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At least 289 records · Page 16Linked to original sources
PubMed1990

High prevalence of rickets in infants on macrobiotic diets.

The vitamin D status of 53 Caucasian infants aged 10-20 mo on a macrobiotic diet and 57 matched control infants on omnivorous diets was studied. In late summer (August-November) physical symptoms of rickets were present in 28% of the macrobiotic group; these infants had lower average plasma 25(OH)D concentrations (34.0 +/- 15.3 nmol/L) (mean +/- SD) than did the macrobiotic infants without such symptoms (49.7 +/- 21.9 nmol/L, p less than 0.02). Follow-up of a subsample of 25 macrobiotic infants in March-April revealed physical symptoms of rickets in 55% of the macrobiotic infants. All concentrations in blood were considerably below those in the preceding summer; the average 25(OH)D concentration was 12.3 +/- 4.3 nmol/L. Further analysis indicated that the low availability of calcium in the macrobiotic diet was an independent factor in causing the high prevalence of rickets in summer. Avoidance of milk products in combination with a high fiber intake may damage bone development in young children.

25-Hydroxyvitamin D 2↗
PubMed1997

Effect of 1,25-dihydroxycholecalciferol, cholecalciferol, and fluorescent lights on the development of tibial dyschondroplasia and rickets in broiler chickens.

Experiments were conducted to determine whether dietary 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] will alleviate a cholecalciferol deficiency induced by low dietary cholecalciferol and no fluorescent lighting and to determine cholecalciferol requirements as influenced by fluorescent lighting or 1,25-(OH)2D3. In each study, nutritionally complete basal diets were fed to broiler cockerels from 1 to 16 d of age. Experiment 1 had a 2 x 2 x 2 factorial arrangement of treatments with 1,25-(OH)2D3 at 0 and 10 micrograms/kg, cholecalciferol at 2.75 and 27.5 micrograms/kg, and fluorescent lights on or off. Experiments 2 to 4 had four levels of dietary cholecalciferol (0, 5.0, 27.5, and 50.0 micrograms/kg) and fluorescent lights on or off (Experiment 2) or 1,25-(OH)2D3 at 0 and 10 micrograms/kg (Experiments 3 and 4). In Experiment 1, fluorescent lighting increased bone ash, and decreased the incidence and severity of rickets at 2.75 micrograms/kg cholecalciferol and 0 microgram/kg 1,25-(OH)2D3 and reduced the severity of TD at both levels of cholecalciferol and 0 microgram/kg 1,25-(OH)2D3. In all cases 1,25-(OH)2D3 improved bone ash. The metabolite also decreased the incidence and severity of TD at both cholecalciferol levels with lights off and decreased the incidence and severity of rickets at 2.75 micrograms/kg cholecalciferol and lights off. In the absence of fluorescent lighting and 1,25-(OH)2D3 27.5 micrograms/kg cholecalciferol reduced the incidence and severity of rickets to levels equivalent to those produced by either fluorescent lighting or 1,25-(OH)2D3 alone (Experiments 2, 3, and 4). However, even 50.0 micrograms/kg cholecalciferol was not as effective as fluorescent lights or 1,25-(OH)2D3 in reducing the incidence and severity of TD.

Animals↗
PubMed1999

Rickets in Nigerian children: response to calcium supplementation.

In a previous study of rachitic children in Jos, Nigeria we concluded that inadequate dietary intake of calcium was the primary contributing factor to the development of their rickets. The objective of the present study was to determine the effect of calcium supplementation in 10 children with radiographically and biochemically proven rickets from the same geographical area. Rachitic children were provided with calcium supplements of 1000 mg/day for a period of 3 months. Serum and urine samples were obtained at baseline and at 24 hours, 1 week, 4 weeks, and 12 weeks after initiation of supplementation. Serum calcium, phosphorus, alkaline phosphatase, intact parathyroid hormone, 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D were measured at each time point. Dietary recalls obtained at two separate times were used to estimate usual daily intakes of calcium and phosphorus. Ten non-rachitic age-matched controls from the same geographical area were recruited for comparison. Nine of 10 rachitic subjects had radiographic evidence of healing after 3 months of calcium therapy. Although serum calcium concentrations returned to control levels, other biochemical data indicated that the rickets of these subjects may have been multifactorial in aetiology, pointing to a possible defect in the synthesis of 25-hydroxyvitamin D.

Anthropometry↗
PubMed2001

Bioelectrical impedance analysis of the body composition of Nigerian children with calcium-deficiency rickets.

Children with calcium-deficiency rickets experience increased urinary excretion of both essential and non-essential amino acids compared to non-rachitic children of the same age. Chronic wastage of amino acids into the urine could lead to a deficit in fat-free mass (FFM) in rachitic children. We therefore determined the FFM of children with calcium-deficiency rickets in northern Nigeria using bioelectrical impedance analysis. Because of the leg deformities present in the rachitic subjects, we calculated a 'corrected' height for each rachitic subject using the relationship between arm length and height in non-rachitic subjects over the same age range (r = 0.94). A total of 28 children (4 male and 24 female), 2-9 years of age with calcium-deficiency rickets and an equal number of age- and gender-matched controls were recruited into the study. Resistance and reactance measurements were obtained for all subjects and the total body water was calculated using age-specific equations. FFM was then calculated using age- and gender-specific hydration constants. No significant differences were found in the weights or FFM between the rachitic subjects and the controls (8.41 kg +/- 2.19 vs. 8.85 kg +/- 1.90, respectively). We conclude that chronic urinary wastage of amino acids by rachitic children does not result in a deficit in FFM.

Amino Acids↗
PubMed1991

Rickets, osteomalacia, and osteopetrosis.

In the field of rickets and osteomalacia, progress has been made mainly in the mapping of vitamin D-dependency rickets or "pseudodeficiency rickets" type I to chromosome 12q14, and the further identification of a variety of abnormalities in the calcitriol receptor complex responsible for hereditary resistance to 1,25-dihydroxyvitamin D. The study of the molecular basis of this latter inherited disorder has important implications for a better understanding of the physiologic role of 1,25-dihydroxyvitamin D. Concerning osteopetrosis, the finding of a reverse transcriptase activity in a patient with the benign form of this disorder opens new perspectives such as the possibility that retroviral infection may be the origin of at least some type(s) of osteopetrosis. Moreover, impairment of macrophage colony-stimulating factor production appears to be a key event in the pathogenesis of the osteopetrotic op/op mutation in rodents.

Drug Resistance↗
PubMed1996

Maternal high calcium diet fails to reverse rickets in the osteosclerotic mouse.

The coexistence of osteopetrosis and rickets (osteopetrorickets) in humans has been described frequently. The osteosclerotic mouse is a unique, lethal osteopetrotic mutation that also has rickets. Attempts to cure this mutation by bone marrow transplantation have been largely unsuccessful, and its resistance to cure presumably is attributable to hypomineralized skeletal tissue that does not support osteoclast neogenesis, differentiation, and function. Current opinion regarding the clinical treatment of patients with osteopetrorickets involves first, the resolution of the rickets, followed by bone marrow transplantation to resolve the osteopetrosis, although this has not been successfully performed in humans. Attempts were made in the current study to reverse the rachitic lesion in the osteosclerotic mouse by feeding female breeders a high calcium (2.0%) diet throughout pregnancy and lactation. Mutant offspring (2 to 3 weeks of age) from such mothers remained hypocalcemic and hypophosphatemic, showed no decrease in growth plate cartilage thickness, and did not have enhanced cartilage or skeletal mineralization. For this unique mutation, efforts should be continued toward developing the appropriate therapies for reversal of its rachitic and skeletal defects; such therapies may yield insights into the clinical care of human infants with osteopetrorickets.

Animals↗
PubMed1989

Rickets in a very low birth weight infant.

A report on a case of rickets in a very low birth weight infant (VLBWI) is presented. The infant had no high-risk factors for rickets and was fed a specialized preterm formula with vitamin D supplementation (200 IU daily) by 10 days of age. Feeds were advanced so that an enteral intake of 120 cal/kg/day was achieved by the 20th day of life. Mean calcium, phosphorus, and vitamin D intakes between the 20th and 61st days of life were 185 mg/kg/day, 93 mg/kg/day, and 367 IU/day, respectively. On the 62nd day of life, a diagnosis of rickets was made, and a nutrient balance study was performed. Urinary calcium excretion was low (1.3 mg/kg/day), suggesting calcium deficiency. However, retention of calcium (127 mg/kg/day) and phosphorus (76 mg/kg/day) was occurring at intrauterine rates. Thus, while calcium absorption was adequate at 10 weeks of age, the same was not true earlier in life. We suggest that there is a limiting role of calcium absorption on bone mineralization during early life in the VLBWI.

Calcification, Physiologic↗
PubMedDate not supplied

Vitamin D deficiency rickets in children: prevalence and need for community education.

Nutritional rickets caused by a deficiency in vitamin D can be a crippling disease and is still prevalent today. Many feel that the vitamin D supplementation present in dairy products prevents any risk of developing vitamin D deficiency rickets. However, a combination of factors such as pigmented skin, inadequate sunlight, breastfeeding past 6 months with no supplementation, and insufficient calcium intake by the nursing mother and her baby often contribute to rickets diagnosed in children. Educating the medical community and those families at risk is critical to eradicate this preventable disease. Steps can be taken using stages of the Organizational Change Theory to involve school nurses, community health centers, and pediatricians in identifying these high-risk children. With prompt diagnosis and treatment, all symptoms can abate, with healthy bone growth resulting.

Child↗
PubMed1982

Hepatobiliary rickets.

Rickets secondary to hepatobiliary disease is a rare condition; however, the skeletal manifestations are similar to simple nutritional rickets. These skeletal changes include epiphyseal plate abnormalities, pseudofractures, bowing of long bones, scoliosis, and fractures. One-hundred and twelve charts and radiographs of patients with chronic hepatobiliary disease admitted to Children's Hospital of Michigan from 1968 to 1978 were reviewed. Nineteen, or 17%, of these patients showed roentgenographic evidence of rickets. Orthopedic management is primarily concerned with the treatment of fractures and prevention or correction of deformities in those children whose longevity justifies treatment.

Biliary Tract Diseases↗
PubMed1978

Copper deficiency and hypocalcemic rickets in a small-for-date infant.

A case of copper deficiency associated with hypocalcemia, radiological features of rickets and hyperparathyroidism is described in a small-for-date infant (gestational age 39 weeks, B.W 1 240 g). Neonatal serum copper (Cu) levels were found between 223 and 138 mumol/l. She was given daily 2 400 U of vitamin D2 and a load dose of 80 000 IU at the age of 55 days. At the age of 79 days, X-rays of the legs and wrist showed spread, cupped and frayed metaphyses. Serum Ca was 1.35 mmol/l, P = 0.99 mmol/l with high alkaline phosphatases (A.P.) 590 IU/ml. But plasma level of 25 hydroxycholecalciferol (25-OH-CC) was normal = 10.8 ng/ml. Serum Cu was low = 3.14 mumol/l and serum immunoreactive parathormone (iPTH) level was elevated: 520 mulEq/ml (N less than or equal to 100). Administration of vitamin D2 (15 mg) induced an immediate normalization of serum Ca, normal serum iPTH (68 mulEq/ml) in one month, normal X-rays in two months and normal A.P. in four months. Serum Cu and ceruloplasmin levels increased slowly without any supplementation to subnormal levels at the age of eight months (14.9 and 1.65 mumol/l. Serum Cu concentrations were found to be normal (16.0--33.7 mumol/l) in five children with hypocalcemic rickets. These results suggest a role of Cu deficiency in the occurrence of this transient vitamin D-resistant rickets.

Calcium↗
PubMed2003

Children with nutritional rickets referred to hospitals in Copenhagen during a 10-year period.

AIM: To describe the prevalence of nutritional rickets among children admitted to three large paediatric departments in the Copenhagen area during a 10 y period. METHODS: Retrospective analysis of cases identified from the diagnosis registers fulfilling the diagnostic criteria for nutritional rickets. RESULTS: Forty cases were identified, distributed in two distinct age groups: 0.5-4 y (n = 31) and 9-15 y (n = 9). All cases were immigrants, of whom 95% were born in Denmark. The main symptoms in the younger age group were bowed legs and clumsy walk, and in the peripubertal group were painful joints. Two children had generalized convulsions. None of the cases had received vitamin D supplementation. CONCLUSION: Nutritional rickets is still present among immigrants in Denmark, and it is likely that the prevalence of mild cases is high. Prevention through vitamin D supplementation is important, but requires a dedicated health education effort.

Child Nutritional Physiological Phenomena↗
PubMed1975

Rickets in Tehran. Study of 200 cases.

Radiologically diagnosed rickets was found to be common in children of the poorer classes in Tehran. It was frequently associated with gastroenteritis or bronchopneumonia and a large proportion of the children were severely underweight for their age. In children below the age of 1 year malnutrition tended to mask the signs of rickets. Convulsions were much less frequent in the malnourished children; the concentration of calcium in the serum was higher and that of alkaline phosphatase was lower than in those who were well nourished. Biochemistry is of little value in the diagnosis of rickets in the presence of malnutrition.

Adolescent↗
PubMed1977

Cystinotic rickets treated with vitamin D metabolites.

A 22-month-old girl with cystinotic rickets was given 1 microgram 1,25-dihydroxycholecalciferol (1,25-DHCC) daily in addition to standard treatment. Her rickets healed and linear growth rate appeared to increase. It is suggested that the effect of 1,25-DHCC and its metabolically active analogues on cystinotic rickets should be further studied.

Cystinosis↗
PubMed1980

Neonatal rickets. Histopathology and quantitative bone changes.

Ribs from 3 preterm infants, who had died after prolonged intravenous feeding and artificial ventilation, were examined histologically and assessed for the degree of osteomalacia and osteoporosis in cancellous bone of the shaft. A grid counting technique was used. Osteomalacia was noted in all 3 cases but to a lesser degree than in classical vitamin D-deficient controls. Osteoporosis was pronounced in the cases of neonatal rickets, but this was not a feature of the vitamin D-deficient controls. Histological features were similar to those reported in experimental phosphate-deficient rickets and vitamin D-resistant rickets.

Bone and Bones↗
PubMed1980

Late presentation of vitamin D-dependent rickets.

An 8 1/2-year-old girl presented with rickets. This had developed despite a normal diet and in the absence of symptoms, signs, or laboratory evidence of malabsorption, hepatic or renal disease. The rickets healed with physiological doses of 1-alpha-hydroxy-cholecalciferol. It is suggested that this case provides evidence for genetic and metabolic heterogeneity in vitamin D-dependent rickets.

Age Factors↗
PubMed1980

Diagnosis of subclinical rickets.

44 randomly selected infants under age one year with suspected lower respiratory infections were investigated for the presence of subclinical rickets. Seven infants had metaphyseal changes at the wrist compatible with a diagnosis of rickets and all of these infants had 25-hydroxy-vitamin D (25-OHD) concentrations less than 12 ng/ml. Serum calcium and phosphorus concentrations were normal in all 44 children. Alkaline phosphatase concentrations did not correlate with the presence of metaphyseal changes. The clinical presence of craniotabes or splaying and loss of definition of the anterior ends of the ribs on x-rays did not correlate with metaphyseal changes at the wrist or with 25-OHD concentrations. An x-ray of the wrist is essential to confirm the presence of subclinical rickets and the at-risk infant can be detected by measuring serum 25-OHD concentrations.

Female↗
PubMed1980

Nutritional rickets in 2 very low birthweight infants with chronic lung disease.

Two very low birthweight infants with rickets are described; one had a low serum 25-hydroxy-vitamin D3 concentration. Similarities in their clinical courses included low birthweights, low calcium intakes, uncertain vitamin D intakes, and chronic administration of frusemide and sodium bicarbonate--all potential aetiological factors in the development of bone undermineralisation. Both infants had a resolution of their chronic lung disease before their treatment for rickets. This experience has led us to the more cautions use of frusemide and sodium bicarbonate in infants at risk for rickets, and shows the need to ensure daily vitamin D supplements.

Bicarbonates↗
PubMed1989

Ultraviolet irradiation for hepatic rickets.

An infant with chronic cytomegalovirus hepatitis and a child with atypical Alagille's syndrome had vitamin D deficiency rickets due to malabsorption. Both received ultraviolet irradiation. This treatment corrected biochemical abnormalities and healed the rickets. In the infant use of a sunlamp at home maintained normal 25 hydroxy-vitamin D for over a year. Our study shows that ultraviolet irradiation is an effective treatment of hepatobiliary rickets.

Child↗