Objective:To determine if psychological stress affects the semen quality.Methods:By searching Chinese and English databases (PubMed, Web of Science, The Cochrane Library, CNKI, WangFang Date, VIP and CBM), literature was screened according to inclusion and exclusion criteria, data were extracted from the included literatures, and various data were analyzed with RevMan 5.3 and Stata 15 software.Results:A total of 9 036 cases were included in 12 literatures. Psychological stress was associated with decreases in sperm density ( WMD=-17.68, 95% CI=-27.53--7.82), progressive sperm motility ( WMD=-5.37, 95% CI=-9.9--0.78), normal sperm morphology ( WMD=-11.62, 95% CI=-19.06--4.18), and total sperm count ( WMD=-28.75, 95% CI=-40.84--16.65). It was not related to semen volume ( WMD=-0.06, 95% CI=-0.22-0.10, P=0.46). Conclusions:Psychological stress has a certain adverse effect on semen quality, psychological stress can reduce sperm density, sperm total, normal sperm morphology and forward sperm percentage.

BACKGROUND:Cross-sensitization of pelvic organs is one theory for why symptoms of gut sickness and interstitial cystitis/bladder pain syndrome overlap. Experimental colitis has been shown to trigger bladder hyperactivity and hyperalgesia in rats. The chemokine receptor CXCR4 plays a key role in bladder function and central sensitization. We aim to study the role of CXCR4 and its inhibitor AMD3100 in colon-bladder cross-organ sensitization.METHODS:The colitis model was established by rectal infusion of trinitrobenzene sulfonic acid. Western blot and immunofluorescence were used to assess the expression and distribution of CXCR4. Intrathecal injection of AMD3100 (a CXCR4 inhibitor) and PD98059 (an ERK inhibitor) were used to inhibit CXCR4 and downstream extracellular signal-regulated kinase (ERK) in the spinal cord and dorsal root ganglion (DRG). Intravesical perfusion of resiniferatoxin was performed to measure the pain behavior counts of rats, and continuous cystometry was performed to evaluate bladder voiding function.RESULTS:Compared to the control group, CXCR4 was expressed more in bladder mucosa and colon mucosa, L6-S1 dorsal root ganglion (DRG), and the corresponding segment of the spinal dorsal horn (SDH) in rats with colitis. Moreover, intrathecal injection of the AMD3100 suppressed bladder overactivity, bladder hyperalgesia, and mastocytosis symptoms caused by colitis. Furthermore, AMD3100 effectively inhibited ERK activation in the spinal cord induced by experimental colitis. Finally, treatment with PD98059 alleviated bladder overactivity and hyperalgesia caused by colitis.CONCLUSION:Increased CXCR4 in the DRG and SDH contributes to colon inflammation-induced bladder overactivity and hyperalgesia partly via the phosphorylation of spinal ERK. Treatment targeting the CXCR4/ERK pathway might provide a potential new approach for the comorbidity between the digestive system and the urinary system.

To investigate the expression and function of CXCL13/CXCR5 in interstitial cystitis/bladder pain syndrome (IC/BPS) and experimental autoimmune cystitis (EAC). The sequencing data from IC/BPS patients GSE11783 were obtained from the GEO database, and data analysis was performed using the R software platform. Female C57BL/6 mice were divided into four groups: the NC group, the NC+TAK-779 group, the EAC group, and the EAC+TAK-779 group. EAC was induced by repeated immunization of mice with bladder homogenates. Subcutaneous injection of TAK-779 was used for EAC model intervention. H&E staining and immunohistochemistry were used for histological assessment. Western blot was used to detect inflammatory factors (IL-6, TNF-α, IL-1β), apoptosis-related proteins (Bax, Caspase-3, Caspase-8) and JNK/JUN and NF-KB signalling pathways. Apoptotic indices were analysed by TUNNEL staining. Urodynamics was used to assess bladder function in mice. CXCL13 and CXCR5 were significantly up-regulated in IC/BPS and EAC. The JNK and NF-κB signalling pathways were activated in IC/BPS and EAC. EAC mice could well mimic the phenotypic and pathophysiologic changes of IC/BPS. Compared with the EAC group, the EAC+TAK-779 group showed significantly lower bladder tissue scores, reduced expressions of inflammatory factors (IL-6, TNF-α, IL-1β) and apoptosis-related proteins (Bax, Caspase-3, Caspase-8), blocked activation of JNK/JUN and NF-KB signaling pathways, and significantly improved bladder function (significant reduction in MF, significant prolongation of ICI). The activation of the CXCL13/CXCR5 axis is involved in the pathophysiology of IC/BPS and EAC. Blocking CXCL13/CXCR5 axis activation by TAK-779 reduces bladder inflammation and improves bladder function in EAC mice.

The abnormal CXCL13/CXCR5 axis is involved in many inflammatory diseases and its selective inhibitor, TAK-799 has exhibited strong anti-inflammatory potency. The sequencing of clinical specimens from interstitial cystitis/bladder pain syndrome (IC/BPS) has shown that CXCL13 and CXCR5 are highly expressed, but the role of CXCL13/CXCR5 axis in IC/BPS has not been rarely reported. Therefore, in this study, we analyzed the GSE11783 sequencing data of IC/BPS patients and investigate the role and mechanism of CXCL13/CXCR5 axis and TAK-779 in the mouse model of experimental autoimmune cystitis (EAC). We verified that CXCL13 and CXCR5 were significantly up-regulated in EAC model. EAC mice exhibited increased bladder inflammatory factors (IL-6, TNF-α, IL-1β), apoptosis-related proteins (Bax, Caspase-3, Caspase-8), frequency of voiding. Using TAK779 to block CXCL13/CXCR5 axis significantly attenuated these inflammatory damages and efficiently improved bladder function (significant reduction in micturition frequency, significant prolongation of inter-contraction interval). Further investigation showed that inhibiton of JNK and NF-kappaB activation, the bioinformatics analysis-indicated downstream signaling of CXCL13/CXCR5 axis, is responsible for the protective effect of TAK779. Taken together, we demonstrate that activation of the CXCL13/CXCR5 axis is involved in the pathophysiology of IC/BPS and EAC. Blocking CXCL13/CXCR5 axis activation by TAK-779 reduces bladder inflammation and improves bladder function in EAC mice.

OBJECTIVE:The aim of the current investigation is to develop a new strategy for evaluating blood loss in the process of transurethral resection of the prostate (TURP).METHODS:318 patients diagnosed with benign prostatic hyperplasia (BPH) that need TURP were enrolled in this study. Hospitalization information including age, height, weight, surgery time, prostate volume, hemoglobin (Hb) concentration, hematocrit (HCT) percentage, and red blood cell count (RBC) was evaluated for each patient. All statistical analysis drawing were conducted using R software.RESULTS:Three methods were employed for calculating blood loss in TURP. Results from a new method display 0 missing value and got higher confidence (0 of 318, Poisson distribution, P < 0.001) compared with blood loss calculated with hemoglobin concentration (20.44%) and hematocrit percentage (19.18%). Also, the new method demonstrated narrow range (0.03~270.03 ml) and approximate normal distribution compared with blood loss calculated with hemoglobin concentration and hematocrit percentage. More importantly, the new method explained positive correlation with prostate volume (R 2 = 0.138, P < 0.001) and also surgery lasting time (R 2 = 0.193, P < 0.001).CONCLUSION:Methods developed for calculating blood loss in TURP in the current study displayed more accurate and reasonable evaluation of bleeding, which can guide the transfusion blood for patients.

Hemorrhagic cystitis is an important complication of cyclophosphamide chemotherapy, and current therapies for the disease are limited. The natural flavonoid luteolin (LUT) has significant anti-inflammatory and antioxidant properties, but its protective effect on cyclophosphamide (CYP)-induced bladder toxicity has yet to be evaluated. This study aims to explore the protective effect of LUT on CYP-induced acute cystitis in rats. Female Sprague-Dawley rats were randomly assigned to the control (CON) group, CON + LUT group, CYP group, and CYP + LUT group. A single intraperitoneal injection of CYP was administered to establish an acute hemorrhagic cystitis model. HE staining was performed to detect the degree of bladder tissue damage, and TUNEL staining was performed to count apoptotic cells. Oxidative stress indicators were measured using commercial kits, and bladder surgery was performed to assess urinary function. The levels of inflammatory cytokines, apoptosis-related indicators, TXNIP/NLRP3 pathway, and NF-κB pathway were detected by western blot. We found that LUT treatment reduced bladder bleeding, congestion, and edema caused by CYP. Compared with the CYP + LUT group, the level of apoptosis was more highly expressed in the CYP group. We also found that caspase-3, caspase-8, and Bax were significantly upregulated and Bcl-2 was downregulated after LUT treatment. In addition, LUT inhibited the activation of NF-κB signal pathway in the rat bladder tissue after CYP exposure. LUT treatment can also reduce the NLRP3 inflammasome (NLRP3, ASC, and caspase-1) and TXNIP in the bladder. Finally, LUT can reduce the increase in the urination frequency and maximum urination pressure caused by cystitis. These results indicate that LUT displays effective anti-inflammatory, antioxidant, and antiapoptotic properties in CYP-induced acute hemorrhagic cystitis rats by inhibiting the TXNIP/NLRP3 and NF-κB pathways. LUT may be a potent therapeutic agent for the prevention and treatment of hemorrhagic cystitis.

Purpose Hyperalgesia and bladder overactivity are two main symptoms of interstitial cystitis/bladder pain syndrome (IC/BPS). Cannabinoid receptors participate in the modulation of pain and bladder function. GPR18, a member of the cannabinoid receptor family, also participates in the regulation of pain and bladder function, but its underlying mechanisms are unknown. In this work, we sought to study the role of GPR18 in IC/BPS. Methods A rat model of IC/BPS was established with cyclophosphamide (CYP). Paw withdrawal threshold (PWT) measurement and cystometry were used to evaluate pain and bladder function, respectively. RT-PCR, Western blotting and immunofluorescence were used to assess the expression and distribution of GPR18. The role of GPR18 in pain and bladder function was studied by intrathecal injection of resolvin D2 (RvD2, a GPR18 agonist) and O-1918 (a GPR18 antagonist). Calcium imaging was used to study the relationship between GPR18 and TRPV1. Results A rat model of IC/BPS, which exhibited a decreased PWT and micturition interval, was successfully established with CYP. The mRNA and protein expression of GPR18 was reduced in the bladder and dorsal root ganglia (DRG) in rats with CYP-induced cystitis. Intrathecal injection of RvD2 increased the PWT and micturition interval. However, O-1918 blocked the therapeutic effect of RvD2. GPR18 was present in bladder afferent nerves and colocalized with TRPV1 in DRG, and RvD2 decreased capsaicin-induced calcium influx in DRG. Conclusion Activation of GPR18 by RvD2 alleviated hyperalgesia and improved bladder function, possibly by inhibiting TRPV1 in rats with CYP-induced cystitis.

Objective To investigate the role of P2X3 receptor in dorsal root ganglion (DRG) in bladder micturition function due to colitis-induced bladder dysfunction in the rat model of 2, 4, 6-trinitrosulfonic acid (TNBS)-induced colitis. Methods Female SD rats were randomly divided into control group, TNBS-3d and TNBS-7d groups. The rat model of colitis was induced with 50% TNBS ethanol solution (100 mg/kg) by clyster, and the rats from the control group were clystered by isopyknic normal saline. In 3 or 7 d after clyster, the colon and bladder tissue of rats were collected for HE staining and Nissl Staining. Cystometry was performed to observe the bladder micturition function. Immunofluorescence staining was carried out to detect the expression of P2X3 receptor in DRG. The effect of P2X3 on colitis-induced bladder dysfunction was observed by intrathecal injection of P2X3 receptor inhibitor A-317491. Results The colons of TNBS-induced colitis rats showed mucosal hyperemia and edema and inflammatory cell infiltration. There were no histopathological changes in the bladder among the 3 groups. Compared to the control group, there were larger number of mast cells observed in the bladder from the TNBS-3d and TNBS-7d groups. The results of cystometry showed that the intercontractile interval of bladder (ICI) was significantly decreased and maximum bladder pressure (MBP) was obviously increased in the TNBS-3d group than the control group (P < 0.01). Similarly, the ICI in TNBS-7d group was significantly decreased (P < 0.01), but MBP did not differ from the control group. The number of P2X3 positive neurons in DRG from the TNBS-3d and TNBS-7d groups was increased significantly compared to the control group (P < 0.01). Intrathecal injection of P2X3 inhibitor A-317491 significantly prolonged the interval of micturition (P < 0.01) in the TNBS-3d and TNBS-7d groups and reduced the maximum bladder pressure in TNBS-3d groups (P < 0.05). Conclusion P2X3 receptor in DRG plays an important role in the pathophysiological process of bladder overactivity induced by colitis, and inhibition of P2X3 receptor in DRG may be an effective treatment strategy for the overactive bladder.

Non-invasive biomarkers to identify patients with bladder outlet obstruction (BOO)-related dysfunction are still needed to guide clinical practice. The current study aims to investigate molecular alterations and biomarkers associated with partial BOO (PBOO) in rats. Sprague–Dawley rats were used to establish the BOO model. Serum samples from 60 patients with benign prostatic hyperplasia (BPH) were used for enzyme-linked immunosorbent assay analysis. RNA sequencing and TMT-labeling proteomic analyses were conducted to identify molecular alterations. Masson’s trichrome, H&E, and immunohistochemical staining and western blotting were conducted by using conventional methods following the manufacturer’s instructions. Rats with PBOO experienced hypertrophy of smooth muscle cells and hyperplasia of interstitial cells during the first 4 weeks after the initiation of obstruction. Four weeks later, rats with PBOO showed activation of the adaptive immune response, cell death and apoptosis. The levels of brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF2) in the serum gradually increased in the first 4 weeks and gradually decreased after week 4. FGF2 levels slightly correlated with prostate volume ( R = 0.156, P = 0.0028) but not with age or BMI in BPH patients. No correlations were found between BDNF levels and prostate volume, age or BMI. BOO induces a change from bladder compensation to decompensation at week 4. FGF2 is involved in the development of hypertrophy in the PBOO bladder and shows a positive correlation with prostate volume in BPH patients.

Acute kidney injury (AKI) is an extremely dangerous clinical syndrome with high morbidity and mortality. Stem cell-based therapies have shown great promise for AKI treatment. Urine-derived stem cells (USCs) are a novel cell source in tissue engineering and cell therapy which provide advantages of simple, noninvasive, and low-cost harvest methods, efficient proliferation, and multi-differentiation potential. Here, we described the therapeutic effects of USCs in a rat model of cisplatin-induced AKI as a novel therapy. In vivo, the intravenous administration of USCs alleviated the renal functional damage in AKI rats, for the levels of blood urea nitrogen (BUN) and serum creatinine (SCr) were significantly decreased. The USCs-treated group also exhibited improved histological and ultrastructural changes, promoted proliferation, and inhibited apoptosis in renal tissues. After the USC therapy, the expression levels of proinflammatory cytokines (TNF- α and IL-6) and apoptosis-related proteins (BAX and cleaved caspase-3) were downregulated. In addition, the presence of a few GFP-labeled USCs was confirmed in rat renal tissues. In vitro, rat tubular epithelial (NRK-52E) cells were incubated with cisplatin to induce cell damage and then cocultured with USCs. After coculture with USCs, the cisplatin-induced NRK-52E cells showed higher cell viability and a lower apoptosis ratio than those of the control group, and cell cycle arrest was improved. In conclusion, our results demonstrated that USC therapy significantly improved the renal function and histological damage, inhibited the inflammation and apoptosis processes in the kidney, and promoted tubular epithelial proliferation. Our study exhibited the potential of USCs in the treatment of AKI, representing a new clinical therapeutic strategy.

Transient receptor potential canonical 3 (TRPC3) is a nonselective cation channel, and its dysfunction is the basis of many clinical diseases. However, little is known about its possible role in the bladder. The purpose of this study was to explore the function and mechanism of TRPC3 in partial bladder outlet obstruction (PBOO)-induced detrusor overactivity (DO). We studied 31 adult female rats with DO induced by PBOO (the DO group) and 40 sham-operated rats (the control group). Here we report that the expression of TRPC3 in the bladder of DO rats increased significantly. Furthermore, PYR10, which can selectively inhibit the TRPC3 channel, significantly reduced bladder excitability in DO and control rats, but the decrease of the bladder excitability of DO rats was more obvious. PYR10 significantly reduced the intracellular calcium concentration in smooth muscle cells (SMCs) in DO and control rats. Finally, Na+/Ca2+ exchanger 1 (NCX1) colocalizes with TRPC3 and affects its expression and function. Collectively, these results indicate that TRPC3 plays an important role in the pathogenesis of DO through a synergistic effect with NCX1. TRPC3 and NCX1 may be new therapeutic targets for DO.

Aims To investigate the clinical characteristics of health care-seeking men presenting with lower urinary tract symptoms (LUTS) in China and to reveal risk factors for symptom severity. Methods This multicenter, hospital-based, cross-sectional study recruited 1477 eligible male subjects, who were at least 45 years, seeking health care at 9 participating hospitals across the mainland China. The general medical information and subjective symptoms were recorded, followed by the measurement of prostate volume, urodynamic indices, and laboratory tests for kidney function, plus glucose/lipid metabolism. Univariate and multivariate linear regression were employed for the detection of risk factors for symptom severity. Results The proportion of mild, moderate, and severe LUTS was 14.6%, 32.6%, and 52.8%, respectively, with 62.2% reporting the triple combination of storage, voiding, and postmicturition symptoms. Median prostate volume was 44.6 ml, and 71.1% were experiencing comorbidities. Thirteen independent risk factors for LUTS severity were identified, namely, nocturnal voiding episodes and the presence of straining and weak steam; the triple combination of symptom subtypes; general and nocturia quality of life; Q(max) and bladder outlet obstruction index; and numbers of comorbidities, hypertension, estimated glomerular filtration rate, and cholesterol and glycosylated hemoglobin. Conclusions The majority of health care-seeking LUTS men present with moderate-to-severe and overlapping symptoms, with a high prevalence of both lower urinary tract dysfunction and systemic comorbidities. The evidence from both urological and nonurological independent risk factors demonstrate the multifactorial nature of LUTS, for which a multidisciplinary management is essential.

2019年12月以来我国武汉市爆发的新冠肺炎疫情目前已逐步发展成为蔓延至全球的爆发性流行性疾病.出于疫情防控需要,我国部分医院的择期外科手术暂停进行.而由泌尿系结石导致的危重患者,往往合并发热、感染性休克等症状,可能需要与新冠肺炎的相关临床表现进行鉴别;另外,在妊娠期肾绞痛合并发热患者中新冠肺炎相关筛查手段中有一部分运用受限,这些都给临床筛查和处理带来了挑战.陆军军医大学第二附属医院泌尿外科在2020年1月18日至2月19日救治了7例泌尿系结石危重患者,我们采用轻重分层模式、严格实施感染防控措施并遵照泌尿外科指南,使所有危重患者均手术顺利平稳出院.本文结合7例诊疗经验,探讨在疫情形势下开展此类临床救治工作的策略.

AimsTransforming growth factor-β (TGF-β) mediated super-activation of urethra fibroblasts contributes to the progression of traumatic urethral stricture (TUS), and the Rho-associated kinase inhibitors, Fasudil, might be a novel therapeutic agent for TUS, but the underlying mechanisms had not been studied.Materials and methodsThe primary urethral fibroblasts (PUFs) were isolated from rabbit urethral scar tissues and cultured in vitro, and the PUFs were subsequently treated with TGF-β (10 μg/L) to simulate the realistic conditions of TUS pathogenesis. Next, the PUFs were exposed to Fasudil (50 μM) and autophagy inhibitor 3-methyladenine (3-MA) treatment. Genes expression was examined by Western Blot and immunofluorescence staining, and cellular functions were determined by MTT assay and Transwell assay.Key findingsTGF-β promoted cell proliferation, migration, autophagy, and secretion of extracellular matrix (ECM), including collagen I and collagen III, which were reversed by co-treating cells with both Fasudil and 3-MA. In addition, TGF-β treatment decreased the expression levels of phosphorylated Akt (p-Akt) and mTOR (p-mTOR) to inactivate the Akt/mTOR pathway in the PUFs, which could be re-activated by Fasudil. Then, the fibroblasts were treated with the Pan-Akt inhibitor (GDC-0068), and we surprisingly found that GDC-0068 abrogated the inhibiting effects of Fasudil on cell autophagy and proliferation in the PUFs treated with TGF-β.SignificanceFasudil regulated Akt/mTOR pathway mediated autophagy to hamper TGF-β-mediated super-activation in PUFs, which supported that Fasudil might be an ideal candidate therapeutic agent for TUS treatment for clinical utilization.

Backgrounds:The mechanism underlying bladder urination pathophysiologies has not been understood yet because the types of interstitial cells present in the bladder are still obscure. Results:Here, we classified the cell types in the bladder without bias using 10x genomics single-cell RNA-seq and identified 35,510 and 19,946 cells from human and rat bladder tissues, respectively. In addition to the major cell clusters including urothelial cells, smooth muscle cells, endothelial cells, neurons, and immune cells, three types of interstitial cells were identified in this study. Fibroblasts and myofibroblasts were shown to occupy large proportions of interstitial cells, located mainly between the epithelial strata and muscle strata. A new type of interstitial cell, Mki67+, which was found both in human and rat bladder tissues, may participate in bladder disease development. Conclusions:Our investigation thus lays the ground work for identifying the cell types in bladder tissues and provides potential clues to understand abnormal bladder functions.

BACKGROUND:Renal cell carcinoma (RCC) has gradually become a severe type of kidney malignant tumor, which warrants an urgent need for highly efficacious therapeutic agents. Morusin, a typical prenylated flavonoid, has been revealed to possess anticarcinogenic effects against several cancers by inhibiting cell proliferation and tumorigenesis.METHODS:Cells proliferation was examined by CCK-8. Migration assays were performed using a 24-well transwell chamber. Apoptotic cells were detected using the Annexin V PE/7-AAD apoptosis detection kit. Cell cycle analysis was carried out by flow cytometry. Western blotting and quantitative real time (qRT) PCR were used to exam the change of target gene in mRNA and protein level. Nude mouse xenograft experiments were performed to identify vivo function of morusin.RESULTS:Here, we evaluated the effect of morusin against RCC. We treated three RCC cell lines, 769-P, 786-O, and OSRC-2, with morusin to study its effects on cell growth, migration, apoptosis, cell cycle and cancer-related pathways. Additionally, we assessed the effects of morusin on tumor growth using a nude mouse model. Morusin could inhibit cell growth and migration, induce cell apoptosis and downregulate apoptosis-related proteins, and disturb the cell cycle arrest in the G1 phase. Additionally, morusin could suppress RCC tumorigenesis in vivo. Moreover, mitogen-activated protein kinase (MAPK) signal pathways were found to be involved in morusin-induced anti-cancer activity. P-p38 and P-JNK levels were up-regulated by morusin, while the ERK phosphorylation level was down-regulated.CONCLUSIONS:Our results show that morusin could inhibit the growth of RCC cells in vitro and in vivo through MAPK signal pathways. Thus, morusin could be a potential anti-cancer agent for RCC.

AIMS:This study aimed to investigate the therapeutic effect and molecular mechanism of chlorogenic acid (CGA) on cyclophosphamide (CYP)-induced rat interstitial cystitis (IC). MATERIALS AND METHODS:An animal model of IC was established by intraperitoneal injection of CYP in female Sprague-Dawley rats. Eighty rats were randomly assigned to four groups: negative control (NC), NC treated with CGA (NC + CGA), IC, and IC treated with CGA (IC + CGA). Bladder urination function was assessed by analyzing urodynamic parameters. The expression of apoptosis-related proteins and inflammatory biomarkers in bladder specimens was detected using western blot and immunohistochemistry analysis. KEY FINDINGS:Compared with the IC group, bladder urinary function was significantly improved in the IC + CGA group. CGA treatment reduced inflammatory damage in the bladder tissue of IC rats. Caspase3 and Bax expression was higher while Bcl-2 expression was lower in the IC group compared to the IC + CGA group. In addition, there were significant differences between the groups in the expression levels of inflammatory biomarkers in the bladder tissue. Furthermore, CGA could inhibit CYP-induced MAPK/NF-κB phosphorylation in the rat bladder tissue. SIGNIFICANCE:In a CYP-induced rat model of IC, CGA could reduce inflammation and apoptosis, thus partially restoring bladder function, and the MAPK/NF-κB pathway was probably involved in it.

目前已证实新冠病毒可以造成泌尿系脏器的损害,在尿液中也已经发现新冠病毒的存在,同时临床证据显示肿瘤合并新冠肺炎的患者更容易发展为危急重症.膀胱癌患者免疫力低下,部分患者需要每周一次的膀胱灌注治疗,且部分患者本身就合并有泌尿系感染等情况,容易出现发热等症状.在疫情期间,如何保证膀胱癌患者得到该有的救治,减少膀胱癌的复发,同时如何最大程度的保护医务人员和患者的安全,我们进行了一些探索,现介绍如下.

Objective: To explore the risk factors, pathogenic bacteria distribution and drug resistance of systematic transrectal ultrasound-guided prostate biopsy (TRUS-Bx), 329 cases of TRUS-Bx were collected, retrospectively, in the Second Affiliated Hospital, Army Military Medical University, from April 2017 to October 2019. Methods: A total of 329 cases were all qualified and grouped into the SIRS group (25 cases) and the non-SIRS group (304 cases). Of all the cases, incidence and risk factors of systemic inflammatory response syndrome (SIRS) were analyzed. Urine and blood samples of patients with SIRS after TRUS-Bx were also collected for bacterial culture and drug sensitivity test. Results: Multivariate logistic regression analysis showed that BMI >= 25 kg/m(2) (OR = 1.66, 95% CI = 1.34-2.12, P < 0.001), history of diabetes (OR = 5.48, 95% CI = 1.53-19.68, P = 0.008), urinary infection before operation (OR = 9.19, 95% CI = 2.92-20.93, P < 0.001) and erythrocyte sedimentation (ESR) >= 20 mm/h (OR = 1.04, 95% CI = 1.01-1.08, P = 0.039) were independent risk factors of SIRS after TURS-PB. Conclusion: The incidence of SIRS and urinary sepsis was 7.59% and 2.13%, respectively, and major pathogens of SIRS after TRUS-Bx were Escherichia coli (58.33%), Klebsiella pneumoniae (12.5%) and Pseudomonas aeruginosa (12.5%). Imipenem, meropenem, tigecycline, piperacillin/tazobactam, teicoplanin, vancomycin, amikacin and cefoperazone/sulbactam had a very strong inhibitory effect to those pathogenic bacteria (sensitivity 85.72%similar to 100%). Levofloxacin, ciprofloxacin, gentamicin, penicillin G, compound neonomine and second-generation cephalosporins showed less but also worked as a good inhibitor to pathogenic bacteria (42.86%similar to 80.95%). Keywords: systematic transrectal ultrasound-guided prostate biopsy, systemic inflammatory response syndrome, prostate cancer, risk factors infection, pathogens