Vitamin B1 is one of the eight B vitamins. It has acquired several names since its discovery, including aneurin and, as of the year 2000, thiamin (thiamine). Because thiamin can only be stored in the body for a short time before excretion, a regular dietary intake of thiamin is necessary to maintain proper blood levels. Moderate amounts of thiamin are present in most foods, yet the food sources richest in thiamin include whole-grains, brown rice, pork, poultry, soybeans, nuts, dried beans, peas, and fortified or enriched grain products such as cereals. The recommended daily intake (RDI) for adults over age eighteen is 1.2 mg/day for men and 1.1 mg/day for women. For children, adequate intake levels are lower, with RDI levels at 0.2 mg/day during early infancy that steadily increase with age. Women of any age who are pregnant or should increase their daily intake of thiamin to 1.4 mg/day.
Vitamin B1 deficiencies may occur if the required daily intake (RDI) is not maintained.; this can happen with alcohol abuse, poor nutrition, fasting, restricted access to food, persistent vomiting, and in cases where the absorption of thiamin becomes hindered. Additionally, individuals with excessive carbohydrate consumption may fail to compensate by increasing their level of thiamin intake, resulting in a thiamin deficiency since thiamin plays a role in carbohydrate metabolism.
Decreased thiamin levels can result in reduced enzymatic activity, altered mitochondrial activity, impaired oxidative metabolism, and reduced energy production. Many cells and organ systems can be affected, and cell death can occur. Neurons have high energy requirements and therefore are especially vulnerable to a thiamin deficit.
Wernicke-Korsakoff syndrome (WKS) and beriberi are the two most common complications that may arise from a thiamin deficiency, though these two syndromes rarely occur simultaneously in an individual. WKS affects the central nervous system, which involves the brain and spinal cord. Its most common cause is alcohol misuse, seen alongside poor nutrition, but can present in individuals who are at risk for thiamin deficiency. Technically, WKS consists of two different syndromes that can often present together. Wernicke encephalopathy occurs early in the disease course and characteristically demonstrates non-inflammatory brain lesions. It can present with ataxia, ophthalmoplegia, punctate hemorrhages in the brain, altered mental status, and balance abnormalities. If left untreated, Wernicke encephalopathy can eventually evolve to include Korsakoff psychosis. Individuals will now present with delirium and permanent memory loss. Treatment should commence emergently to prevent disease progression and irreversible brain damage. Empirically, WKS treatment is with at least 500 mg thiamine hydrochloride per 100mL of normal saline given over 30 minutes. This regimen should be repeated three times a day for 2 to 3 days. Thiamine administration should be before or alongside glucose.
Beriberi is another disorder caused by thiamin deficiency. It most frequently presents in people who abuse alcohol but also can be due to other etiologies resulting in thiamin deficiency. Early on, symptoms of beriberi are nonspecific and include constipation, appetite suppression, nausea, mental depression, fatigue, peripheral neuropathy, anorexia, and weight loss. With progression, chronic symptoms can begin to manifest as either wet beriberi or dry beriberi. Wet beriberi presents with edema, an enlarged heart, cardiac failure, warm extremities, pleural effusions, and pulmonary edema. Meanwhile, complications of dry beriberi are predominantly neurological, with peripheral nervous system involvement. Individuals with dry beriberi may have paresthesia, foot drop, muscle wasting, numbness, and absent ankle reflexes.
Like all B vitamins, vitamin B1 is water-soluble and gets absorbed directly into the blood from the gastrointestinal tract. Once absorbed into the circulatory system, thiamin can circulate freely without carrier molecules in plasma and red blood cells until it eventually gets excreted in the urine. While in the body, it can be stored in the liver, but only for a maximum of eighteen days. It can cross the blood-brain barrier.
Once absorbed into the blood, the thiamin diphosphotransferase enzyme converts thiamin from its provitamin form into its active form, thiamin pyrophosphate (TPP). This reaction requires magnesium as a cofactor. TPP is a coenzyme used for energy metabolism. It is an essential component of the following three reactions:
Individuals at risk of acquiring a thiamin deficiency or individuals who have a non-emergent thiamin deficiency can be instructed to take 50 mg of thiamin by mouth daily or can be given an injection of 50 to 100 mg of thiamin three to four times daily. Oral thiamin supplements may be taken with or without food since food intake does not influence the absorption of vitamin B1. Thiamin supplementation is nontoxic, even in excess.
In individuals receiving Vitamin B1 supplementation, the most commonly reported adverse effects include sensations of warmth, urticaria, pruritus, angioedema, diaphoresis, cyanosis, and anaphylaxis.
Allergic individuals should avoid taking Vitamin B1 supplements to avoid a hypersensitivity reaction. Also, pregnant women should use thiamin with caution as the RDI of thiamin increases during pregnancy and lactation. Finally, some parenteral thiamin products may contain aluminum. Therefore, these products should be used with caution in individuals with renal impairments, particularly in premature infants, to avoid the accumulation of aluminum and subsequent aluminum toxicity.
The best way to measure thiamin levels in patients is with erythrocyte transketolase activity. Thiamin levels also can be obtained from blood and urine; however, these values fail to include the amount of stored thiamin that may be present in the liver. It is important to note that thiamin easily gets destroyed by heat.
All healthcare workers should encourage healthy nutrition in their patients. Vitamin B1 deficiency is not common in North America but can occur in people with malabsorption syndrome, poverty, alcoholism, and restriction to food.
Because thiamin stores in the body are small, it quickly depletes if there is no regular intake. Moderate amounts of thiamin are present in most foods, yet the food sources richest in thiamin include whole-grains, brown rice, pork, poultry, soybeans, nuts, dried beans, peas, and fortified or enriched grain products such as cereals. The recommended daily intake (RDI) for adults over age eighteen is 1.2 mg/day for men and 1.1 mg/day for women. For children, adequate intake levels are lower, with RDI levels at 0.2 mg/day during early infancy that steadily increase with age. Women of any age who are pregnant or should increase their daily intake of thiamin to 1.4 mg/day.
Thiamin therapy should have the efforts of an interprofessional healthcare team behind it. All healthcare team members may make general supplementation suggestions, but for deficiency syndromes, therapeutic dosing will likely come from physicians, dieticians, or nutritionists. Pharmacists can also weigh in on appropriate supplementation, although there is almost no toxicity risk with thiamin. Nursing can verify compliance and also monitor treatment effectiveness. Thiamin therapy becomes optimized with the participation of the entire interprofessional healthcare team, including physicians, nursing, pharmacists, and nutritionists, and/or dieticians. Collaboration among all members will drive optimal outcomes. [Level V]
The outlook for patients with thiamine deficiency is good as long as the patient has not developed moderate to severe neurological and cardiac deficits. In most people, with thiamine supplementation, the outlook is good. [Level V]
|||Sunbol AH,Almaghrabi S,Al Aslany SJ,Aldairi MM,Makhdum SA,Trabulsi N,Almekhlafi MA,Nassif M, Delayed Guillain-Barré Syndrome after Bariatric Surgery: A Report of Three Cases. Case reports in surgery. 2018; [PubMed PMID: 30671275]|
|||Liu K,Zheng J,Wang X,Chen F, Effects of household cooking processes on mineral, vitamin B, and phytic acid contents and mineral bioaccessibility in rice. Food chemistry. 2019 May 15; [PubMed PMID: 30642507]|
|||Olanipekun TO,Bakinde N,Effoe VS,Snyder R, Further Considerations on the Benefits of Thiamine Administration in Patients With Septic Shock. Critical care medicine. 2019 Feb; [PubMed PMID: 30653069]|
|||Doğan İG,Altiokka GU,Türker F,Saka B,Bilgiç B,Orhan EK, Wernicke's Encephalopathy due to Non-Alcoholic Gastrointestinal Tract Disease. Noro psikiyatri arsivi. 2018 Dec; [PubMed PMID: 30622385]|
|||Murate K,Mizutani Y,Maeda T,Nagao R,Kikuchi K,Shima S,Niimi Y,Ueda A,Ito S,Mutoh T, A Patient With Thiamine Deficiency Exhibiting Muscle Edema Suggested by MRI. Frontiers in neurology. 2018; [PubMed PMID: 30619043]|
|||Tinsa F,Hechmi M,Hadj IB,Khalsi F,Chargui M,Kefi R,Azouz H,Boussetta K,Abdelhak S, Thiamine responsive megaloblastic anemia mimicking mitochondrial disorders. Revue neurologique. 2019 Jan 3; [PubMed PMID: 30612703]|
|||Toledo Nunes P,Vedder LC,Deak T,Savage LM, A Pivotal Role for Thiamine Deficiency in the Expression of Neuroinflammation Markers in Models of Alcohol-Related Brain Damage. Alcoholism, clinical and experimental research. 2018 Dec 27; [PubMed PMID: 30589435]|
|||Okafor C,Nimmagadda M,Soin S,Lanka L, Non-alcoholic Wernicke encephalopathy: great masquerader. BMJ case reports. 2018 Dec 27; [PubMed PMID: 30593527]|
|||Pourhassan M,Angersbach B,Lueg G,Klimek CN,Wirth R, Blood Thiamine Level and Cognitive Function in Older Hospitalized Patients. Journal of geriatric psychiatry and neurology. 2018 Dec 20; [PubMed PMID: 30572755]|
|||Saini M,Lin W,Kang C,Umapathi T, Acute flaccid paralysis: Do not forget beriberi neuropathy. Journal of the peripheral nervous system : JPNS. 2018 Dec 19; [PubMed PMID: 30569499]|