Vitamin intoxication

Vitamin D intoxication causes 25-hydroxy vitamin blood levels to go from a normal of 30—50 ng/mL to 200—400 ng/mL. At this high level, the metabohte can compete with 1 a-25-dihydroxy vitamin for receptors in the intestine and bone and induce effects usually attributed to the dihydroxy vitamin D. Thus, 25-hydroxy vitamin is beUeved to be the critical factor in vitamin D intoxication. Vitamin D2 is metabolized slower than vitamin and thus appears to be less toxic (218). 

Vitamin D withdrawal is an obvious treatment for D toxicity (219). However, because of the 5—7 d half-life of plasma vitamin D and 20—30 d half-life of 25-hydroxy vitamin D, it may not be immediately successful. A prompt reduction in dietary calcium is also indicated to reduce hypercalcemia. Sodium phytate can aid in reducing intestinal calcium transport. Calcitonin glucagon and glucocorticoid therapy have also been reported to reduce semm calcium resulting from D intoxication (210). 

One of the major problems In the treatment of patients with vitamin D compounds (l.e., patients with hypoparathyroidism) has been the unpredictable development of hypercalcemia and the syndrome of vitamin D Intoxication. Although this problem may become less serious when some of the faster-acting metabolites and analogues of metabolites of vitamin D become available for clinical use. It Is likely that monitoring of serum levels of... 

Much of the toxicological interest in cyanide relating to mammals has focused on its rapid lethal action. However, its most widely distributed toxicologic problems are due to its toxicity from dietary, industrial, and environmental factors (Way 1981, 1984 Gee 1987 Marrs and Ballantyne 1987 Eisler 1991). Chronic exposure to cyanide is correlated with specific human diseases Nigerian nutritional neuropathy, Leber s optical atrophy, retrobulbar neuritis, pernicious anemia, tobacco amblyopia, cretinism, and ataxic tropical neuropathy (Towill etal. 1978 Way 1981 Sprine etal. 1982 Beminger et al. 1989 Ukhun and Dibie 1989). The effects of chronic cyanide intoxication are confounded by various nutritional factors, such as dietary deficiencies of sulfur-containing amino acids, proteins, and water-soluble vitamins (Way 1981). 

No specific antidote has been shown to be effective in treating 1,2-dibromoethane intoxication once absorption into the bloodstream has occurred (Ellenhorn and Barceloux 1988). Intravenous infusions of glucose may limit the hepatotoxicity of 1,2-dibromoethane (ERA 1989b). During the recovery phase, a diet rich in vitamin B and carbohydrates may limit liver damage (Dreisbach and Robertson 1987 Lawrence and Michaels 1984). Hemodialysis may be needed to regulate extracellular fluid and electrolyte balance and to remove metabolic waste products if renal failure occurs (ERA 1989b). 

Calcium play vital role in excitation - contraction coupling in myocardium. Calcium mediates contraction in vascular and other smooth muscles. Calcium is required for exocytosis and also involved in neurotransmitters release. Calcium also help in maintaining integrity of mucosal membranes and mediating cell adhesions. Hypercalcemia may occur in hyperthyroidism, vitamin D intoxication and renal insufficiency, which can be treated by administration of calcitonin, edetate sodium, oral phosphate etc. Hypocalcemia may occur in hypothyroidism, malabsorption, osteomalacia secondary to leak of vitamin D or vitamin D resistance, pancreatitis and renal failure. Hypocalcemia can be treated by chloride, gluconate, gluceptate, lactate and carbonate salts of calcium. 

Thiamine (vitamin B1 ) Essential vitamin required for synthesis of the coenzyme thiamine pyrophosphate Administered to patients suspected of having alcoholism (those exhibiting acute alcohol intoxication or alcohol withdrawal syndrome) to prevent Wernicke-Korsakoff syndrome Administered parenterally Toxicity None Interactions None... 

When alcoholics have schizophrenia, malvaria, or high HOD scores (uncomplicated by acute intoxication), they will respond well to mega vitamin B3 therapy. 

The major location of calcium in the body is in the skeleton, which contains more than 90% of the body calcium as phosphate and carbonate. Bone resorption and formation keeps this calcium in dynamic equilibrium with ionized and complexed calcium in blood, cellular fluids and membranes. Homeostasis is mainly regulated by the parathyroid hormone and vitamin D which lead to increased blood calcium levels, and by a thyroid hormone, calcitonin, which controls the plasma calcium concentration J5 Increasing the concentration of calcitonin decreases the blood calcium level, hence injections of calcitonin are used to treat severe hyperalcaemia arising from hyperparathyroidism, vitamin D intoxication or the injection of too high a level of parathyroid extract. High levels of calcitonin also decrease resorption of calcium from bone. Hypocalcaemia stimulates parathyroid activity, leading to increased release of calcium from bone, reduction in urinary excretion of calcium and increased absorption of calcium from the intestine. Urinary excretion of phosphate is enhanced. 

Iron is widely used in over-the-counter vitamin preparations and is a leading cause of childhood poisoning deaths. As few as 10-12 prenatal multivitamins with iron may cause serious illness in a small child. Poisoning with other metals (lead, mercury, arsenic) is also important, especially in industry. See Chapter 33 Agents Used in Anemias Hematopoietic Growth Factors and Chapter 58 Heavy Metal Intoxication Chelators for detailed discussions of poisoning by iron and other metals. 

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. 

Wl. Winberg, J., and Zetterstrom, R., Cortisone treatment in vitamin D intoxication. Acta. Paediat. 46, 96-101 (1956). 

Non-response to epoetin alfa therapy should prompt a search for causative factors. These include iron, folate, or vitamin B12 deficiency aluminium intoxication intercurrent infections inflammatory or traumatic episodes occult blood loss haemolysis and bone marrow fibrosis of any origin. 

Correction of fluid acidosis and electrolyte imbalance may be required (Ellenhorn and Barceloux 1988 Stutz and Janusz 1988). At the same time, drug therapy for pulmonary edema should be considered (Bronstein and Currance 1988). Diazepam may be necessary to control seizures (Bronstein and Currance 1988 Haddad and Winchester 1990). However, sedatives such as chlorpromazine may potentiate the action of DNOC (Clarke et al. 1981). However, a study in mice indicated that the effect of chlorpromazine may be dose-dependent. Mice that were pretreated with 8 and 12 mg/kg chlorpromazine were protected against DNOC toxicity, but a dose of 6 mg/kg potentiated the toxicity of DNOC (Tesic et al. 1972). However, the efficacy of chlorpromazine administered after intoxication with DNOC was not evaluated. In the same study, pretreatment with vitamin E, vitamin A and/or glucose 30 minutes before dosing with DNOC prolonged the mean time to death in mice. 

Unfortunately the study did not evaluate the efficacy of vitamin E or vitamin A after DNOC intoxication in mice. 

Q7 The total serum calcium concentration is normally about 9.5 mg dl 1. Approximately half of this is bound to plasma protein, mostly to albumin. Most of the remainder is unbound or ionized calcium, which is the physiologically and clinically important form. Hypercalcaemia, normally defined as a serum concentration of >12 mgdl-1, may sometimes be caused by excessive consumption of calcium in the diet. More important pathologically is malignant disease. Hypercalcaemia occurs when there are bone metastases associated with breast or prostate cancer. However, many tumours can produce a PTH-like protein causing elevated serum calcium levels. Furthermore, intoxication and immobilization of vitamin D or excess vitamin D may also cause hypercalcaemia. 

Haupt R. Akute symptomatische Psychose bei Vitamin A-Intoxikation. [Acute symptomatic psychosis in vitamin A intoxication.] Nervenarzt 1977 48(2) 91-5. 

As the intake of vitamin A increases, there is an increase in the excretion of metabolites in bile, once adequate liver reserves have been established. However, the biliary excretion of retinol metabolites reaches a plateau at relatively low levels, and it seems likely that this explains the relatively low toxic threshold (Olson, 1986). Vitamin A intoxication is associated with the appearance of both retinol and retinyl esters bound to albumin and in plasma lipoproteins, which can be taken up by tissues in an uncontrolled manner the amount of circulating retinol bound to RBP does not increase. Retinol has a membrane lytic action it was noted in Section 2.2.2.3 that one of the functions of RBP binding seems to be to protect tissues against retinol, as well as to protect retinol against oxidation (Meeks et al., 1981). 

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