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Hypervitaminosis

Excessive intake of vitamin D causes abnormally high levels of calcium and phosphorus in the blood, which results in the deposition of calcium salts in the arteries and organs. Symptoms of hypervitaminosis D have been noted in cattle and calves. In the UK, the maximmn amoimt of vitamin D supplement added to diets for farm animals is controlled by legislation. [Pg.101]

Depression in growth and anaemia caused by excessive doses of menadione (vitamin K) have been reported. [Pg.101]

Vitamins are involved in metabolic pathways as coenzymes, and some act as protectors in antioxidant and immune systems. The sources and functions of individual vitamins, and the disorders caused by their deficiencies, are summarised below. [Pg.101]

retinol Fish-liver oil Sight, epithelial tissues Blindness, epithelial infection [Pg.101]

cholecalciferol Fish-liver oil, sun-dried roughage Calcium absorption Rickets [Pg.101]


Hypervitaminosis A is characterized by hepatomegaly, cerebral edema and bone structure alterations. (3-Carotene... [Pg.1076]

Avoid phosphate-containing laxatives (e.g., Fleet s Phospho-Soda), sodium or potassium phosphate solutions, avoid hypervitaminosis D... [Pg.176]

Landy, D. (1985). Pibloktoq [hysteria] and Inuit nutrition Possible implication of hypervitaminosis A. Social Science and Medicine, 21, 173-185. [Pg.183]

The ability to form carbon—carbon bonds in a controlled manner around an alkene is the subject of continuing intense research [49,134—136], These compounds are stable and, due to the considerably different reactivities of the C—Zr and C—B bonds, allow for selective and sequential reactions with a variety of electrophiles. Temarotene 58 is a retinoid of interest [137] because it shows no sign of hypervitaminosis A and it is not teratogenic, presumably due to the lack of a polar group [138,139], The published synthesis of temarotene-type compounds is long and leads to mixtures of diastereo-isomers, from which the desired product is eventually isolated [140—142], However, the synthesis of temarotene 58 by the method of Srebnik et al. [130] is straightforward, as outlined in Scheme 7.18. [Pg.251]

Hypervitaminosis A, 25 789 Hypervitaminosis biotin, 25 800 Hypervitaminosis cobalamin, 25 804 Hypervitaminosis D, 25 792 Hypervitaminosis E, 25 794 Hypervitaminosis folic acid, 25 803 Hypervitaminosis K, 25 795 Hypervitaminosis niacin, 25 798 Hypervitaminosis niacinamide, 25 798 Hypervitaminosis pantothenic acid, 25 799 Hypervitaminosis pyridoxine, 25 799 Hypervitaminosis riboflavin, 25 797 Hypervitaminosis thiamine, 25 796 Hyphenated techniques... [Pg.461]

The effects of the steroid hormone calcitriol (see p. 330) in bone are complex. On the one hand, it promotes bone formation by stimulating osteoblast differentiation (top). This is particularly important in small children, in whom calcitriol deficiency can lead to mineralization disturbances (rickets see p.364). On the other hand, calcitriol increases blood Ca "" levels through increased Ca "" mobilization from bone. An overdose of vitamin D (chole-calciferol), the precursor of calcitriol, can therefore have unfavorable effects on the skeleton similar to those of vitamin deficiency (hypervitaminosis see p.364). [Pg.342]

The activity of vitamin A is related to vision process, tissue differentiation, growth, reproduction, and the immune system. A deficiency of this micronutrient mainly leads to visual problems, impaired immune function, and growth retardation in children. Hypervitaminosis could lead to hepatotoxicity, affect bone metabolism, disrupt lipid metabolism, and teratogenicity [417]. The isomerization of P-carotene, due to technological processes in foods, leads to a reduction of the vitamin A activity it is therefore important to analyze it. [Pg.608]

Excess vitamin D can result in hypervitaminosis D with serious vitamin D toxicity characterized by hypercalcemia and nephrocalcinosis. [Pg.398]

With the exception of the possible development of a hypervitaminosis associated with high-dose administration of vitamin D2 or D3, the compounds discussed in this chapter are relatively safe. Allergic reactions to the injection of calcitonin and PTH have occurred and chronic use of some bisphosphonates has been associated with the development of osteomalacia. The principal side effects of intravenous bisphosphonates are mild and include low-grade fever and transient increases in serum creatinine and phosphate levels. Oral bisphosphonates are poorly absorbed and can cause esophageal and gastric ulceration. They should be taken on an empty stomach the individual must remain upright for 30 minutes after ingestion. [Pg.760]

A varied diet containing a wide range of foodstuffs provides adequate intake of vitamins for most people, and supplementing these amounts will have no beneficial effect and may result in the toxicity associated with hypervitaminosis. The DRI also includes the tolerable... [Pg.777]

The hypercalcemia resulting from hypervitaminosis D is responsible for toxic symptoms such as muscle weakness, bone pain, anorexia, ectopic calcification, hypertension, and cardiac arrhythmias. Toxicity in infants can result in mental and physical retardation, renal failure, and death. [Pg.779]

Contraindications Abnormal sensitivity to toxic effects of hypervitaminosis D, hypercalcemia, malabsorption syndrome... [Pg.888]

Signs and symptoms of hypervitaminosis E, including headache, fatigue, nausea, weakness, and diarrhea... [Pg.890]

The answer is e. (Hardman, p 1533.) Enthusiastic overmedication with vitamin D may lead to a toxic syndrome called hypervitaminosis D. The initial symptoms can include weakness, nausea, weight loss, anemia, and mild acidosis. As the excessive doses are continued, signs of nephrotoxicity are manifested, such as polyuria, polydipsia, azotemia, and eventually nephrocalcinosis. In adults, osteoporosis can occur. Also, there is CNS impairment, which can result in mental retardation and convulsions. [Pg.249]

Most patients with cystic acne respond to 1-2 mg/kg, given in two divided doses daily for 4-5 months. If severe cystic acne persists following this initial treatment, after a period of 2 months, a second course of therapy may be initiated. Common adverse effects resemble hypervitaminosis A and include dryness and itching of the skin and mucous membranes. Less common side effects are headache, corneal opacities, pseudotumor cerebri, inflammatory bowel disease, anorexia, alopecia, and muscle and joint pains. These effects are all reversible on discontinuance of therapy. Skeletal hyperostosis has been observed in patients receiving isotretinoin with premature closure of epiphyses noted in children... [Pg.1295]

Acitretin (Soriatane), a metabolite of the aromatic retinoid etretinate, is quite effective in the treatment of psoriasis, especially pustular forms. It is given orally at a dosage of 25-50 mg/d. Adverse effects attributable to acitretin therapy are similar to those seen with isotretinoin and resemble hypervitaminosis A. Elevations in cholesterol and triglycerides may be noted with acitretin, and hepatotoxicity with liver enzyme elevations has been reported. Acitretin is more teratogenic than isotretinoin in the animal species studied to date, which is of special concern in view of the drug s prolonged elimination time (more than 3 months) after chronic administration. In cases where etretinate is formed by concomitant administration of acitretin and ethanol, etretinate may be found in plasma and subcutaneous fat for many years. [Pg.1296]

Vitamin E deficiency is normally associated with diseases of fat malabsorption and is rare in humans. Deficiency is characterized by erythrocyte haemolysis and prolonged deficiency can cause neuromuscular dysfunction. Hypervitaminosis E is not common, despite an increased intake of vitamin E supplements. Extremely high doses of the vitamin may interfere with the blood clotting process. [Pg.192]

Toverud, S. U., Hammarstrom, L. E., Kristoffersen, U. M. Quantitative studies on acid phosphatase in developing rat bones and teeth during hypervitaminosis D. Arch, oral Biol. 20, 175 (1975)... [Pg.127]

Cholecalciferol [Vitamin D3] (Delta D) [Vitamin/Dietary Supplement] Uses Dietary supl to Rx vit D deficiency Action T Intestinal Ca2+ absorption Dose 400-1000 Int Units/d PO Caution [A (D doses above the RDA), +] Contra T Ca2+, hypervitaminosis, allergy Disp Tabs SE Vit D tox Interactions T Risk of arrhythmias w/ cardiac glycosides X effects w/ cholestyramine, colestipol, mineral oil, orlistat, phenobarbital, phenytoin EMS Can cause vit D tox (Tin serum Ca2+ weakness, AMS, Gl upset and cardiac arrhythmias) OD May cause T risk of vitD tox give IV fluids... [Pg.110]

People with severe hypertriglyceridemia associated with Type V hyperlipoproteinemia may be at increased risk of hypervitaminosis A, even with moderate degrees of vitamin A supplementation (1199). Long-term vitamin A administration is associated with an increase in serum cholesterol and serum triglyceride concentrations (1200) and consequently might be linked with atherosclerosis (SEDA-8, 345) (1201,1202). [Pg.656]

Renkema KY, Nijenhuis T, van der Eerden BC, van der Kemp AW, Weinans H, van Leeuwen JP, Bindels RJ, Hoenderop JG. 2005. Hypervitaminosis D mediates compensatory Ca2+ hyperabsorption in TRPV5 knockout mice. J Am Soc Nephrol 16 3188-95. [Pg.559]

Retinoic acid (vitamin A acid), in which the alcohol group has been oxidized, shares some but not all of the actions of retinol. Retinoic acid is ineffective in restoring visual or reproductive function in certain species in which retinol is effective. Flowever, retinoic acid is very potent in promoting growth and controlling differentiation and maintenance of epithelial tissue in vitamin A-deficient animals. Indeed, all-trans-retinoic acid (tretinoin) appears to be the active form of vitamin A in all tissues except the retina, and is 10- to 100-fold more potent than retinol in various systems in vitro. Isomerization of this compound in the body yields 13-n.v-rctinoic acid (isotretinoin), which is nearly as potent as tretinoin in many of its actions on epithelial tissues but may be as much as fivefold less potent in producing the toxic symptoms of hypervitaminosis A. [Pg.617]

High doses of vitamin A can produce the toxic side effects of the acute or chronic hypervitaminosis A syndrome, which in humans is characterized by the following ... [Pg.620]

Acute hypervitaminosis A in humans requires doses of at least 600 mg in adults and 100 mg in children chronic hypervitaminosis A requires 20 to 50 mg daily for several years (Dawson, 2000). [Pg.621]


See other pages where Hypervitaminosis is mentioned: [Pg.503]    [Pg.104]    [Pg.138]    [Pg.117]    [Pg.95]    [Pg.53]    [Pg.365]    [Pg.110]    [Pg.778]    [Pg.887]    [Pg.966]    [Pg.967]    [Pg.187]    [Pg.191]    [Pg.383]    [Pg.620]    [Pg.200]   
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Calciferols (vitamin hypervitaminosis

Hypervitaminosis A syndrome

Hypervitaminosis acute

Hypervitaminosis biotin

Hypervitaminosis chronic

Hypervitaminosis folic acid

Hypervitaminosis from retinol

Hypervitaminosis niacin

Hypervitaminosis pantothenic

Hypervitaminosis pyridoxine

Hypervitaminosis riboflavin

Hypervitaminosis thiamine

Hypervitaminosis vitamin

Hypo- and hypervitaminosis

Retinol (vitamin hypervitaminosis

Skin toxicity hypervitaminosis

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