Niacin deficiency neuropathy

Introduction to niacin deficiency neuropathy Niacin generally refers to niacin (Nicotinic acid), nicotinamide (nicotinamide), and other biologically active pyridine derivatives. Niacin deficiency is also known as niacin deficiency, also known as pellagra (skin disease) and Pellagra disease. In 1937, niacin deficiency was found to be the cause of the disease. Human organisms can synthesize endogenous niacin, but exogenous intake is necessary to avoid niacin deficiency. The occurrence of this disease is related to the intake of niacin, nicotinamide, tryptophan, decreased absorption and metabolic disorders. It belongs to a chronic wasting disease, with dermatitis, dementia and diarrhea as the main clinical symptoms. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: vaginitis amenorrhea, loss of libido, vitamin B1 deficiency, vitamin B2 deficiency

Niacin deficiency neuropathy

Insufficient intake, congenital defects (25%):

Found in corn-based food, because the niacin contained in corn is mostly combined, it can not be used by the body, and the lack of color amino acid in corn protein. Congenital defects: such as Hartnup disease, due to defects in the transport of tryptophan and several other amino acids in the small intestine and renal tubules.

Alcohol abuse, gastrointestinal disorders (5%):

Insufficient dietary intake during drinking and irregular eating, when there are insufficient intake of other nutrients, it is easy to affect the absorption and metabolism of niacin. Gastrointestinal disorders: long-term diarrhea caused by various causes, pyloric obstruction, chronic intestinal obstruction, intestinal tuberculosis, etc. can cause malabsorption of niacin.

Drugs, others (10%):

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 tryptophan, an important coenzyme in the metabolism of nicotinamide, and also taking valproic acid. Reports of niacin deficiency, some anticancer drugs, especially long-term use of sputum can also lead to niacin deficiency. Carcinoid syndrome: caused by the conversion of a large amount of tryptophan to serotonin without conversion to niacin.

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 (NMN) and 2-pyridone. It is discharged from the urine. The amount of niacin and the nutritional status of human niacin.

About 1.5% 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 (riboflavin) and iron are deficient, the conversion is slowed down when protein, tryptophan, energy and niacin are taken up. When restricted, the conversion of tryptophan increases.

Niacin is converted to nicotinamide, which is essential for nicotinamide adenine dinucleotide (NAD) to maintain cell function and metabolism. NAD (Coenzyme I) is phosphorylated to NADP (Coenzyme II), also color The final product of acid metabolism, about 200 enzymes rely on NAD and NADP for oxidation and reduction. These enzymes are involved in glucose glycolysis, pyruvate metabolism, pentose biosynthesis and metabolism of fats, amino acids, proteins and purines.

Animal experiments showed that zinc absorption rate in niacin deficiency, intestinal zinc, hemoglobin and intrahepatic iron increased significantly lower than the appropriate niacin in the diet, suggesting that niacin plays an important role in improving the utilization of zinc and iron. Acid deficiency may also have potential carcinogenic effects, so niacin deficiency can affect a variety of organs, systemic functions, and diverse clinical manifestations.

Pathological changes include cutaneous vasodilation, epithelial cytoplasmic hyperplasia and perivascular lymphocyte exudation; excessive hyperkeratosis and atrophy of the skin; mucosal edema of the digestive tract, inflammation, and later atrophy; glossitis and tongue atrophy are characteristic changes, pathological changes of the nervous system Found in the brain, spinal cord and peripheral nerves, the brain neurons are centrally Nisslolytic, and the anterior horn cells of the spinal cord have the same changes. The spinal cord is slinged, the spinal cord cerebellar tract and pyramidal tracts are degenerated, and the central and peripheral nerve fibers are patchy. Demyelination and axonal degeneration.

Niacin deficiency neuropathy prevention

The key to niacin deficiency is that the dietary preparation is unreasonable. The recommended daily intake of niacin is 2-6mg for infants, 7-12mg for children and adolescents, 13-14mg for adults, heavy manual workers, pregnant women, and lactators. In corn-based areas, 0.6% sodium bicarbonate can be added to corn flour. After cooking, the combined niacin can be converted into free form for easy use by the human body. Adding 10% soybean in corn can improve the amino acid ratio. It can also achieve the purpose of preventing niacin deficiency. At the same time, it should eat niacin and tryptophan-rich diet. Niacin is widely found in plant and animal foods. Liver, kidney, cow and sheep are rich in niacin. , pork, fish, peanuts, soybeans, wheat bran, rice bran, millet, etc., medium content of beans, hard fruits, rice, wheat, etc., while corn, vegetables, fruits, eggs, milk, low content, due to large Most proteins contain 1% tryptophan, so it is possible to maintain good niacin nutrition by maintaining a diet rich in high-quality protein.

Niacin deficiency neuropathy Complications, vaginitis, amenorrhea, libido, vitamin B1 deficiency, vitamin B2 deficiency

Other symptoms women may have vaginitis and menstrual disorders, amenorrhea; males have a burning sensation during urination, sometimes libido, this disease often with vitamin B1 deficiency, vitamin B2 deficiency and other nutritional deficiencies.

Niacin deficiency neurological symptoms Common symptoms Constipation diarrhea Abdominal pain Nausea dysfunction after redirecting dysfunction Dementia coma

The disease is slow onset, occasionally acute onset, mainly involving the skin, digestion and nervous system. Typical niacin deficiency has three groups (3D) symptoms: dermatitis, diarrhea, dementia, Early symptoms are non-specific, patients are weak, lazy, anorexia, and typical skin lesions, gastrointestinal symptoms and neuropsychiatric symptoms appear soon.

1. Skin changes Skin lesions are mostly on the back of the hand, wrist and foot, nose, cheeks, forehead, neck and other exposed parts, symmetric distribution, manifested as photosensitive dermatitis, skin becomes rough, thick, brown pigmentation, blisters , exfoliation, patients can have itching, pain.

2. Gastrointestinal symptoms 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, a large amount of stench It can also carry blood, bloody or mucous-like stools. If the lesion is close to the anus, it can be urgency and heavy. The diarrhea is often severe and refractory, and can be combined with malabsorption.

Gastritis and gastric mucosal atrophy caused the patient to complain of anorexia, nausea, stomach discomfort, abdominal pain; glossitis caused redness, ulceration and pain in the tongue.

3. Nervous system symptoms Most of the peripheral nerves are accompanied by symmetry stagnation of the limbs, sputum reflexes disappear or disappear, muscle tension is reduced, limbs are terminal type sensation loss, spinal cord damage is not uncommon, and there may be limb paralysis, deep feeling Obstacles and pyramidal tract signs were positive. Early manifestations of brain involvement were depression, anxiety, irritability, and lack of energy. Later, there were disorientation, confusion, paralysis, dementia, and eventually the patient was comatose and stupor.

Niacin deficiency neurological examination

1. Nicotic acid and urine metabolites Determination of N-methylnicotinamide (NMN), the main metabolite of nicotinic acid, was below 5.8 mol/d in 24 hours, and 5.8 to 17.5 mol/d was low.

The ratio of 2-pyridone to NMN in urine was used as an evaluation index, 1.3 to 4.0 was normal, <1.3 was insufficient, but was affected by protein intake level, and the marginal niacin intake was 10 nicotinic acid equivalent per day. The ratio is not sensitive.

2. Determination of plasma niacin metabolites Determination of plasma 2-pyridone is an indicator of niacin deficiency. Determination of 2-pyridone concentration after oral administration of 20 mg of nicotinamide (70 kg body weight) can reflect the nutritional status of niacin, but currently I don't think it is very reliable.

3. The red blood cell NAD content can be used as a sensitive indicator of niacin deficiency. The ratio of red blood cell NAD to NADP <1.0 indicates the risk of niacin deficiency, but there are also different reports that it may not be suggested that the concentration of NAD and NADP in blood may decrease. The lack of niacin, so the value of these biochemical assays is still controversial, the diagnosis still needs to be based on the symptoms and experimental treatment response.

Diagnostic test treatment: The patient was given a standard diet containing 100 mg of nicotinic acid and 1000 mg of tryptophan, and the amount of N-methylnicotinamide and pyridone in the urine of 24 hours was determined, and generally less than 3 mg was diagnosed as lacking.

Diagnosis and identification of niacin deficiency neuropathy

diagnosis

Alcoholism caused by niacin deficiency can be acute encephalopathy, patients with dementia, conscious turbidity, increased limb muscle tone or extensive rigidity, and strong grip and sucking reflex, about 50% with diarrhea, 30% with glossitis There are also varying degrees of spinal cord and peripheral nerve damage, often with vitamin B1 and vitamin B6 deficiency, significant niacin supplementation, autosomal recessive hereditary tryptophan absorption disorder, can show the clinical characteristics of typical pellagra, Niacin treatment is effective, carcinoid syndrome (carcinoid syndrome) due to the conversion of tryptophan to serotonin, can not produce niacin and cause niacin deficiency.

If the niacin deficiency is more serious and the patient has typical clinical manifestations, the clinical diagnosis can be made according to the clinical signs, and the diagnosis can be made in combination with laboratory tests in the early stage of the disease or in the absence of all typical clinical signs.

Differential diagnosis

Niacin deficiency should be distinguished from other causes of dermatitis, glossitis, gastritis and gastric mucosal atrophy, diarrhea, dementia and other neurological symptoms.

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