As a doctor today I prescribe Niacin (Vitamin B3 ) rich foods to eradicate Pellagra.
Prevent the 4 Ds - Dermatitis ; Diarrhea ;Dementia and Death.
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Pellagra is a systemic non-communicable disorder of poverty, caused by deficiency of niacin.
It is still endemic in certain part of Asia and Africa where people mostly consume maize or sorghum (jowar) as staple food.
Niacin refers to two chemically distinct compounds: Nicotinic acid and Niacinamide (nicotinamide).
These biologically active components are derived from dietary niacin or are biosynthesized from available tryptophan.
Niacin plays a major role in the formation of nicotinamide adenine dinucleotide (NAD) and its phosphate (NADP), compounds important in intermediary metabolism and a wide variety of oxidation-reduction reactions.
Source of Niacin in food:
1) Meat 2)Milk 3) Fish 4) Egg 5)Cheese
Animal protein, as found in meat, milk, butter, cheese, eggs, is rich in tryptophan. These are all good source of endogenously synthesized niacin. Niacin is available in many types of grain.
Although different views exist, regarding the etiology of Pellagra, there is general agreement that the major factor is deficiency of certain members of the B group of vitamins, particularly Niacin.
Some investigators believe that niacin deficiency should be regarded as the cause of pellagra, despite the fact that most affected individuals show evidence of multiple dietary deficiencies.
It is seen principally in patients who have been weakened by other diseases and in malnourished alcoholics.
Those who do not eat sufficient protein may suffer a deficiency of tryptophan, which in combination with a lack of exogenous niacin may result in mild pellagra.
Malabsorption of tryptophan, as in Hartnup disease, or excessive utilization of tryptophan for the synthesis of serotonin in the carcinoid syndrome, may also lead to mild symptoms of pellagra.
Pellagra is particularly prevalent in areas where maize is the staple food because the niacin in maize is chemically bound and thus poorly available. Maize is also a poor source of tryptophan.
Deficiencies of pyridoxine and riboflavin increase the requirement for dietary niacin because both of these cofactors are required for the biosynthesis of niacin from tryptophan.
Diphosphopyridine nucleotide and triphosphopyridine nucleotide, which have an abnormally low values in the blood and urine of persons with pellagra, rise to normal levels or higher when niacin is administered.
The pathologic changes of uncomplicated niacin deficiency have not been described in either humans or experimental animals.
Lesions that heal on administration of niacin are assumed to have been caused largely by lack of that compound. Pellagra is apparently a nutritional disease of the "conditioned" type.
Conditioning factors include exposure to sunlight, alcoholism, organic diseases, and infectious diseases.
The patient may have eating disorder like anorexia nervosa.
Other factors, such as mycotoxins, excessive dietary leucine intake , estrogens and progestogens, and various medications, might also lead to the development of pellagra.
Qualitative deficiency in the aminoacid composition of the protein supply is probably a conditioning factor in pellagra.
The relationship of a cornmeal diet to pellagra is probably explainable on the basis of the fact that cornmeal is deficient in tryptophan, which is a precursor of nicotinic acid. There is also some evidence that cornmeal may contain an antagonist of nicotinic acid.
About 50% of persons with pellagra show achlorhydria.
Macrocytic anaemia which is not uncommon, is probably the result of concomitant folic acid deficiency.
Pellagra is characterized by the three Ds of niacin deficiency :dermatitis , diarrhea, and dementia. Severe long-standing pellagra adds another D - death.
The skin changes are characteristic and pathognomonic.
Skin areas exposed to light, such as the face and the hands, and those subjected to pressure, such as the knees and the elbows, exhibit a rough, hyperpigmented, scaly dermatitis.
The lesion has a brown-red coloration, with a sharply demarcated erythematous border, affecting both hands and lower forearms.
The skin lesion around the neck is known as "casal's necklace".
Macroscopically, the lesions are discrete and show areas of pigmentation and / or depigmentation.
Microscopically, there is hyperkeratosis, parakeratosis, epidermal atrophy, vascularization, and a mild superficial infiltrate of lymphocytes.
Vesicles if present are either subepidermal due to edema in the papillary dermis or intraepidermal due to degenerative changes in the epidermis.
Mild keratotic follicular plugging is noted.
In the chronic cases there is subcutaneous fibrosis and scarring and the amount of melanin in the basal layer is increased.
Similar lesions are found in the mucous membranes of the mouth and vagina.
In the mouth, inflammation and edema lead to large, red tongue, which in the chronic stage is fissured and is similar to raw meat.
Anorexia and malabsorbative diarrhea lead to a state of malnutrition and cachexia.
A chronic, watery diarrhea is a typical feature of the disease but occasionally can be bloody and mucoid.
This is probably caused by mucosal atrophy and ulceration in the entire gastrointestinal tract, particularly in the colon.
Brain and spinal cord is affected in some patients. These patients suffer from dementia and in some cases psychosis.
This is characterized by degeneration of ganglion cells in the brain cortex.
Like other deficiencies of the B vitamins, clinical niacin deficiency, pellagra, is rarely seen developed countries except in chronic alcoholics or rarely in those suffering from anorexia nervosa.
Pathology of Vitamin A deficiency:
Importance of Vitamin A in our daily diet
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