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.
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