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.     

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.     

Rickets in Asian immigrants

Although rickets is considered to have practically disappeared in developed countries, there is increasing evidence of widespread vitamin D deficiency among immigrants. Many studies report rickets and osteomalacia in Asian infants, adolescents and pregnant women moving to developed countries with a cooler climate. The etiopathogenesis of this disorder of calcium and D vitamin metabolism depend mainly on environmental and sociocultural factors, associated with low exposure to sunlight and low calcium intake, among other dietary factors. Given the recent increase in the number of immigrants to Spain, the prevention and treatment of this disease in Asian children and adolescents should be reviewed.     

Adolescent rickets in Saudi Arabia: a rich and sunny country

In this retrospective study from Saudi Arabia, which is a rich and sunny country, we report our experience with 34 adolescents (20 females, 10 males) with rickets. The commonest cause was vitamin D deficiency (58.8%) followed by rickets due to low calcium intake (11.8%) and genetic causes, including possible 25-hydroxylase deficiency (8.8%). The etiology of nutritional rickets is multifactorial, including lack of sun exposure and inadequate calcium intake. The clinical symptoms were nonspecific and therefore cases in this country are either underdiagnosed or missed. Vitamin D deficient patients needed an average of 19 months of treatment before recovery. High dose vitamin D plus calcium supplementation are recommended for treatment. Measures to prevent rickets in all age groups including adolescents are suggested. Further studies on nutritional and genetic forms of rickets are recommended.     

Vitamin D-deficient rickets mimicking ankylosing spondylitis in an adolescent girl

Vitamin D-deficient rickets (VDDR) remains an important health problem especially in developing countries. Insufficient dietary intake of vitamin D and inadequate sun exposure increase the risk of vitamin D deficiency. Since their vitamin D requirement is increased, children and adolescents are potentially at higher risk for vitamin D deficiency. In adolescents, vitamin D deficiency causes osteomalacia, osteoporosis and muscle weakness. While osteoporosis is not associated with bone pain, osteomalacia has been associated with isolated or generalized bone pain. The present case suffered from generalized bone pain for three years. She was misdiagnosed as ankylosing spondylitis, which is a seronegative arthropathy, and was treated with corticosteroids and methotrexate, which have potential side effects. Hypocalcemia, hypophosphatemia, elevated alkaline phosphatase level, secondary hyperparathyroidism, and extremely low vitamin D level were consistent with the diagnosis of severe vitamin D deficiency. Complete clinical and biochemical resolution was achieved with vitamin D replacement.     

Vitamin D insufficiency in preadolescent African-American children

To determine the proportion of vitamin D insufficiency in 6- to 10-year-old preadolescent African-American children residing in Pittsburgh, Pennsylvania and to estimate their therapeutic response to vitamin D 400 IU/day for 1-month, an open-label pre- and post-comparison of vitamin D status following vitamin D 400 IU daily for 1 month during winter and early spring was conducted. Outcomes included serum calcium, phosphorus, albumin, 25 hydroxyvitamin D [25 (OH) D], 1, 25 dihydroxyvitamin D [1, 25 (OH) (2) D], parathyroid hormone (PTH), and markers of bone turnover (serum bone-specific alkaline phosphatase, osteocalcin, and urine n-telopeptide crosslinked collagen type 1 [NTX]). Dietary intake of vitamin D was assessed using a food frequency questionnaire. Forty-one of the 42 enrolled subjects (mean age: 8.9 +/- 1.2 yrs [SD]) were analyzed, and 20/41 (49%) were vitamin D insufficient. Vitamin D insufficient group had a suggestive trend of being older (9.2 +/- 1.0 years vs. 8.5 +/- 1.3 years, p = 0.06) and more pubertally advanced (Tanner II: 7/20 vs. Tanner II: 1/21, p = 0.02). Mean dietary intake of vitamin D was 277 ( 146 IU/day (n = 41). Adequate intake for vitamin D (200 IU/day) was not met in 16/41 (39%); however, the dietary intake of vitamin D was not significantly different between the vitamin D insufficient and vitamin D sufficient groups.     

Vitamin D deficiency causes rickets in an urban informal settlement in Kenya and is associated with malnutrition

The commonest cause of rickets worldwide is vitamin D deficiency, but studies from sub‐Saharan Africa describe an endemic vitamin D‐independent form that responds to dietary calcium enrichment. The extent to which calcium‐deficiency rickets is the dominant form across sub‐Saharan Africa and in other low‐latitude areas is unknown. We aimed to characterise the clinical and biochemical features of young children with rickets in a densely populated urban informal settlement in Kenya. Because malnutrition may mask the clinical features of rickets, we also looked for biochemical indices of risk in children with varying degrees of acute malnutrition. Twenty one children with rickets, aged 3 to 24 months, were identified on the basis of clinical and radiologic features, along with 22 community controls, and 41 children with either severe or moderate acute malnutrition. Most children with rickets had wrist widening (100%) and rachitic rosary (90%), as opposed to lower limb features (19%). Developmental delay (52%), acute malnutrition (71%), and stunting (62%) were common. Compared to controls, there were no differences in calcium intake, but most (71%) had serum 25‐hydroxyvitamin D levels below 30 nmol/L. These results suggest that rickets in young children in urban Kenya is usually driven by vitamin D deficiency, and vitamin D supplementation is likely to be required for full recovery. Wasting was associated with lower calcium (p = .001), phosphate (p < .001), 25‐hydroxyvitamin D (p = .049), and 1,25‐dihydroxyvitamin D (p = 0.022) levels, the clinical significance of which remain unclear.     

Current views on requirements for vitamin D, calcium and phosphorus, particularly in formula fed infants

Calcium (Ca) and phosphorus (P) absorption depends on vitamin D. Vitamin deficiency in children results in rickets and osteoporosis in adults. Prematurely born infants are at risk of osteopenia and rickets. Skin synthesis of vitamin D can obtain the level of 10 000 IU (250 ug) when the whole body is exposed to the sun. Recent opinion on vitamin D requirement establishes the level of more than 80 nmol/L of 25(OH)D. There are no recommendations for children but it seems that due to the risk of skin cancer, exposure to the sun in children will be limited and as a result higher dose of vitamin D will be needed. Calcium and phosphorus are the most common minerals of the human body. Calcium concentration in human milk is not related to the intake. Calcium intake of calcium in premature infants is 70-140 mg/100 kcal. Phosphorus content in breast milk, even as low as 15 mg%, can maintain the optimal Ca/P ratio of 2/1. Prolonged breast feeding without additional Ca and P, may result in reduced bone mineralisation. Higher content of calcium in infant formula in comparison to human milk is due to the fact that Ca absorption from breast milk is 60% in comparison to 40% absorption from the formula.     

Symptomatic rickets in adolescence.

AIM: To describe 21 cases of symptomatic rickets in adolescents. METHODS: The setting was a primary and secondary care hospital in Saudi Arabia providing medical care to Saudi Arab company employees and their families. Cases of symptomatic rickets diagnosed between January 1996 and December 1997 in adolescents aged 10 to 15 years were assessed with respect to clinical presentation, biochemical and radiological evaluation, dietary assessment, and estimation of sun exposure. RESULTS: Symptomatic rickets developed in 21 adolescents (20 females), with a prevalence rate of 68 per 100 000 children years. Presentation included carpopedal spasms (n = 12), diffuse limb pains (n = 6), lower limbs deformities (n = 2), and generalised weakness (n = 1). Biochemical findings included hypocalcaemia (n = 19), hypophosphoraemia (n = 9), raised serum alkaline phosphatase (n = 21) and parathormone (n = 7), and reduced 25-hydroxyvitamin D concentrations (n = 7). Radiological studies were suggestive of rickets in only eight children. All children had an inadequate dietary calcium and vitamin D intake. All but one had less than 60 minutes sun exposure per day. CONCLUSION: Even in sunny climates, adolescents, especially females, can be at risk of rickets. Hypocalcaemic tetany and limb pains were the most common presenting symptoms. Radiological evidence was not present in every case.     

Serum concentrations of 25 hydroxyvitamin D in hospitalized infants. Relation to calciuria

In attempt to evaluate the vitamin D status of the infants of our area under the mode of prophylaxis of carential rickets actually used in France, serum 25 hydroxyvitamin D (25 OHD) levels were measured in 65 infants (age 3 - 32 months) during their hospitalisation for acute illness. Most infants were receiving vitamin D either in daily doses (1,200 - 1,600 u) or in unique loading doses (200,000 - 600,000 u every 4 - 6 months). With this prophylaxis serum concentrations of 25 OHD were elevated, i.e. above 75 nmol/l, in more than 50% of the infants, reaching 474 nmol/l in one case. Calciuria estimated by the calcium/creatinine urinary ratio tended to increase in parallel with the serum 25 OHD level. From these data it is concluded that the actual prophylaxis of carential rickets in France frequently uses excessive doses of vitamin D and that new rules have to be established.     

Symptomatic rickets in adolescence

AIM—To describe 21 cases of symptomatic rickets in adolescents.METHODS—The setting was a primary and secondary care hospital in Saudi Arabia providing medical care to Saudi Arab company employees and their families. Cases of symptomatic rickets diagnosed between January 1996 and December 1997 in adolescents aged 10 to 15 years were assessed with respect to clinical presentation, biochemical and radiological evaluation, dietary assessment, and estimation of sun exposure.RESULTS—Symptomatic rickets developed in 21 adolescents (20 females), with a prevalence rate of 68 per 100 000 children years. Presentation included carpopedal spasms (n = 12), diffuse limb pains (n = 6), lower limbs deformities (n = 2), and generalised weakness (n = 1). Biochemical findings included hypocalcaemia (n = 19), hypophosphoraemia (n = 9), raised serum alkaline phosphatase (n = 21) and parathormone (n = 7), and reduced 25-hydroxyvitamin D concentrations (n = 7). Radiological studies were suggestive of rickets in only eight children. All children had an inadequate dietary calcium and vitamin D intake. All but one had less than 60 minutes sun exposure per day.CONCLUSION—Even in sunny climates, adolescents, especially females, can be at risk of rickets. Hypocalcaemic tetany and limb pains were the most common presenting symptoms. Radiological evidence was not present in every case.     

Nutritional and metabolic rickets

Nutritional rickets is casued by vitamin D deficiency due to lack of exposure to sunlight. Neonatal rickets occurs only in infants born to mothers with very severe osteomalacia. Calcium deficiency alone does not cause mineralisation defects. It only causes osteoporosis and secondary hyperparathyroidism with raised plasma, 1,25 (OH)₂D and osteocalcin. Low 25-OHD, increased IPTH, increased alkaline phosphatase in plasma and decreased calcium and increased hydroxyproline in urine are diagnostic of rickets. Low or undetectable plasma levels of 25-OHD, in presence of high plasma 1,25(OH)₂D and IPTH are often observed during treatment with vitamin D. Even the marginal intakes of fluoride (> 2.5 mg/day) cause rickets in calcium deficient children. Indian children often need high dose of vitamin D due to severely depleted D stores, high IPTH and severe bone disease (radiologic and histomorphometric) for treatment.     

Plasma Concentrations of Vitamin D Metabolites before and during Treatment of Vitamin D Deficiency Rickets in Children

ABSTRACT. Plasma concentrations of 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-(OH)₂D), and 24,25-dihydroxyvitamin D (24,25-(OH)₂D) were determined in 17 children with vitamin D deficiency rickets before therapy was started. Thirteen of them also had these tests repeated during treatment. The median 25-OHD concentration was at the lower limit of the reference range before, but increased distinctly within one week of treatment with 1700–4000 IU vitamin D per day (17 vs. 37 nmol/l, p < 0.01). 24,25-(OH)₂D was undetectable in twelve of the patients before therapy. Detectable concentrations were in the range of 1.7 to 3.5 % of the corresponding 25-OHD levels throughout the study, and the two metabolites were closely correlated ( r = 0.84, p < 0.0005). The median l,25-(OH)₂D concentration was near the average of the reference range before, but increased to well above the upper limit of normal within one week of treatment (121 vs. 368 pmol/l, p < 0.01). The levels were largely normal after 10 weeks of therapy, as were the plasma concentrations of calcium, phosphate, and alkaline phosphatase. Parathyroid activity, as judged by serum parathyroid hormone or urinary cyclic AMP concentrations, was stimulated in 11 of 12 children studied prior to treatment. It is concluded that there may be no clear-cut differences between normal nad rachitic values of the different vitamin D metabolites under practical clinical conditions. A low 25-OHD level combined with evidence of a stimulated parathyroid activity, and a rise of l,25-(OH)₂D levels to supernormal values following a few days of vitamin D therapy may be diagnostic clues.     

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.     

Vitamin D levels in children of asylum seekers in The Netherlands in relation to season and dietary intake

Low dietary intake and limited sun exposure during Dutch winters, in particular when combined with highly pigmented skin, could compromise the vitamin D status of asylum seekers’ children in The Netherlands. We determined the vitamin D status of children living in The Netherlands, but originating from Africa, Central Asia, or Eastern Europe. In a subgroup, we reassessed the vitamin D status after the summer, during which the children had been assigned at random to remain unsupplemented or to receive vitamin D supplementation. In total 112 children (median age 7.1 yr, range 2–12 yr) were assessed for serum concentrations of 25-Hydroxyvitamin D [25(OH)D], intact parathyroid hormone (I-PTH) and plasma alkaline phosphatase (ALP). Vitamin D deficiency (VDD) and hypovitaminosis D were defined as 25(OH)D below 30 or 50 nmol/L, respectively. Dietary intake of vitamin D and calcium was estimated using a 24 h recall interview. In mid-spring, 13% of the children had VDD, and 42% had hypovitaminosis D. I-PTH and ALP levels were significantly higher in children with VDD. The dietary intake of vitamin D was below 80% of the recommended daily allowances (RDA) in 94% of the children, but the dietary calcium intake was not significantly related to the s-25(OH)D levels found. After the summer, median s-25(OH)D increased with +35 nmol/L (+85%) and +19 nmol/L (+42%) in children with or without supplementation, respectively. The effect of supplementation was most prominent among African children. VDD and hypovitaminosis D are highly prevalent in mid-spring among asylum seekers’ children in The Netherlands. Although 25(OH)D levels increase in African children during Dutch summer months, this does not completely correct the compromised vitamin D status. Our data indicate that children from African origin would benefit from vitamin D supplementation.     

Effect of season and vitamin D supplementation on plasma concentrations of 25-hydroxyvitamin D in Norwegian infants

Plasma concentrations of 25-hydroxyvitamin D (25OHD) were determined in 81 vitamin D supplemented or unsupplemented infants at the end of winter. The values were compared with maternal levels and with concentrations found in 22 unsupplemented infants at the end of summer. The 25OHD levels of the neonates were lower, but closely related to maternal values (r = 0.95, p less than 0.0005). Unsupplemented breast-fed infants had lower 25OHD levels at 6 weeks than at 4 days (16 +/- 7 vs. 32 +/- 15 nmol/l, mean +/- 1 SD, p less than 0.0005). The mean 25OHD level of vitamin D supplemented 6-12 months old infants was intermediate between those of the unsupplemented nursed groups and the unsupplemented children studied during summer (53 +/- 28 vs. 85 +/- 28 nmol/l, p less than 0.0005). Six weeks old infants who had received a milk formula containing 400 IU vitamin D3 per liter had levels similar to the latter group (92 +/- 21 nmol/l). The data suggest that the vitamin D stores acquired during fetal life, or from ultraviolet light exposure during the summer, may be inadequate to maintain safe levels of 25OHD throughout the winter, but that a daily supplement of 400 IU is adequate to establish concentrations in the summer range.     

Prospective study of vitamin D supplementation and rickets in China.

To determine whether amounts of vitamin D lower than recommended doses are effective in preventing rickets, 256 term infants from two northern and two southern cities in China were studied in a randomized trial of vitamin D supplementation (100, 200, or 400 IU/day) during the first 6 months of life. Cord blood and 6-month blood samples were collected and radiographs were obtained at 3 to 5 days and at 6 months of age. Cord serum 25-hydroxyvitamin D concentrations were lower in the north than in the south (5 vs 14 ng/ml (12.5 vs 35.0 nmol/L); p less than 0.01). Wrist ossification centers were less likely to be present at birth in the northern children than in the southern children (p = 0.009) and were more likely to be present in infants born in the fall who had higher cord serum concentrations of 25-hydroxyvitamin D (p = 0.04). Serum 25-hydroxyvitamin D concentrations were lower in northern children 6 months of age than in southern children (p = 0.005) and were higher with an increasing supplemental dosage of vitamin D (p less than 0.001), particularly in infants in the north. None of the infants had rickets at 6 months of age. Because of the low serum 25-hydroxyvitamin D concentrations, especially among infants in the north, it may be prudent to supplement the diet with vitamin D at a dose of 400 IU/day.     

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.     

Vitamin D metabolism in hypophosphatasia

A 4-month-old boy with the infantile form of hypophosphatasia was followed for 9 months with measurements of serum calcium, phosphate, alkaline phosphatase and various vitamin D metabolites, together with urinary excretion of cyclic AMP. During the initial hypercalcemic stage the serum concentration of 25-hydroxyvitamin D was normal. Urinary cyclic AMP was low and the serum concentration of the dihydroxymetabolites of vitamin D were appropriate to the high serum calcium with low 1,25-(OH)2D and relatively high 24,25(OH)2D and 25,26(OH)2D levels. Due to restrictions of the vitamin D intake and lack of exposure to sun he developed vitamin D-deficiency rickets at 9 months of age with very low serum concentration of 25-hydroxyvitamin D and markedly increased urinary excretion of cyclic AMP. Following vitamin D treatment the serum level of 1,25(OH)2D showed a brisk rise to a considerably elevated value. Initially the serum concentration of alkaline phosphatase was well below the normal range, rose markedly during the stage of active rickets and returned to the characteristic low levels of hypophosphatasia with healing of the rickets.     

Risk factors for nutritional rickets among children in Kuwait

AIM: To assess the risk factors for nutritional rickets among children in Kuwait. METHODS: One hundred and three children with rickets and 102 control children matched for age and socioethnic characteristics were recruited over a 2 year period (January 1995 to January 1997) in Al-Adan Hospital in Kuwait. Diagnosis was made on clinical, radiologic and biochemical parameters. A specially designed questionnaire was administered by one of the investigators to both mothers of patients and mothers of control subjects to assess the role of social, nutritional and other related factors in the pathogenesis of nutritional rickets. Biochemical investigations included estimation of hemoglobin, serum calcium, serum phosphorus, serum alkaline phosphatase and serum 25-hydroxy vitamin D. RESULTS: The mean birthweights of rickets patients and control subjects were 3.20 +/- 0.46 and 3.19 +/- 0.45 kg, respectively. At the time of diagnosis, bodyweights of the patients and controls were 9.36 +/- 1.50 and 10.15 +/- 2.10 kg, respectively. Heights at the time of diagnosis were 73.58 and 77.24 cm for the patients and the controls, respectively. Mean hemoglobin, serum calcium and serum phosphate were significantly lower in the patients compared with the controls. Alkaline phosphatase was higher among the patients (P < 0.0001). The mean serum 25-hydroxy vitamin D level of the patients was 26.5 nmol/L, compared with 83.5 nmol/L in the controls. The mean age of starting semisolid feeds for the patients was 8.12 months, compared with 5.7 months in the controls. The nutritional quality of semisolid feeds was adequate among 71.6% of the controls as opposed to 13.6% of the patients. CONCLUSION: Nutritional rickets is a multifactorial condition. However, several factors seem to make important contributions. Among these, lack of exposure to sunlight, prolonged breast feeding without supplementation and inadequate weaning practices are important. Maternal education is important as it can influence all of the above factors.