Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the case of a 28-year-old man who was admitted in an emergency because of severe abdominal pain with gastrointestinal haemorrhage and shock. Laparotomy showed infarction of the small intestine with mesenteric veins thrombosis. Severe thromboembolic complications occurred during the post-operative period: bilateral femoral deep vein thrombosis with pulmonary embolism, axillary and subclavian vein thrombosis associated with an intravenous catheter, portal hypertension related to portal vein thrombosis and cavernoma, thrombosis of the superior longitudinal sinus. Laboratory investigations performed after thrombotic episodes and repeated 5 years later evidenced a type 1 Heparin Cofactor II deficiency (HCII Ag by EID: 40 percent; functional Tollefsen's method: 60 percent). This heterozygous deficiency was also found in one of the patient's sons. This is the first reported case of HCII deficiency associated with mesenteric infarction and cerebral thrombophlebitis. The relationship between these severe venous thrombotic episodes and the HCII deficiency is discussed in relation to the dermatan sulphate-HCII couple physiology. Vascular injury may act as a triggering factor in patients with HCII deficiency.
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PMID:[Recurrent venous thromboembolism caused by heparin cofactor II deficiency. A case]. 183 93

The authors studied 30 patients with bleeding from esophageal varices due to portal hypertension. They underwent the disconnection of portal and azygos veins and splenectomy. The immediate postoperative complications were: portal thrombosis in four patients (13.3%); subphrenic abscess in two (6.6%); pulmonary embolism in one (3.3%) and esophageal perforation in one (3.3%). The manifestations of portal thrombosis were ascites, and fever (without leukocytosis). One patient with portal thrombosis who had intractable ascite was submitted to peritoneovenous shunting.
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PMID:[Portal thrombosis: early complication of azygo-portal disconnection in the treatment of bleeding esophageal varices]. 213 72

A traumatic venous aneurysm within the greater saphenous vein occurred in a 15-year-old hockey player. The patient had early diagnosis and surgical excision of the lesion. Venous aneurysm is a rare clinical entity and a pathologic curiosity in the absence of varicose veins. It can lead to serious complications, such as pulmonary embolism, portal hypertension, and rupture. Early diagnosis with the use of venography and surgical excision of the lesion can prevent major complications.
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PMID:Traumatic venous aneurysm. Case report. 382 5

Ten patients with clinically and histologically verified Budd-Chiari-Stuart-Bras Syndrome (i.e. occlusive disease of small or large efferent hepatic veins) were re-examined, the examination also including combined ultrasonography and computed tomography. These non-invasive methods help to establish a quick diagnosis by locating and defining the most severe changes, by helping to select the most appropriate invasive diagnostic procedure, and by defining their topographical target. They thus facilitate immediate, optimal therapy. The disease process often starts in the right dorsal lobe of the liver and may cause extreme hyperplasia of the left or middle lobes, causing gross changes in the shape of the liver and considerably displacing the gallbladder in some cases. Thrombosis of the portal vein and pulmonary embolism seem to be most frequent complications or accompanying diseases. We therefore suggest immediate long-term anticoagulation, provided portal hypertension is not too severe; patients with severe portal hypertension should undergo a shunt operation. Our patients were followed up for periods ranging from 3 to 8 years. The very variable prognosis includes complete cure and good compensation over a long period and appears to be much better than has been reported by some authors.
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PMID:Budd-Chiari-Stuart-Bras syndrome: clinical, sonographic, radiological reexaminations in occlusive diseases of hepatic veins. 639 51

The development of an acute pleural effusion during the immediate postoperative period after abdominal or pelvic surgery is not uncommon. In symptomatic patients, pleural effusions often are thought to result from a complication of pulmonary embolism or parapneumonic effusion. We present a patient in whom an acute unilateral hepatic hydrothorax developed after elective total abdominal hysterectomy. Pleural effusion continued to reaccumulate for several days. After extensive efforts failed to reveal the cause of effusion, intraperitoneal radioisotope study confirmed a peritoneopleural communication associated with unsuspected and asymptomatic hepatitis C-induced cirrhosis of the liver with portal hypertension.
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PMID:Acute massive postoperative pleural effusion associated with asymptomatic hepatitis C-induced cirrhosis of the liver. 921 42

After a brief reference to the most important pioneers of angiography, the author describes the techniques performed, lesions treated and future perspectives. The following techniques are performed: embolizations, selective infusion of drugs, placement of inferior vena cava filter, removal of intra-vascular bodies, revascularisation techniques and porta-cava shunt. Reference was made to the following lesions treated: tumours, hemorrhages, arteriovenous malformations, hypersplenism, pulmonary embolism, varicocele, ischemic lesions and portal hypertension.
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PMID:[Therapeutic angiography]. 925 35

This trial represents the Egyptian experience in cyanoacrylate injection for hemostasis of bleeding gastric varices. One hundred patients with portal hypertension due to schistosomal hepatic fibrosis and/or posthepatitic liver cirrhosis were included. All patients presented with bleeding from gastric varices either fundal (80 patients) or inferior extension of esophageal varices (20 patients) were enrolled. Injection therapy was administered as the first active measure. No tamponade or drugs were used. Cyanoacrylate was mixed with lipid and injected through a hand-made probe. A mean of 3 (range 1-9) ampoules of cyanoacrylate were used per injection session. Bleeding stopped at the end of all sessions. Ten patients (12.5%) with fundal varices had rebleeding during the first 24 hours. Reinjection could control bleeding in 6 patients with a total success rate of 95%. Four patients were managed surgically. Fatal pulmonary embolism developed in one patient (1.25%) with fundal varix. Five more patients (6.25%) died from bleeding-related liver failure. In conclusion, injection of cyanoacrylate is highly satisfactory in controlling bleeding from both types of gastric varices.
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PMID:Endoscopic control of gastric variceal bleeding with butyl cyanoacrylate in patients with schistosomiasis. 925 78

Between 1980 and 1996, 16 patients (10 women) with pathologically confirmed insulinomas were operated on; they represents a median of 0.9 per year and 1.1 per cent from the total of pancreatic tumors. Median age was 47.2 (+/- 22.8) years old (range 23-68). Insulinomas occurred with following frequency in: head--2 patients, body and tail--11 patients and diffuse forms (nesidioblastomas)--3 patients. The specific clinical forms only with tumoral syndrome (without hypoglycemic manifestations) and one was an intraoperative discovery. In the case of the four patients two presented with splenic-portal hypertension +/- upper digestive haemorrhages and the other two only tumoral syndrome. The surgical approach was: the midline (ten), uni- or bilateral subcostal (five), and other incisions one. There were performed tumor exeresis through: enucleation (three), segmentary pancreatectomies (two), spleno-left-pancreatectomies (nine) and the extension of an anterior pancreatectomy (one). In one case biopsy alone was done. The tumors were not intraoperatively identified in three cases (blind left spleno-pancreatectomies). The malignancy index was 4/16 (25 per cent). Postoperative mortality rate was 12.5 per cent (two patients: one acute necrotizing pancreatitis and one pulmonary embolism).
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PMID:[Insulinomas--nesidioblastomas. Clinical experience]. 945 52

Azathioprine is a drug commonly used for the treatment of inflammatory bowel disease, organ transplantation and various autoimmune diseases. Hepatotoxicity is a rare, but important complication of this drug. The cases reported to date can be grouped into three syndromes: hypersensitivity; idiosyncratic cholestatic reaction; and presumed endothelial cell injury with resultant raised portal pressures, venoocclusive disease or peliosis hepatis. The components of azathioprine, 6-mercaptopurine and the imidazole group, may play different roles in the pathogenesis of hepatotoxicity. The strong association with male sex, and perhaps with human leukocyte antigen type, suggests a genetic predisposition of unknown type. Many of the symptoms of hepatotoxicity, such as nausea, abdominal pain and diarrhea, can be nonspecific and can be confused with a flare-up of inflammatory bowel disease. As well, the subtype resulting in portal hypertension can occur without biochemical abnormalities. A 63-year-old man with Crohn's disease who is presented developed the rare idiosyncratic form of azathioprine hepatotoxicity, but also had a severe disabling steroid myopathy, peripheral neuropathy, resultant deep venous thrombosis and pulmonary embolism related to immobility, and a nosocomial pneumonia. His jaundice and liver enzyme levels improved markedly on withdrawal of the drug, returning to almost normal in five weeks. Treating inflammatory bowel disease effectively while trying to limit iatrogenic disease is a continuous struggle. Understanding the risks of treatment is the first important step. There must be a low threshold for obtaining liver function tests, especially in men, and alertness to the need to discontinue the drug or perform a liver biopsy should patients on azathioprine develop liver biochemical abnormalities, unexplained hepatomegaly or signs of portal hypertension.
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PMID:Cholestatic hepatocellular injury with azathioprine: a case report and review of the mechanisms of hepatotoxicity. 981 67

Azygos vein enlargement can be detected in congestive heart failure, portal hypertension, inferior vena cava thrombosis, right atrial mural thrombosis, a pulmonary embolism, congenital azygos continuation to the inferior vena cava, and the arteriovenous fistula. Radiography, particularly computed tomography (CT), is very useful, not only in recognition of azygos vein enlargement, but also in evaluation of its etiology for the institution of the appropriate treatment of the diseases.
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PMID:Clinical significance of azygos vein enlargement: radiographic recognition and etiologic analysis. 1063


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