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At least 19 recordsLinked to original sources
PubMed1992

Spatial clustering of simultaneous nonhereditary gastrointestinal angiodysplasia. Small but significant correlation between nonhereditary colonic and upper gastrointestinal angiodysplasia.

Simultaneous nonhereditary colonic and upper gastrointestinal angiodysplasia were spatially clustered in an endoscopic study of 46 consecutive patients. For example, clustering of colonic angiodysplasia was demonstrated using a nonparametric test of clustering (Kruskal-Wallis statistic with 29 degrees of freedom = 76.2, P less than 0.0005), and a parametric test of clustering (F test statistic with 29 and 101 degrees of freedom = 6.91, P less than 0.0005). In accord with spatial clustering, only two of 13 patients (15%) with colonic angiodysplasia who underwent panendoscopy had upper gastrointestinal angiodysplasia. Two of nine patients (22%) with upper gastrointestinal angiodysplasia who underwent colonoscopy had colonic angiodysplasia. These findings suggest that local factors may be important in the pathogenesis of simultaneous nonhereditary angiodysplasia. Possible local factors include intermittent venous obstruction, increased intraluminal pressure, intermittent abnormal arterial flow, and local vascular degeneration. Due to the approximately 20% correlation between upper and lower nonhereditary gastrointestinal angiodysplasia, the upper and lower tract should be examined by endoscopy prior to elective local resection for bleeding from gastrointestinal angiodysplasia.

Aged↗
PubMed1992

Changing epidemiology of gastrointestinal angiodysplasia with increasing recognition of clinically milder cases: angiodysplasia tend to produce mild chronic gastrointestinal bleeding in a study of 47 consecutive patients admitted from 1980-1989.

It is important to recognize patients with gastrointestinal bleeding who are at high risk of having angiodysplasia, because these patients should be evaluated by endoscopy rather than barium studies. Sixty-two clinical and epidemiologic parameters were compared between 47 consecutive patients bleeding from angiodysplasia and 47 consecutive controls bleeding from other lesions admitted to two university teaching hospitals from 1980 through 1989. This study demonstrated statistically significant differences between these two groups. The patients with angiodysplasia generally presented with symptoms and clinical findings compatible with hemodynamically well-compensated, chronic bleeding: they were more likely than other gastrointestinal bleeders to experience weakness or fatigue, less likely to experience dizziness or syncope, and less likely to be orthostatic or hypotensive. They had more prior admissions for gastrointestinal bleeding, particularly for gastrointestinal bleeding of undetermined etiology. They were more likely than other gastrointestinal bleeders to be smokers. Patients with angiodysplasia had a milder hospital course: they had fewer transfusions of packed erythrocytes, shorter hospitalizations, and a lower mortality. The in-hospital mortality of patients bleeding from angiodysplasia was 2.1%. Despite the futility of diagnosing angiodysplasia by barium studies, patients ultimately diagnosed as having angiodysplasia were more often initially evaluated by barium studies than the other gastrointestinal bleeders. The currently identified risk factors for bleeding from angiodysplasia should help to select which gastrointestinal bleeders should be evaluated initially by endoscopy.

Adult↗
PubMed1979

Gastrointestinal angiodysplasia associated with aortic valve disease: part of a spectrum of angiodysplasia of the gut.

Twelve patients with angiodysplasia of the gastrointestinal tract were seen at The Mary Imogene Bassett Hospital are presented. Six share the features of gastric or duodenal angiodysplasia, advanced age, and aortic valve disease. Of these 6 patients, 4 who bled repeatedly were treated with endoscopic coagulation of areas of gastric and duodenal angiodysplasia. Six patients with other types of gastrointestinal angiodysplasia are presented for comparison. Two had gastric angiodysplasia and no aortic valve disease, 2 had hereditary hemorrhagic telangiectasia, 1 had received irradiation, and 1 could not be classified. We suggest that angiodysplasia of the gastrointestinal tract can be regarded as a spectrum with a clearly inherited etiology on one extreme and an acquired etiology on the other. A subset of these patients may be associated with aortic valve disease. Angiodysplasia of the upper gastrointestinal tract may account for a significant fraction of previously unexplained bleeding. It is hoped that this paper will aid in their more frequent recognition.

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PubMed1995

Diffuse microscopic angiodysplasia--a previously unreported variant of angiodysplasia. Report of a case.

PURPOSE: The entity of diffuse microscopic angiodysplasia is described, and a patient with severe gastrointestinal hemorrhage because of this submucosal source of bleeding is reported. METHOD: Case records of a patient with severe gastrointestinal hemorrhage were reviewed, and histologic findings were compared with colonoscopic and operative findings. The patient received 51 units of packed red blood cells over 3.5 months and remained undiagnosed, despite an exhaustive evaluation, until autopsy. RESULTS: Ectatic veins, venules, and capillaries were present within the submucosa in virtually every section of the small and large intestine examined (79 of 86 sections). Histologic evidence of bleeding from these submucosal vessels was identified in three sites (colon, jejunum, and ileum). The absence of endoscopically visible lesions was explained by findings that vessels did not traverse the muscularis mucosa and that mucosal depth was normal. This case of diffuse microscopic angiodysplasia, therefore, represents a unique variant, because the vascular findings were so diffuse and the mucosa remained histologically and endoscopically uninvolved, despite severe bleeding. CONCLUSION: Gastrointestinal bleeding from angiodysplasia is generally assumed to arise from endoscopically recognizable vascular ectasia within the mucosa. Thus, this case helps provide an explanation for some cases in which occult or massive bleeding is assumed to be secondary to angiodysplasia, even when endoscopic verification is not possible. Recognition of this disease process may require segmental resection or deep biopsy of endoscopically normal intestine.

Aged↗
PubMed2006

Macroscopic appearance of intestinal angiodysplasias under antiangiogenic treatment with thalidomide.

BACKGROUND AND STUDY AIMS: Angiodysplasias are the main cause of bleeding from the small intestine. Single lesions may be treated by endoscopic coagulation or surgical resection. However, multiple disseminated angiodysplasias are frequently present, making local therapy an unfavorable choice or impossible. Currently there is no established medical treatment available for these patients. Thalidomide is a potent inhibitor of angiogenesis in experimental models. As angiodysplasias are a result of unregulated vessel growth, antiangiogenic treatment may inhibit growth of angiodysplasias. PATIENTS AND METHODS: We studied the effect of thalidomide on the macroscopic appearance of angiodysplasias in three patients with bleeding due to multiple angiodysplasias of the small intestine. During the previous 12 months patients had experienced 3 - 7 bleeding episodes and had received a mean of 16.7 blood units. RESULTS: After start of treatment with thalidomide at a dose of 100 mg daily, no further bleeding episodes occurred. Although thalidomide was stopped after 3 months, bleeding did not recur and hemoglobin reached and maintained normal levels without further transfusions for the whole observation period (mean follow-up 34 months). Repeat wireless capsule endoscopy after 3 months' thalidomide demonstrated substantial reductions in the number, size, and color intensity of angiodysplasias. CONCLUSION: Thalidomide seems to inhibit growth of intestinal angiodysplasias and may be useful for treatment of patients with bleeding related to angiodysplasias. Wireless capsule endoscopy allows monitoring of the macroscopic effects of antiangiogenic therapy.

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PubMed2005

Increased plasma fibrinolytic activity in bleeding gastrointestinal angiodysplasia.

OBJECTIVE: Gastrointestinal angiodysplasia is a major cause of recurrent bleeding. Haemostatic abnormalities have been implicated in the haemorrhage from these common vascular lesions but their precise contribution remains to be established. Our aim was to investigate whether bleeding angiodysplasia is associated with any specific coagulation disorder. METHODS: Clinical features and blood samples were prospectively obtained from 21 patients with bleeding gastrointestinal angiodysplasia 3 months after the last episode of haemorrhage. Plasma levels of von Willebrand factor, D-dimer, plasminogen activator inhibitor type 1 (PAI-1), tissue-plasminogen activator activity, tissue factor pathway inhibitor and activated factor VII (FVIIa-rTF) were measured. A group of 14 patients with bleeding duodenal ulcer were similarly studied as controls. RESULTS: Mean plasma von Willebrand factor levels were higher in angiodysplasia patients (208+/-12%) than in controls (143+/-11%) (P<0.05). D-dimer levels (661+/-80 ng/ml) and tissue-plasminogen activator activity levels (2.04+/-0.14 IU/ml) were also higher than in controls: 395+/-99 ng/ml and 1.6+/-0.1 IU/ml, respectively (P<0.05), whereas levels of PAI-1, FVIIa-rTF and tissue factor pathway inhibitor were similar in both groups. However, PAI-1 levels (31.5+/-11 ng/ml) were lower in high-bleeding-rate angiodysplasia (more than two bleeding episodes/year) than in low-bleeding-rate angiodysplasia (< or = 2 bleeding episodes/year) (PAI-1 47+/-14 ng/ml) (P<0.05). In a multivariate regression analysis, the plasma level of PAI-1 was a predictor of haemorrhage from angiodysplasia (P<0.05). CONCLUSIONS: Increased plasma fibrinolytic activity may contribute to bleeding from angiodysplasia. Low plasma PAI-1 levels constitute a risk factor for bleeding tendency in patients with angiodysplasia.

Aged↗
PubMedDate not supplied

[Magnetic resonance imaging and ultrasound study in the diagnosis og facial angiodysplasias in children: competition or collaboration?].

This study deals with the capacities of noninvasive magnetic resonance imaging (MRI) with magnetic resonance angiography (MRA) without administration of magnetic resonance contrast substances in the diagnosis of facial soft tissue angiodysplasias in children. Indications for their use are defined. The methodology of the studies is proposed. Their diagnostic role and relationship with the other noninvasive technique of medical visualization--ultrasound study (USS) with Doppler color mapping (DCM) are assessed. As compared with USS, MRI may more accurately and objectively establish the organotopic characteristics of facial soft tissue angiodysplasias and detect lesions of the deep facial parts, maxillary bones, and paranasal sinuses in the diagnosis of these abnormalities. The use of MRI may define the belonging of angiodysplasias to the arterial or venous bed, reveal afferent and efferent vessels, including intracranial ones, and to detect intracranial angiodysplastic changes. USS with DSM was superior to MRI with MRA in defining functional (hemodynamic) parameters of angiodysplasias, which makes this method indispendable in planning treatment and in evaluating its efficiency. Comprehensive examination of patients with large and extensive angiodysplasias of facial soft tissues has indicated that facial angiodysplasias are external manifestations of a more generalized angiodysplastic process in most cases, which, in large and extensive facial angiodysplasias, makes it expedient to perform MRI with MRA of the brain and, if possible, the whole body. The high informative value of MRI with MRA in studying angiodysplasias makes them the method of choice in the diagnosis of this group of diseases.

Adolescent↗
PubMed1995

A prospective controlled evaluation of endoscopic detection of angiodysplasia and its association with aortic valve disease.

BACKGROUND: In view of controversy about the association of aortic stenosis and angiodysplasia of the gut, we performed a prospective, controlled study to evaluate the relationship between aortic valve disease and gastrointestinal angiodysplasia. METHODS: Forty patients who had endoscopy for clinical indications such as gastrointestinal bleeding, anemia, polyps, colon cancer, and dyspepsia, and who were found to have angiodysplasia of the gastrointestinal tract, underwent two-dimensional and Doppler echocardiography. Thirty-seven controls matched for age, sex, indication, and nature of endoscopic examination, but without angiodysplasia, underwent similar echocardiographic examination. RESULTS: None of the patients in either group had aortic stenosis. The prevalence of aortic sclerosis, aortic insufficiency, and low left ventricular ejection fraction was similar in patients with and without angiodysplasia. CONCLUSIONS: This study does not support the role of aortic valve disease as the cause of angiodysplasia of the gastrointestinal tract. A subgroup of patients with angiodysplasia with aortic sclerosis, with or without other valvular disease (but none with aortic stenosis), had increased prevalence of gastrointestinal bleeding when compared with controls. When aortic valve disease or decreased left ventricular ejection fraction were analyzed as independent predictors, none of them in and of itself appeared to be a factor in bleeding from these gastrointestinal lesions.

Aged↗
PubMed1999

Increased expression of angiogenic factors in human colonic angiodysplasia.

OBJECTIVE: Angiodysplasia of the colon is a distinct vascular abnormality characterized by focal accumulation of ectatic vessels in the mucosa and submucosa. To investigate whether angiogenesis contributes to the pathogenesis of human colonic angiodysplasia, we examined the expression of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), and its endothelial cell receptors flt-1 and KDR. METHODS: Immunohistochemistry was performed in sections of specimens obtained from 18 patients with colonic angiodysplasia and from eight patients with colon cancer and its adjacent, histologically normal margins of resection. We used affinity-purified rabbit polyclonal antibodies and a streptoavidin-biotin peroxidase method. RESULTS: We detected strong immunoreactivity for vascular endothelial growth factor, homogeneously distributed in the endothelial lining of blood vessels of all sizes in 16 (89%) specimens of colonic angiodysplasia and in seven (88%) patients with colon cancer. In contrast, very limited immunoreactivity was found in normal colon. Vascular staining for flt-1 was observed in eight (44%) and one (12.5%) of the colonic angiodysplasia or colon cancer specimens, respectively, but not in normal colon. Vascular immunoreactivity for basic fibroblast growth factor was observed in seven (39%) specimens from patients with colonic angiodysplasia, whereas either very limited or no immunostaining was found in sections from specimens of patients with colon cancer and its normal margins. CONCLUSIONS: In human colonic angiodysplasia, increased expression of angiogenic factors is likely to play a pathogenic role.

Adenocarcinoma↗
PubMedDate not supplied

[Bleeding gastrointestinal angiodysplasias: our experience and a review of the literature].

The aim of the present study was to draw an outline of the clinical epidemiology of bleeding gastrointestinal angiodysplasias. The study includes a report of a case and of our series of patients with bleeding gastrointestinal angiodysplasias admitted, between 1993 and 2003, to a ward of Internal Medicine where digestive endoscopy is also performed. A review of the literature is also provided. An 80-year-old cirrhotic woman with aortic stenosis, was referred to our Department because of anemia due to melena. In spite of 13 hospitalizations during which numerous diagnostic procedures including endoscopy, X-ray studies, arteriography, labeled red blood cells scanning and laparotomy with intraoperative ileoscopy, the site and nature of the bleeding lesion remained unidentified. Her red blood cell requirement progressively increased from 6 U in 1993 to 24 U in 1994 to 40 U as of September 1995. Enteroscopy disclosed duodeno-jejunal angiodysplasia. The patient subsequently received 35 additional red blood cell units during 7 new admissions. Between 1993 and 2003, 24 patients were identified. They were mainly women and their average age was 77 years. Angiodysplasias were localized in the large bowel in 92% of cases. Comorbidities included: heart disease (79%), chronic liver disease (29%) and chronic renal failure (21%). One fourth of patients were under anticoagulant drugs or had a hemostatic blood disorder. All patients received blood transfusions and endoscopic treatment was performed in approximately half of the cases. The most relevant updates are related to the pathogenic relationship between aortic stenosis, von Willebrand's disease and bleeding gastrointestinal angiodysplasias, the hemostatic alterations associated with liver cirrhosis or with chronic renal failure and the diagnosis and treatment of bleeding gastrointestinal angiodysplasias. A better understanding of the clinical epidemiology of bleeding gastrointestinal angiodysplasias may facilitate their diagnosis and contribute to an effective clinical management.

Age Factors↗
PubMed1993

Angiodysplasia of the gastrointestinal tract.

Angiodysplasia is an important vascular lesion of the gut and a source of significant morbidity from bleeding. This lesion is probably responsible for approximately 6.0% of cases of lower gastrointestinal (GI) bleeding and 1.2-8.0% of cases of hemorrhage from the upper GI tract. Small bowel angiodysplasia accounts for 30-40% of cases of GI bleeding of obscure origin and represents the single most common cause for hemorrhage in this subset of patients. Lesions in the large bowel occur most often in the right colon. Their cause is unknown but most are probably acquired and the result of a degenerative process associated with aging. The incidence of colonic angiodysplasia among strictly asymptomatic individuals has never been determined and the natural history for these lesions is incompletely understood. Angiodysplasia in the upper GI tract occurs most often in the stomach and duodenum. When affected patients have been evaluated by colonoscopy concomitant lesions have been diagnosed in one-third of instances. Angiodysplasia has been purported to occur with higher frequency in patients with renal failure, von Willebrand's disease, aortic stenosis, cirrhosis, and pulmonary disease. Not all of these associations have been subjected to critical analysis, but available evidence does not support a strong relationship in most instances. Patients with bleeding angiodysplasia are occasionally treated with hormones or, more often, by endoscopic methods. Uncontrolled case studies have reported reduction or cessation of bleeding in subjects managed with conjugated estrogens. However, prospective randomized controlled trials assessing the efficacy of hormonal therapy are limited, and results from two trials conflict. Safety profiles for the endoscopic methods are acceptable, and reported efficacies are high, although not all methods have been extensively evaluated specifically for the treatment of angiodysplasia. Perforation of the right colon is a potential problem, especially for monopolar electrocoagulation and lasers.

Aging↗
PubMed2000

Accuracy of helical computed tomographic angiography for the diagnosis of colonic angiodysplasia.

BACKGROUND & AIMS: The diagnosis of colonic angiodysplasia is often challenging and relies on endoscopy or catheter angiography. We investigated whether computed tomographic angiography (CTA) contributes to the diagnosis of colonic angiodysplasia. METHODS: Twenty-eight patients with suspected bleeding from colonic angiodysplasia were prospectively evaluated. Gastrointestinal bleeding was investigated by colonoscopy plus visceral angiography and by CTA. The level of agreement between CTA and the former procedures was determined. RESULTS: CTA images of diagnostic quality were obtained in 26 patients. Eighteen patients were diagnosed with colonic angiodysplasia by colonoscopy plus visceral angiography, and 14 by CTA (kappa = 0.68; P < 0.001). Sensitivity, specificity, and positive predictive values of CTA for detection of colonic angiodysplasia were 70%, 100%, and 100%, respectively. CTA signs including accumulation of vessels in the colonic wall, early filling vein, and supplying enlarged artery were present in 55%, 50%, and 22% of cases, respectively. None of these signs were present in the 8 patients with obscure gastrointestinal bleeding and negative diagnostic investigation of the digestive tract. CONCLUSIONS: CTA is a sensitive, specific, well-tolerated, and minimally invasive tool for the diagnosis of colonic angiodysplasia.

Aged↗
PubMed1993

Prevalence of aortic valve stenosis in patients affected by gastrointestinal angiodysplasia.

OBJECTIVES: Angiodysplasia is considered to be an important cause of gastrointestinal bleeding in the elderly. An association between idiopathic gastrointestinal bleeding and aortic valve stenosis has been reported in up to 25% of the patients. The association between angiodysplasia mainly of the right colon and aortic valve stenosis has been suggested, but is not proven. The aim of this study was to examine the prevalence of aortic valve stenosis in patients with gastrointestinal angiodysplasia. METHODS: We studied retrospectively 83 patients submitted to gastrointestinal endoscopy and found affected by angiodysplasia. Of them 24 (16M and 8F) had died from causes unrelated to cardiovascular diseases. The 59 patients still alive (27M and 32F) underwent a complete clinical, electrocardiographic and echocardiographic (M-mode, B-mode, pulsed and continuous-wave Doppler) evaluation. RESULTS: Fifteen patients (25%) had a normal examination, both clinical and echocardiographic. Eleven (19%) had minor cardiac abnormalities but had no murmurs. Although no murmurs were present in 15 patients (25%), some echocardiographic abnormalities such as aortic leaflet sclerosis, mitral annular calcification, their association, or trivial mitral regurgitation detectable only at PW-Doppler were found. In 18 patients (31%) both systolic murmurs and valvular abnormalities, as revealed by echocardiographic examination, were detected: 10 had a regurgitant and 8 an ejectional murmur; of these only 1 (1.6%) had a true severe calcified aortic valve stenosis at echo-Doppler examination. CONCLUSIONS: The low prevalence of aortic valve stenosis in patients with gastrointestinal angiodysplasia (1/59 or 1.6%) in this retrospective study argues against the association of gastrointestinal angiodysplasia and aortic valve stenosis.

Aged↗
PubMed1984

[Colorectal angiodysplasias (vascular ectasias). Endoscopic morphology, localization and incidence].

In a prospective study, angiodysplasias were looked for in 824 patients during total coloscopy. Such angiodysplasias were discovered in 30 patients (3.6%). The endoscopic morphology varied, most of the angiodysplasias being smaller than 5 mm (23 patients), with a homogeneous structure in 19, spider-like extensions in only 11 patients. In 13 patients there were multiple angiodysplasias. Two or more segments of the colon were affected in 7 patients. Site of lesions was as follows: in 19 patients in the caecum and/or ascending colon; descending colon, sigmoid and/or rectum in 16; transverse colon in 3 patients. Histological confirmation was obtained in 9 of 20 patients who had a biopsy. Right-sided colectomy for bleeding angiodysplasias (resulting in anaemia) is indicated only if endoscopic coagulation has failed and other colorectal sources of bleeding (neoplasm, diverticulum or polyp) and especially angiodysplasias in the left colon or rectum have been excluded by endoscopy or angiography.

Adolescent↗
PubMed2006

A novel method of treating colonic angiodysplasia.

BACKGROUND: Colonic angiodysplasia is responsible for up to a third of lower-GI bleeding cases. Argon plasma coagulation (APC) is a recognized treatment modality, but active bleeding decreases the ablative efficacy of APC by dissipation of the energy. APC has been associated with colonic perforation. OBJECTIVES: We propose a novel and safe method for the treatment of colonic angiodysplasia by a submucosal injection of a saline epinephrine solution followed by the application of APC. PATIENTS: Three patients with a total of 10 colonic angiodysplasias were treated with this injection-APC method. INTERVENTIONS: Saline adrenaline solution (1:200,000) 2 to 3 mL was injected beneath the angiodysplasia before application of APC. APC 50 W and gas flow 2 L were applied onto the vascular lesion until the sufficient thermal effect was observed. RESULTS: There were no procedure-related complications. CONCLUSIONS: This new injection-APC method was safe for the treatment of colonic angiodysplasia. This may be useful in treating right-sided colonic lesions where the risks of perforation are greater than for the rest of the colon.

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