Thiamine deficiency

Thiamine deficiency
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Thiamine deficiency commonly presents subacutely and can lead to metabolic coma and death. A lack of thiamine can be caused by malnutrition, a diet high in thiaminase-rich foods (raw freshwater fish, raw shellfish, ferns) and/or foods high in anti-thiamine factors (tea, coffee, betel nuts) and by grossly impaired nutritional status associated with chronic diseases, such as alcoholism, gastrointestinal diseases, HIV-AIDS, and persistent vomiting. It is thought that many people with diabetes have a deficiency of thiamine and that this may be linked to some of the complications that can occur.

Well-known syndromes caused by thiamine deficiency include beriberi, Wernicke-Korsakoff syndrome, and optic neuropathy.

Thiamine derivatives and thiamine-dependent enzymes are present in all cells of the body, thus a thiamine deficiency would seem to adversely affect all of the organ systems. However, the nervous system is particularly sensitive to thiamine deficiency, because of its dependence on oxidative metabolism.

Beriberi is a neurological and cardiovascular disease. The three major forms of the disorder are dry beriberi, wet beriberi, and infantile beriberi. A fourth form, gastrointestinal beriberi, was recognized in 2004.

However, it has been recently recognized that peripheral neuropathy (tingling or numbness in the extremities) due to thiamine deficiency could also present with axonal neuropathy (partial paralysis or sensory loss). Peripheral neuropathy can present with subacute motor axonal neuropathy mimicking Guillain–Barré syndrome; or as a large fibre proprioceptive central-peripheral axonal neuropathy presenting as a subacute sensory ataxia.

Following thiamine treatment, rapid improvement occurs, in general, within 24 hours. Improvements of peripheral neuropathy may require several months of thiamine treatment.

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