Vitamin B3 (Niacin, Nicotinic Acid, Nicotinamide, Antipellagra Vitamin): Nutritive Importance, Deficiency And Treatment

Nicotinic acid forms an integral part of nicotinamide adenine dinucleotide (NAD) and its phosphate (NADP) which acts as coenzymes in the metabolic pathways of glucose and proteins. Nicotinic acid and nicotinamide have equal biological potency and are together referred to as niacin. Tryptophan is converted into niacin in the body, 60 mg of tryptophan giving rise to 1 mg niacin.

Dietary sources include liver, pulses, whole cereals, fish, meat, groundnuts, milk, eggs and to a smaller extent, vegetables. Coffee contains appreciable amounts of this vitamin. Rice and other cereals contain this vitamin, major portion of which is lost by milling. In maize, niacin is present in an unabsorbable form “niacytin”. Moreover, maize is poor in its content of tryptophan. One-fourth of the vitamin may be lost in washing and cooking, though cooking alone does not destroy it. Daily requirement is 6 mg/1000 Kcals (15 to 18 mg/day). Deficiency of niacin causes pellagra.

This disease is widely prevalent in maize consuming communities and regions. Consumption of sorghum also predisposes to this deficiency. Newer varieties of maize and sorghum with better nutritive value have helped to reduce the incidence of pellagra. Alcoholism and malabsorption states precipitate pellagra. Inborn disorders of metabolism such as Hartnup disease in which the absorption of tryptophan is impaired, leads to pellagra in rare cases.

Pathology: Dermatitis changes in the oral and intestinal mucosa and degenerative changes in the central nervous system are seen. Ulcers may develop in the intestines. Chromatolysis of ganglion cells occur in the central nervous system. Patchy demyelination occurs in the spinal cord.

Clinical features: Generalised malnutrition is evident in most cases. The most well- known features are the three D’s- dermatitis, diarrhea and dementia, but these characterize the very advanced stage of the disease. Pellagra should be diagnosed much before this classical picture develops, since the advanced stage is associated with high mortality.

Skin Changes: These are seen over areas exposed to sunlight. These start with erythema which may resemble sunburn. This progresses to vesiculation, ulceration, secondary infection and crusting. In chronic pellagra, the skin becomes rough, thickened, scaly and pigmented. In home- bound patients not exposed to the sun, pellagra may develop without the skin changes- “pellagra sine pellagra”

Mucous membrane changes are evident in the mouth and vulva. Skin of the perianal region shows degenerative and inflammatory lesions. The tongue is raw and beefy in appearance. Angulostomatitis may be present.

Alimentary symptoms: Vague alimentary symptoms like anorexia, nausea, vomiting and dyspepsia are invariably seen. Diarrhea is common but not always present. The stools may be watery or rarely dysenteric.

Neurological features: Anxiety, depression, irritability and failure to concentrate are early symptoms. Advanced cases show delirium, dementia and psychiatric manifestation. Mental symptoms may be mistaken for primary psychiatric disorders.

Course And prognosis: Advanced cases are fatal due to diarrhea, secondary infections, or other associated nutritional disorders. Early treatment reverses the symptoms completely.

Treatment

Well balanced diet containing adequate supply of proteins should be instituted. Nicotinamide is well absorbed if given orally. It is given in a dose of 100 mg every 6 hours for 2 to 3 weeks. In the advanced cases, 50 to 100 mg may be given intramuscularly or intravenously. Supplements such as the other B complex vitamins and iron should be concurrently administered. Local application of antihistamine creams and protective clothing gives relief to the skin lesions.