Abstract
Rickets is a disease of growing bone, before fusion of epiphyses. There is defective mineralization of cartilage matrix in the zone of provisional calcification caused either by nutritional vitamin D deficiency and/or low calcium intake or by non-nutritional causes, like hypophosphatemic rickets and rickets due to renal tubular acidosis. In addition, some varieties are due to inherited defects in vitamin D metabolism and are called vitamin D dependent rickets. The diagnosis is made on the basis of history, physical examination, and biochemical testing, and is confirmed by radiographs. Treatment consists of vitamin D supplementation as Stoss therapy or daily or weekly oral regimens, all with equal efficacy and safety, combined with calcium supplements. For renal rickets, the active form of Vit D, 1,25(OH)2 also called Calcitriol is used, treatment is tailored to another type of renal rickets. Routine supplementation starting from the newborn period is being increasingly endorsed by various international organizations. Adequate sunlight exposure, food fortification, and routine supplementation are the currently available options for tackling this nutritional deficiency. In this review article, we discuss the pathophysiology, diagnosis, and management of rickets in detail.
Highlights
Osteoid and hydroxyapatite forms the basic structure of bone
A fasting specimen is recommended, it is not essential; diurnal variations are not so important [24, 25]
From one year onwards till 18 years of age, 3000-6000 IU/ day of vitamin D along with calcium intake of 600-800 mg/day is recommended for a minimum of 3 months
Summary
Osteoid (protein matrix) and hydroxyapatite (mineral phase) forms the basic structure of bone. Hydroxyapatite is mainly composed of calcium and phosphorous. Unmineralized matrix at the growth plates in growing bone is the hallmark of rickets [1]. This form of extreme vitamin D deficiency usually discloses itself between 12-18 months of age. Deficiency state must have been persisting for months before clinical revilement of florid rickets. Vitamin D deficiency can express itself with growth failure, lethargy, irritability, hypocalcemic seizures, and a predilection to respiratory infections during infancy [2, 3]. Sufficient intake of vitamin D has a preventive role for rickets [4]
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