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Rickets, calcium-deficiency

Other Calcium Disorders. In addition to hypocalcemia, tremors, osteoporosis, and muscle spasms (tetary), calcium deficiency can lead to rickets, osteomalacia, and possibly heart disease. These, as well as Paget s disease, can also result from faulty utilization of calcium. Calcium excess can lead to excess secretion of calcitonin, possible calcification of soft tissues, and kidney stones when combined with magnesium deficiency. [Pg.377]

In 1978, on the basis of a few measurements of urine calcium and phosphate excretion as well as an awareness of the previously mentioned work regarding the amounts of calcium and phosphate normally accreted in utero and postnatally, it became apparent that the demineralization, fractures and rickets we were seeing in our infants were caused by calcium deficiency. Consequently we increased the amount of calcium added to the parenteral alimentation solutions. If more than 12.5 mM of the calcium were added to a liter of hyperalimentation solution, gross precipitation would occur in the feeding solution. If 10 mM of calcium were added per liter, crystalline precipitated began to build up on the inside of our barium-impregnated silicone rubber central venous catheters. This crystalline precipitate resulted in gradual occlusion and functional loss of these lines. After several false starts and six lost catheters, chemical and crystal analysis showed that the precipitate inside these catheters was CaHPO. ... [Pg.47]

Mineral deficiencies are not uncommon and can have quite a variety of causes—e. g., an unbalanced diet, resorption disturbances, and diseases. Calcium deficiency can lead to rickets, osteoporosis, and other disturbances. Chloride deficiency is observed as a result of severe Cr losses due to vomiting. Due to the low content of iodine in food in many regions of central Europe, iodine deficiency is widespread there and can lead to goiter. Magnesium deficiency can be caused by digestive disorders or an unbalanced diet—e.g., in alcoholism. Trace element deficiencies often result in a disturbed blood picture—i. e., forms of anemia. [Pg.362]

Vitamin D deficiency (also calcium deficiency) produces a condition known in children as rickets and in adults as osteomalacia. The bones and teeth of children with rickets are poorly formed and soft. A child with rickets frequently has malformed limbs, especially bowlegs. Blood dotting may be impaired, and. in extreme cases, there may be disturbances of the nervous system. An improvement in the level of calcium in the diet, along with vitamin D or parathyroid extract when required, brings about a hardening of the bones, but leaves them misshapen if deformity has already occurred. [Pg.1704]

The site and type of bone deformity seen in rickets depend on the age of the child. In a small infant, deformities of the forearms and anterior bowing of the distal tibias are more common. Clinical features such as craniotabes (areas of thinning and softening in the bones of the skull), hypotonia, and tetany are common in vitamin D-deficiency rickets, which occurs more frequently in infants 1 year old or younger. These features may be absent in calcium-deficiency rickets, which usually presents after the age of 1 year or after the child has been... [Pg.325]

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. [Pg.325]

The dietary history and laboratory findings for this patient pointed to calcium-deficiency as the cause of her rickets a low serum calcium within the normal range secondary hyperparathyroidism with an elevated serum concentration of PTH and a normal serum concentration of 25-hydroxyvitamin with an elevated serum concentration of 1,25-dihydroxyvitamin D, the active hormone form of vitamin D. The patient s calcium-deficiency was due to the fact that she did not have access to milk because of the expense and the lack of adequate storage facilities for fresh dairy products in the home. [Pg.325]

Assume that you are a public health official in northern Nigeria. What actions might you take at the population level to reduce the risk and incidence of calcium-deficiency rickets in the region ... [Pg.333]

The fourth section deals with various aspects Digestion, Absorption, and Nutritional Biochemistry. The chapter Obesity considers current problems with respect to the ever-increasing incidence of imbalance between energy intake and utilization. Key problems of undemutrition are discussed in the chapters Protein-Energy Malnutrition and Vitamin A Deficiency in Children. The chapters Lactose Intolerance, Pancreatic Insufficiency, and Abetalipoproteinemia focus on the biochemical processes underlying food digestion and absorption. Calcium Deficiency Rickets, Vitamin B12 Deficiency, and Hemochromatosis provide discussions of absorption and utilization of vitamin D, vitamin B12, and iron, respectively. [Pg.382]

Cafciiim deficiency Although rare throughout the world, rickets has been found to occur in various parts of Africa due to dietary deficiency in calcium, but w ith sufficient vitamin D (Oginni ft a ., 1996). No amount of vitamin D can prevent the rickets that may develop with calcium deficiency... [Pg.576]

Tsai JR, Yang PH. Rickets of premature infants induced by calcium deficiency. A case report. Changgeng Yi Xue Za Zhi 1997 20(2) 142-7. [Pg.2721]

Osteomalacia—the adult form of rickets—is another calcium deficiency disease. Instead of making bones more brittle and porous as osteoporosis does, osteomalacia makes bones more flexible, resulting in deformities and pain. The cause is usually vitamin D deficiency, and the most effective reversal is short-term use of high dosages of vitamin D, gradually reducing dosages to 400 lU (International Units) daily. This should always be done under the supervision of a doctor since vitamin D is a very potent hormone and can become toxic if improperly used. [Pg.61]

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... [Pg.63]

Vitamin D Vitamin D is produced when ultraviolet light (UV) shines on the skin and triggers the conversion of a steroid known as ergosterol to vitamin D. Its major role is to help the body use calcium, and a deficiency causes rickets in children, the same condition caused by calcium deficiency. Vitamin D supplements are rarely needed, except by those who are almost never exposed to the sun. Both vitamin A and vitamin D are essential to normal growth and development. Overdosage of vitamin D can have serious consequences, however. Calcium deposits can form in the kidney, lungs, or tympanic membrane of the ear (leading to deafness). Infants and small children are especially susceptible to vitamin D toxicity. [Pg.410]

Uses Calcium source, dietary supplement for pharmaceuticals, orals, injections, syrups, low-birth-wt. infants, treatment of hypocalcemia, calcium deficiency, hypoparathyroidism, osteoporosis, rickets Regulatory USP compliance Manuf./Distrib. Calcium Group Shan Par Ind. http //www.shanpar. com... [Pg.681]

The hydroxylated vitamin D derivatives act as hormones in humans and higher animals regulating the absorption of Ca + in the intestine (E 3.1). Reduced hormone levels result in calcium deficiency, which causes rickets. Surplus amounts cause calcification of soft tissues. Vitamin D3 synthesized and stored in certain plants is poisonous to animals (E 5.5.3). [Pg.251]

If calcium is deficient in the diet of young growing animals, then satisfactory bone formation cannot occur and the condition known as rickets is produced. The symptoms of rickets are misshapen bones, enlargement of the joints, lameness and stiffness. In adult animals, calcium deficiency produces osteomalacia, in which the calcium in the... [Pg.112]

Calcium deficiency is manifested by tetany with characteristic carpopedal spasm and, at times, laryngospasm and convulsive seizures. When tetany is present, the concentration of serum calcium is usually less than 8 mg. per 100 ml. Tetany occurs in osteomalacia and often accompanies rickets, sprue, the celiac syndrome, and other steatorrheas. [Pg.539]

Although the effect of vitamin D deficiency is impairment of the absorption and utilization of calcium, rickets (section 11.3.4) does not seem to be simply the result of calcium deficiency. Calcium-deficient children with adequate vitamin D nutritional status do not develop rickets but have a much reduced rate of growth. Nevertheless, calcium deficiency may be a contributory factor in the development of rickets when vitamin D status is marginal. [Pg.408]

Vitamin D [1406-12-2] is a material that is formed ia the skin of animals upon kradiation by sunlight and serves as a precursor for metaboUtes that control the animal s calcium homeostasis and act ki other hormonal functions. A deficiency of vitamin D can cause rickets, as weU as other disease states. This tendency can be a problem wherever animals, including humans, especially kifants and children, receive an kiadequate amount of sunshine. The latter phenomenon became prevalent with the advent of the kidustrial revolution, and efforts to cute rickets resulted ki the development of commercial sources of vitamin D for supplementation of the diet of Hvestock, pets, and humans. [Pg.124]

Disease States. Rickets is the most common disease associated with vitamin D deficiency. Many other disease states have been shown to be related to vitamin D. These can iavolve a lack of the vitamin, deficient synthesis of the metaboUtes from the vitamin, deficient control mechanisms, or defective organ receptors. The control of calcium and phosphoms is essential ia the maintenance of normal cellular biochemistry, eg, muscle contraction, nerve conduction, and enzyme function. The vitamin D metaboUtes also have a function ia cell proliferation. They iateract with other factors and receptors to regulate gene transcription. [Pg.139]

One of the triumphs of the science of nutrition is the careful investigation that linked childhood rickets with vitamin D deficiency. This work, which led to methods for treating the disease, is too familiar to need repetition. A direct consequence of these efforts was the elucidation of the pivotal role played by vitamin D in calcium metabolism, as well as the structural studies that revealed that this compound (102) is in fact a steroid derivative. The past... [Pg.101]

Vitamin D is not strictly a vitamin since it can be synthesized in the skin, and under most conditions that is its major source. Only when sunlight is inadequate is a dietary source required. The main function of vitamin D is in the regulation of calcium absorption and homeostasis most of its actions are mediated by way of nuclear receptors that regulate gene expression. Deficiency—leading to rickets in children and osteomalacia in adults—continues to be a problem in northern latitudes, where sunlight exposure is poor. [Pg.484]

In the vitamin D deficiency disease rickets, the bones of children are undermineralized as a result of poor absorption of calcium. Similar problems occur in adolescents who are deficient during their growth spurt. Osteomalacia in adults results from demineralization of bone in women who have little exposure to sunlight, often after several pregnancies. Although vitamin D is essential for prevention and treatment of osteomalacia in the elderly, there is little evidence that it is beneficial in treating osteoporosis. [Pg.485]

Vitamin A (retinol), present in carnivorous diets, and the provitamin (P-carotene), found in plants, form retinaldehyde, utilized in vision, and retinoic acid, which acts in the control of gene expression. Vitamin D is a steroid prohormone yielding the active hormone derivative calcitriol, which regulates calcium and phosphate metaboUsm. Vitamin D deficiency leads to rickets and osteomalacia. [Pg.497]


See other pages where Rickets, calcium-deficiency is mentioned: [Pg.325]    [Pg.325]    [Pg.639]    [Pg.49]    [Pg.38]    [Pg.323]    [Pg.325]    [Pg.325]    [Pg.326]    [Pg.326]    [Pg.327]    [Pg.329]    [Pg.331]    [Pg.333]    [Pg.333]    [Pg.381]    [Pg.253]    [Pg.225]    [Pg.639]    [Pg.415]    [Pg.1197]    [Pg.481]   


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