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FNO blockers. Tumor necrosis factor: drugs

Drugs that are not tumor necrosis factor (TNF) inhibitors are more effective in treating patients with rheumatoid arthritis who do not respond to anti-TNF drugs, according to a clinical study published in the Journal of the American Medical Association.

Anti-TNF drugs are used worldwide to treat rheumatoid arthritis. They deactivate TNF, molecules produced by immune system and causing inflammation. However, about a third of patients do not respond to this type of therapy.

The study involved 300 patients with rheumatoid arthritis who had an insufficient response to anti-TNF drugs.

All participants were divided into two groups. In the first group, patients received anti-TNF drugs such as adalimumab, etanercept, certolizumab, and infliximab for 52 weeks. In the second group, patients took non-TNF drugs such as tocilizumab, rituximab, and abatacept.

The results of the study showed that 54% of patients who took anti-TNF drugs and 69% of participants who took non-TNF drugs had a moderate response to treatment.

In addition, more patients taking non-TNF drugs had low levels of disease activity at 24 and 52 weeks of the study.

The researchers concluded that patients with rheumatoid arthritis who have not responded to anti-TNF drugs may benefit from non-TNF drugs.

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Drugs for the treatment of polyarthritis: a review of drugs

Polyarthritis is a type of arthritis that affects not one, but several joints at once. In this condition, the diagnosis is extremely difficult, and the treatment of an already diagnosed disease is no less problematic.

This is due to the fact that the symptoms typical of polyarthritis are also inherent in many other joint diseases. Therefore, doctors often make mistakes when diagnosing.

Symptoms characteristic of polyarthritis

Arthritis of any origin is characterized by a large number of common symptoms. The main ones are:

Pain in the joints.
Joint deformity.
impaired mobility.
Temperature jumps.
Swelling at the site of injury.
Change in the color of the periarticular skin.

Arthritis pain can be of different intensity and character. It can then practically disappear, then suddenly become unbearable. Patients usually experience the most severe pain at night and in the morning.

Limitation of mobility in the joints may be the result of excruciating pain (the patient is once again afraid to move his limb or fingers) or degeneration changes in the articular tissues.

With minor lesions of the cartilage, the patient remains able-bodied, mobility is limited only slightly. In severe forms of polyarthritis, the functionality of the affected limb may be completely lost, and the person becomes disabled.

Acute inflammation (reactive arthritis) is treatable. Chronic diseases (rheumatoid arthritis) remain with the patient until the end of life.

Causes of polyarthritis

There are several main causes of polyarthritis:

violation of metabolic processes in the body;
infectious diseases such as viral hepatitis, dysentery, gonorrhea;
various joint injuries;
the presence in the body of autoimmune and allergic processes.

The structure of the synovial membrane includes many blood vessels and nerve endings, which instantly react to both internal and external stimuli with inflammation.

If an infection enters the joint through the blood, the patient may develop severe purulent inflammation joints - a pathology provoked by the waste products of various microorganisms.

Some forms of polyarthritis result from the deposition of salts in the tissues of the joints that injure the articular membrane. Salt crystallization is a consequence of the adverse effects of the environment, a malfunction in the body's immune system, and a genetic predisposition. A striking example of such a disease is gout on the legs, especially its severe form, when more than one joint is affected, but several.

Diagnosis and treatment of this disease is difficult due to its nature. Gout can be triggered by several factors, and its symptoms may be evidence of the development of other equally serious diseases in the patient's body.

Unfortunately, polyarthritis affects people, regardless of age and gender.

Treatment of polyarthritis

Treatment of polyarthritis is based on the appointment of symptomatic medications. In this regard, non-steroidal anti-inflammatory drugs are ideal. Such a medicine for polyarthritis exists in different forms (tablets, injections, liniments, powders).

Non-steroidal anti-inflammatory drugs directly affect the focus of inflammation. This action is due to the inhibition of prostaglandins (substances that provoke inflammation). NSAIDs are no less effective in relieving pain.

The advantage of NSAIDs is that they act quickly and gently. Non-steroidal drugs cause fewer side effects than other stronger, but very toxic drugs, which are also prescribed for polyarthritis.

Here is a small list of these medicines:

Roxicam.
Brufen.
Ortofen.
Flugalin.

However, NSAIDs also have significant side effects that must be taken into account when prescribing treatment. Drugs of the non-steroidal group are contraindicated in numerous diseases of the gastrointestinal tract, for example, with a stomach or duodenal ulcer.

Treatment of polyarthritis involves the appointment of corticosteroid drugs, which, by suppressing the body's immune response, relieve the inflammatory process. This action makes corticosteroids indispensable in the treatment of autoimmune arthritis caused, for example, by systemic lupus. When this diagnosis is confirmed, drugs of the corticosteroid group are prescribed first.

To prevent the development of steroid-induced osteoporosis, doctors recommend that their patients take bisphosphonates. These drugs are an excellent prophylaxis for bone loss.

In addition to corticosteroids and NSAIDs, DMARDs (basic antirheumatic drugs) are prescribed for polyarthritis. With the help of these medicines, it is possible to modify the course of many pathologies that provoke the occurrence of polyarthritis.

As a rule, DMARDs are prescribed in combination with NSAIDs and corticosteroids. This is due to the fact that the effect of DMARDs begins to be felt only two months after the treatment was started, although the therapeutic mechanism of these drugs is also based on the suppression of the body's immune response, as is the case with corticosteroids.

Treatment of polyarthritis is not complete without the drug Methotrexate. This drug has found wide application in chemotherapeutic procedures in cancer patients. However, for the treatment of joint diseases, a much lower dose is required.

Unfortunately, Methotrexate has a serious side effect in the form of liver dysfunction, so patients need to regularly donate blood for analysis.

Patients suffering from polyarthritis are also prescribed other DMARDs: Sulfasalazine and Hydroxychloroquine. Both of these drugs are antimalarial drugs, but they are also effective for arthritis. Medicines can cause side effects on the part of the organs of vision, although this phenomenon is extremely rare.

Dead tissue in polyarthritis provokes the development of various inflammations. In such situations, doctors prescribe anti-TNF to their patients. These are drugs that destroy tumor necrosis factor.

Here is a small list of the most sought after anti-TNF:

Infliximab.
Adalimumab.
Etanercept.

Anti-TNF drugs are administered subcutaneously or intravenously.

Anti-TNF is also not entirely harmless. Treatment with them can provoke chills, fever, dizziness and headache, soreness in the muscles and joints, increased susceptibility to infections.

Non-drug therapy

Treatment of polyarthritis folk remedies acceptable, but it must be agreed with the rheumatologist. This precaution is due to the fact that many folk recipes cause a number of side effects that can radically aggravate the situation.

Physiotherapy plays an important role in the treatment of multiple joint diseases. With the help of physiotherapy procedures, the patient can be relieved of pain, swelling and swelling. Such activities include:

Paraffin treatment.
ultrasonic waves.
Ozokeritotherapy.
Cryotherapy.
Magnetotherapy.

All of the above types of physiotherapy help normalize metabolism, help restore blood flow to diseased joints, and inhibit the process of reducing bone tissue.

Since it is impossible to completely defeat polyarthritis, its treatment becomes continuous. Only thanks to constant maintenance therapy, the patient can maintain natural activity, high quality of life and good health in general for a long time, which can be found in the video in this article.

Suppression of TNF activity leads to a decrease in the synthesis of inflammatory mediators in the body, due to which the necessary therapeutic effect in the treatment of the disease is achieved.

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tumor necrosis factor

Tumor necrosis factor (TNF): determination of TNF; TNF value; treatment with anti-TNF drugs; payback security for higher efficiency

TNF is synthesized by activated macrophages and has cytotoxic, immunomodulatory, and anti-inflammatory effects.
TNF is involved in antiviral, antitumor and transplantation immunity.
In relation to some tumors, TNF has a cytostatic and cytolytic effect.
TNF stimulates macrophages.
At high concentrations, TNF can damage endothelial cells and increase microvascular permeability, causing activation of the hemostasis and complement system, followed by neutrophil accumulation and intravascular microthrombosis (DIC).
The action of TNF extends to lipid metabolism, coagulation, insulin sensitivity and endothelial health, as well as a number of other functions.
TNF inhibits the growth of tumor cells and regulates a number of metabolic processes, as well as the activity of the immune response to infectious agents, which prevents the uncontrolled use of anti-TNF drugs and raises questions about their safety.

What are the mechanisms of antitumor action of TNF:

TNF has a targeted effect on a malignant cell through TNF receptors, provoking programmed cell death or suppressing the process of division; also stimulates the production of antigens in the affected cell;
stimulates "hemorrhagic" tumor necrosis (death of cancer cells).
blocking angiogenesis - suppression of the process of growth of tumor vessels, damage to tumor vessels without harming healthy vessels.

Features of the antitumor effect of TNF:

TNF does not act on all tumor cells; Cytotoxically resistant cells themselves produce endogenous TNF and active nuclear transcription factor NF-kB.
a number of cells show a dose-dependent effect of TNF, the combined use of cytokines TNF and IFN-gamma in many cases gives a much more pronounced effect than when treated with one of these drugs;
TNF acts on tumor cells that are resistant to chemotherapy, and TNF-based therapy in combination with chemotherapy can effectively kill the affected cells.

primary and secondary immunodeficiencies;
AIDS;
severe viral infections;
severe burns, injuries;
treatment with cytostatics, immunosuppressants, corticosteroids.

DIC;
sepsis;
infectious diseases;
allergic and autoimmune diseases;
crisis of rejection of donor organs in recipients;
oncological diseases.

Instrument - Microlab Star ELISA.

Norm: up to 87 pkg / ml

Reference values: 0 - 8.21 pg/ml.

Sepsis (the content may be of a phase nature - an increase at the beginning and a decrease with a pronounced prolonged infection due to the depletion of protective mechanisms).
Septic shock.
DIC syndrome.
Allergic diseases.
The initial period in HIV-infected.
Obesity.
In the acute period of various infections.

Severe and persistent viral infections.
Oncological diseases.
AIDS.
Secondary immunodeficiency states.
Injuries, burns (severe).
Myocarditis.
Taking drugs: immunosuppressants, cytostatics, corticosteroids.

How important are the functions of TNF in the human body?

The following mechanisms of influence of TNF are distinguished:

Cytotoxic effect on both tumor cells and cells affected by viruses.
Stimulates the education of others active substances- leukotrienes, prostaglandins, thromboxane.
It has an immunomodulatory and anti-inflammatory effect (with the activation of macrophages and neutrophils).
Increased membrane permeability.
Increased insulin resistance (an effect leading to the development of hyperglycemia, possibly due to inhibition of the activity of insulin receptor tyrosine kinase, as well as stimulation of lipolysis and an increase in the concentration of free fatty acids).
Damage to the vascular endothelium and increased capillary permeability.
Activation of the hemostasis system.

In-Depth Research immune status in case of severe course of acute, chronic, infectious and autoimmune diseases.
Oncology.
Severe mechanical injuries and burns.
Atherosclerotic lesions of the vessels of the brain and heart.
Rheumatoid arthritis and collagenoses.
Chronic pathology of the lungs.

Inflammatory CD4 T cell activity

Under the conditions of interaction of macrophages with inflammatory T-cells, a more efficient fusion of phagosomes, which captured bacteria, with lysosomes, the custodians of proteolytic enzymes that destroy intracellular pathogens, is observed. The process of phagocytosis is accompanied by the so-called oxygen explosion - the formation of oxygen radicals and nitric oxide, which have bactericidal activity.

Anti-TNF therapy should not be prescribed to debilitated patients, as well as to those who have previously had an infectious disease, because. in both cases, they are at high risk of infection.

Reviews

I would like to see the bibliography

They will not present literature to you. Controversial. Not proven. Experiments.

I underwent a course of treatment with Dr. Ognevoy for psoriasis. By the way, it is quite effective. And now she is forcing the TNF to give up !! Can someone explain why and what he shows with psoriasis. Although the rate has dropped. TNF twice!! And the skin is clean

Where can you buy this drug?

where can i buy tumor necrosis factor

HYBRID POLYPEPTIDE WITH ACTIVITY α1-THYMOSIN-α-TUMORS NECROSIS FACTOR-THYMOSIN a1, METHOD FOR OBTAINING HYBRID POLYPEPTIDE WITH ACTIVITY α1-THYMOSIN- α-TUMORSNECROSIS FACTOR-THYMOSIN a1 , RECOMBINANT PLASMID DNA pThy EXPRESSING A HYBRID POLYPEPTIDE WITH ACTIVITY α1 - THYMOSIN α TUMOR NECROSIS FACTOR - THYMOSIN- a1 Patent of the Russian Federation

Anti TNF preparations

Rheumatology is a specialization of internal medicine dealing with the diagnosis and treatment of rheumatic diseases.

Anti-TNF drugs are used worldwide to treat rheumatoid arthritis. They deactivate TNF, molecules produced by the immune system that cause inflammation. However, about a third of patients do not respond to this type of therapy.

The study involved 300 patients with rheumatoid arthritis who had an insufficient response to anti-TNF drugs.

The results of the study showed that 54% of patients who took anti-TNF drugs and 69% of participants who took non-TNF drugs had a moderate response to treatment.

In addition, more patients taking non-TNF drugs had low levels of disease activity at 24 and 52 weeks of the study.

The researchers concluded that patients with rheumatoid arthritis who have not responded to anti-TNF drugs may benefit from non-TNF drugs.

Treatment with anti-TNF drugs: paying off safety for higher efficacy?

Tumor necrosis factor (TNF) is an extracellular protein, an inflammatory cytokine with a wide spectrum of action, which is synthesized mainly by monocytes and macrophages. Its action extends to lipid metabolism, coagulation, insulin sensitivity and endothelial health, as well as a number of other functions.

For the first time, TNF was detected in the blood serum of mice that were injected with BCG and endotoxin. It turned out that the serum of such mice has a cytotoxic effect, and further study revealed the protein responsible for the development of this effect.

IN last years TNF is becoming increasingly important. Increased interest is associated with the bidirectional action of this cytokine. On the one hand, it plays an important role in the regulation of normal differentiation, growth and metabolism of various cells, and on the other hand, it acts as a mediator of pathological immunoinflammatory processes in various human diseases.

Treatment of polyarthritis

Polyarthritis is a type of arthritis in which the disease affects multiple joints. It affects people of all genders and ages and is often associated with various autoimmune disorders.

Treatment

Basic treatment of polyarthritis (prescribed by a rheumatologist);

Symptomatic treatment (aimed at pain relief).

In the second case, non-steroidal anti-inflammatory drugs (in various forms) are used, for example, brufen, indomethacin-Acri, flugalin, orthofen, roxicam. But it is worth considering the side effects, as well as contraindications to taking these drugs (for example, peptic ulcer).

Medical treatment

Non-steroidal anti-inflammatory

NSAIDs help reduce inflammation. They block the activity of prostaglandins (substances that play an important role in inflammation). They also help relieve mild to moderate pain. NSAIDs are fast-acting and often have fewer side effects than other stronger and more toxic drugs used to treat arthritis. In some cases, taking these medicines can cause indigestion, as well as the formation of ulcers.

Corticosteroids

Treatment of polyarthritis with these medicines helps to relieve inflammation, as well as suppress the immune response. Due to the fact that polyarthritis is often caused by autoimmune disorders, such as systemic lupus, these drugs are used to suppress the immune response that accompanies such disorders.

In most cases, it is corticosteroids that are first prescribed to patients with such diseases. In order to prevent steroid-induced osteoporosis, it is recommended to use, for example, bisphosphonates. These medicines often reduce pain and other symptoms much faster than other medicines.

Basic antirheumatic drugs (DMARDs)

PRPs modify the course of the disease. They can change the course of many diseases that cause polyarthritis. Due to the fact that they begin to act only 6-8 weeks after the start of administration, during this period an additional simultaneous intake of NSAIDs and corticosteroids is often prescribed. DMARDs, like corticosteroids, achieve their therapeutic effect by suppressing the immune system.

Polyarthritis is often treated with methotrexate, the same drug that is sometimes used for chemotherapy in cancer patients (at high doses). Methotrexate sometimes causes liver damage, therefore, during its use, it is necessary to regularly analyze the patient's blood in order to detect this, as well as other possible side effects, as early as possible.

The following DMARDs are also used to treat polyarthritis:

Sulfasalazine.
Hydroxychloroquine (an antimalarial drug). In 1 case, ison causes serious damage to the eyes.

Anti-TNF drugs

In many types of arthritis, including polyarthritis, tumor necrosis factor can cause inflammation. Drugs that block tumor necrosis factor are called anti-TNF drugs.

Treatment of polyarthritis requires the use of the following anti-TNF drugs:

They are administered by subcutaneous injection or intravenously. Taking anti-TNF can cause chills, joint and muscle pain, fever, increased susceptibility to infections, headaches, and other side effects in some cases.

Physiotherapy

Physiotherapy provides an opportunity to reduce pain, inflammation and swelling. This treatment of polyarthritis, such as magnetic therapy, paraffin, ozokerite therapy, ultrasound, cryotherapy, is used simultaneously with drug therapy. They make it possible to restore blood flow to joints that have been damaged, as well as slow down the process of bone loss and normalize metabolism.

It is impossible to completely eliminate this disease. In this regard, the treatment of polyarthritis is always necessary. With the help of continuous treatment, the patient will be able to maintain the quality of his life for a long time, as well as the usual level of activity and excellent well-being.

Please note: the information posted on the site is not a medical recommendation, advice or guide to action. Before using the information presented on our portal, be sure to consult your doctor!

Tumor necrosis factor - Alpha

Tumor necrosis factor alpha (TNF-ᵅ) is a 157 amino acid protein. It is the first multifunctional TFN family cytokine whose properties have been identified for the treatment of cancer. Its biological activity is regulated by TNF-alpha soluble receptors 1 and 2.

The natural effect is directly expressed by the stimulation of the production of interleukin-1, which is capable of recognizing healthy and oncological structures at the cellular level. In this regard, tumor necrosis factor-alpha affects the cancer cell through its surface.

TNF-alpha in the body is mainly produced by active macrophages, T-lymphocytes and natural killer cells of the affected tissues. It plays a key role in apoptosis and cell reproduction.

However, the influence of this natural element is closely related to the toxicity of the substance. Therefore, more effective and less toxic variants of tumor necrosis factor are currently used, for example, such as Thymosin-alpha. Oncologists are also developing ways to directly deliver the necrosis factor to the tumor, without affecting other tissues and without being included in the general circulation.

Tumor necrosis factor-alpha and cancer

To date, the influence of this element, as well as its antagonists and subsequent biological elements, on such forms of oncological lesions as:

Malignant tumors of the stomach and chest:

Tumor necrosis factor-alpha leads to the death of potentially cancerous cells.

Non-small cell lung cancer:

TNF-alpha protects the body from the effects of various pathogens, which prevents the onset of the disease.

Sarcoma and melanoma:

In these types of cancers, a particularly effective tumor necrosis factor-alpha is recombinant.

Cancer of the uterus and ovaries:

Also are sensitive to this element.

Due to its ability to destroy the blood supply of the tumor, tumor necrosis factor-alpha can also be used for clinical therapy of metastatic cancer.

Preparations

Tumor necrosis factor-alpha is a cytokine. They are able to prevent tumor activity not only by counteracting abnormal cells, but also by combining with the main cellular mechanisms. Therefore, when creating drugs, the following types of drugs are used, represented by TNF inhibitors:

Monoclonal antibodies ("Infliximab", adalimumab "Humira", rituximab, represented by the drug "Rituxan");
Recombinant proteins that include immunoglobulin domains and TNF receptors, in particular interferon-1 and 2 (etanercept "Enbrel", golimumab "Simponi").

Among the Russian drugs of the cytokine group, Refnot, Reaferon, Roferon, Intron and others stand out.

The cost of drugs of the cytokinic group directly depends on the country of manufacture. Medicines of European and American origin will be much more expensive than Russian and Ukrainian ones.

However, this does not mean at all that domestic pharmaceuticals will differ from imported ones in terms of the specifics of their action. So, for example, we will direct comparative prices for packages of the drug of the same capacity of 100 yew. unit:

preparations containing monoclonal antibodies (Russia): 1 bottle - from 1500 rubles. up to 2000 rubles; 5 bottles - bran. dorub.;
medicines with monoclonal antibodies (Ukraine): 1 bottle - from 500 UAH. up to 800 UAH; for 5 bottles the price is from 2000 UAH. up to 3500 UAH;
recombinant tumor necrosis factor: the cost in Russia for one bottle is from 2000 rubles. up to 3000 rub. In Ukraine, the price is higher: from 1000 UAH. up to 1800 UAH what is associated with the need for transportation;
the price of imported products containing tumor necrosis factor-alpha per vial ranges from 1000 USD. up to 1300 USD

Where to buy tumor necrosis factor-alpha?

Preparations containing tumor necrosis factor-alpha can be purchased in almost all countries of the world. In domestic pharmacology, drugs of the cytokine group are sold in pharmacies in large cities. But in most cases, drugs are given to the patient only by prescription and pre-order.

Patients from the CIS countries can purchase a drug from a Russian manufacturer, since the price of imported drugs is many times higher.

Reviews

About the drugs in this group, there are different opinions not only of cancer patients and their relatives, but also of the oncologists themselves:

Some point to the ability of drugs with tumor necrosis factor-alpha to fight cancer on their own.
Other experts confirm only the ability of cytokines to enhance the effect of traditional therapy.
Emphasize possible side effects, especially for patients with latent viral infections, tuberculosis, cardiovascular disease, and chronic diseases liver.

In any case, the maximum duration of treatment with tumor necrosis factor-alpha is only 2 courses. It can be carried out at home after a thorough diagnosis and collection of tests.

There are few patient reviews of the drug, but most patients with the therapeutic use of tumor necrosis factor-alpha note an improvement in their general state of health, especially in the presence of advanced or recurrent cancer. Some, in the later stages of the development of the disease, perceive the drug as the only panacea. However, this attitude is not adequate. Even despite the positive reviews, research is still underway in world practice regarding the safety of the product.

Tumor necrosis factor-alpha is one of the newest biological weapons, which is still a lot of discussion in scientific oncology.

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The information on this site is provided for informational purposes only! It is not recommended to use the described methods and recipes for the treatment of cancer on your own and without consulting a doctor!

Tumor necrosis factor (TNF): role in the body, determination in the blood, administration in the form of drugs

Tumor necrosis factor (TNF) is an extracellular protein that is practically absent in the blood of a healthy person. This substance begins to be actively produced in pathology - inflammation, autoimmunization, tumors.

In modern literature, you can find its designation as TNF and TNF-alpha. The latter name is considered obsolete, but is still used by some authors. In addition to alpha-TNF, there is another form of it - beta, which is formed by lymphocytes, but much slower than the first - for several days.

TNF is produced by blood cells - macrophages, monocytes, lymphocytes, as well as the endothelial lining of blood vessels. When a foreign antigen protein (a microorganism, its toxin, tumor growth products) enters the body, TNF reaches its maximum concentration within the first 2-3 hours.

Tumor necrosis factor does not damage healthy cells, but it has a strong antitumor effect. For the first time, such an effect of this protein was proved in experiments on mice in which regression of tumors was observed. In this regard, the protein got its name. Later studies showed that the role of TNF is not limited to the lysis of tumor cells, its action is multifaceted, it takes part not only in reactions in pathology, but is also necessary for a healthy body. At the same time, all the functions of this protein and its true essence still raise a lot of questions.

The main role of TNF is participation in inflammatory and immune responses. These two processes are closely related and cannot be separated. At all stages of the formation of the immune response and inflammation, tumor necrosis factor acts as one of the main regulatory proteins. In tumors, both inflammatory and immune processes, “controlled” by cytokines, also actively occur.

The main biological effects of TNF are:

Participation in immune reactions;
regulation of inflammation;
Influence on the process of hematopoiesis;
Cytotoxic action;
intersystem effect.

When microbes, viruses, foreign proteins enter the body, immunity is activated. TNF promotes an increase in the number of T- and B-lymphocytes, the movement of neutrophils to the site of inflammation, the "sticking" of neutrophils, lymphocytes, macrophages to the inner lining of blood vessels at the site of inflammation. An increase in vascular permeability in the area of development of the inflammatory response is also the result of the action of TNF.

The effect of tumor necrosis factor (TNF) on body cells

Tumor necrosis factor affects hematopoiesis. It inhibits the reproduction of erythrocytes, lymphocytes and white blood cells, but if hematopoiesis is suppressed for any reason, then TNF will stimulate it. Many active proteins, cytokines, have a protective effect against radiation. TNF also has this effect.

Tumor necrosis factor can be detected not only in blood, urine, but also in cerebrospinal fluid, which indicates its cross-system effect. This protein regulates the activity of the nervous and endocrine systems. The beta-type of TNF has a predominantly local effect, and the organism owes its systemic manifestations of immunity, inflammation and regulation of metabolism to the alpha-form of the cytokine.

One of the most important effects of TNF is cytotoxic, that is, cell destruction, which fully manifests itself during the development of tumors. TNF acts on tumor cells, causing their death due to the release of free radicals, reactive oxygen species and nitric oxide. Since single cancer cells are formed in any organism throughout life, TNF is necessary and healthy people for their timely and rapid neutralization.

Transplantation of organs and tissues is accompanied by the placement of foreign antigens into the body, even if the organ is the most suitable for a set of specific individual antigens. Transplantation is often accompanied by activation of local inflammatory reactions, which are also based on the action of TNF. Any foreign protein stimulates an immune response, and transplanted tissues are no exception.

After transplantation, an increase in the content of cytokine in the blood serum can be detected, which indirectly may indicate the onset of a rejection reaction. This fact underlies research on the use of drugs - antibodies to TNF, which can slow down the rejection of transplanted tissues.

The negative effect of high concentrations of TNF can be traced in severe shock against the background of septic conditions. The production of this cytokine is especially pronounced during infection with bacteria, when a sharp suppression of immunity is combined with heart, kidney, and liver failure, leading to the death of patients.

TNF is able to break down fat and deactivate the enzyme involved in the accumulation of lipids. Large concentrations of the cytokine lead to depletion (cachexia), so it was also called cachectin. These processes cause cancer cachexia and malnutrition in patients with long-term infectious diseases.

In addition to the described properties, TNF also plays a reparative function. Following damage in the focus of inflammation and an active immune response, healing processes increase. TNF activates the blood coagulation system, due to which the zone of inflammation is delimited by means of the microvasculature. Microthrombi prevent further spread of infection. Activation of fibroblast cells and their synthesis of collagen fibers contributes to the healing of the lesion.

Determination of the level of TNF and its significance

A laboratory study of the level of TNF does not apply to frequently used analyzes, but this indicator is very important when certain types pathology. The definition of TNF is shown when:

Frequent and prolonged infectious and inflammatory processes;
autoimmune diseases;
malignant tumors;
burn disease;
Injuries;
Collagenosis, rheumatoid arthritis.

An increase in the level of cytokines can serve not only as a diagnostic but also as a prognostic criterion. So, in sepsis, a sharp increase in TNF plays a fatal role, leading to severe shock and death.

For research, venous blood is taken from the patient, it is not allowed to drink tea or coffee before the analysis, only plain water is allowed. At least 8 hours in advance, you should exclude the intake of any food.

An increase in TNF in the blood is observed when:

Infectious pathology;
sepsis;
burns;
Allergic reactions;
Autoimmune processes;
multiple sclerosis;
Meningitis and encephalitis of a bacterial or viral nature;
DIC;
Graft-versus-host reactions;
Psoriasis;
Diabetes mellitus of the first type;
Myeloma and other tumors of the blood system;
Shock.

In addition to an increase, a decrease in the level of TNF is also possible, because normally it should be present, albeit in scanty amounts, to maintain health and immunity. A decrease in the concentration of TNF is typical for:

immunodeficiency syndromes;
Cancer of internal organs;
The use of certain drugs - cytostatics, immunosuppressants, hormones.

TNF in pharmacology

The variety of biological responses mediated by TNF prompted research into the clinical use of tumor necrosis factor preparations and its inhibitors. The most promising are antibodies that reduce the amount of TNF in severe diseases and prevent deadly complications, as well as a recombinant synthetic cytokine prescribed for cancer patients.

Actively used drugs analogues of human tumor necrosis factor in oncology. For example, such treatment, along with standard chemotherapy, shows high efficiency against breast cancer and some other tumors.

TNF-alpha inhibitors have anti-inflammatory effects. With the development of inflammation, there is no need to immediately prescribe drugs of this group, because in order to recover, the body itself must go through all the stages inflammatory process, build immunity and ensure healing.

Early suppression of natural defense mechanisms is fraught with complications, therefore, TNF inhibitors are indicated only with an excessive, inadequate response, when the body is unable to control the infectious process.

TNF inhibitor drugs - Remicade, Enbrel - are prescribed for rheumatoid arthritis, Crohn's disease in adults and children, ulcerative colitis, spondyloarthritis, psoriasis. As a rule, these drugs are not used if standard therapy with hormones, cytostatics, antitumor agents is ineffective, if it is intolerable or if there are contraindications to drugs of other groups.

Antibodies to TNF (infliximab, rituximab) suppress excessive production of TNF and are indicated for sepsis, especially with the risk of developing shock; in advanced shock, they reduce mortality. Antibodies to cytokines may be prescribed in case of long-term infectious diseases with cachexia.

Thymosin-alpha (timaktid) is classified as an immunomodulatory agent. It is prescribed for diseases with impaired immunity, infectious pathology, sepsis, for the normalization of hematopoiesis after irradiation, for HIV infection, and severe postoperative infectious complications.

Cytokine therapy is a separate direction in the treatment of oncopathology, which has been developing since the end of the last century. Cytokine preparations show high efficiency, but their independent use is not justified. The best result is possible only with an integrated approach and the combined use of cytokines, chemotherapy and radiation.

TNF-based drugs destroy the tumor, prevent the spread of metastases, and prevent recurrence after removal of tumors. When used simultaneously with cytostatics, cytokines reduce their toxic effect and the likelihood adverse reactions. In addition, due to the favorable effect on the immune system, cytokines prevent possible infectious complications during chemotherapy.

Among TNF drugs with antitumor activity, refnot and ingaron, registered in Russia, are used. These are drugs with proven effectiveness against cancer cells, but their toxicity is an order of magnitude lower than the cytokine produced in the human body.

Refnot has a direct destructive effect on cancer cells, inhibits their division, and causes hemorrhagic tumor necrosis. The viability of a neoplasm is closely related to its blood supply, and refnot reduces the formation of new vessels in the tumor and activates the coagulation system.

An important property of refnot is its ability to enhance the cytotoxic effect of drugs based on interferon and other antitumor agents. So, it increases the effectiveness of cytarabine, doxorubicin and others, due to which a high antitumor activity of the combined use of cytokines and chemotherapeutic drugs is achieved.

Refnot can be prescribed not only for breast cancer, as indicated in the official recommendations for use, but also for other neoplasms - lung cancer, melanoma, tumors of the female reproductive system

Side effects with the use of cytokines are few, usually a short-term fever, itchy skin. The drugs are contraindicated in case of individual intolerance, pregnant women and nursing mothers.

Cytokine therapy is prescribed exclusively by a specialist, self-medication in this case is out of the question, and drugs can be purchased only by prescription. For each patient, an individual treatment regimen and combinations with other antitumor agents are developed.

Tumor necrosis factor inhibitors - modern drugs for the treatment of rheumatoid arthritis

TNF-α (tumor necrosis factor alpha) plays a key role in starting and maintaining the inflammatory process in rheumatoid arthritis (RA). Suppression of TNF activity leads to a decrease in the synthesis of inflammatory mediators in the body, due to which the necessary therapeutic effect in the treatment of the disease is achieved.

One of the disadvantages of therapy with TNF-α inhibitors is the high cost. However, this method of treatment also has significant advantages: proven effectiveness; safety; persistence of the achieved remission.

Let us consider the use of TNF-α inhibitors in clinical practice using the example of a drug called etanercept, which has been widely used over the past 10 years in the United States, Canada, and European countries. This TNF inhibitor is designed for subcutaneous administration, which allows patients with RA to avoid costly and lengthy hospitalizations.

Etanercept is used in the treatment of rheumatoid arthritis with moderate to high inflammatory activity. The drug has a stimulating effect on the TNF-α receptors present in the patient's body. As a result, receptors more actively capture excess TNF-α, thereby reducing its concentration, which leads to a decrease in the inflammatory process.

Like other TNF-α inhibitor drugs, etanercept differs significantly in its pharmacological action from immunosuppressants also used in some RA treatment regimens. Immunosuppressants affect almost the entire immune system, while TNF-α inhibitors are active against specific targets, which are specific sites in the pathogenesis of rheumatoid arthritis.

The results of etanercept studies have shown that a new drug, a TNF inhibitor, leads to a significant reduction in the severity of symptoms of the disease, the achievement of stable and long-term remissions. Etanercept can be used both as monotherapy for RA (treatment with this drug alone) and as part of complex treatment. TNF inhibitors can be combined with non-steroidal anti-inflammatory drugs (NSAIDs), immunosuppressants (methotrexate), glucocorticoids (GCs), and pain medications.

Etanercept is given by injection under the skin. "Injections" are performed twice a week. Possible injection zones: under the skin of the shoulder, anterior abdominal wall or thigh. Hospitalization of patients for treatment with a TNF inhibitor is not required; injections can be made by a nurse in the treatment room of a polyclinic or at home.

It should be noted that the use of TNF inhibitors may be accompanied by certain undesirable effects: fever, diarrhea, abdominal pain, leukopenia (decrease in the number of leukocytes), headache, dizziness, respiratory disorders. In addition, local reactions sometimes occur at the injection site (skin itching, and rashes).

It has not been established with certainty what effect TNF-α inhibitors have on the protective function of the immune system. Therefore, patients receiving etanercept should be warned that the use of the drug can potentially provoke infection with various infections. Etanercept should not be used in patients with weakened immune systems as in this case, patients may develop serious infectious diseases that are fraught with sepsis and death. Etanercept is also contraindicated in patients with certain heart conditions (the drug can lead to severe cardiovascular failure). TNF-α inhibitors are not intended for the treatment of RA without the participation of a physician.

The introduction of TNF-α inhibitors into wide clinical practice can be considered one of the greatest advances in medicine in the treatment of RA in recent decades. The use of this group of drugs makes it possible to achieve remission of the disease or a significant decrease in the activity of the inflammatory process, even in patients who were resistant (not sensitive) to other types of basic antirheumatic therapy. The use of TNF-α inhibitors for the treatment of RA significantly slows down the progression of the destruction (destruction) of the affected joints, which is confirmed by x-ray methods.

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Arthritis

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