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

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.     

Varying role of vitamin D deficiency in the etiology of rickets in young children vs. adolescents in northern India

The relative importance of calcium vs. vitamin D deficiency in the etiology of nutritional rickets in the tropics may be different in children compared with adolescents. We studied calcium intake, sun exposure, serum alkaline phosphatase, and 25 hydroxyvitamin D in 24 children and 16 adolescents with rickets/osteomalacia. The values were compared with those obtained in control subjects (34 children and 19 adolescents). We found that young children with rickets had lower calcium intake compared with controls (285 +/- 113 vs. 404 +/- 149 mg/day, p < 0.01), but similar sun exposure (55 +/- 28 vs. 56 +/- 23 min x m2/day) and 25 hydroxyvitamin D (49 +/- 38 vs. 61 +/- 36 nmol/l). Sixteen of 24 children with rickets had 25 hydroxyvitamin D above the rachitic range (> 25 nmol/l), in contrast to one of 16 adolescents. Adolescent patients had low calcium intake vs. controls (305 +/- 196 vs. 762 +/- 183 mg, p < 0.001), and lower sunshine exposure (16 +/- 15 vs. 27 +/- 17 min x m2/day, p < 0.01) and serum 25 hydroxyvitamin D (12.6 +/- 7.1 vs. 46 +/- 45.4 nmol/l, p < 0.001). The odds ratio for developing rickets with a daily calcium intake below 300 mg was 4.8 (95 per cent CI, 1.9 - 12.4, p = 0.001). Subjects with rickets were randomized to receive 1 g calcium daily, with or without vitamin D. Children showed complete healing in 3 months, whether they received calcium alone or with vitamin D. Adolescents showed no response to calcium alone, but had complete healing with calcium and vitamin D in 3-9 months (mean 5.3 months). Thus deficient calcium intake is universal among children and adolescents with rickets/osteomalacia. Inadequate sun exposure and vitamin D deficiency are important in the etiology of adolescent osteomalacia.     

Case-control study of factors associated with nutritional rickets in Nigerian children

OBJECTIVE: Because the causes of nutritional rickets in tropical countries are poorly understood, we conducted a case-control study to determine factors associated with rickets in Nigerian children. STUDY DESIGN: We compared 123 Nigerian children who had rickets with matched control subjects. Dietary, demographic, anthropometric, and biochemical data were collected to assess factors related to calcium and vitamin D status, which might predispose children to rickets. RESULTS: Mean (+/- SD) daily dietary calcium intake was low in both children with rickets and control children (217 +/- 88 mg and 214 +/- 77 mg, respectively; P =.64). Children with rickets had a greater proportion of first-degree relatives with a history of rickets (14.6% vs 3.1%; P <.001), a shorter mean duration of breast-feeding (16.0 vs 17.3 months; P =.041), and a delayed age of walking (14 vs 12 months; P <.001). Among children with rickets, biochemical features suggestive of calcium deficiency included hypocalcemia, extremely low calcium excretion, and elevated 1, 25-dihydroxyvitamin D and parathyroid hormone values. Median 25-hydroxyvitamin D concentrations were 32 and 50 nmol/L (13 and 20 ng/mL) in children with rickets and control children, respectively (P <.0001). Only 46 subjects with rickets (37%) had 25-hydroxyvitamin D values <30 nmol/L (12 ng/mL). CONCLUSIONS: Vitamin D deficiency appears unlikely to be the primary etiologic factor of rickets in African children. Moreover, low dietary calcium intake alone does not account for rickets. Insufficient dietary calcium probably interacts with genetic, hormonal, and other nutritional factors to cause rickets in susceptible children.     

Case-control study of diet and sun exposure in adolescents with symptomatic rickets

Dietary intake and sun exposure were compared in a case-control study of 14 adolescent girls diagnosed to have symptomatic nutritional rickets with hypocalcaemia, hypophosphoraemia, elevated serum alkaline phosphatase and serum parathormone and reduced 25-hydroxy vitamin D levels and 20 controls without clinical rickets (ten girls) of the same age group and socio-economic background. In the control group, calorie intake was reduced in seven boys and eight girls, dietary calcium in seven boys and seven girls and vitamin D in six boys and eight girls. All 20 adolescents of both sexes were exposed to the sun for more than 60 min a day. In the group with rickets, calorie intake was reduced in 11 girls, calcium in 14 girls and vitamin D in nine girls). Sun exposure was significantly less in girls with rickets than in controls (p < 0.001). Adolescents in our population, especially females, are at high risk of developing nutritional rickets. Prevention by longer exposure to the sun is simple and cheap but when not practical for social or cultural reasons routine vitamin D supplementation might be indicated.     

Nutritional rickets in African American breast-fed infants

OBJECTIVE: To analyze the characteristics of infants and children diagnosed with nutritional rickets at two medical centers in North Carolina in the 1990s. STUDY DESIGN: The physical and radiographic findings, calcium, phosphorus, alkaline phosphatase, and 25-hydroxyvitamin D levels of infants and children diagnosed with nutritional rickets at two medical centers were reviewed. Breast-feeding data were obtained from the North Carolina Women, Infants and Children Program (WIC). RESULTS: Thirty patients with nutritional rickets were first seen between 1990 and June of 1999. Over half of the cases occurred in 1998 and the first half of 1999. All patients were African American children who were breast fed without receiving supplemental vitamin D. The average duration of breast-feeding was 12.5 months. The age at diagnosis was 5 to 25 months, with a median age of 15.5 months. Growth failure was common: length was <5th percentile in 65% of cases, and weight was <5th percentile in 43%. CONCLUSION: Factors that may have contributed to the increase in referrals of children with nutritional rickets include more African American women breast-feeding, fewer infants receiving vitamin D supplements, and mothers and children exposed to less sunlight. We recommend that all dark-skinned breast-fed infants and children receive vitamin D supplementation.     

Evaluation of serum osteocalcin as an index of altered bone metabolism

Recent evidence suggests that the protein osteocalcin is like the bone alkaline phosphatase produced by osteoblasts and circulates in human blood. With the introduction of a radioimmunoassay for serum osteocalcin it was hoped that this test would provide a useful index of altered bone metabolism. Therefore serum osteocalcin was measured in 88 controls and 112 patients with disorders of calcium and phosphate metabolism, isolated elevation of alkaline serum phosphatase in the absence of disease (isolated hyperphosphatasaemia) and children prone to osteopenia.In the controls serum osteocalcin was higher in children<15 years (median and range: 11.9, 7.7–15.3 ng/ml) than in adults (3.7, 2.6–5.2 ng/ml) and was highly correlated to alkaline serum phosphatase activity (r=0.87, n=88, P<0.01). Osteocalcin was elevated in primary hypoparathyroidism, low in untreated hypoparathyroidism but normal in hypoparathyroidism (including pseudohypoparathyroidism) during vitamin D treatment. The bone protein was low-normal and increased to high-normal levels during vitamin D therapy in vitamin D deficiency rickets and familial hypophosphataemic rickets, but remained low in patients with end organ resistance to 1,25-dihydroxyvitamin D. Osteocalcin (and urinary hydroxyproline) were not elevated in isolated hyperphosphatasaemia, indicating that mechanisms other than increased bone turnover may account for the markedly elevated serum alkaline phosphatase activity in these subjects. Osteocalcin was decreased in children with diabetes mellitus type I and in patients on glucocorticoid treatment, indicating decreased bone formation. It is concluded that the measurement of serum osteocalcin seems to be a reliable index of bone formation provided that the vitamin D status and renal function are normal. Although serum osteocalcin and alkaline phosphatase were generally correlated there were examples of dissociation between both indices. In some circumstances (e.g. rickets) serum osteocalcin may severe as a useful index of an effective therapy.Abbreviations AP alkaline phosphatase activity - Gla gammacarboxy-glutamic acid - 1,25 (OH)₂D₃ 1,25-dihydroxyvitamin - D₃ calcitriol - PTH parathyroid hormone - HP hypoparathyroidism - PHP pseudohypoparathyroidism - I^oHPT primary hyperparathyroidism - VDR vitamin D deficiency rickets - VDDR II vitamin D dependency rickets type II - FHL familial hypophosphataemic rickets - IH isolated hyperphosphatasaemia in the absence of disease     

Comparisons of oral calcium,high dose vitamin D and a combination of these in the treatment of nutritional rickets in children

Nutritional rickets remains a common child health problem in Turkey and many other developing countries. Although vitamin D deficiency is accepted as the basic problem underlying the disease, others postulate that a deficiency of dietary calcium, rather than vitamin D, is often responsible for the nutritional rickets in sunny countries. We conducted a placebo-controlled study to determine the best treatment regimen for nutritional rickets in children residing in lower socioeconomic regions of a sunny city, Istanbul. Forty-two infants (aged 6-30 months) with rickets were divided into three groups and included in the study. In a randomized fashion vitamin D (300 000 units, intramuscularly), calcium lactate (3 g daily) or a combination of vitamin D and calcium were given to the children. Alkaline phosphatase, calcium, albumin, ionized calcium and phosphorus levels were measured each week. X-ray examinations of the left wrist and left knee were undertaken at the beginning of the study and were repeated at the 2nd and 4th weeks and were scored in order to assess the response to treatment. Treatment produced an increase in serum calcium and a decrease in alkaline phosphatase concentration in all three groups, but the most important increase was reached in the vitamin D plus calcium group. We conclude that vitamin D deficiency appears to be the primary etiologic factor of rickets in our study group, but a better response to treatment with vitamin D or in combination with calcium was obtained than to treatment with calcium alone.     

血清25-羟维生素D在佝偻病诊断中的应用价值

目的：探讨血清25 羟维生素D［25（OH）D］在维生素D缺乏性佝偻病早期诊断中的意义。方法：检测对照组（73例）、可疑组（45例）和佝偻病组（65例）的血清25（OH）D、钙、磷、碱性磷酸酶浓度,并通过ROC曲线对血清25（OH）D的诊断价值进行评价。结果：对照组、可疑组和佝偻病组的血清25（OH）D水平分别为112±37、83±30和72±31 nmol/L,后两者均显著低于对照组（F=26.174,P0.05）。可疑组和佝偻病组的维生素D缺乏率均显著高于对照组（χ2=33.346, P0.05）。结论：血清25(OH)D水平在可疑及确诊佝偻病的患儿中显著降低,可以反映维生素D的营养状况,适用于佝偻病的早期筛查。     

Case-control study of breast milk calcium in mothers of children with and without nutritional rickets

Aim: Despite similarly low calcium intakes and normal vitamin D status, only some Nigerian children develop nutritional rickets. We hypothesized that mothers with children who had developed rickets might have lower breast-milk calcium concentration than mothers with normal children and compared the breast-milk calcium concentration of mothers who had had children with rickets with those who had not (controls). Methods: We collected breast milk from 35 Nigerian mothers who had previously had children with nutritional rickets. For each case mother, we collected breast milk from three matched control mothers at the same stage of lactation (±4 weeks) who had had no children with rickets. Data were collected about parity, stage of lactation, and the infant's intake. The mother's bone density was measured. Results: The mean breast milk calcium concentration of mothers of children with rickets (4.30±1.24 mmol/L) was less than that of control mothers (4.65±1.03 mmol/L; P=0.034 in multivariate regression controlling for duration of lactation and resumption of menses). Forearm bone mineral content was significantly related to breast milk calcium concentration (r = 0.20) after adjusting for height, weight, and bone area (P=0.028). Conclusion: : Reduced breast-milk calcium concentration may contribute to a reduced calcium intake in infancy and predispose children to nutritional rickets.     

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.     

Vitamin D Deficiency Rickets and Vitamin B12 Deficiency in Vegetarian Children

ABSTRACT. 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     

Vitamin D deficiency and rickets in the Eastern Province of Saudi Arabia

BACKGROUND: Nutritional rickets remains prevalent in many developing countries, despite the availability of ample sunlight. The aim of this study was to investigate the clinical features and chemical pathology in a group of children with rickets and to compare them with a control group. SUBJECTS AND METHODS: In a case-control study over a 1-year period (March 2004 to February 2005), children clinically diagnosed with rickets (n=61) were age- and sex-matched with controls (n=58). In addition to routine chemical pathology, 25 (OH) vitamin D3 and parathormone (PTH) were determined. Controls were children without clinical rickets attending hospital for other blood investigations. RESULTS: The mean age of children with rickets was 14.8 mths and of controls was 16.5 mths. Mean (SD) body mass index of the children with rickets [16.8 (1.86)] was not significantly different from that of the controls [17.02 (3.16)]. Mean (SD) head circumference of rachitic children [45.41 (3.64) cm] was greater than that of controls [44.39 (5.07) cm, p=0.03]. Eighty per cent of the children with rickets were breastfed compared with 67% of controls. Thirty per cent of children with rickets were hypocalcaemic vs <7% of controls, 89% had phosphorus values <1.5 mmol/L vs 34.5% of controls and 75% had alkaline phosphatise levels >500 IU/L vs 28% of controls. Seventy-five per cent of children with rickets had serum 25 (OH) D3 <20 nmol/L vs 25% of controls. Mean (SD) PTH level was 23.59 (19.03) pmol/L in the rachitic group and 1.9 (1.05) pmol/L in controls (p<0.05). Lack of exposure to sunlight was recorded in 90% of the children with rickets and in 37% of the controls. CONCLUSION: Apparently healthy children living in areas where rickets is prevalent have risk factors for rickets and a small proportion will have evidence of biochemical rickets.     

Homocysteine and other vascular risk factors in patients with phenylketonuria on a diet

The aim of this study was to investigate the known risk factors, such as lipids, homocysteine and endothelin, for the development of coronary artery disease (CAD) in phenylketonuria (PKU) patients, depending on their diet. The PKU patients (n = 74) were divided into two groups. Group A (n = 34; mean age 6.78 +/- 1.5 y) adhered strictly to a diet and group B (n = 40; mean age 8.0 +/- 3.2 y) did not comply with the diet. The control group comprised 50 healthy non-PKU children. All groups were evaluated for blood levels of homocysteine and vitamin B6 by high-performance liquid chromatography, vitamin B12 and folate in serum by a radioassay, lipids by a routine method, and lipoprotein(a) and endothelin-1 with an immunoassay. Homocysteine levels (28.65 +/- 3.3 micromol l(-1)) were increased in group A compared with group B (6.86 +/- 1.6 micromol l(-1)) and the controls (6.9 +/- 2.0 micromol l(-1)) (p < 0.001). Vitamin B6 (10.7 +/- 10.9 nmol l(-1)), vitamin B12 (98.5 +/- 22.3 pmol l(-1)), folate (2.35 +/- 1.3 nmol l(-1)) and lipids were decreased in group A. The other vascular risk factors, which were not dependent on diet [lipoprotein(a) and endothelin-1], did not differ among the three groups. Conclusion: PKU patients on a strict diet had low vitamin B6, vitamin B12 and folate levels resulting in moderate hyperhomocysteinaemia. The evaluation of these vitamins at short intervals and their supplementation could be an early measure in the prevention of CAD.     

Nutritional rickets and z scores for height in the United Arab Emirates: To D or not to D?

Background: Vitamin D deficiency is still prevalent worldwide, including the Middle East. A cohort of patients with nutritional rickets was treated with vitamin D₂ (ergocalciferol) alone. After this intervention, patients were followed to document changes in z scores for height after treatment. The secondary aim was to determine the proportion of affected children who had vitamin D deficiency or calcium deficiency.
Methods: Z score for height was calculated as the difference between the observed value and the median value, divided by the SD of the population. Z scores were compared in patients before and after treatment.
Results: The improvement in z score after treatment was 0.86 ± 0.95. The 95% confidence interval for the mean difference was 1.32–0.40 ( t  = 3.95, P  < 0.001). With a diagnostic cut-off for 25 hydroxyvitamin D₃ (25D) deficiency of <25 nmol/L, only half were diagnosed with severe vitamin D deficiency. The remaining patients had presumable calcium deficiency. The alkaline phosphatase (ALP) was negatively correlated to z scores, implying that higher ALP concentrations predicted severe bone disease (lower z scores). The variables 25D and age were moderately and positively correlated (Pearson's r  = 0.59, 95%CI: 0.15–0.84; P  = 0.01), indicating that younger infants had the lowest 25D levels.
Conclusion: Vitamin D alone was efficient in resolving radiological and biochemical disturbances as well as improving z scores for height in a cohort of children with nutritional rickets, which included patients with 25D deficiency as well as calcium deficiency. The results support the hypothesis of the interplay and continuum of 25D deficiency and calcium deficiency in the pathogenesis of rickets.     

Maternal vitamin D deficiency and vitamin D supplementation in healthy infants

The objective of this study was to evaluate the common effects of maternal vitamin D deficiency, various doses of vitamin D given to newborns and the effects of these on vitamin D status in early childhood. Seventy-eight pregnant women and 65 infants who were followed up in various health centers were included in the sudy. 25-hydroxyvitamin-D (25-OHvitD), calcium (Ca), phosphorus (P) and alkaline phosphatase levels were measured in blood samples drawn from pregnant women in the last trimester. Infants born to these mothers were given 400 or 800 IU of vitamin D subsequently at the start of the second week. 25-OHvitD, Ca, P and alkaline phosphatase levels of the 65 infants who were brought in for controls (May-September 2000) were measured and hand-wrist X-rays were evaluated. We analyzed the relationship between vitamin D status of the mothers and infants and socio-economic status; mothers' dressing habits (covered vs uncovered), educational level, and number of pregnancies; and sunlight exposure of the house. Covered as a dressing habit meant covering the hair and sometimes part of the face and wearing dresses that completely cover the arms and legs. In 40 infants who were breast-fed and received the recommended doses of vitamin D on a regular basis, the relationship between serum vitamin D levels and supplementation doses given was analyzed. Serum 25-OHvitD level of the mothers was 17.50 +/- 10.30 and 94.8% of the mothers had a 25-OHvitD level below 40 nmol/L (below 25 nmol/L in 79.5%). The risk factors associated with low maternal 25-OHvitD were low educational level (p = 0.042), insufficient intake of vitamin D within diet (p = 0.020) and "covered" dressing habits (p = 0.012). 25-OHvitD level of the infants was 83.70 +/- 53.70 nmol/L, and 24.6% of the infants had 25-OHvitD levels lower than 40 nmol/L. Risk factors for low 25-OHvitD levels in infants were a) not receiving recommended doses of vitamin D regularly (p = 0.002) and b) insufficient sunlight exposure of the house (p = 0.033). There was a pour but significant correlation between maternal vitamin D levels and infants' 25-OHvitD levels at four months (r = 0.365, p < 0.05). No significant correlation was found between 25-OHvitD levels and supplementation doses of vitamin D (19 infants were supplemented with 400 IU/day and 21 with 800 IU/day of vitamin D) (p = 0.873). Severe maternal vitamin D deficiency remains a commonly seen problem in Turkey. However, vitamin D deficiency can be prevented by supplementation of vitamin D to newborns (at least 400 IU). Supplementation of 800 IU vitamin D in the areas of maternal vitamin D deficiency has no greater benefits for the infants.     

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.     

Comparison of low and high dose of vitamin D treatment in nutritional vitamin D deficiency rickets

In this study, we compared three different therapy modes (150,000 IU, 300,000 IU, and 600,000 IU vitamin D p.o.) in infants with nutritional vitamin D deficiency rickets (VDR). Our purpose was to determine the most effective dosage of vitamin D with least side effects for treating VDR. The study included 56 patients, 3-36 months of age, with nutritional VDR and 20 age-matched control infants. In all infants, serum calcium, phosphorus, alkaline phosphatase, magnesium, serum 25-hydroxycholecalciferol, plasma intact parathormone levels and urinary Ca/creatine ratio were determined. Of 56 patients, 52 were able to be followed long-term. These patients were reexamined on the 3rd day, 7-10th day, and 25-30th day after treatment. On the 30th day post-treatment, we did not find any difference between the doses in the improvement of rickets. However, hypercalcemia was present in eight infants who had been administered 300,000 IU (two infants) and 600,000 IU (six infants) of vitamin D. In conclusion, our findings showed that 150,000 IU or 300,000 IU of vitamin D was adequate in the treatment of VDR, but 600,000 IU of vitamin D may carry the risk of hypercalcemia.     

Vitamin D status of mothers and their neonates in Kuwait

BACKGROUND: There has been a resurgence of nutritional rickets in children in many developing countries and some of the developed countries. Children between 6 and 18 months old are commonly affected. In order to find out the association between vitamin D and rickets we studied the vitamin D status of the neonates and their mothers in Kuwait. METHODS: Two hundred and fourteen full-term pregnant mothers and their neonates were selected from two hospitals in Kuwait. All mothers had normal vaginal delivery. On the day of delivery 2.5 mL of maternal blood and 2.5 mL of cord blood samples were withdrawn. Serum 25-hydroxyvitamin D (25OHD) was determined in duplicate by radioimmunoassay using an Incstar kit. Quality control analyses were done using several between and within run experiments. RESULTS: A total of 128 mother-neonate pairs were selected from the Al-Adan hospital and 86 from the Maternity Hospital. The mean age and parity of the mothers were similar in both hospitals. The mean (+/- SD) 25OHD levels of the mothers and the neonates in the Adan hospital were 13.3 (6.5) ng/mL and 8.2 (6.5) ng/mL, respectively. The corresponding values in the Maternity Hospital were 17.6 (12.4) and 8.1 (7.3) ng/mL for the mothers and the neonate, respectively. Serum 25OHD of the mothers and their newborn infants were highly correlated (r = 0.790, P < 0.001). CONCLUSIONS: Results demonstrate that 40% of the mothers and 60% of the neonates are vitamin D deficient on the day of delivery. The vitamin D of the mothers and neonates are highly correlated (r = 0.790, P < 0.001).     

Factors causing rickets in institutionalised handicapped children on anticonvulsant therapy.

An epidemiological study on vitamin D-dependent rickets was carried out in severely handicapped institutionalised children on long-term anticonvulsant therapy. Nine (10%) of 94 patients had overt rickets on the basis of roentgenological bone changes and biochemical indices, but 46 patients in hospital without medication, and 50 epileptic patients attending an outpatient clinic and taking anticonvulsants had no sign of rickets. Causative factors for the development of rickets were evaluated. Administration of anticonvulsive drugs depressed the serum 25-hydroxyvitamin D (25-OHD) level, but this was not the major factor in the development of rickets. Vitamin D intake seemed to be about average in these patients and its supplementation increased their serum 25-OHD level. This serum 25-OHD level was not maintained by supplemental vitamin D, unless the children were exposed to sunlight. These results indicate that although several factors--such as anticonvulsants, low vitamin D intake, and inactivity--are concerned in the development of rickets, the main cause is lack of sun in institutionalised handicapped children.     

Vitamin D metabolism in pre-operative extrahepatic biliary atresia

In order to clarify the pathogenesis of rickets in preoperative patients with extrahepatic biliary atresia, we evaluated baseline serum 25-OHD and 1,25(OH)2D levels and correlated serum 25-OHD levels with increase in age and season of birth in 16 preoperative patients. Further, parenteral vitamin D2 tolerance tests were performed in 5 cases. Serum 25-OHD and 1,25(OH)2D levels were significantly lower than those in 15 normal controls. There was a negative correlation between the serum 25-OHD levels and increase in age. The patients born during the winter had lower serum 25-OHD concentrations than those born in summer. The mean value of increased 25-OHD levels after the parenteral vitamin D2 tolerance tests did not differ from that of 6 controls. Since there was no impairment of vitamin D 25-hydroxylation, the reduction in serum 25-OHD may therefore be mainly due to disturbed intestinal vitamin D absorption. It was also concluded that season of birth and increase in age are pathogenic factors in the etiology of rickets in preoperative patients with extrahepatic biliary atresia.