B vitamins B: for diseases

B vitamins B: In diseases.

B vitamins b They are a group of water -soluble vitamins that play a key role in numerous metabolic processes in the human body. Their deficiency can lead to a wide range of diseases, and adequate consumption, especially in certain pathologies, can help improve the condition and accelerate recovery. This article is devoted to the role of each vitamin B in various diseases, focusing on the mechanisms of action, clinical manifestations of deficiency, diagnostic methods and therapeutic strategies, including vitamin therapy.

1. Tiamin (vitamin B1): role in diseases.

Tiamin plays an important role in carbohydrate metabolism, acting as a cooferment in the decarboxylation reactions of α-cutopy acids, such as pyruvat and α-catolutarate. It is also necessary for the function of the nervous system and muscles.

• Tiamine deficit: A classic disease associated with a deficiency of thiamine is since. There are three main forms of Beri Bari:

  • Sukhaaya has since: It is characterized mainly by neurological symptoms, such as peripheral neuropathy (numbness, tingling, weakness in the limbs), encephalopathy of Vernika and psychosis of Korsakov. Vernika encephalopathy is manifested by a triad of symptoms: ophthalmoplegia (paralysis of the eye muscles), ataxia (impaired coordination of movements) and confusion of consciousness. The psychosis of Korsakova is characterized by a memory impairment (anterograd and retrograde amnesia) and confabulations (false memories).
  • Wet Bari-Bari: It is manifested by cardiovascular symptoms such as cardiomegaly (heart enlargement), tachycardia (rapid heartbeat), shortness of breath, peripheral edema and heart failure.
  • Infantile Beri-Bari: It is found in children who are on breast feeding from mothers with a deficiency of thiamine. It is manifested by an acute beginning, with symptoms, including cyanosis, shortness of breath, aphony (voice loss) and heart failure.

• Causes of tiamine deficiency: The most common causes of thiamine deficiency are:

  • Alcoholism: Alcohol disrupts the absorption of thiamine in the intestines, as well as its utilization in the liver. In addition, alcoholics often have poor nutrition, which exacerbates the deficit.
  • Malnutrition: Insufficient consumption of products rich in thiamine, such as whole grain products, legumes and meat.
  • Malibsorption: Diseases that violate the absorption of nutrients in the intestines, such as the disease of the crown and celiac disease.
  • Dialysis: The dialysis procedure can lead to leaching of thiamine from the body.
  • Chronic vomiting and diarrhea: Loss of thiamine with liquid.
  • Some drugs: For example, diuretics can increase thiamine excretion.

• Tiamin for diseases:

  • Alcohol encephalopathy Vernika-Korsakov: Tiamine is a cornerstone of treatment of this condition. High doses of thiamine (usually 500 mg intravenously three times a day) are administered immediately if the vernika encephalopathy is suspected, since irreversible brain damage can occur within a few days. After improving the condition, the dose is reduced and the oral reception is continued.
  • Heart failure: Tiamin can be useful to patients with heart failure, especially if they take diuretics. Studies have shown that some patients with heart failure have a thiamine deficiency, and its replenishment can improve the function of the heart.
  • Diabetical neuropathy: Some studies suggest that thiamine can alleviate the symptoms of diabetic neuropathy. Dismissal, lipid -detected analogue of thiamine, can be more effective in improving the nervous function.
  • Mellori-Weiss syndrome: It is often associated with alcoholism and can lead to a deficiency of thiamine. The replenishment of thiamine is part of the complex treatment.

• Diagnosis Deficit Tiamina:

  • Anamnesis and physical examination: Identification of risk factors for thiamine deficiency and characteristic clinical manifestations.
  • Determining the level of thiamine in the blood: Measurement of the concentration of thiamine in solid blood or plasma.
  • Determining the activity of transcetolas of red blood cells: Transcetolasa is an enzyme that requires thiaminpyrophosphate (TPF) as a coherent. Measurement of transcetolase activity before and after the addition of TPF allows you to evaluate the degree of saturation of the body with thiamine. An increase in transcetolase activity after the addition of TPF indicates a deficiency of thiamine.

• Tiamine therapy:

  • October reception: It is recommended for the treatment of mild thiamine deficiency.
  • Intramuscular or intravenous injections: Showed with severe deficiency of thiamine, encephalopathy of Wernick and if oral administration is impossible.

2. Riboflavin (vitamin B2): role in diseases.

Riboflavin is the predecessor of two important coofers: Flavmononucleotide (FMN) and Flavidenindinindinucleotide (FAD) participating in many redox reactions necessary for the metabolism of carbohydrates, fats and proteins. Riboflavin is also important for the functioning of the antioxidant system.

• Fisheries deficiency: Riboflavin deficiency, known as Ariboflavinosisusually does not arise in isolation and is often combined with a deficiency of other vitamins of group B.

  • Symptoms:
    • Heyrozy: Cracks and redness in the corners of the mouth.
    • Glossit: Inflammation of the tongue, which becomes smooth and red.
    • Seborrheic dermatitis: Peeling of the skin, especially around the nose, lips and ears.
    • Conjunctivitis: Inflammation of the conjunctiva (mucous membrane of the eye).
    • Photophobia: Sensitivity to light.
    • Angular stomatitis: Inflammation in the corners of the mouth.
    • Anemia: In some cases, normochromic normocytic anemia may develop.

• Causes of riboflavin deficiency:

  • Malnutrition: Insufficient consumption of products rich in riboflavin, such as milk, meat, eggs and green vegetables.
  • Malibsorption: Diseases that violate the absorption of nutrients in the intestines.
  • Alcoholism: Alcohol may disrupt the absorption of riboflavin.
  • Some drugs: For example, tricyclic antidepressants and some antipsychotic drugs.
  • Phototherapy of newborns: Treatment of jaundice in newborns with the help of phototherapy can lead to the destruction of riboflavin.

• Riboflavin for diseases:

  • Migraine: High doses of riboflavin (400 mg per day) can be effective in migraine prevention. Riboflavin improves the function of mitochondria, which can be useful for migraine, since mitochondrial dysfunction plays a role in the pathogenesis of this disease.
  • Cataract: Some studies show that adequate riboflavin consumption can reduce the risk of cataracts.
  • Anemia: Riboflavin plays a role in iron metabolism, and its deficiency can contribute to the development of anemia. Riboflavin replenishment can improve the condition of patients with anemia, especially in combination with iron.
  • Brauna-Vialetto-Van Laere syndrome (Brown-Vialetto-Van Laere Syndrome – BVVLS): A rare genetic disease characterized by progressive hearing loss and neurological disorders. BVVLS is caused by mutations in genes encoding riboflavin conveyors. High doses of riboflavin can significantly improve the condition of patients with BVVLS.
  • Precomports: Some studies show that riboflavin deficiency may be associated with preeclampsia.

• Diagnosis Deficit Fisheries:

  • Anamnesis and physical examination: Identification of risk factors for riboflavin deficiency and characteristic clinical manifestations.
  • Determining the level of riboflavin in the blood: Measurement of riboflavin concentration in plasma or red blood cells.
  • Determining the activity of glutationreductase red blood cells: Glutationreductase is an enzyme that requires FAD as a coofer. Measuring the activity of glutationreductase before and after adding FAD allows you to evaluate the degree of saturation of the body with riboflavin.

• Riboflavin therapy:

  • October reception: Recommended for the treatment of riboflavin deficiency. Doses vary depending on the severity of the deficiency.
  • Intramuscular or intravenous injections: Can be used in severe cases or if oral administration is impossible.

3. Niacin (vitamin B3): role in diseases.

Niacin (nicotinic acid and nicotinamide) is the predecessor of two important coofers: nicotinindinindininicoleotide (above) and nicotinindinindininindinininucleotidfosphate (NAS) participating in many redox reactions necessary for the metabolism of carbohydrates, fats and proteins. Niacin also plays a role in DNA reparation and signal transmission.

• Niacina deficiency: Niacin deficiency leads to development Pellagraa classic disease characterized by a triad of symptoms: dermatitis, diarrhea and dementia (known as “three D”).

  • Symptoms:
    • Dermatitis: Symmetric, photosensitive dermatitis, usually affecting open areas of the skin, such as the face, neck, arms and legs. The skin becomes red, peeling and pigmented.
    • Diarrhea: Inflammation of the intestinal mucosa, leading to diarrhea, nausea and vomiting.
    • Dementia: Neurological symptoms, including depression, irritability, headaches, loss of memory and in severe cases dementia.
    • Other symptoms: Glossitis (inflammation of the tongue), stomatitis (inflammation of the mucous membrane of the mouth), anorexia.

• Causes of niacin deficiency:

  • Malnutrition: Insufficient consumption of products rich in niacin, such as meat, fish, poultry, legumes and enriched grain products.
  • Malibsorption: Diseases that violate the absorption of nutrients in the intestines.
  • Alcoholism: Alcohol can disrupt Niacin absorption.
  • Hartnupa disease: A rare genetic disease characterized by a violation of the transport of tripophanes, amino acids, which can be transformed into niacin in the body.
  • Carcinoid syndrome: The condition characterized by excessive production of serotonin, which uses tripophanes, which leads to a decrease in its accessibility for niacin synthesis.
  • Some drugs: For example, isoniazide (anti -TB drug) may disrupt the transformation of a tripophane into niacin.

• Niacin for diseases:

  • Hyperlipidemia: Niacin (in high doses, usually nicotinic acid) is used to reduce the level of LDL cholesterol (low density lipoproteins) and triglycerides, as well as to increase the level of HDL cholesterol (high density lipoproteins). However, the use of niacin in high doses is associated with side effects, such as redness of the skin, hepatotoxicity and hyperglycemia, so its use requires a careful observation of the doctor.
  • Pellagra: Niacin is the main method of treating Pellagra. High doses of niacin (for example, 300 mg per day) are usually prescribed until the symptoms improve.
  • Schizophrenia: Some studies suggest that high doses of niacin can be useful in the treatment of schizophrenia, although further research is needed to confirm these results.
  • Alzheimer’s disease: Some studies show that niacin can reduce the risk of developing Alzheimer’s disease.
  • Osteoarthritis: Niacinamide (one of the forms of niacin) can relieve symptoms of osteoarthritis.

• Diagnosis Niacina Deficit:

  • Anamnesis and physical examination: Identification of risk factors for niacin deficiency and characteristic clinical manifestations.
  • Determining the level of niacin in the blood: Measurement of niacin concentration in plasma or urine.
  • Determining the level of Niacin metabolites in the urine: Measurement of the level of n-methylnicotinamide (NMN) and N-methyl-2-piridon-5-carboxumes (2-Py) in the urine.

• Niacinoma therapy:

  • October reception: Recommended for the treatment of niacin deficiency. Doses vary depending on the severity of the deficiency.
  • Intramuscular or intravenous injections: Can be used in severe cases or if oral administration is impossible.

4. Pantotenic acid (vitamin B5): role in diseases.

Pantotenic acid is a component of cooferment A (COA), which plays a central role in the metabolism of carbohydrates, fats and proteins. COA is involved in the synthesis and oxidation of fatty acids, as well as in the synthesis of cholesterol, steroid hormones and neurotransmitters.

• Pantothenic acid deficiency: Pantothenic acid deficiency is rare, since it is widespread in food.

  • Symptoms (rare):
    • Paresthesias: Numbness and tingling in the limbs.
    • Fatigue: General weakness and fatigue.
    • Headaches:
    • Insomnia:
    • Irritability:
    • Stomach ache:
    • Nausea and vomiting:

• Causes of pantothenic acid deficiency:

  • Severe malnutrition:
  • Genetic disorders: For example, mutations in the pantotenatkinase 2 (PANK2) genes, leading to neurodegenerations with the accumulation of iron in the brain (neurodegeneration associated with pantotentenat-kinase or PKAN).

• Pantotenic acid for diseases:

  • PKAN (neurodegeneration associated with pantoten-kinase): High doses of pantothenic acid can relieve some PKAN symptoms.
  • Acne: Some studies show that pantothenic acid can be effective in treating acne, although further studies are needed.
  • Wound healing: Pantotenic acid can contribute to healing of wounds.

• Diagnosis of pantothenic acid deficiency:

  • Diagnosis of pantothenic acid deficiency is difficult due to the nonspiciency of symptoms and the absence of reliable laboratory tests.

• Pantothenic acid therapy:

  • October reception: It is recommended for the treatment of pantothenic acid deficiency.

5. Pyridoxine (vitamin B6): role in diseases.

Pyridoxine (pyridoxal, pyridoxamine and their phosphorized forms) is a coherent in many enzymatic reactions, especially in amino acid metabolism. It also participates in the synthesis of neurotransmitters (for example, serotonin, dopamine, GABA), hem and nucleic acids.

• Pyridoxine deficiency:

  • Symptoms:
    • Seborrheic dermatitis: Peeling of the skin, especially around the nose, lips and ears.
    • Glossit: Inflammation of the tongue, which becomes smooth and red.
    • Stomatitis: Inflammation of the mucous membrane of the mouth.
    • Neurological symptoms: Depression, irritability, convulsions (especially in children), peripheral neuropathy.
    • Anemia: Microcitic hypochromic anemia (anemia with small and pale red blood cells).

• Causes of pyridoxine deficiency:

  • Malnutrition: Insufficient consumption of products rich in pyridoxine, such as meat, fish, poultry, legumes, nuts and whole grain products.
  • Malibsorption: Diseases that violate the absorption of nutrients in the intestines.
  • Alcoholism: Alcohol can violate the absorption and metabolism of pyridoxine.
  • Some drugs: For example, isoniazide, penicilllammin, contraceptives and some antidepressants.
  • Genetic disorders: For example, homocystinuria.

• Pyridoxine for diseases:

  • Sideroblastic Anemia: Some forms of sideroblastic anemia (anemia characterized by the accumulation of iron in red blood cells) can be sensitive to the treatment of pyridoxin.
  • Homocystinuria: Pyridoxine can reduce the level of homocysteine ​​in blood in patients with homocystinuria, especially those who have mutations in genuine-cyntase genus (CBS).
  • Nausea and vomiting during pregnancy: Pyridoxine is often used to facilitate nausea and vomiting during pregnancy.
  • Premenstrual syndrome (PMS): Some studies show that pyridoxine can relieve PMS symptoms, such as depression, irritability and bloating.
  • Carpal tunnel syndrome: Some studies suggest that pyridoxine can alleviate the symptoms of carpal tunnel syndrome, although additional studies are needed.
  • Autism: Some studies have shown that a combination of pyridoxine and magnesium can improve behavior in children with autism.
  • Izoniazide-induced neuropathy: Pyridoxine is used for the prevention and treatment of neuropathy caused by isoniazide (anti -tuberculosis drug).

• Diagnosis Pyridoxine Deficiency:

  • Anamnesis and physical examination: Identification of risk factors for pyridoxine deficiency and characteristic clinical manifestations.
  • Determination of the level of pyridoxal-5-phosphate (PLF) in the blood: PLF is an active form of vitamin B6 and is the most sensitive indicator of its status.
  • Determination of the level of tryptophan in the urine after the load by a tripophane: In patients with pyridoxine deficiency, increased excretion of xanthuric acid in the urine is observed after the load by tripophane.

• Pyridoxine therapy:

  • October reception: Recommended for the treatment of pyridoxine deficiency. Doses vary depending on the severity of the deficiency and cause.
  • Intramuscular or intravenous injections: Can be used in severe cases or if oral administration is impossible.

6. BIOTIN (vitamin B7): role in diseases.

Biotin is a coherent of carboxylase, enzymes involved in the metabolism of fatty acids, carbohydrates and amino acids. He also plays a role in the regulation of genes expression.

• Biotin deficiency: Biotin’s deficiency is rare.

  • Symptoms:
    • Dermatitis: Peeling of the skin, especially around the nose, mouth and eyes.
    • Alopecia: Hair loss.
    • Conjunctivitis: Inflammation of the conjunctiva (mucous membrane of the eye).
    • Neurological symptoms: Depression, fatigue, paresthesia.

• Causes of biotin deficiency:

  • Excessive use of raw eggs: Raw egg protein contains avidine, which binds biotin and prevents its absorption.
  • Biotinidase deficiency: A rare genetic disease characterized by a deficiency of the enzyme biotinidase necessary for the release of biotin from food.
  • Long -term parenteral nutrition:
  • Malibsorption: Diseases that violate the absorption of nutrients in the intestines.
  • Some drugs: For example, antibiotics.

• Biotin for diseases:

  • Biotinidase deficiency: Biotin is the main method of treating biotinidase deficiency.
  • Fitty nails: Some studies show that biotin can strengthen nails and reduce their fragility.
  • Hair loss: Biotin is sometimes used to treat hair loss, although its effectiveness is not proven in this regard.
  • Diabetical neuropathy: Some studies show that biotin can relieve symptoms of diabetic neuropathy.

• Diagnosis deficiency Biotin:

  • Anamnesis and physical examination: Identification of risk factors for biotin deficiency and characteristic clinical manifestations.
  • Determining the level of biotin in the blood: Measurement of biotin concentration in plasma or urine.
  • Determining the activity of biotinidase in the blood: It is used to diagnose biotinidase insufficiency.

• Therapy Biotinoma:

  • October reception: Recommended for the treatment of biotin deficiency.

7. Folic acid (vitamin B9): role in diseases.

Folic acid (or folate) is a coherent involved in the transfer of single -iron groups in various metabolic reactions, including the synthesis of nucleic acids (DNA and RNA) and amino acids. Folic acid is especially important for rapidly dividing cells, such as blood cells and fetal tissue.

• Folic acid deficiency:

  • Symptoms:
    • Megaloblastic anemia: Anemia characterized by large and immature red blood cells (megaloblasts).
    • Fatigue: General weakness and fatigue.
    • Dyspnea:
    • Glossit: Inflammation of the tongue, which becomes smooth and red.
    • Stomatitis: Inflammation of the mucous membrane of the mouth.
    • Neurological symptoms: Depression, irritability, confusion.
    • Congenital defects of the nervous tube (in the fetus): The deficiency of folic acid during pregnancy increases the risk of developing defects in the nervous tube in the fetus, such as Spina Bifida and anencephaly.

• Causes of folic acid deficiency:

  • Malnutrition: Insufficient consumption of products rich in folic acid, such as green leafy vegetables, legumes, citrus fruits and enriched grain products.
  • Malibsorption: Diseases that violate the absorption of nutrients in the intestines, such as celiac disease and Crohn’s disease.
  • Alcoholism: Alcohol can disrupt the absorption and metabolism of folic acid.
  • Pregnancy: The need for folic acid increases during pregnancy.
  • Some drugs: For example, methotrexate, trimethoprim and phenytoin.

• Folic acid in diseases:

  • Megaloblastic anemia: Folic acid is the main method of treating megaloblastic anemia caused by a deficiency of folic acid.
  • Prevention of defects in the nervous tube: Taking folic acid before and during pregnancy significantly reduces the risk of developing defects in the nervous tube in the fetus. It is recommended that all women of childbearing age take additives with folic acid.
  • Cardiovascular diseases: Folic acid can reduce the level of homocysteine ​​in the blood, which is a risk factor for cardiovascular diseases.
  • Depression: Some studies show that folic acid can be useful in the treatment of depression, especially in combination with antidepressants.
  • Inflammatory diseases of the intestine (BCC): Patients with BCC often experience a deficiency of folic acid due to violation of absorption. Folic acid replenishment can be useful for these patients.
  • Cancer prevention: Some studies show that adequate consumption of folic acid can reduce the risk of developing certain types of cancer, such as colon cancer.

• Diagnosis of folic acid deficiency:

  • Anamnesis and physical examination: Identification of risk factors for folic acid deficiency and characteristic clinical manifestations.
  • Determining the level of folic acid in the blood: Measurement of folic acid concentration in plasma or red blood cells.
  • Determining the level of homocysteine ​​in the blood: An increased level of homocysteine ​​may indicate a deficiency of folic acid or vitamin B12.

• Folic acid therapy:

  • October reception: Recommended for the treatment of folic acid deficiency.
  • Intramuscular or intravenous injections: Can be used in severe cases or if oral administration is impossible.

8. Kobalamin (vitamin B12): role in diseases.

Cobalamine (cyanocobalamin, methylcobalamin and adenosylcobalamin) is a coherent participating in two important enzymatic reactions: the transformation of methylmalonyl-cooa into succinyl-cooa and the transformation of homocysteine ​​into methionine. Cobalamin is necessary for the normal functioning of the nervous system and the formation of red blood cells.

• Cobalamin deficiency:

  • Symptoms:
    • Megaloblastic anemia: Anemia characterized by large and immature red blood cells (megaloblasts).
    • Fatigue: General weakness and fatigue.
    • Dyspnea:
    • Paresthesias: Numbness and tingling in the limbs.
    • Neurological symptoms: Peripheral neuropathy, the demyelinization of the spinal cord (subcortal myelosis), dementia, depression.
    • Glossit: Inflammation of the tongue, which becomes smooth and red.

• Causes of cobalamine deficiency:

  • Malnutrition: Insufficient consumption of products rich in cobalamin, such as meat, fish, poultry, eggs and dairy products. Vegans are at risk of cobalamin deficiency if they do not use enriched products or additives.
  • Personic anemia: Autoimmune disease, characterized by the destruction of the parietal cells of the stomach, which produce the internal factor of casla, necessary for the absorption of cobalamin in the intestine.
  • Malibsorption: Diseases that violate the absorption of nutrients in the intestines, such as the disease of the crown, celiac disease and surgical removal of part of the stomach or small intestine.
  • Atrophic gastritis: Inflammation of the mucous membrane of the stomach, leading to a decrease in the production of hydrochloric acid and the internal factor of casla.
  • Helicobacter pylori infection:
  • Some drugs: For example, metformin, proton pump inhibitors (IPP) and H2-gistamine blockers.
  • Age: With age, the body’s ability to absorb cobalamin decreases.

• Cobalamin for diseases:

  • Megaloblastic anemia: Cobalamin is the main method of treating megaloblastic anemia caused by a deficiency of cobalamin.
  • Procorus myelosis: The replenishment of cobalamin can stop the progression of subcortical myelosis and, in some cases, lead to an improvement in the condition.
  • Dementia: Some studies show that cobalamine deficiency can contribute to the development of dementia. Cobalamin replenishment can improve cognitive functions in patients with deficiency.
  • Depression: Some studies show that cobalamine deficiency may be associated with depression. Filling cobalamin can improve the mood in patients with deficiency.
  • Diabetical neuropathy: Some studies suggest that cobalamin can alleviate the symptoms of diabetic neuropathy.
  • Chronic fatigue syndrome: Some studies show that cobalamin can alleviate the symptoms of chronic fatigue syndrome.

• Diagnosis of cobalamine deficiency:

  • Anamnesis and physical examination: Identification of risk factors for cobalamin deficiency and characteristic clinical manifestations.
  • Determining the level of cobalamine in the blood: Measurement of the concentration of cobalamine in plasma.
  • Determining the level of methylmalonic acid (MMK) in the blood or urine: An increased level of MMK is a more sensitive indicator of cobalamin deficiency than the level of cobalamin in the blood.
  • Determining the level of homocysteine ​​in the blood: An increased level of homocysteine ​​may indicate a deficiency of folic acid or vitamin B12.
  • Shilling test: It is used to determine the cause of cobalamin deficiency (for example, pernicious anemia).

• Kobalamin therapy:

  • Intramuscular injections: It is recommended for the treatment of cobalamin deficiency, especially with pernicious anemia or malabsorption.
  • October reception: Can be effective for