Incidence and Morbidity of Radiation-Induced Hemorrhagic Cystitis in Prostate Cancer.

OBJECTIVE: To determine if reported incidence rates of hemorrhagic cystitis after radiation therapy for prostate cancer are accurate, to investigate the effect of different radiation modalities on the development of hemorrhagic cystitis and to assess its morbidity and treatment. MATERIALS AND METHODS: A retrospective chart review was completed of 709 patients at 2 Detroit Medical Center hospitals who underwent radiation therapy for prostate cancer between January 2000 and September 2015. In patients who developed hemorrhagic cystitis, we analyzed the incidence, radiation modality, morbidity, treatment, and complications. RESULTS: The incidence rate of hemorrhagic cystitis after radiation for prostate cancer was 11.1%. There was no significant difference between external beam and intensity-modulated radiation therapy and the development of hemorrhagic cystitis (P = .18). Patients developed hemorrhagic cystitis an average of 79.1 months (4-230 months) after radiation. The average number of admissions was 2.5 (1-9) with an average length of stay of 7.6 days (1-42 days). Fifty-two percent of patients required blood transfusion with an average of 4.3 units transfused per patient (1-33U). The most common treatment was cystoscopy with fulguration/clot evacuation in 86% of patients. Complications included urinary tract infection, acute kidney injury, urosepsis, and even death. CONCLUSION: The incidence of hemorrhagic cystitis following radiation therapy for prostate cancer is under-reported in the literature. Hemorrhagic cystitis is associated with high morbidity and complications for patients, requiring multiple hospitalizations, blood transfusions, and procedures. Advances in radiation have not significantly reduced the risk of developing hemorrhagic cystitis.

Cellular Microbiology of Mycoplasma canis.

Mycoplasma canis can infect many mammalian hosts but is best known as a commensal or opportunistic pathogen of dogs. The unexpected presence of M. canis in brains of dogs with idiopathic meningoencephalitis prompted new in vitro studies to help fill the void of basic knowledge about the organism's candidate virulence factors, the host responses that it elicits, and its potential roles in pathogenesis. Secretion of reactive oxygen species and sialidase varied quantitatively (P < 0.01) among strains of M. canis isolated from canine brain tissue or mucosal surfaces. All strains colonized the surface of canine MDCK epithelial and DH82 histiocyte cells and murine C8-D1A astrocytes. Transit through MDCK and DH82 cells was demonstrated by gentamicin protection assays and three-dimensional immunofluorescence imaging. Strains further varied (P < 0.01) in the extents to which they influenced the secretion of tumor necrosis factor alpha (TNF-α) and the neuroendocrine regulatory peptide endothelin-1 by DH82 cells. Inoculation with M. canis also decreased major histocompatibility complex class II (MHC-II) antigen expression by DH82 cells (P < 0.01), while secretion of gamma interferon (IFN-γ), interleukin-6 (IL-6), interleukin-10 (IL-10), and complement factor H was unaffected. The basis for differences in the responses elicited by these strains was not obvious in their genome sequences. No acute cytopathic effects on any homogeneous cell line, or consistent patterns of M. canis polyvalent antigen distribution in canine meningoencephalitis case brain tissues, were apparent. Thus, while it is not likely a primary neuropathogen, M. canis has the capacity to influence meningoencephalitis through complex interactions within the multicellular and neurochemical in vivo milieu.