free diet for seven weeks, substituting leavened bread of lower extraction. On this diet serum calcium levels rose to normal or near normal, levels of serum inorganic phosphorus rose slightly but significantly, and serum alkaline phosphatase levels showed a definite rise indicative of healing bone disease. It is concluded that the high phytate content of unleavened bread is the major cause of late rickets and osteomalacia in Pakistani and Indian communities in the United Kingdom. The simplest prophylactic measure seems to be the additional fortification with calcium carbonate of the high extraction flour used in preparing unleavened bread.

Adolescent↗
PubMed2005

Incidental radiological diagnosis of rickets.

Rickets fortunately remains rare in the United Kingdom, although its actual incidence is currently undetermined.1 Many still consider it to be a disease of poverty prevalent during the Victorian era. However, a number of recent articles have highlighted concern among British health professionals about the number of cases still being diagnosed in this country. These cases have nearly all involved non-Caucasian children who are considered to be at high risk due to skin colour, prolonged breast feeding, and low maternal vitamin D levels. Their presentations are variable ranging from failure to thrive, bone deformities, seizures, and even stridor. The diagnosis is usually made in babies and toddlers.We present a series of patients attending our accident and emergency (A&E) department, over a five month period, where the diagnosis of rickets was primarily a radiological diagnosis.

Arabs↗
PubMed1978

Rickets in growing pigs and response to treatment.

The clinical, radiological and pathological findings in a natural outbreak of rickets affecting 82 pigs are described. An interesting feature was the presence of gross articular abnormalities including resorption of subchondral bone with folding and ulceration of the articular cartilage. The diet was deficient in calcium and vitamin D. A diagnosis of rickets complicated by nutritional secondary hyperparathyroidism was made. The results of treatment and the economics of the outbreak are discussed.

Animals↗
PubMed2002

Vitamin-D-dependent rickets type 2.

Vitamin-D-dependent rickets type 2 results from autosomal recessive mutations of the vitamin D receptor gene. With congenital total body alopecia and onset of rickets during the second half of the first year of life, patients display rapidly progressing rachitic bone changes, hypocalcemia and secondary hyperparathyroidism. This article describes extensive personal experience with about one third of the world's reported cases, their clinical course, the physiological consequences, diagnostic steps, molecular findings and therapeutic approach, as they developed over the course of the last 25 years.

Adolescent↗
PubMed2006

Vitamin D receptor polymorphisms in hypocalcemic vitamin D-resistant rickets carriers.

BACKGROUND/AIMS: Hypocalcemic vitamin D-resistant rickets (HVDRR) is a rare autosomal recessive disorder characterized by severe rickets, hypocalcemia, secondary hyperparathyroidism, elevated levels of 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)], and occasionally, alopecia. In most cases, the disease is associated with mutations in the gene of the vitamin D receptor (VDR), the mediator of 1,25(OH)(2)D(3) action. The apparently healthy HVDRR heterozygotes express both normal and mutant VDR alleles, and they present higher levels of 1,25(OH)(2)D(3) than their respective controls. Because VDR function, except for the disease-causative mutations, might be influenced by the presence of certain polymorphisms, we investigated the distribution of four common VDR polymorphisms--BsmI, ApaI, TaqI and FokI--in HVDRR carriers compared with their respective controls. METHODS: Sixty-seven relatives of 2 HVDRR patients, all members of an extended Greek kindred, were included in the study. VDR allelic polymorphisms were assessed by restriction fragment length polymorphisms after specific polymerase chain reaction amplification. RESULTS: The distribution of genotypic and allelic frequencies differed between HVDRR carriers and their respective controls regarding BsmI and TaqI polymorphisms. The bb genotype and the T allele (presence of BsmI and absence of TaqI polymorphisms) were less frequent in the HVDRR carrier group than in the control group in a statistically significant manner (p = 0.029 and p = 0.025, respectively). CONCLUSIONS: Our findings showed that the apparently healthy HVDRR carriers present a different distribution of BsmI and TaqI VDR polymorphisms than their controls, suggesting that further investigation of the HVDRR carrier population may elucidate the implication of VDR alleles in VDR function and the vitamin D endocrine system.

Adolescent↗
PubMed1985

Yogurt. Contributory factor in development of nutritional rickets.

Vitamin D deficient rickets occurred in a 15-month-old black girl for whom yogurt had been substituted for milk products. Investigation determined that commercially available yogurt contains no vitamin D, and that this fact is not generally recognized by lay persons and health professionals. Use of yogurt as a major source of nutritional intake in infants and young children may be a contributory factor in development of vitamin D deficiency rickets.

Dairy Products↗
PubMedDate not supplied

Rickets in premature infants receiving parenteral nutrition: a case report and review of the literature.

There is a multifactorial etiology for rickets in premature infants receiving total parenteral nutrition. As an example of this, we describe a premature infant fed almost exclusively parenterally for the first 8 months of life who developed biochemical and radiologic evidence of rickets despite receiving vitamin D, calcium, and phosphorus at presently recommended levels. From our experience and a review of previous literature, there appears to be considerable uncertainty regarding the intravenous requirements of calcium, phosphorus, and vitamin D, particularly in low-birth weight infants. Therefore, measurements of serum 25-hydroxyvitamin D levels, vitamin D, and mineral intakes, and calcium and phosphorus excretion might be clinically useful for monitoring premature infants receiving total parenteral nutrition. Further research delineating more precisely the vitamin D, calcium, and phosphorus requirements of such infants is also suggested.

Calcium↗
PubMed1995

Hypophosphatemic rickets in rheas (Rhea americana).

Rickets was diagnosed in 11 rheas from four flocks in Ohio. At necropsy, had pliable bones with prominent valgus or varus deformation of the femoral bone and/or the tibiotarsal bone, marked thickening of the metaphyseal plates, and frequent fractures. Histopathologically, bones of rachitic birds showed marked retention of cartilage core within the growth plate, mainly because of a significant lengthening of the hypertrophied zone of the growth plate in relationship to the remaining zones. Feed analysis showed that rachitic birds were fed diets having higher calcium/phosphorus (Ca/P) ratios (1.38-4.32) than that of the diet fed to nonrachitic birds from a different flock (0.65 Ca/P ratio). Serum analysis of blood from clinically rachitic birds from the affected flocks revealed a marked hypophosphatemia (3.0-4.7 mg/dl), mild hypocalcemia, and normal 25-(OH)-vitamin D concentrations as compared with values in nonrachitic birds, which had serum phosphorus concentrations of 8.5-8.7 mg/dl. These findings suggest that rickets in growing rheas was associated with marked hypophosphatemia and improper Ca/P ratios.

Animals↗
PubMed2002

Hurler's syndrome, West's syndrome, and vitamin D-dependent rickets.

Mucopolysaccharidosis I is a metabolic disease of autosomal recessive inheritance caused by deficient activity of alpha-L-iduronidase. The clinical phenotype presents a wide spectrum of signs in the first year of life. We report a child with clinical features and laboratory data consistent with mucopolysaccharidosis I who precociously developed hydrocephalus and flexion spasms with hypsarrythmia in the electroencephalographic registration characteristic of West's syndrome. His radiologic and biochemical data suggested vitamin D-dependent rickets. To our knowledge, this is the first report of a patient demonstrating an association among mucopolysaccharidosis 1, West's syndrome, and vitamin D-dependent rickets.

Chromosome Aberrations↗
PubMed2002

Severe congenital rickets secondary to maternal hypovitaminosis D: a case report.

We report a full-term baby boy who presented soon after birth with severe congenital rickets. Maternal and neonatal vitamin D levels were very low and the infant responded well to oral vitamin D. Transient secondary hyperparathyroidism normalised on treatment. The mother's vitamin D deficiency was attributed to the region's cultural dress code which prevents exposure to sunlight. There has not been a previous report of severe congenital rickets from this region.

Adult↗
PubMed1981

Hypocalcemic, hypophosphatemic rickets in rat pups suckling vitamin D-deprived mothers.

The effects of maternal vitamin D deprivation on rat pups were examined in terms of serum levels of Ca, phosphorus (P), and 25-hydroxyvitamin D (250HD), ash content, and histological appearance of long bones. In each of 10 experiments, litters of 8--10 young were examined at 2 or 3 different ages within the range of 5--57 days. Pregnant mothers were fed a diet containing 0.4% Ca, and 0.4% P and either no vitamin D(--D) or 5 IU D3/g diet (+D). Mothers fed the --D diet developed marked hypocalcemia (4--5 mg/dl) during lactation, but no change in milk Ca or P. The earliest changes in pups suckled by mothers on --D diets compared to pups suckled by mothers on +D diets were significant reductions at 8 days in serum P (6--12% in 3 of 5 experiments) and in serum 250HD3. By the 15th day, serum 250HD3 was undetectable, body weight was reduced by 26%, serum Ca was reduced by 9%, and serum P was reduced by 15%. During the following 10 days, when gradual weaning took place, serum Ca decreased progressively, serum P returned to normal, serum Mg became elevated, bone ash (as percent of dry weight of tibia) was decreased, and decalcified sections of the proximal end of the tibia revealed irregularity and widening (1.5- to 3-fold) of the hypertrophic cartilage layer and the metaphyseal trabeculae. All of these changes were also prominent in 8-week-old --D rats. The results indicate that rat pups suckling vitamin D-deprived mothers can develop biochemical evidence (including hypophosphatemia) as well as histological evidence of vitamin D deficiency similar to that of human vitamin D deficiency rickets. This is in contrast to rats deprived of vitamin D after weaning, who do not develop hypophosphatemia or characteristic histological evidence of rickets unless deprived of P as well as vitamin D.

25-Hydroxyvitamin D 2↗
PubMed1998

Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice.

1,25-Dihydroxyvitamin D3 plays a major role in intestinal calcium transport. To determine what phenotypic abnormalities observed in vitamin D receptor (VDR)-ablated mice are secondary to impaired intestinal calcium absorption rather than receptor deficiency, mineral ion levels were normalized by dietary means. VDR-ablated mice and control littermates were fed a diet that has been shown to prevent secondary hyperparathyroidism in vitamin D-deficient rats. This diet normalized growth and random serum ionized calcium levels in the VDR-ablated mice. The correction of ionized calcium levels prevented the development of parathyroid hyperplasia and the increases in PTH messenger RNA synthesis and in serum PTH levels. VDR-ablated animals fed this diet did not develop rickets or osteomalacia. However, alopecia was still observed in the VDR-ablated mice with normal mineral ions, suggesting that the VDR is required for normal hair growth. This study demonstrates that normalization of mineral ion homeostasis can prevent the development of hyperparathyroidism, osteomalacia, and rickets in the absence of the genomic actions of 1,25-dihydroxyvitamin D3.

Alopecia↗
PubMed1980

Pseudohypoparathyroidism presenting with rickets.

Pseudohypoparathyroidism (PHP) is a condition characterized by hypocalcemia, hyperphosphatemia, and an impaired phosphaturic response to exogenous parathormone (PTH). A minority of patients with PHP have associated bone disease, and in some the radiological appearances have been suggestive of rickets. We report a patient with PHP who had epiphyseal enlargement and bowing of the long bones similar to that seen in rickets. Radiology showed generalized osteomalacia with failure of epiphyseal calcification and several pseudofractures. Bone biopsy showed increased osteoid seams. The phalanges of both hands showed subperiosteal erosions consistent with hyperparathyroidism. Biochemically, he had persistent hypocalcemia, hyperphosphatemia, and an elevated alkaline phosphatase. Plasma calcitonin, magnesium, and 25-hydroxycholecalciferol levels were normal. The 1,25-dihydroxycholecalciferol level was within the normal adult range but was probably inappropriately low for an adolescent. Plasma parathormone was elevated (1.3--1.7 microgram/liter; normal, < 0.73). His diet was not deficient in vitamin D. Gastrointestinal function was normal. Renal function was normal, apart from an increase in the maximum tubular reabsorption of phosphate (46--52.6 mg/liter glomerular filtration rate; normal, 38 +/- 5). Intravenous PTH infusion tests were performed on the patient and a control subject before and 6 months after serum calcium levels had returned to normal. The maximum increases in cAMP excretion in the patient were 0.03 and 0.05 mmol/g creatinine before and after treatment, respectively (control, 0.53 and 0.24); the maximum increases in phosphate excretion in the patient were 0.14 and 0.04 mmol/g creatinine before and after treatment, respectively (control, 0.32 and 0.07). He responded to initial treatment with a high dose of calciferol and later to 1,25-dihydroxycholecalciferol in a dose of 1 microgram/day. It is considered that renal resistance to PTH is his primary abnormality, with the bone disease representing a secondary phenomenon.

Adult↗