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Cipro 500mg 14 Tabs, Ciprofloxacino

Cipro 500mg 14 Tabs, Ciprofloxacino
Model:DF, EQ, FA
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Price:$9.00

Cipro 500mg 14 Tabs, Ciprofloxacino

INDICATIONS: Deficiency of the components of the formula. Neurobion is indicated as part of the treatment of various painful conditions such as back pain, muscle pain, sciatica, radiculitis, alcoholic polyneuropathy, diabetic neuropathy, torticollis, peripheral neuralgia, facial neuralgia, trigeminal neuralgia, intercostal neuralgia, postherpetic neuralgia.

Human Pharmacokinetics: vitamins B1, B6 and B12 are involved in the metabolism of all cells in the body and show particularly significant activity in hematopoiesis and the functioning of the nervous system cells, therefore they have been termed vitamins neurotropic.

Thiamin (vitamin B1): Thiamine is absorbed in the small intestine by two mechanisms: a) by active transport, and b) by passive diffusion. There appears to be a specific carrier and energy-dependent sodium. The active absorption of thiamine is greater in the jejunum and ileum. The intestinal transport of thiamine radiolabeled human has a Vmax of 31.5 micromol (8.3 mg) and 45.6 km mol (12.0 mg).

Thiamine is carried by the blood to the portal vein to the liver. From 20 to 30% of thiamine present in the plasma of normal adults is protein bound in the form of thiamine pyrophosphate. The average total amount in the normal adult is about 30 mg, with high concentrations in the heart, liver, kidneys, brain and skeletal muscle. Approximately 50% of the total body thiamine is present in muscles. The biological half life of the radiolabeled thiamine is 9 to 18 days. Since Thiamine is not stored in tissues in large quantities, it requires a continuous supply of this vitamin.

About 80% of the total body thiamine is thiamine pyrophosphate, 10% is thiamine triphosphate and the remainder is as thiamine monophosphate. Found 25 to 30 urinary metabolites of thiamine in humans of which override the pyrimidine-carboxylic acid, acid and acid thiazoleacetic tiaminacético.

Thiamine and its metabolites are primarily excreted in the urine and a small amount is excreted in the bile. When administered orally or parenterally, it is rapidly converted to vitamin thiamine pyrophosphate, thiamine triphosphate and tissues. Thiamine tissue needs exceeding the storage capacity and is rapidly excreted in the urine in free form. The fabrics perform total degradation of thiamine approximately one milligram daily amount corresponding to the daily. When intake is less than that amount, thiamine in the urine does not appear or does it in very small amounts.

Thiamine pyrophosphate functions as a coenzyme in the decarboxylation and transcetolación of a-keto acids. In a more functional, thiamin participates in various neurophysiological processes.

Thiamin is involved in various processes of neurotransmission. Preclinical studies have shown that in thiamine deficiency, replacement of acetylcholine and their use are decreased in the cerebral cortex, midbrain, diencephalon and brain stem; decreases the synthesis of catecholamines in the brain, including significant reductions noradrenaline content in the cerebral cortex, the hippocampus and olfactory bulbs, the uptake of serotonin by synaptosomes cerebellar decreases, 5-hydroxyindoleacetic acid (catabolite serotonin), is significantly increased without altering the concentrations of tryptophan and are reduced concentrations of glutamate, aspartate, and glutamine gamma-aminobutyrate.

Irrespective of its function as a coenzyme were observed other important actions of thiamine. Thiamine antagonists affect the impulse conduction in peripheral nerves after stimulation of thiamine is released from membrane preparations of brain, spinal cord and sciatic nerves, phosphorylated derivatives of thiamin are related proteins sodium channel. The thiamine may play a fundamental role in controlling the sodium conductance axon membranes as well as in other neurophysiological processes.

Pyridoxine (vitamin B6): The process of absorption of the three primary forms of vitamin B6 is performed primarily by a passive transport process nonsaturable, mainly in the jejunum. After hydrolysis of the phosphorylated forms and uptake by the intestine, each is then phosphorylated and retained. However, the forms of vitamin B6 which are released from the basolateral side of the membrane of the intestine are mainly unphosphorylated forms.

In general, human studies show an inverse correlation between the amount of pyridoxine glucoside diet and bioavailability. Nearly 58% of pyridoxine glucoside is bioavailable. The digestion of food and the presence of fiber in the diet may limit the bioavailability of vitamin B6. Vitamin B6 is transported in the blood plasma and erythrocytes.

Pyridoxal and less pyridoxal phosphate are bound to albumin and hemoglobin.

The liver is the organ responsible for most of the metabolism of vitamin B6. As a result, the body provides the active form of vitamin B6 (pyridoxal phosphate) transit and other tissues. The three unphosphorylated forms are converted to their respective shapes pyridoxine-phosphorylated by the kinase, which uses zinc as cofactors and ATP. Pyridoxamine phosphate and pyridoxine phosphate can be processed by pyridoxal phosphate oxidase flavin mononucleotide. Pyridoxal coming from this dephosphorylation and nourishing sources derivative or drug, may be converted to 4-pyridoxic acid in a non-reversible reaction where participates adenyl flavin dinucleotide and aldehyde oxidase. This reaction occurs in the human liver, but whether the case in other tissues.

Pyridoxal phosphate and pyridoxal comprise about 75 to 80% of the total circulating vitamin B6 in the plasma, after these forms, pyridoxine is the most common form, which is absorbed by the tissues to be converted to phosphate pyridoxine, however, lack many tissues oxidase activity sufficient to convert pyridoxine phosphate pyridoxal phosphate.

The various functions of vitamin B6 in humans are complex and interrelated. Because the reactivity of pyridoxal phosphate and amino acids with various nitrogen compounds, the biochemical functions of vitamin B6 are concentrated around these molecules. In these functions pyridoxal phosphate acts as a catalyst for many reactions.

Pyridoxal phosphate is involved in gluconeogenesis through its participation in transamination reactions and the action of glycogen phosphorylase. The activities of the glycogen phosphorylase in the liver and muscle are decreased in rats with vitamin B6 deficiency, but a vitamin deficiency, by itself, does not produce mobilization of vitamin B6 stored in muscle. In experimental animals were observed increased concentrations of linoleic and linolenic acids d-and low concentrations of arachidonic acid in liver phospholipids. This effect is accompanied by alterations in amino acid metabolism (homocysteine) and changes in the phospholipids and fatty acids associated with them.

The correlation between vitamin B6 and cholesterol also remains unclear. In humans, a deficiency of vitamin B6 is not accompanied by significant changes in serum cholesterol.

In the erythrocyte pyridoxal phosphate functions as a coenzyme of transaminases. Both pyridoxal phosphate as pyridoxal bind to hemoglobin. Pyridoxal phosphate attached to the alpha chain of hemoglobin, increases the affinity of the molecule by oxygen, while pyridoxal phosphate loosely bound to beta chain decreases the binding affinity for oxygen. Severe and chronic deficiency of vitamin B6 can cause microcytic-hypochromic anemia.

Some patients with sideroblastic anemia and other forms of anemia respond favorably to therapy with pyridoxine.

Pyridoxal phosphate is a coenzyme which participates in the enzymatic reactions leading to the synthesis of various neurotransmitters, such is the case of serotonin (from tryptophan), taurine, dopamine, norepinephrine, histamine and alpha-aminobutyric acid. Neurological disorders have been reported in infants and animals deficient in vitamin B6. Children fed formula lacking vitamin B6 show abnormal electroencephalograms and convulsions. Treatment with vitamin B6 can correct EEG abnormalities. Adults fed diets low in vitamin B6 for three to four weeks have also presented electroencephalographic abnormalities.

Studies in animals receiving intake of vitamin B6 deficient progeny showed that the vitamin D deficient rats had alterations in fatty acid levels in the cerebellum and brain. Other changes were observed in nerve cells are low concentrations of alpha-aminobutyric acid and altering the concentration of amino acids. These observations point out the need for an adequate supply of vitamin B6 during nervous system development.

The intake of vitamin B6 has a significant impact on immune function. In animal and human studies found that a low intake of vitamin B6 is accompanied by immune disorders.

Production of interleukin-2 (IL-2) and lymphocyte proliferation in humans are reduced with vitamin B6 deficiency.

Pyridoxal phosphate binds to the steroid receptor. In one of the binding sites, pyridoxal phosphate inhibits steroid receptor binding to DNA.

Vitamin B6 is stored mainly in the liver and to a lesser extent in muscle and brain.

The total body reservoir of vitamin B6 was estimated at 1.000 mol, of which 800 to 900 mol are present in muscle.

The parts of pyridoxal phosphate in the plasma is related to a dual-compartment model and has been estimated that the slow replacement of the stored portion occurs in 25 to 33 days.

The biological half-life of pyridoxine appears to be 15 to 20 days, the liver is oxidized to pyridoxal pyridoxic acid, which is excreted in the urine.

Cyanocobalamin (vitamin B12): The cobalamins are linked with high affinity with the glycoproteins present in all mammalian tissues. One is the intrinsic factor, which is necessary to be carried out the normal absorption of Vitamin B12.

Other glycoproteins are haptocorrinas (Hc, also called linkers R, TC I and III) and transcobalamin II (TC II). Transcobalamin II binds to vitamin B12 in the terminal ileum cells and the plasma conveyed by the body cells.

Intrinsic factor is secreted by gastric parietal cells, but is also present in the cells of the fund, in antral G cells of the gastric mucosa and salivary glands.

For cobalamins bind to intrinsic factor and TC II requires a rearrangement of the Co-N bond, this implies that both intrinsic factor and CT II can not join the corrinoids cobalamínicos not.

In the stomach, vitamin B12 from the diet is liberated from its union with other organic compounds by the action of gastric acid and pepsin. The vitamin, which is predominantly methylcobalamin (MCB) and adenosylcobalamin (AdoCb), binds to haptocorrinas immediately.

Up to 0.2% of total body reservoir of cobalamin is excreted in the bile and day is bound to haptocorrin. Also, apoptosis of intestinal mucosal cells containing cobalamin occurs at constant speed.

The partial proteolytic removal of cobalamin from haptocorrin and subsequent reabsorption cobalamin receiver terminal ileal enterocyte can constitute the enterohepatic cycle of vitamin B12 when the amounts of vitamin B12 are greater than 1.0 g per day.

This may explain why the absorption of vitamin B12 occurs specifically at the end of the ileum 60 centimeters.

Once inside the cell the ileum by endocytosis mechanism, cobalamin is released and the intrinsic factor is degraded by separate mechanisms which are associated with the acidic region prelisosomal. Cobalamin absorbed is converted to methylcobalamin and adenosylcobalamin, probably within the mitochondria of the cell of the ileum.

In humans, 90% of the cobalamin is bound to circulating transcobalamin I wherein has a half life of 9.3 to 9.8 days. The cobalamin bound to TC I probably the only available form of vitamin B12 that is stored in the liver cells and the reticuloendothelial system.

The total content of vitamin B12 in the adult organism is 3 to 5 mg, of which 50% is in the liver. The adenosylcobalamin constitutes more than 70% of cobalamin in the liver, erythrocytes, brain and kidney, while methylcobalamin formed only 1 to 3%.

Plasma cobalamin is mainly methylcobalamin (60-80%), the remainder is hydroxocobalamin and adenosylcobalamin.

Excretion of cobalamin occurs through a process of cell apoptosis within the gastrointestinal tract, kidneys and skin. This is an exceedingly slow process, since in case of total gastrectomy, which reduces the absorption of cobalamin virtually zero, only a deficiency of cobalamin megaloblastic anemia sufficient to produce after a period of 4 to 7. This is due to enterohepatic circulation.

In cells B12 vitamin functions as a coenzyme for methylmalonyl-CoA and methionine synthetase.

The methionine synthetase establishes a connection between two important metabolic processes: the synthesis of DNA and RNA purines and pyrimidines. Another function of this enzyme is to act as a gatekeeper for folate entry into cells.

Unlike what was thought some years ago, the body has no way to control the effects of vitamin B12 deficiency, so that the gap resulting in a number of complications in that differentiates the association may have a possible and have a well defined relationship. Among those with a definite association is megaloblastic anemia and neuropathy associated with vitamin B12 deficiency and a possible association are atheroma formation that can cause thrombosis, cerebral vascular disease and peripheral neural tube defects and hepatic steatosis.

Particularly neuropathy associated with vitamin B12 deficiency is associated with changes in the rate of methylation. When the methionine synthase is inhibited due to vitamin B12 deficiency, occurs an increase of homocysteine ​​and adenosylhomocysteine, which impairs the synthesis of methionine and adenosylmethionine, causing reduction of the methylation rate, this hypomethylation state deteriorates synthesis of myelin basic protein.

Organs such as liver and kidney remetilar to produce methionine homocysteine ​​methyltransferase through, however, this enzyme is not available in the brain.

Hypersensitivity to the components of the formula.

The administration of any compound with stimulatory activity on hematopoiesis is contraindicated in polycythemia vera.

PRECAUTIONS: The administration of megadoses of pyridoxine has been associated with the presentation of neuropathic syndromes, which reversed upon discontinuation of therapy.

RESTRICTIONS OF USE DURING PREGNANCY AND LACTATION: This product contains benzyl alcohol and therefore should not be used during pregnancy or lactation or in newborns.

ADVERSE REACTIONS: Adverse reactions include burning at the site of application, may be observed rarely hypersensitivity reactions (in people susceptible to the components of the formula) consisting of respiratory distress, pruritus, abdominal pain and shock.

Some of these reactions may occur after prolonged application.

It has been reported the onset of peripheral neuropathy with prolonged administration of pyridoxine.

Other side effects include gastrointestinal disorders, folic acid deficiency, and children hypotonia and respiratory distress, and skin reactions.

The administration of vitamin B complex to treat megaloblastic anemia may mask a picture of polycythemia vera.

DRUG INTERACTIONS AND OTHER GENDER: 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 investment can be overridden carbodopa concomitant 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 pyridoxine daily 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.

The absorption of vitamin B12 in the gastrointestinal tract may be decreased by aminoglycosides (by mouth, such as neomycin), colchicine, potassium preparations extended release aminosalicylic acid and its salts, anticonvulsants (phenytoin, phenobarbital, primidone), irradiation cobalt in the small intestine, and excessive alcohol intake for more than two weeks.

In vitro, the ascorbic acid can destroy substantial amounts of vitamin B12 and intrinsic factor and this possibility must be considered when given large doses of ascorbic acid within the first hour was orally administered Vitamin B12.

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, so it must be carefully monitored and should be considered alternate antimicrobial.

Some data show that colestipol can join the cyanocobalamin-intrinsic factor complex so that concomitant administration of this compound may reduce the bioavailability of preparations based on vitamins and minerals.

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 by cyanocobalamin supplementation in patients 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.

It has been reported that ascorbic acid, even at low doses, may destroy over 80% of cyanocobalamin in foods, which does not occur with parenteral administration of vitamin B12.

CHANGES IN RESULTS OF LABORATORY TESTS: It has been reported that pyridoxine can produce a false-positive reaction when used urobilinogen Ehrlich's reagent.

PRECAUTIONS IN RELATION TO EFFECTS Carcinogenesis, Mutagenesis, Impairment of Fertility: In animal studies, there are no reports of carcinogenicity, mutagenicity, teratogenicity or impaired fertility.

DOSAGE AND ADMINISTRATION: Intramuscular deep. 2 ml (one vial or prefilled syringe) every 24 or 48 hours.

MANIFESTATIONS AND MANAGEMENT OF OVERDOSE OR ACCIDENTAL INGESTION Regarding thiamine no danger of overdosing.

About pyridoxine, although as has been considered relatively nontoxic, long-term (eg two months or more) the administration of megadoses of pyridoxine (example: 2 g 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 reported rarely, some adverse neurological level due to chronic administration to approximate dose of 500 mg pyridoxine. Although pyridoxine causal relationship was not established, reported a case of sensory neuropathy with subsequent axonal degeneration in a patient who received a single dose of 10 g of intravenous pyridoxine.

Manifestations: reported impairment of position sense and vibration of the distal limbs, and progressive ataxia in several patients. The sense of touch, temperature and pain were less affected, and there was widespread weakness nor condition of deep reflexes.

Nerve conduction studies and somatosensory captured responses indicative of dysfunction distal portions of peripheral sensory nerves. Nerve tissue biopsies showed no axonal damage. By discontinuing pyridoxine gradually improved neurological dysfunction and after a monitoring period, patients were successfully retrieved. As for vitamin B12 is no danger of overdosage.
Drug Name: CIPROFLOXACINO
Comparative CIPRO
Active ingredient: CIPROFLOXACINO
Presentation: TAB CON 8
Concentration: 500MG
Laboratory MAVER, S. A. de CV
Box of 8 TAB
Manufactured in: Mexico


   
   
   
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