Rickets can be referred to as the softening, as well as weakening of bones, commonly due to an extreme and extended deficiency in vitamin D. Vitamin D enhances phosphorus and calcium absorption from the digestive tract. A vitamin D deficiency renders maintenance of proper levels of phosphorous and calcium difficult resulting in rickets. Addition of calcium or vitamin D or o the diet in general corrects any resulting problems for a child. Rickets resulting from a genetic condition may need extra or other medications. A number of skeletal deformities resulting from rickets may require restorative surgery.
Symptoms of rickets include tenderness or pain in the bones of the legs, arms, spine, or pelvis. Teeth deformities, delayed formation of tooth, a high number of cavities, defects or abscesses in the teeth structure and holes in the enamel. Other symptoms include impaired growth, as well as short stature, muscle cramps, bone fractures, skeletal deformities such as pelvic deformities, a protruding breastbone, bowlegs, oddly shaped skull as well as a curved spine.
Cholecalciferol or vitamin D-3 is usually made in the skin from a steroid called 5-dihydrotachysterol. This steroid goes through a 2 steps hydroxylation. The initial hydroxylation takes place in the liver at position 25, forming calcidiol that spreads in the plasma as the most plentiful of the metabolites of vitamin D and is beloved to be a good signal of the overall status vitamin D. The second step of hydroxylation occurs at the first position in the kidney, where it is hydroxylated to the active metabolite calcitriol. Calcitriol serves at 3 cognized sites to tightly modulate metabolism of calcium. It does this by promoting phosphorus and calcium absorption of from the intestine, increasing phosphate reabsorption in the kidney, as well as acting on bone to produce phosphate and calcium. Calcitriol may as well directly aids in calcification. These actions lead to a rise in the calcium and phosphorus concentrations in extracellular fluid. This rise in calcium and phosphorus results in the osteoid calcification, primarily at the metaphyseal bones’ growing ends but also all over all skeleton osteoid. Parathyroid hormone enhances the first step of hydroxylation in metabolism of vitamin D.
In the state of deficiency of vitamin D, hypocalcaemia develops leading to stimulation of excess parathyroid hormone secretion. Successively, loss of renal phosphorus is increased, further lowering calcium deposition in the bone. Excess parathyroid hormone also causes changes in the bone, which are the same as those taking place in hyperparathyroidism. During the early course of rickets, there is a decrease in the concentration of calcium in the serum. Following the parathyroid reaction, the concentration of calcium goes back to the reference range, although levels of phosphorus remain low. Alkaline phosphatase that is secreted by overactive osteoblast cells, outflows into the extracellular fluids, such that its concentration increases to anywhere between moderate rise to very high levels.
Fat and diseases intestinal malabsorption of the kidney or liver may show the clinical, as well as secondary biochemical image of nutritional rickets. Anticonvulsant drugs speed up calcidiol metabolism that may result in insufficiency, as well as rickets, especially in children with darkly pigmented skin together with those who primarily stay indoors(Yuen and Jablonski). Intakes of calcium and vitamin D are low in infants who are fed vegetarian diets, especially in the lactovegans, and it is essential to monitor their status of vitamin D. Studies have demonstrated that disorders of enhanced fibroblast growth factor 23 function are linked to rickets (McKay and Portale). Prevalence
Prevalence
Lack of reporting on rickets cases has resulted in lack of credible data on the prevalence of the disease. Between 1986 and 2000, of all the children reported to have rickets, a third of them were due to nutritional deficiencies. The rest of the cases were caused by genetic or other disease. Outside United States, the major cause of rickets that are reported is nutritional deficiency, lack of vitamin D in the diet, resistance to vitamin D and as a result of renal disease. In the absence of surveillance on the disease prevalence, there is no current information that can be used to predict the chances of a child visiting a hospital for rickets treatment. Prevalence of rickets caused by nutritional deficiency is estimated to be 9 cases in every one million children. Most of the children affected by the disease are African (Nield, et al., 2006).
Medications
In the treatment of rickets, the administration of a single dose consisting of 15,000 mcg of vitamin D may be done daily to the patient for a number of months. The administration is normally continued until recovery is perfectly established. Recovery can be monitored by the restoration of the alkaline phosphate amount in the blood (Shah & Finberg, 1994 ). In addition to vitamin D, increased intake of calcium and phosphates is also employed in the treatment of rickets. Some of the sources of vitamin D that are utilized include viosterol, ultraviolet light, and cod liver oil among others. Rickets treatment mainly depends on cause of the disease. The easiest form of rickets to treat is the one caused by nutritional deficiencies. Other forms of rickets such as renal and hypophosphatemic rickets caused by renal disease and vitamin D–resistance respectively are more difficult to treat (Nield, et al., 2006).
Works Cited
McKay, C. P. and A. Portale. "Emerging topics in pediatric bone and mineral disorders 2008." Semin Nephrol. 29.4 (2009): 370-8.
Nield, L. S., et al. "Rickets: not a disease of the past." Am Fam Physician 74.4 (2006): 619-626.
Shah, B. R. and L. Finberg. "Single-day therapy for nutritional vitamin D-deficiency rickets: a preferred method." J Pediatr 125.3 (1994 ): 487-490.
Yuen, A.W.C. and N.G. Jablonski. "Vitamin D: In the evolution of human skin colour." Medical Hypotheses 74.1 (2010): 39–44.
