Beriberi

The patients with beriberi do not report any signs or symptoms of thiamine deficiency. Signs and symptoms at the early stage are often nonspecific, such as fatigue, thigh failure of high cardiac-output can direct the diagnosis to thiamine deficiency.

Some of the neurological symptoms of beriberi are: poor memory, sleep disturbances, Korsakoff syndrome, irritability, muscle cramps, muscle atrophy, and foot drop. Beriberi also manifests with some cardiovascular symptoms such as tachycardia, heart failure, chest pain, hypotension and shock. The gastroenterologic symptoms of beriberi are anorexia, constipation, dysphagia, and abdominal discomfort [6] [7].

Replacing of thiamine is the first step to ascertain the diagnosis of the disease. If the patient responds to the treatment, it would be safe to measure the thiamine deficiency as the cause of the trouble. Since thiamine is non-toxic at higher levels, this method of managing the condition offers little risk.

Measuring blood thiamine pyruvate, glyoxylate levels and alpha-ketoglutarate levels, urinary excretion of thiamine and its metabolites provides the correct diagnosis of the condition.

Thiamine loading test has been considered as the best indicator of thiamine deficiency. If there is an increase of more than 15% of the enzyme activity is seen, it is indicative of a deficiency of the vitamin. This test, however, is both expensive and time-consuming.

Urinary methylglyoxal levels: Measuring methylglyoxal levels and thyroid-stimulating hormone (TSH) also helps to rule out thyrotoxicosis-induced heart failure.

Troponin I: Higher levels of troponin I is seen in patients with heart failure induced by thiamine deficiency.

Metabolic acidosis is also caused by thiamine deficiency because of the increased lactic acid production. In gastrointestinal beriberi, patients report abdominal pain caused due to lactic acidosis [8] [9][10].

The goal of the treatment of beriberi is to substitute the deficiency of thiamine, reduce the morbidity associated with such deficiency and prevent complications. If the correct diagnosis is ascertained, there must be prompt administration of parenteral thiamine. Thiamine substitution therapy must be continued until all the symptoms associated with beriberi are gone [11].

Beriberi, if not cured on time, can be fatal. In this disease, the patient is robbed of the energy even for the daily activities making them lethargic. Beriberi is treatable even in the severe cases. Thus, the prognosis of the patient with beriberi is good. In case of wet beriberi, the improvement is observed within 12 hours.

Development of beriberi is caused by the deficiency of thiamine. There are several mechanisms by which this can occur, such as lack of thiamine intake, increased consumption of thiamine, and decreased absorption.

Lack of thiamine intake: A diet with high levels of thiaminases (milled rice, raw freshwater fish, ferns), anti-thiamine factor (tea, coffee, or betel nuts), or high levels of sulfite causes a lack of thiamine. There are some diet-related factors that can cause a reduction in the thiamine intake are alcoholic state, starvation state and gastric bypass surgery or parental nutrition devoid of adequate thiamine levels.

Increase in the consumption of thiamine: The increase in the metabolism of thiamine can result from having a diet rich in carbohydrate or saturated fat, hypothyroidism, pregnancy, lactation, fever with severe infections. Increased depletion of thiamine occurs in patients with diarrhea, or one who are undergoing diuretic therapies, hemodialysis, or peritoneal dialysis. Thiamine loss is often associated with the increase in the rate of urine flow.

Decrease in the absorption of thiamine: Reduction in the absorption of thiamine is observed in patients with chronic intestinal disease, malnutrition, gastric bypass surgery, folate deficiency, and alcoholism. Folate deficiency causes indirect thiamine deficiency as thiamine of the body is not activated.

Infantile beriberi: Infantile beriberi occurs in the infants who are 2-4 months of age and are exclusively fed with mother’s milk, whose mother is thiamine deficient.

Patients with chronic alcoholism must be administered parenteral thiamine as alcohol is a direct neurotoxin and causes low and impaired thiamine intake and storage. It also leads to the accelerated destruction of the thiamine diphosphate. When the person is dieting, he often neglects the correct intake of micronutrients, and hence leads to several vitamin deficiency diseases [3] [4].

The population of developing countries is at a higher risk of vitamin deficiency diseases. Though no accurate data is available, beriberi is reported in the refugees who are dependent on the emergency food aid, rich in carbohydrate and saturated fats. There is a lack of micronutrient supplementation in such diet [5].

When the person is devoid of thiamine, the stores of this vitamin in the body get depleted within a month, after which there are several symptoms such as resting tachycardia, decrease in the deep tendon reflexes, or peripheral neuropathy. Beriberi is categorized into two types: dry beriberi and wet beriberi.

Dry beriberi: When the thiamine deficiency involves the nervous system, it is termed as dry beriberi. This type of beriberi is seen in patients with poor calorie-intake and higher physical inactivity. The manifestations of the disease are peripheral neuropathy (impairment of the sensory, motor or reflex functions of the extremities), or degeneration of the myelin in muscle sheaths.

One of the significant presentations of dry beriberi is Wernicke encephalopathy. In this condition, there is an orderly sequence of symptoms such as vomiting, horizontal nystagmus, fever, ataxia, and progressive mental impairment. All these symptoms lead to Korsakoff syndrome. Only 50% of the patients who reach this stage recover completely [7].

Wet beriberi: When beriberi involves the cardiovascular system, it is referred to as wet beriberi. There is peripheral vasodilation causing high cardiac output. Salt-water retention mediated by renin-angiotensin-aldosterone system is also observed. With vasodilation, the kidneys detects the loss of volume and thus starts conserving the salt.

When salt retention occurs, more fluid is absorbed causing edema of the extremities. This puts extra burden on the heart and it is severely overworked. Parts of the heart, thus, undergo injury and the patient starts showing physical symptoms of tachycardia, edema and myocardial injury.

Shoshin beriberi is a rapid form of wet beriberi causing predominant injury to the heart, and the inability of the heart muscles to fulfill its functions. In this case, edema is absent, however, cyanosis of the hands and feet, tachycardia, and anxiety is observed. If no treatment is initiated, death is almost certain within hours or days [6].

Complications: Some of the severe complications of beriberi are coma, congestive heart failure, psychosis and death.

Correct dose of thiamine through diet daily can help prevent beriberi.

Beriberi is a disease that occurs due to deficiency of thiamine pyrophosphate. Thiamine pyrophosphate is the active form of the vitamin thiamine or vitamin B1. The functions of the active form of thiamine are that it acts as a coenzyme in the metabolism of carbohydrate by decarboxylation of alpha-ketoacids and in the pentose monophosphate pathway.

Thiamine is a water-soluble vitamin (which the body cannot produce) and is concentrated in the skeletal muscles, brain, kidneys, liver and heart. It is excreted by the kidneys. If the proper amount of Vitamin B1 is not taken through diet, it can lead to deficiency of this vitamin. In hyperthyroidism, pregnancy, severe liver disease and lactation, there is an excessive use of the vitamin contributing to the deficiency. Food is an excellent source of vitamin B1. Some of the food-items that are rich in thiamine are whole grain foods, milk and milk products, green leafy vegetables, juices (orange and tomato), and legumes [1] [2].

Patients must know that vitamins are very important for the working of the body. These micronutrients must be provided to the body in adequate amount in order to combat deficiency.

Beriberi is asymptomatic but as it progresses, its manifestations are severe. Alcohol and fad diet worsens the condition in such patients. Once the problem is addressed, the patients are advised to maintain the appropriate diet.

1. Wooley, JA. Characteristics of thiamin and its relevance to the management of heart failure. Nutr Clin Pract. Oct-Nov 2008;23:487-93.
2. Masumoto K, Esumi G, Teshiba R, et al. Need for thiamine in peripheral parenteral nutrition after abdominal surgery in children. JPEN J Parenter Enteral Nutr. Jul-Aug 2009;33(4):417-22. [Medline].
3. Matrana MR, Davis WE. Vitamin deficiency after gastric bypass surgery: a review. South Med J. October/ 2009;102:1025-31.
4. Weise Prinzo Z, de Benoist B. Meeting the challenges of micronutrient deficiencies in emergency-affected populations. Proc Nutr Soc. May 2002;61(2):251-7. Weise Prinzo Z, de Benoist B. Meeting the challenges of micronutrient deficiencies in emergency-affected populations. Proc Nutr Soc. May 2002;61(2):251-7.
5. Shenoy VV, Patil PV, Nagar VS, et al. Congestive cardiac failure and anemia in a 15-year-old boy. J Postgrad Med. Jul-Sep 2005;51(3):225-7.
6. Zuccoli G, Gallucci M, Capellades J, et al. Wernicke encephalopathy: MR findings at clinical presentation in twenty-six alcoholic and nonalcoholic patients. AJNR Am J Neuroradiol. Aug 2007;28(7):1328-31.
7. Tran HA. Increased troponin I in "wet" beriberi. J Clin Pathol. May 2006;59(5):555. 
8. Falder S, Silla R, Phillips M, Rea S, Gurfinkel R, Baur E, et al. Thiamine supplementation increases serum thiamine and reduces pyruvate and lactate levels in burn patients. Burns. Mar 2010;36(2):261-9. 
9. Donnino M. Gastrointestinal beriberi: a previously unrecognized syndrome. Ann Intern Med. Dec 7 2004;141(11):898-9. 
10. Hamilton Wright. The Cause, Course, Prevention, and Treatment of Beriberi. Public Health Pap Rep. 1905; 31(Pt 1): 289–299.