We aimed to study the correlation between leukocyte counts in semen and bacterial pathogens in seminal samples of infertile men, and to establish the minimum leukocyte count associated with significant bacteriospermia. A total of 116 patients who underwent evaluation of fertility were investigated using routine semen analysis according to the guidelines of the WHO and bacterial pathogens analysis by culture and in-house PCR assay. The overall prevalence of bacteriospermia in semen samples was 56.9% independent of the presence of leukocytes. The most common bacterial species detected were Chlamydia trachomatis (41.4%), Ureaplasma urealyticum (15.5%) and Mycoplasma hominis (10.3%). The receiver operating characteristic curve analysis demonstrated that the sensitivity/specificity for detecting bacteria at a cut off level of >or=1 x 10(6) leukocytes per ml (which is the WHO defined level for leukocytospermia) was 20.3%/81.5%. The highest sensitivity/specificity ratio was found in semen samples with a cut-off level of >or=0.275 x 10(6) leukocytes per ml, which is best shown with the odds ratio of 2.47. A significant correlation was found between bacteriospermia and leukocytospermia at the cut-off level of >or=0.275 x 10(6) leukocytes per ml of semen samples (P = 0.032). We proposed that this is a possible new cut-off level to predict the presence of bacteria in semen of infertile men.
Primary renal lymphangioma is exceedingly rare. Medical imaging has certain limits for the diagnosis which required histological confirmation. The treatment of choice is surgical.
Toll-like receptor (TLR) genetic polymorphisms may modify their expression causing inflammatory disorders and influencing both susceptibility and severity of lupus erythematosus. We aim to determine whether TLR-5 and TLR-9 gene polymorphisms are implicated in the susceptibility to systemic lupus erythematosus (SLE) and lupus nephritis (LN) and to evaluate their expressions and distributions in renal LN patients' biopsies. The frequencies of two SNP in the TLR-9 gene and one in the TLR-5 gene was examined in 106 SLE patients (among them 37 LN patients) and in 200 matched controls by polymerase chain reaction-restriction fragment-length polymorphisms (PCR-RFLP) analysis. TLR-9 and TLR-5 expressions were assessed by reverse transcription (RT)-PCR and immunohistochemistry carried on LN renal biopsies compared to healthy renal tissue. A significant genotypic and allelic association was revealed between TLR-9-rs352140 and both SLE and LN (P < 0·05). The TLR-9 transcript level was significantly higher in LN biopsies compared to control (P < 0·05). This increase was observed histochemically in the tubulointerstitial compartment. TLR-9 was detectable in LN glomeruli patients but not in normal control glomeruli. No allelic nor genotype association was found with TLR-5-rs5744168 in SLE. but the T allele and the TT genotype were raised significantly in the LN group (P < 0·05). A significant increase in TLR-5 gene expression in LN biopsies, which contrasted with normal kidneys (P < 0·05), was confirmed by an intense and diffuse staining for TLR-5 only in LN tubules (P < 0·05). Our data show that TLR-5 and TLR-9 are susceptible genes to LN and that their expression is dysregulated in LN patients' kidneys, supporting a role of these mediators in the pathogenesis of LN.
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