Actilyse in Prostatitis Treatment
ROLE OF TISSUE PLASMINOGEN ACTIVATOR (t-PA) IN ENZYME THERAPY OF ANTIBIOTIC- RESISTANT CHLAMYDIAL PROSTATITIS

Pavels Ivdra, Aija Zilevica, Alfreds Miltins, Inara Ancupane
Riga Clinical Hospital No.7, Head doctor: E. Platkajis
LSU Medical Faculty, Latvian Association of Physicians - Chlamydiologists

Pavels Ivdra	Aija Zilevica	Alfreds Miltins	Inara Ancupane

Antibiotic- resistance in chlamydial prostatitis treatment is still one of the unsolved medical problems. Antibiotic- resistance is the microorganism's ability to survive despite the antibiotic presence. Microorganism, intracellulary persisting chlamydial resistance turns antibiotic therapy ineffective.

In the last years resistant microorganisms seem to have become much more aggressive. A correct choice of the method to test the antibacterial sensitivity is of great importance. The interpretation and choice of the antibacterial drug is significant in the treatment of chronic chlamydial prostatitis.

In the period from 1981 to 1999 (18 years) the Urology Department of Riga Clinical Hospital No.7 has treated 1842 chronic antibiotic- resistant prostatitis patients, aged 15 to 80 years. From the hospitalized prostatitis patients, almost 90% of cases were diagnosed chlamydial infection. Patients were administered enzyme therapy with fibrinolysin, streptokinase and, since 1994, urokinase and tissue plasminogen activator Actilyse in 103 cases { 1, 2, 3, 4, 5, 6, 7}.

Diagnostic possibilities for enzymatic activities of proteolytic and fibrinolytic enzyme ystems in dynamics proved to be an objective grounds for an optimal choice of enzyme therapy and the ability to determine the presence of positive sanogenous reaction.

Chlamydia are, as a rule, parasitic and the host cell-energodependant prokaryote-type bacteria which can develop only in the vertebrate and non-vertebrate cell cytoplasm and cause human and animal diseases.

Facilities of microbiological laboratories of to-day do not allow us to study chlamydial sensitivity against antibiotics in vitro.

The treatment of diseases, caused by intracellulary persisting chlamydia, is one of the most difficult tasks of enzyme-antibiotic therapy to solve, because it calls for the activation of prolteolytic and fibrinolytic anzyme systems at the cellular level.

The task and goal of the enzyme therapy is to achieve the regression of destructive changes in the cells caused by antibiotic- resistant, intracellulary persisting chlamydial infection and to restore the cell's energoresources by activating proteolytic and fibrinolytic enzyme system at the cellular level and not so much at the peripheral blood circulation level.

Single of recurrent activation of fibrinolytric enzyme system of peripheral blood circulation by streptokinase (SK) alone does not guarantee any positive sanogenous reactions of etiopathogenetic anzyme therapy nor does induce the tissue plasminogen activation.

When starting an enzyme therapy by SK, one can quite often see a secondary-induced hypercoagulaemia and hyperfibrinogenaemia. In such cases it is necessary to have a tissue plasminogen activator (t-PA) or urokinase.

When treating by SK, fibrinolytic enzyme system activation can be achieved only after the desensibilization course against SK applying the same SK in small doses. A desensibilization course lasts on average 30-35 days, while SK antibody titre reaches its maximum level and the concentration, and then starts to decrease. By achieving elimination of SK antobodies, the blockage of antibody induction and complete blockage of genesis, streptase in the dose from 750 000 - 1 000 000 e.u. provides the activation of fibrinolytic enzyme system { 7}.

In order to decrease the length of treatment, one should indicate SK (t-PA) Actilyse together with streptase.
The aim of the enzyme therapy is the induction of intracellular sanogenous reaction.

The next aim of the enzyme therapy is to resore the destroyed cellular energoresources resulting from a chlamydial infection and to provide the eradication of chlamydial antigene structures and the elimination of antichlamydial antibodies.
In clinic the chronic chlamydial prostatitis patients are seen to have two different antibiotic- resistances - dependant on microorganisms and macroorganisms. Microorganism-dependant antibiotic- resistance may commonly be observed in 1-2 phases of prostatitis.

Macroorganism-dependant chlamydial antibiotic- resistance is most commonly seen in 3-4 inflammation phases of the prostatic gland, mainly due to complications: scarring deformation of the prostate, paraprostatitis, inflammation of urogenital vein plexus, dyscoagulaemia, hypercoagulaemia, cell and humoral immunodefficiency.
Secondary antibiotic- resistance can be related also to the enzymatic defect of tissue plasminogen activation in cells. The cause of the enzymatic defect of plasminogen activation is the result of being run out of energoresources of infected cells, resulting in depression of proteolytic and fibrinolytic enzyme system activity.

Chlamydia by parasiting in the host's cells and consuming cellular energoresources establish plsminogena-activation enzymatic defect at the tissue level. This, in turn, causes the exhaustion of the patient's immune system defense.
The immune system loses its ability to recognize strange antigen structures - chlamydia, nor can induce the synthesis of chlamydial antibodies.

Problems of antibiotic- resistance may be solved by encouraging proteolytic and fibrinolytic enzyme system activation not only at the level of peripheral blood circulation and microcirculation level but, mostly, at the intracellurlar level.

The significance of intracellular proteinases and their proteolytic activities in protein change are being investigated and are well-known to biochemists and biologists. The tissues contain active proteolytic enzymes - proteinases and peptidases. Intracellular proteinases take part in hydrolysis of physiologically active substances right in the cells {8}.

In cases of intracellular persistence of chlamydia, the influence of proteinases on the cell enzymatic apparatus, cellular energoresources, zymogen activation may be inhibited. An enzymatic defect is formed at the tissue plasminogen activation level and secondary resistance against streptokinase.

There is no plasminogen deficit in the blood circulation and in the tissues, however, there is no optimal activation observed either. In clinic one can observe the depression of fibrinolytic enzyme system activity in coagulogram.

Plasmin is the second important proteolytic enzyme ( the next important after thrombin), which can hydrolyze a wide prectre of proteins, fibrinogen and fibrin.

Chlamydia, being an intracellular infection, have a destructive effect on macroorganic cells, causing a more or less marked enzymatic defect and tissue plasminogen activation insufficiency or deficit.

Clinically it is seen as dyscoagulaemia, dysfibrinogenaemia, hyperfibrinogenaemia and dysaminoacidaemia with a secondary antibiotic- resistance.
Clinical selection of antibiotic-resistant chlamydia prostatitis patients and differential diagnostics, in fact, takes place ex juvantibus, i.e., in a long run of months and even years, patients being treated by different physicians without any positive results.

In cases of physicians' incompetence, the disease progressing, there may develop complications of extragenital localization via hematogenous, lymphogenous and translocal ways, for instance, Reiter's syndrome, chlamydial polyarthritis, mesadenitis,etc.
Not uncommonly the secondary induced complications are considered by physicians as the basic disease, i.e. the main diagnosis ( example 1).

In cases of antibiotic-resistant chlamydial prostatitis, physicians indicate routine etiopathogenetic therapy, prescribing antichlamydial antibiotics together with the so-called "systemic enzyme therapy" (SET) enterally (per os or per rectum). These combined polyenzyme drugs (Wobenzym, Wobe-Mugos, Flogenzym) in various combinations contain hydrolases of animal and plant origin (proteolytic enzymes). The above-mentioned proteolytic enzymes break up plasma proteins which enter the interstitial space, thus fibrin and detrite wear away, the evacuation of these metabolites and other inflammatory products increase from the local inflammation foci, and the inflammatory process ends much faster {9}. However, tissue plasminogen (t-PA) activation does not give a clinical effect to SET.

The so-called "systemic enzyme therapy" (SET) cannot be claimed to be a universal pathogenetic therapy because it cannot cause plasminogen activation neither in peripheral blood circulation, nor at the level of microcirculation or tissues, it does not promote the induction of proteolytic and fibrinolytic enzyme system activities in all 3 of the above-mentioned levels and, especially, intracellular level.

In cases of dyscoagulaemia, hypercoagulaemia and hyperfibrinogenaemia, the effect of SET on peripheral blood circulation is of little effectiveness.
"Systemic enzyme therapy" for antibiotic-resistant chlamydial prostatitis patients can be indicated extra, either per os or per rectum. But, in order to provide an optimal pathogenetic therapy, the enzyme drugs Actilyse, urokinase and streptokinase may be drugs of choice.
Tissue plasminogen activator (t-PA) was first used in the world by the USA cardiologists {10,11}. Latvian urologists {12,13} were the first to use Actilyse for prostatitis therapy.

Physicians' incompetence quite often results in patients' extragenital complications and disabilities.

Example 1

Patient - K.G. - 19 yrs.old, treated in the Department No.11 for 47 days (case history No. 4456-99). On admission at the Urology Department - the patient complained of pains in both knee and foot joints. There was edema of IV toe,sometimes pains in the pelvic girdle and the kidney area. No complaints of urogenital character were expressed due to the latent course of the prostate inflammation.

Case history. Patient with chronic chlamydial prostatitis, has been suffering from reactive chlamydial polyarthritis for more than 5 years. From the age of 14 yrs. had been treated at Rūjiena (Latvia) hospital. Treatment at the Republican Children Clinical Hospital from 22.01.95. - 23.02.95. (Case history No.1327).

Pediatricians' diagnosis: reactive arthritis. Chlamydiosis.

The child was screened for chlamydiosis - clinically, serologically and cytologically - Chlamydia trachomatis antibodies were found in titre 1:16 (++). In direct immunofluorescence method chlamydial antigene structures were found (+). In cytogram - vakuolized cells. The findings prove the process to be induced by chlamydia. Therapy - ineffective.

During 31.07.95.-18.08.95. the patient was treated at P.Stradiņš Republican Clinical Hospital, Department No. 26 with a diagnosis: oligoarthritis of reactive urogenital etiology. Therapy - ineffective, because the prostate was not sanated. In 1995 he was treated in the Rehabilitation centre "Līgatne". Repeatedly in 1996 he was treated in the Republican Children Clinical Hospital. In 1997 the knee joint arthroscopy was performed at the Traumatology Institute.Plasmophoresis was performed 4 times at the Riga Maternity Home. During 23.02.98. - 06.03.98. (case history No. 6610) he was repeatedly treated at P.Stradiņš Republican Clinical Hospital, Dep. No. 26 with a diagnosis: reactive oligoarthritis. Right side sacroileitis.

The patient was indicated antibacterial therapy with antichlamydial antibiotics and "systemic enzyme therapy" - Wobenzym 2 tabl. 3 times a day for 1,5 months. Treatment outcome - negative.

Another time , the third time, the patient was treated at P.Stradiņš Republican Clinical Hospital, Dep. No.26 from 06.01.00. - 15.01.00. (case history No. 766). Repeatedly a general examination and all necessary clinical tests were done. X-ray pictures did not show any knee or foot joint pathological changes.

Conclusion: The patient's clinical diagnosis was correct: reactive arthritis of urogenital etiology. However, within 5 years period he has not been examined per rectum! When undergoing treatment at the leading clinics, the prostate was not palpated rectally, thus chlamydial prostatitis with a marked paraprostatitis was not diagnosed. As a result, the patient did not get an adequate treatment. Due to antibiotic- resistance, the so-called (SET) etiopathogenetic therapy which was administered together with Wobenzym tablets was ineffective.

Thanks to Rujiena hospital physicians, in February 1999 the patient was examined per rectum and by palpation prostatitis with marked signs of paraprostatitis was diagnosed.

That was transferred to Riga Clinical Hospital No. 7, Urology Dep. for prostatitis enzyme antibiotic therapy, i.e. pathogenetic therapy with streptase and Actilyse.

Objective signs: Examining rectally - the prostate is deformed, sickle-type or half-moon-type, due to a marked paraprostatitis on both sides, the lateral borders of the lobes converge with the surrounding tissues and pelvic bones, smoothed posterior fissure, rigid, hard, very painful when pressing diffusely. In the right lingual region one can feel enlarged peripheral lymph nodes 0,5-0,8 in diameter.

Clinical diagnosis made at Urology Department:

- Urogenital chlamydiosis
- Chronic chlamydial prostatitis, III inflammation phase
- Paraprostatitis
- Inguinal lymphadenitis
- Reactive polyarthritis of urogenital etiology
- Hyperfibrinogenaemia
- Secondary enzynomatic defect of tissue plasminogen activation at the cell level ( because of intracellular chlamydial persistence)
- Antibiotic- resistance

The patient had received the following enzyme antibiotic therapy:

Streptase - 15 000 u. - 750 000 u. x 1 a day, i/v, 44 days = 16 435 000 u
Actilyse - 10 mg - 20 mg x 1 a day, i/v. 6 days = 100 mg
Heparin - 5 000 u. x 1 a day, i/v, 42 days = 210 000 u.
Because of paraprostatitis - sol. Metrogyl - 0,5% - 100,0 x 3 a day, i/v,10 days = 20 vials
Erythromicin - 0,1 x 2 a day, i/v, 15 days = 30 ampoules
Amoxicillin - 500 mg x 3 a day, 30 days
Doxicillin - 0,1 x 2 a day, 45 days = 90 capsules
Cefazolin - 1,0 x 2 a day, i/v, 14 days = 28 ampoules
Abaktal - 400 mg x 2 a day, i/v, 9 days = 17 ampoules
Physical procedures

During the enzyme therapy the patient was given streptase in the doses up to 750 000 e.u. i/v one time a day.
It was not possible to indicate larger doses of streptase because of (SK side-effects) arthralgias and hyperpyrexia.

By the 30th treatment day there was a constant hyperfibrinogenaemia 5,8-4,9 g/l, fibrinogen B (++), positive etanol test, but antistreptokinase titre reached 1800 a.v. level I ml plasma. The inflammatory process in the prostate and its surrounding tissues (paraprostatitis) did not regress. Clinically there was a marked resistance to streptase with a fibrinolytic enzyme system enzymatic defect in the peripheral blood circulation,at microcirulation level and in the tissues intracellulary. The treatment was indicated by applying tissue plasminogen activator Actilyse or Alteplaze. On the 30th enzyme therapy day the patient did not get SK but Actilyse i/v 20 mg. 15 min. after Actilyse infusion, after doing a coagulogram, we registered a marked hypocoagulaemia. Spontanous fibrinolysis reached 95%, plasma euglobulin fraction fibrinlysis occurred within 3 days, but fibrinogen concentration in blood was still 4,9 g/l. And only on the 44th day, when the patient had received 20 mg Actilyse for 6 times, the fibrinogen concentration in blood normalized per 4,0 g/l, though a spontanous fibrinolysis was 85% and plasma euglobulin fraction fibrinolysis 16.

The antibody elimination against SK started and antistreptokinase titre decreased per 1400 a.v. 1 ml plasma. After receiving the etiopathogenetic enzyme-antibiotic therapy, the deformation of the prostate with a half-moon form (sickle-shaped) disappeared, the paraprocess completely regressed, the lateral outlines and the posterior fissure appeared.

The prostate was cured. Arthralgias - polyarthritis of urogenital etiology - disappeared too. Structures of chlamydial antigenes and antibodies in blood in the control test after 6 weeks were not found due to their complete elimination.

Conclusion: Due to side-effects, streptase did not provide even the enzyme system activation of peripheral blood circulation. It called for administration of t-PA extra to streptase. On the day of tissue plasminogen activation, 20 mg t-PA showed an immediate sanogenous reaction in a form of hypocoagulaemia which had not been achieved by streptase within 30 days. Actilyse i/v 10-20 mg once a day for 6 days calatyzed the activation of peripheral blood circulation and tissue fibrinolytic enzyme system. A higher tissue and cell fibrinolytic activity provided the elimination of persisting chlamydial infection intracellulary. Extra SK Actilyse optimized the regression of antibiotic- resistance and the inflammation, increased the abilities for repair and healing. Actilyse gave a possibility to shorten the length of the therapeutic course.

Example 2.

Patient - Z.B., 45 yrs.old. He was treated at the Urology Department for 28 bed days. (Case history No. 6315-99). On admission the patient complained of the pain in the sacrum, in the lower part of the abdomen, fatigue, prostration, decreased libido and potency.

The patient had been suffering for 2 years. He was treated in the district hospital by a neurologist and internist. He was examined in the Nephrology Department, where chlamydial antigene structures were found by using monoclonal antibodies with DIF method and the urologist diagnosed: chlamydial prostatitis, paraprostaitis, the inflammation of urogenital venous plexus with secondary dyscoagulaemia and antibiotic- resistance,

The patient was given enzyme antibiotic therapy with streptase, Actilyse and antichlamydial antibiotics.
The treatment was started with SK in the doses from 5000 - 500 000 e.u. and heparin 5000 u. a day. Due to SK side-effects, it was impossible to indicate larger doses. On the 20th enzyme therapy day, dyscoagulaemia with SK did not regress, the inflammation process in the prostate did not diminish. The therapy seemed to be ineffective.

Actilyse of 10-20 mg per day was indicated for 6 days together with SK 500 000 e.u. with an aim to reduce the length of treatment. As a result marked hypocoagulaemia was achieved. Within next 8 days, the inflammation of the prostate and around it, disappeared. The antibiotics which seemed ineffective so far (doxicillin, erythromicin, surlid, klafovan) became effective. On disacharge from the hospital, the patient felt well. The prostate regained its usual size, well-outlined, symmetrical, deep posterior fissue and lateral outlines appeared again, the surface of the lobes - smooth, elastic, painless. Signs of the inflammation of urogenital venous plexus disappeared, coagulogram indices normalized (table nr 1). The patient was cured. For the purpose to restore sexual functions, there was prescribed Viagra 50 mg x 1 a day. If necessity arises - control at the urologist's.

Table No. 1

Test results

Dyscoagulaemia during the enzyme therapy course with SK and Actilyse completely disappeared and proved the sanogenous reaction of t-PA at intracellular level with a following eradication of persisting chlamydia and the elimination of antibodies.

CONCLUSIONS:

1. Plasminogen activator (t-PA) Actilyse has to be indicated extra with an aim to shorten the length of treatment in cases of chlamydia trachomatis induced antibiotic- resistant urogenital inflammation.

2. Enzyme and antibiotic therapy with Actilyse is the method of choice.

3. 24 hours dose of Actilyse and the length of the treatment course depend on the patient's individual sensitivity and the phase of the prostate inflammation.

4. An individually optimal t-Pa dose is decided upon the indices of coagulogram which characterize the changes of fibrinolytic activity in peripheral blood circulation and tissues.

5. As a result of proteolytic and fibrinolytic enzyme system activation, the antichlamydial antibiotics previously ineffective become effective.

6. Actilyse can also be indicated simultaneously with streptokinase. First of all streptase is introduce i/v, and then t-PA.

7. Actilyse monotherapy is very expensive and therefore is not available for all patients.

8. Streptokinase is very cheap, its resources are not limited and therefore is available for all patients.

9. Actilyse administered simultaneously with streptokinase weakens or even completely prevents SK- caused allergic and anaphylactic reactions. There can be observed the regression of SK hyperergic reactions.

10. In the treatment of intracellulary persisting chlamydial infections, Actilyse in the interaction with SK is incomparably more effective than proteolytic plant, animal and microorganism enzymes and their activators, but the latter can be used in the out-patient practice before the hospitalization period.

11.Patients with intracellulary persisting chlamydial infection lose the antigen-specific immunological memory, but the enzyme therapy with SK and Actilyse can restore the antigene-specific immunological memory. Patients with the negative antichlamydial antibody titre are restored antigene-specific response to chlamydial antigene and antichlamydial antibodies begin to form.

12. Actilyse give a possibility to refuse from SK desensibilization course and, beginning with the 1st enzyme therapy day, to indicate the antibiotics, thus shortening the enzyme therapy course by for at least 25-30 days.

13. After introducing Actilyse i/v, the main indicator for sanogenous reaction is shortening of plasma euglobulin fraction fibrinolysis time for more than once, even in secondary induced hypercoagulaemia and hyperfibrinogenaemia cases.

14. After the enzyme therapy with t-PA the plasma fibrinogene proteolytic resistance decreases.

15. In 2, 3 and 4 prostate inflammatory phase Actilyse has a strongly expressed antiinflammatory effect. After 2 - t-PA infusions, the prostate swelling disappears. Actilyse is contraindicated in the prostatitis 1st or alteration phase.

16. Optimal results in the treatment of antibiotic-resistant intracellulary persisting chlamydial infection are achieved only in the case if, simultaneously or alternately, there are used streptokinase, urokinase, Actilyse and other proteplytic or fibrinolytic entzymes of animal and plant or microorganism origin and their activators, affecting all three enzymatic defect levels.

17. The use of plasminogen activator opens new ways for the treatment of reactive arthritis ( Reiter's disease too).

REFERENCES

1. Pavels Ivdra.
   Indications for Chronic Prostatitis Enzyme Therapy and Possibilities for Regression of Antibiotic-Resistance.
   Latvijas Arsts, 1994, 2; 120-122

2. Pavels Ivdra.
   Urokinase in Treatment of Antibiotic-Resistant Urogenital Chlamydiosis.
   Latvijas Arsts, 1995, 3; 30 - 35

3. Pavels Ivdra., Gertrude Enina, Alfreds Miltins.
   Treatment of Chlamydia-Infected MS Patients by Using Streptokinase, Urokinase and Antichlamydial Antibiotics.
   Latvijas Ārsts 1996, 1; 34 - 41

4. Pavels Ivdra.. Inara Ancupane, Ilze Katlapa.
   Possibilities of Differetial Diagnosis and Treatment of Chlamydial Induced Female Infertility by Means of Streptase and Urokinase.
   Latvijas Arsts 1996, 5; 361 - 365

5. Pavels Ivdra., Edvins Platkajis.
   Tissue Plasminogen Activator in Climacteric Virile and Prostatitis Treatment.
   Latvijas Arsts 1997, 6; 351 - 355

6. Pavels Ivdra.
   Indications for Enzyme Therapy in Chlamydial Induced Prostatitis.
   Latvijas Arsts 1998, 6; 16 - 20

7. Pavels Ivdra, Alfreds Miltins, Ivars Geldners, Inara Ancupane.
   Clinical Value of Dynamics or Streptokinase Antibody Level in Antibiotic-Resistant Chlamydial Prostatitis Patients During Enzyme Therapy with Streptokinase.
   Latvijas Arsts 1999, 5; 42 - 46

8. V.V.Mosolov
   Proteoliteckije fermenti.
   Moskva, 1971

9. Janis Baltkajs, Vladimirs Fatejevs.
   Biologic Availability of Systemic Enzyme Therapy Drugs.
   Latvijas Arsts 1999, 3; 20 - 22

10. Mueller H.S., Rao A.K., Forman S.A. and the TIMI investigators.
    Thrombolysis in Myocardial Infarction (TIMI):
    Comparative Studies of Coronary Reperfusion and Systemic Fibrinogenolysis with Two Forms of Recombinant Tissue- Type Plasminogen Activator.
    J.Amer.Coll.Cardiol. 1987, vol. 10, p. 490 - 497

11. Sherry S.
    Recombinant Tissue Plasminogen Activator (t-PA). Is It the Thrombolytic Agent of Choice for an Evolving Acute Myocardial Infarction.
    Amer. J.Cardiol. 1987, vol. 59, p. 984 - 989

12. Pavels Ivdra, Edvins Platkajis.
    Usage of Tissue Plasminogen Activator in Treatment of Men Pathological Climacteric and Prostatitis.
    1998, http://www.expo.lv/gailes/climax.htm

13. Pavels Ivdra, Edvins Platkajis, Ivars Geldners.
    Indications for Enzyme Therapy with Streptase, Urokinase and Tissue Plasminogen Activator - t-PA in Chlamydial Prostatitis.
    1998, http://www.expo.lv/gailes/prostatitis.htm

14. Edvins Platkajis, Pavels Ivdra, Alfreds Miltins, Ivars Geldners, Inara Ancupane.
    Clinical Value of Dynamics of Streptokinase Antibody Level in Antibiotic-Resistant Chlamydial Prostatitis Patients During Enzyme Therapy with Streptokinase.
    1999, http://www.expo.lv/gailes/streptokinase.htm

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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