Immard tab. cover captivity. about. 200 mg per blister. in pack №10x3 (hydroxychloroquine)

Immard instructions

Indications for use

• - malaria: treatment of acute attacks and suppressive therapy of malaria caused by Plasmodium vivax, Plasmodium ovale and Plasmodium malariae (excluding hydroxychloroquine-resistant cases) and susceptible strains of Plasmodium falciparum; radical treatment of malaria caused by susceptible strains of Plasmodium falciparum; - rheumatoid arthritis; - systemic lupus erythematosus, discoid lupus erythematosus; - photodermatosis; - bronchial asthma; - Sjögren's syndrome

All indications for use

Contraindications

• - pregnancy; - lactation period; - children under 3 years of age; - long-term therapy in childhood; - hypersensitivity to the components of the drug. Use with caution in patients with retinopathy (including a history of maculopathy), disorders of bone marrow hematopoiesis, diseases of the central nervous system and cardiovascular system, psychosis (including a history), porphyria, psoriasis, glucose deficiency 6-phosphate dehydrogenase, with liver and/or renal failure.

All contraindications

pharmachologic effect

An antimalarial drug that actively suppresses erythrocyte forms (hematoschizotropic drug). Compacts lysosomal membranes and prevents the release of lysosomal enzymes, disrupts DNA replication, RNA synthesis and hemoglobin utilization by erythrocyte forms of plasmodium. It also has an immunosuppressive and anti-inflammatory effect, suppresses the processes in which free radicals are formed, weakens the activity of proteolytic enzymes (protease and collagenase), leukocytes, and lymphocyte chemotaxis.

Genetically engineered drugs: addition to basic therapy

monoclonal antibodies has provided new insight into the treatment of autoimmune diseases [11]. A fundamentally new class of drugs has been obtained thanks to the achievements of genetic engineering. To understand the mechanism of action of these drugs, it is worth remembering how immune cells work in health and disease [1], [12].

The immune system is a complex mechanism consisting of many “cogs” - immune cells. Each of them has its own functions and occupies a certain place in the overall structure of the protective system. In response to the arrival of an “enemy” agent (antigen), components of the innate immune system—nonspecific protective factors—are activated. These are neutrophils, eosinophils and basophils, which are the first to stand in the way of harmful effects.

The cogs turn and new components of the immune system are activated. T- and B-lymphocytes enter the fight against the pathogen. They include more subtle defense mechanisms - specific cytotoxicity. Antibodies are produced, T-killers look for their “victim”... Fine regulation of the process with the help of cytokines allows you to quickly achieve your goal. The coordinated action of all components of immunity leads to the implementation of the program - the destruction of the pathological agent.

During the selection of suitable “parts” for the mechanism - during the selection of lymphocytes - errors inevitably arise. The immune system produces autoreactive clones—cells that are specific to body tissue antigens. Normally, they are eliminated in the “workshops” - the thymus and lymph nodes. Those clones of lymphocytes that do not distinguish between self and foreign antigens are immediately destroyed even before they begin to perform their function. But what happens when the cogs fall out of the immune machine? The breakdown occurs in a specific part of the mechanism - in the work of T- and B-lymphocytes. If the selection process is disrupted, autoreactive cells are released into the blood. They look for their “victims” and find them in the normal elements of their own tissues.

Depending on the type of reaction, the pathophysiological process underlying autoimmune aggression differs. T-lymphocytes can kill body cells on their own, or they can work “by proxy” - activating the production of autoantibodies by B-lymphocytes. When B-cell immunity is damaged, autophagy is realized through the complement system, as well as through the formation of cytotoxic immune complexes [13], [14]. You can read more about the mechanisms of normal and altered immune responses on Biomolecule [1], as well as in articles [15], [16].

In autoimmune diseases, it is possible to suppress the entire complex mechanism of immunity at once, which is what classical therapy drugs do. But this leaves a person without protection from enemy agents - bacterial infections, viruses and other pathogens. Therefore, it is preferable to preserve the activity of the immune system as a whole, saving a person from auto-aggression of certain of its components. This is exactly how new drugs—monoclonal antibodies—work.

Biological agents affect individual “cogs” of the immune defense mechanism. Their targets may be cytokines and their receptors, membrane molecules of lymphocytes. Depending on the point of application of the drug, monoclonal antibodies are divided into groups (Fig. 4):

1. TNF (tumor necrosis factor) inhibitors - infliximab, etanercept, certolizumab, golimumab, adalimumab.
2. Interleukin receptor blockers - tocilizumab (IL-6R), canakinumab (IL-1R), secukinumab (IL-17R).
3. Anti-B-cell antibodies (antibodies to membrane molecules CD20) - rituximab, belimumab [17].
4. Anti-T-cell antibodies (antibodies to CD80 and CD86 molecules) - abatacept [18].

Figure 4. Pathophysiological “victims” of monoclonal antibodies - interleukins, TNF, surface proteins of lymphocytes.

“Individualization of treatment for rheumatoid arthritis: a course to achieve optimal results”

TNF inhibitors

Tumor necrosis factor inhibitors are the first monoclonal antibodies introduced into rheumatological practice. This group includes infliximab, etanercept, certolizumab, golimumab, adalimumab.

Tumor necrosis factor ( TNF ) is a pro-inflammatory cytokine (a substance that stimulates the development of an inflammatory response). Normally, when it is released, vascular cell proliferation, macrophage activation, and lysis of tumor agents occur. These effects play an important role in protecting the body from pathogens. Inflammation can be considered a response to damaging factors.

However, the effect of TNF on joints in rheumatic diseases cannot be called positive. Thus, in rheumatoid arthritis, the cytokine stimulates the proliferation of synovial fibroblasts - cells of the joint lining. This leads to the formation of pannus - growths of aggressive tissue. As the disease progresses, the process of inflammation and destruction spreads to the articular cartilage and underlying bones (Fig. 5). The joint tissues are filled with immune cells - macrophages, T- and B-lymphocytes, neutrophils. These mechanisms underlie the development of chronic inflammation. You can refresh your knowledge about the pathogenesis of rheumatoid arthritis in the article “Rheumatoid arthritis: change the composition of the joints” [3].

Figure 5. Pathological changes in the joint in rheumatoid arthritis. The autoimmune process causes erosions, synovitis (inflammation of the synovial membrane), and destruction of articular cartilage.

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One of the TNF inhibitors is the drug infliximab. It has "human" and "mouse" areas. Approximately 25% of all amino acids in the monoclonal antibody are derived from mice. This is a Fab fragment - a specific region responsible for binding to TNF. The Fc fragment of the protein is formed from IgG1, a human antibody.

This structure is associated with the mechanism for obtaining the drug. Initially, an antibody to tumor necrosis factor is synthesized in the mouse. The resulting immunoglobulin is specific to TNF and can already neutralize it, but completely foreign proteins, of course, cannot be introduced into the patient’s body. This will cause an active immune reaction - the production of antibodies against therapeutic agents. Therefore, mouse immunoglobulin domains are replaced with similar regions of human proteins. Antibodies that have fragments of different origins are called chimeric. In fact, they take the best qualities of their predecessors. The mouse part provides high sensitivity to TNF, and the human fragments reduce immunogenicity - the likelihood of developing an immune response.

The mechanism of action of infliximab is clear from its structure. The Fab fragment of the molecule binds tumor necrosis factor, forming a stable complex with it. This interaction completely blocks the activity of the cytokine, preventing its connection with the membrane receptors p55 and p57. Infliximab “neutralizes” both soluble and membrane-associated forms of TNF (Fig. 6). The content of other pro-inflammatory factors, such as IL-1, IL-6, and nitrogen monoxide, also decreases in joint cells.

Figure 6. Main effects of TNF and monoclonal antibodies blocking it (infliximab and etanercept). The targets for monoclonal antibodies are free and membrane-associated forms of tumor necrosis factor. The drugs prevent the cytokine from binding to the receptor, thereby reducing the activity of rheumatoid arthritis.

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Another effective drug from the group of TNF inhibitors, etanercept, . It contains the extracellular part of the receptor for tumor necrosis factor. It “connects” to human IgG1. The hybrid molecule enters into fierce competition for free TNF and neutralizes it before the cytokine has time to contact receptors and trigger an inflammatory response. An additional effect of etanercept that other TNF inhibitors do not have is the neutralization of lymphotoxin. This substance also belongs to pro-inflammatory cytokines. The production of lymphotoxin stimulates proliferative processes in the joints. Accordingly, blocking its action reduces the activity of inflammation in rheumatological diseases [18].

TNF inhibitors have shown good results not only in the treatment of rheumatoid arthritis, but also in other autoimmune pathologies. For example, new drugs are widely used in patients with ankylosing spondylitis. Slowing the progression of pathology in this case is very important, since auto-aggression is aimed at the joint and bone formations of the spine. Over time, the disease turns the spinal column into a “bamboo stick” - a monolithic, rigid formation. Ankylosis develops gradually, but inevitably. Every year the motor abilities of patients become more and more limited. The use of biological drugs can reduce the activity of inflammation in the spine. This slows down the process of ankylosis formation [19].

Interleukin receptor blockers

Interleukins play an important role in the development of autoimmune inflammation , which, like TNF, are proinflammatory cytokines (Fig. 7). The main representatives of this group are IL-6, IL-1, IL-17. The function of interleukins is the control of the processes of differentiation, proliferation and death (apoptosis) of immune cells, which is carried out through the corresponding target genes [20].

Figure 7. The mechanism of action of interleukins in autoimmune inflammation (using the example of IL-6). The cytokine affects T- and B-lymphocytes, hematopoietic cells, and hepatocytes. It stimulates the production of autoantibodies by B cells, as well as the formation of autoreactive T clones, which are directly involved in the autoimmune process. The effect on the bone marrow is to stimulate the production of new blood cells - the number of leukocytes and platelets increases. Inflammation is accompanied by a response of liver cells, the appearance of characteristic symptoms of an autoimmune disease.

[21]

The influence of interleukins is one of the “triggers” of the inflammatory process. Therefore, blocking their activity improves the condition of patients with autoimmune diseases. You can stop the work of interleukins by binding their receptors - molecules that transmit a signal to immune cells. This is the basis of the mechanism of action of monoclonal antibodies from the group of interleukin receptor inhibitors.

Tocilizumab is a drug that blocks IL-6. The receptor for this substance consists of two components: membrane IL-6R (α chain) and glycoprotein g130 (β chain). The membrane part of the receptor binds to IL-6, forming a stable complex. Together they activate the g130 component, causing a change in its structure (homodimerization). A receptor complex of two g130 molecules is formed, which in turn activates JAK1 kinase. This enzyme triggers a cascade of reactions in the cell, which leads to the appearance of the biological effect of the cytokine - the development of inflammation. In some cases, IL-6 binds not the membrane, but the soluble form of the α-chain (Fig. 8). The mechanism of action of the receptor does not change in this case [21].

Tocilizumab works by competitive inhibition. Signaling molecules actively bind to the monoclonal antibody. The vacant place is filled - interleukin cannot form a complex with the receptor, which means it is not able to activate the inflammation process.

Figure 8. Mechanism of action of tocilizumab. The drug binds soluble and membrane IL-6 receptors, blocking signal transmission.

"Modern targets for targeted therapy of rheumatoid arthritis: from monoclonal antibodies to signal molecule blockers"

Tocilizumab is considered one of the safest drugs in the group of monoclonal antibodies. This allows it to be used for juvenile idiopathic arthritis, which occurs before the age of 16 years. Children react particularly acutely to toxic effects, so the drugs used in their treatment should have a minimum number of adverse reactions. The use of tocilizumab allows one to achieve the desired treatment effect without causing severe complications.

Anti-B cell therapy

One of the main elements involved in autoimmune inflammation are B lymphocytes . They produce autoantibodies that bind to healthy cells in the body. The resulting complex of antibody and autoantigen attacks the complement system or cytotoxic lymphocytes. This process underlies the inflammatory response in rheumatic diseases such as systemic lupus erythematosus. A separate article on “Biomolecule” is devoted to it: “Systemic lupus erythematosus: a disease with a thousand faces” [2].

Anti-B cell therapy drugs ( rituximab and belimumab ) block the activity of B cells by binding to their membrane CD20 molecules. Only certain categories of B cells have these substances. They are specific for pre-B lymphocytes and mature B lymphocytes. CD20 is not present in stem elements and pro-B cells, from which new lymphocytic elements will be formed. Membrane molecules of this type are not found in plasma cells that produce immunoglobulins [22].

Thanks to this feature, the CD20 protein is an ideal “victim” for biological drugs. When its activity is “turned off,” neither the formation of new lymphocytes nor the production of normal antibodies is disrupted. One drug with this mechanism of action is rituximab. The monoclonal antibody binds to the CD20 molecule. This leads to the launch of immunological reactions in relation to B-lymphocytes, which ensure the destruction (lysis) of these cells (Fig. 9).

Figure 9. Mechanism of action of rituximab. The Fab fragment of the monoclonal antibody binds to CD20 on the surface of the B lymphocyte. This triggers cell lysis, which can occur in several ways: through the complement system, the apoptosis program, or the aggression of natural killer cells and macrophages.

"Modern targets for targeted therapy of rheumatoid arthritis: from monoclonal antibodies to signal molecule blockers"

Anti-T cell therapy

Blocking the action of T-lymphocytes is possible due to the peculiarities of their activation. In order for a T lymphocyte to enter the autoimmune process and bind to an antigen, it must receive two signals from antigen presenting cells (APCs). The first signal ensures recognition of a specific autoantigen by T-cell receptors. The second signal is a nonspecific process of binding of membrane molecules CD80 and CD86 on the surface of APC with the CD28 receptor of the lymphocyte. The combination of these interactions causes activation of T cells, which in turn stimulate the production of proinflammatory cytokines. This is the main contribution of T lymphocytes to the autoimmune process.

Knowledge of the mechanism of T cell activation was used in the development of monoclonal antibodies. The main representative of anti-T-cell agents is abatacept . The drug is a protein consisting of two parts. The specific part is formed by the CTLA-4 molecule (cytotoxic lymphocyte antigen 4). The nonspecific region is the Fc fragment of human immunoglobulin G1 [23].

The effect of abatacept is aimed precisely at a nonspecific (costimulatory) signal. The CTLA-4 component binds the CD80 and CD86 proteins on the surface of antigen-presenting cells. The CD28 lymphocyte receptor can no longer interact with them, which is why the activation of the T cell is not completed (Fig. 10).

Figure 10. Mechanism of action of abatacept. Abatacept modulates the immune response through binding to CD80/CD86 on antigen presenting cells. This prevents CD80/CD86 from binding to CD28 T cells, i.e. T cell activation is abolished through blocking costimulation.

"Modern targets for targeted therapy of rheumatoid arthritis: from monoclonal antibodies to signal molecule blockers"

Pharmacokinetics

Absorption Absorption of the drug is variable. The half-absorption period is 3.6 hours (1.9-5.5 hours). Bioavailability - 74%. Tmax in blood plasma is 3.2 hours (2-4.5 hours). After taking the drug orally at a dose of 155 mg, Cmax in blood plasma is 948 ng/ml, at a dose of 310 mg - 1895 ng/ml. Distribution Plasma protein binding - 45%. It accumulates in tissues with a high level of metabolism (in the liver, kidneys, lungs, spleen - in these organs the concentration exceeds the plasma concentration by 200-700 times; in the central nervous system, erythrocytes, leukocytes) and in tissues rich in melanin. It is found in very low concentrations in the walls of the gastrointestinal tract. Penetrates the placental barrier and is detected in breast milk in small quantities. Vd in blood - 5,522 l, in plasma - 44,257 l. Metabolism Partially metabolized in the liver to form active deethylated metabolites. Elimination T1/2 - 50 days, from plasma - 32 days. Excreted by the kidneys (23-25% unchanged) and with bile (less than 10%). It is excreted very slowly and can be detected in urine for a long time after cessation of treatment.

Use of the drug Immard

Orally during meals or with a glass of milk. The course dose for adults in the treatment of malaria is 2 g: on the 1st day - 800 mg for the 1st dose, after 6-8 hours - another 400 mg; on the 2nd and 3rd days - 400 mg in one dose. Children weighing more than 40 kg are prescribed a daily dose of 25 mg/kg body weight for 3 days according to the following scheme: 1st dose - 10 mg/kg (in a single dose no more than 620 mg); 2nd dose - 5 mg/kg (in a single dose no more than 310 mg) 6 hours after taking the 1st dose; 3rd dose - 5 mg/kg 18 hours after taking the 2nd dose; 4th dose - 5 mg/kg 24 hours after the 3rd dose. For systemic connective tissue diseases, adults are usually prescribed a dose of 400–600 mg/day in 1–2 doses. After the progression of the disease has stopped, the dose can be reduced to 200 mg/day. According to indications, the maintenance daily dose can be reduced by 50%. It is recommended to take the drug in the minimum effective dose, which does not exceed 6.5 mg/kg per day, especially in children weighing more than 30 kg. The starting dose for adults for systemic lupus erythematosus is 400 mg 1–2 times daily for several weeks or months, depending on response to therapy. For long-term treatment, a dose of 200–400 mg/day is considered adequate. The duration and frequency of taking the drug is determined individually. For rheumatoid and juvenile arthritis, systemic lupus erythematosus, the course of treatment should be stopped if the effect is not achieved within 6 months.

Special conditions

Before starting and during therapy, it is necessary to conduct an ophthalmological examination at least once every 6 months. During therapy, constant monitoring of the cellular composition of the blood and the condition of skeletal muscles (including tendon reflexes) is necessary. Effect on the ability to drive vehicles and operate machinery During the treatment period, care must be taken when driving vehicles and other potentially dangerous activities that require increased concentration and speed of psychomotor reactions.

Special instructions for the use of the drug Immard

Before starting treatment, consultation with an ophthalmologist is necessary. Ophthalmological examination is repeated every 6 months (determining visual acuity, performing ophthalmoscopy). If any violations are detected, treatment should be stopped immediately. The likelihood of developing retinopathy is directly proportional to the daily dose. In patients with severe renal or hepatic impairment, plasma levels of hydroxychloroquine should be monitored. The cellular composition of peripheral blood should be periodically monitored and if pathological changes are detected, the course of treatment should be stopped. Patients with psoriasis may develop a skin rash. Particular caution is required when treating patients with glucose-6-phosphate dehydrogenase deficiency. During treatment with the drug, you should refrain from driving vehicles and servicing potentially dangerous mechanisms.

Side effects

From the musculoskeletal system: myopathy or neuromyopathy, leading to increasing myasthenia gravis and atrophy of proximal muscle groups. From the central nervous system and peripheral nervous system: sensory disturbances, decreased tendon reflexes, abnormal nerve conduction; headache, dizziness, nervousness, psychosis, emotional lability, convulsions. From the senses: tinnitus, hearing loss, photophobia, impaired visual acuity, impaired accommodation, swelling and clouding of the cornea, scotoma; with long-term use in high doses - retinopathy (including with pigmentation disorders and visual field defects), optic nerve atrophy, keratopathy, ciliary muscle dysfunction. From the cardiovascular system: with long-term therapy with the drug in high doses - myocardial dystrophy, cardiomyopathy, AV block, decreased myocardial contractility, myocardial hypertrophy. From the digestive system: nausea, vomiting (rarely), loss of appetite, spastic abdominal pain, diarrhea, hepatotoxicity (impaired liver function, liver failure). From the hematopoietic system: neutropenia, aplastic anemia, agranulocytosis, thrombocytopenia, hemolytic anemia (in patients with glucose-6-phosphate dehydrogenase deficiency). Metabolism: loss of body weight, worsening of porphyria

Side effects of the drug Immard

Retinopathy, deposits in the cornea with reversible photophobia and opacification, disturbance of accommodation; disorders of the digestive tract (nausea, diarrhea, anorexia, intestinal spasms, vomiting); muscle weakness, dizziness, tinnitus, hearing loss, headache, emotional disorders, toxic psychosis, convulsions, cardiomyopathy, impaired myocardial contractile function, impaired neuromuscular conduction, myelosuppression, decreased appetite, hair loss, weight gain; anemia, thrombocytopenia.

Drug interactions

With simultaneous use, hydroxychloroquine increases the concentration of digoxin in plasma, aminoglycosides enhance the blocking effect on neuromuscular conduction. Hydroxychloroquine enhances the effect of hypoglycemic drugs (reducing the dose of the latter is required). When used simultaneously with antacids, the absorption of hydroxychloroquine is reduced (the interval between taking the antacid and Immard should be at least 4 hours). Alkaline drinking and alkalis speed up the elimination of hydroxychloroquine from the body. Hydroxychloroquine increases plasma concentrations of penicillamine and increases the risk of side effects from the hematopoietic system, urinary system and skin reactions. Hydroxychloroquine increases the side effects of corticosteroids, salicylates, class IA antiarrhythmic drugs, hemato-, hepato- and neurotoxic drugs.

Is there any result from using it?

Reviews from patients with rheumatoid arthritis are mostly positive. Patients claim that the drug is effective:

• eliminates pain;
• reduces inflammation;
• prolongs the period of remission;
• It becomes easier to walk, the quality of life improves.

“Thanks to French studies, Immard’s effectiveness against coronavirus has been proven, and the drug has shown good results specifically in the treatment of patients with severe symptoms of respiratory tract infection. On the 6th day of therapy, the number of those cured who took Immard was 70%, without it – 12%.”

Today, Immard is also actively used to treat patients with coronavirus. Moscow doctors were even asked to take it to prevent COVID-19. Research is still being conducted on its effectiveness, but the practice of other countries has shown that hydroxychloroquine is effective against coronavirus infection.

Pharmacodynamics

An antimalarial drug that actively suppresses erythrocyte forms (hematoschizotropic drug).
Compacts lysosomal membranes and prevents the release of lysosomal enzymes, disrupts DNA replication, RNA synthesis and hemoglobin utilization by erythrocyte forms of plasmodium. It also has an immunosuppressive and anti-inflammatory effect, suppresses the processes in which free radicals are formed, weakens the activity of proteolytic enzymes (protease and collagenase), leukocytes, and lymphocyte chemotaxis.

Literature

1. Immunity: fight against strangers and... one's own;
2. Systemic lupus erythematosus: a disease with a thousand faces;
3. Rheumatoid arthritis: change the composition of the joints;
4. Nasonov E.L., Alexandrova E.N., Novikov A.A. (2015). Autoimmune rheumatic diseases - problems of immunopathology and personalized therapy. Bulletin of the Russian Academy of Medical Sciences. 2, 169–182;
5. Babaeva A.R., Kalinina E.V., Zvonorenko M.S. (2016). New opportunities to improve the effectiveness and safety of treatment of rheumatoid arthritis. Medical alphabet. 22, 5–12;
6. Josef S Smolen, Robert Landewé, Ferdinand C Breedveld, Maya Buch, Gerd Burmester, et. al.. (2014). EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2013 update. Ann Rheum Dis
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   73 , 492-509;
7. Nasonov E.L. (2015). Methotrexate for rheumatoid arthritis - 2015: new facts and ideas. Scientific and practical rheumatology. 4, 421–433;
8. Kanevskaya M.Z. and Gurskaya S.V. (2013). Methotrexate in the treatment of rheumatic diseases. Modern rheumatology. 4, 47–53;
9. D. T. Felson, J. S. Smolen, G. Wells, B. Zhang, L. H. D. van Tuyl, et. al.. (2011). American College of Rheumatology/European League Against Rheumatism Provisional Definition of Remission in Rheumatoid Arthritis for Clinical Trials. Annals of the Rheumatic Diseases
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   70 , 404-413;
10. Patrick Durez, Jacques Malghem, Adrien Nzeusseu Toukap, Geneviève Depresseux, Bernard R. Lauwerys, et. al.. (2007). Treatment of early rheumatoid arthritis: A randomized magnetic resonance imaging study comparing the effects of methotrexate alone, methotrexate in combination with infliximab, and methotrexate in combination with intravenous pulse methylprednisolone. Arthritis Rheum
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    56 , 3919-3927;
11. Monoclonal antibodies;
12. 12 methods in pictures: immunological technologies;
13. Autophagy, protophagy and others;
14. Nobel Prize in Medicine or Physiology 2021: for self-criticism;
15. Zaichik A.M., Poletaev A.B., Churilov L.P. (2013). Recognition of “One’s own” and interaction with “One’s own” as the main form of activity of the adaptive immune system. Bulletin of St. Petersburg State University. Episode 11. Medicine. 1;
16. Autoimmunity. Modern views on the physiological and pathological aspects of autoimmunity. NSU Electronic Archive;
17. For the first time in half a century, there is a new drug for lupus;
18. Nasonov E.L. and Karateev D.E. (2013). The use of genetically engineered biological drugs for the treatment of rheumatoid arthritis: general characteristics (lecture). Scientific and practical rheumatology. 2, 163–169;
19. Logvinenko S.I., Shcherban E.A., Pridachina L.S., Pridachina A.N., Maslova Yu.Yu., Kashichkina A.A. (2016). Genetic engineering in the treatment of ankylosing spondylitis (Bechterew's disease). Scientific bulletins of BelSU. Series: Medicine. Pharmacy. 19, 179–182;
20. Masahiko Mihara, Misato Hashizume, Hiroto Yoshida, Miho Suzuki, Masashi Shiina. (2012). IL-6/IL-6 receptor system and its role in physiological and pathological conditions. Clin.
    Sci. .
    122 , 143-159;
21. Nasonov E.L., Alexandrova E.N., Avdeeva A.S., Panasyuk E.Yu. (2013). Inhibition of interleukin 6 - new possibilities for pharmacotherapy of immunoinflammatory rheumatic diseases. Scientific and practical rheumatology. 4, 416–427;
22. Suponitskaya E.V., Alexandrova E.N., Aleksankin A.P., Nasonov E.L. (2015). The effect of therapy with genetically engineered biological drugs on B-lymphocyte subpopulations in rheumatic diseases: new data. Scientific and practical rheumatology. 1, 78–83;
23. Babaeva A.R., Cherevkova E.V., Galchenko O.E., Solodenkova K.S. (2012). Biological agents in the basic therapy of rheumatoid arthritis. Medicinal Bulletin. 7, 3–9;
24. Muravyov Yu.V. and Muravyova L.A. (2016). Untimely thoughts on the use of genetically engineered biological drugs for rheumatic diseases. Scientific and practical rheumatology. 3, 361–366;
25. Psoriasis: at war with your own skin.

Take generic Immard with caution.

Review left by Rinat
Rating: 2

(out of 5)

Advantages:

For various diseases, price, there is a positive trend

Flaws:

Overdose can cause death

My mom takes Immard for arthritis. It helps her flawlessly, but you just need to strictly adhere to the doses that the doctor prescribes. I used these tablets for malaria and it also worked like a charm. So I recommend it. In addition, the price is only pleasing, unlike its analogues.

• Review #1
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• Review No. 7

Immard is my salvation

Review left by Regina
Rating: 5

(out of 5)

Advantages:

Cost, effectiveness

Flaws:

No complaints

I have rheumatoid arthritis. I treated him with Plaquenil before, but it turns out to be very, very expensive, I can no longer afford to spend so much money on drugs. I turned to the pharmacist at the pharmacy who recommended a cheaper analogue and she said that there is Immard, but I need to consult a doctor. I immediately called the rheumatologist and she approved it. As a result, I drank Immard for about 2 months, but intermittently. This is how the doctor drew up a treatment regimen for me and said that there would be no side effects. Yes, that’s what happened, and the arthritis stopped bothering me. And saved money)))

Is there any point in taking Immard?

Review left by Claudrine

Grade: 4

(out of 5)

Advantages:

Heals

Flaws:

You're losing a lot of weight

I go in for sports on my own, often on horizontal bars. Because of this, he suffered a knee injury. The pain did not go away for a long time, so after a few months I went to the hospital. After examination, a diagnosis of rheumatoid arthritis was made. Damn, and this is at my age!

The doctor prescribed Immard for a long course of 2 tablets per day with a dosage of 200 mg. I tolerated the medicine normally, only after a couple of months insomnia began and something wrong happened with my psyche. But I continued to drink, as a result of which, after six months, improvement began. The only thing that really upsets me is losing weight, but I was in great shape. When I complained about taka. I told the doctor, he gave me recommendations on taking other medications to increase appetite. What can I say, it worked and now I’m gaining weight.

Take generic Immard with caution.

Review left by Rinat
Rating: 2

(out of 5)

Advantages:

For various diseases, price, there is a positive trend

Flaws:

Overdose can cause death

My mom takes Immard for arthritis. It helps her flawlessly, but you just need to strictly adhere to the doses that the doctor prescribes. I used these tablets for malaria and it also worked like a charm. So I recommend it. In addition, the price is only pleasing, unlike its analogues.

Immard

Review left by Natalie
Rating: 3

(out of 5)

Advantages:

Accumulation effect, cost

Flaws:

Adverse reactions

I took Immard for rheumatoid arthritis. I took the pills for a long time, so I can tell you all the details. But first, let me draw your attention to the fact that the drug has a prolonged effect, which means that you should not expect positive dynamics after 2-3 days. It takes several months. But this is only true in the case of arthritis, since my sister took Immard for malaria, and 4 days was enough for her. So, the active substances accumulate in the body and then begin to act rapidly. I used to think that maybe to speed up this process, I could increase the dosage, but the doctor said that it was life-threatening. Then I read in the instructions for use that an overdose leads to disturbances in the heart muscle and the heart in general, and also negatively affects vision and that even death is possible. After that, I took the treatment regimen that the doctor gave me with all seriousness. So, initially I took the maximum dosage - 600 mg, then reduced it to 400, and in the last couple of months to 200. I will say this - there was no relief for three months, so the rheumatologist additionally prescribed me Meloxicam to relieve the pain, but when the cumulative effect from Immard began to manifest itself, I stopped taking non-steroids.

If anyone thinks that Immard will completely cure rheumatoid arthritis, then I want to disappoint you - this disease is incurable, but drugs such as Immard help restore joint mobility and get rid of other symptoms. To put it simply, they make life easier. This is not the only remedy, but it is the most budget-friendly and at the same time effective. The only warning is that to reduce the level of adverse reactions, be sure to adhere to the dosages and all doctor’s instructions.