This happens because latitude affects the zenith angle of the sun, and subsequently, the amount of the ultraviolet B (UVB) radiation. In higher latitudes, there are more chances to develop vitamin D deficiency and rickets. Latitude also plays an important role in vitamin D deficiency and rickets. Pregnant mothers who have a vitamin D deficiency may predispose their babies to rickets and hypocalcemia. Risk factors for nutritional vitamin D deficiency include prolonged exclusive breastfeeding without vitamin D supplementation, excessive juice rather than fortified milk consumption, and inadequate intake of vitamin D fortified foods. A study revealed 89% of the patients with rickets had no or minimal sun exposure. The main causes of rickets worldwide in older infants and toddlers are due to vitamin D deficiency, either due to nutritional deficiency or due to insufficient sun exposure. It is characterized by a pathology in the renal tubules that causes phosphate transport defects. (more details in pathophysiology section)įGF-23-independent hypophosphatemic rickets: This type of rickets is not phosphatonin-dependent. Both calcipenic rickets and phosphopenic rickets are characterized by hypophosphatemia, which eventually causes the clinical and radiological bone changes characteristic of rickets (rachitic changes). Both conditions increase the urinary phosphate loss resulting in chronic hypophosphatemia. (2) increased urinary phosphate loss due to mutations that cause inactivation of sodium-dependent phosphate transporters in the kidneys. In premature children, dietary phosphate deficiency can result in osteopenia of prematurity. Low serum phosphate levels occur in (1) conditions that increase the production or decrease degradation of fibroblast growth factor 23 (FGF23), a hormone that reduces the reabsorption and increases the excretion of phosphate in the renal tubules. Phosphate is abundant in our regular food, so phosphate deficiency does not usually occur from dietary insufficiency in healthy individuals. Phosphopenic rickets, on the other hand, is caused by conditions that cause chronic low serum phosphate levels, either from impaired intestinal absorption or, more commonly, from increased renal loss. Subsequently, it causes renal phosphate loss and hypophosphatemia. In the long term, this secondary hyperparathyroidism results in the internalization of sodium-dependent phosphate co-transporter proteins in the renal tubules. Low serum calcium is a common phenomenon in calcipenic rickets that stimulates the secretion of parathyroid hormone (PTH), which may result in the normalization of serum calcium. Additionally, calcipenic rickets may result from a genetic defect of vitamin D metabolism, either from a failure of vitamin D to switch to its active form (1,25-dihydroxy vitamin D) or due to end-organ resistance. Rickets can be the first presenting manifestation in patients with celiac disease. Calcipenic rickets may also result from poor calcium absorption, such as in children with malabsorption syndromes, especially celiac disease and cystic fibrosis. Calcipenic rickets may result from inadequate dietary calcium intake, which is reported in a few developing countries. Deficiency of calcium results in calcipenic rickets, and vitamin D deficiency is the most common etiology for calcipenic rickets.
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