Abstract

62 years old male patient underwent routine screening colonoscopy. He was found to have diffuse erythema, friability and colitis along with multiple large polyps. Biopsies suggested vascular ectasia without dysplasia. He had no symptoms and no history of gastrointestinal (GI) bleeding. He denied family or personal history of liver disease. Two months later, he underwent an EGD and another colonoscopy. Large polyps were found throughout the colon (see figures). Adenomatous tissue was reported on biopsies. He also had new esophageal and rectal varices as well as ectatic vessels in the stomach. Liver CT showed marked intraabdominal varices in the jejunum and gastric wall. Findings were consistent with portal hypertension. Full workup including viral hepatitis, autoimmune liver disease, iron overload, HIV, giardia, cryptosporidium, schistosomiasis and parasites were all negative. Endoscopies were performed again 5 months later. There was an extensive, diffuse, pan-colonic polypoid hypervascular lesions. Findings appeared nearly identical to initial exam. There were multiple patches of vascular ectasia lesions in the duodenum. Biopsies were all negative for dysplasia. Liver biopsy was pursued and showed minimal to mild portal inflammation with mild macrovesicular steatosis.Figure 1Figure 2Figure 3Discussion: Portal hypertension is characterized by vascular ectatic changes in stomach and colon termed portal gastropathy and colopathy, respectively. Vascular ectasias are the most common vascular lesions in the GI tract and probably the most frequent cause of recurrent or chronic lower GI bleeding in the elderly population. Endoscopically, they appear as flat or slightly elevated bright red lesions. There are only few cases of polypoid vascular ectasias reported. These were manly solitary and usually located in the transverse, descending and sigmoid colon. Portal hypertensive colopathy (PHC) is prevalent in 25-70% of patient with cirrhosis. The incidence of vascular ectasia detected by colonoscopy has been reported to range from 1% to 6%. There is no established standard treatment of PHC. There might be a role for β-blockers for primary or secondary prophylaxis for lower GI bleeding caused by PHC. In summary, polypoid vascular ectasias and portal hypertensive gastropathy are important clinically because they may lead to chronic and/or acute GI bleeding. Careful investigation is essential to accurately delineate the proper diagnostic needs and to start specific treatment.

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