Development and validation a simple model for identify malignant ascites.

The differential diagnosis of benign ascites and malignant ascites is incredibly challenging for clinicians. This research aimed to develop a user-friendly predictive model to discriminate malignant ascites from non-malignant ascites through easy-to-obtain clinical parameters. All patients with new-onset ascites fluid were recruited from January 2014 to December 2018. The medical records of 317 patients with ascites for various reasons in Renmin Hospital of Wuhan University were collected and reviewed retrospectively. Thirty-six parameters were included and selected using univariate logistic regression, multivariate logistic regression, and receiver operating characteristic (ROC) curve analyses to establish a mathematical model for differential diagnosis, and its diagnostic performance was validated in the other groups. Age, cholesterol, hypersensitivity C-reactive protein (hs-CRP) in serum, ascitic fluid adenosine deaminase (AF ADA), ascitic fluid lactate dehydrogenase (AF LDH) involvement in a 5-marker model. With a cut-off level of 0.83, the sensitivity, specificity, accuracy, and area under the ROC of the model for identifying malignant ascites in the development dataset were 84.7%, 88.8%, 87.6%, and 0.874 (95% confidence interval [CI], 0.822-0.926), respectively, and 80.9%, 82.6%, 81.5%, and 0.863 (95% CI,0.817-0.913) in the validation dataset, respectively. The diagnostic model has a similar high diagnostic performance in both the development and validation datasets. The mathematical diagnostic model based on the five markers is a user-friendly method to differentiate malignant ascites from benign ascites with high efficiency.

Causative bacteria associated with a clinically relevant postoperative pancreatic fistula infection after distal pancreatectomy.

PURPOSE: Clinically relevant postoperative pancreatic fistulas (CR-POPF) occurring after distal pancreatectomy often cause intra-abdominal infections. We monitored the presence of bacterial contamination in the ascitic fluid after distal pancreatectomy to clarify the bacterial origin of intra-abdominal infections associated with CR-POPF. METHODS: In 176 patients who underwent distal pancreatectomy, ascitic fluid bacterial cultures were performed on postoperative days (POD) 1-4 and when the drainage fluid became turbid. The association between postoperative ascitic bacterial contamination and CR-POPF incidence was investigated. RESULTS: CR-POPF occurred in 18 cases (10.2%). Among the patients with CR-POPF, bacterial contamination was detected in 0% on POD 1, in 38.9% on POD 4, and in 72.2% on the day (median, day 9.5) when the drainage fluid became turbid. A univariate analysis revealed a significant difference in ascitic bacterial contamination on POD 4 (p < 0.001) and amylase level on POD 3-4 (p < 0.001). A multivariate analysis revealed the amylase level and ascitic bacterial contamination on POD 4 to be independent risk factors. CONCLUSIONS: In the CR-POPF group, ascitic bacterial contamination was not observed in the early postoperative stage, but the bacterial contamination rate increased after pancreatic juice leakage occurred. Therefore, CR-POPF-related infections in distal pancreatectomy may be caused by a retrograde infection of pancreatic juice.

Use of adenosine deaminase (ADA) to diagnose suspected peritoneal tuberculosis in Rwanda: a cross-sectional study.

BACKGROUND: Peritoneal tuberculosis is the most common cause of low albumin gradient ascites in developing countries, but it can be easily confused with other causes of ascites. Peritoneal tuberculosis requires early recognition of symptoms and signs in order to make a quick diagnosis for appropriate treatment. Measurement of adenosine deaminase (ADA) level > 39 in ascites fluid is an established test to diagnose peritoneal tuberculosis. Many low-income countries do not currently test for adenosine deaminase in ascites fluid, including Rwanda. METHOD: Cross-sectional, descriptive study conducted through the Internal Medicine Department of three university teaching hospitals in Rwanda. Participants were patients older than 16 years presenting to tertiary referral hospitals with ascites of unknown cause. RESULTS: Of 103 ascites fluid samples collected, 52 of them (50.5%) had an elevated ADA, consistent with a presumptive diagnosis of peritoneal TB. Among those 52 subjects diagnosed with peritoneal TB, 39 out of 52 (75%) did not receive anti-TB medications. Among the 17 subjects who were treated with anti-TB medications, 4 of 17 (23.6%) did not have peritoneal TB based on ADA level. Samples with low-albumin gradient ascites were more likely to have high ADA ≥39 IU/L (p = 0.039). CONCLUSION: Our findings suggest that 3out of 4 patients with PTB in Rwanda are not getting TB treatment and 1 in 4 patients who are taking TB medications do not need it. Even if the true number of Rwandans who are being undertreated and overtreated is less than our study suggests, these results should prompt a larger study of peritoneal tuberculosis. Adding adenosine deaminase (ADA) to the diagnostic tools available to clinicians could help achieve the goal of correctly putting every Rwandan with tuberculosis on treatment, while avoiding unnecessary tuberculosis medications in those who do not have the disease.

Soluble AXL is ubiquitously present in malignant serous effusions.

OBJECTIVE: The objective of this study was to analyze the expression level and clinical role of soluble AXL (sAXL) in cancers affecting the serosal surfaces, with focus on ovarian carcinoma. METHODS: sAXL protein expression by ELISA was analyzed in 572 effusion supernatants, including 424 peritoneal, 147 pleural and 1 pericardial specimens. RESULTS: sAXL was overexpressed in peritoneal effusions compared to pleural and pericardial specimens (p < 0.001). sAXL levels were additionally significantly higher in effusions from patients with ovarian carcinoma, malignant mesothelioma and breast carcinoma compared to specimens from patients with other cancers (predominantly carcinomas of lung, gastrointestinal or uterine corpus/cervix origin) or benign reactive effusions (p < 0.001). sAXL was further overexpressed in high-grade serous carcinoma (HGSC; n = 373) compared to low-grade serous carcinoma (LGSC; n = 32; p = 0.036). In HGSC, sAXL levels were significantly lower in post-chemotherapy effusions compared to primary diagnosis pre-chemotherapy specimens (p = 0.002). sAXL levels in HGSC were unrelated to chemoresponse at diagnosis, progression-free survival or overall survival. Levels were similarly unrelated to survival in LGSC and breast carcinoma. CONCLUSIONS: sAXL is widely expressed in malignant effusions, particularly in ovarian and breast carcinoma and in malignant mesothelioma. sAXL is overexpressed in HGSC compared to LGSC and its levels are lower following exposure to chemotherapy. However, sAXL levels are not informative of chemoresponse or survival.

The IL-1-dependent sterile inflammatory response has a substantial caspase-1-independent component that requires cathepsin C.

The sterile inflammatory response to cell death and irritant crystals is medically important because it causes disease. Although these stimuli are structurally distinct, they cause inflammation through a common pathway that requires the cytokine IL-1. In vitro, the inflammasome, and in particular its generation of active caspase-1, is absolutely required to produce bioactive IL-1ß. However, in this study, we report that caspase-1 is not required in vivo for much of the IL-1ß-dependent sterile inflammatory response. Furthermore, we find that cathepsin C, which controls the activity of a number of leukocyte serine proteases capable of processing IL-1ß, plays a major role in this caspase-1-independent pathway. Mice that are deficient in cathepsin C have reduced inflammatory responses to dying cells and silica crystals. In the absence of cathepsin C, caspase-1 becomes rate limiting such that mice doubly deficient in both of these proteases make little IL-1ß in vivo and have markedly attenuated inflammatory responses to the sterile stimuli. In contrast, these mutant mice generate normal inflammation in response to exogenous IL-1ß, indicating that cathepsin C and caspase-1 function upstream of IL-1ß, and, in their absence, all components of the pathway downstream of mature IL-1ß are intact.

Role of MAP kinases and PI3K-Akt on the cytokine inflammatory profile of peritoneal macrophages from the ascites of cirrhotic patients.

AIMS: Several new approaches targeting inflammation associated with different diseases are in clinical development. OBJECTIVE: To explore the role played by MAPK and PI3K-Akt pathways on the release of cytokines in monocyte-derived macrophages (M-DM) obtained from the ascites of cirrhotic patients to identify novel targets for pharmaceutical intervention to prevent hepatic damage. METHODS: M-DM were isolated from the ascites of cirrhotic patients and stimulated in vitro with LPS and heat-killed Candida albicans in the presence or absence of the inhibitors for MEK1, p38 MAPK, JNK and PI3K. The MAPK phosphorylation levels were determined by Western Blot. Cell culture supernatants were assayed by ELISA for TNF-α, IL-6 and IL-10. RESULTS: The release of the pro-inflammatory cytokines IL-6 and TNF-α at baseline was more effectively reduced by the MAPK inhibitors, while the basal IL-10 anti-inflammatory cytokine secretion was only and strongly (90.3%) affected by the PI3K inhibitor. The incubation of peritoneal M-DM in the presence of LPS and C. albicans increased the release of IL-6, TNF-α and IL-10. LPS-induced pro-inflammatory cytokines secretion was more sensitive to MAPK inhibitors, whereas that induced by C. albicans was more susceptible to inhibition of PI3K. Finally, inhibition of PI3K almost completely suppressed the secretion of IL-10 in stimulated M-DM. CONCLUSIONS: These results demonstrate that pro-inflammatory cytokines release in M-DM from this clinical setting strongly depends on the MAPK signalling pathways, differs depending on the microbial stimulus added and confirms the prominent role of the PI3K-Akt pathway in the modulation of IL-10-mediated anti-inflammatory function.

Radiofrequency is a secure and effective method for pancreatic transection in laparoscopic distal pancreatectomy: results of a randomized, controlled trial in an experimental model.

BACKGROUND: Postoperative pancreatic fistula (PPF) is the most frequent and serious complication after laparoscopic distal pancreatectomy (LDP). Our goal was to compare the performance, in terms of PPF prevention, and safety of a radiofrequency (RF)-assisted transection device versus a stapler device in a porcine LDP model. METHODS: Thirty-two animals were randomly divided into two groups to perform LDP using a RF-assisted device (RF group; n = 16) and stapler device (ST group; n = 16) and necropsied 4 weeks after surgery. The primary endpoint was the incidence of PPF. Secondary endpoints were surgery/transection time, intra/postoperative complications/deaths, postoperative plasmatic amylase and glucose concentration, peritoneal liquid amylase and interleukin 6 (IL-6) concentrations, weight variations, and histopathological changes. RESULTS: Two clinical and one biochemical PPF were observed in the ST and RF groups respectively. Peritoneal amylase concentration was significantly higher in the RF group 4 days after surgery, but this difference was no longer present at necropsy. Both groups presented a significant decrease in peritoneal IL-6 concentration during the postoperative follow-up, with no differences between the groups. RF group animals showed a higher postoperative weight gain. In the histopathological exam, all RF group animals showed a common pattern of central coagulative necrosis of the parenchymal surface, surrounded by a thick fibrosis, which sealed main and secondary pancreatic ducts and was not found in ST group. CONCLUSIONS: The fibrosis caused by an RF-assisted device can be at least as safe and effective as stapler compression to achieve pancreatic parenchyma sealing in a porcine LDP model.

MGST1 expression in serous ovarian carcinoma differs at various anatomic sites, but is unrelated to chemoresistance or survival.

OBJECTIVE: To investigate the expression of MGST1 in primary tumors, solid metastases and metastatic effusions in advanced-stage serous ovarian carcinoma (OC) and analyze the association with clinicopathologic parameters, including chemotherapy resistance and survival. METHODS: MGST1 mRNA expression was investigated in 178 tumors (88 effusions, 38 primary carcinomas, 52 solid metastases) from 144 patients using real-time quantitative PCR (qRT-PCR). Forty-two of the 88 effusions were additionally analyzed for MGST1 protein expression by Western blotting. RESULTS: mRNA expression of MGST1 was higher in primary carcinomas and solid metastases compared to effusions (p=0.008 and p=0.012, respectively). In patient-matched samples, mRNA expression of MGST1 was higher in solid metastases compared to effusions (p=0.023), and a trend for higher MGST1 levels in solid metastases compared to primary tumors was observed (p=0.06). Biopsies from primary carcinomas obtained from patients with >200 ml ascites at diagnosis had higher mRNA expression of MGST1 compared to samples from patients with <200 ml ascites (p=0.037). MGST1 mRNA expression was not associated with age, histological grade, tumor stage, residual disease volume, response to chemotherapy, chemotherapy resistance or survival. Western blot analysis of patient-matched effusions showed high concordance between MGST1 protein and mRNA levels measured by qRT-PCR (p<0.001). CONCLUSIONS: The present study documents frequent MGST1 mRNA and protein expression in OC. The data suggest increased activity of oxidative response pathways, reflected by higher mRNA expression, in solid OC tumors compared to metastatic effusions. Additionally, a tumor microenvironment consisting of ascites may induce antioxidant activity.

Chitotriosidase levels in patients with severe endometriosis.

OBJECTIVE: To study the levels of chitotriosidase activity in the peritoneal fluid and the plasma of patients with severe endometriosis and control subjects. MATERIALS AND METHODS: Twenty-five women with laparoscopically and histopathologically confirmed endometriosis (study group) and 27 control patients who had undergone laparoscopic surgery were included. Peritoneal fluid and peripheral blood were obtained from all the patients before the surgery. Chitotriosidase activities were measured. RESULTS: Analysis of chitotriosidase activity in the peritoneal fluid of patients with endometriosis showed that there was no significant difference between endometriosis and control group, respectively (32.04 ± 64.20 vs. 15.25 ± 31.17 nmol/mL/h; p > 0.05). Analysis of chitotriosidase activity in plasma of patients with endometriosis showed significantly increased levels of chitotriosidase levels compared with the control group (74.81 ± 60.54 vs. 14.10 ± 26.17; p < 0.001), respectively. CONCLUSION: We found that the activity of chitotriosidase in plasma was statistically higher in severe endometriosis patients than women without endometriosis.

Adenosine deaminase activity in patients with ovarian neoplasms.

PURPOSE: The aim of this study was to investigate the serum and peritoneal fluid adenosine deaminase (ADA) activity in patients with benign and malignant ovarian neoplasms. METHODS: This is a prospective cross-sectional study performed in Cukurova University, Department of Gynecologic Oncology. Eighty-four patients with ovarian mass were included in this study within 13 months. The levels of serum and peritoneal fluid ADA levels were measured and compared in patients with benign and malignant ovarian neoplasms and also low- and high-grade malignant tumors. RESULTS: Serum and peritoneal fluid ADA levels were found to be significantly higher in patients with ovarian cancers as compared with benign ovarian tumors (p = 0.001). Additionally, ADA levels were found to be significantly different according to the histopathological subtypes and grade of ovarian cancers. However, there was no significant difference for ADA levels between the benign and low-grade malignant tumors. There was an important correlation between the peritoneal fluid and serum ADA levels. CONCLUSIONS: Serum and peritoneal fluid ADA levels were found to be higher in malignant ovarian neoplasms. This finding may be useful to understand the biochemically characteristics of malignant ovarian tumors and ADA may be a useful biomarker in diagnosis and management of ovarian tumors.

Circulating biomarker tissue kallikrein-related peptidase KLK5 impacts ovarian cancer patients' survival.

BACKGROUND: Effective cancer biomarkers for early detection, prognosis, or therapy response prediction are urgently needed in ovarian cancer. Kallikrein-related peptidases, including KLK5, have been reported to play an important role in the course of the disease. PATIENTS AND METHODS: KLK5 antigen content was determined by enzyme-linked immunosorbent assay in ovarian cancer patients' [FIGO (International Federation of Gynecology and Obstetrics) stages I-IV, n = 52] serum as well as ascitic fluid and compared with KLK5 content in serum of patients with benign ovarian tumors (n = 45). RESULTS: KLK5 antigen content was significantly elevated in the serum of ovarian cancer patients compared with the serum of patients with benign ovarian tumors. Forty-two of 52 ovarian cancer serum samples, 42 of 43 benign ovarian tumor serum samples, and all 41 ascitic fluid samples were KLK5 positive. Elevated KLK5 antigen in serum and ascitic fluid of ovarian cancer patients was a prognostic factor for progression-free survival. CONCLUSIONS: Our data support the finding that ovarian cancer patients release significant amounts of KLK5 into serum and ascitic fluid but KLK5 antigen is low in serum of patients with benign ovarian tumors. Increased serum and ascitic fluid KLK5 levels are associated with poor patient outcome, thus underlining the importance of KLK5 as a biomarker for early detection as well as for disease management in ovarian cancer.

A new highly sensitive point of care screen for spontaneous bacterial peritonitis using the leukocyte esterase method.

BACKGROUND & AIMS: Urine reagent strips measuring leukocyte esterase activity have been studied to screen spontaneous bacterial peritonitis (SBP) but are insensitive. We calibrated a strip specifically for ascitic fluid to achieve high sensitivity in this diagnosis. METHODS: Experiments were conducted on ascitic fluid from patients with cirrhosis. Samples with SBP were diluted with native acellular ascitic fluid to achieve PMN counts below, above, and close to the diagnostic threshold of 250 PMN/microl. A model of SBP was created by spiking negative ascitic fluid samples (<250 PMN/microl) with activated PMN from blood of patients with sepsis, and diluted to achieve a range of PMN. Aliquots were tested at 2, 3, 4, and 10 min with the Periscreen leukocyte esterase strip. PMN/microl was correlated to timings and color scales: white defined negative (PMN <250/microl); and shades of brown, purple, and pink defined positive. Ascitic fluid samples were obtained from 58 patients. Negative ascitic fluid was used from 32 to generate the model SBP. RESULTS: One thousand three hundred and four experiments were performed with a median PMN count of 492/microl (0-7510). After exclusion of uninterpretable colorimetric results, 1089 experiments were analyzed [PMN of 444/microl (0-7510)]. The best result was obtained at 3 min (n=299), with Se: 100%, Sp: 57.9%; NPV: 100%, PPV: 76.5%. The test was not interpretable in bloody, chylous or bilious ascitic fluid, or concurrent imipenem treatment. CONCLUSIONS: This new leukocyte esterase strip calibrated to an ascitic fluid PMN count 250/microl is a robust screening tool when the strip turns any hue of tan/brown at 3 min.

Elevated intraperitoneal matrix metalloproteinases-8 and -9 in patients who develop anastomotic leakage after rectal cancer surgery: a pilot study.

OBJECTIVE: Experimental studies suggest that matrix metalloproteinase (MMP) enzymes mediate the early tissue breakdown that leads to a decrease in intestinal anastomotic strength. Patients with upregulation of MMPs in intestinal biopsies have an increased rate of anastomotic leakage. We measured MMPs and their inhibitors [tissue inhibitors of metalloproteinases (TIMPs)] in postoperative intraperitoneal fluid after rectal cancer surgery, and hypothesized that they would be elevated in patients who later would develop anastomotic leakage. METHOD: Twenty-nine patients with rectal carcinoma underwent low anterior resection of the rectum for cancer. Intraperitoneal fluid was collected via a pelvic drain at a median of 4 h postoperatively. MMP-1, -2, -3, -7, -8, -9 and -13 were determined using particle-based multiplex flow-cytometry. TIMP-1 and -2 were measured by enzyme-linked immunosorbent assays. MMP-9 was considered the main outcome variable. RESULTS; Ten patients developed anastomotic leakage. These patients had increased intraperitoneal MMP-9 [median difference (m.d.) 29%; P = 0.03] and MMP-8 (m.d. 58%; P = 0.02), compared with patients who did not develop leakage. There were no differences between the groups for other MMPs and TIMPs. CONCLUSION: Matrix metalloproteinase-8 and -9 appear to have an important role in the development of anastomotic leakage and may be promising pharmacological targets to protect anastomotic integrity. We suggest further investigation of MMPs as markers for anastomotic leakage.

Cytochemical localization of acid phosphatase activity in granule fractions from rabbit polymorphonuclear leukocytes.

When rabbit peritoneal exudates (97% polymorphonuclear [PMN] leukocytes, 2% mononuclear cells) were fractionated by zonal sedimentation or isopycnic centrifugation, four fractions (A, B, C, and D) were obtained, as reported earlier. "A" consisted largely of PMN azurophil granules, "B" of PMN specific granules, and "D" of membranous elements. The source of the more heterogeneous "C" fraction (containing acid hydrolases) was uncertain. To gain further information on the nature of this fraction, cytochemical tests for acid phosphatase (AcPase) were carried out on the starting cells and on the fractions. In intact PMN, lead phosphate reaction product was found in Golgi complexes, perinuclear cisternae, and some azurophil granules (immature forms or disrupted mature forms) of a few cells. The specifics and the intact azurophils were not reactive. Reaction product was also found within Golgi cisternae, secondary lysosomes, and some of the azurophil granules of mononuclear cells. Observations on the A and B fractions confirmed those in situ regarding the localization of reaction product in disrupted PMN azurophils, its absence from specifics, and the latency of the enzyme activity in intact azurophils. In the C fraction, AcPase was found in three structures (a) Golgi cisternae, (b) dense bodies, and (c) small pleomorphic granules Comparison with the starting cells indicates that the Golgi complexes are probably derived from both PMN leukocytes and mononuclear cells, whereas the remaining elements resemble (in size, shape, and density) secondary lysosomes and azurophil granules of mononuclear cells. The results indicate that the bulk of the cytochemically detectable AcPase present in the C fraction is derived from mononuclear cells, rather than from PMN leukocytes

Nicotinamide adenine dinucleotide splitting enzyme: a characteristic of the mouse macrophage.

Murine macrophages are endowed with nicotinamide adenine dinucleotide splitting activity that is markedly higher than that of other cells, tissues, or organs of the mouse. This enzyme therefore can be used as a biochemical marker for distinguishing macrophages from other cells of the lymphoreticular system and from polymorphonuclear leukocytes.

Pelvic-peritoneal tuberculosis simulating peritoneal carcinomatosis: high clinical suspicion and a minimally invasive procedure.

Peritoneal tuberculosis (TB) is still a major health problem in developing countries. We describe a 26-year-old woman with peritoneal TB presenting with lower abdominal pain and distention, weight loss, and night sweats. There are no pathognomonic clinical, laboratory, or radiologic findings for peritoneal TB. Therefore, it can be easily confused with peritoneal carcinomatosis and advanced ovarian carcinoma. Adenosine deaminase activity in ascitic fluid combined with a high clinic suspicion is an effective and minimally invasive procedure for the differential diagnosis of pelvic-peritoneal TB simulating peritoneal carcinomatosis, and may obviate the need for unnecessary extensive surgery and rapidly initiate appropriate therapy.

Clinical significance of telomerase activity in gastric carcinoma and peritoneal dissemination.

Telomerase activity is responsible for telomere maintenance and is believed to be crucial in most cancer cells, but its significance in gastric cancer remains unknown. This observational study investigated whether there is a relationship between telomerase activity and the development of gastric cancer, and between telomerase activity and peritoneal dissemination. Telomerase activity was measured in primary gastric cancers and in peritoneal washings from the same patients, and findings were compared with those of conventional cytology and an immunoassay for cancer antigen 125 (CA125). Positive cytological examination and telomerase activity in peritoneal washings both correlated with the histological grade, depth of tumour invasion, area of serosal invasion and peritoneal metastasis. The detection of free cancer cells in peritoneal washings by the telomeric repeat amplification protocol/enzyme-linked immunosorbent assay (TRAP-ELISA) was significantly more sensitive than cytology or the CA125 immunoassay, suggesting that this could be used to diagnose early peritoneal dissemination.

Amifostine increases cure rate of cisplatin on ascites hepatoma 22 via selectively protecting renal thioredoxin reductase.

It has been demonstrated via in vitro experiments that the anti-cancer drug cisplatin (CDDP) can inactivate thioredoxin reductase (TrxR), a molecular target for cancer therapy. The present study in mice revealed that CDDP at pharmacological doses inhibited TrxR activity in both ascitic hepatoma 22 (H22) cells and kidney, leading to suppression of H22 cells proliferation along with nephrotoxicity. Amifostine, a clinical used cytoprotective agent, protected against CDDP-induced TrxR inactivation in kidney but not in H22 cells. Such an excellent selective modulation of amifostine on TrxR led us to exploit the potential of amifostine in increasing cure rate of CDDP on cancer. In mice, CDDP at the doses of 5 and 7.5 mg/kg once weekly for 4 weeks could not completely control H22 ascites development and the cure rate was no more than 12.5%; CDDP 9 mg/kg by the same schedule prominently suppressed the ascites development, but finally resulted in 87.5% mortality caused by CDDP toxicity. Thus, these dose-dependent therapeutic results well recapitulated the clinical dilemma of chemotherapy on cancer. However, co-treatment of CDDP (9 mg/kg) and amifostine largely reduced CDDP toxicity, and obtained a cure rate as high as 87.5%. Overall, the present study demonstrates both pharmacological and toxicological effects of CDDP involve TrxR inactivation, and the large enhancement on CDDP cure rate in H22 ascites model by using amifostine is, at least in part, ascribed to its selective modulation on TrxR.

Myeloperoxidase assay in plasma and peritoneal fluid of horses with gastrointestinal disease.

Gastrointestinal disorders, especially strangulating intestinal obstructions, are still a major cause of illness and death in the horse. Circulating lipopolysaccharides may activate both neutrophils and monocytes. The activated neutrophils release myeloperoxidase (MPO), a specific enzyme with strong oxidative activity. The aim of this study was to evaluate MPO concentrations in the plasma and peritoneal fluid (PF) of horses with colic and to check the hypothesis that these concentrations would be higher in a case of strangulating obstruction than in cases of nonstrangulating disease. By using a specific enzyme-linked immunosorbent assay for equine MPO, we determined the MPO concentrations in horses admitted to a clinic for colic. Horses with nonstrangulating or strangulating obstruction of the large intestine (NSLI or SLI), strangulating obstruction of the small intestine (SSI), or inflammatory bowel disease (IBD) were compared with healthy horses. The horses with SLI, SSI, or IBD had significantly higher MPO levels in plasma and PF than did those in the other 2 groups. The mean plasma level was significantly higher in the horses with NSLI than in the healthy horses. High MPO values in PF indicated necrotic bowel. These results show that neutrophil activation occurs during nonstrangulating and strangulating intestinal obstruction in horses and that the plasma and PF MPO concentrations may be a marker of the severity of the disease.

The diagnostic role of BAP1 in serous effusions.

The aim of this study was to analyze the diagnostic role of BAP1 in effusion cytology. Effusions (n = 258), consisting of 53 malignant mesotheliomas and 205 other cancers, the majority carcinomas (62 breast, 60 ovarian, 31 lung, 51 carcinomas of other origin, 1 melanoma), were analyzed for BAP1 expression using immunohistochemistry. BAP1 was lost in 46 (87%) mesotheliomas compared with 4 (2%) of 205 other cancers (P < .001), resulting in sensitivity and specificity of 87% and 98%, respectively. There was no significant difference between peritoneal (n = 14) and pleural (n = 39) mesotheliomas. The 4 carcinomas with loss of BAP1 included 1 ovarian, 1 breast, 1 uterine cervical, and 1 gastric carcinoma. The present study supports the role of BAP1 as a highly sensitive and specific marker for malignant mesothelioma in serous effusions and argues for inclusion of this test in all specimens in which this diagnosis is considered.