Procalcitionin as a diagnostic marker to distinguish upper and lower gastrointestinal perforation

AIM To assess the accuracy of serum procalcitionin(PCT)as a diagnostic marker in verifying upper and lower gastrointestinal perforation(GIP).METHODS This retrospective study included 46 patients from the surgical intensive care unit(ICU)of the Second Affiliated Hospital of Harbin Medical University who were confirmed to have GIP between June 2013 and December 2016.Demographic and clinical patient data were recorded on admission to ICU.Patients were divided into upper(n=19)and lower(n=27)GIP groups according to the perforation site(above or below Treitz ligament).PCT and WBC count was obtained before laparotomy and then compared between groups.Meanwhile,the diagnostic accuracy of PCT was analyzed.RESULTS Patients with lower GIP exhibited significantly higher APACHE II score,SOFA score and serum PCT level than patients with upper GIP(P=0.017,0.004,and0.001,respectively).There was a significant positive correlation between serum PCT level and APACHE II score or SOFA score(r=0.715 and r=0.611,respectively),while there was a significant negative correlation between serum PCT level and prognosis(r=-0.414).WBC count was not significantly different between the two groups,and WBC count showed no significant correlation with serum PCT level,APACHE II score,SOFA score or prognosis.The area under the receiver operating characteristic curve of PCT level to distinguish upper or lower GIP was 0.778.Patients with a serum PCT level above 17.94 ng/d L had a high likelihood of lower GIP,with a sensitivity of 100%and a specificity of 42.1%.CONCLUSION Serum PCT level is a reliable and accurate diagnostic marker in identifying upper or lower GIP before laparotomy.

Can mean platelet volume play a role in evaluating the severity of acute pancreatitis?

AIM To investigate serum mean platelet volume(MPV) levels in acute pancreatitis(AP) patients and assess whether MPV effectively predicts the disease severity of AP.METHODS We included 117 consecutive patients with AP as the AP group and 34 consecutive patients with colorectal polyps(before endoscopic treatment) as the control group. Complete blood counts, liver function, platelet indices(MPV), coagulation parameters, lactate dehydrogenase(LDH) and C-reactive protein(CRP) were measured on days 1, 2, 3 and 7 after admission. Receiver operating characteristic curves were used to compare the sensitivity and specificity of MPV, white blood cell(WBC), LDH and CRP in predicting AP severity. The Modified Glasgow Prognostic Score(m GPS) and the 2012 revised Atlanta criteria were used to evaluate disease severity in AP.RESULTS MPV levels were significantly lower in the AP group than in the control group on day 1(P = 0.000), day 2(P = 0.029) and day 3(P = 0.001) after admission.In addition, MPV values were lower on day 1 after admission than on day 2(P = 0.012), day 3(P = 0.000) and day 7(P = 0.002) in all AP patients. Based on the m GPS, 78 patients(66.7%) were diagnosed with mild and 39 patients(33.3%) with severe AP. There was no significant difference in mean MPV levels between patients diagnosed with mild and severe AP based on the m GPS(P = 0.424). According to the 2012 revised Atlanta criteria, there were 98 patients(83.8%) without persistent organ failure(OF) [non-severe acute pancreatitis(non-SAP) group] and 19 patients(16.2%) with persistent OF(SAP group). MPV levels were significantly lower in the SAP group than in the non-SAP group on day 1 after admission(P = 0.002). On day 1 after admission using a cut-off value of 6.65 f L, the overall accuracy of MPV for predicting SAP according to the 2012 revised Atlanta criteria(AUC = 0.716) had a sensitivity of 91.8% and a specificity of 47.4% and was superior to the accuracy of the traditional markers WBC(AUC = 0.700) and LDH(AUC = 0.697).CONCLUSION MPV can be used at no additional cost as a useful, noninvasive biomarker that distinguishes AP with persistent OF from AP without persistent OF on day 1 of hospital admission.

ESTABLISHMENT OF K562/ADM/VER CELL SUBLINE RESISTANT TO VERAPAMIL AND ITS RESISTANT MECHANISM

Objective: To understand whether verapamil (VER) resistance development in the multidrug-resistant cell line and its mechanism. Methods: K562/ADM/VER cell subline resistant to verapamil was established through a gradual increase of VER concentration in the media. MTT method was used to assay resistance to VER, cross resistance to dipyriamole (DPM), cyclosporin A (CsA) in the cells, and HPLC and spectrofluorometer to detect intracellular accumulation of VER or ADM respectively, as well as S-P immunocytochemical technique for detection of genes expression. Results: It were observed that 7.9-fold increase in VER resistance, significantly reduced intracellular accumulation of VER or ADM and also develop across resistance to DPM and CsA in K562/ADM/VER cells, compared with its parent cell, K562/ADM. High-level of p-glycoprotein(pgp), middle-level of p53, p16, was present in two cell lines without expression of GSTPI, C-myc, C-myc, C-fos and C-erbB-2. Bc1-2 protein expression was found only in K562/ADM cells. Conclusion: K562/ADM cells were capable of being induced to develop resistance to VER.

Pure Total Flavonoids from Citrus paradisi Macfad InduceLeukemia Cell Apoptosis In Vitro

Objective: To investigate the potential effect of pure total flavonoids from Citrus paradisi Macfad peel(PTFC) on the proliferation and apoptosis of human myeloid leukemia cells Kasumi-1, HL-60 and K562, and the underlying mechanisms. Methods: PTFC was extracted from Citrus paradisi Macfad peel and was identified by high performance liquid chromatography. The effect of PTFC on the proliferation and apoptosis of leukemia cells were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, fluorescent microscopy and flow cytometry, respectively. The effect of PTFC on the expression levels of apoptosis-related regulators was determined by Western blot assay. Results: Treatment with PTFC inhibited leukemia cell proliferation in a dose-and time-dependent manner and triggered Kasumi-1 cell apoptosis. Treatment with PTFC significantly increased the levels of activated poly adenosine diphosphate-ribosepolymerase and caspase-3/-9, but reduced the levels of Mcl-1 expression in Kasumi-1 cells. However, PTFC did not obviously induce HL-60 cell apoptosis. Conclusion: PTFC inhibited leukemia cell proliferation and induced their apoptosis by modulating apoptosisrelated regulator expression in leukemia cells in vitro.