Infants calcium deficiency

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. ... 

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... 

Phosphates are important because they affect the absorption of calcium and other elements. The absorption of inorganic phosphorus depends on the amount of calcium, iron, strontium, and aluminum present in the diet. Chapman and Pugsley (1971) have suggested that a diet containing more phosphorus than calcium is as detrimental as a simple calcium deficiency. The ratio of calcium to phosphorus in bone is 2 to 1. It has been recommended that in early infancy, the ratio should be 1.5 to 1 in older infants, 1.2 to 1 and for adults, 1 to 1. The estimated annual per capita intake in the United States is 1 g Ca and 2.9 g P, thus giving a ratio of 0.35. The danger in raising phosphorus levels is that calcium may become unavailable. 

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. 

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. 

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... 

Animal studies indicate that nutritional deficiencies in a number of essential elements (e.g., calcium, iron, zinc, copper, phosphorus) may impact the toxicokinetic and toxicological behavior of lead (ATSDR 1993 Chaney et al. 1989). In infants and children, lead retention has been shown to be inversely correlated with calcium intake (Johnson and Tenuta 1979 Sorrell et al. 1977 Ziegler et al. 1978). Zinc has been shown to have a protective effect against lead toxicity in a number of animal species (Goyer 1986 Haeger-Aronsen et al. 1976 Brewer et al. 1985 Cerklewski and Forbes 1976). 

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). 

Parathyroid Hormone Parathyroid hormone raises plasma calcium by direct effects on bone resorption and renal reabsorption of calcium, and indirectly by regulating the metabolism of vitamin D. It is a peptide and acts via cell surface G-protein receptors linked to adenylate cyclase. The parathyroid glands have G-protein cell surface calcium receptors linked to phospholipase G, and parathyroid hormone is secreted in response to hypocalcemia. Magnesium is required for secretion of the hormone, which may explain the development of hypocalcemia in premature infants who are magnesium deficient. 

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

Rickets, which is diagnosed by X-rays of leg bones, heals promptly with 4000 lU of oral vitamin D per day, with treatment for a month. In performing this treatment, the physician needs to monitor plasma 25 hydroxyvitamm D to make certain that they are raised to the normai range. The bone abnormalities (visible by X-ray) disappear gradually over the course of 3-9 months. Parents are instructed to take their infants outdoors for about 20 minutes per day with their faces exposed in order to prevent deficiency. Osteomalacia is treated by eating 2500 ID/day for about three months. Measurements of 25-hydroxyvitamin D, calcium, and parathyroid hormone are also part of the treatment process. 

Metabolic bone disease in children receiving parenteral nutrition manifests primarily as osteopenia and, on occasion, fractures (5). The etiology is multifactorial calcium and phosphate deficiency play a major role in the preterm infant but the part played by aluminium toxicity in this population is unknown. Lack of reference values of bone histomorphometry in the premature infant, as well as lack of reference data for biochemical markers of bone turnover in these patients, contributes to the uncertainty. Other factors that may play a role in the pathogenesis of bone disease associated with parenteral nutrition include lack of periodic enteral feeding underljdng intestinal disease, including malabsorption and inflammation the presence of neoplasms and drug-induced alterations in calcium and bone metabohsm. However, the true incidence and prevalence of parenteral nutrition-associated bone abnormalities in pediatric patients are unknown. 

The RDA for calcium in adults over the age of 24 is 0.8 g. The RDA for women during pregnancy and lactation is 1.2 g. The increased level of 1.2 g is required to supply the fetus with the 30 g of calcium present in the newborn and to provide the 0.24 g of calcium secreted in the milk each day. The RDA for persons from 11 to 24 years of age is 1.2 g the RDAs for children (0.8 g) and infants (0.6 g) are lower. Eggs supply about 30% of dietary calcium and 30% of dietary phosphate for the overall population in the United States. Meat, poultry, and fish supply 20-25% of our phosphate, but only 10% of our calcium. Milk and dairy products supply 20-25% of our phosphate, and 50% of our calcium (Calvo and Park, 1996). A dietary deficiency in calcium is quite rare, though calcium nutrition receives much attention because of mainstream health concerns related to calcium, such as osteoporosis, hypercalcemia, and hypocalcemia. 

PN solutions therefore may need to be modified by clinicians to provide supplemental amounts of CEAAs. Cysteine is a CEAA in preterm and term infants that may be added to PN solutions at the time of compounding. An additional benefit of including cysteine is that it enhances calcium and phosphate solubility in PN solutions by decreasing the solution s pH. Carnitine is a qnarternary amine required for transport of free fatty acids into the mitochondria for beta-oxidation and energy prodnction. Newborns are at risk for carnitine deficiency becanse of their immature synthetic and conservation mechanisms. Decreased plasma carnitine concentrations are associated with impaired lipid metabolism in patients receiving intravenous lipid emulsion (TVLE). ... 

C19. Gifuentes, R. F., Kooh, S. W., and Radde, I. C, Vitamin D deficiency in a calcium-supplemented very low-birth-weight infant. /. Pediatr. 96, 252-255 (1980). 

The work of Harrison and Harrison (1941) is best discussed in connection with the tabulated data on metabolic studies in children (Table I). The following quotation from Harrison and Harrison is instructive Careful examination of the data from metabolic studies in the rachitic infant leads to the conclusion that deficient absorption of phosphate from the intestinal tract cannot wholly explain the diminished concentration of phosphate in the plasma. In infants developing rickets on a cow s milk diet high in both calcium and phosphate, the amount of phosphate absorbed from the intestinal tract would be sufficient for the needs of the infant were the phosphate retained rather than excreted in the urine. ... 

The primary as well as the secondary effects may vary widely in intensity in different species, with the consequence that the rachitic symptoms may vary from hardly recognizable, as in rats on a diet rich in calcium and phosphate, to severe deficiency symptoms, as in puppies or infants in spite of an abundance of calcium and phosphorus in the food. 

Infants with severe cholestasis due to 3jff-HSDH deficiency may have hypo-calcaemia due to malabsorption of vitamin D or severely deranged clotting due to malabsorption of vitamin K. Vitamins D and K should be given either parenterally or orally in a form that is absorbed despite intestinal bile salt deficiency (e.g. la-hydroxy-cholecalciferol or 1,25-dihydroxy-chole-calciferol). Fresh frozen plasma and intravenous calcium supplement may occasionally be required. 

The calcium content of human milk is only about 30 mg per 100 ml, but, provided that the volume produced by the mother is sufficient, the infant s need will be covered. Milk is low in iron but infants accumulate a store of iron during intrauterine life, and this is usually sufficient for the first 4-6 months of independent existence. After this time it is important to supplement the milk diet with iron-containing foods such as strained meat and vegetables. Milk is also relatively deficient in vitamins C and D. The vitamin C content of breast milk is usually adequate, but infants fed on cow s milk may need a supplementary source. Although fresh orange juice and rose hip syrup are good sources, it is undesirable to accustom children to sweet drinks at an early age since later on these can have disastrous effects on the teeth. 

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. 

Deficiencies of Vitamin D. People who have moderate intakes of calcium, but who live in northern areas, seem to have more osteoporosis than people who eat diets low in calcium, but live in sunny, tropical areas. Furthermore, considerable effort is made in most countries to provide infants and children with adequate levels of the vitamin by either diet or exposure to sunlight, but there is often a lack of attention to the needs of adults, many of whom are kept indoors by either their occupations or the circumstances under which they live. 

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. 

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