Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162871 (abdominal aortic aneurysm)
 8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A unique case of a Chinese boy with Wiskott-Aldrich syndrome (WAS) associated with Takayasu's arteritis is reported. He had eczema, epistaxis and recurrent infections since early infancy and was found to have thrombocytopenia, negative delayed-type skin hypersensitivity, low T cell number and impaired lymphocyte proliferation to phytohaemagglutinin and concanavalin A. He had high normal serum immunoglobulin (Ig)G and IgA with low IgM and isohaemagglutinin. He presented with hypertensive encephalopathy at 5.5 years of age and an aortogram demonstrated abdominal aortic aneurysm with bilateral stenosis of renal arteries resulting in renovascular hypertension. His hypertension was difficult to control medically and autotransplant of his kidneys to the iliac arteries was performed, but he died in the immediate postoperative period. The relationship between immunodeficiency and collagen-vascular disease was discussed.
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PMID:Takayasu's arteritis associated with Wiskott-Aldrich syndrome. 135 86

A 71-year-old male with disseminated intravascular coagulation (DIC) caused by abdominal aortic aneurysm was successfully treated surgically. He had aortic regurgitation, an old myocardial infarction, and nephrotic syndrome. The infrarenal part of the inferior vena cava, which was on the left side of the aneurysm, was temporarily transected during the surgical procedure. Preoperative heparin therapy was insufficient, but infusion of blood components during the operation and minimal dissection of the aneurysm were effective in controlling intraoperative hemorrhage. Hypofibrinogenemia and thrombocytopenia were normalized immediately after operation, and hemorrhagic diathesis was completely cured. In this case, the definitive treatment of DIC caused by an abdominal aortic aneurysm war removal of the lesion and the infusion of coagulation factors during the operation was effective in minimizing blood loss.
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PMID:Disseminated intravascular coagulation caused by abdominal aortic aneurysm. 341 54

Four patients with ruptured abdominal aortic aneurysm developed thrombocytopenia and marked megaloblastic changes within 3-10 days of surgery. In 2 patients, direct evidence of folate deficiency within marrow cells was obtained by measuring deoxyuridine suppression in short-term bone marrow cultures. The results suggest that folate deficiency was limited to marrow tissue. Folate deficiency localized to the bone marrow offers an explanation for the extremely rapid onset of thrombocytopenia in these patients. The significance of these findings with regard to folate metabolism is discussed. The importance of recognizing this potentially fatal complication of critical illness is emphasized, because it should be readily prevented by folic acid therapy.
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PMID:Acute onset of folate deficiency in patients under intensive care. 741 25

A patient with chronic idiopathic thrombocytopenic purpura (ITP), chronic disseminated intravascular coagulation (DIC) and abdominal aortic aneurysm is described. He had severe thrombocytopenia and his platelet life span was shortened (29 h). Indium 111-labeled platelet scintigraphy demonstrated an increased accumulation of radioactivity over the aneurysm and the spleen. Following preoperative heparin therapy for DIC, the platelet count remained low (10 x 10(9)/l), while the DIC improved. Because of the elevated platelet-associated IgG, we considered that the patient had complicated chronic ITP. After intravenous immunoglobulin therapy, his platelet count increased. The aneurysm was successfully replaced with an artificial Y-graft vessel and a splenectomy was performed at the same time. The platelet count was maintained at about 60 x 10(9)/l after the operation and the patient is quite well now.
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PMID:Chronic idiopathic thrombocytopenic purpura complicated by chronic disseminated intravascular coagulation associated with abdominal aortic aneurysm. 823 72

The authors report a case of a 70-year-old man, with repeating episodes of systemic subdermal hematoma due to consumption coagulopathy associated with abdominal aortic aneurysm and the bilateral femoral arterial aneurysms. Prior to the first operation for abdominal aortic repair, anticoagulation therapy was applied to treat thrombocytopenia and hypofibrinogenemia. Five years following the first surgery, the same treatment was required before resection of the femoral lesions. Consumption coagulopathy is seen in approximately 1-4% population of aortic aneurysms, however, repeated appearance of symptomatic coagulopathy is rarely reported. Anticoagulation therapy was effective to normalize the coagulation and fibrinolytic system and followed by uneventful surgical resection of the aneurysms.
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PMID:Consumption coagulopathy associated with aneurysms of the abdominal aorta and the bilateral femoral arteries. Report of a case. 1129 44

A 71-year-old man was diagnosed as having an abdominal aortic aneurysm when he was treated for idiopathic interstitial pneumonia (IIP). Three years later, he developed severe thrombocytopenia and had disseminated intravascular coagulation (DIC) that was associated with the inflammatory abdominal aortic aneurysm (IAAA). The coagulation abnormalities were corrected by low-molecular weight heparin, however the platelet count remained low. Bone marrow showed normocellularity with an increase of immature and mature forms of megakaryocytes. Platelet-associated IgG level was high. These findings suggested that the patient had severe thrombocytopenia caused by unusual complications of immune thrombocytopenic purpura and IAAA-associated DIC.
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PMID:Inflammatory abdominal aortic aneurysm followed by disseminated intravascular coagulation and immune thrombocytopenia. 1248 85

Perioperative hemorrhage is one of the principal causes of death in patients with ruptured abdominal aortic aneurysm (AAA). This study examines perioperative coagulation and fibrinolysis in patients undergoing ruptured AAA repair complicated by coagulopathy. Eight patients (8 men of median age 74, range 69-87, years) who developed clinical and laboratory evidence of coagulopathy during attempted repair of ruptured infrarenal AAA were prospectively studied. Platelet count, fibrinogen, clotting times, prothrombin fragment (PF) 1+2, and tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) activities were measured preoperatively, immediately before, and 5 min and 24 hr after aortic declamping. Six patients died, three intraoperatively, one within 24 hr, and two in the late postoperative period. All patients had thrombocytopenia and prolonged clotting times intraoperatively with evidence of increased thrombin generation (as demonstrated by elevated PF 1+2). Five patients had increased systemic fibrinolysis (as demonstrated by elevated t-PA activity) preoperatively and/or before aortic declamping and all of these patients died. Three patients had perioperative inhibition of systemic fibrinolysis (as demonstrated by elevated PAI activity) and two survived. These data demonstrate that coagulopathy in ruptured AAA repair may be associated with a hyperfibrinolytic state. Further research is required to determine if (a) a causal relationship exists between hyperfibrinolysis and coagulopathy and (b) whether antifibrinolytic agents can improve outcome if targeted at this group of patients.
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PMID:Coagulopathy and hyperfibrinolysis in ruptured abdominal aortic aneurysm repair. 1553 37

We experienced excessive anticoagulation induced by argatroban for the treatment of heparin-induced thrombocytopenia (HIT). A 74-year-old man was scheduled for elective abdominal aortic aneurysm resection. During the surgery, both femoral arteries were found non-pulsatile requiring thrombectomy. The next day, second laparotomy was needed because of superior mesenteric artery occlusion. After the surgery, acute renal failure and hypoxemia continued with progressive thrombocytopenia necessitating frequent administration of platelet concentrates. Considering possibility of HIT, we stopped heparin and began argatroban. Due to his mild liver dysfunction, we initiated argatroban at 0.5 microg x kg(-1) x min(-1) one-fourth of standard initial dose, according to its drug information approved by FDA. Although expected APTT level was from 50 to 60 sec, it increased immediately up to 93 sec. Excessive anticoagulation continued more than 24 hours after cessation of argatroban and bleeding occurred from the tracheostomy site. When APTT decreased to the target range, we restarted argatroban and found the adequate dosage at 0.08 microg x kg(-1) x min(-1). After argatroban treatment, platelet count recovered immediately and no thromboembolism was observed. We recommend that argatroban should be initiated at a lower dosage than the dose shown in its drug information for HIT patients after cardiovascular surgery with frequent monitoring of APTT.
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PMID:[A case of heparin-induced thrombocytopenia associated with unexpected excessive argatroban anticoagulation after abdominal aortic aneurysm resection]. 1649 97

The antiphospholipid syndrome is characterized by recurrent fetal loss, venous and/or arterial thrombosis, and thrombocytopenia associated with elevated titers of lupus anticoagulant and anticardiolipin antibodies. Although thrombosis is the characteristic vascular involvement in APS, the development of vascular aneurysms in patients with APS has been reported. We describe four patients with established APS who developed abdominal aortic aneurysm, and review the literature on previous published cases of arterial aneurysms developing in patients with APS. In addition, we discuss the possible pathophysiological association between APS and the development of this vascular abnormality.
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PMID:Coexistence of the antiphospholipid syndrome and abdominal aortic aneurysm. 1830 May 73

Heparin-induced thrombocytopenia is an immune-mediated syndrome that results from unfractionated heparin or low molecular weight heparin exposure. It often remains unrecognized and undertreated and can cause limb and/or life-threatening thrombosis. The authors present 2 cases of thrombosis: one arterial and the other venous that occurred following endovascular abdominal aortic aneurysm repair. To the authors' knowledge, this is only the second report of arterial thrombosis and the first of deep vein thrombosis as a result of heparin-induced thrombocytopenia developing following endovascular abdominal aortic aneurysm repair. This underscores the importance of considering heparin-induced thrombocytopenia as a potential cause for postendovascular thrombotic complications in the patient who develops thrombocytopenia following this procedure.
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PMID:Heparin-induced thrombocytopenia with thrombosis after endovascular aneurysm repair. 1879 98


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