Clinical value of dynamics of streptokinase antibody level in antibiotic-resistant chlamydial prostatitis patients during enzyme therapy with streptokinase

Edvins Platkajis, Pavels Ivdra, Alfreds Miltins, Ivars Geldners, Inara Ancupane
Riga Clinical Hospital No.7, Head doctor: E. Platkajis
Latvian Association of Physicians - Chlamydiologists

Edvins Platkajis	Pavels Ivdra	Alfreds Miltins	Ivars Geldners	Inara Ancupane

According to the immunologists' point of view, streptokinase is an antigene, which, if introduced intravenously, may cause the formation of antibodies. Biochemists and enzymologists consider streptokinase (SK) to be an enzyme - streptococcal peptidasis A.The investigations on streptokinase began in 1933 when Tillet W and Garner R.found out that by mixing human plasma or fibrinogenous clots with hemolytic streptococcal culture or filtrate, one can observe very quick dissolution of the clot (lysis) [1]. In 1945 Christensen L. and MacLeod C. stated that the bacterial factor, which was named - streptokinase, acted as a plasminogenous activator (2). SK and its proenzyme (zymogene) in the crystallyzed form was first extracted by Elliot S. in 1950 (3).

In the last 30 years SK has been used in medicine as fibrinolytic enzyme system - plasminogenous activator. SK is used for myocardial infarctions, vein thrombosis, lung artery emboly, occlusions of extremity arteries, retinal blood-vessel thrombosis and priapism.

Streptokinase in the treatment of chronic inflammatory diseases, i.e. chronic prostatitis was first used by professor V.Purmalis, P.Ivdra and professor I.Silins at the Riga Clinical Hospital No.7, receiving the USSR patent certificate for the invention n#1066604, 1984 [4]. P.Ivdra, professor V.Purmalis and E.Smiltens delivered a report on the results of chronic prostatitis treatment with streptokinase at the USSR All-Union III Congress of Urologists in Minsk in 1984 (5).

Due to occurrence of rather frequent complications, allergic and anaphylactic reactions, SK has not gained the necessary approval and evaluation from the clinicists' side. With no definite reason, physicians try to avoid using SK, giving preferance to urokinase and tissue plasminogen activator (t-PA), which are not endangered by allergic and anaphylactic complications, but are expensive and not available to broader public. One should take into consideration the fact that the resources of urokinase and tissue plasminogen activator - Alteplaze (Actilyse) are and will be limited, as a result, physicians will not be able to indicate them keeping to to the principle " what is best for the patient", but only to an elite patient group.

Low-income patients have also to be treated and they can be treated not worse than those who are well off, the only difference being the length of treatment which on average is by 30-35 days longer, most often at expense of SK desensibilization course.

SK is an enzyme drug - plasminogen activator of microbiological origin, which is and will be the main and most available fibrinolytic since its output resources are unlimited, production costs - very low, the medium for culture being the broth or milk whey plus pure hemolytic streptococcal culture.

Fibrinolytic enzymes and their activators are the basis for the enzyme therapy of inflammatory antibiotic-resistant prostatitis. Plasminogen activator SK is the cheapest and at the same time a sufficiently effective enzyme drug. Antibiotic therapy does not cause any problems since so far being ineffective, cheap antichlamydial antibiotics become effective at the background of fibrinolytic enzyme activation - antibiotic resistance disappears [6]. The length of treatment with SK depends on the clinical effect. Clinicians are of the opinion that thrombolytic therapy with SK should not exceed 5-6 days due to a considerable increase of antibody titre within this period and, as a result, there may develop severe anaphylactic reactions or some other complications.

The disadvantage of the conventional thrombolytic therapy with SK is its dissatisfying treatment results observed in more than 50% of patients in the above-mentioned 5-6 days treatment period.

How to overcome the drawbacks of enzyme therapy with SK and the complications?

The experience (18 years) we have had with SK has pointed to the necessity to make the treatment course longer. Starting with individually small SK doses, one can achieve the desensibilization effect on streptokinase. To prevent allergic and anaphylactic reactions, SK desensibilization course by enlarging the doses from 5000 - 50.000 e.u. on average lasts for 20-30 days. Small SK doses are sufficient for providing SK antibody induction, synthesis and increase of the concentration level. In this way, antibodies for SK can reach an individually maximal level and concentration, giving no rise to complications. After the desensibilization course for SK, when the antibody elimination begins, the therapy should be continued with individually maximal SK doses achieving normocoagulaemia or hypocoagulaemia.

Antistreptokinase titre, i.e., positive dynamics of the antibody level and concentration in inflammatory prostatitis has to be considered as sanogenous reaction and good prognosis for reconvalescence. V. Korzans, P.Ivdra, V.Purmalis and J.Prombergs were the first to discover the above-mentioned SK antibody dynamics and it got published in 1986 - the USSR patent certificate of inventions n# 1237213 (7).

Our experience of many years' standing prove that if the patient has received a desensibilization course with small SK doses, then the high antistreptokinase titre in a repeated enzyme therapy course with SK is rarely to cause allergic or anaphylactic complications. In 38% of patients with chronic antibiotic resistant chlamydial prostatitis, while treating them with SK, they do not develop antibodies against SK and remain at their natural background within the range of 50 - 150/200 a.b. 1 ml plasma. These patients' immune system has lost their abilities to recognize an alien agent-antigene.Allergic and anaphylactic reactions in the above-mentioned group of 38% of patients are encountered as frequently as in patients with a positive antistreptokinase titre dynamics. Patients' resistance to SK, allergic etc. complications, enzyme dose, length of the treatment depend not only on the level of SK antibody level and concentration in blood, but also on the physically-chemical properties and complement of fibrinogen molecule.

The Urology Department of Riga Clinical Hospital No.7 has been using SK for chlamydial prostatitis treatment since 1982. SK antibody induction, formation differences and dynamics have been analyzed on 800 patients, aged 16 - 18 yrs., who have undergone treatment within the last 10 years.

Patients can be divided into three basic groups depending on the formation of antistreptokinase titre.

I group.

In 342 chlamydial prostatitis patients (38%), treated with SK on average for 30-35 days, the antibodies against SK were seen not to form and they remained at the level of the natural background.

We, doctors from Riga Clinical Hospital No.7, have been the first in the world to register humoral immunodeficiency in chronic chlamydial prostatitis patients when no antibodies are formed against SK-antigen if introducing it regularly i/v, nor any adequate immune system response is seen. The patients of the above-mentioned 1 group are difficult to be treated.

I case. Patient Z.P., 59 yrs.old, case report n#6556-98, has been suffering from chronic chlamydial prostatitis for 10 years. He had been treated as an out-patient and in hospital, but the remission did not exceed 0,5-1 year.

On admission the patient complained of frequent and painful urination, pain in the genitals, pain in the back, fatigue, weakness and pressure at the nape. Using direct immunofluorescence (DIF) method with monoclonal antibodies, (+) chlamydial antigene structures were diagnosed. Using indirect immunofluorescence (IIF) method, Chlamydia trachomatis antibodies in blood (-) were not diagnosed due to immunodeficiency.

When starting enzyme therapy, the prostate gland was flat, poorly outlined due to paraprostatitis,with smoothed posterior fissure, hard consistency, rigid, diffusely - tender. USS of pelvic organs detected g.prostatae 5,5 x 5,5 cm with tiny calcinates in parenchyma.

CLINICAL DIAGNOSIS:
1) Relapse of urogenital chlamydiosis;
2) Chronic calculous chlamydial prostatitis in the 3rd -4th inflammatory stage;
3) Paraprostatitis;
4) Antibiotic-resistance.

Before the enzyme therapy, antistreptokinase titre - 150 a.v. 1 ml plasma. Coagulogram indices - in norm.

During the enzyme therapy, the patients received SK doses from 10.000 to 350.000 e.u. i/v once a day for 44 days. Total dose of SK course - 11.790.000 e.u. Simultaneously the patients were given antibiotics against chlamydia: doxicillin in capsules, macropen pills, erythromycin i/v, abaktal i/v/, cephalosporin i/v and vitamins.

On every seventh day of the course we were determining the antibodies against streptokinase. Antistreptokinase titre in plasma from 1-44th day did not exceed 100 a.u. 1 ml plasma ( Table n#1). The patient was registered to have negative antistreptokinase titre dynamics. It pointed to humoral immunodeficiency and doubtful prognosis for treatment results. At the end of the therapy the patient felt well, complaints expressed on admission, had completely disappeared. By palpating the prostate gland it was found to be flat, with smoothed posterior fissure, rigid, unpainful. The inflammation had regressed, remission stage - achieved. A repeated enzyme therapy course was planned considering the length of the remission period.

Remission period lasted only for 6 months and a new exacerbation of chronic calculous chlamydial prostatitis was diagnosed. This issue does not mean the dead-lock with SK. Negative dynamics of antistreptokinase titre and short periods of remission call for urokinase and tissue plasminogene activator (t-PA) [8;9]to be extra indicated to SK.

Table n#1

ANTISTREPTOKINASE TITRE DYNAMICS
(abtibody units in 1 ml of plasma)

II group.

184 chlamydial prostatitis patients (20,5%) were registered to have a poorly marked SK antibody formation. During the enzyme therapy with SK, the antibody level did not exceed 250 - 500 a.u. 1 ml plasma (Table n#1).

III group.

During the enzyme therapy with SK the antibody level in 374 (41.5%)chlamydial prostatitis patients increased from 50 a.u. to 1000 - 3000 and more a.u. 1 ml plasma. The patients of this group havd a marked positive dynamics of antistreptokinase titre with antibody induction, synthesis and storage level and consequent elimination abilities at the final stage of the enzyme therapy course. The patient's immune system responded to i/v SK antigene with an adequate antibody formation. Thus, only less than a half - 41,5% of chlamydial prostatitis patients had not lost the abilities to recognize i/v antigene - SK and responded with sufficient antibody formation. The higher was the increase of antistrepotokinase titre in dynamics, the better were the reconvalescence perspectives, which was contrary to regular thrombolytic therapy.

In cases of chlamydial reinfection or relapse, one could observe and register the loss of SK antigene- specific response, antibody formation blockage with a negative dynamics of antistrptokinase tire, if the patient had earlier (some months or years) undergone SK therapy.

Doctors P.Ivdra, A.Miltins, prof. V.Purmalis, J.Prombergs and V.Pakalne of Riga Clinical Hospital No.7 were the first to detect secondary induced SK antibody formation blockage and registered this priority by USSR patent certificate of inventions n# 1534785, ........ 05.05.88. P.Ivdra delivered a report on the peculiarities of antistreptokinase titre dynamics in chronic prostatitis patients at the 4th All-Union Urologists Congress in Moscow in 1990 (10;11).

The organism of chlamydial patients makes use of specific immune system defence mechanism which is formed by T cells and B-ly lymphocytes created by the bone marrow.

B-ly cells are capable of forming antibodies against streptokinase, chlamydia, viruses, bacterial components and other alien agents, defined as antigenes. (P.Ivdra, prof. I.Silins. IV All-Union Urologists Congress, 10-12 October, 1990, pp.359-360, Moscow) (12).

Antigenes stimulate the formation of antibodies. An antibody, after combining with an antigene, make up an immune complex which activizes macrophages. The immune complex acts as an activator for the enzyme system - complement. An activized complement can destroy chlamydial antigene structures. By combining with a great number of antigenes and antibodies, it forms the network, the conglomerates that are hard to be split (hydrolized), the ones that macrophages cannot phagocytize. The aim of the enzyme therapy pathogenetic mechanism of chlamydial prostatitis patients is to achieve the activation of fibtinolytic enzyme system with an aim to activize macrophages and destroy the immune complex by hydrolyzing and phagocytizing them.

Contrary to that, by using antiinflammatory and immunosuppressive drugs, including the hormones, a considerable improvement can be achieved because the chlamydial formation is reduced.

In chronic chlamydial patients, when using IIF method to determine Chlamydia trachomatis antibodies in blood, they are found in the low titre (+) 1:16 or they are not diagnosed at all. More reliable are the cases when the antigene structures are diagnosed, but chlamydial antibodies in blood cannot be found. As a result, fewer immune complexes are formed and the disease activity decreases. Antibody formation, however, is the basis for specific immune system defence mechanism. Therefore, the treatment with hormones, antiinflammatory and immunosuppressive drugs weaken the immune system which is not able to react normally to any antigene structures further on. The immune complexes do not become hydrolyzed, they remain in their places, and the complement. in its turn, may continue its destructive effect. This is why the antiinflammatory drugs do not cure inflammations caused by chlamydial infections but only lessen some of their manifestations.

Such enzyme drugs as streptokinase, urokinase and tissue plasminogen activator (t-PA) activate fibrinolytic processes and hydrolysis of immune complexes, improve resistance of macroorganisms, fastens the regression of the inflammation, shortens the time needed for the treatment.

Not uncommonly, the course of the disease at the beginning of the treatment gets worse for a while. There may be the evidence of some seeming complications: hyperpyrexia, arthralgias, abdominal pain syndrome and thoracal (between ribs) pain syndrome. The main attention to be paid to is: while infusing SK i/v, one should be aware of collapse and anaphylactic shock due to formation of vasoactive peptides. SK use deals with an intensified hydrolysis of immune complex, as well as their riddance of tissues.

As a result, blood circulation seems to have a greater number of immune complexes, hyperergic responses appear, temperature runs up to 38-39 C, fever, etc. If therapy is continued and SK dose is sufficient, in a short while the reconvalescence begins.Transitory allergic reactions are not the contraindications for the enzyme therapy with streptokinase.

II case. Patient I.P., 38 yrs.old, case report n# 233741-98, has been suffering from chronic chlamydial prostatitis for more than 5 years. Accompanying disease - vulgar psoriasis for 20 years,due to which he has got II disability class. In the last 1,5 year he has been hospitalized and treated at the leading Riga clinics for 5 times: Railway Hospital "Bikernieki" ( 3 times), clinic "Linezers" and State Infectology Centre - 65 days altogether. The prescribed antibiotic therapy had been ineffective. Due to antibiotic resistance he had been hospitalized at the Urology Department of Riga Clinical Hospital No.7, where the enzyme therapy with fibrinolytic enzyme system activator - streptokinase (SK) was administered. On admission, the prostate gland was deformed, with smoothed posterior fissure, asymmetrical because of paraprocesses on both sides, hard and rigid and painful in the centre.

By using direct immunoflurescence method (DIF) with monocloncal antibodies, there were diagnosed (+) chlamydial antigene structures. By indirect immunofluorescence method (IIF) Chlamydia trachomatis antibodies in blood -2(+) titre 1:16.

In the exacerbation stage psoriasis covered almost all the body.

Clinical diagnosis:
1) Urogenital chlamydiosis;
2) Chronic chlamydial prostatitis in the 3rd inflammatory stage;
3) Paraprostatitis;
4) Antibiotic resistance;
5) Vulgar psoriasis in exacerbation stage.

Before the enzyme therapy, antistreptokinase titre 50 a.u. 1 ml plasma. The treatment was started with streptokinase in small, incrementing doses, starting with 15.000 e.u. i/v once a day. On the 8th enzyme therapy day, antistreptokinase titre reached 300 a.u. 1 ml plasma. Therapy was continue by increasing SK dose up to 150.000 e.u. On the 29th enzyme

therapy day, streptokinase titre was 1200 a.u. - the same as in the previous time on the 22nd day. It seemed to be the maximal SK antibody level and the enzyme therapy was continued.

On the 36th enzyme therapy day we registered the beginning of SK antibody elimination, because antistreptokinase titre decreased to 800 a.u. 1 ml plasma. Antibody dynamics during the enzyme therapy with a subsequent antibody elimination could be considered as a positive sanogenous reaction. The patient received SK for 37 days with the total course dose of 3.200.000 e.u.

After the treatment, the prostate gland was well-outlined, posterior fissure could be distinguished, the lobes -symmetrical, smooth, unpainful. The prostate gland - cured. One should mention that signs of psoriasis disappeared completely and there was achieved a convincing remission stage of vulgar psoriasis.

The enzyme therapy course of chronic chlamydial prostatitis can be cancelled only if SK antibody formation and concentration in blood have received an individually maximal level, and stopped with a successive antibody elimination, otherwise, there may develop a relapse of chlamydial infection.

Chlamydia trachomatis induced prostatitis may be not only a local inflammatory process, but most commonly the cause for various complications, for example, paraprostatitis, urogenital venous plexus inflammation, inguinal lymphadenitis, conjunctivitis, Reiter's syndrome, polyarthritis and other diseases. Prostatitis may proceed in a latent form and in such a case the complications quite often may prevalent as the basic disease. If chlamydial prostatitis is not treated, it is impossible to cure complications caused by the disease and one may get an impression of an antibiotic resistance.

III case. Patient I., 47 yrs.old, case record n# 24491-98, had been suffering from chlamydial prostatitis and polyarthritis for 4 years. Daugavpils doctors diagnosed the chlamydial infection, but the antichlamydial antibiotic therapy proved to be ineffective. Due to the exacerbation of polyarthritis, the patient was transferred to Riga Clinical Hospital No.7, the Neurology Department. Diagnosis: reactive arthropaty and arthralgias of unclear genesis.The patient underwent treatment at the Neurology Department for 8 days and then was transferred to the Therapeutic Department.

Therapeutists' differential diagnosis was rheumatoid arthritis. The patient complained of pains in the joints, limited range of movements in general in all joints - more painful in the left wrist and knee joints. In the knee joints - the exudate with a marked ballotation of the patella. Swelling of the joints of the left hand.

Roentgenologist's conclusion: Articulatio radiocarpea arthrosis, wrist bone osteoporosis with marked sclerosis at the articulation surface, dystrophic changes similar to the deformative arthrosis in the metacarpal bones of the right hand. Initial changes like in ligamentoses in both knee joints.

Despite the dominating clinical picture of polyarthritis, specialists in the Therapeutic Department succeeded in making the exact diagnosis: chronic calculous chlamydial prostatitis and chlamydial polyarthritis. Diagnosis of prostatitis was confirmed by USS, because in the ultrasonoscopy there were diagnosed calcinates in the prostate gland. On the 9th day the patient was transferred to the Urology Department.

On examination the prostate gland seemed to be asymmetrical due to paraprostatitis - deformed at the right side,with shallow posterior fissure, polymorphous consistency, diffusely - painful. Inguinal lymphadenitis was diagnosed. The diameter of lymh nodes was 0,5-0,8 cm.

Clinical diagnosis:
1) Urogenital chlamydiosis;
2) Chronic calculous chlamydial prostatitis;
3) Paraprostatitis;
4) Exacerbation of chlamydial polyarthritis;
5) Inguinal lymphadenitis.

In coagulogram there were definite hypercoagulaemia signs. Antistreptokinase titre 50 a.u. 1 ml plasma, i.e. within the borders of the natural background. (Table n#2). Except for coagulogram indices, ultrasonoscopic findings and roentgenogramms, the other clinical analyses and rheumatism tests were in norm. During 42 days of hospitalization at the Urology Department the patient was receiving the enzyme therapy course of antibiotics with streptase, heparin and antichlamydial antibiotics.Taking into consideration the patient's individual sensitivity and arthralgias, streptase dose round the clock did not exceed 5000 - 450.000 e.u. Steadily increasing SK dose, the pain in the joints got more severe. During the treatment course the patient received streptase of 7.345.000 e.u.

The results of the treatment were evaluated assessing the patient's feeling, coagulogram indices, antistreptase titre dynamics and the eradication of chlamydial antigene structures.

The faster the antibodies were forming against streptase, the better was prognosis. When reaching the patient's individually maximal antistreptase titre level of 1000 a.u. 1 ml plasma, the antibody formation stopped and their elimination began. This type of antistreptase titre dynamics was considered to be a sanogenous response.

It was typical for the antibody titre to grow much slower than it was in the cases of thrombolytic therapy.

For the patient I.L. the antistreptase titre from 50 a.u. reached the level of 400 a.u. on the 12th day of the enzyme therapy. On the 20th day the antibody titre was 800 a.u. And only on the 27th enzyme therapy day the individually maximal 1000 a.u. level of antistreptase titre was achieved. On the 34th anzyme therapy day, the antistreptase titre decreased to 600 a.u., which pointed to the beginning of antibody elimination. On the 41st enzyme therapy day, the antibody titre fell down to 400 a.u. 1 ml plasma. It meant that the patient had a positive antistreptase titre dynamics with the maximal rise of antibody level and the subsequent elimination, which demonstrated positive sanogenous response, complete reconvalescence and good prognosis. As a result of the enzyme therapy, the prostate gland regained its usual size, well-outlined, symmetrical, with deep posterior fissure, smooth, elastic, unpainful. Paraprostatitis had completely regressed. While treating chlamydial prostatitis, the clinical signs of polyarthritis had also disappeared during 42 days. The patient was cured. Working abilities restored.

 

CONCLUSIONS:

1. In inflammatory prostate gland diseases, if treated with SK, positive dynamics of antistreptase titre level should be considered a sanogenous response and prognosis for reconvalescence.

2. During repeated enzyme therapy course with SK, the high antistreptase titre is rarely the cause of anaphylactic complications.

3. In 38% of cases, if treated with SK, no antibodies form against SK and remain within the limits of their natural background, but the allergic and anaphylactic responses are seen as often as in patients with a high antistreptokinase level.

4. Negative dynamics of antistreptase titre requires that SK is combined with either urokinase or tissue plasminogene activator (t-PA) and then SK being repeatedly administered in individually maximal doses.

5. Only 41,5% of chronic chlamydial prostatitis patients have normal SK antibody induction, synthesis and storage abilities. Reaching the maximal antibody level, their elimination starts already at the final stage of the enzyme therapy.

6. The greater is the rise of SK antibody level, the better are the prognosis for sanation.

7. In reinfections or relapse of chlamydial infections, when being repeatedly treated by SK, one can observe and register the loss of SK antigene-specific response and the blockage of antibody formation. We have been the first to discover the blockage of secondary induced SK antibody formation.

8. During SK i/v infusion one should be aware of the collapse and anaphylactic shock which ia due to hydrolysis of the immune complexes and the formation of vasoactive peptides.

9. SK antibody rise in chlamydial prostatitis patients to the maximal level is comparatively longer - on average 25-30 days - and it determines the length of the anzyme therapy course.

10. The enzyme therapy with SK for chronic chlamydial prostatitis patients can be stopped only if SK antibody formation and concentration have reached the individually maximal level and have stopped there, and the antibody elimination has begun. In other case there may be a relapse of chlamydial infection.

 

December,1998                                      Urologist: P.Ivdra

Table n#2

COAGULOGRAM

List of Literature:

1. Tillet W.S., Garner R.L.
   The fibrinolytic activity of hemolitik streptococci.- Jornal Exptl.Med., 58, 485, 1933.
   
   
2. Christensen L.R., MacLeod C.M.
   A proteolytic enzyme of serum: characterization, activation, and reaction with inhibitors.Jornal Gen.Physiol., 28, 559, 1945.
   
   
3. Elliott S.D.
   The crystallization and serological differentiation of a streptococcal proteinase and its precursor.
   Jornal Exptl.Med., 92, 204, 1950.
   
   
4. Purmalis V.R, Ivdra P.P., Silins I.A.
   "Sposob lecenia hroniceskogo prostatita streptokinazoi"
   Avt. svid. SSSR N#1066604, 15.01.84.Bjul.N#2.
   
   
5. P.P.Ivdra, V.R.Purmalis, E.E.Smiltens.
   "Fermoterapija hroniceskogo prostatita streptokinazoi"
   v knige Vsesojuznogo sjezda urologov (18-21 ijuna, 1984g.),
   Minsk, 1984. str.251-252.
   
   
6. Pavels Ivdra.
   Hroniska prostatita enzimoterapijas indikacijas un antibiotiku rezistences regresijas iespejas.
   Latvijas Arsts, 1994/2, 120-122 lpp.
   
   
7. V.A.Korzans, P.P.Ivdra, V.P.Purmalis, J.B.Promberg.
   "Sposob lecenia hroniceskogo prostatita"
   Avt. svid. SSSR N#1237213, 15.06.86. Bjul. N#22.
   
   
8. P.Ivdra, E.Platkajis, I.Geldners.
   Indications for Enzyme therapy with Streptase, Urokinase and Tissue Plasminogen Activator - t-PA in Chlamydial Prostatitis
   http://www.expo.lv/gailes/prostatitis.htm
   
   
9. Pavels Ivdra, Edvins Platkajis.
   Usage of Tissue Plasminogen Activator in treatment of Men Pathological Climacteric and Prostatitis
   http://www.expo.lv/gailes/climax.htm
   
   
10. P.P.Ivdra, A.P.Miltins, V.R.Purmalis, J.B.Prombergs, V.A.Pakalne.
    "Sposob lecenia urogenitalnogo hlamidioza"
    Avt.svid.SSSRN#1534785, DSP 05.05.88.
    
    
11. P.P.Ivdra.
    "Antitelegonez antitel k streptokinaze pri enzimoterapii osloznennih form hroniceskogo  prostatita"
      Materiali Vsesojuznogo sjezda urologov 10-12 oktabra 1990., Moskva.
    
    
12. P.P.Ivdra, I.A.Silins.
    "Diagnostika i lecenije V-kletocnoi imunnoi nedostatocnosti u bolnih hroniceskom prostatitom"
    Materiali Vsesojuznogo sjezda urologov 10-12 oktabra 1990., Moskva, str.359-360.

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• PROTEINASES IN ENZYME THERAPY OF CHRONIC PROSTATITIS
• TREATMENT OF CHLAMYDIAL SPONDYLITIS
• STREPTOKINASE IN GERONTOLOGY
• SPECIFICITY OF ENZYME THERAPY IN TREATMENT OF LATE INFLAMMATORY FORMS OF PROSTATITIS
• POSSIBILITIES OF ENZYME THERAPY IN PAIN SYNDROME
• CHRONIC FATIGUE SYNDROME, FIBROMYALGIA ENZYME THERAPY
• ENZYME THERAPY OF ANTIBIOTIC-RESISTANT AND UROGENITAL CHLAMYDIOSIS
• STREPTOKINASE AS PLASMINOGEN ACTIVATION
• VIAGRA IN PROSTATITIS TREATMENT 
• ENZYME THERAPY WITH STREPTOKINASE
• CHLAMYDIAL PROSTATITIS
• ACTILYSE IN PROSTATITIS TREATMENT
• ENZYME THERAPY IN CHLAMYDIAL POLYARTHRITIS
• MEN PATHOLOGICAL CLIMACTERIC