Vitamin B1

VITAMIN B1

General Monograph

Thiamine

Vitamin

Pharmacology: Vitamin B1 is a water soluble B complex vitamin. In vivo, vitamin B1 combines with adenosine triphosphate (ATP) to form thiamine pyrophosphate, also known as cocarboxylase, a coenzyme. Its role in carbohydrate metabolism is the decarboxylation of pyruvic acid and alpha-ketoacids to acetaldehyde and carbon dioxide. Increased levels of pyruvic acid in the blood indicate vitamin B1 deficiency.

Vitamin B1 depletion can occur after approximately 3 weeks of total absence of the vitamin from the diet. Deficiency may occur in alcoholics and food faddists or in special clinical situations such as hemodialysis, chronic peritoneal dialysis, or after administration of glucose to a vitamin B1-depleted patient. Requirements may be increased due to burns, chronic fever, gastrectomy, intestinal disease, liver disease and hyperthyroidism.

Deficiency of vitamin B1 eventually leads to beriberi and Wernicke’s encephalopathy. The cardiovascular or nervous system, or both, may be affected. Cardiovascular involvement is manifested by high output, biventricular heart failure and edema. CNS symptoms include peripheral neuropathy and an encephalopathy syndrome characterized by nystagmus, ophthalmoplegia, fever, ataxia and progressive mental deterioration which may ultimately result in coma and death.

Pharmacokinetics: Orally administered vitamin B1 is absorbed mainly from duodenum, by both active and passive processes. The total amount which can be absorbed following administration of a large dose is 4 to 8 mg. Body stores are approximately 30 mg, with a 1 mg daily turnover. Storage is mainly in skeletal muscles, heart, liver, kidneys and brain.

Vitamin B1 is metabolized in the liver and excreted in the urine. When large doses are administered, body stores may become saturated and unchanged vitamin B1 may be excreted in the urine.

Indications: Prophylaxis and treatment of vitamin B1 deficiency states including beriberi and Wernicke’s encephalopathy.

Contraindications: Hypersensitivity to vitamin B1 or any component of a product containing vitamin B1.

Precautions: Serious sensitivity reactions can occur. Deaths have resulted from i.v. use. Some manufacturers recommend an intradermal test dose prior to i.v. administration in patients with suspected hypersensitivity.

Simple vitamin B1 deficiency is rare. Multiple vitamin deficiencies should be suspected in any case of dietary inadequacy.

Pregnancy: No adverse effects have been reported with intake of normal daily requirements.

Lactation: No adverse effects have been reported with intake of normal daily requirements.

Adverse Effects: Feeling of warmth, pruritus, urticaria, weakness, sweating, nausea, restlessness, tightness of the throat, angioneurotic edema, cyanosis, pulmonary edema, hemorrhage into the gastrointestinal tract, collapse and death have been rarely reported, mainly following repeated i.v. administration of the drug.

Dosage: In preventing vitamin deficiencies, adequate dietary intake is preferred over supplementation whenever possible. For a listing of food sources of vitamin B1, see Vitamin Food Sources in the Clin-Info section.

For a listing of the daily requirements of vitamin B1, see Recommended Nutrient Intake in the Clin-Info section.

In the treatment of deficiency, vitamin B1 is usually administered orally. When oral administration is not feasible, when malabsorption is suspected, or in patients with Wernicke’s encephalopathy or high output heart failure secondary to beriberi, vitamin B1 may be administered i.m. or i.v.

Oral: Usual adult dose to treat deficiency is 5 to 30 mg daily given as a single dose or in 3 divided doses.

Parenteral: Wernicke’s encephalopathy and high output cardiac failure secondary to beriberi must be treated as emergencies. Critically ill patients or those with malabsorption syndromes should also be treated by the i.v. or i.m. route.

In the treatment of beriberi, 5 to 100 mg 3 times daily may be given by the i.v. or i.m. route. Dosage should then be reduced depending on patient response, followed by oral therapy for 1 month.

In Wernicke’s encephalopathy 100 mg i.v. is given initially followed by 50 to 100 mg i.m. or i.v. daily until the patient is eating a well balanced diet. I.V. dextrose solutions increase thiamine requirements and thiamine should be given parenterally before administering these solutions to the patient with Wernicke’s. Following clinical improvement and resumption of a regular diet, oral therapy may be instituted.

VITAMIN B1 General MonographThiamineVitamin

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