Protein-losing enteropathy, deep venous thrombosis and pulmonary embolism in a patient with generalized inflammatory polyposis in remission stage of ulcerative colitis

Kawaguchi, Yoshindo; Mine, Tetsuya; Kawana, Ichiro; Umemura, Satoshi

doi:10.1007/s12328-008-0060-x

Cited by 5 publications

(2 citation statements)

References 13 publications

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“…In particular, many patients with IBD have a clinically significant protein-losing enteropathy due to increased lymphatic and mucosal permeability [43–45]. As in nephrotic syndrome, hypercoagulability in protein-losing enteropathy is probably driven by the loss of antithrombin III and, to a lesser extent, protein C and protein S [46–48]. This mechanism is similar to that which occurs in patients with protein-losing enteropathy secondary to Fontan-type cardiac procedures [49, 50].…”

Section: Discussionmentioning

confidence: 99%

Ménétrier’s disease presenting as recurrent unprovoked venous thrombosis: a case report

Greenblatt

Nguyen

2019

J Med Case Reports

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BackgroundAcquired thrombophilia is a potential sequela of malignancy, chronic inflammation, and conditions characterized by severe protein deficiency (for example, nephrotic syndrome, protein-losing enteropathy). As such, venous thrombosis is often a feature, and occasionally a presenting sign, of systemic disease. Ménétrier’s disease is a rare hyperplastic gastropathy that may lead to gastrointestinal protein loss and hypoalbuminemia. To date, reports of venous thrombosis associated with Ménétrier’s disease are exceedingly scarce.Case presentationWe report the case of a 40-year-old white man who presented with unprovoked deep venous thrombosis, pulmonary embolism, and renal vein thrombosis. Upon receiving therapeutic anticoagulation, he developed severe gastrointestinal bleeding, and endoscopic evaluation led to a diagnosis of Ménétrier’s disease. A laboratory workup revealed deficiency of protein C, protein S, and antithrombin III, as well as markedly elevated levels of factor VIII. He was determined to have an acquired thrombophilia as a direct result of Ménétrier’s disease.ConclusionsThis case describes an acquired thrombophilic state in a patient with Ménétrier’s disease and profound hypoalbuminemia. Although this association is rarely described, we discuss the probable mechanisms leading to our patient’s thrombosis. Specifically, we posit that his gastrointestinal protein loss led to a deficiency of several anticoagulant proteins and a compensatory elevation in factor VIII, as occurs in nephrotic syndrome and inflammatory bowel disease. Of note, this patient’s recurrent venous thrombosis was the initial clinical sign of his gastrointestinal pathology.

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Section: Discussionmentioning

confidence: 99%

Ménétrier’s disease presenting as recurrent unprovoked venous thrombosis: a case report

Greenblatt

Nguyen

2019

J Med Case Reports

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“…Albumin can interact with fibrinogen resulting in impaired fibrinogen activity [13]. Protein-losing enteropathy can increase the risk of thrombosis by perpetuating the loss of anticlotting factors, namely antithrombin III, protein C, and protein S [14]. The presence of GIP in IBD patients leads to an increase in the colonic mucosal surface area, cell turnover, and permeability.…”

Section: Discussionmentioning

confidence: 99%

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

Amini

Vaezi

Talebian

et al. 2019

Case Rep Gastroenterol

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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.

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Nutritional screening and assessment in inflammatory bowel disease

Singh

Wall

Levine

et al. 2022

Indian J Gastroenterol

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Protein-losing enteropathy, deep venous thrombosis and pulmonary embolism in a patient with generalized inflammatory polyposis in remission stage of ulcerative colitis

Cited by 5 publications

References 13 publications

Ménétrier’s disease presenting as recurrent unprovoked venous thrombosis: a case report

Ménétrier’s disease presenting as recurrent unprovoked venous thrombosis: a case report

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

Nutritional screening and assessment in inflammatory bowel disease

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