Testicular microlithiasis is not a risk factor for the production of antisperm antibody in infertile males.

Testicular microlithiasis (TM) is a pathological event characterised by the presence of microliths within the testicular entities, and such calcium deposition is thought to have deleterious impacts on the structure of blood-testis barrier (BTB). Breaches in the BTB appear to be a risk factor for antisperm antibody (ASA) production, which is reported to have negative influence on human fertility. Thus, the theories are provocative that ASA formation is elicited in TM men, and the resultant ASA will accordingly affect the fecundity in these men. To illustrate these hypotheses, this study enrolled 22 infertile men incidentally diagnosed with TM by testicular ultrasound evaluation. Sperm samples were collected, and direct immunobead test was used to determine the ASA levels. None of the infertile men with TM were found to display significant levels of ASA, whilst relatively abnormal sperm parameters in these cases were revealed by semen analysis. These observations suggest that TM exposure does not increase the risk of ASA production in infertile men, and therefore, ASA is discarded as an active participant in the development of infertility in TM men. Nevertheless, disrupted spermatogenesis resulting from TM may, at least in part, have certain implications for the pathogenesis of TM-associated infertility.

The distribution of secretory immunoglobulin A in the liver of patients with hepatolithiasis.

Patients with hepatolithiasis are known to be complicated with bile stasis and bacterial infections in the stone-containing ducts. It has been suspected that a decrease in portal venous flow is important in the progression of hepatolithiasis. This study was done to find if the affected liver in hepatolithiasis is inflamed or has lowered local immunity by an examination of the distribution of secretory immunoglobulin A and proliferating cell nuclear antigen in the intrahepatic biliary tracts in operative specimens of 36 patients with hepatolithiasis. The number of biliary epithelia stained for the immunoglobulin was greater when the cholangitis was more severe up to a point; in advanced cholangitis, with severe parenchymal atrophy or proliferating epithelia, there were fewer cells stained for the immunoglobulin than in mild cholangitis. In hepatolithiasis, secretory immunoglobulin A decreases when inflammatory changes become severe and there is parenchymal atrophy caused by stenosis or obstruction of portal branch.

Immunohistochemical demonstration of MET overexpression in human intrahepatic cholangiocarcinoma and in hepatolithiasis.

Expression of MET, the c-met-encoded receptor for hepatocyte growth factor, has not been investigated in proliferative biliary diseases of human liver, including hepatolithiasis and cholangiocarcinoma. Comparatively, we analyzed by immunohistochemistry the expression of MET in normal adult human livers (n = 20), normal postnatal preadult livers (n = 21), fetal livers (n = 36), hepatolithiatic livers (n = 32), and intrahepatic cholangiocarcinomas (n = 26). In normal adult livers, obvious MET immunoreactivity was not found in any cell types. In fetal liver, MET was weakly expressed in primitive biliary cells (ductal plate and immature bile ducts) and immature hepatocytes during 8 to 30 gestational weeks but was essentially negative thereafter. In hepatolithiasis, a condition of risk for cholangiocarcinoma development, MET was overexpressed in proliferated biliary cells in 26 of 32 cases (81%). In this nonneoplastic proliferative biliary condition, MET immunoreactivity was observed to be most prominent in the hyperplastic septal and large bile ducts of liver, and in the proliferated peribiliary glands associated with intrahepatic large bile ducts. In intrahepatic cholangiocarcinoma, MET overexpression in neoplastic biliary epithelium was observed in 15 of 26 cases (58%) and correlated with the degree of tumor differentiation, being highest in well-differentiated tumors and relatively low in poorly differentiated tumors. These data show for the first time that overexpression of MET is a common feature of hyperplastic and neoplastic biliary epithelial cells in human liver and suggest that MET/hepatocyte growth factor may be playing an important role in human biliary hyperplasia and in cholangiocarcinogenesis in vivo.