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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Duplex Doppler sonography (DS) and color-flow Doppler sonography (FDS) are noninvasive diagnostic methods for the evaluation of a patient with suspected vascular disease of the abdomen. They represent a useful adjunct to realtime sonography in the identification of normal and variant visceral vascular anatomy. Aneurysms and pseudo-aneurysms of visceral arteries are readily differentiated from other cystic lesions. DS and FDS have a high sensitivity in the detection of portal vein thrombosis and stenosis. Both methods allow the observation and measurement of splanchnic hemodynamics in patients with chronic liver disease and portal hypertension. Hence, DS and FDS already play an important role in the pre- and postoperative assessment of patients undergoing liver or pancreas transplantation. The possibility that DS and FDS may enable discrimination between hypovascular and hypervascular tumors is under clinical investigation. FDS facilitates an excellent anatomic display of the abdominal vasculature and allows easy placement of the Doppler sample volume. Consequently, quantitative data acquired with DS are accomplished within short scanning times. However, the diagnostic impact of both modalities depends to a great extent on the experience of the investigator.
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PMID:[Duplex ultrasound and color-coded Doppler ultrasound of visceral blood vessels in abdominal diseases]. 160 75

A 24-year-old patient suffered from acute intestinal haemorrhage three times within 10 years. After the last bleeding coloscopy demonstrated mesenterial varices in the terminal ileum and in the colon between the caecum and the left flexure. There were no signs of portal hypertension or obstruction of the superior mesenteric vein either by sonography or by angiography. Arteriovenous malformations of the vascular ectasia type were identified as other potential causes of haemorrhage when selective digital subtraction angiography of the superior mesenteric artery was performed segmentally in the proximal jejunum. Since the bleeding stopped spontaneously, no curative therapeutic consequences resulted from the combined vascular disorder. The patient was advised to submit to treatment immediately if bleeding recurred, to enable an angiography to be performed in the acute stage.
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PMID:[Vascular anomalies as the cause of recurrent intestinal hemorrhages]. 232 64

Severe hepatic vascular disease developed in two patients 4 and 8 years after kidney transplantation, while receiving combined immunosuppressive therapy with prednisone and azathioprine. Portal hypertension and marked liver failure were observed in both cases. The diagnosis was established by histological examination of liver biopsies showing typical veno-occlusive disease of the liver associated with peliosis in both cases. Azathioprine was discontinued. Two years later one patient was asymptomatic and liver function tests were normal. The second patient died 3 years later from liver failure. Early recognition of hepatic vascular disease arising in kidney transplant recipients would be of utmost importance, as substitution of another immunosuppressive agent for azathioprine could halt the process leading to portal hypertension.
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PMID:Hepatic vascular disease after kidney transplantation: report of two cases and review of the literature. 311 79

Malformations of the extrahepatic portal vein are quite rare. A 6-cm aneurysmal malformation of the extrahepatic portal vein, thought to be congenital in origin, is described. An English language literature review yielded only six similar cases, each of which was associated with portal hypertension, primary hepatocellular disease, or both. The patient reported herein had cholelithiasis with chronic cholecystitis, but no primary liver disease or vascular disease. We believe this is the first report of such an anomaly.
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PMID:Aneurysmal malformation of the extrahepatic portal vein. 352 72

Patients with portal hypertension of varying etiology may develop pulmonary artery hypertension. In the present autopsy study, pulmonary and hepatic tissue was studied in 12 patients in whom pulmonary and portal hypertension coexisted. Plexogenic pulmonary arteriopathy was present in 10 patients, 7 of whom had coexistent thromboembolic lesions. One patient had isolated medial hypertrophy, which may be an early stage in the plexogenic category, whereas isolated thromboembolic pulmonary vascular disease was observed in one subject. Hepatic disease was consistent with alcoholic cirrhosis in seven patients, cryptogenic cirrhosis in four and extrahepatic portal hypertension without cirrhosis in one. Thrombocytopenia was present in all 10 patients whose platelet count was determined. This study suggests that pulmonary hypertension associated with portal hypertension commonly has a plexogenic appearance on histologic examination. However, thrombosis (whether embolic or in situ) may also contribute to vascular obstruction.
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PMID:Coexistent pulmonary and portal hypertension: morphologic and clinical features. 368 Jul 90

Vascular disorders of the liver except portal hypertension are rare. They can be visualised via ultrasound, as demonstrated by two cases of cavernous transformation of the portal vein, one case of Osler's disease of the liver, and one case of Budd-Chiari's syndrome. The cavernous transformation and the occlusion of the hepatic veins can be diagnosed by ultrasound, while Osler's disease cannot be differentiated with certainty from other disorders.
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PMID:[Vascular diseases of the liver: cavernous transformation of the portal vein, Osler disease and Budd-Chiari syndrome]. 647 45

Fibrous thickening of the splenic capsule is often seen in patients with hepatic cirrhosis or portal hypertension from other causes. However, most cases of capsular thickening have been considered idiopathic, with no obvious abnormality of the portal circulation. The possibility that these "idiopathic" cases also have evidence of portal hypertension was examined in a retrospective study. The splenic capsule thickness was measured in 434 consecutive autopsy specimens. Various clinical and autopsy parameters relevant to vascular disease were recorded and correlated with splenic capsular thickness. Thickened capsules were significantly more frequent in patients with advanced age, clinical history of severe congestive heart failure, cirrhosis, and hepatic portal sclerosis. It is suggested that most cases of splenic capsular thickening are caused by splenic congestion with organization of capsular and subcapsular hemorrhages.
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PMID:Fibrous thickening of the splenic capsule. A response to chronic splenic congestion. 668 17

Three autopsy cases of systemic lupus erythematosus with unique association of multiple nodular hyperplasia (MNH) of the liver, portal hypertension, and hypertensive pulmonary vascular disease are reported. None of the patients had received oral contraceptive or androgenic steroid, but they were treated with glucocorticoids for 2 to 11 years. Raynaud's phenomenon, sclerodactyly, and mild impairment of the kidney were the common clinical features. Macroscopically, MNH is characterized by many nodules scattered throughout the non-cirrhotic liver, and histologically, each nodule is made up of normal-appearing hepatocytes and not encapsulated. Portal tracts are scanty in the nodules. MNH seems to be a regenerative-hyperplastic process, but its true nature still remains unclear. Relationships between MNH and portal hypertension, MNH and pulmonary hypertension, and collagen disease and pulmonary hypertension are discussed. A brief review of the literature concerning multiple benign hepatocellular tumors similar to MNH is also presented.
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PMID:Systemic lupus erythematosus associated with multiple nodular hyperplasia of the liver. 710 12

Pulmonary arterial hypertension with severe pulmonary vascular disease is a rare association of portal hypertension in man, be it the result of cirrhosis of the liver or obstruction of the portal vein. We induced portal hypertension in 23 rats by partially ligating the portal vein or by totally occluding it in two stages. The rats were killed between one and 15 months after operation. A collateral circulation of varicose, anastomotic vessels was established, and in six animals well-marked oesophageal varices developed. Despite this evidence of sustained portal hypertension, hypertrophy did not develop in the right ventricle or in the media of the pulmonary trunk or muscular pulmonary arteries in any of the animals. This suggests that mechanical obstruction of the portal vein per se is not responsible for the development of pulmonary hypertension. Other factors, perhaps of a humoral nature, appear to be required to induce this rare association of portal hypertension but we have been unable to identify these. In particular, blood levels of oestrogen were not raised after ligation of the portal vein.
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PMID:Observations on the rare association between portal and pulmonary hypertension. 726 72

This paper presents a review of the literature on hepatic circulation and circulatory disorders of the liver in the dog and cat, and also includes a number of our own not previously published data. Circulatory disorders of the liver are frequently observed in dogs and cats. These disorders can be divided into congenital portosystemic shunts, disorders associated with outflow disturbances, and disorders associated with portal hypertension. Outflow disturbances result in passive congestion of the liver and in both species are mainly due to cardiac failure. Portal hypertension with resultant portosystemic collateral circulation and ascites mainly results from chronic liver disease, particularly cirrhosis. The main vascular disorder resulting in portal hypertension and ascites in the dog is primary hypoplasia of the portal vein.
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PMID:Circulatory disorders of the liver in dogs and cats. 757 Dec 84


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