Niacin deficiency

Introduction to niacin deficiency Nicotic acid deficiency (nicohic acid deficiency), also known as niacin deficiency, ecdysis, rough skin disease or pellagra, caused by the lack of niacin in the human body, the main clinical manifestations of rash, digestive system and nervous system symptoms. The main food sources of niacin are liver, kidney, lean meat, poultry, fish, peanuts, beans, etc. When these foods are insufficiently ingested, the lack of vitamin B1 and vitamin B2 can cause niacin deficiency. basic knowledge The proportion of sickness: 0.01% Susceptible people: no special people Mode of infection: non-infectious Complications: epilepsy schizophrenia peripheral neuritis

Cause of niacin deficiency

(1) Causes of the disease

Insufficient intake (20%):

The main food sources of niacin are liver, kidney, lean meat, poultry, fish, peanuts, beans, etc. When these foods are insufficient, lack of vitamin B1 and vitamin B2 can cause niacin deficiency. Because most of the niacin contained in corn is a combination type, it can not be used for the body without decomposition, and the lack of tryptophan in corn protein is prone to niacin deficiency.

Drugs (20%):

Some drugs can interfere with the metabolism of niacin, the most well known is isoniazid, which interferes with the action of pyridoxine, while pyridoxine is a tryptophan, an important coenzyme in the metabolism of nicotinamide, and some anticancer drugs. In particular, long-term use of sputum can lead to niacin deficiency.

Alcohol abuse (10%):

Insufficient dietary intake during drinking and irregular eating, it is easy to affect the absorption and metabolism of niacin when other nutrients are insufficient.

Gastrointestinal disorders (15%):

Long-term diarrhea caused by various reasons, pyloric obstruction, chronic intestinal obstruction, intestinal tuberculosis, etc. can cause malabsorption of niacin.

Congenital defects (5%):

Such as Hartnup disease, due to small intestinal and renal tubules caused by transport defects of tryptophan and several other amino acids.

Carcinoid syndrome (10%):

Due to the conversion of a large amount of tryptophan to serotonin without conversion to niacin.

(two) pathogenesis

Niacin and nicotinamide are almost completely absorbed in the stomach and small intestine. At low concentrations, they are dependent on the easy absorption of Na. At high concentrations, they are mainly passive diffusion. The main form in the bloodstream is nicotinamide, and nicotinic acid is present in all cells. Only a small amount can be stored in the body. Excessive niacin is methylated in the liver to N-mononucleotide (N'MN) and 2-pyridone is excreted from the urine. The amount of niacin intake and the nutritional status of human niacin.

About 15% of the tryptophan in the diet can be converted to niacin, 60mg of food tryptophan can be converted to 1mg of human niacin, so the niacin intake of the diet should include both niacin and tryptophan, color ammonia The efficiency of acid conversion to niacin is affected by various nutrients. When vitamin B6, vitamin B2 and iron are deficient, the conversion is slowed down. When the intake of protein, tryptophan, energy and niacin is limited, color ammonia The conversion of acid is increased.

Nicotinic acid in the form of nicotinamide adenine dinucleotide (NAD), coenzyme adenine dinucleotide phosphate (NADP) as a coenzyme of dehydrogenase acts as a hydrogen donor in biooxidation, involved in glucose glycolysis, pyruvate Salt metabolism, pentose biosynthesis and metabolism of fats, amino acids, proteins and strontium, animal experiments show that zinc absorption rate in niacin deficiency, intestinal zinc, hemoglobin and intrahepatic iron increase significantly lower than dietary nicotinic acid In mice, it is suggested that niacin plays an important role in improving the utilization of zinc and iron, and niacin deficiency may also have potential carcinogenic effects.

Niacin deficiency prevention

Active treatment of primary diseases, exclusion of drugs affecting corn-based foods can add 0.6% sodium bicarbonate to corn flour, after cooking, combined niacin can be converted into free form for human use, added to corn 10% soybean can improve the amino acid ratio, and can also prevent niacin deficiency. At the same time, it should eat niacin and tryptophan-rich diet. The foods rich in niacin are liver, kidney, cow, sheep, pork. Fish, peanuts, soybeans, wheat bran, rice bran, millet, etc., medium-sized beans, hard fruits, rice, wheat, etc., while corn, vegetables, fruits, eggs, milk, low content, due to most proteins Containing 1% tryptophan, it is possible to maintain good niacin nutrition by maintaining a diet rich in high quality protein.

Niacin deficiency complications Complications, epilepsy, schizophrenia, peripheral neuritis

Niacin deficiency can progress to insanity, disorientation, seizures, tension schizophrenia, hallucinations, confusion, paralysis, and even death, symptoms of peripheral neuritis such as limb numbness, burning sensation, gastrocnemius tenderness and reflex abnormalities, etc. Both can occur, sometimes with subacute spinal posterior column combined degeneration symptoms, may be related to other vitamin B deficiency.

Symptoms of niacin deficiency Common symptoms Abdominal pain, itching, constipation, diarrhea, inattention, edema, swelling, depression, depression, coma

Patients in the early performance may not be obvious, often have loss of appetite, fatigue, weight loss, abdominal pain, discomfort, indigestion, excitement, inattention, insomnia and other non-specific diseases, when the disease progresses, can appear more typical symptoms, performance It occurs during sun exposure in summer and autumn, and can sometimes be induced by radiation and physical damage to the skin.

1. Skin: dermatitis is the most typical symptom of this disease. It is often present symmetrically in the exposed parts of the limb. It is the most common in the back of the hand, the back of the foot, the wrist, the forearm, the fingers, the ankle, etc., followed by the friction of the limb, the initial lesion of the skin. When the color is red and itchy, it is like sunburn, but there is a clear boundary with the surrounding skin, the edge is slightly higher, the center is more lesions; after that, the skin color changes rapidly to reddish brown, with obvious edema, may be accompanied by herpes and The epidermis ruptures and forms a oozing wound. It is easy to induce secondary infection. When the condition improves, the edema and red can gradually recede. When it is cured, there is a large piece of peeling, and then the new pink skin is thickened. It is also thin and atrophic. The edges are pigmented.

Chronic edema is mild or insignificant, but pigmentation is deeper, and the skin tends to be thicker in areas prone to wear such as elbows, knuckles, knees, etc., hyperkeratosis, dark complexion, different from its surroundings, and dry , the phenomenon of desquamation, another manifestation of fish scale-like skin changes in the front and outside of the calf, the lesion often has pigmentation.

2. Digestive system: The most prominent is glossitis and diarrhea.

(1) glossitis: early tongue tip and edge congestion and redness, and sacral papilla enlargement, followed by full tongue, oral mucosa, pharynx and esophagus can be red and swollen, epithelial shedding, and superficial ulcer, causing tongue Pain and difficulty in eating hypopharynx, increased salivation, atrophy of the tongue when the disease is long, the tongue is smooth and dry, often accompanied by vitamin B2 deficiency of keratitis.

(2) diarrhea: early constipation, followed by intestinal wall, digestive gland, intestinal wall and mucous membrane, villus atrophy and enteritis often occur diarrhea, stool is watery or mushy, the amount is more than stench, Can also bring blood, such as lesions close to the anus can appear in the urgency and heavy, diarrhea is often severe and refractory, can be combined with absorption disorders.

3. Neuropsychiatric system: Early symptoms are mild, may have dizziness, vertigo, irritability, anxiety, depression, forgetfulness, insomnia and paresthesia, but this disease is different from beriberi, this disease affects the central nervous system The latter is dominated by peripheral nerves.

Other symptoms women may have vaginitis and menstrual disorders, amenorrhea; males have a burning sensation when urinating, sometimes libido, this disease often with beriberi, 2 deficiency vitamin B2 deficiency and other nutritional deficiencies, niacin deficiency Clinical manifestations can be described by four English letters D: dermatitis, diarrhea, dementia, and death.

Niacin deficiency check

1. Analysis of gastric juice: Gastric acid is reduced, even absent.

The determination of niacin metabolite N-methylnicotinamide and -pyridone-N'-methylnicotinamide in urine was significantly reduced (normal human excretion was >5 mg/d).

3. Plasma tryptophan content is reduced (normal).

4. Load test: After urinating in the morning, the patient enters a standard meal containing 10 mg of nicotinic acid and 100 mg of tryptophan. The urine is collected for 24 hours, and N-methylnicotinamide and -pyridone-N'-methyl are determined. Nicotinamide, the normal amount of these two metabolites is 7.0 to 37.0 mg, and the niacin deficiency is often less than 3.0 mg.

Diagnostic identification of niacin deficiency

diagnosis

1. History: Dietary history is extremely important. This disease is easy to occur in areas where corn is the staple food, while non-staple foods (especially animal foods) are insufficient. Children with partial eclipse habits, refused to eat meat, food is monotonous, pregnant women, and lactating mothers Increased demand, insufficient supplementation, etc., can lead to niacin deficiency.

2. Clinical manifestations: Typical symptoms of this disease are diarrhea, dermatitis and dementia, commonly referred to as "three D".

(1) Early indigestion, loss of appetite, diarrhea constipation, indifferent sleepiness, dizziness and insomnia, burning and numbness in the limbs.

(2) Skin damage: Starting from erythema, it is like sunburn, burning and itching, followed by exudation, formation of herpes and bullae, then scab, pigmentation, rough skin and scaly.

(3) digestive system symptoms: there are angular keratitis, oral mucosa, tongue mucosa and gum swelling, accompanied by ulcers and secondary infections, loss of appetite, nausea, vomiting, diarrhea and so on.

(4) symptoms of the nervous system: start with headache, dizziness, irritability, restlessness, etc., such as the progression of the disease can appear mental depression, illusion, auditory hallucinations, mental disorders, paralysis and coma, check abnormalities, limb numbness, body Pain, sputum reflexes early, and later disappeared.

Differential diagnosis

The disease should be identified with toxic dermatitis, lupus erythematosus, impetigo, eczema, purpura, sunburn, enteritis, dyspepsia, peripheral neuritis and psychosis.

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