346 Background: Clinically localized prostate cancer can be treated with prostatectomy, radiation or focal therapy, with known impacts on sexual function. We sought to characterize long term sexual function in a large cohort of men treated with primary EBRT and to differentiate between those who have high vs low sexual function scores at baseline. Methods: Patients enrolled in CaPSURE, a national registry of men diagnosed with prostate cancer, from 1995 - 2017 with clinically localized prostate cancer (cN0M0/X, PSA < = 50) and treated with primary EBRT were included. Sexual function (SF) was self-reported using the UCLA Prostate Cancer Index (PCI). We performed repeated measures mixed models to evaluate SF after EBRT, stratified by baseline SF and adjusted for age, BMI, comorbidities, smoking, clinical risk, receipt of brachytherapy and/or hormonal therapy, and type of clinical site. Results: 1193 patients were included for analysis. Mean age was 70, mean number of comorbidities was 2, and median PSA was 7.5 at diagnosis. Baseline PCI scores were available for 43% of the cohort (data not collected before 1998). The mean PCI score was 38 out of 100 at baseline and after EBRT, declined gradually to 16 by 10 years. When only those men with good SF at baseline were assessed (scores 80 – 100), the initial rate of decline was more severe, but the nadir in this group was higher than those with lower baseline scores. Unadjusted mean PCI scores showed a similar decline amongst both groups, although those with good baseline SF consistently had better scores. 63% of patients were treated for erectile dysfunction (PDE5 inhibitors, intracavernosal injections or both), 13% of whom started therapy before EBRT. In the repeated measures mixed models analysis, we found that SF changed significantly over time and scores differed significantly by age, comorbidities, baseline SF, receipt of brachytherapy boost and concurrent ADT. Conclusions: SF after EBRT declines and persists. The most affected are those who had better PCI scores at baseline, although their overall PCI scores are consistently higher compared to those with baseline scores less than 80. Among both groups however, there was a similar decline that was statistically significant.

393 Background: Radiation therapy is a common form of treatment for men with prostate cancer. Biochemical recurrence (BCR) is most commonly defined using the Phoenix definition of PSA nadir + 2. We sought to characterize long term rates of biochemical recurrence in a large, well-characterized and well-followed cohort of men treated with primary EBRT. Methods: Patients enrolled in CaPSURE, a national registry of men diagnosed with prostate cancer, from 1995 - 2017 with clinically localized prostate cancer (cN0M0/X, PSA<=50) treated with primary EBRT were included. Cancer risk was defined by NCCN criteria. Cox proportional hazards regressions were used to assess associations between patient characteristics and BCR as defined by PSA nadir + 2. Results: 1193 patients were included. Mean age at diagnosis was 70 (SD 6.82), median PSA at diagnosis was 7.6 and mean number of follow up PSA tests was 5. Overall rates of BCR were 17.4% at 5 years and 39.4% at 10 years. Rates of BCR were significantly associated with NCCN risk with high-risk patients having the highest rates of recurrence, followed by intermediate- and low-risk groups (61.5%, 36.4% and 28.5% respectively at 10 years). NCCN high vs low clinical risk was significantly associated with likelihood of BCR (HR 4.8, CI 2.5 – 9.2). Rates of salvage treatment, usually ADT, were 16% at 5 years and 19% at 10 years and these were also significantly associated with NCCN high vs low clinical risk (HR 3.7, CI 2.3 – 6) and concurrent ADT (HR 1.83, CI 1.2 – 2.7). Overall rates of bone metastases were 2.6% at 5 years and 4% at 10 years. Overall prostate cancer specific mortality was 3% at 5 years and 7% at 10 years. Conclusions: In this analysis, rates of BCR were fairly high and consistent with published RTOG studies, but rates of salvage treatment were relatively low in comparison, indicating that not all patients who recur need, are offered or want treatment. The limitations of this analysis include incomplete information on radiation dose and field size. The strengths of this analysis include the size of the cohort and the length of follow-up. Furthermore, as this cohort largely represents treatment in community settings, the results may be broadly applicable.

Introduction Certain sexual disorders are under-reported, under-researched, and rarely discussed. Many patients have suffered from ailments such as vulvodynia, a subset of vulvodynia called vestibulodynia, post-orgasmic illness syndrome (POIS), and interstitial cystitis (IC) without clear and optimal treatment strategies. To bring more awareness to these conditions, researchers and other medical professionals are working to elucidate their pathophysiologies in order to provide patients with therapeutic solutions. Mast cell dysfunction is one proposed mechanism of disease for these conditions. Mast cells are CD34+/CD117+/CD13 pluripotent progenitors of hematopoietic stem cells. They serve as innate immune cells that play a significant role in allergic responses, inflammation, and tissue homeostasis. They undergo maturation via growth factors and interleukins in the periphery and are heavily implicated in processes such as anaphylaxis, arthritis, coronary artery disease, autoimmune disorders, and cancer. As the body of research grows surrounding the function of mast cells and mast cell activation, researchers are finding that they may be implicated in multiple disease processes, even in genitourinary disorders. We know little about the etiology of disorders that affect sexual function like vulvodynia, POIS, and IC, but when considering their inflammatory and/or allergic-type symptoms, such as itching, burning, and congestion, we hypothesize that their pathophysiology may be correlated to mast cell function impairment. Objective The purpose of this study is to determine if mast cell dysfunction correlates with the pathophysiology of vulvodynia, POIS, and IC based on a literature review. Methods The authors reviewed existing literature published from January 2010 - June 2022 that explored the histopathological, pathophysiological, and etiological nature of vulvodynia, POIS, and IC. The selection criteria for this narrative review included: original articles (randomized and non-randomized clinical trials, including prospective observational studies, retrospective cohort studies, and case-control studies), review articles, and Cochrane analyses concerning the relationship between sexual disorders and allergens and/or immunology. Eighteen articles met the inclusion criteria. Results From the studies evaluated, it is reasonable to infer that vulvodynia, POIS, and IC have an immunological component to their pathophysiology. The inflammatory nature of all the diseases above indicates a definite immunological involvement, but as more research emerges, several medical providers and authors alike are noting that immunology and, certainly, mast cells may play a more significant role than initially hypothesized. While mast cells are likely not the sole cause of disease, it would be in the patient’s and provider’s best interest to consider their involvement in multifactorial pathophysiology for sexual disorders. Conclusions The pathophysiology of sexual disorders like vulvodynia, POIS, and IC is not currently well understood. However, review of existing literature supports that mast cell activation and, to a lesser extent, Toll-like receptors (TLRs) and lymphocytes may play a cardinal role in the pathophysiology of the sexual disorders described. Further research needs to be conducted on the possible pathophysiology of sexual disorders broadly so healthcare practitioners can provide effective, evidence-based treatment that will provide patients optimal relief. Disclosure No

No abstract