Vitamin B1

Chemistry: also known as thiamine, is a water-soluble vitamin, the best active form is thiamine pyrophosphate (TPP), a coenzyme in the catabolism of sugars and amino acids. Thiamine is used in the biosynthesis of the neurotransmitter acetylcholine and gamma-aminobutyric acid (GABA).


Sources: Legumes (ie, lentils, soybeans, nuts, seeds), Whole-grain foods, Vegetables (ie, green, leafy vegetables; beets; potatoes), Meat/fish/poultry/eggs, Milk and milk products and

Orange and tomato juices.

 

 

Daily allowance:

The RDAs for various age groups are as follows:

• Boys 9-13 years 0.9 mg
• Men >14 years 1.2 mg
• Girls 9-13 years 0.9 mg
• Women 14-18 years 1.0 mg
• Women >19 years 1.1 mg
• Pregnant/lactating women 1.4 mg
• Children 1-3 years 0.5 mg
• Children 4-8 years 0.6 mg

 

Adequate Intakes (AIs):

 

Infant 0-6 months 0.2 mg

Infant 7-12 months 0.3 mg

 

 

Causes of Thiamine (Vit B1 ) deficiency:

 

1-malnutrition.

2-a diet high in thiaminase-rich foods (raw freshwater fish, raw shellfish, ferns and milled rice)

3-a diet high in anti-thiamine factors (tea, coffee, betel nuts)

4-chronic diseases, such as alcoholism, gastrointestinal diseases, HIV-AIDS.

5-persistent vomiting. or diarrhea

 

Clinical presentations, signs and symptoms of vitamin B1 deficiency:

 

Can be asymptomatic or present with vague symptoms as fatigue. If the patient present with nervous system involvement alone the disease is called Dry Beriberi. If the patient has cardiovascular involvement this is called Wet Beriberi.

 

1-Neurologic symptoms include: Poor memory, irritability, sleep disturbance, Wernicke encephalopathy, Korsakoff syndrome, bilateral, symmetrical lower extremities paresthesias, burning pain, muscle cramps, decreased vibratory position sensation, absent knee and ankle jerk, muscle atrophy and Foot drop (late stage).

 

2-Cardiovascular symptoms include: tachycardia, chest pain, wide pulse pressure, heart failure with warm skin due to vasodilation, hypotension and shock.

 

3-Gastroenterologic symptoms are as follows: anorexia, abdominal discomfort and constipation.

4- Eyes: Optic neuropathy characterized by bilateral visual loss, cecocentral scotomas and impaired colour perception. The ophthalmological findings usually can show a bilateral oedema of the optic disk in the acute phase, followed by a bilateral optic atrophy.

 

5-Infantile beriberi symptoms are as follows: CHF, aphonia and absent deep tendon reflex.

 

Terms doctors should be aware of:

 

Wet Beriberi: peripheral vasodilation leads to a high cardiac output state which leads to salt and water retention mediated through the renin-angiotensin-aldosterone system in the kidneys. Further vasodilation make the kidneys interpret a relative loss of volume and respond by further salt retention which also drives the fluid to absorbed into the circulatory system. This leads to volume overload and peripheral edema. This in turns lead to increased heart work loud and hence demand ischemia which leads to myocardial injury.

 

Acute fulminant cardiovascular beriberi, or Shoshin beriberi: Is a rapid form in which the predominant injury is to the heart, and rapid deterioration follows the inability of the heart muscle to satisfy the body's demands because of its own injury. In this case, edema may not be present. Instead, cyanosis of the hands and feet, tachycardia, distended neck veins, restlessness, and anxiety occur. Treatment with thiamine causes low-output cardiac failure, because systemic vasoconstriction is reinstated before the heart muscle recovers. Support of heart function is an added requirement at this stage.

 

Persons with known alcoholism should be administered parenteral thiamine as a routine action when they present to a medical facility before administration of any IV fluids to avoid encephalopathy ppted by glucose administration.

 

Wernicke encephalopathy presents with a classic triad: encephalopathy, ataxic gait, and some variant of oculomotor dysfunction. All 3 features of the triad are recognized in only about one third of cases.
Consideration for Wernicke encephalopathy should be given to patients with any evidence of long-term alcohol abuse or malnutrition and any of the following: acute confusion, ataxia, ophthalmoplegia, memory disturbance, hypothermia with hypotension, and delirium tremens.

A high proportion of patients with acute Wernicke encephalopathy who survive develop Korsakoff psychosis, also called Korsakoff syndrome, characterized by potentially irreversible retrograde amnesia (inability to recall information) and anterograde amnesia (inability to assimilate new information), with varying degrees of other cognitive deficits.


Laboratory findings and workup::
In most instances specific workup is not necessary and clinical response to treatment is diagnostic. However if dealed necessary then the low levels of the following markers can sufficiently indicate thiamine deficiency: blood thiamine, pyruvate, alpha-ketoglutarate, lactate, and glyoxylate levels. Also, measure urinary excretion of thiamine and its metabolites. In conjunction with whole blood or erythrocyte transketolase activity preloading and postloading, a thiamine loading test is the best indicator of thiamine deficiency. An increase of more than 15% in enzyme activity is a definitive marker of deficiency. However, this test is expensive and time consuming. Checking TSH is advised to r/o hyperthyroidism as a cause for high output cardiac failure.


Prevention:
Eleminating the causes of vomiting and diarrhea. Managing chronic illnesses. Advicing the patient about balanced diet.


Treatment:

Outpatient:
Initially start with 50 mg of IM daily for several days then switch to 2.5 mg PO daily unless the patient requires higher doses due to malabsorption. Thiamine is not toxic in high doses in people with normal renal function.

Inpatient:
These patients present to the ED with other problems like alcohol withdrawal or related illnesses that may raise the possibilty of Wernicke's. Strat with 100mg IV daily then switch to same PO dose. If Wernicke is highly suspected then see below.

Wernicke encephalopathy
100 mg of parental (intravenous or intramuscular) thiamine for 3-7 days (treatment period), followed by oral thiamine indefinitely as long as the patient is consuming alcohol. In symptomatic patients, especially in the ICU, 500 mg intravenously 3 times a day for 2-3 days is recommended. If no response is noted, discontinue supplementation and assess for supportive care (unless the patient is comatose). If there is a partial response, continue at 250 mg parenterally for 5 days or as long as improvement continues in patients with neuropsychiatric symptoms. Administering dextrose to an individual in a thiamine-deficient state exacerbates the process of cell death by providing more substrate for biochemical pathways that lack sufficient amounts of coenzymes. So it is very important to start any alcoholic patient or any patient suspected with thiamine deficiency by IV thiamine infusion before administration of any IV fluids.