Fatty degeneration of the vertebrae and methods of its treatment. How to Treat Fatty Bone Marrow Degeneration

Doctors say that the condition of the entire body largely depends on the health of the spine. But a person often does not take care of his musculoskeletal system, subjecting it to heavy loads, leading an inactive lifestyle, and sitting at the computer for a long time. As a result of this, degenerative-dystrophic changes occur in the spine, subsequently causing osteochondrosis.

Fatty degeneration bone marrow The vertebral bodies are called tissue changes, accompanied by the accumulation of a lot of fat in the cells. At the same time, the protoplasm of the cell can be converted into it due to the fact that fat grains get inside it. Such disturbances cause the death of the cell nucleus, and subsequently it dies.

In most cases, fatty degeneration occurs in the liver and blood vessels, but can also occur in other parts of the body. When fat replaces the cartilage of the intervertebral discs, they lose their ability to provide flexibility and springiness to the spine.

Even human bones can be replaced by fat. As a result, the vertebrae become less strong, which adversely affects the health of the spine as a whole. The vertebrae acquire excessive mobility, that is, they become unstable. These pathological abnormalities are clearly visible to doctors when performing magnetic resonance imaging.

Based on the nature of the pathological changes, the forms of degeneration can be different. If the spine is affected by this pathology, then there is a high probability of developing osteochondrosis.

Classification of degenerative-dystrophic changes in the spine

The course of pathology is divided by specialists into several stages, each of which is characterized in its own way. Thus, they highlight next stages dystrophy in the vertebrae:

1. First stage. It shows no changes in the intervertebral disc yet, but upon examination one can already see that there are small tears inside the layers of the fibrous ring.
2. Second stage. At this stage, the outer layers of the annulus fibrosus are still preserved and can prevent the disc from bulging. But the patient already feels pain in the back area, which can radiate to the leg and knee.
3. Third stage. Extensive ruptures of the fibrous ring occur on it, resulting in protrusion intervertebral disc. Painful sensations in lumbar region become even stronger.

Reasons for the development of the disease

The main cause of fatty degeneration is poor nutrition vertebral cells. They are the ones who are most sensitive to the fact that a small amount of oxygen and glucose is supplied and changes occur acid-base balance in blood. All this provokes the development of disc disorders.

Deterioration in performance circulatory system can occur for various reasons, for example, due to anemia, spinal overload and poor nutrition. Deviations can also develop due to age.

Changes can even occur as a result of poisoning with a substance, such as alcohol. Certain infectious pathologies can also cause fatty degeneration.

Treatment methods for fatty degeneration of the bone marrow of the vertebral bodies

Fatty degeneration of the vertebrae is treated with both conservative and surgical method. If the pathology appears due to the aging of the body, then the process cannot be cured, since it is irreversible.

Whenever unpleasant symptoms, processes of inflammation and compression of nerves, experts prescribe the following medications:

• non-steroidal anti-inflammatory drugs aimed at relieving inflammation and relieving pain;
• muscle relaxants to eliminate spasms of muscle tissue;
• blockades with novocaine in the form of injections;
• chondroprotectors that help restore damaged cartilage.

Except medicines patients are prescribed physiotherapeutic procedures, for example, magnetic therapy and electrophoresis. Also great help physiotherapy, but it can only be used during remission. Good methods of treatment are massage and acupuncture.

Surgery is performed only if narrowing is observed spinal canal. In this case, without the help of a doctor, the patient risks losing sensitivity and acquiring paralysis.

Restore bone tissue in in this case is possible only in the first stages of the disease, but basically therapy can only stop the development of the pathological process.

The rhythm of life of a modern person dictates its conditions. The average resident of a large city does not have the opportunity to devote several hours a day to eating: our contemporary is too busy. In order to somehow satisfy the need for food, a person resorts to fast food, small snacks, etc. As you know, “piecemealism” never leads to good things. The lack of a rational and thoughtful diet certainly leads to various diseases of the gastrointestinal tract. The least you can get away with is gastritis, but there are also more serious diseases. One of them is fatty liver hepatosis.

Fatty liver hepatosis is a degenerative disease of the organ with the gradual destruction of hepatocyte cells. Instead of hepatocytes, fat cells - lipocytes - take their place in the liver. Over time, lipocytes are destroyed, liver fibrosis begins, and this is a direct path to cirrhosis and death.

What do you need to know about fatty liver hepatosis so as not to miss the trouble?

Fatty liver hepatosis: causes

In the vast majority of cases, the causes of fatty liver hepatosis lie in the nutritional factor. This means that the disease itself develops due to poor nutrition. However, not always. Among the factors leading to the disease are:

Alcohol abuse. Approximately 80% of all patients with hepatosis are people who do not know the limits of alcohol consumption. The problem of alcoholism is especially common in men, so they are the main patients of the gastroenterologist. In women, hepatosis develops more rapidly and has a worse prognosis, especially against the background of alcoholism.

Drug use and psychoactive substances. This includes not only drugs, but also the notorious energetic drinks, caffeine in general and even tea, due to the tannins it contains (you can drink tea without fear, we are talking about isolated cases).

Another risk group consists of people with poor nutrition. In this case we speak of a deficit normal food. This includes vegetarians and people suffering from anorexia. The body is not designed for such extreme stress. With prolonged poor nutrition, the body begins to think that the “hunger year” has come and it’s time to stock up on fat. This is extremely harmful not only to the liver, but also to the heart.

Disorders of the lungs and heart can lead to hepatosis.

Diseases associated with lipid metabolism disorders in the body. The most important culprit of hepatosis among diseases is diabetes mellitus (especially type 2). It causes both external and internal obesity affecting the organs.

The effects of toxins on the body.

There are many causes of fatty liver disease. Almost always the person himself is to blame for violations of its work.

Fatty liver hepatosis: first symptoms

Liver hepatosis is a silent disease. Often, until the process becomes advanced, a person develops cirrhosis of the liver, nothing is noticeable. However, this is only an appearance. If you listen carefully to your own body, you can notice something that was not observed before. The first symptoms of fatty liver disease include:

Mild pain in the right side under the ribs. This is where the liver is located. At initial stages lesions, hepatocyte cells die. This is accompanied by inflammation and pain. The pain is dull and aching in nature and is almost unnoticeable if hepatitis or cholecystitis is not added in parallel to hepatosis.

Peptic phenomena. Common signs fatty liver hepatosis. Since the liver ceases to function normally, there is a high risk of developing problems from other organs of the gastrointestinal tract: nausea, vomiting, abdominal pain, heartburn, belching. Pain may be observed in the left side, in the center of the abdomen in the epigastric region.

Phenomena of dysbacteriosis. Usually manifested in the form of constipation, diarrhea, or their alternation. The stool takes on a greenish tint.

Dry skin. The skin with hepatosis becomes dry, hot and flabby. If we are talking about the later stages of the disease, then it completely turns yellow from the release of bile into the bloodstream.

Disorders of the sensory organs, in particular decreased vision.

All this - nonspecific signs fatty liver hepatosis. You can put an end to it only after going through a full diagnosis.

Diagnosis of fatty liver hepatosis

At the first suspicion of the development of hepatosis, you should immediately consult a doctor. Gastroenterologists deal with problems with the gastrointestinal tract. On initial appointment The doctor conducts a survey of the patient regarding complaints, their nature and duration. This is how the specialist draws up a diagnostic strategy.

The list of necessary events for staging accurate diagnosis includes:

Ultrasound of the liver. Traditionally, ultrasonography the liver helps to identify its enlargement, and this almost always indicates problems with the organ.

Tomographic research. MRI allows you to evaluate the structure of the liver. If fat is deposited in an organ, this will be visible on an MRI.

Blood chemistry. ALT and AST indicators are assessed. When they increase, we are talking about liver disease.

Biopsy. It doesn't happen that often. Allows you to find out whether fat is present in the structure of the organ.

In most cases, doctors are faced not with hepatosis, but with hepatitis or cholecystitis. However, you cannot diagnose yourself. The doctor will do this. The patient’s task is to clearly and consistently talk about his complaints.

Treatment of fatty liver hepatosis

Treatment of fatty liver hepatosis presents many difficulties. To solve the problem once and for all, an integrated approach is required. Treatment includes a number of important aspects:

Eliminating the root cause of fat deposition in the liver. The most important step, without which the treatment will have no effect. The first thing to do is to identify the root cause. It could be alcoholism, then you cannot do without completely giving up alcohol, at least for the period of treatment, it could be an unhealthy diet, then you should give up fatty, fried and excessively salty foods. At this stage, the main role is played by the patient’s willpower and discipline.

Compliance with nutrition, diet and physical activity. If fat is broken down, it will not be deposited in the liver. But in order for fat to be broken down, effort is required. Firstly, it is necessary to refuse fatty foods and foods rich in “bad” cholesterol. This includes fatty varieties meat, sausages, baked goods, etc. Secondly, it is necessary for the reserves that have penetrated the body to be broken down. Therefore, physical inactivity should be avoided.

Taking medications. The main group of drugs used to treat hepatosis are the so-called hepatoprotectors.

In addition to avoiding factors that cause fatty liver disease and following a specialized diet, it is possible to take hepatoprotectors. Among them, preparations based on silymarin (milk thistle flavonoid) are very trusted. For example, Legalon, an original German preparation containing milk thistle flavonoids (silymarin), which have undergone a special purification and standardization procedure.

Compared to analogues, Legalon has increased content active component. It helps the liver cope with the load, strengthens its structure and prevents destruction by stabilizing cell membranes and additional synthesis of phospholipids. Legalon actively fights toxic substances, preventing their excess from harming the liver and the entire body.

In addition to the protective effect, the hepatoprotector Legalon has a restorative effect and helps reduce inflammatory factors. Also, Legalon is suitable for the prevention of liver dysfunction, since it significantly reduces the load on the organ when taking medications, fatty foods and alcohol. In addition, the drug helps prevent the occurrence of fibrosis and other degenerative changes in the liver.

These medications stop destructive processes in the liver and help restore already dead cells. Antioxidant medications have also proven themselves to be effective in preventing liver cells from dying and being replaced by scar or fatty tissue.

Contrary to popular opinion on the Internet, hepatosis should be treated with herbs with great care. Only milk thistle is suitable. The reason lies in the fact that this disease is often accompanied by cholecystitis: choleretic drugs may cause gallbladder rupture.

Prevention of fatty liver hepatosis

Prevention of fatty liver hepatosis is not difficult. It is enough to follow the following recommendations:

Eat often and in small portions. This way the liver will not be overstrained.

Reduce your consumption of animal fats to a minimum. Complete refusal from them is also unacceptable.

Drink alcohol with caution, and never abuse it.

Maintain at least a minimum level of physical activity: physical inactivity has an extremely negative effect on liver function.

All these tips will help you avoid liver problems in the future.

Fatty liver hepatosis is characterized by high danger due to the risk of degeneration into cirrhosis. To prevent problems, you should rationalize your diet and physical activity regimen. And if trouble does occur, you should urgently consult a doctor for advice. It is much easier to treat hepatosis in the initial stages. This way the patient will help both himself and the doctor.

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Nutrition for fatty liver

One of the factors in the development of fatty liver is sedentary lifestyle life combined with overeating. Therefore, it is very important to monitor your diet and maintain a normal weight. If the patient is obese, then he is recommended to follow a diet (but not strict) with a weight loss of approximately 0.5 kg per week. Moderates welcome physical exercise: exercise on an exercise bike, swimming, walking.

Diet for fatty liver is not just important - it plays a leading role in the effectiveness of treatment for patients. IN medical institutions Usually, dietary table No. 5 is prescribed, with the consumption of protein foods up to 120 g per day, limiting animal fat, as well as a sufficient amount of liver-healthy foods - cottage cheese, cereals (oatmeal, buckwheat, millet, wild rice). Plant foods are welcome - fruits and vegetables, greens, all types of cabbage.

Instead of meat products, it is recommended to eat fish and seafood. It is advisable to avoid fried foods - steam, boil or bake dishes, with minimum quantity butter (it is better to replace it with vegetable oil).

We must not forget about drinking regime: in the absence of contraindications, you should drink at least 2 liters of water per day, mainly in the first half of the day.

It is necessary to limit or exclude fatty dairy products: whole milk, sour cream, cheeses. Low-fat kefir, fermented baked milk, and yogurt are allowed for consumption.

Alcoholic drinks will have to be eliminated completely! In addition to alcohol, carbonated drinks are also prohibited.

It is also recommended to avoid sweets, white pastries, store-bought and fatty sauces, margarine, sausages, fatty meats and lard. Try to eat only natural, fresh foods, with a minimum amount of sugar.

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Causes of fatty liver

Various reasons can lead to fatty liver degeneration: alcohol abuse, improper and inadequate nutrition, and especially protein starvation; endocrine disorders (lesions of the diencephalic-pituitary system, islet apparatus of the pancreas), long-term infections (tuberculosis) and intoxications (phosphorus, chloroform, carbon tetrachloride, etc.), treatment with corticosteroids and antibiotics.

Symptoms and signs of fatty liver

On early stage the disease is asymptomatic; hepatomegaly is possible without noticeable functional abnormalities. The liver is smooth and soft to the touch. In this still reversible period, elimination of the cause leads to normalization of the size of the liver. As the disease progresses, the liver becomes sensitive and dense. Determined high level choline in the blood serum, acetylcholinesterase activity increases. The content of total fats in the blood serum is often increased, and the first stage of the polarographic wave shows a tendency to increase. Emphasize increased sensitivity and vulnerability of the liver during fatty degeneration, a decrease in its glycogen content.

During the terminal period of the disease, severe complications are possible: fat embolism, vascular thrombosis, hemorrhagic diathesis, hepatic coma. There is no convincing evidence that stenosis can lead to cirrhosis in humans.

Diagnosis. One should think about fatty liver degeneration in cases where an enlarged liver of soft consistency is detected, in the absence of noticeable functional disorders, especially when it comes to alcoholics, patients with diabetes mellitus, ulcerative colitis, tuberculosis or nutritional disorders, etc. The pathology of fat metabolism and the presence of fatty degeneration of the liver is indicated by a high level of choline in the blood serum, increased activity acetylcholinesterase, high content total fats and an increased first stage of the polarographic wave. A reliable diagnosis can be made by histological examination of biopsy material from the liver.

Fatty liver degeneration is differentiated from liver prolapse, chronic hepatitis and compensated inactive cirrhosis.

Treatment of fatty liver

First of all, the cause that led to fatty liver should be eliminated. The diet should be rich in animal proteins, vitamins, lipotropic substances with a limited amount of fat. You can prescribe vitamin B6 due to the unconditional dapottropic effect inherent in the drug, as well as choline chloride, lipocaine, folic acid, empirically methionine and choline (the use of the latter in the clinic has been disappointing).

Fatty liver degeneration of non-alcoholic etiology

Fatty liver degeneration of non-alcoholic etiology is called liver damage of varying severity, histologically resembling alcohol impairment liver, but occurs in those who do not abuse alcohol. It includes fatty liver degeneration itself, damage to hepatocytes, necrosis and fibrosis; liver cirrhosis with portal hypertension and other complications, including hepatocellular carcinoma. Life expectancy with fatty liver is lower than in the general population.

In practice, the diagnosis of fatty liver of non-alcoholic etiology is made by exclusion. It should be suspected in a patient with chronic liver damage who does not abuse alcohol, if negative results serological tests for viral hepatitis and the absence of congenital or acquired liver diseases.

Associated diseases and conditions

Fatty liver of non-alcoholic etiology often occurs in type 2 diabetes mellitus, obesity and dyslipoproteinemia, which, in turn, are closely related to the presence metabolic syndrome.

Obesity. It is obesity that most often accompanies fatty liver disease that is not associated with alcohol consumption. The presence of obesity is noted in 40-100% of cases of fatty liver with signs of hepatitis, and fatty liver with signs of hepatitis is detected in 9-36% of obese individuals. In addition, the type of obesity matters.

Hyperlipoproteinemia(hypertriglyceridemia, hypercholesterolemia, or both) is detected in 20-80% of cases of fatty liver with signs of hepatitis.

As a rule, with fatty liver with signs of hepatitis There are several risk factors at once.

In addition, risk factors include female gender, rapid weight loss, acute starvation, small intestinal diverticulosis.

To hereditary diseases in which fatty liver develops, include Wilson's disease, homocystinuria, tyrosinemia, abetalipoproteidemia and hypobetalipoproteidemia, as well as spontaneous Weber-Christian panniculitis.

Fatty liver degeneration (especially with signs of hepatitis) can lead to surgical interventions, for example gastroplasty, jejunoileal anastomosis, biliopancreatic bypass.

Medicines and other substances. Fatty liver disease can be caused by a number of medications and other chemical compounds. These include glucocorticoids, amiodarone, synthetic estrogens, tamoxifen, diethyphene (used in the past cardiovascular drug), isoniazid, methotrexate, perhexiline, tetracycline, puromycin, bleomycin, dichloroethylene, ethionine, hydrazine, hypoglycine A, asparaginase, azacitidine, azauridine, azaserine. Constant contact with petroleum products at work is also a risk factor for fatty liver disease.

Symptoms. Most often, fatty liver disease is asymptomatic; Sometimes patients complain of weakness, malaise, and mild pain.

Physical examination. Almost three quarters of patients have hepatomegaly, and a quarter have splenomegaly.

Laboratory research. In the absence of signs of hepatitis laboratory research uninformative. If they are present, the main change in biochemical indicators of liver function is an increase in the activity of ALT and AST. Usually these abnormalities are discovered during the next medical examination or when visiting a doctor for another reason. There is no clear connection between enzyme activity, on the one hand, and histological parameters and the severity of inflammation or fibrosis, on the other. The activity of ALT is often higher than the activity of AST, which distinguishes fatty liver of non-alcoholic etiology from liver damage due to alcoholism, when the activity of AST is higher than ALT, and the activity of ALP may be slightly increased; Serum bilirubin and albumin levels are usually normal. Prolongation of PV indicates decompensated liver failure. In some patients, a low titer of antinuclear antibodies is determined. However, there are no antimitochondrial antibodies, antibodies to the hepatitis C virus or HBsAg in the blood, and serum levels of ceruloplasmin and α 1 -antitrypsin are within normal limits. Elevated serum ferritin levels and increased transferrin saturation are common. In men, excess iron in the body is more pronounced than in women. In a third of patients with fatty liver degeneration with signs of hepatitis, a homozygous or heterozygous mutation in the HFE gene is detected, leading to the replacement of cysteine ​​at position 282 with tyrosine (a genetic marker of hemochromatosis). Liver fibrosis in the presence of this mutation is usually more severe.

Instrumental studies. To diagnose fatty liver, various non-invasive radiation diagnostic methods are used, including ultrasound abdominal cavity, CT and MRI of the abdomen. None of them are sensitive enough to detect liver inflammation and fibrosis. CT and MRI can detect only extrahepatic manifestations of cirrhosis and portal hypertension. Thus, these methods lack both sensitivity and specificity to confidently diagnose fatty liver with signs of hepatitis and determine its severity.

Liver biopsy- a method that allows you to confirm the diagnosis of fatty liver, with or without signs of hepatitis, to assess the activity of hepatitis and the degree of fibrosis. It is still unclear whether all patients should undergo a biopsy, since the results do not always influence treatment. A biopsy is indicated if patients have metabolic syndrome and if the activity of liver enzymes is constantly elevated, despite proper treatment.

Histological picture In case of fatty liver degeneration, alcoholic and non-alcoholic etiologies are the same. Histologically, there are 3 stages of fatty liver. The first stage is fatty infiltration of hepatocytes without their inflammation and destruction. At the same time, fat accumulates in large drops in hepatocytes. The second stage is fatty infiltration of hepatocytes with signs of necrosis and inflammation. Fatty degeneration can be diffuse, or it can be concentrated in the central zones of the liver lobules. Inflammation of the parenchyma of varying degrees is always observed; the cellular infiltrate consists of neutrophils, macrophages and lymphocytes. Necrosis of hepatocytes with areas of devastation of the parenchyma is possible; Mallory and Councilman bodies may be detected.

In 15-65% of patients, iron deposits are detected in hepatocytes. In case of fatty degeneration with signs of hepatitis, in 35-85% of cases fibrosis is found around individual hepatocytes, around the sinusoids and portal tracts. The degree of fibrosis can vary greatly, from mild fibrosis around small veins and groups of cells to severe, extensive fibrosis. In 7-16% of patients with fatty liver with signs of hepatitis, liver cirrhosis is detected at the first biopsy; histologically it is indistinguishable from portal cirrhosis.

Causes of liver dystrophy of non-alcoholic etiology

The pathogenesis of fatty liver of non-alcoholic etiology is complex; Apparently, not only the liver is involved in it, but also fat, muscle and other tissues. The leading role in the pathogenesis of the disease is played by adipose tissue and insulin resistance. It is known that fats are stored in adipose tissue internal organs. With excess caloric intake of food, the process of normal fat storage is disrupted, which affects the rate of both lipogenesis and lipolysis and leads to an increased supply of free fatty acids from adipose tissue into the blood. This, in turn, promotes the accumulation of fats in the liver and striated muscles. This releases cytokines, which disrupts intracellular signal transmission when insulin binds to receptors and reduces insulin-mediated glucose uptake into muscle. At the same time, utilization is suppressed and glucose production in the liver is stimulated. In addition, the availability of fatty acids in the liver stimulates their esterification and de novo lipogenesis. At the same time, the level of apoprotein B 100l of VLDL increases. All this taken together leads to the accumulation and oxidation of fats in the liver, stimulates free radical oxidation, the release of inflammatory cytokines and the activation of Ito cells.

In general, although the specific mechanisms for the development of inflammation and necrosis of hepatocytes in fatty liver are not entirely clear, they are most likely based on two processes: fatty infiltration of the liver, on the one hand, and free radical oxidation and release pro-inflammatory cytokines, which cause progressive liver damage, on the other. Increasing evidence suggests that a second mechanism in the pathogenesis of fatty liver disease is mediated by adipokines released from adipose tissue.

Adiponectin is an adipokine with anti-inflammatory properties. There is a significant connection between low levels of adiponectin and an increase in the amount of fatty tissue in internal organs, hyperlipoproteinemia and insulin resistance. Another adipokine, leptin, on the contrary, has a pro-inflammatory effect. It promotes liver fibrosis by increasing the expression of transforming growth factor beta and stimulating Ito cell activation. Proinflammatory cytokines produced by the fatty tissue of internal organs also include FIO and IL-6. They play a leading role in the development of insulin resistance because they disrupt intracellular signal transmission when insulin binds to receptors and promote inflammation. In addition, they have a negative effect on the immune system.

Course and prognosis of liver dystrophy of non-alcoholic etiology

The course of the disease depends on the histological picture. If there is no inflammation and destruction of hepatocytes, the disease usually does not progress, but in the presence of signs of hepatitis, approximately 20% of patients develop cirrhosis over time. In the presence of signs of hepatitis, fatty liver degeneration is considered a stable condition in most cases, but in some patients it progresses and leads to severe cirrhosis of the liver. Risk factors for cirrhosis include old age, the presence of metabolic syndrome, obesity, diabetes mellitus, and higher activity of AST than ALT.

There is currently no treatment for fatty liver of non-alcoholic etiology; Available methods are aimed at eliminating factors associated with the development of the disease. Patients are recommended to lose weight and abstain from alcohol, correct hyperglycemia and hyperlipoproteinemia, and discontinue hepatotoxic drugs (glucocorticoids, estrogens, amiodarone, perhexiline). In cases of severe obesity, surgical treatment is indicated. In a number of small short-term studies, ursodeoxycholic acid, vitamin E, gemfibrozil, betaine (a choline metabolite), acetylcysteine, and metformin improved biochemical parameters of liver function and reduced the severity of liver fatty infiltration, but did not have a significant effect on inflammatory activity or fibrosis.

Thiazolidinedione derivatives (pioglitazone and rosiglitazone) increase the sensitivity of fat and muscle tissue to insulin and improve the absorption of glucose by their cells.

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Liver pathology

Symptoms

As a rule, patients with fatty degeneration or hepatosis in the liver do not complain about deteriorating health. The disease has a mild course, but continues to progress slowly. Subsequently, persistent dull pain develops in right side hypochondrium, accompanied by nausea with vomiting and stool disorders.

IN in rare cases fatty liver degeneration of various etiologies develops with pronounced severe symptoms — strong pain in the abdomen, weight loss, jaundice and itching of the skin.

Causes

“> The main reason for damage to the body is the insusceptibility of liver cells to the effects of insulin on them. The main function of this hormone is to transport glucose into cells from tissue fluid and blood. When insulin resistance develops, cells in the liver do not receive vital glucose and die, and are subsequently replaced by useless fatty tissue.

Insulin resistance can develop as a hereditary pathology, and also often occurs due to improper metabolism and can be triggered by improper immune aggression towards the hormone insulin.

To the accompanying factors that have beneficial influence on the development of the disease are: intoxication, high concentration fat in foods and insufficient physical activity.

Treatment

For treatment, patients are advised to take multivitamins and drugs that protect the liver. It is also recommended to ensure sufficient physical activity. Treatment for fatty liver degeneration is usually long-term and takes at least two to three months. Subsequently in mandatory An ultrasound of the peritoneum and a biochemical blood test are performed.

As for nutrition, it should include vegetable oils with the non-vegetables they contain. fatty acids. With the concomitant development of diabetes and obesity, it is necessary to limit the amount of carbohydrates consumed.

Courses of treatment for pathology must be carried out at least twice a year. This disease indicates a metabolic disorder, which provokes the accumulation of excess fat in the cells in the form of droplets.

If the causes of the pathology are not treated in a timely manner, fatty degeneration will lead to the complete loss of damaged organs and ultimately to death. In this regard, you should not ignore the recommendations of a specialist and strictly adhere to the course of treatment.

Pathology of the pancreas

“> Regardless of the location of the lesion, the pathology disrupts the normal functioning of the organ. The same thing happens in the pancreas, where fat cells begin to push out healthy structures and prevent proper operation the remaining ones. Fatty infiltration in the pancreas indicates a disruption of metabolic processes in the human body.

Most often, fatty degeneration of the pancreas occurs in patients with acute or chronic pancreatitis due to alcohol abuse. Usually in such situations this pathology combined with infiltration in the liver. At the same time, in the process of carrying out ultrasound examination The gland practically does not change its size and has smooth contours. Neglect of pathology can lead to serious and unpleasant consequences.

Causes

Often, fatty infiltration in the pancreas develops due to improper treatment or poor nutrition in patients with chronic pancreatitis. Against the background of obesity, all the negative manifestations of the disease intensify several times, since normal functioning is disrupted, healthy tissues are replaced by fat, and the process itself is considered irreversible.

Degeneration does not necessarily develop against the background inflammatory pathology, and the process of inflammation in the pancreas will not always cause degeneration in it. Usually like this pathological changes people with overweight, elderly patients.

Treatment

Degeneration in the pancreas can only be treated conservative ways or through surgical intervention. Conservative treatment is carried out provided that small fat cells are distributed throughout the gland and do not compress its ducts. When fat cells begin to merge into groups, compress the ducts and interfere with the production of secretions, a surgical intervention- namely, removal of lipomatous nodes.

The essence of conservative treatment is to organize the following activities:

• Strict diet with limited fat intake.
• Reducing body weight in the presence of excess fat deposits. According to statistics, most people who suffer from fatty degeneration also suffer from overweight bodies. Therefore, this measure will remove excess fats from the lipid layer in the pancreas.

“> Due to the fact that fatty degeneration is considered an irreversible process, it will no longer be possible to cure the damaged areas of the organ, and the main goal therapeutic treatment What remains is the prevention of subsequent progression of fat cell proliferation. At this stage of treatment, proper nutrition plays an important role, because a correctly chosen diet, which is strictly followed by the patient, helps to avoid surgical intervention in case of progression of the disease process.

Diet is based on rules fractional meals. This is not just the basis of the diet, but an indisputable algorithm for proper nutrition in general. Unfortunately, in the modern world, even such an inalienable norm is becoming an exception.

You need to eat four to five times a day. The nutrition itself is based on diet No. 5, which must be followed by all patients affected by pancreatic pathologies. Patients are required to avoid eating fried foods, smoked and salty foods, sweets, baked goods, alcoholic drinks and chocolate. Doctors recommend cooking all dishes by steaming or in a double boiler. It is especially useful to eat dairy products and cereals.

As for meat, it is better to give preference to lean poultry, but whenever possible replace them with vegetables. It is also useful to drink pre-prepared infusions from medicinal herbs, such as chamomile, mint, St. John's wort, blueberry leaves and cranberries.

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Why does pathology develop?

Most often, the pathology develops after 46-50 years.

Impaired metabolism leads to the fact that the liver cannot secrete the required amount of enzymes to process fats.

As a result, they begin to accumulate in the organ cavity.

Such changes can occur under the influence of the following factors:

1. Eating disorder. Sweets, processed foods and fast foods, preservatives, dyes and other toxins are especially harmful to the liver.
2. Prolonged fasting or, conversely, constant overeating. Starvation diets or an incorrectly composed diet, vegetarianism are the enemies of the liver. They lead to organ obesity.
3. Hereditary factor. If there were relatives in the family with liver diseases, then the person will develop dystrophic pathology in 89%.
4. Uncontrolled and prolonged use of medications.
5. Drinking too much alcohol (alcoholic fatty liver).
6. Drug use.
7. Professional activity involving work at industrial enterprises where they produce different kinds chemicals.
8. Passive lifestyle.
9. Failure of the hormonal system.
10. Neoplasms affecting the pituitary gland.

The mechanism of formation of fatty degeneration is actually very simple. Fats enter the gastrointestinal tract ( gastrointestinal tract) and are susceptible to the process of splitting. If a lot of these components enter the liver, and disposition factors are present, fats undergo synthesis and accumulate in liver cells. The same thing happens under the influence of carbohydrate-containing substances that enter the liver in large quantities.

Fatty degeneration can be classified as follows:

Type I – fatty inclusions are sporadic, they are randomly located in the liver. Clinical manifestations are missing.

Type II – fat molecules are arranged tightly. The person feels worse and experiences pain in the liver area.

Type III – there is a local location of fat capsules, they are located in certain areas of the organ. The symptoms are pronounced.

Type IV - fatty molecules are located almost throughout the liver or occupy one of the lobes. The symptoms are vivid.

Fatty degeneration can also be classified depending on the stage:

I – contained in liver cells a small amount of fat molecules, but they do not affect the functioning of the organ, although the destructive mechanism has already been launched.

II – fat completely fills the cells, they are destroyed, and an inflammatory process can develop around each cell.

III – the processes are irreversible, necrosis develops, in most cases at this stage it is impossible to restore liver function.

How does the disease manifest itself?

Signs of the disease appear already in the second stage:

1. Drawing, aching pain in the liver area, which becomes stronger after eating fatty foods, smoked foods, spicy foods and alcoholic drinks. In this case, the pain can be constant or intermittent.
2. Bitterness in the mouth, belching with a bitter aftertaste.
3. Nausea, almost always ending in vomiting.
4. Flatulence.
5. Enlargement of the liver.
6. A yellow coating appears on the tongue, it is dense.
7. Constipation followed by diarrhea. They are permanent.

Signs of the third stage of damage cause very great discomfort and are expressed in:

• increased irritability;
• sleep disturbance;
• fatigue;
• memory impairment;
• tendency towards depression;
• accumulation large quantity(up to 25 l) free fluid (the stomach becomes very large

Painful sensations in the back are the most common complaint of patients when visiting a traumatologist and orthopedist. Without the necessary treatment, acute diseases of the spine develop into chronic form and can significantly reduce the patient’s quality of life.

The intervertebral disc is located between the vertebral bodies and consists of three structures - the fibrous ring surrounding the intervertebral joint, the nucleus pulposus and two hyaline plates that close the disc and adjacent to the adjacent vertebrae. The fibrinous ring is needed to hold the nucleus in the correct position, because it is a kind of shock absorber spinal column when walking, jumping, bending, turning.

Intervertebral discs make up almost a third of the entire spinal column. The gelatinous nuclei contained within it are very hydrophilic (they love water), they need it for elasticity and resilience, thanks to which they can serve as a shock absorber.

How does vertebral degeneration develop?

When the spinal column is malnourished, various degenerative diseases develop and lead to a decrease in height intervertebral disc and movement disorders in the spine. Gradually, surrounding structures - joints, muscles, ligaments - are also involved in the process. A major role in the pathological process is played by fatty degeneration of the vertebrae, or rather the yellow ligaments that hold the spine. As a result, the spinal canal that runs inside the vertebrae begins to narrow. It is this stenosis (narrowing) that causes back pain.

Due to the fact that the vertebrae do not have their own innervation and blood supply system (it is present only in the outer plates of the fibrous ring), and also due to the fact that during life the greatest pressure is exerted on the spinal column, degenerative processes in it begin much earlier than in other large joints.

This fact is also associated with the fairly young age of the majority of patients; this process gradually intensifies and leads to the fact that by the age of 60–70, more than half of the population has vertebral degeneration to one degree or another. The gradual erasure of the border between the fibrous ring and the nucleus leads to a decrease in the height of the spine and infringement of the inner part of the intervertebral disc - the nucleus pulposus.

Besides, age-related changes occur in blood vessels, due to which delivery deteriorates necessary substances(protein glycans) to the internal structures of the ligamentous apparatus of the spine. A complex of factors - deterioration of trophism and compression of the vertebrae, leads to the formation of cracks in the nucleus pulposus, it loses moisture and its elastic properties decrease. In addition, prolapse (protrusion) of the disc occurs in spinal canal. This is how degeneration of the intervertebral discs develops, and now the vertebrae are not sufficiently cushioned, any careless, and sudden movements may cause pain.

However, the process is not limited to spinal disc degeneration. A decrease in the height of the spinal column contributes to the involvement of neighboring formations in the process - ligaments, facet joints, this leads to their overstrain and increased removal of calcium from them and the development of osteoporosis. Naturally, the yellow ligaments, which fill the spaces between the vertebrae and are attached to the vertebral arches, weaken, because the spine has become shorter. The yellow ligaments, or as they are also called fatty ligaments, lose their elasticity, thicken and wrinkle. Due to the fact that serious pathological processes occur in the yellow (fatty) ligaments, the disease is called fatty degeneration of the spine.

As a result of long-term studies, it has been proven that protrusion of the disc into the intervertebral canal is not always the only cause of pain. The spinal cord, which is represented by the roots of the spinal nerves, passes through the spinal canal. When there is a protrusion at any level of the intervertebral disc, compression of the root occurs and the appearance of pain is quite logical. However, scientists have found that pain also appears due to “sterile” autoimmune inflammation of the root. The source of inflammation is a crushed vertebral disc that is in contact with the root.

The main reason for the degeneration of intervertebral discs is the deterioration of the nutrition of their cells - they are more sensitive to a decrease in the amount of oxygen, glucose and changes in the acid-base balance in the blood. This in turn initiates degenerative processes in the disc.

What causes eating disorders? There are a lot of reasons, this includes, in addition to metabolic changes, various blood diseases, for example, anemia, also atherosclerotic changes, insufficient or excessive loads on the spine, and unhealthy diet.

Classification of degenerative-dystrophic changes in the spine

Degenerative-dystrophic changes in the vertebrae occur in several stages.

Thus, at stage 0, disturbances in the disc are not yet registered, but at the first stage it is already possible to see small gaps in the disc during the study. inner layers fibrous ring.

During the transition to the second stage, the outer layers of the fibrous ring are still preserved (which still prevents the protrusion of the disc into the intervertebral canal), however, back pain appears, which can radiate to the lower limb and knee joint.

The third stage is characterized by extensive ruptures of the fibrous ring along the entire perimeter, as a result of which the disc prolapses into the spinal canal, and lumbar pain intensifies. A tear of the longitudinal ligament is visible.

Treatment of pain caused by vertebral degeneration

To relieve pain, surgical and conservative methods. They are aimed at alleviating the patient’s condition, and therefore can only be considered palliative.

1. Bed rest for the period of the most intense pain. Getting up late aggravates the situation and leads to less recovery of the spine;
2. Non-steroidal anti-inflammatory drugs - ibuprofen, diclofenac, piroxicam, indomethacin, naproxen, ibuprol, nimesulide, diclofenac patch;
3. Muscle relaxants - baclofen, tizanidine, cyclobenzaprine, tolperisone, methocarbamol;
4. Local anesthesia - novocaine blockades are most often used;
5. Chondroprotectors - chondroitin sulfate, glycosamine sulfate and diacerein.
6. Physical therapy - dosed load on the spine, special strength exercises, warming up, electrical stimulation. Often, the complex of these effects has a more significant result than long-term pharmacological treatment.
7. A specially selected set of exercises, massotherapy, in some cases manual therapy.

As for the surgical treatment of this pathology, the attitude towards it in most leading countries of the world is rather restrained; it is used only for a small percentage of patients.

Among the surgical treatment methods that can be used:

• Discectomy with arthrodesis;
• Intradiscal injection of steroids;
• Intradiscal decompression;
• Laser therapy.

In recent years, widespread minimally invasive methods Treatments: electrothermal plasty of the fibrous ring, laser disc decompression, percutaneous endoscopic disc removal. Methods for replacing the nucleus pulposus with restoring the integrity of the fibrous disc have also begun to be used.

Bone marrow occupies approximately 5% of the total body mass and plays active role in hemapoiesis (blood formation). Bone marrow consists mainly of stem cells (all types of cellular elements of the blood), surrounding supporting cells - macrophages, adipocytes and large number others involved in nutrition, proliferation (growth) and differentiation of stem cells. Red bone marrow contains about 40% fat, yellow bone marrow contains up to 80%. This feature helps in identifying various pathologies associated with changes in this ratio during MRI of the spine.

T1-weighted MRI is most sensitive to adipose tissue. They are the basis of the MRI protocol. In addition, T2-weighted MRI with fat suppression is used. Below we will focus on the main pathologies that appear on MRI of the spine, such as bone marrow pathology in the first place.

• Hemangioma, single or multiple, accounts for 10-12% of changes in the vertebrae. It refers to vascular anomalies and has characteristic features on MRI of the spine - round or trabecular, light on T1-weighted and T2-weighted MRI, does not change MRI with signal suppression techniques from fat.
• Local fat deposits appear with age and are a variant of the norm. Fatty deposits are also observed in osteochondrosis along the endplates (fatty degeneration, or Modic type 2). They are bright on T1-weighted MRIs of the spine and become dark on fat-suppressed MRIs. Sometimes there are mixed variants of bone marrow changes in osteochondrosis, which are not completely suppressed when using the STIR MRI sequence.
• Paget's disease is a metabolic disorder and is observed in 1-3% of people over 40 years of age. Damage to the vertebrae ranks second after the pelvic bones. In diagnosing Paget's disease, identifying lytic foci in the bones of the skull is very helpful. Paget's disease goes through 3 stages - lytic, mixed and blastic. In accordance with these stages, MRI of the spine shows different picture. In the lytic stage, the lesion signal is bright on T2-weighted MRI and low on T1-weighted MRI, then becomes hypointense on both types of MRI as sclerosis and fibrosis increase. MRI of the spine also reveals other character traits Paget's disease - thickening of the cortical plates of the vertebral bodies, fatty degeneration on late stage and during successful treatment.

MRI of the spine. T1-weighted sagittal MRI of the lumbosacral region. Replacement of sacral bone marrow with fat in Paget's disease.

• Lipoma refers to benign tumors of adipose tissue. They make up about 1% of all primary bone tumors and no more than 4% of them are localized in the vertebrae. On MRI of the spine, lipomas are difficult to distinguish from fat deposits, however, they are more clearly defined and may undergo internal necrosis and calcification
• hemorrhages in the vertebrae occur with injuries. MRI of the spine reveals characteristic blood dynamics depending on the duration of the hemorrhage.
• The consequences of radiation therapy are reduced to replacing red bone marrow with yellow one. When the absorbed dose exceeds 36 Gy, this process becomes irreversible. MRI of the spine shows diffuse signal enhancement on T1-weighted MRIs with a clear border corresponding to the irradiation field. After radiation therapy and chemotherapy, myelofibrosis - bone marrow replacement - can also develop fibrous tissue. In MRI of the spine, the signal is very low on both T1-weighted and T2-weighted MRIs.

MRI of the spine. T1-weighted sagittal MRI of the thoracic region. Fatty bone marrow degeneration after radiation therapy.

• Osteoporosis leads to a decrease in cellular composition bone marrow and increased fat. MRI of the spine often shows diffuse increased signal from the vertebral bodies on T1-weighted MRI. There are also focal changes that require differential diagnosis with hemangiomas using MRI of the spine. MRI diagnostics for osteoporosis is also presented in a separate article.
• Spondyloarthropathy on MRI of the spine often manifests as “glowing” angles on T2-weighted MRI. This is especially true for the acute stage of ankylosing spondylitis. The change from the acute phase to the chronic phase leads to the transformation of the inflammatory reaction into a depot of adipose tissue, which is light on T1-weighted MRI. MRI of the spine with various diseases related to the group of spondyloarthropathies, a special article on our other website is devoted.
• Anorexia is accompanied by various changes in the body, including osteoporosis and decreased signal intensity on T1-weighted MRI, as well as bone marrow edema, which is referred to as “gelatinous transformation.” On T2-weighted MRI (especially fat-suppressed MRI), there is a slight diffuse increase in signal from the vertebrae. MRI of the spine with contrast shows amorphous signal enhancement.

MRI of the spine. T2-weighted sagittal MRI. Gelatinous transformation due to malnutrition.

• Hemosiderosis is a phenomenon observed in hemolytic anemia. MRI of the spine shows low signal in the bone marrow. In differential diagnosis, it is important that the liver and spleen acquire the same low signal.
• Gaucher disease is an autosomal recessive hereditary disease classified as sphingolipidosis and manifests itself in the accumulation of glucocerebrosides in histiocytes. The diagnosis is made based on puncture of the spleen and detection of specific cells. On MRI of the spine, red bone marrow is replaced by Gaucher cells, which are hypointense on T1- and T2-weighted MRI. In addition, bone infarcts are often observed on MRI of the spine.

MRI of the spine. T1-weighted MRI of the thoracic spine. Gaucher's disease.

• Myeloproliferative and myelodysplastic syndromes, which include chronic myeloid leukemia and others chronic leukemia, polycythemia, mastocytosis, essential thrombocytopenia on MRI of the spine manifest as a uniformly reduced signal on T1-weighted MRI. On T2-weighted MRIs of the spine, a “reverse” brightness of the intervertebral discs is often observed; they become lighter than the vertebral bodies. MRI of the brain for tumors of the hematopoietic system can also reveal its damage.

MRI of the spine. T2-weighted sagittal MRI of the cervical spine. Chronic myeloid leukemia.

• Sarcoidosis affects the bone marrow in 1-3% of cases. Damage to the brain and spinal cord is much more common in sarcoidosis. MRI of the spine reveals sclerotic foci that closely resemble metastases, often multiple. The lesions can be mixed lytic with sclerotic rims. MRI of the spine with contrast may show increased signal from lesions.
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Fatty degeneration of the bone marrow is a natural age-related process, which is characterized by the replacement of hematopoietic tissue with adipose tissue. Bone marrow degeneration can be caused by both pathological and physiological reasons. Treatment methods depend on the causative disease and the patient's health status. Symptoms are nonspecific, and sometimes the disorder is asymptomatic. The prognosis depends on the degree of fatty tissue degeneration, the patient’s age and concomitant diseases.

Age-related degeneration of yellow bone marrow increases the likelihood of developing spinal osteochondrosis

Bone marrow is a spongy red substance that is located in the inside of the bones. It plays an important role in the formation bone tissue. It contains multipotent stem cells. They form white blood, red blood cells and platelets.

Yellow bone marrow is composed primarily of fat cells (hence the color), which increase in content as each person ages. Red bone marrow is the site of formation of cellular components of blood. In a child, bone marrow fills all the bones. Over time, red bone marrow turns yellow. In adults, red is found only in flat bones: sternum, vertebral bodies, ribs, cranial bones, pelvic bones. In case of anemia, yellow bone marrow can be replaced with red bone marrow.

The prevalence of early fatty degeneration caused by hypoplastic or aplastic anemia is low in the United States and Europe: 2–6 cases per million people. Much more often, fatty degeneration of the bone marrow occurs as a result of acute myelogenous leukemia and multiple myeloma: 27-35 cases per 1,000,000 people. The incidence of myelodysplasia has increased from 143 cases reported in 1973 to 15,000 cases annually in the United States.

In Japan and the Far East, the incidence of fatty bone marrow degeneration is at least 3 times higher than in the United States and Europe. Mexico and Latin America also have high performance morbidity, which are explained by the liberal use of chloramphenicol. Factors environment and widespread use of insecticides have been seen as causes of this disease. The incidence of myelodysplasia is estimated to be approximately 4-5 cases per 100,000 people per year in Germany and Sweden.

IN international classification diseases of the 10th revision (ICD-10), fatty degeneration in the bone marrow is indicated by code M42.

Symptoms

Age-related degeneration of yellow bone marrow increases the likelihood of developing osteochondrosis (dystrophy) of the vertebral bodies (in the spinal region). In most cases pathological process is asymptomatic or manifests minor symptoms. Symptoms depend on the rate of lipoid bone marrow degeneration and the underlying disease.

Causes

Deficiency of folic acid in the body leads to fatty degeneration of the bone marrow

Degenerative bone marrow diseases can be inherited or acquired during life.

Main reasons:

• Decreased concentration or damage to hematopoietic stem cells, leading to hypoplastic or aplastic anemia.
• Deficiency of folic acid or vitamin B12.
• Myelodysplasia.

Damage to hematopoietic stem cells can be caused by congenital or acquired disorders. The main mechanisms of stem cell destruction:

• Acquired damage to stem cells is caused by viruses, toxins or chemicals (chloramphenicol, insecticides), which leads to quantitative or qualitative change cellular composition.
• Abnormal humoral or cellular control of hematopoiesis.
• Antibody, T cell, or lymphokine-mediated suppression of hematopoiesis.
• Mutations in genes that accelerate fatty degeneration of the bone marrow. The identification of these mutations has led to progress in determining the precise functions of the corresponding proteins in normal cells
• Hereditary syndromes.

Hereditary syndromes that accelerate bone marrow degeneration:

• Fanconi anemia.
• Congenital dyskeratosis.
• Shwachman-Diamond syndrome.
• Diamond-Blackfan anemia.
• Amegakaryocytic thrombocytopenia.
• Congenital neutropenia.

Constitutional aplastic anemia is associated with chronic bone marrow failure, congenital anomalies, familial morbidity, or thrombocytopenia at birth.

Red bone marrow aplasia may be a consequence of thymoma. Sometimes it occurs as a result viral infection. Bone marrow aplasia can also be permanent, for example as a result of viral hepatitis. In rare cases, aplasia is caused malignant neoplasms lymphoid tissue or collagen vascular diseases(for example, systemic lupus erythematosus).

Decreased concentrations of all 3 types of blood cells are the most common manifestation of a bone marrow disorder. Aplastic or hypoplastic anemia can develop due to secondary causes. Myelodysplastic may also reduce all types of blood cells.

Dangerous complications

Severe bone marrow degeneration requires rapid initiation of therapy - early search for donors for bone marrow transplantation

The morbidity and mortality from fatty bone marrow degeneration is caused by low levels of mature blood cells. Severe anemia can cause heart failure and fatigue. Neutropenia can predispose people to bacterial and fungal infections. A decrease in platelet count can increase the risk of severe bleeding.

The severity and extent of fatty degeneration determine the prognosis. Severe multiple bone marrow degeneration is an emergency medical situation, requiring a quick start of therapy - an early search for donors for bone marrow transplantation.

Long-term transfusion of donor red cells increases total load per patient. Elevated iron levels are toxic to various organs, including the heart. High dosages can cause arrhythmia, diabetes mellitus and cirrhosis of the liver. Iron can also produce a bronze coloration in people with soft skin. Therefore, it is necessary to measure the patient's reserves of the element (in the form of ferritin).

The introduction of a chelating agent is effective method removing excess iron. Chelating agents are made up of molecules that bind tightly to free iron and remove it.

Monitoring serum ferritin levels and measuring total urinary excretion may determine the effectiveness of therapy. Most bone marrow tissue damage can be reversed with timely treatment.

Diagnostics

First, a physical examination is performed and a medical history is taken. The doctor then orders blood tests that show the quality and quantitative composition blood. Red blood cells are morphologically normal in tests. The reticulocyte count is usually less than 1%, indicating a lack of red blood cell production. Sometimes the average cell volume increases.

The platelet count is lower than usual, and sometimes there is a severe decrease in platelet count. The platelet size is normal, but low platelet levels can lead to bleeding.

There is a decrease in all granular leukocytes, including neutrophils, eosinophils and basophils, as well as a decrease in monocytes. Sometimes relative lymphocytosis occurs. Folic acid, vitamin B12 and serum erythropoietin levels are usually elevated in fatty bone marrow degeneration.

Fanconi anemia should be considered in all young adults and children with hypoplastic or aplastic anemia, unexplained macrocytosis, myelodysplastic syndrome, acute myeloid leukemia, or cutaneous malignancies.

Bone marrow tests help confirm the diagnosis. Pure red cell aplasia characteristically affects red blood cell progenitor cells; amegakaryocytic thrombocytopenia is confirmed by the absence of megakaryocytes. Detection of bone marrow hypoplasia distinguishes aplastic anemia from aleukemic leukemia.

Classification

To assess changes in the bone marrow of the vertebral bodies using magnetic resonance imaging, the Modic classification is used:

• Type I: areas of low magnetic resonance signal intensity on T1-weighted images and high-intensity areas on T2-weighted images. Patients experience bone marrow changes due to inflammation and swelling.
• Type II: high signal intensity on T1- and T2-weighted images due to fatty degeneration of the bone marrow.
• Type III: low signal intensity on T1- and T2-weighted images. Sclerotic changes are visible in the spongy substance of the vertebral bodies.

Treatment

The choice of treatment method (conservative or surgical) depends on many factors - technical capabilities, age and health status of the patient, prognosis for the success of a specific method of therapy

Infections leading to neutropenia should be treated as an emergency medical conditions. After taking blood and other biological materials broad-spectrum antibiotics are prescribed. The choice of antibiotic may be changed later, depending on the results of the microbiological analysis.

Sepsis, pneumonia, infections urinary tract and cellulite are common complications of neutropenia.

Patients with severe aplastic anemia who receive antithymocyte or antilymphocyte globulin have a 1-year survival rate of 55%. Androgen supplementation increases treatment response rates to 70%, with a 1-year survival rate of 76%. Although their mechanism of action is unknown, antithymocyte or antilymphocyte globulin should be given with corticosteroids to prevent serum sickness.

Forecast

The prognosis of bone marrow degeneration depends on the underlying disease. Most inherited syndromes, such as Fanconi anemia, can develop into leukemia after a few years. Acquired idiopathic aplastic anemia is usually a permanent and life-threatening blood disorder. Half of patients die within the first 6 months.

If fatty degeneration of the bone marrow is caused by harmless causes - aging - the prognosis is favorable and life expectancy does not decrease.