Rickets phosphorus deficiency

The biochemical features of calcium-deficiency and vitamin D deficiency are very similar. Both disorders result in a low-to-normal serum calcium concentration, an elevated PTH level, a decreased or normal phosphorus concentration, and increased alkaline phosphatase activity. The serum concentration of 25-hydroxyvitamin D is normal or slightly decreased in calcium-deficiency rickets but is markedly decreased in vitamin D deficiency. On the other hand, the serum concentration of 1,25-dihydroxyvitamin D is greatly elevated in calcium-deficiency rickets but is normal or even slightly decreased in vitamin D-deficiency rickets. 

In children, bone deformities, soft flexible bones (rickets), and stunted growth result from calcium deficiency (or vitamin D or phosphorus deficiency). Early signs of adult deficiency are... 

Like calcium, phosphorus is required for bone formation and a deficiency can also cause rickets or osteomalacia. Pica, or depraved appetite, has been noted in cattle when there is a deficiency of phosphorus in the diet the affected animals have abnormal appetites and chew wood, bones, rags and other foreign materials. Pica is not specifically a sign of phosphorus deficiency, since it may be caused by other factors. Evidence of phosphorus deficiency may be obtained from an analysis of blood serum, which shows a phosphorus content lower than normal. In chronic phosphorus deficiency, animals may have stiff Joints and muscular weakness. 

Phosphorus Disorders. Phosphoms nutrient deficiency can lead to rickets, osteomalacia, and osteoporosis, whereas an excess can produce hypocalcemia. Faulty utilisation of phosphoms results in rickets, osteomalacia, osteoporosis, and Paget s disease, and renal or vitamin D-resistant rickets. 

As a brief introductory summary, vitamin D substances perform the following fundamental physiological functions (1) promote normal growth (via bone growth) (2) enhance calcium and phosphorus absorption from the intestine (3) serve to prevent rickets (4) increase tubular phosphorus reabsorpiion (5) increase citrate blood levels (6) maintain and activate alkaline phosphatase m bone (7) maintain serum calcium and phosphorus levels. A deficiency of D substances may be manifested in the form of rickets, osteomalacia, and hypoparathyroidism. Vitamin D substances are required by vertebrates, who synthesize these substances in the skin when under ultraviolet radiation, Animals requiring exogenous sources include infant vertebrates and deficient adult vertebrates, Included there are vitamin D (calciferol ergocalciferol) and vitamin D< (activated 7-dehydrocholesterol cholecalciferol). 

Calcitriol is the main active metabolite of vitamin D, and synergizes with parathormone in mobilizing bone calcium and Increasing calcium absorption from the intestine. Vitamin D occurs in a number of sterol forms. These include vitamin D3 (cholecaldferol - the form in foods and made in the skin by the action of UV) vitamin Dj (ergocalciferol -also from plants). These forms are 25-hydroxylated in the kidney, and then la-hydroxylated in the kidney (under the control of parathormone), to make the most active form. This is available as calcitriol. Vitamin D facilitates the absorption of calcium and to a lesser extent, phosphorus, from the intestine and promotes deposition into the bones. A deficiency of vitamin D therefore results in bone deficiency disorders, e.g. rickets in children. Therapeutic replacement of vitamin D in cases of severe deficiency requires quantities of the vitamin best provided by one of the synthetic vitamin D analogues (e.g. alfacalcidol and dihydrotachysterol). 

Deficiency conditions Rickets, deficit of phosphorus and calcium in blood... 

Vitamin D is essential for bone formation. Without vitamin D, calcium and phosphorus could not be assimilated into the body or deposited onto the bones. In centuries past, deficiency of vitamin D caused a bone-softening disease called rickets in children and osteomalacia in adults. In this country, milk was fortified with vitamin D in the first half of the last century to put an end to the deficiency diseases, and it almost succeeded. Doctors still run into a case every now and then. 

Vitamin D and its metabolites play an important role in the maintenance of extracellular calcium concentrations and in normal skeletal structure and mineralization. Vitamin D is necessary for the optimal absorption of calcium and phosphorus. On a worldwide basis, the most common cause of hypocalcemia is nutritional vitamin D deficiency. In malnourished populations, manifestations include rickets and osteomalacia. Nutritional vitamin D deficiency is uncommon in Western societies because of the fortification of miUc with ergocalciferol. " The most common cause of vitamin D deficiency in Western societies is gastrointestinal disease. Gastric surgery, chronic pancreatitis, small-bowel disease, intestinal resection, and bypass surgery are associated with decreased concentrations of vitamin D and its metabolites. Vitamin D replacement therapy may need to be administered by the intravenous route if poor oral bioavailability is noted. Decreased production of 1,25-dihydroxyvitamin D3 may occur as a result of a hereditary defect resulting in vitamin D-dependent rickets. It also can occur secondary to chronic renal insufficiency if there is insufficient production of the 1 -a -hydroxylase enzyme for the... 

Vitamin D contributes to the calcemic action of the parathyroid hormone (C2, N14). Deficiency of vitamin D therefore results in a fall in ionic calcium concentration which stimulates the parathyroids. Parathyroid hypertrophy is seen in vitamin D-deficient animals (C3, H7, S7) and man (PI) and can be prevented by exposure to ultraviolet light (H7). A low plasma phosphorus concentration and high Cp/Ca are characteristic of osteomalacia and rickets, and the FEl is of the same order as that in parathyroid tumor (Nil) (Fig. 10). However, this high phosphate clearance, unlike that of parathyroid tumor, can be reduced to a normal or subnormal value by intravenous infusion of calcium (N5). 

Rickets is a disorder of young children caused by a deficiency of vitamin D. Low levels of calcium and phosphorus in the blood are associated with skeletal deformities in these patients. 

A deficiency of vitamin D in the yoxmg animal results in rickets, a disease of growing bone in which the deposition of calcium and phosphorus is disturbed as a result the bones are weak and easily broken and the legs may be bowed. In young cattle the symptoms include swollen knees and hocks and arching of the back. In pigs the symptoms are usually enlarged joints, broken bones, stiffness of the joints and occasionally... 

Vitamin D has long been recognized as an essential factor in the absorption of calcium from the gut. As mentioned in Chapter 12, deficiency of this vitamin in infants and children causes rickets, which is characterized by abnormal endochondral calcification, resulting in bones that are hypocalcified and soft. Rickets can be induced experimentally in rats fed on diets lacking vitamin D or low in phosphorus. 

Mellanby in 1918 first described experimental rickets, using the puppy as his experimental animal, and shortly afterwards McCollum et aZ. described the same disease in the rat. It is of interest that Mellanby later found that confinement of his dogs predisposed them toward development of rickets. Also, it is of interest that the rat is normally resistant to vitamin D deficiency and for such a condition to express itself in this animal there must be concomitant unbalance of the calcium-phosphorus ratio or else a deficiency of these elements (Shohl and Wolbach ). McCollum and his co-workers showed that cod-liver oil added to the diet of vitamin D-deficient rats induced calcification to take place. 

In an adequate, well-balanced diet the ratio of calcium to phosphorus is of little significance from the nutritional viewpoint, but in less-balanced diets this ratio assumes some importance. At the pH of the intestine calcium phosphate is difficultly soluble, and excessive amounts of calcium will render most of the phosphate insoluble and thus not available for absorption a high ratio of phosphate to calcium has a similar effect upon the calcium. This effect is enhanced when there is a deficiency of vitamin D, the incidence of rickets being directly related both to the actual amount ingested and to the calcium-phosphorus ratio. 

F vitamin D3 Vitamin D3 is the most abundant of the D vitamins. Strictly speaking, it is not a vitamin because it can be synthesized in the body from cholesterol. Nevertheless, it is classified as such, and many foods (particularly milk) are fortified with vitamin D3 so that we get enough of this vital nutrient. Vitamin D helps regulate both calcium and phosphorus metabolism. A deficiency of vitamin D causes rickets, a bone disease characterized by knock-knees, spinal curvature, and other deformities. 

Rickets— This disease of infancy and childhood, which is usually due to a deficiency of vitamin D, is characterized by poor utilization of dietary calcium and phosphorus for the mineralization of bones. A similar condition, which may occur in adults, is called softening of the bonesor osteomalacia. 

Also see BONE, section on "Bone Disorders" CALCIUM, section on "Calcium Related Diseases" PHOSPHORUS, section on "Phosphorus Related Diseases" VITAMIN D, section on "Deficiency Symptoms" and RICKETS.)... 

Severe and prolonged deficiencies of phosphorus may be manifested in rickets and phosphorus related diseases (see subsequent section headed "Phosphorus Related Diseases"). 

Prevention of rickets and osteomalacia is usually achieved by the provision of adequate dietary calcium (a daily amount equivalent to that in 1 1/2 pints [720 ml] of milk) and making certain that vitamin D is obtained from the diet or from the effect of sunlight on the skin. There is usually sufficient phosphorus present in the diets of people that a deficiency occurs only when there is an abnormally high level of urinary excretion of this element. Therefore, there have been worldwide efforts to promote the fortification of all milk with 400 lU of vitamin D per quart (950 ml). Should this prophylactic measure be unfeeisible in some instancies, calcium and vitamin D might be administered in the form of a mineral and vitamin supplement It is noteworthy that in some areas of the Middle East, infants are fitted with miniature goggles (to proted their eyes) and placed out in the sun in bassinets. 

The deficiency of phosphorus leads to poor mineralisation of bones and teeth, rickets, loss of appetite, vomiting, weakness, weight loss, liver diseases etc. 

Vitamin D Vitamin D enhances the efficiency of the small intestine to absorb calcium and phosphorus from the diet and thus helps to maintain normal serum levels of these minerals. Vitamin D deficiency in infants and children results in inadequate mineralization of the skeleton, causing rickets, which is characterized by various bone deformations. The major source of vitamin D is its formation in the skin as a result of exposure to sunlight. Dietary sources include fortified foods, such as milk and cereals, and certain fish. Infant formula is fortified with vitamin D in many countries. Because human milk contains only low amounts of vitamin D, breast-fed infants who do not receive either supplemental vitamin D or adequate exposure to sunlight are at risk for developing vitamin D deficiency. Subclinical vitamin D deficiency can be assessed by measuring serum 25-hydroxyl-vitamin D deficiency occurs months... 

Vitamin D deficiency in young children causes rickets. As a child becomes vitamin D deficient, this results in a decrease in the efficiency of intestinal calcium absorption. There is a decline in blood-ionized calcium, which causes the parathyroid glands to produce and secrete more parathyroid hormone (PTH). PTH tries to conserve calcium by enhancing tubular reabsorption of calcium in the kidney. However, in the face of developing hypocalcemia, which could disturb neuromuscular function and a wide variety of metabolic and cellular processes, the body calls upon l,25(OH)2D and PTH to mobilize stem cells to become functional osteoclasts, which, in turn, mobilize calcium from the skeleton. In addition, PTH causes a loss of phosphorus into the urine causing hypophosphatemia. Thus, in early vitamin D deficiency the serum calcium is normal it is the low serum phosphorus that causes the extracellular CaXP04 to be too low for normal mineralization of... 

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