Transurethral microwave thermotherapy of benign prostatic hyperplasia : mechanisms of action and clinical outcome

Background. The therapeutic value of transurethral microwave thermotherapy (TUMT) in benign prostatic hyperplasia (BPH) is a matter of debate. Aims. Evaluation of the clinical effect of TUMT and of various duration of the treatment; investigation of the kind and extent of tissue lesions induced by TUMT and of the mechanisms behind the therapeutic effect; investigation of the effect of heat on human prostate stromal cells in cell culture. Material and methods. Patients were evaluated before and after TUMT with respect to symptoms, micturition frequency, and urodynamic parameters. Selfassessment was done after one year. Sham therapy was compared to 30 or 60 minutes of TUMT. Effects of TUMT on prostate innervation were studied by immunohistochemical staining of specimens from transurethral resection (TURP). Sensitivity thresholds in posterior urethra were measured before and after TUMT. Morphological alterations in prostatic adenomas following TUMT were studied. Cultures of prostatic cells were studied for apoptosis following exposure to moderate heat. Results. TUMT significantly improved symptom scores, voiding frequency, and maximum urinary flow rates (Qmax). TUMT was superior to sham therapy; 30 and 60 min of TUMT were equally successful. TUMT markedly reduced nerve fibres in the smooth muscle layer of posterior urethra. TUMT was followed by elevated sensory thresholds in posterior urethra, in conjunction with decreased urge. TUMT produced necrosis in a limited part of the prostate, surrounded by areas of apoptotic cell death, confirmed by TUNEL staining technique. Heat induced extensive apoptosis in cultured prostatic stromal cells. Conclusion. TUMT does have beneficial effect in uncomplicated BPH. Decrease in obstructive symptoms may be due to denervation in periurethral prostatic tissue, causing diminished tension in smooth muscle cells, plus tissue ablation in a limited area. Decrease of urge may be due to weakened excitatory signals to the bladder caused by sensory denervation of posterior urethra. TUMT produced necrotic lesions in the adenoma, surrounded by apoptototic cell death in areas of lower temperature elevation. The latter process was confirmed in cell culture studies