Diseases and disorders occur due to many reasons such as bacterial or viral infections, can genetically be inherited or they can be linked to nutritional deficiencies. One such disease linked with nutritional deprivation is termed as Rickets or Osteomalacia. It is an illness which has been around for many centuries and mainly affects children. However, the prevention of rickets has been made possible with research and discovering the factors which can help improve bodily health. Yet, the disease is a commonly recurring one in developing countries where infants and young children are exposed to a nutritional deficiency of Vitamin D. The disease is more common in babies who are being breastfed or those who are dark-skinned and belong to an immigrant background. Moreover, it is common amongst Middle Eastern developing countries and in the tropics and sub-tropics (Pettifor, 2004).The cause for Vitamin D deficiency amongst infants and young children in these regions and countries lies in the low content of the vitamin in breast milk and due to certain social or religious norms, the covering of the body does not permit ultraviolet radiation from reaching the skin, which is also a cause of production for Vitamin D. However, for cases where the Vitamin D content is low in sunny countries relates to nutritional deficiencies in the mother and the child, which is a common cause of rickets (Pettifor, 2004).
Rickets or Osteomalacia is a disease which causes the softening and deformation of the bones, often leading to bowed legs and other deformed bones in the body. Diagnosing Rickets is usually common from four to fifty-four months of age, while many are below thirty months. In the United States, about 83% of the children with rickets are African American in origin, and out of these, 96% are being breastfed (Pettifor, 2004).
There is a very specific role of Vitamin D especially if it is in scarce amounts in breast milk. While the recommended need of an infant is 200IU/d, breast milk contains about 22IU/d. Vitamin D is not abundantly available in diet hence it is developed by the photochemical action of UV light from the sun, through 7-hydrocholesterol present in the skin. A deficiency in its production has factors such as low skin exposure, excess melanin in the skin as well as the application of sunscreen. A low-calcium intake along with other mineral deficiencies can also result in rickets, while the most common case is Vitamin D deficiency rickets (Breyer, 2008).
Rickets does not show up as an immediately detectable disorder; rather it is revealed in three stages. Vitamin D and the parathyroid (PTH) hormone work together to regulate calcium concentration in the body (Breyer, 2008). The first stage is where there is a lowered level of Vitamin D, a decreased calcium concentration, but phosphorus levels remain stable. However lowered calcium levels cause the PTH to increase in amount, causing the release of calcium and phosphorus from the body and the kidneys reabsorb calcium and decrease reabsorption of phosphorus. Calcium is also not absorbed in the intestines (Breyer, 2008). The second stage is when calcium levels are constant, but phosphorus levels go down because of excretion by the kidneys (Breyer, 2008). This process causes the bones to lose calcium, while the alkaline phosphatase goes up and it is not possible to upkeep calcium levels. In the final stage, both calcium and phosphorus levels drop very low while the phosphatase is high. PTH level is also high along with the other chemical abnormalities which present the symptoms of the disease. Children suffer from seizures, stunted growth, extended abdomen, being unable to walk, bone deformities like widening of ankles and wrists, bowing of legs and fractures are common (Breyer, 2008).
The prevention of the disease is simply a richer and more nutritious diet for children and infants. Infants must receive milk with high calcium content and mothers should regulate their levels of Vitamin D by getting moderate sun exposure. Feeding cereals and foods with high calcium and phosphorus content with help maintain better calcium content in the body. Young children must also get exposure to sunlight for Vitamin D (Glorieux, 2014).
Treatment for Rickets is to reverse the cycle of the bodily chemical changes by re-regulating the same dietary intake. The treatment is either provided on a daily basis as a regular dose or over a period of several months over time. A single dose of Vitamin D is given at about 15,000 mcg or 600,000 U. If several months’ treatment plan is chosen, then about 125-250 mcg which is 5000 till 10,000 U is administered (Glorieux, 2014).This is given for a period of two to three months until the bones are healed and other symptoms dissipate. Moreover, the alkaline phosphatase levels need to reach normal levels as well. With daily treatment, obeying the plan is crucial for treating rickets. On a daily basis, there are about four to six oral doses of Vitamin D while intramuscular injections are also administered (Glorieux, 2014). Vitamin D is then stored in the body and released gradually with the passage of time. While it is possible that a reversal of diet can cure the disease, there are still concerns regarding the deformation of the bones. Severe deformities will have to be dealt with by an orthopedic surgeon who might have to adjust and align bones. Moreover, seeing a pediatric endocrinologist is also recommended (Glorieux, 2014).
For clinical relevance, a physical exam is most important for rickets. Craniotabes are prominent in infants, while an enlarged skull is visible for young children with progressed disease. Knobby deformities are also commonly seen in the later stage and bowing of legs is perceptible. A protruding forehead, pigeon chest, and curved humerus can be observed too. In the clinic, other symptoms such as the seizures which relapse into sleepiness, running blood tests for calcium and phosphorus levels and asking the patient history make the disease diagnosable in the clinic.
References
Breyer, P. (2008, March ). Pediatric Clips. Retrieved September 4, 2016, from
http://www.childrensdayton.org/cms/resource_library/pediatric_clips/c71a5cec3daca26d/pediatric_clips_vitamin_d_deficiency_rickets.pdf
Glorieux, F. H. (2014). Vitamin D/dietary calcium deficiency rickets and pseudo-vitamin D
deficiency rickets. BoneKEy Reports, 3, doi:10.1038/bonekey.2014.19
Pettifor, J. M. (2004). Nutritional rickets: Deficiency of vitamin D, calcium, or both? The
American Journal of Clinical Nutrition, 80(6), 1725–1729. Retrieved from http://ajcn.nutrition.org/content/80/6/1725S.full
