Vitamin D And Deficiency

It is deficiency is rarely observed in adults and is becoming uncommon in infants due to the widespread use of dietary supplements in the early months of life. A unique feature of vitamin D metabolism is the formation of this vitamin in the skin on exposure to sunlight or ultraviolet rays and, consequently, only partial dependence of the body on a dietary supply. Actually, only small amounts of vitamin D are present in the average diet.

In several animal species, the susceptibility to rickets is influenced by dietary changes, such as the inclusion of cereals containing phytic acid which decreases absorption of calcium. Phytate also appears to interfere with the absorption of calcium in man. Since vitamin D is fat soluble, absorption is impaired in conditions associated with decreased absorption of fats as when bile is absent from the intestinal tract or in the steatorrheas.

Vitamin D consists of a group of sterol derivatives including vitamin D2, activated ergosterol, which is derived from plants and vitamin D3, activated dehydrocholesterol, which is found in animal tissues. Vitamin D is measured in International Units, one unit being equivalent to the activity of 0.025 ,ug. of calciferol ( crystalline vitamine D2 ). In infancy, maximum retention of calcium will be attained with administration of 300 – 400 I.U. of vitamin D daily if the diet contains an ample supply of calcium and phosphorus (150). Larger amounts of vitamin D are not beneficial and a daily dose of more than 1800 I.U. may be deleterious. Maximum retention of calcium is associated with good skeletal growth and early dentition. The majority of children probably require supplementary vitamin D throughout the period of growth and practically all need it during adolescence. The recommended allowance for vitamin D is 400 I.U. daily from birth to 20 years of age.

Supplements of vitamin D would seem desirable during pregnancy and lactation in view of the increased need of calcium and phosphorus in these conditions. In adults, the need for supplemental vitamin D appears to be minimal except in unusual circumstances in which occupation or habits prevent exposure to sunlight.

Vitamin D functions by increasing absorption of calcium from the intestinal tract, possibly increasing the absorption of phosphorus as well, and decreasing the urinary excretion of phosphorus by enhancing reabsorption in the renal tubule. The renal influence may be due, in part, to diminished activity of the parathyroid glands which follows a rise in serum calcium induced by vitamin D. In addition to maintaining levels of calcium and phosphorus in blood which are suitable for deposition of bone, vitamin D is believed to exert some direct effect at the site of bone formation. Recent investigation suggests that vitamin D may activate alkaline phosphatases of bone, kidney and intestine but this enzymatic role of the vita-min needs confirmation. Normal bone formation requires an adequate supply of calcium and phosphorus as well as vitamin D.

Vitamin D Deficiency

Vitamin D deficiency is characterized by poor retention of calcium and phosphorus and retarded skeletal growth, particularly in infancy and early childhood, and by osteomalacia in adult life. The clinical signs of rickets vary greatly depending on the severity of the process and on the age, rate of growth and stage of physical development when the disease is active. The earliest findings are deformities of the skeleton which have been described so well by Park (151). Craniotabes, which may be seen as early as the second month, consists of areas of softening of the skull usually involving the occipital and parietal bones along the lambdoidal suture. The anterior fontanel does not close at the usual time and the margins are soft, as are the margins of the cranial bones that form the sutures. In severe rickets, the skull can become very thick particularly at the frontal and parietal eminences, resulting in the so-called rachitic “bossing” of the skull. Thickening may occur concomitantly with thinning and craniotabes in the back of the skull.

Another early sign of rickets is enlargement of the costochondral junctions, often referred to as beading of the ribs or the rachitic rosary. Other deformities of the thorax include pigeon breast and Harrison’s grooves. The latter are depressions at the sides of the chest at the level of the diphragmatic attachments which develop as a result of muscle pull. Abdominal distention commonly accompanies rickets and accentuates these grooves.

The rachitic child shows postural kyphosis on sitting and lordosis on standing. The long bones become enlarged at the ends, most readily seen at the wrists and ankles. The shafts of the bones may be curved, the direction of curvature being dependent on the age at which rickets occurs. Anterior bowing of the tibia or “saber shin,” occurs before weight bearing while lateral deformity, bow legs and knock knees, develop following standing and walking. The waddling gait in severe rickets is due to a twist in the tibia and femur (151). Narrowing of the pelvic outlet may occur but injury is rarely permanent except in rickets of long duration.

Primary dentition is delayed in rickets and the permanent teeth may show serious defects in enamel formation. The muscles are hypotonic and motor development is delayed; the child is slow in sitting and walking. This muscular relaxation is also responsible for the pot belly. Tetany due to low serum calcium concentration may complicate the clinical picture of rickets.

Roentgenographic examination of the bones will reveal abnormalities except in early rickets, and healing may be followed by serial roentgenograms. Characteristic changes are observed at the cartilage-shaft junctions and in the shafts of the long bones (151). The end of the shaft appears cupped in the x-ray, first visible at both ends of the fibula and the lower end of the ulna, later in the ends of the tibia and the lower ends of the radius and femur. Cupping occurs also in scurvy and in chondrodystrophy.

Spreading of the end of the shaft is another common finding in rickets as is fringing, which appears as thread-like shadows extending from the end of the shaft into the transparent cartilage. The end of the shaft may have an irregular, dotted or stippled appearance. The trabecular network of the shaft becomes coarse and there is a marked decrease in bone density in severe rickets. In advanced stages of the disease, the cortex may be thin or non-visible or it may be thickened and appear reduplicated. Curvatures of the bones are another characteristic finding.

In vitamin D deficiency, fecal excretion of calcium and phosphorus is increased while urinary excretion of calcium is decreased and that of phosphorus increased. The concentration of inorganic phosphorus in the serum de-creases to less than 4 mg/100 ml. (2.5 mEq/1) while the concentration of calcium may remain normal or de-crease. Determination of alkaline phosphatase in serum is the most important single procedure for diagnosing rickets in its early stages. Normal concentration in young children ranges from 5 to 15 Bodansky units. Elevation of alkaline phosphatase above 20 units is highly suggestive of rickets since few other conditions influence phosphatase activity in this age group. Such elevation occurs before clinical rickets is evident. Serial determinations of serum phosphatase are useful in following therapy since the return to normal is delayed until healing is complete.

Rickets which is refractory to treatment is observed occasionally, especially in children over the age of three. The metabolic defect in this condition is not understood; there seems to be interference with the normal calcifying action of vitamin D. Massive doses of the vitamin may promote healing but some of the metabolic abnormalities may not be corrected. Relationships between rickets and the Fanconi syndrome have been discussed previously.

Osteomalacia is an uncommon disease which presumably is the adult counterpart of rickets. It occurs most frequently during pregnancy and lactation and is characterized by osteoporosis, deformity and fracture of bones and tetany. The first symptom is usually pain in the back and sacral area. Muscular weakness is an associated finding which may be pronounced in the adductor muscles of the thighs. Stiffness and contractures of the extremities have been reported. When deformity develops, it is seen first in the areas in which pain occurs, that is, in the spine and pelvis. X-ray examination will show extensive de-mineralization with dislocation and fractures. The concentration of serum calcium decreases, often to levels below 7mg/100 ml., (3.5mEq/1) and the level of alkaline serum phosphatase rises above the normal adult value of 3 to 5 Bodansky units. Since a number of diseases influence phosphatase concentration in the blood in adults, a high level should not be considered evidence of osteomalacia in the absence of other findings.

Osteoporosis and tetany may occur in association with sprue, the celiac syndrome and idiopathic steatorrhea. In these conditions both calcium and vitamin D are poorly absorbed from the intestinal tract.

Massive doses of vitamin D given over long periods of time may lead to toxic reactions. These include elevation of serum calcium, metastatic calcification, loss of weight, vomiting and diarrhea. Death may occur from renal failure. Intoxication may be detected at an early stage by serum calcium determination, a rise above 11.5 mg/100 ml. (6 m Eq/1) being indicative of excessive dosage.