Rickets

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By Medifit Education

 

RICKETS

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RICKETS DEFINITION

Rickets is the softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency.

Vitamin D promotes the absorption of calcium and phosphorus from the gastrointestinal tract. A deficiency of vitamin D makes it difficult to maintain proper calcium and phosphorus levels in bones, which can cause rickets.

If a vitamin D or calcium deficiency causes rickets, adding vitamin D or calcium to the diet generally corrects any resulting bone problems for your child. Rickets due to a genetic condition may require additional medications or other treatment. Some skeletal deformities caused by rickets may need corrective surgery.

RICKETS CAUSES

Lack of vitamin D – the main cause of rickets. Our bodies need vitamin D in order to absorb calcium from the intestines. Ultraviolet light (from sunlight) helps our skin cells convert vitamin D from an inactive into an active state.

If we do not have enough vitamin D, calcium that we get from the food we eat is not absorbed properly, causing hypocalcemia (lower-than-normal blood calcium) to develop. Hypocalcemia results in deformities of bones and teeth, as well as neuromuscular problems.

The following foods are known to be rich on vitamin D: eggs, fish oils, margarine, some fortified milks and juices, some oily fishes, and some soymilk products that have vitamin D added.

Genetic defect – hypophosphatemic rickets is a rare genetic fault that undermines the way the kidneys process phosphates. Phosphate blood levels are too low, leading to weak and soft bones.

Some diseases – some renal (kidney), hepatic (liver) and intestinal diseases can interfere with the way the body absorbs and metabolizes minerals and vitamins, resulting in rickets.

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RICKETS PATHOPHYSIOLOGY

Cholecalciferol (ie, vitamin D-3) is formed in the skin from 5-dihydrotachysterol. This steroid undergoes hydroxylation in 2 steps. The first hydroxylation occurs at position 25 in the liver, producing calcidiol (25-hydroxycholecalciferol), which circulates in the plasma as the most abundant of the vitamin D metabolites and is thought to be a good indicator of overall vitamin D status.

The second hydroxylation step occurs in the kidney at the 1 position, where it undergoes hydroxylation to the active metabolite calcitriol (1,25-dihydroxycholecalciferol). This cholecalciferol, which circulates in the bloodstream in minute amounts, is not technically a vitamin but a hormone.

Calcitriol acts at 3 known sites to tightly regulate calcium metabolism: (1) it promotes absorption of calcium and phosphorus from the intestine; (2) it increases reabsorption of phosphate in the kidney; and, (3) it acts on bone to release calcium and phosphate. Calcitriol may also directly facilitate calcification. These actions result in an increase in the concentrations of calcium and phosphorus in extracellular fluid.

This increase of calcium and phosphorus in extracellular fluid, in turn, leads to the calcification of osteoid, primarily at the metaphyseal growing ends of bones but also throughout all osteoid in the skeleton. Parathyroid hormone facilitates the 1-hydroxylation step in vitamin D metabolism.

In the vitamin D deficiency state, hypocalcemia develops, which stimulates excess secretion of parathyroid hormone. In turn, renal phosphorus loss is enhanced, further reducing deposition of calcium in the bone.

Excess parathyroid hormone also produces changes in the bone similar to those occurring in hyperparathyroidism. Early in the course of rickets, the calcium concentration in the serum decreases. After the parathyroid response, the calcium concentration usually returns to the reference range, though phosphorus levels remain low. Alkaline phosphatase, which is produced by overactive osteoblast cells, leaks into the extracellular fluids, so that its concentration rises to anywhere from moderate elevation to very high levels.

Intestinal malabsorption of fat and diseases of the liver or kidney may produce the clinical and secondary biochemical picture of nutritional rickets. Anticonvulsant drugs (eg, phenobarbital, phenytoin) accelerate metabolism of calcidiol, which may lead to insufficiency and rickets, particularly in children who have darkly pigmented skin and those who are kept primarily indoors (eg, children who are institutionalized).

Calcium and vitamin D intakes are low in infants who are fed vegan diets, particularly in those who are lactovegans, and monitoring of their vitamin D status is essential.

Studies have noted that disorders of increased fibroblast growth factor 23 (FGF-23) function are associated with rickets.

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RICKETS SYMPTOMS

Signs and symptoms of rickets may include:

  • Delayed growth
  • Pain in the spine, pelvis and legs
  • Muscle weakness

Because rickets softens the growth plates at the ends of a child’s bones, it can cause skeletal deformities such as:

  • Bowed legs
  • Thickened wrists and ankles
  • Breastbone projection

RICKETS DIAGNOSIS

Blood tests – serum calcium may reveal inadequate levels of calcium and phosphorus. Serum alkaline phosphatase levels may be high.

Metabolic acidosis may be revealed by arterial blood gases.

X-rays – these may reveal calcium loss in bones, or alterations in the structure or shape of the bones.

Bone biopsy – this can confirm rickets (rarely used).

RICKETS TREATMENT

Most cases of rickets can be treated with vitamin D and calcium supplements. Follow your doctor’s directions as to dosage, which may vary by the size of your child. Too much vitamin D can be dangerous.

Surgical and other procedures

For some cases of bowlegs or spinal deformities, your doctor may suggest special bracing to position your child’s body appropriately as the bones grow. More severe skeletal deformities may require surgery.

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By Medifit Education

www.themedifit.in