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At least 307 records · Page 17Linked to original sources
PubMed1996

Rickets and soil strontium.

The subjects of this study were children aged 6-60 months living in villages in the Ulas Health Region, Sivas. The villages were divided into two groups according to the amount of strontium in the soil: region 1, > 350 ppm, 650 children; region 2, < 350 ppm, 1596 children. Overall, the prevalence of one or more clinical signs of rickets was 22.9%. The prevalence in region 1 was 31.5% and that in region 2, 19.5%. These values were significantly different (p < 0.001). When other variables which may be relevant to the occurrence of rickets were taken into account, the difference in prevalence persisted. The results suggest that in villages where nutrition is mainly based on grain cereals the presence of strontium in the soil will increase the prevalence of rickets significantly. As a preventive measure, a greater proportion of the foods given to children in these villages should be derived from animal origin, and cereals and drinking water supplies should be obtained from villages with a low soil strontium content, or calcium supplements should be given.

Age Distribution↗
PubMed2003

Radiological and biochemical resolution of nutritional rickets with calcium.

AIMS: To determine the response to oral calcium in Nigerian children with rickets. METHODS: In a teaching hospital in Western Nigeria, 26 children (13 boys, 13 girls, aged 2-5 years) with confirmed rickets received calcium lactate (2.7 g/day). RESULTS: Within one month of treatment leg pain was relieved and the children were more active. The mean x ray score improved from 3.3 at baseline to 1.7 at three months and 0.9 at six months (arbitrary scoring system, 0-6). Twelve cases were healed radiologically after six months, 11 others improved considerably, two showed no significant improvement, and a non-compliant patient was worse. There was progressive reversal of biochemical features. Median plasma alkaline phosphatase fell from 519 (range 178-1078) to 283 (209-443) IU/l (p = 0.04) in four months, while mean 1,25-dihydroxyvitamin D fell from 473 (251-1057) to 281 (155-481) pmol/l (p = 0.04), and mean plasma calcium increased from 2.26 (1.63-2.54) to 2.37 (2.06-2.54) mmol/l (p = 0.13). Parathyroid hormone fell from 5.3 (0.4-21.5) to 1.7 (0.45-7.4) pmol/l. Type I collagen carboxy terminal cross linked telopeptide was very high at baseline (20 (7.2-103) to 14 (11-24) micro g/l) (p = 0.03) and fell promptly to normal. CONCLUSION: Calcium supplementation alone effected healing of rickets in most of these Nigerian children and may provide sufficient treatment in this environment.

Calcium↗
PubMed1985

Screening Rastafarian children for nutritional rickets.

We examined 42 Rastafarian children under 5 years of age who were registered with a single inner city general practice to determine the prevalence of nutritional rickets. Twenty children were receiving a strict vegan(I-tal) diet and were considered to be at high risk of developing rickets and were referred for biochemical and radiological investigation. Seven of 20 children investigated had rickets, giving an overall prevalence of 7/42. Treatment with oral cholecalciferol was successful in all seven children. Fourteen out of 18 children had evidence of iron deficiency, with low haemoglobin concentrations and hypochromic-microcytic blood films. Before this study Rastafarian children rarely attended the well baby clinic, received no vitamin supplements, and few had been immunised. They now regularly attend the clinic, receive vitamin and iron supplements, and all have completed primary immunisation.

Alkaline Phosphatase↗
PubMed1985

Relationships between radiological and biochemical evidence of rickets in Asian schoolchildren.

One hundred Asian schoolchildren provided evidence of the relationships between radiological and biochemical evidence of rickets in a vitamin D-deficient population. In a retrospective study of the X-rays of 56 children the variables serum alkaline phosphatase, inorganic phosphorus and age provided a discriminant function which correctly classified 10 of 11 children with radiological evidence of rickets and 44 of 45 children with negative or marginally abnormal X-rays. When the discriminant function was applied to a prospective study of 44 children, three children with radiological evidence of rickets were correctly classified together with 38 of the remaining 41 children with negative or marginally abnormal X-rays. Serum alkaline phosphatase was the most important variable in the discriminant analysis, followed by serum inorganic phosphorus and age. Low levels of serum 25-hydroxy vitamin D (25-OHD) are of little value in predicting the severity of radiological evidence of rachitic bone disease in a vitamin D-deficient population.

Adolescent↗
PubMed1982

Rickets associated with cholestasis and parenteral nutrition in premature infants.

Fourteen premature infants on prolonged total parenteral nutrition (TPN) exhibited radiographic evidence of rickets. All had received supplementary doses of vitamin D that, in retrospect, may have been inadequate. Cholestasis and rickets resolved in the 10 surviving infants after they were started on oral feelings, which corrected their hypophosphatemia. On the assumption that they might be deficient in vitamin D, they were given high doses of it. In retrospect, it appears probable that rickets in such cases is caused by hypophosphatemia, due to inadequate phosphorus intake, and that vitamin D deficiency is of little or no importance.

Cholestasis↗
PubMed2006

Rickets with Dorfman-Chanarin syndrome.

BACKGROUND: Dorfman-Chanarin syndrome is a rare, autosomal recessive, inherited, lipid storage disease. It is characterized by nonbullous congenital ichthyosiform erythroderma, leukocyte vacuoles and variable involvement of the liver, muscles and central nervous system, due to errors of triacylglycerol metabolism. To date only 32 cases of this syndrome have been described worldwide. AIMS: To report the case of a boy with Dorfman-Chanarin syndrome with rickets. CASE REPORT: A boy of Turkish origin was born of a nonconsanguineous marriage after an uncomplicated perinatal period. On examination the patient had failure to thrive, diffuse erythroderma and ichthyosis and clinical features suggesting rickets. A light-microscopic examination of peripheral smear revealed vacuolated leukocytes typical of Jordans' anomaly. Lipid analysis showed an increase in triacylglycerol and very low density lipoprotein. A radiographic study of the wrist revealed rickets. CONCLUSION: The clinical progression in these patients ranges from mild to fatal. We believe that patients with ichthyosis should be evaluated bearing in mind the possibility of Dorfman-Chanarin syndrome. This may increase the number of reported Dorfman-Chanarin syndrome cases, and the pathogenesis and progression of the disease will become clearer.

Brain↗
PubMed1985

Hypercalciuric rickets: metabolic studies and pathophysiological considerations.

Extensive metabolic studies were performed in a 14-year-old boy suffering from the rare clinical entity known as childhood idiopathic hypercalciuria associated with dwarfism, renal tubular abnormalities and bone lesions. The salient features were: hyperphosphaturia with hypophosphatemia, hypercalciuria with normocalcemia, elevated serum 1,25-dihydroxycholecalciferol[1,25(OH)2D3] levels, marked intestinal hyperabsorption of calcium and phosphorus, with low serum parathyroid hormone (PTH) and urinary adenosine 3':5'-cyclic monophosphate (c-AMP). Bone biopsy confirmed the clinical and radiological diagnosis of rickets. It appears that the following pathophysiological sequence is operating: primary renal phosphate leak with hypophosphatemia, increased 1,25(OH)2D3 synthesis, enhanced intestinal calcium absorption which in turn inhibits release of PTH and c-AMP. Hypercalciuria is seen to be secondary to both avid intestinal calcium absorption and depressed PTH activity, and rickets the result of phosphate depletion. Treatment with oral phosphorus only resulted in an acceleration of growth rate, cure of rickets, and return of urinary calcium excretion to normal values.

Adolescent↗
PubMed1986

Plasma alkaline phosphatase activity and its relation to rickets in pre-term infants.

Sequential measurements of plasma alkaline phosphatase activity were made in 84 pre-term infants delivered before 38 weeks gestation. In 67% of infants, without evidence of rickets but in whom three or more measurements were made and the peak activity was less than 10 times the adult reference range, the activity rose to a peak and declined to previous levels, or lower. The time taken for these changes varied greatly. The range of values was inspected at each week of age, and in all but six cases the level did not exceed 10 times the upper limit of the adult reference range. Three infants had radiological evidence of rickets, and of the six cases in whom higher levels were found, only one had radiological evidence of rickets; the remainder did not. It is recommended that in the latter, the high plasma alkaline phosphatase activity should be regarded as evidence of subclinical bone disease.

Age Factors↗
PubMed2001

Antacid-induced rickets in infancy.

A 3-month-old premature infant presented with a "soft skull." Clinical and radiologic findings confirmed the diagnosis of rickets. Biochemistry revealed normal serum parathyroid hormone (PTH) and undetectable urine phosphate. These findings combined with a history of 5-6 weeks' treatment with high-dose aluminum-rich antacid established the diagnosis of antacid-induced rickets. Discontinuation of the medicine combined with phosphate and vitamin D supplementation resulted in quick resolution of all clinical, radiologic, and biochemical abnormalities. Our patient demonstrates that in premature infants antacid-induced rickets can develop within a few weeks; normal serum PTH concentration and hypophosphaturia are highly indicative of the diagnosis, and contrary to the situation in adults in whom hypercalciuria has been often described, in infants hypocalciuria is more commonly observed. Pediatricians should avoid or minimize the use of aluminum-containing antacids, and when used, carefully monitor mineral metabolism.

Antacids↗
PubMed1986

Pycnodysostosis with visceral manifestation and rickets.

Pycnodysostosis is a rare bone disease. Visceral manifestations associated with anemia and/or rickets have been reported in pycnodysostosis. Five children with typical findings of pycnodysostosis with hepatosplenomegaly, anemia with rickets, one with visceromegaly and anemia, and another with rickets alone are reported here. These findings strongly suggest that extramedullary erythropoiesis does occur in pycnodysostosis.

Anemia↗
PubMed1992

The effects of hypocalcemia/hypophosphatemia on porcine bone and dental hard tissues in an inherited form of type 1 pseudo-vitamin D deficiency rickets.

The effects of Vitamin D deficiency rickets on the formation of mineralized dental tissues were studied in a breed of pigs which had moderate and marked hypocalcemia because of an inherited defect in the renal production of the biologically-active Vitamin D metabolites. Affected piglets developed classical symptoms of rickets which were fatal unless Vitamin D supplements were given. The dissected mandibles of homozygous (rickets) and heterozygous (normal) pigs were photographed and radiographed. Compared with those of normal pigs, the mandibles of homozygous pigs demonstrated slowed development/eruption of permanent teeth, under-mineralized bone, underdeveloped dentin (enlarged pulp chambers), interglobular dentin, and enamel hypoplasia. Enamel defects in rachitic pig teeth were difficult to observe radiographically, but could be detected visually and by SDS-PAGE analysis of the enamel protein components of developing and maturing enamel. There was significant retention of amelogenins in the enamel maturation zones of developing molars taken from rachitic pigs, but there was no obvious difference in the patterns of amelogenin processing.

Amelogenin↗
PubMed1982

High incidence of rickets in children with wheezy bronchitis in a developing country.

The incidence of rickets in 100 Iraqi infants with wheezy bronchitis (24%) exceeded by two and a half times that found in age-matched controls (9%), and by ten times when only those with severe rickets were considered. The reason for this is not entirely clear, but could be related to the fact that the infants with wheezy bronchitis weighed more and therefore had grown faster than the control group. This itself could be related to the higher incidence of breastfeeding in the infants with wheezy bronchitis. We wish to stress the importance of screening for rickets, particularly in those with wheezy bronchitis.

Body Weight↗
PubMed2006

Case report of 5 siblings: malnutrition? Rickets? DiGeorge syndrome? Developmental delay?

BACKGROUND: Parents of six children are facing a trial on charges of aggravated manslaughter in the care a 5 1/2 month old infant who died suddenly and neglect of their four older children for causing them to be malnourished by feeding them all an exclusively raw foods vegan diet. Both parents declined plea bargains and plan to defend themselves in court. CASE PRESENTATION: The fifth child born to a married couple was breast-fed until 2 1/2 months. Subsequently, the parents fed the baby an exclusively raw foods diet prepared in a blender at home. The four older children, ages 18 months-6 1/2 years also ate an exclusively raw foods vegan diet. None of the four older children had significant previous injuries or serious illnesses. At autopsy, the infant weighed 3180 mg (6.99 pounds) and appeared emaciated. The thymus gland was absent and parathyroid glands were not located. The lungs were "congested." DiGeorge anomaly cannot be ruled out from these findings. Although, the coroner ruled that "malnutrition" was the sole cause of death, malnutrition, according to the World Health Organization definition, cannot be diagnosed in this infant. Compared with standard growth charts, the older children fell 2.1-4.1 standard deviations below the mean for North American children in height and weight. Labs were normal except for a low cholesterol level in all and a low prealbumin in one of three children tested. Therefore, malnutrition cannot be diagnosed in these children. The pediatrician diagnosed rickets in the four-year-old. However, chest x-rays were normal in all and long bone x-rays showed minimal changes in one child--no sign of rickets. The clinical diagnosis of rickets was not confirmed by the Center for Disease Control's criteria. A psychologist diagnosed the 18-month-old as developmentally delayed to the level of a 15-month-old, but this diagnosis is questionable. CONCLUSION: The raw foods vegan diet and possibly inherited small stature from the father's side account for their relatively low heights and weights. Catch-up growth will probably occur on the standard American diet but would have also been expected if they had remained on a vegan diet.

Body Height↗
PubMed2003

Nutritional rickets with normal circulating 25-hydroxyvitamin D: a call for reexamining the role of dietary calcium intake in North American infants.

The incidence of nutritional rickets appears to be increasing in North American infants and toddlers; it is widely assumed that this is due to vitamin D deficiency. Thus, records of 43 children with nutritional rickets from greater New Haven, Connecticut, from 1986-2002 were identified. The mean age of presentation was 20 months; 86% were of African-American, Hispanic, or Middle Eastern descent. More than 93% of children had been breastfed; however, 15% had received vitamin D supplementation. Eighty-six percent of those with food histories available were weaned to diets with minimal dairy content after nursing. Serum 25-hydroxyvitamin D was 20.9 +/- 11.5 ng/ml and was less than 15 ng/ml in only 22% of patients. Three representative case histories suggest that dietary calcium intake may play a contributory role in the development of disease; 1 case documents radiographic and biochemical resolution of rachitic abnormalities after calcium treatment, but no vitamin D therapy. Clinicians should be aware that low dietary calcium intake after weaning may result in the development of nutritional rickets, and that attention to calcium intake as well as that of vitamin D is important in the establishment of optimal dietary practices for North American infants and children.

Black or African American↗
PubMed2002

Nutritional rickets: an old disease returns.

Nutritional rickets, an ancient disease that was thought to have been cured in the early part of the 20th century, has made an unexpected comeback in recent years throughout the world. Although the frequency of its occurrence is poorly documented, increasing case reports of rickets are apparently related to low dietary intake of vitamin D and calcium and decreased sunshine exposure. Greater awareness of this problem is needed, as are further data regarding vitamin D status and incidence of rickets among infants and toddlers. Routine provision of supplemental vitamin D to all breastfed infants remains controversial, but may become more widely recommended.

Child, Preschool↗
PubMed1996

Early detection of infants with hypophosphatemic vitamin D resistant rickets (HDRR).

The onset of physical signs in infants with hypophosphatemic vitamin D resistant rickets (HDRR) has generally been considered to be at the age of 12 months, but the time of appearance of hypophosphatemia and rachitic signs on radiographs remains unclear. We report a prospective study in three neonates whose mothers were HDRR. At birth, despite a low maternal serum inorganic phosphorus (Pi) level, the serum Pi level was normal together with a negligible renal Pi leak in one neonate. At age 3 months, their serum Pi levels, percentages of tubular reabsorption of Pi, and renal tubular maximal rates of Pi reabsorption in relation to the glomerular filtration rate were low except for one infant. Radiographically, their rickets were not apparent at birth but at age 3 months in all. A premature born infant, born at 28 weeks' gestation weighing 1240 g, was diagnosed as HDRR based on hypophosphatemia due to low renal tubular maximal rate of phosphorus reabsorption in relation to the glomerular filtration rate (TmP/GFR) and normal urine Ca excretion at age 5 months. They were initially treated with 1 alpha-hydroxyvitamin D3 (1 alpha OHD3) and later with 1 alpha OHD3 in combination with Pi, which results in healing of the rickets and a normal increase in height. Thus, early detection and treatment of patients born from mothers with HDRR before physical signs of bow-leg and short stature is possible, but the outcome of early treatment requires further study.

Age of Onset↗
PubMed1993

Nutritional rickets: thoughts about pathogenesis.

The pathogenesis of nutritional rickets is not well-understood. While the etiologies include deficiencies of vitamin D, calcium (Ca) or phosphate (PO4), and perhaps aluminium toxicity, the role these nutrients play in the development of tissue level anomalies characteristic of rachitic cartilage and bone has yet to be defined. Reported alterations in the biochemistry of rachitic bone and cartilaginous matrix which could adversely affect mineralization and endochondral ossification are of questionable significance since the tissues mineralize rapidly when exposed to Ca and PO4 salts in vivo and in vitro. The low Ca and PO4 concentrations of the extracellular fluid (ECF) bathing rachitic cartilage and bone matrix suggest that local mechanisms operate to impair mineralization. In healing rickets, the Ca and PO4 content of these tissue fluids increases in the same time-frame it takes to experimentally remineralize the matrices. However, it is not certain what determines the Ca and PO4 content of the ECF. Cytokines which may play a role in the cellular regulation of Ca and PO4 and maintain processes which contribute to normal patterns of endochondral ossification could provide a mechanism common to the pathogenesis of rickets from a variety of causes.

Animals↗
PubMedDate not supplied

Epidermolytic hyperkeratosis with rickets.

A 6-year-old child presented with generalized hyperkeratosis, most marked over the flexures; windswept deformity of the legs; and limping since 3 years. On the basis of the clinical, histopathologic and biochemical findings, he was diagnosed as a case of epidermolytic hyperkeratosis with rickets. He was treated with parenteral vitamin D3 and calcium supplements orally. Nutritional rickets has been reported in children with various types of ichthyosis like lamellar and X-linked types. We report this case of epidermolytic hyperkeratosis with rickets for its rarity.

Child↗