What Is the Connection Between Thiamine and Alcoholism?

The structural formula of vitamin B1 contains sulfur and amino groups, so it is also called thiamine. Because it cannot be synthesized in the central nervous system, it must be supplied from the blood

Vitamin B1 deficiency neuropathy

Nutrient deficiency caused by various reasons, especially lack of specific nutrients (such as vitamins), can affect some functions of the central nervous system and / or peripheral nerves or cause pathological damage, resulting in some neuropsychiatric symptoms. Vitamin B1 (ie thiamine) deficiency was once clinically called "beriberi", a systemic disease caused by insufficient intake of vitamin B1 in food, which mainly affects the digestive, nervous and circulatory systems clinically. The incidence of this disease is relatively low, but it still occurs frequently in areas where cereals are the staple food of China.

Vitamin B1 deficiency neuropathy review

Vitamin B1 deficiency neuropathy Should enter the brain or cerebrospinal fluid through the blood-brain and blood-cerebrospinal fluid barriers. Brain cells have a system that takes up and releases thiamine, and regulates thiamine levels throughout the body through the intestine and kidneys. After thiamine enters the body, the liver and brain thiamine pyrophosphate kinase quickly converts it into active thiamine pyrophosphate (TPP), which becomes an important coenzyme. In addition to participating in the oxidative decarboxylation of pyruvate, TPP may also play a role in nerve conduction. TPP or its derivative, thiamine triphosphate, aggregates in the membrane of peripheral nerves and may play a role in the synthesis of acetylcholine. Thiamine is the most abundant in all kinds of unmilled grains and is generally not easy to lack. According to different clinical types, vitamin B1 deficiency neuropathy caused by thiamine deficiency is more common in famine years; but thiamine deficiency disorders due to acute and chronic alcoholism, such as Wernicke encephalopathy and alcoholic peripheral neuropathy, are not uncommon .

Vitamin B1 deficiency neuropathy is more common in chronically malnourished people. Due to insufficient long-term intake of thiamine, it often causes paralysis of symmetrical peripheral nerves in the limbs, and often has heart damage.

Wernicke encephalopathy (Wernicke encephalopathy, WE) was first described by Wernicke in 1881, and later known to be caused by alcoholism

Caused by thiamine deficiency. Acute or subacute onset, combined with alcoholism, mainly affect the upper midbrain gray matter and hypothalamus including the papillary body, hyperemia and punctate hemorrhage and capillary pathological changes. Clinical features of mental consciousness disorder, ataxia and paralysis of extraocular muscles. Severe memory and orientation disorders, as well as mental symptoms such as hallucinations and delusions, are often referred to as Wernicke-Korsakoff syndrome; the chronic phase is also known as Korsakoff's psychosis (KP). Currently, no authoritative comprehensive statistics on incidence rates have been found. There are reports in the US that vitamin B1 deficiency accounts for 17% of elderly hospitalized patients. There is no statistical report on incidence rates in China.

Causes of vitamin B1 deficiency neuropathy

Subacute vitamin B1 deficiency caused by chronic inadequate thiamine intake or alcoholism is the direct cause of vitamin B1 deficiency.

1, insufficient intake-whole wheat, brown rice, beans, fresh vegetables, meat and animal liver and kidney foods are rich in vitamin B1. Food is the human dimension

Vitamin B1 deficiency neuropathy The main source of biotin B1, the bacteria in the intestine can synthesize a small amount of vitamin B1, but the amount is not enough to meet the needs. Vitamin B1 is not stored in the body for a long time, and the storage amount is not much (about 30 mg). This disease is prone to occur when inadequate intake. Vitamin B1 deficiency often occurs in areas where cereals are a staple food. The reason is that the loss of vitamin B1 is large during the removal of bran and bran; vitamin B1 is a large amount of water-soluble vitamins that can be washed away; vitamin B1 is at high temperatures. It is very easy to destroy, especially in alkaline solution. Adding alkali and discarding rice soup during cooking will also cause serious loss. In addition, appetite loss caused by various reasons can cause insufficient vitamin B1 intake.

2. Increasing demand-children grow vigorously, women are pregnant, and breastfeeding. Physical conditions such as physical exertion and athletes; or diseases with an increased metabolic rate, such as hyperthyroidism, long-term fever, and some chronic wasting diseases, will increase the demand for vitamin B1. Without proper supplementation, it can cause Relatively lacking.

3. Absorption and utilization disorders-Long-term diarrhea or frequent use of laxatives and gastrointestinal obstruction can cause malabsorption.

4. Increased decomposition and excretion-some foods contain factors that can change the structure of vitamin B1 and reduce vitality, such as thiaminase in freshwater fish and shellfish, and heat-resistant factors in plants such as coffee and tea. Therefore, when vitamin B1 is already insufficient, eating too much of this kind of food can easily promote the occurrence of vitamin B1 deficiency. The use of diuretics, peritoneal or hemodialysis may accelerate the excretion of vitamin B1, resulting in vitamin B1 deficiency.

5. Causes of vitamin B1 deficiency caused by alcoholism.

(1) Alcohol metabolism consumes vitamin B1 reserves.

(2) Alcohol affects the absorption of vitamin B1 in the small intestine.

(3) Partial or inadequate eating results in insufficient vitamin B1 intake.

Pathogenesis: It is generally believed that vitamin B1 deficiency will lead to a decrease in thiamine pyrophosphate in the body, which affects the catalytic action of enzymes such as pyruvate dehydrogenase and transketolase.

Alcoholism Use, the glucose metabolism is inhibited, excessive accumulation of pyruvate in the blood, which leads to nervous system poisoning. It is also believed that a deficiency of vitamin B1 will increase the permeability of the cell membrane to Na, thereby causing dysfunction and causing disease. In addition, an increase in pyruvate and lactic acid in the blood can cause high expansion of the arterioles, leading to small bleeding in the central nervous system. Vitamin B1 deficiency neuropathy mainly involves movement, sensory and autonomic nerve fibers in the peripheral nervous system, and is particularly damaged distally. Axonal lesions are the main causes, and secondary myelin sheaths are lost. In severe cases, spinal cord horn cells have different degrees of secondary Nissl body lysis. The muscle showed degenerative neuron degeneration, and the extensor muscles of the wrists, fingers, ankles, and toes were the most severe. In wet patients, the skin and subcutaneous tissues were edema. The right ventricle is enlarged, the myocardium degenerates and the striated muscle disappears and muscle fibers swell. Liver and spleen chronic venous stagnation.

Pathophysiology caused by vitamin B1 deficiency:

The pathological changes of Wernicke encephalopathy mainly damage the 3rd and 4th ventricles and the area around the aqueduct of the brain and the papillary body. Gross specimens showed gray matter in the surrounding ventricles and aqueducts, and a bit of hemorrhage in the thalamus and inferior olive nucleus, so Wernicke was first pathologically called acute superior hemorrhagic policencephalitis. These areas also show hemorrhagic necrosis or softening, which are old injuries.

Under the light microscope, the characteristic changes in the acute phase are increased capillaries and dilatation, and the number of vascular endothelium and adventitia cells increased and thickened. Capillary blood

Rich in Vitamin B1 Fruit Thickening of the tube is particularly significant. Nerve cell degeneration spinal cord fibers are particularly prone to damage. In addition, the anterior hypothalamus and optic cross are also damaged and have severe glial hyperplasia. Advanced pathological changes vary according to the degree of injury and survival time. In the worst cases, the tissue is completely necrotic and can form a capsule cavity. Nerve cells are lost to varying degrees, especially those who surround the papilla, with severe disappearance of myelinated fibers and an increase in reactive microglia, histiocytes, and macrophages. Significant glial hyperplasia in the old damaged area, and heme-containing macrophages can be seen, indicating that there has been bleeding in the past, cerebellar Purkinje cells lost, granulosa cells were sheet-shaped, and astrocytes became thinner and were all found in Anterior (upper) earthworm.

In patients with Korsakoff syndrome, the papillary body can be roughly seen, and severe neuronal loss and glial fibrosis can be seen under the microscope.

Vitamin B1 deficiency neurological symptoms

Clinical manifestation

In clinical practice, people with neurological damage are called "dry" vitamin B1 deficiency neuropathy, and those with edema and heart damage are called "wet"

Vitamin B1 deficiency neuropathy Vitamin B1 deficiency neuropathy. Vitamin B1 deficiency in children is common in infants and can affect the digestive, nervous, and circulatory systems. Clinically, those with neurological symptoms as the "brain type" and those with sudden heart failure are called "brain type". "Heart-shaped". Older children often show edema and polyneuritis as the main manifestations. 1. Vitamin B1 deficiency neuropathy is a multiple-onset disease with early manifestations of fatigue, headache, muscle aches, loss of appetite, nausea and vomiting, and abdominal pain Non-specific symptoms such as diarrhea or constipation, weight loss, and typical symptoms and signs can appear as the disease worsens.

(1) Symptoms of the nervous system: The peripheral nervous system lesions of adults with vitamin B1 deficiency neuropathy are manifested by ascending symmetry of sensory, motor, and reflex dysfunction. The onset usually starts from the distal end of the limb, and is more common in the lower limbs than in the upper limbs. Or a strange feeling, showing a sock-like distribution, gradually progressing to the proximal end of the limb, muscle tenderness. In addition, the allergic area gradually became dull and painful, and the temperature sensation gradually disappeared, accompanied by decreased muscle strength, myalgia (by gastrocnemius muscles), difficulty in ascending and descending stairs, and then the foot, toe sagging, and knee tendon reflexes disappeared or disappeared. Severe upper arm can also be affected.

Younger children first show irritability, and then become unresponsive to surroundings, drowsiness and even coma, sometimes with convulsions. Patients with neuritis show ascending peripheral paralysis, coughing after feeding, and tendon reflexes disappear. Skin sensation may be reduced, but routine examination of cerebrospinal fluid is normal.

(2) Circulatory system symptoms: often in the prodromal or seizure phase of acute heart failure. Adults can develop side-to-side breathing and cyanosis. Examination revealed that the heart rate was accelerated, the heart dullness range was enlarged, and the right heart was enlarged mainly. There was a systolic murmur in the anterior region of the heart. Heart failure can lead to an enlarged liver. Child patients showed signs of sudden crying, cold sweats, cough with shortness of breath, cyanosis, tachycardia, weak heart sounds, enlarged heart, pulmonary edema, and enlarged liver and spleen. Electrocardiogram showed low voltage, low ST segment, flat T wave, two-phase or inverted QT interval. If not rescued in time, severe cases can be fatal.

(3) Edema and serous exudation: Different degrees of edema can occur in different parts. The first severe cases of lower limbs can affect the whole body, and pericardial and pleural effusions can occur.

2. Wernicke's encephalopathy (Wernicke'sencephalopathy WE) patients, symptoms often occur suddenly, manifested as mental and conscious disorders, cerebellar ataxia and eye movement disorders triad. In addition, about half of patients can be accompanied by polyneuropathy. It is also known as the Wernicke quadrilateral sign. Eye movement disorders and ataxia can occur a few days before the onset of mental symptoms.

Vitamin B1 deficiency neuropathy

(1) Mental and conscious disorders: manifested as disorientation, computational difficulties, hallucinations, delusions, restlessness, or depression. Brain Stem Reticulum

Vitamin B1 degrading enzyme in fish Structural involvement, recent forgetfulness and fiction are related to papillary body damage. It is similar to Kosakoff's psychosis due to its fiction and forgetting, and the latter persists after treatment. In addition, there may be symptoms such as unresponsiveness, lack of concentration, headache, insomnia, lethargy, or coma. Kosakoff's mental illness not only creates new learning content memory disorders (antegrade amnesia), but also impairs the memory of past events (retrograde amnesia). Because patients have the most severe near-memory disorders, patients often have time and place disorientation. Patients' memories of distant events are relatively complete. Fiction is a typical manifestation of early prominent. Patients often don't know about memory deficits and they are kept away. (2) Eye movement disorders: There are a variety of eye movement disorders, which are caused by damage to the abductor nerve, oculomotor nerve, and hypothalamus. Abduction dyskinesia is most common. Followed by vertical dyskinesia and gaze paralysis, there may be eyeball floating, pupil shrinkage and abnormal response to light. Patients are often accompanied by horizontal nystagmus, but also vertical nystagmus, drooping eyelids and internucleus ophthalmoplegia, with occasional radial disturbances.

(3) Cerebellar ataxia: caused by damage to the medulla vestibular nucleus and cerebellum, and the cerebellar vermiform part is more severe than the hemisphere. Therefore, the ataxia of the trunk and lower limbs is obvious. There may be spontaneous horizontal or vertical nystagmus, and a few are rotational nystagmus. Language barriers are rare.

(4) Polyneuropathy: manifested as limb weakness and muscle pain. Paresthesia may have parotid dysfunction, and tendon reflexes weaken or disappear. There may be foot droop, wrist droop, and calf muscle atrophy, as well as limb autonomic symptoms, such as sweating in hands and feet, redness, and so on.

Complications include weight loss, hypothermia, hypotension, orthostatic hypotension, abnormal antidiuretic hormone secretion, and other manifestations of chronic alcoholism.

Vitamin B1 deficiency diagnosis of neuropathy

1. Vitamin B1 deficiency neuropathy-It is not difficult to diagnose multiple nerves based on paralysis of motor neurons and peripheral sensory disorders under symmetry of the extremities.

Vitamin B1 rich in tea Disease, if systemic malnutrition and edema are significant, and blood pyruvate levels increase, and the symptoms improve after thiamine supplementation is more conducive to diagnosis. Adults with chronic alcoholism should consider this disease, but should pay attention to the identification of polyneuropathy caused by certain metal poisoning. 2. Wernicke encephalopathy-According to the typical symptoms and signs of drinking history, the diagnosis of serum pyruvate is not difficult. However, autopsy confirmed that only a few patients had a typical triad during their lifetime. That is, the diagnosis is only based on a typical triad, and a considerable amount of WE will be missed. Therefore, when the etiology of WE is accompanied by unexplained neuropsychiatric symptoms, ophthalmia, or ataxia, the disease should be vigilant. may.

Differential diagnosis should pay attention to the identification of polyneuropathy caused by some metal poisoning. The diagnosis of Wernicke encephalopathy should also exclude cerebrovascular disease, brain tumors, multiple sclerosis, and sporadic encephalitis. If diagnosis is difficult, large doses of vitamin B1 can be used for diagnostic treatment.

Vitamin B1 deficiency neurological examination

Laboratory tests 1. Determination of blood vitamin B1 levels-whole blood vitamin B1 levels <40 & micro; g / L suggest deficiency. The level of vitamin B1 in the blood is relatively stable and cannot accurately reflect the level of vitamin B1 in the tissue. It decreases only when the symptoms are significant, so it is rarely used in practice.

2. Determination of gram of creatinine and thiamine excretionVitamin B1 excretion in urine throughout the day is a better indicator to evaluate and diagnose vitamin B1 deficiency. However, it is necessary to collect 24 hours of urine, and the actual operation is difficult. The total amount of vitamin B1 excretion is 40 100 & g; g is the normal measurement of creatinine thiamine excretion, as long as the relative relationship between vitamin B1 and creatinine in fasting urine is measured once B1 (& micro; g) / creatinine (g)] can evaluate the nutritional status of vitamin B1 in the body, which is more accurate and does not need to collect 24h urine, which is more practical in clinical.

3. Determination of erythrocyte transketolase activity (E-TKA)-E-TKA measurement is an effective indicator to evaluate the nutritional status of vitamin B1 in the body, and it can be diagnosed before the clinical symptoms of vitamin B1 deficiency appear. Vitamin B1 is partly present in red blood cells as a coenzyme of transketolase. Deficiency of vitamin B1 results in a decrease in transketolase activity. E-TKA measures transketolase by adding exogenous thiamine pyrophosphate (TPP). Activity, using the percentage of TPP effect as an index to determine the results is more accurate and sensitive.

4, increased blood pyruvate; liver function can be abnormal.

Other auxiliary examinations 1. ECG-When there is a dimension B1 deficiency neuropathic heart disease or alcoholic cardiomyopathy, the ECG may have reduced ST segments or reduced T waves or inverted.

2. B ultrasound-may have chronic liver disease, cirrhosis or fatty liver.

3. Electroencephalography-most of them are diffuse rhythm slowdown, and wave bursts can also occur.

4, evoked potentials-may have somatosensory, auditory and visual evoked potential abnormalities. It shows that the potential between each peak is prolonged, and the higher the condition, the higher the positive. Some patients develop abnormalities early.

5. Imaging-some patients may have changes in cerebral atrophy such as cortical atrophy and ventricular enlargement.

Vitamin B1 deficiency treatment for neuropathy

B1() Vitamin B1 deficiency neuropathy given vitamin B1 (thiamine)

1. Vitamin B1 deficiency neuropathy mainly provides vitamin B1 (thiamine) and other B vitamins to improve the nutritional status of the whole body. Paralyzed limb

Cucumbers are rich in e-vitamin B1 Physical therapy, massage and acupuncture should be used. Pay attention to improving your heart condition.

Wernicke Vitamin B1 deficiency neuropathy Wernicke encephalopathy

(1) Vitamin B1 treatment should be given immediately, 50 to 100 mg intravenously or intramuscularly. Thereafter, 50 mg / d was administered orally or intramuscularly for 3 days. But some people advocate large doses of vitamin B1400 600mg / d, intramuscular injection. Severe patients should be given both niacin and other B vitamins. Most patients disappeared quickly after treatment, followed by improvement of ataxia, but the recovery of psychiatric symptoms was slow, and some patients remained with sequelae and turned to Kosakoff psychosis.

(2) Vitamin B1 is a cofactor for glucose metabolism, so before applying vitamin B1, application of glucose may trigger WE. Therefore, in any person with vitamin B1 deficiency, including patients of unknown cause and coma, 50 to 100 mg of vitamin B1 should be given before intravenous glucose injection, or intramuscular or intravenous injection. Otherwise, the patient may fall into a coma or even cause respiratory heartbeat. .

(3) Corticosteroids can inhibit pyruvate oxidation, therefore, it should not be used in patients with WE. Pay attention to vitamin B1 and other B vitamin supplements, avoid alcoholism, and gradually quit alcohol is necessary to prevent alcoholic WE. In addition, patients often have deficiencies of folic acid, pyridoxine, magnesium nicotinate, calcium, potassium zinc, and phosphate, and multiple vitamins and minerals should be given.

(4) All patients with Kosakoff Psychiatry (KP) should be given vitamin B1 to treat WE that may coexist to prevent the progression of forgetfulness. If KP has sympathetic nerve excitement or anxiety, sweating, and insomnia, it can be treated with -blockers and clonidine (Kronin) to improve symptoms.

Vitamin B1 deficiency prevention for neuropathy

Prognosis Early treatment has a good prognosis. Alcoholics should avoid alcohol. However, KP's mental disorders did not improve after treatment with vitamin B1.

Prevent reasonable diet and alcohol. Should not eat refined white rice food for a long time. Avoid cooking methods that may lose vitamin B1 to ensure adequate vitamin B1 is obtained. Pregnant women and nursing mothers should eat foods rich in vitamin B1. Supplementary foods should be added appropriately to infants who are fed artificially or after weaning.

Vitamin B1 (ie thiamine) deficiency was once clinically called "beriberi", a systemic disease caused by insufficient intake of vitamin B1 in food, which mainly affects the digestive, nervous, and circulatory systems clinically. The incidence of this disease is relatively low, but it still occurs frequently in areas where cereals are the staple food of China.