[A trial of suppressing secondary hyperparathyroidism by oral high dose therapy of 1, 25-dihydroxyvitamin D3].

We reported a successful treatment of secondary hyperparathyroidism by intermittent oral administration of high dose of 1, 25 dihydroxycholecalciferol [1.25-(OH)2D3] in three patients on maintenance hemodialysis. Dialysis durations were 4 months in case 1, 6.5 years in case 2 and 12.5 years in case 3. The levels of c-PTH ranged from 4.7 ng/ml to 94.2 ng/ml. 1, 25-(OH)2D3 in dosages up to 8.0 micrograms was given once a week just after hemodialysis. Before the administration and after 48 hours, serum Ca, serum Pi, serum Mg, c-PTH and highly sensitive PTH were assayed. There was a significant correlation between max. plasma concentration of 1, 25-(OH)2D and logarithm of the dose in all patients. The max. plasma level of 1, 25-(OH)2D reached 25-(OH)2D reached to 200 pg/ml at 4 hours after the oral administration of 8.0 micrograms. Their thresholds of 1, 25-(OH)2D level which could decrease the PTH levels were elevated proportionally to their dialysis durations. Case 1 required 4.0 micrograms to suppress secondary hyperparathyroidism, whereas, case 2 and 3 did 8.0 micrograms of 1, 25-(OH)2D3. Severe hypercalcemia was not observed during a high dose treatment. In conclusion, we have succeeded in treating refractory secondary hyperparathyroidism by intermittent oral administration of high dose 1, 25-(OH)3D3. This therapy is recommended to start in the earlier stage of a long-term dialysis in order to prevent severe secondary hyperparathyroidism and bone disease.

Bone mineral content, serum vitamin D metabolite concentrations, and ultraviolet B light exposure in infants fed human milk with and without vitamin D2 supplements.

OBJECTIVE: To monitor ultraviolet B light exposure in human milk-fed infants both with and without supplemental vitamin D2, and to measure longitudinally the bone mineral content, growth, and serum concentrations of calcium, phosphorus, 25-hydroxyvitamin D3, 25-hydroxyvitamin D2, 1,25-dihydroxyvitamin D, and parathyroid hormone. DESIGN: Longitudinal, randomized, double-blind, placebo-controlled study of 6 months' duration. SETTING: Patients from private pediatric practice, Madison, Wisconsin. PATIENTS: Sequential sampling of 46 human milk-fed white infants; 24 received 400 IU/day of vitamin D2, and 22 received placebo. An additional 12 patients were followed who received standard infant formula. Eighty-three percent of patients completed a full 6 months of the study. MEASUREMENTS AND RESULTS: Ultraviolet B light exposure and measurements of growth did not differ between groups. At 6 months, the human milk groups did not differ significantly in bone mineral content or serum concentrations of parathyroid hormone or 1,25-dihydroxyvitamin D, although total 25-hydroxyvitamin D values were significantly less in the unsupplemented human milk group (23.53 +/- 9.94 vs 36.96 +/- 11.86 ng/ml; p less than 0.01). However, 25-hydroxyvitamin D3 serum concentrations were significantly higher in the unsupplemented human milk-fed group compared with the supplemented group (21.77 +/- 9.73 vs 11.74 +/- 10.27 ng/ml, p less than 0.01) by 6 months of age. CONCLUSION: Unsupplemented, human milk-fed infants had no evidence of vitamin D deficiency during the first 6 months of life.

Bone disease in chronic childhood cholestasis. I. Vitamin D absorption and metabolism.

Metabolic bone disease is common in children and adults with chronic cholestasis. We evaluated baseline vitamin D (vitamin D2 and D3), 25-OH vitamin D2 and D3, 1,25(OH)2 vitamin D, vitamin D-binding protein, bone mineral content and dietary mineral content in six children (mean age: 12.1 years) with cholestasis since infancy. Absorption of 25-OH vitamin D3 and vitamin D2 was evaluated by measuring serial serum concentrations after a test dose. Bone mineral content was reduced by greater than 2 S.D. in five of six subjects compared to age-specific controls; none had radiographic evidence of rickets but all had osteopenia. Dietary Ca and P content in the subjects was comparable to the recommended daily allowance for age-specific children. Baseline serum vitamin D2 concentrations were undetectable in all but one cholestatic subject despite oral supplementation with 2,500 to 50,000 IU per day vitamin D2. Baseline serum 25-OH vitamin D was 33.2 +/- 6.0 ng per ml (mean +/- S.E.) and comparable to our laboratory norms (15 to 50 ng per ml). Serum 1,25(OH)2 vitamin D and "free" 1,25(OH)2 vitamin D were both significantly (p less than 0.05) reduced compared to controls. A significantly blunted rise and reduced area under the absorption curve (both p less than 0.001) after 1,000 IU per kg vitamin D2 was found in cholestatic children (0.8 ng +/- 0.5 ng per ml and 18.0 +/- 14.3 ng hr per ml, respectively) compared to controls (59.5 +/- 10.0 ng per ml and 1,780 +/- 253 ng hr per ml, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Intermittent high-dose vitamin D prophylaxis during infancy: effect on vitamin D metabolites, calcium, and phosphorus.

In infants receiving intermittent high dose vitamin D prophylaxis (600,000 IU ergocalciferol per dose orally) every 3-5 mo, the serum concentrations of vitamin D metabolites, calcium (Ca), and phosphorus (P) were determined before and 2 wk after each dose. The 25-hydroxyvitamin D (OHD) concentrations increased to well above normal but the values returned to the normal range before each subsequent dose. The 24,25- and 25,26-dihydroxyvitamin D ([OH]2D) levels followed a pattern similar to that of 25-OHD, and both were closely related to the latter (r = 0.85, p less than 0.005, and r = 0.84, p less than 0.005, respectively). The 1,25-(OH)2D concentrations did not vary in a consistent pattern and remained largely within the normal range. All infants had normal Ca levels before the first dose but 14 infants (34%) later had one or both Ca values above the upper normal limit of 2.80 mmol/L (2.81-3.32 mmol/L), indicating that the vitamin D doses were excessive despite the lack of accumulative increases in serum vitamin D concentrations.

Treatment effects of parenteral vitamins in total parenteral nutrition patients.

To determine the prevalence of abnormal vitamin levels in an adult hospitalized population requiring total parenteral nutrition (TPN) and to assess the effect of routine parenteral vitamin therapy on vitamin levels, we studied 35 general surgical patients. Assays for 12 vitamins were performed both before and after a standard 10-day course of TPN. Patients were given nothing by mouth. The first 25 patients received a daily parenteral vitamin mixture tailored to the recommendations of the Nutrition Advisory Group of The American Medical Association (maintenance dose). The final 10 patients were given a parenteral multivitamin dose providing substantially greater amounts of most vitamins (repletion dose). Only 58% (190/324) of pre-TPN vitamin levels were normal, 25% were low, and 17% were high. No patient had fewer than two abnormal baseline levels. Vitamin levels did not correlate with serum albumin, body weight, or nitrogen balance. After 10 days of treatment, only 39% of low pre-TPN vitamin levels improved; most (45/62) of the low posttreatment levels were low at baseline. The higher repletion dose resulted in a significantly (p less than 0.01) greater percent increase in vitamin A, C, and pyridoxine levels. The prevalence of abnormal vitamin levels in this population is high (42%). Standard parenteral vitamin therapy leads to marginal improvement in abnormally low pre-TPN vitamin levels.

Hypercalcemia in infants with congenital hypothyroidism and its relation to vitamin D and thyroid hormones.

The circulating concentrations of calcium, phosphorus, and vitamin D metabolites were measured in 25 infants (fifteen to 30 days of age) with congenital hypothyroidism before treatment or during the first 6 months of thyroxine therapy. Five of the children before treatment and four during the early 3 months of treatment had mild hypercalcemia (10.8 to 12.4 mg/dl). Hypercalcemia before treatment did not appear to be related to the vitamin D status of the infant nor to an alteration in vitamin D metabolism, but to the presence of a residual thyroid secretion. In contrast, hypercalcemia during thyroxine therapy was related to vitamin D supplementation, even though the serum calcium concentration could not be correlated with the circulating concentration of any of the vitamin D metabolites assayed and obvious changes in vitamin D metabolism could not be demonstrated.

Vitamin D supplementation during pregnancy: effect on neonatal calcium homeostasis.

We assessed whether modification of vitamin D nutritional status during the last trimester of pregnancy affects maternal and neonatal calcium homeostasis. At the end of the first trimester, 40 pregnant women were randomly assigned to either of two groups, and blood taken to assess the basal values of Ca, Pi, Mg, iPTH, 25-OHD, and 1,25(OH)2D. From the sixth month on, group 1 (+D) received 1000 IU vitamin D3 daily; group 2 (-D) served as control. At the time of delivery, maternal serum 25-OHD was higher in the +D group (P less than 0.0005). Ca, Pi, iPTH, and 1,25(OH)2D were not affected. At term, venous cord 25-OHD levels were also higher in the +D group (P less than 0.0005), and 1,25(OH)2D levels slightly lower (P less than 0.05), but neither Ca, Pi, nor iPTH differed between the two groups. Serum CaT dropped significantly (P less than 0.002) at 4 days of age in the infants from both groups, although to a lesser extent in these from the +D group (P less than 0.05). Circulating iPTH increased in both groups. Serum 25-OHD remained low in the -D group, and dropped slightly in the +D group; 1,25(OH)2D remained stable during the first 4 days of life in the -D group, and increased in the +D group (P less than 0.001). Our data demonstrate the importance of providing adequate maternal vitamin D stores to ensure better perinatal handling of calcium. This is of particular importance for populations at risk for hypovitaminosis D.

Relationship between bone GLA-protein (BGP) and calcidiol (25-hydroxycalciferol) in serum of breast-fed infants.

The aim of this investigation was to study the bone metabolism in early infancy by establishing the relationship between serum osteocalcin levels and the hormonal vitamin D status of exclusively breast-fed infants during their first month of life. Calcium, phosphorus, alkaline phosphatase, 25-hydroxycalciferol (calcidiol), 1,25-dihydroxycalciferol (calcitriol) and osteocalcin (BGP or GLA-protein) were measured in 22 healthy lactating women and their paired breast-fed infants before and after supplementation (400 IU vitamin D per day). Prior to supplementation calcidiol, calcitriol and osteocalcin remained unchanged. Following supplementation there was an increase in all the parameters with the exception of calcitriol. The administration of vitamin D to breast-fed infants should in fact have an effect on bone activity as reflected by the increase in osteocalcin levels.

Parameters related to 25-OH-D levels in a population-based study of women.

We surveyed calcidiol levels (25-OH-D) in a geographically-defined population of 373 women, ages 20-80 yr to test for an association between occult osteomalacia and excess bone loss. Bone mass was measured by photon densitometry and an estimate of vitamin D was determined by measuring dietary and supplemental intake as well as sunlight exposure equivalent. The relationship of smoking practices, alcohol use, exogenous estrogen use, and medications to calcidiol level was assessed. Calcidiol levels were not associated with bone mass levels observed at two different forearm sites. Low levels of calcidiol, indicative of generalized vitamin D deficiency, were not observed in this population though mean estimates of vitamin D intakes from food 119 +/- 148 IU) or food and supplements (319 +/- 463 IU) were less than the Recommended Dietary Allowance (400 IU). Calcidiol was significantly associated with estimates of vitamin D intake from food (r = 0.11), supplement use (r = 0.21), and sunlight equivalent exposure (r = 0.26). Calcidiol levels were negatively related to age (p = 0.0020) and positively related to exogenous estrogen use and premenopausal state independent of age.

Effect of race and diet on human-milk vitamin D and 25-hydroxyvitamin D.

Vitamin D-deficiency rickets continues to be reported in infants fed human milk, and the importance of human milk as a source of vitamin D for infants is controversial. Furthermore, effects of race and of normally consumed maternal vitamin D intake on human-milk vitamin D have not been reported. Milk, serum, and three-day-diet diaries were obtained from 25 mother-infant pairs. Human-milk vitamins D3 and D2 and 25-hydroxyvitamin D3 were lower in blacks vs whites, whereas 25-hydroxyvitamin D2 did not differ. Total-milk vitamin D, but not 25-hydroxyvitamin D, correlated with vitamin D intake. Milk vitamin D2 specifically was correlated with vitamin D intake even after controlling for race. Infant serum 25-hydroxyvitamin D did not correlate with milk vitamin D or 25-hydroxyvitamin D; we speculate that the contribution of vitamin D from human milk in these infants is insignificant relative to the contribution from sunshine exposure.

Vitamin D prophylaxis in the elderly: a simple effective method suitable for large populations.

A comparison of two regimens of vitamin D prophylaxis in elderly institutionalized subjects has been made. Sixty-six subjects received 2.5mg vitamin D2 by mouth in December 1982; a further group of 62 received the same dose in December 1982 and again in June 1983. Blood samples have been analysed for 25-hydroxyvitamin D2 [25(OH)D2] in 10 subjects from each group over a 12-month period. The serum 25(OH)D2 was maintained at normal concentrations for most of the year in the once-a-year dosage group but at the end of 12 months only 60% were fully protected. The twice-per-year regimen offered complete protection maintaining the serum 25(OH)D2 above the threshold associated with osteomalacia. It is concluded that a twice-yearly regimen of vitamin D supplementation is a practical method for prophylaxis in institutionalized elderly people.

Serial serum 25-hydroxyvitamin D and mineral homeostasis in very premature infants fed preterm human milk.

Fourteen very low birthweight infants (mean +/- SD 1,070 +/- 180 g and 29.3 +/- 1.9 weeks gestation) fed their own mother's milk were clinically followed until 3-4 months of age with frequent measurements of serum calcium, phosphorus, magnesium, 25-hydroxyvitamin D (25-OHD), parathyroid hormone, alkaline phosphatase, and albumin, and urine calcium, phosphorus, and magnesium. These infants were matched for birthweight and gestation with 14 infants (1,075 +/- 152 g and 29.0 +/- 1.7 weeks) who had been similarly followed during concomitant studies of infants fed standard formula (Similac 20 cal/oz). Urine phosphorus was markedly lower in the breast milk-fed group from initiation of feedings, and serum phosphorus became significantly lower at and after 6 weeks of age. The fall in serum phosphorus was accompanied by a marked calciuria. Parathyroid hormone was suppressed in the breast milk-fed group, although serum calcium was not elevated and did not differ from formula-fed infants. A high incidence of moderate-severe hypomineralization on radiographs was seen in both breast milk- and formula-fed groups. Six of 14 breast-fed infants required phosphorus supplementation at 8-10 weeks of age because of significant hypophosphatemia, hypercalciuria, and hypomineralization. These infants differed from those not requiring phosphorus supplements by being smaller at birth but not of lower gestation, and having persistently low serum 25-OHD at and after 6 weeks of age.

Late infantile tetany and secondary hyperparathyroidism in infants fed humanized cow milk formula. Longitudinal follow-up.

Five full-term infants with birth weights appropriate for gestational age presented with hypocalcemic tetany at 5 to 9 days of age. All infants had been fed Similac 20, a cow milk formula. Initial mean serum calcium (Ca), phosphorus (P), and magnesium (Mg) levels of the tetanic infants were 6.8, 9.5, and 1.6 mg/dL, respectively. The mean serum parathyroid hormone (PTH) level was elevated at 79 mu LEq/mL (adult normal values, less than or equal to 57 mu LEq/mL). Following restoration of normocalcemia with Ca supplements, feeding was reinstituted with Similac 20 in two infants and Similac PM 60/40 in three infants. Serum biochemical and hormonal values were compared with those of 18 exclusively breast-fed infants followed up from three weeks to six months and 14 Similac 20-fed full-term infants followed up from one week to six months. In tetanic infants, serum Ca concentrations became elevated (10.4 +/- 0.05 mg/dL; mean +/- SEM) by six weeks (vs 9.2 +/- 0.3 mg/dL in breast-fed infants) (P less than .001) and serum Mg concentrations (2.26 +/- 0.01 mg/dL) by four weeks (vs 1.92 +/- 0.07 mg/dL in breast-fed infants) (P less than .01). Mean serum P concentrations declined progressively. Mean serum PTH concentrations were elevated and ranged from 74 to 143 mu LEq/mL at two to 16 weeks (vs mean 28 to 35 mu LEq/mL in breast-fed infants (P less than .0001). In 14 formula-fed-nontetanic full-term infants, serum PTH concentrations were intermediate between formula-fed-tetanic and breast-fed infants, mean serum Ca concentrations ranged from 10.2 to 10.4 mg/dL, and mean serum P concentrations declined from 8.3 to 7.1 mg/dL. We speculate that acute hypocalcemic tetany in the study infants was induced by the relatively high P load in cow milk formulas (vs human milk); with the continued P load, secondary hyperparathyroidism continued, maintaining P, Ca, and Mg homeostasis.

The relations between vitamin D2 and D3 in the diet and plasma 25OHD2 and 25OHD3 in elderly women in Great Britain.

Vitamin D2 and D3 intake and plasma 25OHD2 and 25OHD3 were measured in 70 elderly women; 13 living at home and 57 long-stay patients with no access to sunlight. Vitamin D2 intake and plasma 25OHD2 were correlated in the whole group (p less than .005) and vitamin D3 intake and plasma 25OHD3 and total D intake and total 25OHD were significantly correlated (p less than .005) in the patients. In the whole group the plasma 25OHD2 increased by 4.5 nmol/l for every 1 microgram increase in vitamin D2 intake. This was also the increase observed in a longitudinal study of vitamin D2 supplements in 11 patients. Vitamin D intake is a significant determinant of plasma 25OHD and the relation between them suggests that stores of vitamin D can be maintained at 20 nmol/l in the elderly by a daily intake of 4 micrograms of vitamin D, even in the absence of sunlight.

Effects of vitamin D. A comparison of 1 alpha OHD2 and 1 alpha OHD3 in rats.

The effect of 1 alpha OHD2 and 1 alpha OHD3 have been studied in rachitic, normal, and prednisolone-treated male rats. The healing of rickets, the stimulation of intestinal Ca and P transport, the effect on bone mineral, and the induction of renal calcifications have been examined. The two 1-hydroxylated compounds are equally potent in healing rickets, and by comparison with previous data are equivalent to 100-200 IU/micrograms. 1 alpha OHD2 and 1 alpha OHD3 stimulated intestinal Ca and P transport to the same extent and were antagonistic to prednisolone in this respect. 1 alpha OHD2 reduced the number of osteoclasts and increased bone mineral in normal rats in contrast to 1 alpha OHD3, which increased osteoclasts and slightly reduced bone mineral. Prednisolone-induced osteopenia was more effectively counteracted by 1 alpha OHD2 than by 1 alpha OHD3. Mortality rate was higher in rats intoxicated with 1 alpha OHD3 than for rats given 1 alpha OHD2. LD50 was estimated to be five to fifteen times higher for 1 alpha OHD2. Renal calcification were more pronounced after dosing with 1 alpha OHD3 than after treatment with 1 alpha OHD2. When prednisolone was given together with 1 alpha OHD2 or 1 alpha OHD3, renal calcifications were further increased. These observations demonstrate physiological dissimilarities between vitamin D2 and vitamin D3 in rats which are in accordance with a different metabolism of the two vitamins. The findings, in particular that 1 alpha OHD2 is less toxic than 1 alpha OHD3, are of potential clinical importance.

Relative contributions of diet and sunshine to the overall vitamin D status of the grazing ewe.

Circulating concentrations of 25-hydroxyvitamin D2 (25OHD2) and 25-hydroxyvitamin D3 (25OHD3) provide, respectively, a measure of the contributions of the diet and sunshine to the overall vitamin D status. These indices were measured in grazing sheep over a 16 month period which included their first pregnancy. Seasonal fluctuations in 25OHD3 concentrations were very marked, demonstrating both the dominance of photobiosynthesis as a source of vitamin D in the summer and also the lack of an effective storage mechanism. The concentration of 25OHD2 was subject to much smaller fluctuations, but when young grass was being consumed it was significantly lower than when mature grass or hay was fed. Supplementation in winter maintained circulating concentrations at a satisfactory level and may be a wise precaution in practice.

25-Hydroxyvitamin D and 1,25-dihydroxyvitamin D of D2 and D3 origin in maternal and umbilical cord serum after vitamin D2 supplementation in human pregnancy.

Serum concentrations of 25-hydroxyvitamin D (25-OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] of vitamin D2 and D3 origin were determined separately in 10 women before vitamin intake in early pregnancy, and repeated in maternal and cord serum obtained at delivery after 20 to 30 wk of vitamin D2 supplementation in a dose of 400 IU/day. Before supplementation 25-OHD2 and 1,25-(OH)D2D2 were present in just traceable or nondetectable concentrations, but the levels increased in all to a mean +/- 1 SD of 7.3 +/- 3.7 ng/ml and 37.2 +/- 18.1 pg/ml, respectively (p less than 0.0025), by the time of delivery. At delivery the total 25-OHD and 1,25-(OH)2D levels were always lower in the cord than in the maternal serum (30.7 +/- 14.2 versus 20.1 +/- 9.1 ng/ml, and 90.1 +/- 31.2 versus 37.3 +/- 11.6 pg/ml, p less than 0.0025). The paired concentrations of 25-OHD were closely related (r = 0.89, p less than 0.0005), while the association for 1,25-(OH)2D was not statistically significant (r = 0.53, p less than .01). The 25-OHD of D2 and D3 origin accounted for a similar proportion of the total 25-OHD in the maternal and cord serum (ratio of 25-OHD2 to 25-OHD3: 0.40 +/- 0.28 versus 0.45 +/- 0.29, p = NS), as did the respective 1,25-(OH)2D metabolites [ratio of 1,25-(OH)2D2 to 1,25-(OH)2D3: 0.73 +/- 0.35 versus 0.90 +/- 0.50, p = NS].(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence that 1,25-dihydroxyvitamin D3 inhibits the hepatic production of 25-hydroxyvitamin D in man.

Previous in vitro studies in rachitic rat liver suggested that 1,25-dihydroxyvitamin D inhibits the hepatic production of 25-hydroxyvitamin D (25-OHD). An investigation therefore was carried out in eight normal subjects to determine whether concomitant administration of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] would alter the response of serum 25-OHD to challenge with vitamin D. In control studies, vitamin D, 100,000 U/d for 4 d, significantly increased mean serum 25-OHD, from 26.3 +/- 2.9 to 66.7 +/- 12.6 ng/ml (P less than 0.01). In contrast, 1,25(OH)2D3, 2 micrograms/d for 4 d, completely prevented an increase in serum 25-OHD in response to the same dose of vitamin D in the same individuals (25.1 +/- 2.2 vs. 27.4 +/- 5.3 ng/ml, NS). In a post-control study in seven of the normal subjects, vitamin D again significantly increased mean serum 25-OHD, from 18.2 +/- 3.1 to 42.8 +/- 4.7 ng/ml (P less than 0.001). In each of the three studies, mean serum calcium, phosphorus, and creatinine did not change and remained within the normal range. Whereas mean urinary calcium did not change in response to vitamin D alone during the 4 d of the two control studies, it increased significantly in the study in which vitamin D and 1,25(OH)2D3 were given together. A dose-response inhibition of the response of serum 25-OHD to vitamin D by 1,25(OH)2D3 was demonstrated in two of the normal subjects. The results provide evidence that 1,25(OH)2D3 inhibits the hepatic synthesis of its precursor 25-OHD in man.

Persistence of parathyroid hypersecretion after vitamin D treatment in Asian vegetarians.

An investigation into plasma calcium concentrations and the biochemical factors which regulate it in vegetarian Asian subjects without clinical or radiological features of osteomalacia revealed the presence of low serum 25-hydroxyvitamin D concentrations and elevated PTH concentrations, even in the presence of calcium levels in the normal range (up to 2.35 mmol/liter). These elevated PTH concentrations, though not as high as those in osteomalacic patients with hypocalcemia, often persisted despite treatment with vitamin D, normalization of 25-hydroxyvitamin D, and an increase in calcium concentrations. In one patient the PTH concentration remained high even when the plasma calcium concentration became supranormal. Therefore, secondary hyperparathyroidism is commonly associated with vegetarianism, and may play an important role in maintaining calcium concentrations within the normal range. Persistent elevation of PTH despite normalization of 25-hydroxyvitamin D also points to autonomous PTH hypersecretion, which may result in osteolysis in the long term, and raises the question of the need for vitamin D supplementation in vegetarians with low dietary intake of vitamin D.

Vitamin D nutrition in pregnant women at term and in newly born babies in Saudi Arabia.

A survey to assess the vitamin D nutritional state in 119 pregnant women at term and in their newborns was undertaken in Riyadh, Saudi Arabia. Concentrations of 25-hydroxy vitamin D (25-(OH)D) were below 4 ng/ml in 30 of 119 maternal sera, in 11 of which they were undetectable. The median concentration of 25-(OH)D was 5.7 ng/ml, which is comparable to that found in Asian vegetarian women at term in London. Fifty of 119 cord samples had undetectable 25-(OH)D, and a total of 81 samples had 25-(OH)D concentrations of less than 4 ng/ml. Despite the low 25-(OH)D concentrations cord bloods had calcium concentrations higher than those in maternal blood, while serum albumin concentration was similar in maternal and cord samples. Higher socioeconomic background of women, antenatal care, and vitamin D supplementation were associated with significantly higher concentrations of 25-(OH)D. Vitamin D supplementation, however, had no significant effect on 25-(OH)D concentration in cord samples or on the weight of the newborns. This study shows the high prevalence of marginal vitamin D nutrition in women in Saudi Arabia, which may predispose babies to rickets during infancy. In a country endowed with plentiful sunshine, the exclusion of sunshine by thick dark veils and bad housing probably contribute to this marginal state of vitamin D nutrition.