Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The liver of Syrian hamsters was studied after exposure to dimethylnitrosamine (DMN) in drinking water for, respectively, 8, 12 and 16 weeks. One additional group of animals was offered DMN for 8 weeks, but maintained for further 8 weeks after removal of the compound. The changes consisted of a narrowing portal venopathy, probably arising, initially, from toxic pylephlebitis, being followed by widespread subendothelial prolapse of hepatocytes encroaching upon the lumen of terminal hepatic veins, which generally were free of inflammatory fibrosing lesions. The venous lesions were unrelated to malignant processes in the biliary duct system, which occurred after 16 weeks. Dilatation of sinusoids and small venules was associated with the presence of prolapsed hepatocytes around their openings into involved larger veins. At the end of 12 and 16 weeks of continuous ingestion of DMN, but also where the agent was withdrawn already at 8 weeks, phlebectasis and transitional stages in the formation of teleangiactatic type of peliosis were demonstrated, probably resulting from progressively impeded blood flow due to partial occlusion by prolapsed hepatocytes in terminal veins. The mechanism enabling hepatocytes to penetrate the venous wall was not clarified. There was no indication of invasive malignancy. Hepatocyte prolapse appeared more likely to result from some unknown mechanism of benign infiltration, promoted by regenerative stimulation. This may have been initiated by mild persistent ischemia due to the demonstrated portal venopathy. No endothelial hyperplasia was seen at any stage of the experiments thus eliminating the probability of peliosis being a source of vascular neoplasia, which has previously been described following more prolonged exposure to DMN. Certain parallelisms of the experimental results with hepatic vascular lesions in man subjected to drug therapy are discussed.
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PMID:Venoocclusive disease of the liver and phlebectatic peliosis in the golden hamster exposed to dimethylnitrosamine. 373 74

Thirty-four adult patients with portomesenteric venous occlusion (PVO) were reviewed. In 11 with hepatic cirrhosis, PVO was usually heralded by worsening ascites often with varix hemorrhage; mortality was high. Four with isolated portal block had varix hemorrhage without ascites. All of these patients survived despite recurrent hematemesis when portal decompression was not feasible in two patients. Eight others (5 agnogenic and 3 with hypercoagulability), experienced sudden abdominal pain with a clot typically propagated into mesenteric tributaries with ileojejunal infarction; survival was related to the promptness of operation and the extent of bowel ischemia. Of five patients with intraabdominal sepsis and pylephlebitis, only one survived. In the final six patients, PVO occurred with intraabdominal carcinoma. Five had progressive ascites, cachexia, and an early death. Imaging techniques included plain and contrast roentgenograms, ultrasonography, and for definitive diagnosis direct portography (operative or splenoportogram), indirect portography (splanchnic arteriovenogram), and computed tomography. Thirteen of 34 patients had ascites, and in nine of 11 patients examined, protein concentration of ascitic fluid was extremely low (less than 0.6 g/dl). Clinical presentation of PVO varies, depending on acuteness and extent of visceral venous blockade, severity of portal hypertension, auxiliary venous collateralization, and regional lymph flow. Inciting factors include endothelial damage and blood hypercoagulability from trauma, infection, stagnant circulation, blood dyscrasia, and malignancy. Improved imaging now allows early diagnosis.
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PMID:Protean manifestations of pylethrombosis. A review of thirty-four patients. 387 12

Pylephlebitis--suppurative thrombophlebitis of the portal and/or mesenteric veins--is a rare complication of abdominal infections, especially diverticulitis. It can lead to severe complications such as hepatic abscess, sepsis, peritonitis, bowel ischemia, etc., which increase the mortality rate. Here we present a case of suppurative thrombophlebitis of the inferior mesenteric vein, as a complication of sigmoid diverticulitis. The epidemiology, clinical and radiological features as well as treatment strategies are discussed. We also review the anatomy of the mesenteric vein given its anatomic variation in the present case and how this anatomic knowledge might influence the operative approach should surgery be necessary.
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PMID:Pylephlebitis of a variant mesenteric vein complicating sigmoid diverticulitis. 2496 18