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Rickets remains a common problem among infants and children in many countries worldwide. Although the classical presentation associated with bone abnormalities is well known, paediatricians need to be aware of atypical presentations, especially in the first 6 months of life. Furthermore, although vitamin D deficiency rickets remains the commonest form of rickets in most countries, health care providers need to be aware of other possible causes and their typical clinical and biochemical presentations. This article discusses these and highlights the characteristic features of various forms of rickets and possible pitfalls clinicians should be aware of when confronted with a patient with suspected rickets. In conclusion, the recent advances made in understanding the underlying pathogeneses of the various forms of rickets has helped to delineate the diagnostic tests that assist in the diagnosis and management of the disease in children.

It has been previously documented that alphacalcidol (1alpha-hydroxyvitamin D3) is inefficient in healing rickets, partly because it results in a suboptimal rise in 1,25-dihydroxyvitamin D (1,25-(OH)2D) and partly because it fails to replenish the store of 25-hydroxyvitamin D (25-OHD). However, very few studies have actually documented this outcome. The aim was to document biochemically the response to alphacalcidol and subsequently the change in response to ergocalciferol. This study was conducted at our institution from January 2005 till December 2008. We included all patients referred to our clinic with active rickets after a failed course of alphacalcidol. At baseline the median (IQR) for PTH l7.1 (4.5-35.3) pmol/L, 25-OHD 29.0 (18-66.2) nmol/L, 1,25-(OH)2D 205 (158.2-311.2) pmol/L and ALP 676 (462.5-1101.7) IU/L. After 3 months treatment with ergocalciferol the concentrations changed markedly with biochemical healing: PTH 4.5 (3.9-7.5), 25-OHD 143.5 (101.5-206.5), 1,25-(OH)(2)D 277 (221.0-572.7), ALP 369 (302.2-438.0). The results confirm the biochemical and physiological basis for using ergocalciferol (or cholecalciferol) in nutritional rickets. Unfortunately these forms are not readily available in many geographic areas. This supply problem together with marketing strategies forces physicians to make an incorrect choice of medication. Treatment with ergocalciferol was either with intramuscular stosstherapy or drops for 3 months. The former ensures compliance and is associated with higher 25-OHD and 1,25-(OH)2D concentrations., (Copyright (c) 2010 Elsevier Ltd. All rights reserved.)

Background: Vitamin D deficiency is still prevalent worldwide, including the Middle East. A cohort of patients with nutritional rickets was treated with vitamin D(2) (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 D(3) (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.

Abstract: It has been previously documented that alphacalcidol (1α-hydroxyvitamin D3) is inefficient in healing rickets, partly because it results in a suboptimal rise in 1,25-dihydroxyvitamin D (1,25-(OH)2D) and partly because it fails to replenish the store of 25-hydroxyvitamin D (25-OHD). However, very few studies have actually documented this outcome. The aim was to document biochemically the response to alphacalcidol and subsequently the change in response to ergocalciferol. This study was conducted at our institution from January 2005 till December 2008. We included all patients referred to our clinic with active rickets after a failed course of alphacalcidol. At baseline the median (IQR) for PTH l7.1 (4.5–35.3)pmol/L, 25-OHD 29.0 (18–66.2)nmol/L, 1,25-(OH)2D 205 (158.2–311.2)pmol/L and ALP 676 (462.5–1101.7)IU/L. After 3 months treatment with ergocalciferol the concentrations changed markedly with biochemical healing: PTH 4.5 (3.9–7.5), 25-OHD 143.5 (101.5–206.5), 1,25-(OH)2D 277 (221.0–572.7), ALP 369 (302.2–438.0). The results confirm the biochemical and physiological basis for using ergocalciferol (or cholecalciferol) in nutritional rickets. Unfortunately these forms are not readily available in many geographic areas. This supply problem together with marketing strategies forces physicians to make an incorrect choice of medication. Treatment with ergocalciferol was either with intramuscular stosstherapy or drops for 3 months. The former ensures compliance and is associated with higher 25-OHD and 1,25-(OH)2D concentrations. [ABSTRACT FROM AUTHOR]