Vitamin B2 (riboflavin) deficiency diseases

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What is vitamin B2?
Vitamin B2 (riboflavin) is a water-soluble micronutrient belonging to the B-complex group of vitamins. Vitamin B2 deficiency results in ariboflavinosis diseases with manifestations
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such as normocytic anemia, congenital heart defects and limb deformities in neonates and stomatitis. Riboflavin is the central component of flavoproteins.

Flavoproteins, flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), contain a nucleic acid derivative of riboflavin. They are cofactors for a variety of enzyme reactions including, removal of radicals contributing to oxidative stress, biosynthesis and metabolism of carbohydrates, amino acids and lipids, conversion of pyridoxine (vitamin B6) and folic acid (vitamin B9) into their coenzymes, activation of other vitamins, DNA repair and apoptosis.

Food sources

Bacteria, fungi and plants can produce riboflavin, but humans and mammals, have lost the ability to synthesize it. Vitamin B2 is widely available in food sources, such as milk, cheese, yoghurt, leafy green vegetables, organ meat, liver, kidney, yeast and eggs.
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Whole grains contain moderate amounts of riboflavin in the bran and germ. The bacteria in the colon synthesize riboflavin, which is an important source and is available for absorption in the free form. The daily recommended dietary allowances (RDAs) of riboflavin for men is 1.3 mg and for women is 1.1 mg.

Flavoproteins

The dietary riboflavin is mostly available as flavoproteins and their coenzyme forms. The flavoproteins can withstand high temperatures and are stable after cooking. However they undergo rapid degradation on exposure to light. These flavoproteins are hydrolyzed by intestinal proteases and luminal phosphatases into riboflavin for absorption. After reaching systemic circulation, vitamin B2 is imported and converted into FAD and FMN inside the tissues. Liver is the main storage organ and stores nearly 30% of the body's flavoproteins.

Flavin mononucleotide (FMN)

FMN (riboflavin-5′-phosphate) is a flavoprotein produced from vitamin B2 by the enzyme riboflavin kinase. FMN is the major form of riboflavin stored in the cells and tissues. Its production requires ATP and is an energy-intensive reaction. Flavin mononucleotide is more soluble than riboflavin in water. FMN plays a major role as an enzyme cofactor along with adenine dinucleotide (FAD), another molecule synthesized from riboflavin.

Flavin adenine dinucleotide (FAD)

FAD consists of an adenine nucleotide (adenosine monophosphate) and a flavin mononucleotide bridged together through their phosphate groups. As described earlier, riboflavin kinase adds a phosphate group to riboflavin to produce flavin mononucleotide (FMN). Flavin adenine dinucleotide synthase (FAD synthase) attaches an adenine nucleotide to FMN to synthesize FAD. Both the reactions are energy-intensive and require ATP.

Functions of vitamin B2

Vitamin B2 is important for maintaining cellular health and functions. Riboflavin is critical for normal growth and repair.
  • The vitamin B6 is available in the food in the form of pyridoxine, pyridoxal and pyridoxamine. They have to be converted into the metabolically active form, Pyridoxine 5'-phosphate (PLP). Pyridoxine 5'-phosphate oxidase brings about the conversion. Pyridoxine 5'-phosphate oxidase is FMN dependent for its activity.
  • FAD is required for oxidation of pyruvate, α-ketoglutarate and branched-chain amino acids.
  • FAD is required to convert retinol (vitamin A) to retinoic acid.
  • FAD is required for synthesis of active form of folate.
  • FAD is required to conversion of tryptophan into niacin.
  • Vitamin B2 is required for blood cell production and utilization of iron in the body.

Vitamin B2 deficiency causes

The primary cause of inadequacy of the vitamin B2 in the body is nutritional insufficiency of the nutrient. As a water soluble vitamin, riboflavin is continuously excreted in the urine. Its deficiency usually arises along with that of other water-soluble vitamins. Diuretics, antacids, chemotherapy, anticonvulsants, certain antibiotics and thyroid hormone therapy can deplete the vitamin B2 from the body.

The use of oral contraceptives, old age related diseases, chronic alcoholism, HIV, inflammatory bowel disease, diabetes, cancer therapy and chronic heart disease may cause secondary or subclinical deficiency. Phototherapy to treat jaundice in infants degrades riboflavin in the body and the infant may develop ariboflavinosis.

Vitamin B2 deficiency symptoms

Riboflavin insufficiency in the body causes several disease symptoms involving, skin, hair, mucous membranes, vision, nervous system and metabolism. Some of the symptoms are:
  • glossitis (tongue inflammation),
  • chapped and fissured lips (cheilosis),
  • inflammation of the corners of the mouth (angular stomatitis),
  • dermatitis,
  • greasy, scaly inflammation of the skin,
  • dry itchy eyes,
  • pruritus,
  • alopecia,
  • general weakness,
  • photophobia (sensitivity to light),
  • visual impairment,
  • anemia,
  • depression,
  • dementia,
  • behavioral abnormalities,
  • growth retardation,
  • neurodegeneration and
  • neuropathy.

Vitamin B2 deficiency diagnosis

The measurement of the activity coefficient of erythrocyte glutathione reductase (EGR) is the preferred method for assessing the nutrient status. This method provides a measure of tissue saturation and long-term riboflavin status. An activity coefficients (AC) of 1.4 or more suggests deficiency.

Vitamin B2 deficiency diseases

Vitamin B2 deficiency disease, ariboflavinosis, manifests as glossitis, cheilosis, angular stomatitis, neuropathy, seborrhea-like dermatitis, pruritus, lenticular cataracts, photophobia, visual impairment, corneal opacity, growth retardation, alopecia, fatty degeneration of liver and kidney and degenerative changes of the nervous system. Certain systemic or genetic diseases can reduce the availability of flavoproteins for cellular functions.

Riboflavin-responsive multiple acyl-coenzyme A dehydrogenase deficiency (glutaric acidemia type 2) is an autosomal recessive inheritance characterized by a decrease in fatty acid beta-oxidation capacity. Muscle uncoupling protein-3 (UCP3) is upregulated under conditions that either increase the levels of circulating free fatty acid and/or decrease fatty acid beta-oxidation. There is accumulation of muscle fatty acid/acylCoA. Treatment with riboflavin restores the normal parameters. In patients with amyotrophic lateral sclerosis (ALS), the synthesis of FAD is markedly decreased.

Normochromic normocytic anemia is caused due to vitamin B2 insufficiency in the body. The red blood cell size and hemoglobin content are normal whereas the insufficiency of folic acid or cyanocobalamin causes megaloblastic anemia wherein the blood cells are larger than normal. Vitamin B2 deficiency during pregnancy can affect the fetus leading to birth defects, limb deformities and congenital heart diseases. Treatment of riboflavin deficiency and related diseases is by giving the patient appropriate doses of vitamin B2 supplements.
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References:
1.Zhao H, Yang X, Zhou R, Yang Y. Study on vitamin B1, vitamin B2 retention factors in vegetables.We Sheng Yan Jiu. 2008;37(1):92-96.
2.Uma Sundaram. Regulation of intestinal vitamin B2 absorption Focus on “Riboflavin uptake by human-derived colonic epithelial NCM460 cells”. American Journal of Physiology - Cell Physiology Published 1 February 2000 Vol. 278 no. 2, C268-C269.
3.Powers HJ. Riboflavin (vitamin B-2) and health. Am J Clin Nutr. 2003 Jun;77(6):1352-60.
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Current topic on nutrition, deficiency and diseases: Vitamin B2 deficiency diseases.