Vitamin D deficiency has emerged as one of the most significant micronutrient deficiencies worldwide, particularly affecting growing children under five years of age. Despite abundant sunlight in tropical and subtropical regions, a paradoxical rise in hypovitaminosis D and nutritional rickets has been increasingly reported in South Asian populations [1-5]. Vitamin D plays a central role in calcium–phosphorus homeostasis, skeletal mineralization, and immune modulation; its deficiency during early childhood may result in bone deformities, delayed growth, increased susceptibility to infections, and long-term adverse outcomes such as reduced peak bone mass [2,3]. Globally, vitamin D deficiency affects nearly one billion individuals, with the highest prevalence among infants, preschool children, and women of reproductive age [4]. In India, estimates suggest that 50–90% of children are vitamin D deficient, with significantly higher burden in northern regions compared to the south [5]. This disparity is attributed to geographic latitude, cultural practices of clothing, skin pigmentation, dietary inadequacies, and limited outdoor activity of young children [6]. In northern India, particularly, prolonged winters, atmospheric pollution, and urbanization further limit effective sun exposure, thereby compounding the risk [7]. Nutritional rickets remains a critical public health issue in developing countries, reflecting the intersection of vitamin D deficiency, inadequate dietary calcium intake, and poor socio-economic conditions [8]. Clinical manifestations include bowing of legs, widening of wrists and ankles, delayed motor milestones, and, in severe cases, hypocalcemic seizures [9]. Although rickets is preventable, the persistent occurrence among under-five children signals gaps in awareness, preventive supplementation policies, and dietary practices. In recent years, several clinical studies from India have highlighted a resurgence of rickets, once considered largely controlled, with cases presenting both in rural and urban healthcare centers [10]. The re-emergence is thought to result from rapid urbanization, reduced traditional outdoor play, and exclusive breastfeeding without adequate vitamin D supplementation during infancy. This trend poses significant challenges for pediatric health services, as untreated cases may lead to permanent skeletal deformities and impaired growth. Understanding the burden of vitamin D deficiency and rickets in under-five children in northern India is crucial, as this population represents a vulnerable window of growth and development. Moreover, the clinical evaluation of such cases provides insights into early recognition, socio-demographic determinants, and therapeutic outcomes, which can guide region-specific preventive strategies. A systematic clinical study in this context is therefore warranted, not only to assess the magnitude of the problem but also to inform public health interventions such as supplementation programs, fortification policies, and parental education on sun-exposure practices. This study aims to evaluate vitamin D deficiency and its clinical manifestation as rickets in children under five years of age in northern India, emphasizing the clinical spectrum, risk factors, and implications for pediatric care. By documenting the current status, the findings can contribute to national strategies for the prevention and management of this preventable disorder.

Study Design and Setting This was a hospital-based, cross-sectional clinical study conducted in a tertiary care pediatric hospital in North India. The region experiences distinct seasonal variations with prolonged winters and high atmospheric pollution, both of which are known to influence cutaneous synthesis of vitamin D. Study Population Children aged 6 months to 59 months attending the pediatric outpatient department and admitted to the inpatient services with clinical suspicion of nutritional rickets or symptoms suggestive of hypovitaminosis D were recruited. Exclusion criteria included children with chronic renal disease, hepatic disorders, endocrine abnormalities, malabsorption syndromes, or those receiving vitamin D or calcium supplementation within the past three months. Sample Size Based on previous prevalence data suggesting vitamin D deficiency rates of approximately 60–80% among under-five children in northern India, a minimum sample size of 200 participants was calculated using the formula for prevalence studies with a 95% confidence interval and 10% allowable error. Data Collection After obtaining written informed consent from parents or guardians, demographic details including age, sex, socio-economic status, nutritional history, duration of exclusive breastfeeding, and outdoor activity were recorded using a pre-structured proforma. Anthropometric measurements such as weight, height/length, and mid-arm circumference were taken following WHO guidelines. Clinical Examination All enrolled children underwent thorough clinical examination by a pediatrician to assess for signs of rickets such as frontal bossing, widening of wrists and ankles, rachitic rosary, bowing of legs, delayed dentition, and motor developmental delay. Laboratory Investigations Venous blood samples were collected for estimation of: • Serum 25-hydroxyvitamin D [25(OH)D] (by chemiluminescent immunoassay) • Serum calcium, phosphorus, and alkaline phosphatase (ALP) (using standard automated analyzers) • Parathyroid hormone (PTH) levels where feasible Vitamin D status was defined as: • Deficiency: <20 ng/mL • Insufficiency: 20–30 ng/mL • Sufficiency: >30 ng/mL Radiological Assessment X-rays of wrist and knee joints were performed in children with clinical features of rickets to confirm metaphyseal changes, cupping, and fraying. Radiological scoring was done according to established criteria. Ethical Considerations The study protocol was approved by the Institutional Ethics Committee. Written informed consent was obtained from parents or guardians prior to enrollment. Confidentiality and ethical principles were strictly maintained throughout the study. Statistical Analysis Data were analyzed using SPSS version 25 (IBM Corp., Armonk, NY). Continuous variables were expressed as mean ± standard deviation, while categorical variables were presented as proportions. Associations between vitamin D deficiency and clinical or demographic variables were evaluated using chi-square test or Fisher’s exact test. A p-value <0.05 was considered statistically significant.

Demographic Profile A total of 200 children aged 6–59 months were enrolled. The mean age was 32.4 ± 14.7 months, with a slight male predominance (56% boys, 44% girls). The majority (62%) belonged to lower socio-economic status, and 71% had limited outdoor exposure (<2 hours/day). Table 1 Prevalence of Vitamin D Deficiency Overall, 68.5% of children were found to have vitamin D deficiency (<20 ng/mL), while 21% had insufficiency (20–30 ng/mL), and only 10.5% had sufficient levels (>30 ng/mL). Table 2 Clinical Manifestations Among vitamin D deficient children, the most frequent clinical signs were wrist widening (48%), frontal bossing (39%), and bowing of legs (31%). Hypocalcemic seizures were reported in 8% of cases. Table 3 Biochemical Findings Children with deficiency had significantly lower mean serum calcium (7.6 ± 0.9 mg/dL) and phosphorus (3.2 ± 0.7 mg/dL) compared to those with sufficient vitamin D levels. Alkaline phosphatase levels were markedly elevated (mean: 820 ± 215 IU/L). Table 4 Radiological Findings Radiographic evaluation of wrist and knee joints in symptomatic children (n=120) revealed metaphyseal cupping and fraying in 74%, generalized osteopenia in 62%, and growth plate widening in 55%. Table 4 Tables Table 1. Demographic characteristics of study participants (N=200) Variable Frequency (%) Age <24 months 72 (36.0) Age 24–59 months 128 (64.0) Male 112 (56.0) Female 88 (44.0) Lower socio-economic 124 (62.0) Middle/upper class 76 (38.0) Outdoor exposure <2 hr/day 142 (71.0) Outdoor exposure ≥2 hr/day 58 (29.0) Table 2. Vitamin D status distribution among study population Vitamin D Status Serum 25(OH)D (ng/mL) Number (%) Deficient (<20) Mean 12.6 ± 4.8 137 (68.5) Insufficient (20–30) Mean 24.1 ± 3.2 42 (21.0) Sufficient (>30) Mean 36.4 ± 5.1 21 (10.5) Table 3. Clinical features observed in vitamin D deficient children (n=137) Clinical Sign Frequency (%) Wrist widening 66 (48.2) Frontal bossing 54 (39.4) Bowing of legs 43 (31.4) Rachitic rosary 29 (21.2) Delayed dentition 25 (18.2) Hypocalcemic seizures 11 (8.0) Table 4. Biochemical and radiological parameters in children with and without vitamin D deficiency Parameter Deficient (n=137) Non-deficient (n=63) p-value Serum calcium (mg/dL) 7.6 ± 0.9 9.1 ± 0.6 <0.001 Serum phosphorus (mg/dL) 3.2 ± 0.7 4.6 ± 0.8 <0.001 ALP (IU/L) 820 ± 215 345 ± 120 <0.001 Radiological changes (%) 74.2 11.1 <0.001

The present clinical study highlights the high prevalence of vitamin D deficiency and nutritional rickets among children under five years of age in North India. Nearly seven out of ten children were vitamin D deficient, confirming previous reports from northern states where limited effective sun exposure, cultural clothing practices, and high atmospheric pollution restrict cutaneous synthesis of vitamin D [11,12]. Despite abundant sunlight in tropical countries, hypovitaminosis D is increasingly recognized as a widespread public health problem, underscoring the importance of regional determinants of deficiency [13]. The predominance of deficiency in lower socio-economic groups observed in this study is consistent with earlier findings that nutritional inadequacies, inadequate fortified foods, and poor healthcare access contribute significantly to childhood rickets [14]. Exclusive breastfeeding without supplementation, limited outdoor activity, and lack of awareness about preventive strategies further exacerbate the risk [15,16]. Clinical features such as wrist widening, frontal bossing, and bowing of legs were comparable to classical manifestations reported in South Asian pediatric cohorts [17-20]. Importantly, hypocalcemic seizures in a subset of children indicate that vitamin D deficiency can have acute and life-threatening consequences if unrecognized [18]. Biochemical parameters in this study demonstrated the classical triad of hypocalcemia, hypophosphatemia, and elevated alkaline phosphatase, which reflect impaired mineralization and compensatory secondary hyperparathyroidism. Radiological evidence of metaphyseal cupping and fraying further confirmed active rickets, findings that remain gold-standard markers for diagnosis in resource-limited settings [21-25]. The significant differences in laboratory values between deficient and sufficient groups highlight the reliability of biochemical screening in early detection. These findings have important implications for pediatric health policy. Routine supplementation of vitamin D during infancy, dietary fortification, and parental education on safe sun exposure are recommended preventive strategies [25-30]. Furthermore, urbanization and lifestyle transitions necessitate renewed guidelines adapted to regional epidemiology. Strengthening surveillance, integrating screening in primary care, and conducting large-scale community-based studies are crucial to address this preventable disorder.

Vitamin D deficiency and nutritional rickets remain highly prevalent among North Indian children under five, particularly in socio-economically disadvantaged groups. Clinical, biochemical, and radiological evidence confirms significant morbidity, with classical skeletal deformities and metabolic derangements. Preventive measures including vitamin D supplementation, food fortification, and public awareness on sun exposure are urgently required. Early recognition and targeted interventions can substantially reduce the burden of rickets, prevent long-term skeletal consequences, and improve child health outcomes in resource-limited settings.

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