In-hospital outcomes of splanchnic vein thrombosis including Budd Chiari syndrome associated with GI malignancies.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e16503-e16503
Author(s):  
Shivani Handa ◽  
Kamesh Gupta ◽  
Ahmad Khan ◽  
Kathan Mehta ◽  
Anup Kasi

e16503 Background: Patients with gastrointestinal (GI) malignancies are at increased risk of developing splanchnic vein thrombosis (SVT). However, there is a dearth of information about the epidemiology of splanchnic vein thrombosis associated with specific GI malignancies. We sought to compare the differences in hospitalizations and mortality related to SVT among various GI malignancies. Methods: We included the top three discharge diagnoses to identify cases of splanchnic vein thrombosis (portal/mesenteric/hepatic and splenic vein thrombosis) along with a secondary diagnosis of a GI malignancy, namely esophagus, gastric, hepatic, colorectal, pancreatic and cholangiocarcinoma within the 2010-2014 Nationwide Inpatient Sample (NIS). Outcomes including mortality, hospitalization charges and length of stay were compared for different types of GI malignancies for SVT hospitalizations using the chi-square test. Complications related to SVT were also identified. Data was analyzed using STATA 15. Results: There were 320,804 total weighted admissions for SVT, of which 33,556 or 11.6% occurred in patients with GI malignancies. Hepatic cancer was the most common GI malignancy associated with SVT, responsible for 5.1% of all cases, followed by pancreatic cancer (2.76% cases). Hepatic vein thrombosis was the commonest type of SVT occurring in patients with GI malignancy. Hospitalizations for SVT in GI malignancies increased from 5743 in 2010 to 8415 in 2014, representing an increase of 46% over 5 years. On univariate analysis, patients with esophageal cancer and SVT had higher rates of cardiac arrest (3.5% vs 0.7% average for other cancers, p = 0.03), but there were no significant differences in rates of other complications studied including intracranial hemorrhage, requirement for blood transfusion, mechanical ventilation or variceal bleeding. Inpatient mortality rate for admission with SVT was the highest for esophageal cancer (21.1%), followed by gastric cancer (17%) against an average of 9.3% for all GI malignancies (p < 0.05).The median cost of an admission for a patient with SVT were highest for esophageal cancer $102,452, followed by colorectal cancer ($97,491) and the least for hepatic cancer ($67,007). Conclusions: We found that hospitalizations for splanchnic vein thrombosis in patients with GI related malignancies has been steadily increasing and represent a significant burden. Hospitalizations for SVT in esophageal, gastric and colorectal cancer patients bear poorer outcomes as compared to hepatic cancer.

2021 ◽  
Vol 104 (2) ◽  
pp. 003685042110106
Author(s):  
Walid Alam ◽  
Youssef Bouferraa ◽  
Yolla Haibe ◽  
Deborah Mukherji ◽  
Ali Shamseddine

The Coronavirus (COVID-19) pandemic had a huge impact on all sectors around the world. In particular, the healthcare system has been subject to an enormous pressure that has surpassed its ability in many instances. Additionally, the pandemic has called for a review of our daily medical practices, including our approach to colorectal cancer management where treatment puts patients at high risk of virus exposure. Given their higher median age, patients are at an increased risk for severe symptoms and complications in cases of infection, especially in the setting of immunosuppression. Therefore, a review of the routine colorectal cancer practices is needed to minimize risk of exposure. Oncologists should weigh risk of exposure versus the patient’s oncologic benefits when approaching management. In addition, treatment protocols should be modified to minimize hospital visits and admissions while maintaining the same treatment efficacy. In this review, we will focus on challenges that colorectal cancer patients face during the pandemic, while highlighting the priority in each case. We will also discuss the evidence for potential modifications to existing treatment plans that could reduce infectious exposure without compromising care. Finally, we will discuss the impact of the socio-economic difficulties faced by Lebanese patients due to a poor economy toppled by an unexpected pandemic.


2008 ◽  
Vol 23 (1) ◽  
pp. 18-23 ◽  
Author(s):  
P.V. Pereira Serafim ◽  
I.D. Cotrim Guerreiro da Silva ◽  
N. Manoukian Forones

Aims and background The enzyme cytochrome P450 plays an important role in the metabolization and detoxification of various compounds. CYP1A1 is a polymorphic enzyme and some of its alleles have been correlated with an increased risk of developing various types of cancer. The aim of this study was to investigate the incidence of the polymorphism A→G (Ile462Val, exon 7) in colorectal cancer patients and the correlation of this polymorphism with others risk factors. Patients and methods 114 Brazilian patients with colorectal cancer were matched by age and sex to 114 healthy individuals. DNA was extracted from peripheral blood and the genotypes of the polymorphisms were assessed by PCR-restriction fragment length polymorphism. Results In the case group 64 subjects were male, 53 were alcohol users and 68 were smokers. In the control group 61 were male, 67 were alcohol users and 53 smokers. There were 14 subjects with wild-type homozygous A/A, 97 with heterozygous A/G, and 3 with homozygous mutated G/G in the cancer group versus 81 subjects with wild-type homozygous A/A and 33 with heterozygous A/G in the control group. The presence of the G allele (OR 5.14, 95%CI 3.15–10.80) was associated with an increased risk of colorectal cancer (p=0.001). The prevalence of smokers was higher in the cancer group (p=0.047, OR 1.71, 95%CI 1.03–3.11). Conclusion These results suggest a positive association between the A→G polymorphism and the risk of colorectal cancer. In addition, smoking was also a colorectal cancer risk. We did not find any correlation between this polymorphism and sex, grade of differentiation, stage, or evolution of the disease.


2017 ◽  
Vol 53 (3) ◽  
pp. 185-192 ◽  
Author(s):  
Ana M. L. Jacinto ◽  
Alison E. Ridyard ◽  
Itamar Aroch ◽  
Penny J. Watson ◽  
Linda R. Morrison ◽  
...  

ABSTRACT Dogs with protein-losing enteropathy (PLE) are suggested to be at increased risk of developing thromboembolic events. However, with some exceptions, there are very few reports of thromboembolism in such dogs. This multicentre retrospective observational study describes a case series of thromboembolism (TE) in eight dogs with PLE secondary to non-neoplastic, chronic small intestinal disease. Seven dogs had poorly controlled PLE when the thromboembolic event occurred. Pulmonary thromboembolism (PTE) occurred in six dogs, while one dog developed splenic vein thrombosis and another had concurrent splenic vein and aortic TE. Six dogs died, all with PTE. Antithrombin activity was decreased in one of two dogs in which it was measured. Serum cobalamin and folate concentrations were measured in three dogs and cobalamin was subnormal in all three. Serum magnesium, measured in two dogs, was low in both. Dogs with uncontrolled chronic small intestinal disease and PLE are at risk for developing serious life-threatening TE, mostly PTE.


2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 390-390
Author(s):  
Pilar Garcia Alfonso ◽  
Andres J. Muñoz ◽  
Montse Blanco Codeisido ◽  
Daniel Lopez-Trabada Ataz ◽  
Lucia Cortejoso-Fernandez ◽  
...  

390 Background: 5-fluorouracil and capecitabine are the gold standards in colorectal cancer (CRC) treatment and are often combined with oxaliplatin (FOLFOX and XELOX chemotherapy, respectively). Our purpose was to analyze associations between severe adverse reactions to these regimes and polymorphisms in genes related to these drugs Methods: Retrospective study with 47 adult CRC patients treated with adjuvant FOLFOX/XELOX. 20 polymorphisms in 14 genes were selected: 6 genes [XRCC1 (rs25487), ERCC2 (rs131181), ERCC1 (rs11615), GSTP1 (rs1695), EGFR (rs4559542) and GSTT1 (copy number variation)] related to the pharmacokinetics and dynamics of oxaliplatin and 8 related to fluoropyrimidines [MTHFR (rs1801131 and rs1801133), DPYD (rs2297595 and rs3918290), TYMS (rs34743033 and rs34489327), ABCB1 (rs1128503, rs2032582 and rs1045642), ABCC4 (rs4148551 and rs3742106), ABCC5 (rs3805114), CYP2A6 (rs3742106 ) and CDA (rs2072671)]. Linear by linear association chi-square test (SPSS v.18.0.) was used to study associations. A multivariate analysis including sex and performance status was also conducted. p< 0.05 was considered significant. Results: Mean age was 62 (SD: 12) years and 78.7% male. Univariate analysis: statistically significant associations were obtained between rs11615 (ERCC1), neutropenia and hand-foot syndrome; rs3742106 (CYP2A6) and neutropenia; rs34743033 and rs34489327 (TYMS) and nausea/vomiting; and CNV of GSTT1 and neutropenia. Multivariate analysis: statistically significant associations were obtained between rs3742106 (CYP2A6) and neutropenia (GT vs. TT: OR, 0.042, 95% CI, 0004-0499, p = 0.012); rs2297595 (DPYD) and nausea/vomiting (GA vs AA: OR, 0.051, 95% CI, 0003-0772, p = 0.032); and rs11615 (ERCC1) and neutropenia (CC vs CT / TT: OR, 0.099, 95% CI, 0016-0615, p = 0.013) Conclusions: These results could help oncologists reduce adverse reactions associated to FOLFOX and XELOX chemotherapy by giving patients the best possible option, thus, improving their quality of life. Bigger cohorts are needed to verify the polymorphisms in ERCC1, CYP2A6, TYMS, DPYD and GSTT1 prior application in clinical practice.


2021 ◽  
Vol 108 (Supplement_9) ◽  
Author(s):  
K Thejasvin ◽  
Sara-Jane Chan ◽  
Chris Varghese ◽  
Wei Boon Lim ◽  
Gemisha Cheemungtoo ◽  
...  

Abstract Background There is paucity of data on the incidence, risk factors and role of anticoagulation for splanchnic vein thrombosis (SVT) in acute pancreatitis (AP). Methods A retrospective review of AP admissions between 2018-2021 across North East England was undertaken. Data on demographics, etiology, severity of AP and SVT was collected. In addition, a selective anticoagulation policy for portal vein thrombosis (PVT) and progressive splenic vein thrombosis was explored. Results 401 patients were included with a mean age of 57.0 and M:F ratio of 1.6:1. 152 patients developed intestinal oedematous pancreatitis and 249 developed necrotising pancreatitis based on Revised Atlanta criteria (RAC). 109 patients (27.2%) developed SVT of which 27 developed a PVT and splenic vein thrombus, 36 PVT only and 46 splenic vein thrombus only.  On univariate analysis, alcoholic aetiology, severe pancreatitis, necrotising pancreatitis with &gt;50% necrosis and elevated CRP at 2 weeks were risk factors for developing SVT. On multivariable analysis, alcohol aetiology (OR 2.6, p = 0.002), and &gt;50% pancreatic necrosis (OR 14.6,p = 0.048) increased the risk of developing SVT . 58 patients received anticoagulation for SVT, with a median duration of 90 days of anticoagulation. Recanalization rates were higher for PVT when compared to splenic vein thrombosis. 6 patients developing bleeding complications whilst on anticoagulation therapy.  Conclusions A third of patients with AP develop SVT, particularly those with severe AP secondary to alcohol and with extensive pancreatic necrosis. A selective anticoagulation policy was associated with improved recanalization rates and fewer bleeding complications.


2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e22192-e22192
Author(s):  
Weijia Fang ◽  
Milan Radovich ◽  
Anwu Zhou ◽  
Yulong Zheng ◽  
Peng Zhao ◽  
...  

e22192 Background: The frequency and poor prognosis of metastasis colorectal cancer (mCRC) emphasizes the need of better markers for both treatment and prognosis. Here we describe an approach of identifying somatic variants in exonic regions of key cancer genes. Methods: Formalin-fixed paraffin embedded (FFPE) tissues biopsied from mCRC patients were collected. DNA was extracted and sequenced on the Ion Torrrent Personal Genome Machine.For targeted amplification, we used the Ion AmpliSeq Cancer Panel which is designed to detect 739 mutations in 604 loci from 46 oncogenes and tumor suppressor genes with as little as 10ng of input DNA.Sequencing results were then analyzed using the Ampliseq Variant Caller plug-in within Ion Torrent Suite Software. Ingenuity Pathway Software was used to do pathway analysis. Cox regression was tested regarding the potential relationship between the alteration numbers and the clinical factors including response rate, disease free survival and overall survival, etc. Results: Among 10 specimens, we identified 66 genetic alterations in 24 genes after excluding the germline mutations according the dbSNP database. 41% of those alterations were also present in the COSMIC database (Catalogue of Somatic Mutations in Cancer). No clinical factor was found to be significantly associated with the alteration numbers by univariate analysis. Notably, there are 11 genes including the expected APC, BRAF, KRAS, PIK3CA and TP53 that were mutated in at least 2 samples. Pathway analysis identified “Colorectal Cancer Metastasis Signaling” as the top mutated canonical pathway. This analysis further revealed mutated genes in the classic signal pathways of Wnt, PI3K/AKT, and TGF-beta/SMAD as significantly present. Interestingly, 90% of specimens harbored at least one “druggable” alteration (range from 1 ~ 6)that has been linked to a target treatment or is currently being investigated in clinical trials. Those pairs of drug and targeted genes are vemurafenib to BRAF; cetuximab to EGFR; palifermin to FGFR2; pazopanib to FGFR3; AEE 788 to KDR and BEZ235 to PIK3CA. Conclusions: DNA deep sequencing of key cancer related genes enables identification of “druggable” mutations for individual colorectal cancer patients.


2014 ◽  
Vol 32 (3_suppl) ◽  
pp. 462-462
Author(s):  
Gerald Prager ◽  
Alexandra Schuler ◽  
Cihan Ay ◽  
Clemens Pausz ◽  
Heinz-Josef Lenz ◽  
...  

462 Background: Patients with colorectal cancer are at increased risk of venous thromboembolism (VTE). Integrin beta-3 are involved in tumor biology as well as platelet aggregation, thus, we tested as a primary endpoint whether a comprehensive panel of germline single nucleotide polymorphisms (SNPs) in the integrin beta-3 gene could predict the risk of VTE in colorectal cancer patients. Methods: The study population comprises patients recruited into the Vienna Cancer and Thrombosis Study (CATS) (Ay, C et al; JCO 2011 vol. 29 no. 15), an ongoing prospective observational cohort study initiated in October 2003 at the Medical University of Vienna. In 114 out of 139 patients diagnosed with colon cancer DNA was assessable for integrin beta-3 germline SNPs rs3809865, rs5918, rs4642 characterization. Whole blood samples were analyzed using PCR-RFLP or direct DNA-sequencing. VTE events were statistical analyzed using one-way Anova testing. Results: The patient’s demographics and tumor characteristics were balanced between groups. VTE occurred in 14 patients (12.28%). In colorectal cancer patients with an rs3809865 A/A allele profile a statistical significant (p=0.0015) increased risk of VTE events was observed as 12 (25%) of 48 patients experienced VTE. Only 2 of 52 patients (3.85%) harboring an A/T allele VTE was diagnosed. None (0%) of the T/T subgroup had any VTE. Other SNPs revealed no predictive value for VTE. In multivariable analysis including age, sex, chemotherapy, and anti-VEGF therapy rs3809865 A/A allele profile remained a statistical significant risk factor for VTE. Conclusions: This study identifies germline polymorphisms in integrin genes as independent prognostic markers for VTE in colorectal cancer. These data may help to select subgroups of patients who may benefit from an enforced prophylaxis of venous thromboembolism (VTE).


2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e18281-e18281
Author(s):  
Matthew Blake Lockwood ◽  
Krishna Prasad Joshi ◽  
James Mobley ◽  
Suneetha Sampath ◽  
Eric R Siegel ◽  
...  

e18281 Background: Peripheral sensory neuropathy (PN) is a known dose limiting toxicity of oxaliplatin, used to treat patients with colorectal cancer. Patients with rectal cancer receive radiation therapy (RT) in addition to oxaliplatin in adjuvant setting. Pelvic radiation causes plexopathy due to demyelination, ischemia due to blood-vessel injury, and nerve fibrosis. To assess if RT increases the incidence of peripheral neuropathy, we conducted an analysis of patients with colorectal cancer treated with oxaliplatin alone vs. oxaliplatin and radiation. Methods: A retrospective analysis of subjects with stages II, III, and IV rectal (R) and colon (C) cancer from 2005 to 2014 was conducted. Only subjects receiving O with or without RT were included. The incidence of PN was compared for increase in subjects receiving both O and RT compared to O alone via one-sided chi-square tests at 5% alpha, both overall and after subgrouping by stage. Results: Out of 261 subjects analyzed, 158 met the study’s criteria. There were 97 C (all received only O) and 61 R (10 received only O; 51 received O+RT). PN occurred in 37% (19/51) of subjects receiving O+RT compared to 22% (24/107) receiving only O ( P= 0.025). In Stage II-III disease, PN occurred at nearly equal rates of 36% (14/39) in subjects receiving O+RT and 33% (16/46) in subjects receiving O only ( P= 0.457). However, in Stage IV disease, PN occurred in 42% (5/12) of subjects receiving O+RT compared to 13% (8/61) of subjects receiving only O ( P= 0.009). Conclusions: In our study, the incidence of PN was higher in subjects receiving both RT and O compared to O alone. Although our study did not show higher PN in stages II and III disease, patients with rectal cancer may have residual neurotoxicity from previous radiation and the subsequent exposure to oxaliplatin may be contributing to the cumulative toxicity. [Table: see text]


2018 ◽  
Vol 36 (4_suppl) ◽  
pp. 595-595
Author(s):  
Junjie Gu ◽  
Zhao Sun ◽  
Chunmei Bai ◽  
Fei Luo

595 Background: Colorectal cancer(CRC) is the fourth most prevalent cancer and the leading cause of cancer mortality worldwide. Drug resistance remains the main obstacle to the success of cytotoxic therapies. It is reported that soluble factors released by carcinoma-associated fibroblasts(CAFs) can induce the translocation of AKT, Survivin, P38 to the nucleus of tumor cells, which might be the mechanism of microenvironment-mediated drug resistance to nonspecific conventional chemotherapeutic agents, such as platinum compounds or 5-FU. Methods: Clinicopathological data of colorectal cancer patients who underwent chemotherapy (XELOX or FOLFOX) were collected, followed up and evaluated. p-AKT and survivin expression were assessed by immunohistochemical (IHC) staining. The relationships between p-AKT and survivin expression and patients’ resistance to chemotherapy were analyzed by Chi square respectively. The expression between p-AKT and survivin expression and progression-free survival(PFS) of patients were analyzed by Kaplan-Meier. Results: 51 CRC patients were enrolled in our research. Among them, 21 patients were resistant to chemotherapy(PD), and 30 patients were sensitive to chemotherapy(PR). P-AKT and survivin were assessed by IHC in 47 patients. Among them, 17 patients were p-AKT positive, and 29 patients were survivin positive. Patients of progressive disease(resistant to chemotherapy) were significantly associated with p-AKT positive and survivin positive(p = 0.009, 0.000). Poorer progression-free survival(PFS) was observed in patients with survivin positive compared to those with survivin negative(6.323±0.9m, 13.857±2.664m, Breslow chi square = 4.885, p value = 0.027). There is no significant difference between p-AKT expression and PFS(Breslow chi square = 2.403, p value = 0.121). Conclusions: CRC patients with p-AKT positive or survivin positive were more likely to be resistant to chemotherapeutic agents. CRC patients with survivin positive had a shorter DFS.


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