The etiopathogenesis of this medical condition is not consensual among specialists but its study is still continuing his development.
Peyronie disease is a local idiopathic fibrosis of the penile tunica albuginea and/or the areolar tissue conjunctive located between the tunica albuginea and the corpus cavernosum. This condition develops itself through a multifocal structural degeneration of the penile tunica albuginea and the adjacent cavernous tissue, presenting the following significant symptoms:
- Pain in 50 to 70% of patients;
- Pathological curvature of the penis during erection in 80 to 100% of the patients;
- Erectile dysfunction in approximately 30% of the patients [W. Weidner et al., 1997];
The etiopathogenesis of Peyronie disease is arguable. Some researcher´s understand that the traumatism or the excessive torsion of the erectile penis can generate bleeding in the space beneath the tunica albuginea, consequently affecting its structure [C.J. Devine et al., 1997]. In this case, the microlesions of the blood vessels are closed by the means of the fibrin, which anticipates the formation of the plaques [V.E. Mazo, 1985; K.D. Somers, D.M. Dawson, 1997].
It has not yet been discovered the genetic propensity for Peyronie disease but some authors tend to associate this pathology to the Paget´s disease of the bone [K.W. Lyles et al., 1997], to the Dupuytren contracture [L.M. Nyberg et al., 1982] and to some subtypes of HLA´s [M.S. Ltffell, 1997].
According to D. Schiavino and their collaborators (1997), the autoimmune component takes part in the pathogenesis of this disease. The elevated content of antielastin antibodies in the blood plasma that we find in Peyronie patients can also be seen as a sign of the autoimmune character of this disease [S. Stewart et al., 1994]. Thus, we have subpopulations with a genetic background with propensity to create Peyronie plaques during the cicatrization of lesions.
Initial histologic stages of this disease are characterized by a perivascular inflammatory infiltration of the lymphocytes of the tunica albuginea and the formation of the conjunctive tissue between this last one and the corpus cavernosum [W. Weidner et al., 1997]. This inflammatory phase produces the activation of fibroblast´s, followed by a structural alteration of the tunica albuginea and the adjacent tissue. Hence we can observe an excessive and pathologic deposit of collagen (mainly type III), the growth of fibrin concentration and the decrease or fragmentation of the elastic fibers [G. Brock et al., 1997]. X-rays also show dystrophic calcification in approximately 30% of these patients [M.R. Gelbard, 1998]. 1478
The synthesis of normal collagen and the fibrosis process are both sensible to biological active substances like the case of interleukin-1, to the tumor necrosis factor, the epidermal growth factor and finally the transforming growth factor beta (TGF- β)(A.I. El-Sakka et al, 1998).
The insertion of the transforming growth factor beta or its analogous the cytomodulin, into the tunica albuginea, creates histologic reactions in the form of chronic cellular infiltrations, focal or diffuse elastosis, thickening, disorganization and aggregation of collagenous fibers. This scenario proves the transformational growth factor beta´s role in the pathogenesis of Peyronie disease [A.I. El-Sakka et al., 1997].
The above data indicates us the existence of four major conditions in the development of Peyronie disease, in individuals with a genetic predisposition:
Penile closed trauma;
• Bleeding within the multi-layer structure of the tunica albuginea;
• Fibrin and inflammatory cells deposits;
• Elevated expression of cytokines and growth factors, which stimulate the production of excessive quantities of extracellular matrix proteins, inhibiting the action of metalloproteinases.
Growth factors like the transformational growth beta can lure more inflammatory cells, thus creating a vicious circle. The outcome is a long-lasting and inflammatory process of the extracellular matrix, accompanied by the excessive formation of elastic and collagenous fibers which are incorrectly organized, thus leading to the focal loss of elasticity in the tunica albuginea.
Taking in consideration the etiopathogenesis and the histologic alteration of the disease, we defend that the traditional treatment of the pathologic collagenous deposit in the penile tunica albuginea, is of the utmost importance. It is now known that the interferon alfa-2b has the ability to modify the metabolic activity of the in vitro fibroblasts, therefore causing the decrease of collagen production and the increment of collagenase [M.R. Duncan et al., 1991].
Laser therapy should be combined with the injection of interferon alfa-2b [L.P. Ivanchenko et al., 2003]. These injections are administrated twice a week, in a dosage of 1 to 3 million ME.
The totality of patients included in the study of indicators related with interferon, showed a significant decrease of induced alfa interferon and gama interferon. After the treatment, all these parameters and their positive dynamics got normalized.
Therefore, the combination of magneto-laser and the administration of interferon alfa-2b was indeed an effective one in the treatment of the 2nd stage Peyronie disease, mainly by eliminating pain and diminishing the curvature of the penis.
By the virtue of its analgesic, inflammatory and immunomodulatory effects, the low frequency laser radiation is recommended for the treatment of the Peyronie disease in the 1st and 2nd stages. For the 3rd and 4th stages, the recommended treatment is chirurgic intervention, however, it´s possible to use magneto-laser therapy to decrease the perifocal inflammation surrounding the plate during the pre-operative period and also using it to prevent recurrences.
We still haven´t discovered the genetic tendency of Peyronie disease but we suspect that that may be its source. Nonetheless, laser therapy remains an effective treatment.