Most patients have no symptoms and signs of thiamine deficiency; therefore, it must be suspected in the appropriate clinical setting.
Early symptoms and signs are often nonspecific and vague, such as fatigue. Other common symptoms and signs are listed under the major organs that are affected.
* Tachycardia * Chest pain * Wide pulse pressure * Heart failure12 (orthopnea with or without edema, warm skin due to vasodilation) * Hypotension, shock
Persons with chronic alcoholism have low thiamine intake, impaired thiamine uptake and storage, accelerated destruction of thiamine diphosphate, and varying degrees of energy expenditure.
Alcohol is a direct neurotoxin.
The effects on the body's supply of thiamine and on brain tissue are detrimental.
Persons with known alcoholism should be administered parenteral thiamine as a routine action when they present to a medical facility.
Fad diets often do not contain the necessary amounts of thiamine.
Dialysis also robs thiamine from the circulation.
Persons with a history of gastric bypass may also have beriberi.13, 14 For bariatric surgery, it is believed that deficiency can occur most during the first 6 months after surgery, when there is the most rapid weight loss.
States of high energy consumption, such as hyperthyroidism, pregnancy, or severe illness, require more thiamine and other nutrients.
Physical
High-output cardiac failure should prompt investigation of thiamine deficiency as a cause. The same applies to neuropathic symptoms, particularly in the distal extremities. Causes
* Lack of thiamine intake * o Diets consisting mainly of the following: o + Food containing a high level of thiaminases, including milled rice, raw freshwater fish, raw shellfish, and ferns + Food high in anti-thiamine factor, such as tea, coffee, and betel nuts + Processed food with a content high in sulfite, which destroys thiamine o Alcoholic state o Starvation state * Increased consumption states * o Diets high in carbohydrate or saturated fat intake o Pregnancy o Hyperthyroidism15 o Lactation o Fever - severe infection o Increased physical exercise * Increased depletion * o Diarrhea o Diuretic therapies o Peritoneal dialysis o Hemodialysis o Hyperemesis gravidarum8
Loss of thiamine through renal excretion can occur with most, if not all, diuretics.
It has been seen with the use of such diuretics as mannitol, acetazolamide, chlorothiazide, amiloride, and loop diuretics.16
Thiamine loss is associated with the increase in urine flow rate, but it is not related to sodium excretion.
This suggests that patients with polyuria, even if the condition is unrelated to diuretics, may benefit from thiamine supplementation.
One cross-sectional observational study showed that up to 33% of patients admitted with a diagnosis of CHF had a thiamine deficiency due to chronic loop diuretic use, usually for more than 1 month.17
Risk factors for the development of thiamine deficiency in the study's patients consisted of the following:
* Normal renal function * Lack of thiamine supplementation (as little as 1.5 mg thiamine/day has been effective in the prevention thiamine deficiency) * Preadmission spironolactone therapy (indicating more advanced disease)
Repletion of thiamine in patients with CHF has been shown to improve left ventricular function.
* Decreased absorption * o Chronic intestinal disease o Alcoholism o Malnutrition o Gastric bypass surgery o Malabsorption syndrome - Celiac and tropical sprue o Folate deficiency - For example, in patients undergoing chemotherapy with high-dose methotrexate
o + Thiamine serves as a coenzyme (in the form of thiamine pyrophosphate) in a variety of metabolic processes. In these processes, thiamine pyrophosphate is regenerated via the donation of a proton from the reduced form of nicotinamide adenine dinucleotide (NADH).
+ Folic acid is essential to having enough dihydrofolate reductase to regenerate NADH from its oxidative form. This regeneration allows NADH to continue to be present to regenerate thiamine pyrophosphate without being consumed in the process.
+ If folic acid is deficient in cells, it causes an indirect thiamine deficiency, because thiamine is present but cannot be activated.