scholarly journals Does the Presence of Giant Pseudopolyps in a Patient with Newly Diagnosed Inflammatory Bowel Disease Increase the Risk of Major Thrombotic Events?

2019 ◽  
Vol 13 (3) ◽  
pp. 468-474
Author(s):  
Afshin Amini ◽  
Zahra Vaezi ◽  
Amirsina Talebian ◽  
Elliott Koury ◽  
Elie Chahla

Giant inflammatory polyp and thromboembolism are uncommon complications in inflammatory bowel disease (IBD) patients. Colon mucosal inflammation is possibly the main mechanism of pathogenesis for these two complications. IBD has long been associated with hypercoagulability and thromboembolism. In fact, thromboembolism has been noted in 0.7% to 7.7% of IBD patients, with the deep veins of the legs and the pulmonary veins accounting for 90% of the cases. The proposed mechanism of this hypercoagulability involves the promotion of hemostasis that results from the inflammatory process underlying the IBD, as well as the loss of proteins, including antithrombotic factors, resulting from the inflamed bowel and increased permeability of the colonic mucosa. This process may be exacerbated by the presence of giant inflammatory polyps, which are defined as polyps in the setting of IBD with dimensions greater than 1.5 cm. The presence of these polyps leads to an increase in inflamed colonic surface area, which can accelerate the rate of protein loss, leading to an increased incidence of thrombosis. Here, we report the case of a 21-year-old female with inferior vena cava and left renal vein thromboses secondary to a newly diagnosed IBD and the presence of severe giant inflammatory polyposis. These thromboses were detected incidentally in this patient after 1 week of hospitalization. She had presented with hypoalbuminemia and elevated inflammatory markers, which raised the suspicion for possible giant inflammatory polyposis as a potential risk for her major thromboembolic events. More studies are required to explore this plausible correlation further.

2013 ◽  
Vol 1 (4) ◽  
pp. 333-343 ◽  
Author(s):  
Michele Herzer Maddux ◽  
Julie A. Bass ◽  
Christy Geraghty-Sirridge ◽  
Ellen Carpenter ◽  
Kathy Christenson

Author(s):  
Juan Hernandez ◽  
Elodie Rouillé ◽  
Florian Chocteau ◽  
Marie Allard ◽  
Karine Haurogné ◽  
...  

Abstract Background The incidence of inflammatory bowel disease (IBD) is increasing worldwide, emphasizing the need of relevant models, as dogs spontaneously affected by IBD may be, for better knowledge of the disease’s physiopathology. Methods We studied 22 client-owned dogs suffering from IBD without protein loss and 14 control dogs. Biopsies were obtained from the duodenum, ileum, and colon. Inflammatory grade was assessed by histopathology, immunohistochemistry, and chemokine analysis. The expression of Toll-like receptors (TLR) in mucosa was immunohistochemically evaluated. Antibody levels against bacterial ligands (lipopolysaccharide [LPS] and flagellin) were measured in sera using enzyme-linked immunoassay. Results Dogs with IBD showed low to severe clinical disease. Histopathologically, the gut of dogs with IBD did not exhibit significant alterations compared with controls except in the colon. The number of CD3+ T lymphocytes was decreased in the ileum and colon of dogs with IBD compared with controls, whereas the numbers of Foxp3+, CD20+, and CD204+ cells were similar in the 2 groups. Three chemokines, but no cytokines, were detected at the protein level in the mucosa, and the disease poorly affected their tissue concentrations. Dogs with IBD exhibited higher serum reactivity against LPS and flagellin than controls but similar immunoreactivity against the receptors TLR4 and TLR5. In addition, TLR2 and TLR9 showed similar expression patterns in both groups of dogs. Conclusions Our data described dysregulated immune responses in dogs affected by IBD without protein loss. Despite fairly homogeneous dog cohorts, we were still faced with interindividual variability, and new studies with larger cohorts are needed to validate the dog as a model.


2021 ◽  
Vol 8 (1) ◽  
pp. 01-06
Author(s):  
Marilena Stoian

We present a case of a 38-year -old man was admitted to the hospital with biliary obstruction and Clostridium Difficile infection. He presented with moderate increases in the aminotransferase and bilirubin levels suggesting the diagnosis of an autoimmune hepatobiliary disease; intestinal protein loss needs to evaluate an associated inflammatory bowel disease. The clinical diagnosis of autoimmune hepatobiliary disease associated with inflammatory bowel disease is based on the patients symptoms and the presence of a protein-losing enteropathy which are more suggestive of Crohn disease, while moderate increases in the aminotransferase levels in proportion to the increase in the bilirubin level suggesting the diagnosis of primary sclerosing cholangitis. The pathological and positive diagnosis needs an endoscopic retrograde cholangiopancreatography and a biopsy of gastric and duodenum mucosae who showed severe inflammation findings that are diagnostic of Crohn disease.


2018 ◽  
Vol 2018 ◽  
pp. 1-4 ◽  
Author(s):  
Antoine Abou Rached ◽  
Jowana Saba ◽  
Leila El Masri ◽  
Mary Nakhoul ◽  
Carla Razzouk

We report two cases of giant inflammatory polyposis (GIP) with totally different presentation and evolution. The first patient had two giant pseudopolyps after one year of the diagnosis of UC. The second patient had one obstructive giant pseudopolyp secondary to CD at the level of the transverse colon, being totally asymptomatic years before the presentation. GIP is a rare complication of inflammatory bowel disease (IBD). It consists of numerous filiform polyps that look like a “mass of worms” or a “fungating” mass. Surgical resection is inevitable when GIP presents with obstructive symptoms.


2001 ◽  
Vol 121 (2) ◽  
pp. 504-505 ◽  
Author(s):  
Asghar Qasim ◽  
John Seery ◽  
C.A.O. Morain

2018 ◽  
Vol 154 (6) ◽  
pp. S-1028
Author(s):  
Ritika Rampal ◽  
Mohamad Nahidul Wari ◽  
Amit K. Singh ◽  
Ujjwal K. Das ◽  
Sawan Bopanna ◽  
...  

2021 ◽  
Vol 46 ◽  
pp. S757-S758
Author(s):  
D. Kofinova ◽  
R. Shentova ◽  
P. Hadzhiyski ◽  
H. Naydenov ◽  
P. Yaneva ◽  
...  

2018 ◽  
Vol 12 (supplement_1) ◽  
pp. S518-S518
Author(s):  
H S Lee ◽  
S J Yeo ◽  
E S Kim ◽  
B I Jang ◽  
Y J Lee ◽  
...  

2019 ◽  
Vol 26 (8) ◽  
pp. 1283-1290 ◽  
Author(s):  
Victoria Grossi ◽  
Jeffrey S Hyams ◽  
Nicole C Glidden ◽  
Brittany E Knight ◽  
Erin E Young

Abstract Background There is often dissociation between inflammatory activity and abdominal pain in children with inflammatory bowel disease (IBD), suggesting other factors may play a role in the pain experience. Methods Patients (8 to 17 years) newly diagnosed with IBD were enrolled in the ALLAY Study: Assessing Risk Factors for Abdominal Pain in Children with Inflammatory Bowel Disease (NCT02984059). At diagnostic colonoscopy, 3 rectal biopsies were collected, and gene expression analysis was performed using Qiagen RT2 Profiler Neuropathic and Inflammatory Pain PCR Array. Relative fold difference in gene expression for 84 pain-associated genes was calculated using the 2-ΔΔ Cq method compared with pain-free controls. Factors affecting pain burden (Pain Burden Interview; PBI) were analyzed, including age, sex, rectal inflammation, and gene expression. Data were analyzed using multiple stepwise linear regression and 2-tailed t tests (P ≤ 0.05). Results Thirty-nine newly diagnosed IBD patients were included (65% male, mean age 12.75 years [SD 2.63], 23 Crohn’s disease, 16 ulcerative colitis), along with 3 controls. Mean PBI score was 7.73 (SD 6.4, range 0 to 23) for all patients. Age and sex were not predictive of pain burden, but disease activity score was (P = 0.03). Expression of TRPV3, OPRM1, P2X3, SCN9A, PTGS2, and MAPK14 were associated with PBI score. Subsequent 2-tailed t tests comparing patients with no pain (PBI score ≦ 2, N = 11) to those with pain (PBI > 2, N = 28) confirmed differential expression of TRPV3, PTGS2, and MAPK14 was in patients with pain (all P < 0.05). Conclusion Pain burden in newly diagnosed IBD patients may be linked to TRPV3, PTGS2, and MAPK14 expression, suggesting potential therapeutic targets for managing pain in IBD.


2018 ◽  
Vol 154 (6) ◽  
pp. S-132-S-133
Author(s):  
Jason M. Shapiro ◽  
José C. Clemente ◽  
Noah Palm ◽  
Marcel de Zoete ◽  
Yaro Laenen ◽  
...  

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