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Increased COX-2 and decreased 15-hydroxyprostaglandin dehydrogenase (15-HPGD) expression promote prostaglandin-mediated inflammation and colorectal carcinogenesis. Experimental studies suggest that vitamin D and calcium may inhibit these pathways, but their effects on colorectal tissue COX-2 and 15-HPGD expression in humans are unknown. We tested the effects of supplemental vitamin D (1,000 IU/day) and/or calcium (1,200 mg/day) on COX-2 and 15-HPGD expression in the morphologically normal rectal mucosa from 62 paients with colorectal adenoma in a placebo-controlled chemoprevention trial. We measured biomarker expression using automated IHC and quantitative image analysis at baseline and 1-year follow-up, and assessed treatment effects using mixed linear models. The primary outcome was the COX-2/15-HPGD expression ratio, because these enzymes function as physiologic antagonists. After 1 year of treatment, the mean COX-2/15-HPGD expression ratio in full-length crypts proportionately decreased 47% in the vitamin D group (P = 0.001), 46% in the calcium group (P = 0.002), and 34% in the calcium + vitamin D group (P = 0.03), relative to the placebo group. Among individuals with the functional vitamin D–binding protein isoform DBP2 (GC rs4588*A), the COX-2/15-HPDG ratio decreased 70% (P = 0.0006), 75% (P = 0.0002), and 60% (P = 0.006) in the vitamin D, calcium, and combined supplementation groups, respectively, relative to placebo. These results show that vitamin D and calcium favorably modulate the balance of expression of COX-2 and 15-HPGD—biomarkers of inflammation that are strongly linked to colorectal carcinogenesis—in the normal-appearing colorectal mucosa of patients with colorectal adenoma (perhaps especially those with the DBP2 isoform). Prevention Relevance: Supplemental calcium and vitamin D reduce indicators of cancer-promoting inflammation in normal colorectal tissue in humans, thus furthering our understanding of how they may help prevent colorectal cancer.

Gut barrier dysfunction promotes chronic inflammation, contributing to several gastrointestinal diseases, including colorectal cancer. Preliminary evidence suggests that vitamin D and calcium could prevent colorectal carcinogenesis, in part, by influencing gut barrier function. However, relevant human data are scarce. We tested the effects of supplemental calcium (1,200 mg/day) and/or vitamin D3 (1,000 IU/day) on circulating concentrations of biomarkers of gut permeability (anti-flagellin and anti-lipopolysaccharide IgA and IgG, measured via ELISA) from baseline to 1 and 3 or 5 years postbaseline among 175 patients with colorectal adenoma in a randomized, double-blinded, placebo-controlled clinical trial. We also assessed factors associated with baseline concentrations of these biomarkers. We found no appreciable effects of supplemental vitamin D3 and/or calcium on individual or aggregate biomarkers of gut permeability. At baseline, a combined permeability score (the summed concentrations of all four biomarkers) was 14% lower among women (P = 0.01) and 10% higher among those who consumed >1 serving per day of red or processed meats relative to those who consumed none (Ptrend = 0.03). The permeability score was estimated to be 49% higher among participants with a body mass index (BMI) > 35 kg/m2 relative to those with a BMI < 22.5 kg/m2 (Ptrend = 0.17). Our results suggest that daily supplemental vitamin D3 and/or calcium may not modify circulating concentrations of gut permeability biomarkers within 1 or 3–5 years, but support continued investigation of modifiable factors, such as diet and excess adiposity, that could affect gut permeability. Prevention Relevance: Calcium and vitamin D may be involved in regulating and maintaining the integrity of the intestinal mucosal barrier, the dysfunction of which results in exposure of the host to luminal bacteria, endotoxins, and antigens leading to potentially cancer-promoting endotoxemia and chronic colon inflammation. While our results suggest that daily supplementation with these chemopreventive agents does not modify circulating concentrations of gut permeability biomarkers, they support continued investigation of other potential modifiable factors, such as diet and excess adiposity, that could alter gut barrier function, to inform the development of treatable biomarkers of risk for colorectal neoplasms and effective colon cancer preventive strategies.

Chronic inflammation in the colorectum, a significant contributor to colorectal carcinogenesis, can be triggered by the activation of proinflammatory signaling pathways such as those initiated by Toll-like receptors (TLR) and nuclear factor κB (NF-κB). Although experimental evidence supports calcium and vitamin D potentially modifying these proinflammatory pathways in the colorectum, human data in these regards are scarce. We investigated supplemental calcium (1,200 mg daily) and/or vitamin D3 (1,000 IU daily) effects on inflammatory signaling pathway-related biomarkers in a subset of 105 participants from a colorectal adenoma recurrence chemoprevention clinical trial. We assessed expression of TLR4 and TLR5, which recognize the bacterial components lipopolysaccharides and flagellin, respectively, and phospho-IKKα/β (pIKKα/β), a biomarker of inflammation, in the normal-appearing rectal crypt epithelium and stroma using standardized, automated immunohistochemistry and quantitative image analysis. Following 1 year of treatment, TLR4, TLR5, and pIKKα/β expression in the rectal mucosa did not statistically significantly change with vitamin D or calcium supplementation, taken alone or in combination. Several baseline participant characteristics, including body mass index, history of sessile serrated adenomas, high red/processed meat intake, and high levels of rectal epithelial cell proliferation (as measured by MIB-1/Ki-67), were associated with higher baseline expression of TLRs or pIKKα/β. Our findings suggest that vitamin D and calcium may have no substantial effect on the investigated biomarkers. However, several modifiable lifestyle factors may be associated with TLRs and pIKKα/β expression in the normal rectal mucosa, supporting their future investigation as potentially treatable, preneoplastic risk factors for colorectal neoplasms. Cancer Prev Res; 11(11); 707–16. ©2018 AACR.

Introduction/Background Rates of colorectal cancer screening are improving but remain suboptimal. Limited information is available regarding how patients are diagnosed with colorectal cancer (for example, asymptomatic screened patients or diagnostic workup because of the presence of symptoms). The purpose of this investigation was to determine how patients were diagnosed with colorectal cancer (screening colonoscopy, diagnostic colonoscopy, or emergent surgery) and tumor stage and size at diagnosis. Patients and Methods Adults evaluated between 2011 and 2014 with a diagnosis of colorectal cancer were identified. Clinical notes, endoscopy reports, surgical reports, radiology reports, and pathology reports were reviewed. Sex, race, ethnicity, age at the time of initial diagnosis, method of diagnosis, presenting symptom(s), and primary tumor size and stage at diagnosis were recorded. Colorectal cancer screening history was also recorded. Results The study population was 54% male (265 of 492) with a mean age of 58.9 years (range, 25-93 years). Initial tissue diagnosis was established at the time of screening colonoscopy in 10.7%, diagnostic colonoscopy in 79.2%, and during emergent surgery in 7.1%. Cancers diagnosed at the time of screening colonoscopy were more likely to be stage 1 than cancers diagnosed at the time of diagnostic colonoscopy or emergent surgery (38.5%, 7.2%, and 0%, respectively). Median tumor size was 3.0 cm for the screening colonoscopy group, 4.6 cm for the diagnostic colonoscopy group, and 5.0 cm for the emergent surgery group. At least 31% of patients diagnosed at the time of screening colonoscopy, 19% of patients diagnosed at the time of diagnostic colonoscopy, and 26% of patients diagnosed at the time of emergent surgery had never undergone a screening colonoscopy. Conclusion Nearly 90% of colorectal cancer patients were diagnosed after development of symptoms and had more advanced disease than asymptomatic screening patients. Colorectal cancer outcomes will be improved by improving rates of colorectal cancer screening.

To clarify the roles of vitamin D and calcium as potential chemopreventive agents against colorectal cancer in humans, and to develop “treatable”, pre-neoplastic, phenotypic biomarkers of risk for colorectal neoplasms, we estimated the effects of supplemental vitamin D3 (1,000 IU/day [25 μg/day]) and calcium (1,200 mg/day), alone and in combination, on biomarkers of proliferation (mib-1), differentiation (p21), and apoptosis (bax [apoptosis-promoting] and bcl-2 [apoptosis-inhibiting]), in the normal-appearing rectal mucosa in a subsample of participants (n = 104) in a larger randomized, double-blind, placebo-controlled clinical trial among colorectal adenoma patients. The biomarkers were measured in rectal biopsies at baseline and after one year of follow up, using automated immunohistochemistry and quantitative image analysis. In the vitamin D plus calcium group relative to control, in the crypt differentiation zone (upper 40% of crypts), mib-1 expression decreased 24% (P = 0.28); p21 expression alone and relative to mib-1 expression increased 29% (P = 0.06) and 73% (P = 0.06), respectively; and bax expression relative to mib-1 expression increased 58% (P = 0.21). The estimated vitamin D alone treatment effects were similar but of lesser magnitudes, and those for calcium alone were mixed. All estimated treatment effects on bcl-2 expression were close to the null. These pilot study results support further investigation of whether 1) vitamin D and calcium promote colorectal epithelial cell differentiation, reduce proliferation, and promote apoptosis in the normal-appearing human colorectal mucosa, 2) vitamin D and calcium act as chemopreventive agents against colorectal neoplasms, and 3) mib-1, p21, and bax are potential “treatable”, pre-neoplastic, biomarkers of risk for colorectal neoplasms.

APC/β-catenin pathway perturbation is a common early event in colorectal carcinogenesis and is affected by calcium and vitamin D in basic science studies. To assess the effects of calcium and vitamin D on adenomatous polyposis coli (APC), β-catenin, and E-cadherin expression in the normal appearing colorectal mucosa of sporadic colorectal adenoma patients, we conducted a randomized, double-blinded, placebo-controlled 2 × 2 factorial clinical trial. Pathology-confirmed colorectal adenoma cases were treated with 2 g/day elemental calcium and/or 800 IU/day vitamin D3 versus placebo over 6 months (N = 92; 23/group). Overall APC, β-catenin, and E-cadherin expression and distributions in colon crypts in normal-appearing rectal mucosa biopsies were detected by standardized automated immunohistochemistry and quantified by image analysis. In the vitamin D3-supplemented group relative to placebo, the proportion of APC in the upper 40% of crypts (Φh APC) increased 21% (P = 0.01), β-catenin decreased 12% (P = 0.18), E-cadherin increased 72% (P = 0.03), and the Φh APC/β-catenin ratio (APC/β-catenin score) increased 31% (P = 0.02). In the calcium-supplemented group Φh APC increased 10% (P = 0.12), β-catenin decreased 15% (P = 0.08), and the APC/β-catenin score increased 41% (P = 0.01). In the calcium/vitamin D3-supplemented group, β-catenin decreased 11% (P = 0.20), E-cadherin increased 51% (P = 0.08), and the APC/β-catenin score increased 16% (P = 0.26). These results support (i) that calcium and vitamin D modify APC, β-catenin, and E-cadherin expression in humans in directions hypothesized to reduce risk for colorectal neoplasms, (ii) calcium and vitamin D as potential chemopreventive agents against colorectal neoplasms, and (iii) the potential of APC, β-catenin, and E-cadherin expression as modifiable, preneoplastic risk biomarkers for colorectal neoplasms. Cancer Prev Res; 5(10); 1247–56. ©2012 AACR.

In cancer cell lines and rodent models, calcium and vitamin D favorably modulate cell proliferation, differentiation, and apoptosis in colonic epithelia. These effects may be modulated by local expression of the calcium receptor (CaR), the vitamin D receptor (VDR), and the P450 cytochromes, CYP27B1 and CYP24A1; however, they have yet to be investigated in humans. To address this gap, we conducted a randomized, double-blinded, placebo-controlled 2 × 2 factorial clinical trial. Patients with at least one pathology-confirmed colorectal adenoma were treated with 2 g/d elemental calcium and/or 800 IU/d vitamin D3 versus placebo over 6 months (n = 92; 23 per group). CaR, VDR, CYP27B1, and CYP24A1 expression and distribution in biopsies of normal appearing rectal mucosa were detected by standardized, automated immunohistochemistry and quantified by image analysis. In the calcium-supplemented group, CaR expression increased 27% (P = 0.03) and CYP24A1 expression decreased 21% (P = 0.79). In the vitamin D3-supplemented group, CaR expression increased 39% (P = 0.01) and CYP27B1 expression increased 159% (P = 0.06). In patients supplemented with both calcium and vitamin D3, VDR expression increased 19% (P = 0.13) and CaR expression increased 24% (P = 0.05). These results provide mechanistic support for further investigation of calcium and vitamin D3 as chemopreventive agents against colorectal neoplasms, and CaR, VDR, CYP27B1, and CYP24A1 as modifiable, preneoplastic risk biomarkers for colorectal neoplasms. Cancer Res; 71(2); 413–23. ©2010 AACR.

Purpose To retrospectively evaluate the efficacy of spectral presaturation attenuated inversion-recovery (SPAIR) fat-suppressed (FS) partial Fourier single shot (SSH) T2-weighted (T2W) and gadolinium-enhanced (Gd) FS 3D-gradient echo (3DGRE) T1-weighted (T1W) delayed phase MRI to differentiate active bowel inflammation from fibrotic disease in patients with Crohn's disease (CD). Materials and Methods MRI studies of 81 patients (mean age, 43 years; range, 22–77 years; M:F ratio 33:48) had T2W and T1W imaging including SPAIR-SSH and delayed Gd-3DGRE. The ability to assess disease activity in bowel segments affected were retrospectively evaluated by a grading scheme based on subjective analysis of signal intensities. These results were compared against the standard clinical parameters of disease activity. Results SPAIR-SSH images correlated better (r = 0.74, P < 0.0001) with activity than delayed Gd-3DGRE (r = 0.39, P = 0.0003), with a significant difference between the two techniques (P < 0.0001). SPAIR-SSH images showed higher specificity in detection of severely active disease in per patient (98%) and segmental (98%) analysis compared to Gd-3DGRE (57%, 70%). Gd-3DGRE technique showed significantly higher sensitivity (P = 0.01) in identifying active disease in per patient (83%) and segmental (85%) analysis compared to SPAIR-SSH (70%, 64%). Conclusion SPAIR-SSH detects actively diseased CD bowel segments with a high level of specificity. Noninflammatory bowel fibrosis corresponds to abnormal uptake on delayed phase Gd-3DGRE images but without associated elevated abnormal signal on SPAIR-SSH. J. Magn. Reson. Imaging 2008;28:1133–1140. © 2008 Wiley-Liss, Inc.

To further clarify and/or develop calcium and vitamin D as chemopreventive agents against colorectal cancer in humans, understand the mechanisms by which these agents reduce risk for the disease, and develop “treatable” biomarkers of risk for colorectal cancer, we conducted a pilot, randomized, double-blind, placebo-controlled, 2 × 2 factorial clinical trial to test the effects of calcium and vitamin D3, alone and in combination on markers of apoptosis, in the normal colorectal mucosa. Ninety-two men and women with at least one pathology-confirmed colorectal adenoma were treated with 2.0 g/d calcium or 800 IU/d vitamin D3, alone or in combination, versus placebo over 6 months. Overall expression and colorectal crypt distributions of Bcl-2 (an apoptosis inhibitor) and Bax (an apoptosis promoter) in biopsies of normal-appearing rectal mucosa were detected by automated immunohistochemistry and quantified by image analysis. After 6 months of treatment, Bax expression along the full lengths of crypts increased 56% (P = 0.02) in the vitamin D group and 33% in both the calcium (P = 0.31) and calcium plus vitamin D (P = 0.36) groups relative to the placebo group. The vitamin D treatment effect was more pronounced in the upper 40%, or differentiation zone, of crypts (80%; P = 0.01). There were no statistically significant treatment effects on Bcl-2 expression. Overall, these preliminary results suggest that calcium and vitamin D, individually or together, may enhance apoptosis in the normal human colorectal epithelium, and the strongest treatment effects may be vitamin D related and in the upper sections of the colorectal crypts.

Introduction: Epstein–Barr virus (EBV) infection frequently involves the liver, presenting as elevations in transaminases. EBV infection associated hepatitis, presenting with hyperbilirubinemia is rare. We describe a case of infectious mononucleosis that presented with cholestatasis, and summarize 23 cases from the literature to categorize this increasingly recognized clinical spectrum of EBV infection induced cholestatic hepatitis. Methods: We conducted an extensive literature review of all cases of EBV in pediatric and adult literature with cholestatasis using MEDLINE and EMBASE. We also included information on one case from our institution. Results: We identified 24 cases. Median age was 20 years (range 1–72 years), with 14 (58%) females. On presentation, fever (72%), jaundice (67%) and splenomegaly (62%) were the most common signs. Laboratory data revealed the median asparate aminotransferase (AST), or alanine aminotransferase (ALT) level was 179 IU/L (range 56–2518 IU/L), median serum bilirubin level 12.6 mg/dL (range 2.2–47.5 mg/dL) and median alkaline phosphatase level 749 IU/L (range 31–3105 IU/L). Diagnosis was confirmed using EBV viral capsid antigen IgM in 20 (83%) patients. HIV testing was done in 7 (29%) of the cases, and was negative. One patient died from the illness, while full recovery was reported in all other cases, with median follow-up of 30 days (range 5–180 days). Conclusions: Cholestatasis is associated with EBV infection, and should be part of the differential diagnosis in all age groups, presenting with hyperbilirubinemia.

We report the case of a patient in whom bacterial endocarditis developed on a native valve after variceal sclerotherapy. We are concerned about the discrepant recommendations for antibiotic prophylaxis in the literature and consider that our report, which we take to be the first, suggests reasons for prophylactic antibiotic treatment in selected patients undergoing sclerotherapy.

Increased concentrations of inflammatory biomarkers predict antidepressant nonresponse, and inflammatory cytokines can sabotage and circumvent the mechanisms of action of conventional antidepressants.To determine whether inhibition of the inflammatory cytokine tumor necrosis factor (TNF) reduces depressive symptoms in patients with treatment-resistant depression and whether an increase in baseline plasma inflammatory biomarkers, including high-sensitivity C-reactive protein (hs-CRP), TNF, and its soluble receptors, predicts treatment response.Double-blind, placebo-controlled, randomized clinical trial.Outpatient infusion center at Emory University in Atlanta, Georgia.A total of 60 medically stable outpatients with major depression who were either on a consistent antidepressant regimen (n = 37) or medication-free (n = 23) for 4 weeks or more and who were moderately resistant to treatment as determined by the Massachusetts General Hospital Staging method.Three infusions of the TNF antagonist infliximab (5 mg/kg) (n = 30) or placebo (n = 30) at baseline and weeks 2 and 6 of a 12-week trial.The 17-item Hamilton Scale for Depression (HAM-D) scores.No overall difference in change of HAM-D scores between treatment groups across time was found. However, there was a significant interaction between treatment, time, and log baseline hs-CRP concentration (P = .01), with change in HAM-D scores (baseline to week 12) favoring infliximab-treated patients at a baseline hs-CRP concentration greater than 5 mg/L and favoring placebo-treated patients at a baseline hs-CRP concentration of 5 mg/L or less. Exploratory analyses focusing on patients with a baseline hs-CRP concentration greater than 5 mg/L revealed a treatment response (≥50% reduction in HAM-D score at any point during treatment) of 62% (8 of 13 patients) in infliximab-treated patients vs 33% (3 of 9 patients) in placebo-treated patients (P = .19). Baseline concentrations of TNF and its soluble receptors were significantly higher in infliximab-treated responders vs nonresponders (P.05), and infliximab-treated responders exhibited significantly greater decreases in hs-CRP from baseline to week 12 compared with placebo-treated responders (P.01). Dropouts and adverse events were limited and did not differ between groups.This proof-of-concept study suggests that TNF antagonism does not have generalized efficacy in treatment-resistant depression but may improve depressive symptoms in patients with high baseline inflammatory biomarkers.clinicaltrials.gov Identifier: NCT00463580.

Increased inflammatory markers predict antidepressant treatment non-response in patients with depression, and inflammatory cytokines can sabotage and circumvent mechanisms of action of conventional antidepressants. We therefore endeavored to determine whether inhibition of the inflammatory cytokine tumor necrosis factor (TNF)-alpha would reduce depressive symptoms in patients with treatment resistant depression (TRD) and whether baseline inflammation would predict response. Sixty outpatients with major depression participated in a double-blind, placebo-controlled trial involving random assignment to three infusions of the TNF-alpha antagonist infliximab (5 mg/kg) ( n = 30) or placebo ( n = 30) at baseline and weeks 2 and 6 of a 12-week trial. The 17-item Hamilton Depression Rating Scale (HAM-D-17) was the primary outcome variable. No differences in change of HAM-D-17 scores between groups across time were found. Interestingly, however, there was significant interaction between treatment, time and log baseline hs-CRP ( p = 0.01) with the change in HAM-D-17 scores at Week 12 favoring infliximab-treated patients at a baseline hs-CRP > 5 mg/L. Treatment response (⩾50% reduction in HAM-D-17 at any time during treatment) in patients with a baseline hs-CRP > 5 mg/L ( n = 22) was 62% in infliximab-treated patients versus 33% for placebo. Baseline concentrations of TNF-alpha and its soluble receptors were significantly higher in infliximab-treated responders versus infliximab non-responders ( p

Background: Evidence suggests that calcium and vitamin D have anti-neoplastic effects in the colorectal mucosa; and that many of these effects are modulated by the calcium receptor (CaR) and vitamin D receptor (VDR); however, this has not been investigated in humans. To evaluate differences of effects of calcium and vitamin D according to CaR and VDR expression, we conducted a secondary analysis of data from a clinical trial of the effects of supplemental calcium and vitamin D3 on biomarkers of risk for colorectal adenomas. Methods: Ninety-two men and women with at least one pathology-confirmed sporadic colorectal adenoma were treated with calcium 2 g/day or vitamin D3 800 IU/day, alone or in combination vs. placebo over six months. A panel of potential biomarkers of risk in colon crypts was detected in biopsies of normal-appearing colorectal mucosa using standardized automated immunohistochemistry and novel image analysis methods. Participants were stratified based on the median treatment effects on CaR and VDR expression in the study population. Treatment effects relative to the placebo group were calculated using a MIXED effects model as implemented in SAS v9.2. Results: Relative to the placebo group, those in the calcium treatment (calcium) group who had greater than the median increases in CaR expression (CaR high), had greater mean increases in p21, TGFβ1, and MSH2 expression than those with a lower than the median increase in CaR expression (CaR low). Among those in the vitamin D3 treatment (D3) group who were CaR high, there were greater mean increases in E-cadherin, APC, p21, TGFβ1, and MSH2 expression, and greater mean decreases of the Bax/Bcl2 expression ratio than in those who were CaR low. Among those in the calcium + vitamin D3 (Ca+D3) treatment group who were CaR high, there were greater mean increases in TGFβ1 and MSH2 expression than in those who were CaR low. Relative to the placebo group, those in the calcium group who had greater than the median increases in VDR expression (VDR high), had greater mean increases in APC, p21, TGFβ1, MLH1, and MSH2 expression, and a greater mean decrease in the Bax/Bcl2 expression ratio than were seen in those with a lower than the median increase in VDR expression (VDR low). Among those in the D3 group who were VDR high, there were greater mean increases in E-cadherin, APC, p21, TGFβ1, and MSH2 expression than in those who were VDR low. Among those in the Ca+D3 group who were VDR high, there were greater increases in APC, p21, MLH1, and MSH2 expression than in those who were VDR low. Discussion: These preliminary results suggest that anti-neoplastic effects of calcium and vitamin D3, individually or in combination on the normal colorectal mucosa may depend on CaR and VDR expression, and provide additional support for CaR and VDR as modifiable biomarkers of risk for colorectal neoplasms. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 842. doi:10.1158/1538-7445.AM2011-842

AIM: To determine factors affecting the outcome of patients with cirrhosis undergoing surgery and to compare the capacities of the Child-Turcotte-Pugh (CTP) and model for end-stage liver disease (MELD) score to predict that outcome. METHODS: We reviewed the charts of 195 patients with cirrhosis who underwent surgery at two teaching hospitals over a five-year period. The combined endpoint of death or hepatic decompensation was considered to be the primary endpoint. RESULTS: Patients who reached the endpoint had a higher MELD score, a higher CTP score and were more likely to have undergone an urgent procedure. Among patients undergoing elective surgical procedures, no statistically significant difference was noted in the mean MELD (12.8 ± 3.9 vs 12.6 ± 4.7, P = 0.9) or in the mean CTP (7.6 ± 1.2 vs 7.7 ± 1.7, P = 0.8) between patients who reached the endpoint and those who did not. Both mean scores were higher in the patients reaching the endpoint in the case of urgent procedures (MELD: 22.4 ± 8.7 vs 15.2 ± 6.4, P = 0.0007; CTP: 9.9 ± 1.8 vs 8.5 ± 1.8, P = 0.008). The performances of the MELD and CTP scores in predicting the outcome of urgent surgery were only fair, without a significant difference between them (AUC = 0.755 ± 0.066 for MELD vs AUC = 0.696 ± 0.070 for CTP, P = 0.3). CONCLUSION: The CTP and MELD scores performed equally, but only fairly in predicting the outcome of urgent surgical procedures. Larger studies are needed to better define the factors capable of predicting the outcome of elective surgical procedures in patients with cirrhosis.