Testosterone Replacement Therapy in Hypogonadal Men Following Prostate Cancer Treatment: A Questionnaire-Based Retrospective Study among Urologists in Bavaria, Germany.

BACKGROUND: Several reports suggest testosterone replacement therapy (TRT) may be an option in selected hypogonadal patients with a history of prostate cancer (PCa) and no evidence of disease after curative treatment. Our aim was to assess TRT experience and patient management among urologists in Bavaria. MATERIALS AND METHODS: Questionnaires were developed and mailed to all registered urologists in Bavaria (n = 420) regarding their experience with TRT in patients with treated PCa. RESULTS: One hundred and ninety-three (46%) urologists returned the questionnaire and reported their experience with TRT in hypogonadal patients after curative treatment for PCa. Complete data was available for 32 men. Twenty-six patients (81%) received TRT after prostatectomy, 1 patient after external beam radiation, 3 patients after high-dose brachytherapy and 2 patients after high-intensity focused ultrasound. Of the PCa cases, 88.5% (23/26) were organ confined (pT2a-c), and 3 were pT3 tumors. All patients were pN0/cN0, and only 1 patient (pT3a) had a positive surgical margin status postoperatively. After a mean follow-up of 39.8 months, no biochemical relapse was observed. CONCLUSION: To date, there is no clear evidence to withhold TRT from hypogonadal men after curative PCa treatment. Our findings, although with limitations, fit in with the available data showing that TRT does not put patients at an increased risk after curative treatment of PCa.

Solitary metastasis of a Merkel cell tumor to the urinary bladder.

The primary Merkel cell carcinoma, a neuroendocrine tumor, mostly appears on skin areas exposed to light. Complete excision with a safety margin plus local lymphadenectomy is the basic therapy. In cases of relapse or metastasis, surgical treatment is also the first choice. Chemotherapy or radiotherapy are used only for a palliative purpose. To date, in no case of metastasis has healing occurred. Lymphogenic and hematogenic metastasizing to the urinary bladder is rare, however infiltrating tumor growth into the urinary bladder occurs more frequently. In urology, the Merkel cell tumor has been detected only sporadically, while infiltration of the bladder has been described in three cases worldwide. We report the case of a patient with a single metastasis of a Merkel cell tumor in the urinary bladder, after excision of the femoral primary cancer two years earlier.

DNA double-strand break induction and repair in irradiated lymphoblastoid, fibroblast cell lines and white blood cells from ATM, NBS and radiosensitive patients.

BACKGROUND AND PURPOSE: DNA double-strand breaks (dsbs) in lymphoblastoid cell lines (LCLs), fibroblasts and white blood cells from healthy donors, cancer patients with and without late effects of grade 3-4 (RTOG) as well as donors with known radiosensitivity syndromes were examined with the aim to detect dsb repair ability as a marker for radiosensitivity. MATERIAL AND METHODS: LCLs from six healthy donors, seven patients with a heterozygous or homozygous genotype for ataxia-telangiectasia (ATM) and Nijmegen breakage syndrome (NBS), two patients with a late toxicity of grade 3-4 (RTOG), and one cell line with a ligase IV-/- status and its parental cell line were examined. Furthermore, fibroblasts from patients with ATM, NBS, two healthy control individuals, and leukocytes from 16 healthy and 22 cancer patients including seven patients with clinical hypersensitivity grade 3 (RTOG) were examined. Cells were irradiated in vitro with 0-150 Gy. Initial damage as well as remaining damage after 8 and 24 h were measured using constant field gel electrophoresis. RESULTS: In contrast to cells derived from patients homozygous for NBS, impaired dsb repair ability could be detected both in fibroblast and lymphoblastoid cells from ATM and ligase IV-/- patients. The dsb repair ability of all 38 leukocyte cell lines (patients with grade 3-4 late effects and controls) was similar, whereas the initial damage among healthy donors was less. CONCLUSION: Despite showing a clinically elevated radiosensitivity after irradiation, the DNA repair of the patients with clinical hypersensitivity grade 3 (RTOG) appeared to be normal. Other mechanisms such as mutations, altered cell cycle or defective apoptosis could play a critical role toward determining radiosensitivity.