Vitamin hypervitaminosis

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). 

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. 

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

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. 

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... 

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. 

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. 

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... 

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). 

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. 

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 ... 

Harrison (H5) has reported that serum citrate is increased above the normal range in hypervitaminosis D. Winberg and Zetterstrom (Wl) found it to be low in an 11-month-old infant suffering from vitamin D intoxication. Forfar et al. (F7) have reported that during the active phase of idiopathic hypercalcemia, serum citrate levels are low. 

It is widely accepted that retinoids inhibit tumor growth and development, or the promotional phase of tumorigenesis (1J5) since it is well known that vitamin A plays a marked, as yet ill-defined, role in controlling the growth and differentiation of epidermis and epidermally-derived structures (16-18). Experimental evidence for this hypothesis rests primarily on the observation that conditions of hypervitaminosis A significantly inhibit tumor production even when initiated after application of the carcinogenic insult. Thus, 13-cis-retinoic acid inhibits the induction of transitional cell... 

Vitamin A deficiency is characterized by xerophthalmia, follicular hyperkeratosis (phrynoderma), and generalized xerosis.29 In hypervitaminosis A the skin becomes dry, rough, pruritic, and scaly and the lips become cracked. 

The fat-soluble vitamins can dissolve in the fats of our bodies, in which they can be stored. Too large a concentration of these can lead to an illness called hypervitaminosis. Seal livers, for example, are extremely rich in vitamin E. This makes them toxic if eaten in too large a quantity by most people. The metabolism of the Inuit people, who eat seal liver, has adapted to cope with this. The water-soluble vitamins cannot be retained in the body for long periods. They are flushed out and excreted and so must be constantly taken in by eating fruit and fresh vegetables. 

The fact that vitamin D3 toxicity results from primarily uncontrolled intestinal calcium absorption suggests that it is dietary calcium and not vitamin D3 that exacerbates the hypervitaminosis D3 toxicity effect [119]. This was tested by the interaction of excess vitamin D3 and calcium restriction [113]. Rats fed a calcium-deficient diet and given 25,000 IU of vitamin D3 three dmes/week for 2.5 weeks did not succumb to overt hypervitaminosis D3. Simple calcium restriction increased intestinal but not renal 24-OHase activity, presumably because of the absence of parathyroid hormone regulation in the intestine [113]. Coupled with vitamin D3, excess intestinal 24-OHase increased several fold more. However, when dietary calcium was adequate, vitamin D3 excess increased intestinal 24-OHase activity only slightly because of a suppressive mechanism regulated in part by increased blood calcitonin [120],... 

Retinoic acid modulates gene expression and tissue differentiation, acting by way of nuclear receptors. Historically, there was confusion between the effects of deficiency of vitamins A and D by the 1950s, it was believed that the confusion had been resolved. Elucidation of the nuclear actions of the two vitamins has shown that, in many systems, the two act in concert, forming retinoid-vitamin D heterodimeric receptors hypervitaminosis A can antagonize the actions of vitamin D. 

There are few dietary sources of cholecalciferol. The richest sources are oUy fish (especially fish liver oUs), although eggs also contain a relatively large amount, and there is a modest amount in mUk fat and animal liver. In many countries, margarine is fortified with vitamin D. No common plant foods contain vitamin D, although some tropical plants contain calciferol glucuronides that are hydrolyzed in the intestinal lumen and are a source of the vitamin. Indeed, this can be a cause of hypervitaminosis and calcinosis in grazing animals. 

Because of their solubility characteristics, the fat-soluble vitamins can build up in the fatty tissues of the body. This buildup has both positive and negative effects. Since these vitamins can be stored, the body can temporarily tolerate a diet deficient in vitamins A, D, E, or K. Conversely, if excessive amounts of these vitamins are consumed, their buildup can lead to the illness hypervitaminosis. 

Patients with sarcoidosis are intolerant of vitamin D possibly even to the tiny amoimt present in a normal diet, and to that synthesised in their skin by sunlight. The intolerance may be due to overproduction of calcitriol (see above) by macrophages activated by interferon the overproduction is reversed by corticosteroid, which is also used in the treatment of severe hypervitaminosis D (see below). 

---