Vitamin conditioned deficiency

In humans, vitamin A deficiency manifests itself in the following ways night blindness, xerophthalmia, Bitot s spots, and corneal involvement and ulceration. Changes in the skin have also been observed. Although vitamin A deficiency is seen in adults, the condition is particularly harmful in the very young. Often, this results from malnutrition (56). 

On a vitamin A-deficient diet, mucus-secreting tissues become keratinized. This condition tends to occur in the trachea, the skin, the saUvary glands, the cornea, and the testes. When this occurs in the cornea, it can be followed by blindness. Vitamin A deficiency is the principal cause of blindness in the very young. This problem is particularly acute in the third world (8). 

For acute symptomatic hypocalcemia, 200 to 300 mg of elemental calcium is administered IV and repeated until symptoms are fully controlled. This is achieved by infusing 1 g of calcium chloride or 2 to 3 grams of calcium at a rate no faster than 30 to 60 mg of elemental calcium per minute. More rapid administration is associated with hypotension, bradycardia, or cardiac asystole. Total calcium concentration is commonly monitored in critically ill patients. Under normal circumstances, about half of calcium is loosely bound to serum proteins while the other half is free. Total calcium concentration measures bound and free calcium. Ionized calcium measures free calcium only. Under usual circumstances, a normal calcium level implies a normal free ionized calcium level. Ionized calcium should be obtained in patients with comorbid conditions that would lead to inconsistency between total calcium and free serum calcium (abnormal albumin, protein, or immunoglobulin concentrations). For chronic asymptomatic hypocalcemia, oral calcium supplements are given at doses of 2 to 4 g/day of elemental calcium. Many patients with calcium deficiency have concurrent vitamin D deficiency that must also be corrected in order to restore calcium homeostasis.2,37,38... 

Renal osteodystrophy Altered bone turnover that results from sustained metabolic conditions that occur in chronic kidney disease, including secondary hyperparathyroidism, hyperphosphatemia, hypocalcemia, and vitamin D deficiency. 

The nutritional experiments with carotene and fish oils led to the conclusion that a second fat-soluble compound was essential for normal rat growth. Rickets, the condition caused by vitamin D deficiency, is a disease afflicting children where, because of impaired calcification, bone formation is disturbed and the bones become bowed and otherwise deformed. In adults, especially multiparous women, vitamin D deficiency produced osteomalacia—demineralization of bone, leading to tenderness over the bones, pain, and muscle weakness. Rickets was particularly prevalent in slum areas. Glasgow, Vienna, and Lahore were notorious for the high incidence of the disease. 

Vitamin Bg deficiency, iron deficiency, and lead poisoning all can cause anemia. These three conditions are summarized and compared in Ihble 1-17-6. 

Oral As a dietary supplement when calcium intake may be inadequate. Conditions that may be associated with calcium deficiency include the following Vitamin D deficiency, sprue, pregnancy and lactation, achlorhydria, chronic diarrhea, hypoparathyroidism, steatorrhea, menopause, renal failure, pancreatitis, hyperphosphatemia, and alkalosis. Some diuretics and anticonvulsants may precipitate hypocalcemia, which may validate calcium replacement therapy. Calcium salt therapy should not preclude the use of other corrective measures intended to treat the underlying cause of calcium depletion. 

Hypocalcemia - To correct plasma calcium levels (eg, neonatal tetany and tetany due to parathyroid deficiency, vitamin D deficiency, alkalosis) prevention of hypocalcemia during exchange transfusions conditions associated with intestinal malabsorption. 

Stofft, E., Biesalski, H. K., Niederauer, U., Zschabitz, A., and Weiser, H. (1992b). Morphological changes in the tracheal epithelium of guinea pigs in conditions of "acute" vitamin A deficiency. Int. J. Vitam. Nutr. 62,143-147. 

The answer is B. This patient s greasy, foul-smelling stools indicate steatorrhea. Her vision problems may be a manifestation of vitamin A deficiency due to fat malabsorption. The most likely explanation is biliary insufficiency, ie, decreased bile salt production leading to poor emulsification of dietary fats. Active ileal disease is a possibility, but the WBC count would likely be elevated unless her condition was in remission. Infection with Giardia is less likely due to the absence of pathogenic organisms in her stool. Lactose intolerance can produce diarrhea but not steatorrhea. 

Vitamin B deficiency is a rare condition, but it is prevalent in persons with chronic alcoholism due to low dietary Intake and impaired conversion ofpyridoxine to the active coenzyme pyridoxal phosphate. 

D. There is no evidence that affinity for D3 with its receptor is altered during aging. Aging is associated with vitamin D deficiency for several reasons. It is important for the elderly to receive vitamin D supplementation to prevent osteoporosis and the other problems associated with hypocalcemia. If they have chronic liver or renal conditions, use of one of the specific metabolites should be used, such as cal-citriol. 

Since vitamin A is a fat-soluble vitamin, any disease that results in fat malabsorption and impaired liver storage brings with it the risk of vitamin A deficiency these conditions include biliary tract disease, pancreatic disease, sprue, and hepatic cirrhosis. One group at great risk are children from low-income families, who are likely to lack fresh vegetables (carotene) and dairy products (vitamin A) in the diet. 

The most common causes of vitamin B12 deficiency are pernicious anemia, partial or total gastrectomy, and conditions that affect the distal ileum, such as malabsorption syndromes, inflammatory bowel disease, or small bowel resection. 

Deficiency of vitamin K A true vitamin K deficiency is unusual because adequate amounts are generally produced by intestinal bacteria or obtained from the diet. If the bacterial population in Ihe gut is decreased, for example by antibiotics, the amount of endogenously formed vitamin is depressed, and can lead to hypoprothrombinemia in the marginally malnourished individual (for example, a debilitated geriatric patient). This condition rcaj require supplementation with vitamin K to correct the bleeding tendency. In addition, certain second generation cephalosporins (for example, cefoperazone, cefamandole, and moxalactam) cause hypoprothrombinemia, apparently by a warfarin-like mechanism. Consequently, their use in treatment is usually supplemented with vitamin K. 

Vitamin A is necessary for growth and reproduction, resistance to infection, maintenance and differentiation of epithelial tissues, stability and integrity of membrane structures, and the process of vision. In terms of the last function, vitamin A is a component of rhodopsin or visual purple, a photosensitive pigment in the eye that is needed for vision in dim light. An early mild clinical symptom of vitamin A deficiency is night blindness a severe deficiency of this fat-soluble vitamin results in xerophthalmia, an eye condition leading to blindness. 

In this hereditary disease up to 1 - 2 g of methylmalonic acid per day (compared to a normal of <5 mg/day) is excreted in the urine, and a high level of the compound is present in blood. Two causes of the rare disease are known/ One is the lack of functional vitamin B12-containing coenzyme. This can be a result of a mutation in any one of several different genes involved in the synthesis and transport of the cobalamin coenzyme.6 Cultured fibroblasts from patients with this form of the disease contain a very low level of the vitamin B12 coenzyme (Chapter 16), and addition of excess vitamin B12 to the diet may restore coenzyme synthesis to normal. Among elderly patients a smaller increase in methylmalonic acid excretion is a good indicator of vitamin B12 deficiency. A second form of the disease, which does not respond to vitamin B12, arises from a defect in the methylmalonyl mutase protein. Methylmalonic aciduria is often a very severe disease, frequently resulting in death in infancy. Surprisingly, some children with the condition are healthy and develop normally.3 1... 

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. 

Observations on deficiency symptoms in the cardiovascular system were also made [29, 30]. In chicks, exudative diathesis, a condition in which plasma moves from the capillaries into surrounding, particularly subcutaneous, tissue, was studied and found to be associated with lipid peroxidation [31]. In cardiac muscle, a necrotizing myopathy was found in vitamin-E-deficient mice [32], rats [33], rabbits [34] and ruminants [35], Blood abnormalities, associated with increased susceptibility of erythrocytes to haemolysis, figure among reports of the effects of vitamin E deficiency [36, 37]. 

Plasma malondialdehyde-like material, an indicator of lipid peroxidation, is increased in conditions of ischaemia, such as stroke [83, 84] and myocardial infarction [85]. Mitochondria extracted from hearts of vitamin-E-deficient rabbits showed a decreased mitochondrial function and an increased formation of oxygen radicals associated with a reduced superoxide dismutase activity. This was partially reversed by addition of vitamin E in vitro [86]. Measurement of in vitro susceptibility to lipid peroxidation in cardiac muscle from vitamin-E-deficient mice showed a highly significant negative correlation between the concentration of vitamin E and in vitro lipid peroxidation. The results indicate that short-term vitamin E deficiency may expose cardiac muscle to peroxidation injuries [ 87 ]. In rats, treatment for 2 days with isoprenaline increased lipid peroxide activity, as measured by malondialdehyde levels, in the myocardium. Vitamin-E-deficient animals were even more sensitive to this effect, and pretreatment with a-tocopheryl acetate for 2 weeks prevented the effect induced by isoprenaline. The authors [88] propose that free-radical-mediated increases in lipid peroxide activity may have a role in catecholamine-induced heart disease. 

Much has been said about the positive effects of vitamin E (a-tocopherol) on sexual performance and ability in humans. Unfortunately, there is little scientific rationale to substantiate such claims. The primary reasons for attributing a positive role in sexual performance to vitamin E come from experiments on vitamin E deficiency in laboratory animals. In such experiments the principal manifestation of this deficiency is infertility, although the reasons for this condition differ in males and females. In female rats there is no loss in ability to produce apparently healthy ova, nor is there any defect in the placenta or uterus. However, fetal death occurs shortly after the first week of embryonic life, and fetuses are reabsorbed. This situation can be prevented if vitamin E is administered any time up to day 5 or 6 of embryonic life. In the male rat the earliest observable effect of vitamin E deficiency is immobility of spermatozoa, with subsequent degeneration of the germinal epithelium. Secondary sex organs are not altered and sexual vigor is not diminished, but vigor may decrease if the deficiency continues. 

Because of experimental results such as these, vitamin E has been conjectured to restore potency or to preserve fertility, sexual interest, and endurance in humans. No evidence supports these contentions, but because sexual performance is often influenced by mental attitude, a person who believes vitamin E may improve sexual prowess may actually find improvement. The only established therapeutic use for vitamin E is for the prevention or treatment of vitamin E deficiency, a condition that is rare in humans. 

Anyone with the condition phenylketonuria (PKU), a metabolic disorder, should be particularly careful about nitrous oxide use. Individuals with PKU require a diet that is high in protein in low in animal fats, which frequently results in a vitamin B12 deficiency. Nitrous oxide can remove even more B12 from these individuals bloodstreams, possibly causing mental impairments, as well as severe nerve and brain damage. 

There is little in the literature relative to vitamin A and colon cancer in human populations. Experimental animal studies, however, strongly suggest that vitamin A deficiency may have a role in this type of cancer. We have shown that a deficiency of vitamin A increased DMH-induced tumors and shortened the lag time for induction, compared to normally supplemented controls (72). More recently (73) we have confirmed a protective role for vitamin A in colon carcinogenesis (Table XVII). Furthermore, we have shown (74) that vitamin A deficiency can result in colon tumors in rats given aflatoxin (AFB ) which is normally a liver carcinogen (Table XVIII). The colon tumors associated with the hepatocarcinogen AFB.. appear to be a result of differences in metabolism and binding of AFB or its metabolite ) to colon DNA under conditions of vitamin A deficiency (75). 

Clinical Conditions Associated with Vitamin B12 Deficiency. 185... 

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