Vitamin B Complex Deficiency and Excess

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Chapter 46 Vitamin B Complex Deficiency and Excess

Vitamin B complex includes a number of water soluble nutrients, including thiamine (B1), riboflavin (B2), niacin (B3), pyridoxine (B6), folate, cobalamin (B12), biotin, and pantothenic acid. Choline and inositol are also considered part of the B complex and are important for normal body functions, but specific deficiency syndromes have not been attributed to a lack of these factors in the diet.

B-complex vitamins serve as coenzymes in many metabolic pathways that are functionally closely related. Consequently, a lack of one of the vitamins has the potential to interrupt a chain of chemical processes, including reactions that are dependent on other vitamins, and ultimately can produce diverse clinical manifestations. Because diets deficient in any one of the B-complex vitamins are often poor sources of other B vitamins, manifestations of several vitamin B deficiencies usually can be observed in the same person. It is therefore a general practice in a patient who has evidence of deficiency of a specific B vitamin to treat with the entire B-complex group of vitamins.

46.1 Thiamine (Vitamin B1)

Thiamine (vitamin B1) consists of thiazole and pyrimidine rings joined by a methylene bridge. Thiamine diphosphate, the active form of thiamine, serves as a cofactor for several enzymes involved in carbohydrate catabolism such as pyruvate dehydrogenase, transketolase, and α-ketoglutarate. These enzymes also play a role in the hexose monophosphate shunt that generates nicotinamide adenine dinucleotide phosphate (NADP) and pentose for nucleic acid synthesis. Thiamine is also required for the synthesis of acetylcholine and gamma-aminobutyric acid (GABA), which have important roles in nerve conduction. Thiamine is absorbed efficiently in the gastrointestinal (GI) tract, and may be deficient in persons with GI or liver disease. The requirement of thiamine is increased when carbohydrates are taken in large amounts and during periods of increased metabolism, for example, fever, muscular activity, hyperthyroidism, and pregnancy and lactation. Alcohol affects various aspects of thiamine transport and uptake, contributing to the deficiency in alcoholics.

Pork (especially lean), fish, and poultry are good nonvegetarian dietary sources of thiamine. Main sources of thiamine for vegetarians are rice, oat, wheat, and legumes. Most ready-to-eat breakfast cereals are enriched with thiamine. Thiamine is water soluble and heat-labile; most of the vitamin is lost when the rice is repeatedly washed and the cooking water is discarded. The breast milk of a well-nourished mother provides adequate thiamine; breast-fed infants of thiamine-deficient mothers are at risk for deficiency. Most infants and older children consuming a balanced diet obtain an adequate intake of thiamine from food and do not require supplements.


Deficiency of thiamine is associated with severely malnourished states, including malignancy and following surgery. The disorder (or spectrum of disorders) is classically associated with a diet consisting largely of polished rice (oriental beriberi), it can also arise if highly refined wheat flour forms a major part of the diet, in alcoholics, and in food faddists (occidental beriberi). Thiamine deficiency has often been reported from inhabitants of refugee camps consuming the polished rice–based monotonous diets. Thiamine-responsive megaloblastic anemia (TRMA) syndrome is a rare autosomal recessive disorder characterized by megaloblastic anemia, diabetes mellitus, and sensorineural deafness, responding in varying degrees to thiamine treatment. The syndrome occurs because of mutations in the SLC19A2 gene, encoding a thiamine transporter protein, leading to abnormal thiamine transportation and vitamin deficiency in the cells. Thiamine and related vitamins can improve the outcome in children with Leigh encephalomyelopathy and type 1 diabetes mellitus.

Clinical Manifestations

Thiamine deficiency can develop within 2-3 mo of a deficient intake. Early symptoms of thiamine deficiency are nonspecific such as fatigue, apathy, irritability, depression, drowsiness, poor mental concentration, anorexia, nausea, and abdominal discomfort. As the condition progresses, more-specific manifestations of beriberi such as peripheral neuritis (manifesting as tingling, burning, paresthesias of the toes and feet), decreased deep tendon reflexes, loss of vibration sense, tenderness and cramping of the leg muscles, congestive heart failure, and psychic disturbances develop. Patients can have ptosis of the eyelids and atrophy of the optic nerve. Hoarseness or aphonia caused by paralysis of the laryngeal nerve is a characteristic sign. Muscle atrophy and tenderness of the nerve trunks are followed by ataxia, loss of coordination, and loss of deep sensation. Later signs include increased intracranial pressure, meningismus, and coma. The clinical picture of thiamine deficiency is usually divided into a dry (neuritic) type and a wet (cardiac) type. The disease is wet or dry depending on the amount of fluid that accumulates in the body due to factors such as cardiac and renal dysfunction, even though the exact cause for this edema has not been explained. Many cases of thiamine deficiency show a mixture of the 2 main features and are more properly termed thiamine deficiency with cardiopathy and peripheral neuropathy.

The classic clinical triad of Wernicke encephalopathy (mental status changes, ocular signs, ataxia) is rarely reported in infants and young children with severe deficiency secondary to malignancies or feeding of defective formula. An epidemic of life-threatening thiamine deficiency was seen in infants fed a defective soy-based formula that had undetectable thiamine levels. Manifestations included emesis, lethargy, restlessness, ophthalmoplegia, abdominal distention, developmental delay, failure to thrive, lactic acidosis, nystagmus, diarrhea, apnea, and seizures. Intercurrent illnesses that resembled Wernicke encephalopathy often precipitated the symptoms.

Death from thiamine deficiency usually is secondary to cardiac involvement. The initial signs are slight cyanosis and dyspnea, but tachycardia, enlargement of the liver, loss of consciousness, and convulsions can develop rapidly. The heart, especially the right side, is enlarged. The electrocardiogram shows an increased Q-T interval, inverted T waves, and low voltage. These changes as well as the cardiomegaly rapidly revert to normal with treatment, but without prompt treatment, cardiac failure can develop rapidly and result in death. In fatal cases of beriberi, lesions are located principally in the heart, peripheral nerves, subcutaneous tissue, and serous cavities. The heart is dilated, and fatty degeneration of the myocardium is common. Generalized edema or edema of the legs, serous effusions, and venous engorgement are often present. Degeneration of myelin and axon cylinders of the peripheral nerves, with wallerian degeneration beginning in the distal locations, also is common, particularly in the lower extremities. Lesions in the brain include vascular dilation and hemorrhage.

46.2 Riboflavin (Vitamin B2)

Riboflavin is part of the structure of the coenzymes flavin adenine dinucleotide (FAD) and flavin mononucleotide, which participate in oxidation-reduction reactions in numerous metabolic pathways and in energy production via the mitochondrial respiratory chain. Riboflavin is stable to heat but is destroyed by light.

Milk, eggs, organ meats, legumes, and mushrooms are rich dietary sources of riboflavin. Most commercial cereals, flours, and breads are enriched with riboflavin.


The causes of riboflavin deficiency are mainly related to malnourished and malabsorptive states, including GI infections. Treatment with some drugs, such as probenecid, phenothiazine, or oral contraceptives, can also cause the deficiency. The side chain of the vitamin is photochemically destroyed during phototherapy for hyperbilirubinemia, as it is involved in the photosensitized oxidation of bilirubin to more polar excretable compounds. Isolated complex II deficiency, a rare mitochondrial disease manifesting in infancy and childhood, responds favorably to riboflavin supplementation and thus can be termed a dependency state.

Clinical Manifestations

Clinical features of riboflavin deficiency include cheilosis, glossitis, keratitis, conjunctivitis, photophobia, lacrimation, corneal vascularization, and seborrheic dermatitis. Cheilosis begins with pallor at the angles of the mouth and progresses to thinning and maceration of the epithelium, leading to fissures extending radially into the skin (Fig. 46-1). In glossitis, the tongue becomes smooth, with loss of papillary structure (Fig. 46-2). Normochromic, normocytic anemia may also be seen because of the impaired erythropoiesis. A low riboflavin content of the maternal diet has been linked to congenital heart defects, but the evidence is weak.


Figure 46-1 Angular cheilosis with ulceration and crusting.

(Courtesy of National Institute of Nutrition, Indian Council of Medical Research, Hyderabad, India.)


Figure 46-2 Glossitis as seen in riboflavin deficiency.

(From Zappe HA, Nuss S, Becker K, et al: Riboflavin deficiency in baltistan (website). Accessed May 23, 2010.)


The recommended daily allowance (RDA) of riboflavin for infants, children and adolescents is presented in Table 46-1. Adequate consumption of milk, milk products, and eggs prevents riboflavin deficiency. Fortification of cereal products is helpful for those who follow vegan diets or are consuming inadequate amounts of milk products because of other reasons.


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