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Proton boost of 20 Gy in daily 5 Gy fractions followed by external beam radiotherapy (EBRT) of 50 Gy in daily 2 Gy fractions were given to 278 patients with prostate cancer with T1b to T4N0M0 disease. Fifty-three percent of the patients received neoadjuvant androgen deprivation therapy (N-ADT). The medium followup was 57 months. The 5-year PSA progression-free survival was 100%, 95%, and 74% for low-, intermediate-, and high-risk patients, respectively. The toxicity evaluation was supported by a patient-reported questionnaire before every consultant visit. Cumulative probability and actuarial prevalence of genitourinary (GU) and gastrointestinal (GI) toxicities are presented according to the RTOG classification. N-ADT did not influence curability. Mild pretreatment GU-symptoms were found to be a strong predictive factor for GU-toxicity attributable to treatment. The actuarial prevalence declined over 3 to 5 years for both GU and GI toxicities, indicating slow resolution of epithelial damage to the genitourinary and gastrointestinal tract. Bladder toxicities rather than gastrointestinal toxicities seem to be dose limiting. More than 5-year followup is necessary to reveal any sign of true progressive late side effects of the given treatment. Hypofractionated proton-boost combined with EBRT is associated with excellent curability of localized PC and acceptable frequencies of treatment toxicity.

The 5-year estimated biochemical progression rates were 31% for Arm A and 28% for Arm B. Febrile neutropenia occurred in 16% of the docetaxel patients. No deaths were related to the docetaxel treatment. There were 43 deaths during the trial, including 20 in Arm A and 23 in Arm B, of which 9 and 7, respectively, were due to PCa. The Hazard Ratio from Cox multivariate analysis for PSA progression of Arm A (docetaxel) vs Arm B (surveillance) was 1.14 (95% CI 0.79 to 1.64, p=0.5). Conclusions: Adjuvant docetaxel without prednisone did not improve BDFS after radical radiotherapy with ADT for intermediate-or high-risk prostate cancer.

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ABSTRACT. This report concerns two patients, a 43‐year‐old woman and a 53‐year‐old man, who developed clinical as well as laboratory signs of permanent gonodal and thyroid failure following an acute intracranial infection—in the woman a meningoencephalitis of unknown origin, and in the man an encephalitis caused by Coxsackie B5. Endocrine investigations were compatible with hypothalamicpituitary dysfunction, with some of the results favoring a hypothalamic lesion. Perhaps hormone deficiency of hypothalamic and/or pituitary origin is a more common sequel of acute meningoencephalitis than has hitherto been reported.