Rickets

Alternative names:

deficiency - vitamin D; osteomalacia in children; pediatric osteomalacia; renal osteodystrophy; renal rickets; vitamin D deficiency

Definition:

A disorder involving softening and weakening of the bones of children, primarily caused by lack of vitamin D and/or lack of calcium or phosphate.

Causes, incidence, and risk factors:

Rickets is a disorder caused by insufficiency or inefficient action of activated vitamin D in the body during childhood. Vitamin D is a fat-soluble vitamin that may be absorbed from the intestines or may be produced by the skin when the skin is exposed to ultraviolet light (particularly sunlight). It is converted to its active form by the body in 2 steps, occurring first in the liver and completed in the kidneys. In its active form, vitamin D acts as a hormone to regulate calcium absorption from the intestine and to regulate levels of calcium and phosphate in the bones. Active vitamin D is assisted by the actions of other body hormones.

Because vitamin D is fat soluble, conditions that reduce digestion or absorption of fats will decrease the ability of vitamin D to be absorbed from the intestines. Sunlight is important to skin production of vitamin D, and environmental conditions where sunlight exposure is limited may reduce this source of vitamin D. Lack of vitamin D production by the skin may occur with indoor confinement or working indoors during the daylight hours, or it may occur in climates with little exposure to sunlight.

When the body is deficient in vitamin D, it is unable to properly regulate calcium and phosphate levels. If the blood levels of these minerals becomes low, the other body hormones may stimulate release of calcium and phosphate from the bones to the bloodstream.

Rickets is a bone disease of children. It causes progressive softening and weakening of the bone structure. There is a loss of calcium and phosphate from the bone, which eventually causes destruction of the supportive matrix. The parathyroid gland may increase functioning to compensate for decreased levels of calcium in the bloodstream, resulting in even more loss of calcium and phosphorous as it is reabsorbed from the bones. In severe cases, cysts may develop in the bones.

Rickets is fairly rare. It is most likely to occur during periods of rapid growth where the body demands high levels of calcium and phosphate. It is usually seen in young children 6 to 24 months old and is uncommon in newborns.

Nutritional causes of rickets occur with a lack of vitamin D in the diet or with malabsorption disorders characterized by poor fat absorption, including steatorrhea, sprue, and short bowel syndrome. A dietary lack of vitamin D may occasionally occur in people on a vegetarian diet who do not drink milk products or in people who are lactose intolerant (those who have trouble digesting milk products). A dietary lack of calcium and phosphorous may also play a part in nutritional causes of rickets. Rickets from a dietary lack of these minerals is rare because calcium and phosphorous are present in milk and green vegetables. A dietary lack of calcium causes osteoporosis (an adult disorder causing brittle bones) more often than it causes rickets.

Hereditary rickets is a vitamin D-resistant form of rickets caused when the kidney is unable to retain phosphate. It is an inherited, sex-linked disorder.

Rickets may also be caused by kidney disorders involving renal tubular acidosis. The acidic condition of the body causes the calcium in the bones to dissolve, leaving soft, weak bones.

Occasionally, rickets may be caused in children with disorders of the liver or biliary (liver secretion) system, when fats and vitamin D are inadequately absorbed or when the vitamin D is not converted to its active form.

Renal osteodystrophy occurs in people with chronic renal failure. The manifestation is virtually identical to that of rickets in children, and that of osteomalacia or osteoporosis in adults.