Search

Two patients with xanthogranulomatous inflammation are described, one with involvement of the spermatic cord and the other with 1 testicle and epididymis affected. To our knowledge, only 12 cases of xanthogranulomatous orchiepididymitis have been reported previously, one of which also presented a xanthogranulomatous funiculitis. Clinically, our patients presented with spermatic cord enlargement (case 1) and chronic orchitis that did not respond to treatment with antibiotics (case 2). Histopathologically, both cases showed extensive xanthogranulomatous inflammation with numerous foamy macrophages that were associated with colonies of microorganisms suggestive of actinomyces in case 1. Additionally, Escherichia coil was cultured from the surgical specimen of case 2. The possible underlying pathology may be diabetes in case 1 and phlebitis associated with chronic orchitis in case 2. Differential diagnoses with other lesions that are rich in macrophages, such as malakoplakia, and those testicular neoplasms without serologic tumor markers are discussed. [ABSTRACT FROM AUTHOR]

Purpose: Polyamines are important regulators of cell growth and death. The polyamine modulated factor-1 (PMF-1) is involved in polyamine homeostasis. After identifying an enriched CpG island encompassing the PMF1 promoter, we aimed at evaluating the clinical relevance of PMF1 methylation in bladder cancer., Experimental Design: The epigenetic silencing of PMF1 by hypermethylation was tested in bladder cancer cells (n = 11) after azacytidine treatment. PMF1 methylation status was evaluated in 507 bladder tumors and 118 urinary specimens of bladder cancer patients and controls. PMF1 protein expression was analyzed by immunohistochemistry on tissue arrays containing bladder tumors for which PMF1 methylation was assessed (n = 218)., Results: PMF1 hypermethylation was associated with gene expression loss, being restored in vitro by a demethylating agent. An initial set of 101 primary frozen bladder tumors served to identify PMF1 hypermethylation in 88.1% of the cases. An independent set of 406 paraffin-embedded tumors also revealed a high PMF1 methylation rate (77.6%). PMF1 methylation was significantly associated with increasing stage (P = 0.025). Immunohistochemical analyses revealed that PMF1 methylation was associated with cytoplasmic PMF1 expression loss (P = 0.032). PMF1 protein expression patterns were significantly associated with stage (P < 0.001), grade (P < 0.001), and poor overall survival using univariate (P < 0.001) and multivariate (P = 0.011) analyses. Moreover, PMF1 methylation in urinary specimens distinguished bladder cancer patients from controls (area under the curve = 0.800)., Conclusion: PMF1 was identified to be epigenetically modified in bladder cancer. The association of PMF1 methylation with tumor progression and its diagnostic ability using urinary specimens support including PMF1 assessment for the clinical management of bladder cancer patients.

Despite the knowledge and histological classification of testicular lesions, epididymal lesions associated with cryptorchidism are not well defined and only macroscopic alterations have been reported. We have evaluated the alterations in the growth of both the epithelium and muscular wall of efferent ducts and epididymis in human patients with cryptorchidism from infancy to adulthood. In addition, by cytokeratin immunostaining we have also evaluated the stage of differentiation of each segment along the human postnatal life in these patients. A decrease is shown in the size of efferent and epididymal ducts in cryptorchid children compared with normal, age-matched controls. The height of the epithelium, muscular wall, and lumen of the cryptorchid epididymis were reduced at every age studied. This decrease in all regions was seen even in the testicular quiescent period (1 to 4 years of age). In addition, the cryptorchid epididymis grows more slowly during the transition to the pubertal period. The smaller size of the cryptorchid epididymis in pubertal and adult men compared with that of normal men is due primarily to underdevelopment of the muscular wall and a reduction in epithelial height. The pattern of growth of cryptorchid efferent ducts and ductus epididymides parallels that in normal men, except that development of the lumen and muscular layer in the cauda epididymis region are delayed. Epithelial differentiation, monitored by cytokeratin expression, is minimal in efferent ducts and throughout the epididymis of the cryptorchid male, and this is already seen in children. In conclusion, our immunohistochemical and morphometric results show a reduced development of the human cryptorchid epididymis that is already evident in childhood. They indicate that cryptorchidism is a primary congenital illness of the testis and spermatic ducts, with evident lesions from the first years of life, and suggest that surgical descent would probably not be able to completely reverse these alterations.