Rickets-Vitamin D Deficiency

Rickets-Vitamin D Deficiency

Rickets occurs mainly in children. It results from calcium or phosphate deficiency in the extracellular fluid, usually caused by lack of vitamin D. If the child is adequately exposed to sunlight, the 7-dehydrocholes-terol in the skin becomes activated by the ultraviolet rays and forms vitamin D₃, which prevents rickets by promoting calcium and phosphate absorption from the intestines.

Children who remain indoors through the winter in general do not receive adequate quantities of vitamin D without some supplementation in the diet. Rickets tends to occur especially in the spring months because vitamin D formed during the preceding summer is stored in the liver and available for use during the early winter months. Also, calcium and phosphate absorption from the bones can prevent clinical signs of rickets for the first few months of vitamin D deficiency.

Plasma  Concentrations  of  Calcium  and  Phosphate  Decrease in Rickets The plasma calcium concentration in ricketsis only slightly depressed, but the level of phosphate is greatly depressed. This is because the parathyroid glands prevent the calcium level from falling by pro-moting bone absorption every time the calcium level begins to fall. However, there is no good regulatory system for preventing a falling level of phosphate, and the increased parathyroid activity actually increases the excretion of phosphates in the urine.

Rickets Weakens the Bones During prolonged rickets, themarked compensatory increase in PTH secretion causes extreme osteoclastic absorption of the bone; this in turn causes the bone to become progressively weaker and imposes marked physical stress on the bone, resulting in rapid osteoblastic activity as well. The osteoblasts lay down large quantities of osteoid, which does not become calcified because of insufficient calcium and phosphate ions. Consequently, the newly formed, uncal-cified, and weak osteoid gradually takes the place of the older bone that is being reabsorbed.

Tetany in Rickets In the early stages of rickets, tetanyalmost never occurs because the parathyroid glands continually stimulate osteoclastic absorption of bone and, therefore, maintain an almost normal level of calcium in the extracellular fluid. However, when the bones finally become exhausted of calcium, the level of calcium may fall rapidly. As the blood level of calcium falls below 7 mg/dl, the usual signs of tetany develop, and the child may die of tetanic respiratory spasm unless intravenous calcium is administered, which relieves the tetany immediately.

Treatment of Rickets. The treatment of rickets depends onsupplying adequate calcium and phosphate in the diet and, equally important, on administering large amounts of vitamin D. If vitamin D is not administered, little calcium and phosphate are absorbed from the gut.

Osteomalacia—“Adult Rickets”. Adults seldom have aserious dietary deficiency of vitamin D or calcium because large quantities of calcium are not needed for bone growth as in children. However, serious deficien-cies of both vitamin D and calcium occasionally occur as a result of steatorrhea (failure to absorb fat) because vitamin D is fat-soluble and calcium tends to form insoluble soaps with fat; consequently, in steator-rhea, both vitamin D and calcium tend to pass into the feces. Under these conditions, an adult occasionally has such poor calcium and phosphate absorption that adult rickets can occur, although this almost never proceeds to the stage of tetany but often is a cause of severe bone disability.

Osteomalacia and Rickets Caused by Renal Disease. “Renalrickets” is a type of osteomalacia that results from prolonged kidney damage. The cause of this condition is mainly failure of the damaged kidneys to form 1,25-dihydroxycholecalciferol, the active form of vitamin D. In patients whose kidneys have been removed or destroyed and who are being treated by hemodialysis, the problem of renal rickets is often a severe one.

Another type of renal disease that leads to rickets and osteomalacia is congenital hypophosphatemia, resulting from congenitally reduced reabsorption of phosphates by the renal tubules. This type of rickets must be treated with phosphate compounds instead of calcium and vitamin D, and it is called vitaminD–resistant rickets.