Thiamine

Low circulating levels of thiamine have been described in 80% of patients with alcoholic cirrhosis. Thiamine pyrophosphate is a coenzyme in the intermediary metabolism of carbohydrates, in particular for transketolases, which play a role in cardiac and neurological functions. While alcoholic beverages are essentially devoid of thiamine, acute exposure to alcohol decreases the activity of intestinal transporters required for thiamine absorption. The major neurological signs and symptoms of thia-mine deficiency in alcoholics include peripheral neuropathy, partial paresis of ocular muscles, wide-based gait secondary to cerebellar lesions, cognitive defects, and severe memory loss. The presence of peripheral neuropathy is sometimes referred to as 'dry beriberi,' while the other symptoms constitute the Wernicke-Korsokoff syndrome. Whereas abnormal eye movements can be treated acutely by thia-mine injections, the other signs are often permanent and contribute to the dementia that often afflicts

Table 3 Micronutrient deficiencies in chronic alcoholic patients

Deficiency

Cause

Effect

Thiamine

• Poor diet

• Peripheral neuropathy

• Intestinal malabsorption

• Wernicke-Korsokoff syndrome

• High output heart failure

Folate

• Poor diet

• Megaloblastic anemia

• Intestinal malabsorption

• Hyperhomocysteinemia

• Decreased liver storage

• Neural tube defect

• Increase urine excretion

• Altered cognition

Pyridoxine (vitamin B6)

• Poor diet

• Peripheral neuropathy

• Displacement from circulating albumin promotes

• Sideroblastic anemia

urine excretion

Vitamin A

• Malabsorption

• Night blindness

• Increased biliary secretion

• May promote development of alcoholic liver disease

Vitamin D

• Malabsorption

• Calcium deficiency

• Decteased sun exposure

• Metabolic bone disease

Zinc

• Poor diet

• Night blindness

• Increaded urine excretion

• Decreased taste

• Decreased immune funtion

Iron

• Gastrointestinal bleeding

• Anemia

alcoholics after years of drinking. 'Wet beriberi' refers to the high-output cardiac failure that can also occur in thiamine-deficient alcoholics, and is responsive to thiamine therapy in addition to conventional treatment. Since endogenous thiamine is used during carbohydrate metabolism, acute cardiac failure can be precipitated by the administration of intravenous glucose to malnourished and marginally thiamine-deficient patients by depletion of remaining thiamine stores. This process can be prevented by the addition of soluble vitamins including thiamine to malnourished chronic alcoholic patients who are undergoing treatment for medical emergencies.

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