What are common risk factors for angiodyplasia?
Sporadic angiodysplasias most commonly occur as (acquired) lesions in older adults. They are believed to arise as degenerative lesions of aging caused by chronic, intermittent, low-grade obstruction of veins and capillaries. They most commonly occur in the cecum or proximal right colon. This predilection is explained by the greater cecal mural tension owing to its larger luminal diameter, according to Laplace’s law. Exposure to greater mural tension tends to stretch the vessel wall and promote angiodysplasia.
Angiodysplasias are sometimes associated with the following syndromes or diseases:
• Hereditary hemorrhagic telangiectasia (HHT): HHT is a genetic vascular disorder caused by mutations of the endoglin (ENG) gene (type 1 HHT), or the ACVRLI gene (type II HHT). These mutations impair blood vessel endothelial growth and repair, which result in tortuous blood spaces lined by a single layer of endothelial cells. These mutations lead to widening of small vessels that eventually create angiodysplasia. Because these patients have a diathesis for angiodysplasia, they can develop extensive angiodysplasia in several organs, most commonly the nasal mucosa, GI mucosa, or oropharynx and lips. Nasal angiodysplasia may present as recurrent epistaxis (nosebleeds) that are difficult to treat because of the extensiveness of these lesions. Oropharyngeal angiodysplasia may be identified on physical examination. GI angiodysplasias tend to bleed significantly and repeatedly because of their thin and fragile vascular wall that lacks a muscular layer. Patients often present with the clinical triad of telangiectasia, recurrent epistaxis, and a compatible family history. Patients with HHT are differentiated from sporadic angiodysplasias by clinical presentation at a much younger age, multiplicity of GI lesions, positive family history, and chronic epistaxis.
• Chronic renal failure: Patients with chronic renal failure have a much higher frequency of bleeding from GI angiodysplasia than the general population.
• Collagen vascular disease: A number of case reports have associated GI angiodysplasia with scleroderma or related disorders such as calcinosis cutis, Raynaud’s phenomenon, esophageal dysfunction, sclerodactyly, and telangiectasia (CREST) syndrome.
• Aortic stenosis: Although somewhat controversial, numerous studies have associated aortic stenosis with chronic GI bleeding from angiodysplasia. The bleeding may not reflect an increased risk of developing angiodysplasia in patients with aortic stenosis, but an increased risk of bleeding from preexisting angiodysplasia caused by destruction of multimers of von Willebrand factor from high shear forces across a stenotic aortic valve.