Riboflavin is widely distributed throughout all plant and animal cells. Good sources are dairy products, offal and leafy vegetables. Riboflavin is not destroyed appreciably by cooking, but is destroyed by sunlight. Riboflavin is a flavoprotein that is a cofactor for many oxidative reactions in the cell.
Riboflavin deficiency, which is rare in developed countries, is virtually always accompanied by other deficiencies and many features previously attributed to riboflavin deficiency are probably due to multiple deficiencies:

• Angular stomatitis or cheilosis (fissuring at the corners of the mouth)
• A red, inflamed tongue
• Seborrhoeic dermatitis, particularly involving the face (around the nose) and the scrotum or vulva Riboflavin (5 mg) daily can be tried for the above conditions, usually given as vitamin B complex.


This is the generic name for the two chemical forms: nicotinic acid and nicotinamide, the latter being found in the two pyridine nucleotides, nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). Both act as hydrogen acceptors in many oxidative reactions and in their reduced forms (NADH and NADPH) act as hydrogen donors in reductive reactions. Many oxidative steps in the production of energy require NAD, and NADP is equally important in the hexose monophosphate shunt for the generation of NADPH, which is necessary for fatty-acid synthesis.

Niacin is found in many foodstuffs, including plants, meat (particularly offal) and fish. Niacin is lost by removing bran from cereals but is added to processed cereals and white bread in many countries. Niacin can be synthesized in humans from tryptophan, 60 mg of tryptophan being converted to I mg of niacin. The amount of niacin in food is given as the niacin equivalent which is equal to the amount of niacin plus one-sixtieth of the tryptophan content.


This is now rare and is found in people who virtually only eat maize, e.g. in parts of Africa. Maize contains niacin in the form of niacytin, which is biologically unavailable, and has a low content of tryptophan. Many of the features of pellagra can be explained purely by niacin deficiency; some, however, are probably due to multiple deficiencies, including proteins and other vitamins.


The classical features are of dermatitis, diarrhoea and dementia. Although this is an easily remembered triad, not all are always present and the mental changes are not a true dementia.


Initially there is a redness of the skin in the areas exposed to sunlight. This is followed by cracks in the skin, with occasional ulceration. Chronic thickening, dryness andpigmentation develop. The lesions are always symmetrical and often affect the dorsal surfaces of the hands. The perianal skin and vulva are frequently involved. Casal’s necklace or collar is the term given to the skin lesion around the neck, which is confined to this area by the clothes worn.


This is often a feature but constipation is occasionally seen. Other gastrointestinal manifestations include painful red raw tongue, glossitis and angular stomatitis.Recurring mouth infections occur.


This occurs in chronic disease. In milder cases there are symptoms of depression, apathy and sometimes thought disorders. Tremor and an encephalopathy frequently occur. Hallucinations and acute psychosis are seen with more severe cases.
Pellagra may also occur:
THERAPY WITH ISONIAZID, as this can lead to a deficiency of vitamin B6, which is needed for the synthesis of nicotinamide from tryptophan; vitamin B6 is now given concomitantly with isoniazid
HARTNUP DISEASE, a rare inborn error whereby basic amino acids including tryptophan are not absorbed by the gut and there is also loss of this amino acid in the urine

ALCOHOL-DEPENDENT patients who do not eat
VERY LOW PROTEIN DIETS given for renal disease or taken as a food fad
CARCINOID SYNDROME and phaeochromocytoma, in which tryptophan metabolism is diverted away from the formation of nicotinamide to form amines

The oxidative pathway of tryptophan metabolism.
The oxidative pathway of
tryptophan metabolism.


In endemic areas this is based on the clinical features, remembering that other vitamin deficiencies can produce similar changes, e.g. angular stomatitis. Nicotinamide (approximately 300 mg daily by mouth) with a maintenance dose of 50 mg daily is given. Mostly, however, vitamin B complex is given, as other deficiencies are often present. An increase in the protein content of the diet and treatment of malnutrition and other vitamin deficiencies is essential. Mild cases respond well but dementia is often permanent.


Vitamin B6 exists as pyridoxine, pyridoxal and pyridoxamine, and is found in plant and animal foodstuffs. Pyridoxal phosphate is involved in the metabolism of aminoacids. Dietary deficiency is extremely rare. Some drugs are antagonistic to B6, e.g. isoniazid, hydralazine and  penicillamine. The polyneuropathy occurring after isoniazid usually responds to vitamin B6. Sideroblastic anaemia occasionally responds to vitamin B6

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