RU2580301C1 - Method for treatment of human systemic lupus erythematosus - Google Patents

Abstract

FIELD: medicine.

SUBSTANCE: invention refers to medicine, namely to therapy and Immunology, and concerns treating Systemic Lupus Erythematosus. That is ensured by integrated treatment, consisting of two ten-days stages. First stage involves intramuscular introduction of preparations of interferon, anti aggregants and/or detoxification therapy combined autohemotherapy in form of mixture in one syringe of auto blood in amount of 2 ml and human immunoglobulin normal in amount of 1.5 ml for following 5 days. Second stage involves oral introduction of interferon inductors and intravenous infusion therapy with hepatoprotectors. Such courses of treatment is carried out once in three months. Therapeutic courses are repeated to normalize immunological, laboratory values and improving clinical presentation of patient.

EFFECT: method provides the stable remission at decrease of dependence of cytostatic agents and glucocorticosteroids.

3 cl, 2 ex

Description

The invention relates to medicine, in particular to methods for treating autoimmune diseases such as human systemic lupus erythematosus.

Human systemic lupus erythematosus (SLE) is a chronic polysyndromic disease that affects mainly young women, develops against the background of genetic imperfection of immunoregulatory mechanisms, characterized by early disability and high mortality. SLE affects mainly women of reproductive age in whom fertility does not suffer. Numerous studies confirm the adverse effect of SLE on pregnancy, its maternal and perinatal outcomes. So the frequency of spontaneous abortions in SLE is 50%, stillbirths - 35%, preterm births - 25%, and about 5% of infants suffer from intrauterine growth retardation.

Human SLE is characterized as a systemic autoimmune rheumatological disease of unknown etiology, accompanied by overproduction of a wide range of organ-specific autoantibodies to various components of the nucleus and immune complexes that cause immuno-inflammatory damage to internal organs. SLE is known as an autoimmune disease, which is quite widespread and fatal due to damage to many organs and systems. Under conditions of deficiency of T-suppressor function of lymphocytes, the production of a large number of autoantibodies is noted: antinuclear, to DNA, microsomes, lysosomes, mitochondria, blood cells, etc. Antibodies to native DNA (nDNA), which bind to nDNA, form the most immune pathogens. complexes and activate complement. They are deposited on the basement membranes of various internal organs and skin, causing inflammation and damage. At the same time, lysosomal permeability increases, inflammatory mediators are released, and the kinin system is activated. (Systemic lupus erythematosus, A manual for clinical residents, interns and cadets, Compiled by N. B. Osipok, Irkutsk, 2012).

SLE is central to the group of autoimmune diseases and is a classic example of human immunocomplex disease.

Known drugs (PM) used in the treatment of SLE: glucocorticosteroids (GA), cytostatic drugs (azathioprine, cyclophosphamide), hydroxychloroquine, non-steroidal anti-inflammatory drugs. (Systemic lupus erythematosus, Textbook for clinical residents, interns and cadets, Compiled by N.V. Osipok, Irkutsk, 2012).

A known method of treating lysozyme in the complex treatment of patients with lupus erythematosus, including aminoquinoline derivatives (delagil), presocyl and nicotinic acid preparations (Application No. 94017960 publ. 05/10/1996).

A known method of treating an autoimmune disease (for example, systemic lupus erythematosus), comprising administering to the subject of treatment an effective amount of histone hyperacetylating agent or a pharmaceutically acceptable salt thereof. (Patent US 2010204322, publ. 08/12/2010).

A known method of treating an individual, comprising co-administration of calcitonin as an agent and as a DHEA agent. (Patent WO 0135975 (A2), publ. 25.05.2001).

A known method of treating SLE of a patient, comprising administering to a patient with SLE an amount of vitamin D effective to reduce the symptoms of SLE. (RF patent WO 0066098 (A2), publ. 09.11.2000).

A known method of treating an inflammatory or autoimmune disease in a subject, which includes the introduction of mefloquinine. (Patent WO 0219994 (A2), publ. 14.03.2002).

A known method of treating a patient with an autoimmune disease or chronic immune system disorder, comprising the following steps: administering a therapeutically effective amount of an anti-CD40L compound to a patient during the first therapeutic period, in doses separated by an interval of less than about 3 weeks, and then administering a therapeutically effective amount of an anti -CD40L compounds to the patient during the second therapeutic period, in doses separated by intervals of at least about 3 weeks. (Patent EA 001426 (B1), publ. 02.26.2001.)

A known method of treating systemic lupus erythematosus (SLE), including taking an effective amount of a pharmaceutically active form of dehydroepiandrosterone (DHEA) to patients with SLE, determining, after the appointment of DHEA, indicators of disease activity and general symptoms of the process characterizing the condition of a patient with SLE: SLE activity index (IASC), degree activity of systemic lupus erythematosus (SAS), visual analogue scale (VAS) of the patient and the coefficient of severity Krupna (KSTK), the determination of the difference between the values of the indicators IASKV, SASV, VA Ш and КСТК obtained before the start of treatment and the values taken during treatment, and a decrease in three of these four indicators and either a decrease or stabilization or an increase of not more than 5% of the fourth indicator indicates that the patient is responding to DHEA intake. SLE patient is human. A patient with SLE has an IASC value higher than 2. DHEA is taken in doses and over a period of time necessary to reduce three of the four indicators of disease activity and general symptoms of the process and either reduce or stabilize or increase the fourth indicator by no more than 3% of the initial values. The above administration includes a daily oral dose of at least 100 mg of pharmaceutically active DHEA to a patient with SLE. The dose is at least 200 mg of DHEA per day for at least 40 weeks. A patient with SLE takes an orally medication from the group consisting of: a glucocorticoid, a non-steroidal anti-inflammatory agent, an immunosuppressant and an antimalarial agent until DHEA is prescribed, and this method involves continuing to take the above medication for the duration of DHEA. The above medicine is prednisone at a daily dose of at least 2 mg. A method for the treatment of systemic lupus erythematosus (SLE), including the administration of a pharmaceutically active form of dehydroepiandrosterone (DHEA) by a patient with SLE having an IASC value of more than 2, determination of disease activity indicators and general symptoms of the process characterizing the condition of a patient with SLE after the appointment of DHEA: IARCS), the degree of activity of systemic lupus erythematosus (CACS), the patient’s visual analogue scale (VAS) and Krupp severity coefficient (CCCT), determining the difference between the values of the IACCS indicators, DIA, VAS and KSTK obtained before treatment and values taken during treatment, and a decrease in three of these four indicators and either a decrease or stabilization or an increase of not more than 5% of the fourth indicator indicates that the patient responds to the reception of DHEA, in which at least 85% of the received DHEA is either in polymorphic form I, characterized by peaks of solid-state nuclear magnetic resonance at carbon-13 at 14.1 and 14.8 ppm for carbon atom No. 18 and 118.9 and 120.4 ppm for carbon atom number 6, or in polymorphic form II, characterized by peaks of solid-state nuclear magnetic resonance for carbon-13 at 13.1 ppm for carbon atom No. 18 and 119.9 ppm for carbon atom No. 6, or in a mixture thereof. At least 95% of the DHEA taken is in polymorphic form I, in polymorphic form II, or in a mixture thereof. At least 95% of the DHEA taken is in polymorphic form I. At least 95% of the DHEA taken is in polymorphic form P. A method for treating systemic lupus erythematosus (SLE), comprising administering a pharmaceutically active form of dehydroepiandrosterone (DHEA) to a person with SLE having the value of IAASC is higher than 2, the determination after the appointment of DHEA of indicators of disease activity and general symptoms of the process that characterize the condition of a patient with SLE: the index of activity of SLE (IASC), the degree of activity of systemic lupus erythematosus (SLE), the patient’s analogue analogue scale (VAS) and Krupp severity coefficient (KSTK), determining the difference between the values of the IASKV, SASV, VAS and KSTK indicators obtained before treatment, and the values taken during treatment, with a decrease in three of these four indicators and either a decrease, or stabilization, or an increase of no more than 5% of the fourth indicator indicates that the patient is responding to DHEA, in which DHEA is taken at the doses necessary to reduce the risk of an SLE outbreak for approximately 200 days at ma DHEA at least 5%. (RF patent No. 2248207, publ. March 20, 2005).

A known method of treating systemic lupus erythematosus, including drug therapy, in which, in order to increase the effectiveness of treatment while reducing the side effects of drug therapy, manual therapy is preliminarily performed, including simultaneous pushing of the spinous process of the underlying vertebra and both transverse processes of the adjacent superior vertebra at the level of C2 - Jh10, Jh12 - S3 with an effort of 20-40 kg / cm ² daily once for 30-50 days, after 1-1.5 hours hemosorption is carried out twice a day with an interval of 1 2 hours for 30-50 days, and then polysorb is used as a medicine for 30-60 days. (RF patent No.2008926, publ. March 15, 1994).

There is a method of treating patients with lupus erythematosus by administering aminoquinoline preparations or presocyl and nicotinic acid, characterized in that they additionally intramuscularly administer 5 cm ^{3 of} autologous blood saturated with 15 cm ^{3 of an} ozone-oxygen mixture with an ozone concentration of 30 μg / ml in one syringe twice a week up to 10 injections and intramuscularly injected once a day 10 cm ^{3 of an} ozone-oxygen mixture with an ozone concentration of 30 μg / ml three times a week up to 10 injections. (RF patent No. 2158129, publ. 27.10.2000).

The common disadvantages of the known methods of treating systemic lupus erythematosus of a person, which impede the achievement of the claimed technical result, include the development of the body’s dependence on the drugs administered, which provokes an increase in doses to achieve a therapeutic effect.

The main method for the pathogenetic treatment of systemic lupus erythematosus remains treatment with glucocorticosteroids and cytostatics, with long-term and fairly high doses, which often develop addiction, which provokes an increase in doses. The positive effect of therapy is achieved due to the progressive increase in therapeutic doses, which has a number of negative side effects, expressed in the development of Itsenko-Cushing syndrome with pituitary type obesity, hypertrichosis, arterial hypertension, asthenia, damage to arteries due to impaired cholesterol metabolism, increased blood sugar, infections easily join, and finally, the early development of cataracts. Characteristically, the higher the dose of glucocorticosteroids, the more severe the side effects. Also, the longer they are taken, the greater the risk of side effects. In addition, while taking glucocorticosteroids, stomach and duodenal ulcers often develop, the risks of exacerbation of chronic infections, the risk of osteoporosis, fractures and aseptic bone necrosis, and internal bleeding increase. Another undesirable effect of glucocorticosteroids is associated with the development of adrenal atrophy.

The toxic effects of hormones and cytostatics are known. The danger of their use may be in the occurrence of the so-called "rebound syndrome."

Other existing treatments for human systemic lupus erythematosus are auxiliary.

The aim of this invention is to increase the therapeutic effectiveness of the treatment of systemic lupus erythematosus in humans.

The technical result manifested in the implementation of the claimed method of treatment is to reduce the toxic effect and the absence of the body's dependence on the use of drugs, the absence of clinical and immunological signs of exacerbation of SLE, the reduction in the frequency of relapses, the onset of persistent remission, complete recovery and maximum restoration of damaged organs, restoration of reproductive function the body of women, a decrease in dependence on cytostatics and glucocorticosteroids.

The technical result is achieved by a method of treating systemic lupus erythematosus of a person, including drug therapy, in which the treatment is carried out in therapeutic courses, each of which consists of two ten-day steps, the first step involving the parallel administration of intramuscular injections of reaferon 500000-1000000 ME per day for 10 days , infusion administration of a trental antiplatelet agent and / or detoxification drug reopoliglukin in an amount of 200 ml during the first 5 days and autohemotherapy as a mixture in one spray Ace autologous blood in an amount of 2 ml and normal human immunoglobulin in an amount of 1.5 ml over the next 5 days; the second ethane includes the parallel oral administration of an interferon inducer of lycopide at a dose of 10 mg / day or galavit at a dose of 100 mg / day and intravenous administration of a heptral hepatoprotector at a dose of 400 mg in 200 ml of saline. Therapeutic courses of treatment are carried out once every three months. Therapeutic courses are carried out to normalize immunological, laboratory parameters and improve the clinical picture of the patient.

Applicants for the first time proved the reliability of the therapeutic effect of the claimed method for the treatment of systemic lupus erythematosus in humans.

When creating a treatment regimen, the following factors were taken into account:

- one cytokine can be produced by different types of cells;

- one cell can produce several different cytokines;

- one cytokine can act on several types of cells;

- several cytokines can induce the same function in a particular type of cell.

The interferon system, being the most important factor of nonspecific resistance, is present in almost every cell of the body and is aimed at recognizing and eliminating foreign genetic information. Interferons block the translation of foreign proteins. Interferonogenesis consists of three clearly following successive stages: induction - production-action and is a kind of chain reaction in response to an alarm, in this case, autoimmune processes. Interferons stimulate phagocytosis, the activity of natural killers, the expression of antigens of the main histocompatibility complex. They inhibit the formation of antibodies, the development of inflammation, delayed hypersensitivity, proliferation of lymphocytes, the complement binding reaction.

Antiplatelet agents prevent less venous and more arterial thrombosis. They disrupt the synthesis of the L-factor, necrotic tumor, help the accumulation of c-AMP in platelets, which prevents thrombosis, i.e. improve rheological properties of blood. Red blood cells become soft, supple, which is necessary for passage through the capillaries. Blood viscosity decreases, with SLE the blood is thick. Antiplatelet agents have a small vasodilating effect, thereby improving microcirculation and oxygen supply to the tissue.

Detoxification therapy includes drugs: reamberin, reopoliglyukin, polyglukin, etc.

The pathological process leads to the formation of free radicals, which provoke the development of peroxide processes, the latter circumstance leads to the final blockade of membrane pumps, tissue ischemia is aggravated. This is called "oxidative stress." Here is another important, in practical terms, biochemical equivalent that damages “oxidative stress” - the activation of polymerase reactions as a result of which free radicals “unzip” DNA, thereby blocking transcription processes. This circumstance leads to a slowdown in the rate of chemical synthesis of plastic and signal proteins in SLE.

It has been established that succinic acid, which is part of reamberin, activates the glutathione system - one of the most powerful endogenous antioxidant systems in the human body.

Reamberin enhances tissue oxygenation by increasing lung ventilation. Reamberin strengthens the diuretic component even without the use of diuretics. In SLE, a serious complication is severe kidney damage (lupus nephritis). The use of reamberin reduces hyperfermentemia, endogenous intoxication, reduces the dose of hormones. Reamberin inhibits cellular cytolysis of the liver, which is often observed with prolonged use of hormones, non-steroidal anti-inflammatory drugs, aminoquinoline derivatives, and cytostatics.

Polyglukin has a pronounced anti-adhesive and anti-aggregate effect on platelets, leading to an improvement in the rheological properties of blood. Non-toxic, prescribed in the absence of chronic renal failure (CIN).

Reopoliglyukin is used in cases of impaired capillary blood flow (the syndrome accompanying SLE), including renal blood flow, is quite effective in patients with stage II-III chronic renal failure.

Interferon inducers are used to reduce the time of administration of recombinant interferon, which, with prolonged use, can itself produce antibodies. Interferon inducers do not have the ability to induce autoimmune processes. They increase the formation of active forms of O _{2 by} phagocytes, contributing to complete phagocytosis, which causes an increase in the level of NK cells in peripheral blood. Interferon inducers thereby correct immunity. They are a family of high and low molecular weight natural and synthetic compounds. Combined use with other drugs often leads to potentiation of effects, does not lead to hyperinterferonemia, and ensures a long circulation of interferons at a therapeutic level. Interferon inducers include: cycloferon, amixin, neovir, half-dan, IL-2, IL-12, galavit, thymopoietins, lycopid, etc.

Outside the countries of the former USSR, interferon inducers are not registered as medicines.

Infusion therapy with hepatoprotectors with prolonged use of the cytostatics of patients with SLE often leads to a cytostatic disease, which is characterized by cell death. A frequent manifestation of it is liver damage, which exacerbates thrombocytopenia, reduces immunity, and increases the likelihood of bleeding. To this end, hepatoprotectors are used that inhibit the irreversible degeneration of hepatocytes. They are designed to restore the liver, its protection against intoxication.

The class of hepatoprotectors exists only in Russia and in the CIS countries.

In SLE, the main histocompatibility complex, HLA, MHC, has general biological significance:

- transplantation antigens during autohemotherapy are involved in intercellular interactions in the implementation of the immune response (a foreign antigen is presented for recognition by T-lymphocytes);

autohemotherapy regulates the immunological activity of the body.

With the help of autohemotherapy, an information signal is formed, blood is dynamized according to the principle of auto vaccine. This leads to the fact that the products of the disease and endotoxins contained in the blood of a patient with SLE lose their toxic properties and are actively excreted from the body. With the claimed method of treating SLE, autohemotherapy helps:

- mobilization of all defense mechanisms;

- increase the overall reactivity of the body;

- stimulation of blood formation;

- the formation of non-specific immunity;

- correction of the homeostatic system.

Immunoglobulins perform a protective function in the body:

- recognize a foreign substance, such as an antigen

- bind to antigen

- participate in the removal or destruction of the formed immune complexes. The use of immunoglobulin enhances the therapeutic effect of autohemotherapy.

The advantage of the claimed method lies in the fact that the dependence of the body on hormonal and non-steroidal anti-inflammatory drugs (NSAIDs) and cytostatics before microdoses is reduced, while their full cancellation is possible, damaged organs with systemic lupus erythematosus are restored as much as possible.

The claimed quantitative characteristics of the drugs are sufficient and necessary to provide them with therapeutic efficacy and prevent dose-dependent toxicity.

The method is as follows.

Treatment is carried out with therapeutic courses, each of which consists of two ten-day stages. At the first stage, parallel administration of intramuscular injections of reaferon 500000-1000000 ME per day for 10 days, infusion of trental antiplatelet and / or detoxification drug reopoliglukin in an amount of 200 ml for the first 5 days, and autohemotherapy in the form of a mixture in one autologous syringe in the amount of 2 ml and normal human immunoglobulin in an amount of 1.5 ml over the next 5 days. At the second stage, 10.0 mg / day interferon inducers of lycopide or 100 mg / day galavit are simultaneously taken orally and intravenous infusion of heptoprotectant heptral in a dose of 400 mg in 200 ml of saline is carried out. Therapeutic courses of treatment are carried out once every three months. Therapeutic courses are carried out until the normalization of immunological and laboratory parameters.

Results proving the effectiveness of the claimed method for the treatment of systemic lupus erythematosus in humans.

Example 1

A 29-year-old woman in 2009 entered the Institute of Rheumatology of the Russian Academy of Medical Sciences.

Until this time, a woman for two years was constantly taking prednisone at a dosage of 2 tablets / day for the treatment of rheumatoid arthritis. The patient's condition did not improve and in 2009 she was admitted to the Research Institute of Rheumatology in Moscow with a diagnosis of systemic lupus erythematosus in combination with Sjogren’s syndrome. Upon admission, she complained of pain in the small joints of the hands, nonspecific skin rashes, alopecia, general weakness, high fever (38-39 ° C), weight loss, and enlarged lymph nodes. During the examination: hypergammaglobulinemia, HB 102 g / l, ESR - 80 mm / h, anti-DNA 45.9 IU / ml, RF in high titers - 273.3 IU / ml, CRP - 80 mg / d. Before receiving treatment at the Research Institute of Rheumatology RAMS, the patient was constantly taking prednisone and methotrexate for two years.

The patient underwent therapeutic courses of treatment according to the claimed methodology during the year (i.e. 4 therapeutic courses, each of which included two stages) with a gradual decrease in the dose of prednisolone. At the first stage of the therapeutic course, intramuscular injections were administered in the form of EC 500000-1000000 ME peraferon per day for the first 10 days, infusion therapy with polyglucin was carried out, from the group of antiplatelet agents - trental, in the amount of 200 ml for the first 5 days and autohemotherapy as a mixture in one syringe autologous blood in the amount of 2 ml and normal human immunoglobulin in the amount of 1.5 ml over the next 5 days. After the first therapeutic course, the patient during the second stage (next 10 days) orally took interferon inducers - lycopid in the amount of 10 mg / day every other day, along with intravenous infusion therapy with hepatoprotectors (heptral 400 mg in 200 ml of saline).

After a one-year course of therapeutic treatment, the patient complained of periodic non-intense pain in the small joints of the hands. The temperature returned to normal, the lymph nodes, rashes on the skin, alopecia disappeared. Disability has fully recovered. Nevertheless, a reduced HB remained - 113 g / l, ESR - 37 mm / h, CRP - 12 mg / l, anti-DNA - 12.2 IU / ml Less than 20 - negatively), CEC - 188 Units.

In the second year of treatment according to the claimed methodology, the clinical and immunological signs of SLE completely disappeared. HB - 131 g / l, ESR - 11 mm / hour, CRP - negatively, RF - negatively, anti-DNA - negatively.

After two years of intensive treatment according to the claimed method, the patient became pregnant twice with an interval of one year and safely gave birth to two healthy children (2011 and 2013).

Since 2011, the patient every year passed immunological and laboratory tests, which showed no signs of exacerbation of SLE. No complaints at this time. The patient began full-time work.

The given clinical case allows us to evaluate the result of treatment of a patient with SLE according to the claimed method, such as a decrease in the toxic effect and the absence of an organism's dependence on the use of drugs, the absence of clinical and immunological signs of exacerbation of SLE, a decrease in the frequency of relapses, the onset of persistent remission, full recovery and maximum restoration of damaged organs, restoration of the reproductive function of the woman’s body.

Example 2

A patient aged 66 was admitted for treatment to the city clinical hospital named after Botkin with a diagnosis of long-term SLE with damage to the joints, kidneys, lungs, blood. Until that time, from 33 years old, she suffered from pains in the knee and ankle joints, accelerated ESR was noted. Diagnosed with infectious and allergic polyarthritis, was treated with penicillin drugs. Since 2004, a sharp deterioration began. The patient was diagnosed with hemolytic anemia, myeloid, dysplastic syndrome, two-growth cytopenia, hyperazotemia, liver enlargement: +6 cm below the edge of the costal arch, an increase in lymph nodes. HB - 60 g / l, platelets 82 × 109 l, ESR - 70 mm / h, proteinuria 1-1.5 g / l, leukocyturia, erythrocyturia. CRP-10 mg / l, anti-DNA - 3.312 IU / ml, ECHO-KG FV - 46, creatinine - 220 μmol / l, bilirubin 35 units, ALT - 70 units, LDH - 535 units, echo KG: ejection fraction - 46%, sinus fluid, chest x-ray - congestion in the lungs. The diagnosis of long-term SLE with the defeat of joints, blood, kidneys, lungs, lupus nephritis, anemia was first established. The patient was treated with a metipred 250 mg / day intravenously, prednisone inside at a dose of 30 mg / day with a gradual decrease to 20 mg / day. Discharged with improvement. From 2005 to 2008, the patient constantly took prednisolone in the amount of 4 tablets / day. With an independent reduction in the dosage of hormones, the condition worsened sharply and the patient returned to the previous dosage. In 2008, trophic ulcers on the legs joined the above complaints. The conclusion of the rheumatologist: “The patient has a systemic lupus erythematosus with a long course with immunological activity (hypocomplementemia, increased titers of antibodies to DNA, antibodies to phospholipids), anemia of mixed origin. Since 2008, treatment has been carried out according to the claimed methodology. At the first stage of the therapeutic course, intramuscular injections with drugs from the group of interferons Reaferon EC 500000-1000000 ME per day were administered, infusion therapy with drugs from the detoxification group - reopoliglukin in the amount of 200 ml for the first 5 days and autohemotherapy as a mixture in one syringe autologous blood in an amount of 2 ml and normal human immunoglobulin in an amount of 1.5 ml over the next 5 days. After the first therapeutic course, the patient during the second stage (next 10 days) orally took interferon inducers - galavit in the amount of 100 mg / day, along with intravenous infusion therapy with hepatoprotectors No. 5 (heptral 400 mg in 200 ml of saline), reamberin 200 ml / day intravenously No. 5. The treatment of the patient was well tolerated.

After five courses of the claimed method of treating SLE: HB - 127 g / l, platelets 174 × 10 ⁹ l, ESR - 7 mm / h, proteinuria in the urine protein 0.09 g / l, erythrocytes 1-2 in the field of view, anti- DNA - 83.37 IU / ml, creatinine - 158 μmol / L, ECHO-KG FV - 46%, bilirubin - 15 units, ALT - 26 units, ACT - 29 units, ultrasound of the liver - normal sizes. Treatment with prednisone decreased to 1 tablet / day, azathioprine to 1 tablet / day.

After a five-year treatment period, in 2013, the conclusion of the rheumatologist is as follows: in a patient with a prolonged course of SLE, the clinical and immunological manifestations of activity are currently minimal. Renal failure does not progress. Anemia without signs of iron deficiency does not require correction. Treatment with prednisone and azathioprine remained unchanged.

During the period from 2005 to 2015, the patient constantly underwent a detailed examination in the city clinical hospital named after Botkin.

In 2014, against the background of constant declared therapy, the patient had the following indicators: HB - 119 g / l, platelets 105 × 10 ⁹ l, ESR - 22 mm / h, proteinuria in the urine protein 0.47 g / l, red blood cells negative, anti-DNA - 7.6 IU / ml, creatinine - 156 μmol / l, liver biochemical parameters are normal, liver sizes are normal, ECHO-KG EF - 64%. Treatment with prednisone and azathioprine remained unchanged. The patient's condition remains stable. There were no clinical and immunological signs of exacerbation of SLE. There were also no signs of exacerbation of urinary tract infection.

In 2015, after a survey at the city clinical hospital named after Botkin’s conclusion of a rheumatologist: “The patient has no clinical and immunological signs of exacerbation of SLE. There are also no signs of an exacerbation of urinary tract infection. The patient's condition is relatively satisfactory, there is no edema. The condition is stable. ”

The given clinical case allows us to evaluate the result of treatment of a patient with SLE according to the claimed method as reducing the toxic effect and the absence of the body's dependence on the use of drugs, the absence of clinical and immunological signs of exacerbation of SLE, reducing the frequency of relapses, the onset of persistent remission, restoration of damaged organs, reducing dependence on cytostatics and glucocorticosteroids.

The shown results of clinical studies suggest a significant improvement in clinical and immunological efficacy and apply the claimed method for the treatment of systemic lupus erythematosus in humans.

Thus, the proposed method for the treatment of human systemic lupus erythematosus reduces the toxic effect, the absence of clinical and immunological signs of exacerbation of SLE, the rate of relapse is reduced, the onset of persistent remission, the full recovery and restoration of damaged organs, the restoration of the reproductive function of the female body, the dependence on cytostatics and glucocorticosteroids is reduced .

Claims (3)

1. A method of treating systemic lupus erythematosus of a person, including drug therapy, characterized in that the treatment is carried out in therapeutic courses, each of which consists of two ten-day steps, the first step involving the parallel administration of intramuscular injections of reaferon 500000-1000000 ME per day for 10 days, infusion administration of a trental antiplatelet agent and / or detoxification drug reopoliglukin in an amount of 200 ml during the first 5 days and autohemotherapy as a mixture in one autologous syringe in an amount of 2 ml and normal human immunoglobulin in an amount of 1.5 ml over the next 5 days; the second stage includes the parallel oral administration of an interferon inducer of lycopide at a dose of 10 mg / day or galavit at a dose of 100 mg / day and intravenous administration of a heptral hepatoprotector at a dose of 400 mg in 200 saline. 2. A method of treating systemic lupus erythematosus of a person according to claim 1, characterized in that the therapeutic courses of treatment are carried out once every three months. 3. A method of treating systemic lupus erythematosus of a person according to claim 1, characterized in that the therapeutic courses are carried out to normalize immunological, laboratory parameters and improve the clinical picture of the patient.