Diabion 30 Caps
THIS IS A BRAND MEDICATION
INDICATIONS: Deficiency of the components of the formula.
Pharmacokinetics in humans:
Vitamin A: Vitamin A is a fat-soluble compound chemically related to several retinoids possess the biological activity of transretinol. The natural forms of Vitamin A including retinol, alpha, gamma carotene and beta cryptoxanthin. Vitamin A exist in the body as retinol, retinyl ester, retinal and retinoic acid.
Prior absorption of vitamin A should be converted to retinol, whereupon it is absorbed by the mucosal cells of the small intestine to enter the systemic circulation and be subsequently stored in the liver, containing approximately 90% of the vitamin A body. The half-life of the vitamin A is several days.
Normal serum concentrations of vitamin A are 30 to 80 ug / dl. Women generally show lower concentrations of vitamin A than men or children over 15 years.
Vitamin C (ascorbic acid): Vitamin C is an essential vitamin for the human metabolism. When vitamin C is administered in pharmaceutical preparations reaches maximum levels two to three hours after ingestion. Urinary excretion of vitamin C supplementation na 1 g per day is 400 mg. Hemodialysis and peritoneal dialysis removed significant amounts of vitamin C. The anticancer activity of vitamin C may be related to the ability to prevent intercellular communication through gap junction of the hydrogen peroxide, which does not occur with other free radical scavengers. The vitamin C protects endothelial cells stimulated by various cytokines apoptosis.
Vitamin E Vitamin E is alpha-tocopherol or a fat soluble vitamin which is variably absorbed in the gastrointestinal tract in the presence of bile.
Vitamin E is distributed to all tissues and is metabolized primarily in the liver. When administered intramuscularly at half-life is 44 hours when using the intravenous route is 282 hours.
Vitamin E acts as an antioxidant in the membrane to prevent the spread of oxidative processes of unsaturated fatty acids. Research indicates that vitamin E prevents oxidative changes in low density lipoprotein (LDL). Oxidized LDL particles are converted to foam cells more readily than non-oxidized LDL particles. These foam cells are in the fatty streaks of early atherosclerosis. May promote atherogenesis by the chemotactic action of oxidized LDL on monocyte cytotoxicity by endothelial cells, stimulating the release of growth factors and cytokines and their potential vasoconstrictive actions.
Vitamin B1 (thiamine): Thiamine or Vitamin B1 is a water soluble vitamin essential. After absorption is fully distributed to all tissues.
When higher doses are administered, thiamine excess is excreted in the urine as unchanged thiamine or pyrimidine.
Thiamin is converted to the active coenzyme, thiamin pyrophosphate, by the tiamindifosfocinasa. The functions of thiamine pyrophosphate in carbohydrate metabolism are decarboxylation of alfacetoácidos and is involved in the hexose monophosphate pathway.
Vitamin B6 (pyridoxine): pyridoxine, pyridoxal and pyridoxamine are natural compounds known collectively as vitamin B6. These compounds are readily absorbed in the gastrointestinal tract and are metabolized in the liver, particularly pyridoxal phosphate (the active form of the vitamin). 4-pyridoxic acid is the primary form of vitamin excreted in the urine. The half life of pyridoxine is 15 to 20 days.
The various compounds known as vitamin B6 have the same biological activity and are functionally interrelated metabolic. The metabolism of tryptophan to niacin and the conversion of methionine to cysteine are pyridoxal phosphate dependent. Furthermore, pyridoxal phosphate is a coenzyme involved in several metabolic transformations of amino acids and proteins, such as decarboxylation, desulfurization, synthesis, degradation and racemization. The reactions catalyzed by pyridoxal phosphate are important in the metabolism of nitrogen, so that the requirement for vitamin B6 are related to the total protein nitrogen load to be metabolized. Pyridoxal phosphate is a cofactor of glycogen phosphorylase and participates in the metabolism of serotonin, norepinephrine, dopamine, polyunsaturated fatty acids and phospholipids.
Vitamin B12 (cyanocobalamin): Cyanocobalamin is a form of vitamin B12 used in the prevention and treatment of conditions of deficiency of this vitamin. The oral absorption of vitamin B12 requires the presence of intrinsic factor, however, small amounts are absorbed by simple diffusion.
The plasma vitamin B12 binds to transcobalamin II and transported in this form of complex tissues, mainly the liver. Most of the vitamin B12 is excreted in the urine and only small amounts are excreted in the bile with subsequent enterohepatic recirculation.
Both vitamin B12 and folic acid are necessary for purine synthesis and metabolism of certain amino acids, ie Vitamin B12 is essential for normal growth and replication. The deficiency results in defective synthesis of DNA and cellular maturation disorders, these are more evident in cells with high turnover rates, including the hematopoietic system.
In U.S. cyanocobalamin is preferred because the administration of hydroxocobalamin induces antibodies transcobalamin II complex vitamin B12, in some patients.
Folic acid: Folic acid is an essential vitamin, which after oral administration are absorbed in the proximal small intestine. The metabolism takes place in the liver to its active metabolite, 5-methyltetrahydrofolate, 30% is excreted unchanged in the urine.
After absorption, folic acid is reduced to tetrahydrofolic acid which acts as an acceptor of one-carbon units, they come together in different positions to form six major counterparts, which play a specific role in intracellular metabolism. Coenzymes formed from folic acid participating in the following processes: conversion of homocysteine to methionine, conversion of serine to glycine, thymidylate synthesis, histidine metabolism, synthesis of purines. The methyltetrahydrofolate is a methyl donor in the conversion of homocysteine to methionine. This reaction requires vitamin B12 as a cofactor. Persons with elevated homocysteine are at high risk of coronary disease.
Chromium: There is evidence that chromium may play an important role in carbohydrate metabolism and glucose tolerance, possibly as a result of disorders of metabolism and elimination of this element.
The propelling effect of chromium has been clearly demonstrated in animal models of chromium deficient. Although the mechanism of action is unknown, it has been hypothesized that chromium facilitates activation of the insulin receptor by forming a ternary complex.
Selenium: Selenium is an antioxidant nutrient that can act in parallel with vitamin E. Selenium deficiency is associated with reduced insulin secretory capacity and reduction of the activity of glutathione peroxidase, catalase, superoxide dismutase and peroxidase enzymes has a protective role against tissue damage caused by free radicals.
The increased lipid peroxidation and the antioxidant status reduction can contribute to the development of diabetic complications. It has also been observed that selenium induce a sustained improvement of glucose homeostasis in diabetic patients, by an action similar to insulin.
Magnesium: magnesium is an essential component of several enzymes is important in the maintenance of the action potential in nerve and muscle membranes also involved in glucose homeostasis, since the magnesium modulates glucose transport through the cell membranes and is a cofactor of various enzymatic pathways involved in glucose oxidation.
Hypomagnesemia appears to be a characteristic of diabetes, both type 1 and type 2, the reasons for this are not fully understood, but it has been proposed to cause increased urinary losses of magnesium and a low intake of the mineral. In addition the interrelationship has been found between magnesium and metabolic control as hypomagnesaemia is more common in diabetics with inadequate metabolic control and has been attributed to hypomagnesemia an important role in the development of acute and chronic metabolic complications of diabetes . In some studies it has been observed that administration of magnesium improves the response to insulin.
Zinc Zinc is an essential constituent of various enzymes in various metabolic pathways, is also forming part of nucleic acids and bone. The role of zinc in the metabolism of carbohydrates is of considerable interest, about 0.65% of the corresponding crystalline zinc insulin.
Zinc deficiency has been associated with reduced insulin secretion and increased tissue resistance to the action of the hormone. It has also established that diabetic patients, especially those with inadequate control of blood glucose are at risk of zinc deficiency.
Hypersensitivity to any component of the formula.
The administration of any compound with stimulatory activity on hematopoiesis is contraindicated in polycythemia vera.
Because vitamin A is contraindicated in patients with hypervitaminosis A.
Due to the content of zinc administration is contraindicated in patients with glaucoma.
PRECAUTIONS: Patients with kidney stones.
Glucose-6-phosphate dehydrogenase deficiency, hemochromatosis, thalassemia and sideroblastic anemia.
Concomitant treatment with levodopa.
History of neonatal seizures.
Leber's disease (hereditary optic atrophy).
Treatment with vitamin B12 deficiency can mask folic acid.
The administration of vitamin B12 can mask and delay the diagnosis of pernicious anemia.
Doses of folic acid greater than 0.1 mg can mask vitamin B12 deficiency and cause remission of haematological disorders, while there is progression of neurological symptoms.
Due to the low doses used in formulating reports no problems secondary to the administration of the mineral content in the formula, except in cases of severe renal insufficiency.
RESTRICTIONS OF USE DURING PREGNANCY AND BREASTFEEDING
Vitamin A: Pregnancy limit intake to 5,000 units per day, including vitamin A in the diet.
Studies have shown that some components of the formulation (vitamin C) or embryocidal exert teratogenic in animals, however, no controlled studies in women substantiate these results, whereas for other elements no report of adverse effects pregnancy (thiamine).
Other micronutrient supplementation may be desirable during pregnancy to reduce the risk of malformations and low birth weight (folic acid).
ADVERSE REACTIONS: Most of the effects described below have been reported in patients receiving high doses and for prolonged periods of vitamins and minerals, which does not occur with the indicated dose of Diabion.
Macrocytic normochromic anemia and hypoprothrombinemia. It has been reported the appearance of thrombocytopenic purpura, neuropathy and sedation after prolonged administration of high doses and pyridoxine. It can also occur irritability, insomnia, diplopia and blurred vision, seizures, weakness, headache, hepatotoxicity, diarrhea, nausea, flatulence, and skin disorders.
Doses greater than 4.5 g per day of vitamin C can cause hyperglycemia. Doses greater than 500 mg a day can cause gastritis and esophagitis. Megadoses (2.5 to 60 g) of vitamin C can cause calcium oxalate crystalluria.
Anaphylactic reactions by the use of thiamin are presented primarily for the parenteral administration.
Vitamin E can prolong prothrombin time and paradoxically may increase the risk of thrombophlebitis.
DRUG INTERACTIONS AND OTHER GENDER: Concomitant cholestyramine administration with fat-soluble vitamins can cause malabsorption of these.
When administering minocycline vitamin A may increase the risk of development of pseudotumor cerebri.
Concomitant administration of anticoagulants with some components Diabion formula may increase the risk of bleeding.
Chronic administration of acetylsalicylic acid may increase the requirements for vitamin C.
Orlistat can inhibit up to 60% absorption of some vitamins.
Although the clinical significance is unknown, it has been reported that thiamine may increase the effect of neuromuscular blocking agents. Pyridoxine hydrochloride reverses the therapeutic effects of levodopa.
This effect can be overridden by the concomitant administration of carbidopa with levodopa.
Pyridoxine hydrochloride should not be administered at doses of 5 mg daily in patients receiving levodopa alone.
In a study that received 200 mg of pyridoxine hydrochloride, for a month, there was a reduction of approximately 50% in the serum concentration of phenobarbital and phenytoin, as well as interactions with hydralazine, cycloserine and penicillamine.
Simultaneous administration of pyridoxine and isoniazid oral contraceptives may increase or pyridoxine requirements.
Concomitant administration of pyridoxine and amiodarone may increase photosensitivity reactions induced by the latter.
Absorption of vitamin B12 in the gastrointestinal tract may be decreased by aminoglycosides (oral, such as neomycin), colchicine, potassium preparations extended release aminosalicylic acid and its salts, anticonvulsants (phenytoin, phenobarbital, primidone), cobalt irradiation the small intestine, and alcohol intake for more than two weeks.
It has been reported that prednisone increases the absorption of vitamin B12 and intrinsic factor secretion in some patients with pernicious anemia, but not in patients with partial or total gastrectomy. The clinical significance of these findings is unknown.
Concomitant administration of chloramphenicol and vitamin B12 may antagonize the hematopoietic response of vitamin B12 in patients receiving both drugs simultaneously, so alternating antimicrobials should be considered.
Some data show that colestipol can join cyanocobalamin-intrinsic factor complex so that concomitant administration of this compound may reduce the bioavailability of the vitamin and mineral preparations.
In one study found that treatment with omeprazole for two weeks up to 90% may decrease the absorption of protein-bound cyanocobalamin. Therefore, when required supplementation of cyanocobalamin in a patient receiving omeprazole should be preferred parenteral administration. A similar effect was observed with ranitidine and cimetidine, without these changes were due, apparently, to an alteration of the intrinsic factor.
CHANGES IN RESULTS OF LABORATORY TESTS: Vitamin C may interfere with the determination of paracetamol in urine and cause false elevations in SGPT tests, bilirubin and creatinine.
It can alter the results of the determination of glucose when using reduction methods and copper oxidase. It may also interfere with the determination of uric acid, at least enzymatic methods are used.
It has been reported that pyridoxine may cause a false positive reaction when used urobilinogen Ehrlich's reagent.
PRECAUTIONS IN RELATION TO EFFECTS Carcinogenesis, Mutagenesis, Impairment of Fertility: The administration of vitamin A in doses higher than the recommended daily intake has been associated with fetal abnormalities and increased risk of spontaneous abortion. As for the other components of Diabion, no controlled studies in humans or animals which show potential teratogenic, causing embryocidal or fertility disorders.
DOSAGE AND ADMINISTRATION: Oral.
One capsule a day.
MANIFESTATIONS AND MANAGEMENT OF OVERDOSE OR ACCIDENTAL INGESTION Overdoses of vitamin A, are rare in the clinic because they require higher doses of 300,000 IU in children and one million U.I. in adults. Clinical manifestations are pseudotumor cerebri, headache, blurred vision, diplopia, bone pain, rash, hepatitis, increased transaminases, rarely hypercalcemia and renal failure and convulsions.
Where this occurs in children is recommended decontamination with activated carbon, whereas in adults.
It must carry out supportive measures, monitoring of intracranial pressure, electrolyte balance, and vital signs. In chronic overdose monitor levels of transaminases, bilirubin and calcium.
With respect to vitamin C, vitamin E, thiamine, cyanocobalamin, selenium, no danger of overdose.
About pyridoxine, although as has been considered relatively nontoxic, long-term (eg two months or more) the administration of megadoses of pyridoxine (example: 2 grams or more per day) can cause sensory neuropathy or neuropathic syndromes.
The pathogenesis and biochemical basis pyridoxine induced neurotoxicity not been determined. This has suggested that sensory syndrome produced by megadoses of pyridoxine can be of any vulnerability of neurons in the dorsal root ganglion.
Have been observed, rarely, some adverse neurological level due to chronic administration of approximate dose of 500 mg pyridoxine, although pyridoxine causal relationship has not been established.
It is reported impairment of position sense and vibration of the distal limbs and progressive ataxia in several patients. The sense of touch, pain and temperature were less affected and no generalized weakness nor deep reflexes condition. Nerve conduction studies and somatosensory captured responses indicative of dysfunction distal portions of peripheral sensory nerves. Nerve tissue biopsies showed no axonal damage. When discontinuing pyridoxine, neurological dysfunction gradually improved and after a follow-up period, patients recover satisfactorily.
An overdose of magnesium can result in ECG changes as prolongation of the PR interval, QRS and QT, hypotension, bradycardia, respiratory and CNS depression or electrolyte disorders.
Management includes gastric lavage decontamination, because the activated carbon adsorbs not effectively magnesium salts.
Measures should be established to support. If respiratory depression is indicated administration of calcium gluconate or epinephrine in case of hypotension. The most effective management is hemodialysis.