Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Acute renal failure (ARF) can occur as a complication of cocaine abuse. We present a case of microangiopathic hemolytic anemia, ARF, and thrombocytopenia after inhalation of crack cocaine in a 38-year-old woman. Her renal failure ultimately required dialysis. She underwent renal biopsy because of persistent renal failure, hematuria, and thrombocytopenia. The biopsy findings consisted of thrombotic microangiopathy and glomerular ischemia. After treatment with fresh frozen plasma, her platelet count and bleeding resolved. The possible mechanisms involved in cocaine-induced thrombotic microangiopathy include: (1) endothelial injury, (2) vasoconstriction and/or impairment of vasodilatation, (3) procoagulant activity, and (4) antiplatelet activity. Although our patient survived after hemodialysis and transfusion of fresh frozen plasma, she continued to have residual renal insufficiency. One month later, the patient again used cocaine and presented with worsening ARF, anemia, and thrombocytopenia.
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PMID:Cocaine-induced acute renal failure, hemolysis, and thrombocytopenia mimicking thrombotic thrombocytopenic purpura. 1062 May 64

The most common anticoagulant used for cardiopulmonary bypass is heparin. An alternate form of anticoagulant therapy is needed for patients who have immune-mediated heparin-associated thrombocytopenia (HIT). Thrombocytopenia causes bleeding and may lead to serious arterial and venous thrombosis. HIT or heparin-induced thrombocytopenia with thrombosis type II (HITT) are both described as adverse reactions to heparin. They are diagnosed with a platelet count less than a 100,000/mcl for 2 consecutive days. HITT, the severe form, is characterized with the thrombocytopenia in combination with thromboembolic complications, such as strokes, myocardial infarctions, and limb ischemia. Two cases are presented in which r-hirudin was used for anticoagulation for aortocoronary bypass surgery and mitral valve replacement. The activated partial prothrombin time (aPTT) was used to monitor coagulation. In the first case, the aPTT was maintained greater than 100 seconds, and at the termination of cardiopulmonary bypass, some clot was noted in the cardiopulmonary bypass circuit. In the second case, a longer cardiopulmonary bypass run was anticipated, the hirudin bolus and infusion rate were increased, and the aPTT was maintained at greater than 200 sec. Adequate coagulation resulted, and, at the end of bypass, no clot was noted. These case studies seem to suggest a higher dosage of r-hirudin may be required for the use of cardiopulmonary bypass and a need to maintain aPTT values greater than 200 sec to help monitor anticoagulation.
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PMID:The emergency use of recombinant hirudin in cardiopulmonary bypass. 1091 79

A 60-year-old man was admitted to the hospital with aortic dissection. An operative excision and replacement with a Y-graft was performed. Postoperatively he developed multiple organ dysfunction and required intermittent haemofiltration (anticoagulation with heparin). An ischemia of the left leg occurred at the third postoperative day. The initial platelet count was 99,000/microliter. Continuous haemofiltration (CVVH) was started three days later. Thrombotic obstructions of haemodialysis filters and catheters occurred frequently and heparin-induced thrombocytopenia (HIT II) was suspected. Antibodies against heparin were found in the HIPA test. Despite heparin free citrate dialysis and anticoagulation with danaparoid thrombotic obstructions of filters and catheters continued. Therefore the anticoagulation therapy during CVVH was changed to recombinant hirudin (lepirudin). Starting dose was a bolus of 0.01 mg/kg bw followed by the same amount as maintenance dose per hour. Anticoagulation was adjusted to an increase of aPTT (activated partial thromboplastin time) to 1.5-2 times its normal value. A dose of 0.005 mg/kg bw/h lepirudin was sufficient to maintain adequate anticoagulation. After changing to lepirudin no further catheter obstructions were observed and the platelets recovered slowly. Renal function improved and five weeks after admission endogenous creatinine clearance showed a value of 25 ml/min. We conclude that lepirudin is an effective anticoagulant during CVVH in patients with HIT II. In partly permeable polysulfon filters a dose of 0.005 mg/kg bw/h lepirudin is sufficient to maintain adequate anticoagulation. Monitoring anticoagulation by measuring the increase of aPTT (factor 1.5-2.0) seems to be safe. However, optimally the r-hirudin concentration should be measured directly using the Ecarin clotting time.
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PMID:Continuous haemofiltration with r-hirudin (lepirudin) as anticoagulant in a patient with heparin induced thrombocytopenia (HIT II). 1095 74

Clinical experience suggests that patients treated with the glycoprotein (GP) IIb/IIIa inhibitor abciximab (ReoPro , Eli Lilly and Company, Indianapolis, Indiana) may be at increased risk of thrombocytopenia. This case report details the successful use of the GP IIb/IIIa inhibitor eptifibatide (Integrilin , COR Therapeutics, South San Francisco, California) in a patient who developed acute thrombocytopenia (platelet count: 67,000/mm3) approximately 10 hours after initiation of abciximab therapy. Five hours after abciximab was discontinued, platelet count returned to normal (191,000/mm3) and eptifibatide was started because of persistent electrocardiographic evidence of ischemia. The patient underwent diagnostic catheterization during eptifibatide therapy, which was administered for approximately three days. Four days after the initial course of therapy with eptifibatide was discontinued, percutaneous revascularization with adjunct eptifibatide was performed. During both courses of eptifibatide therapy, platelet counts remained in the normal range (> 100,000/mm3) and no adverse ischemic or bleeding events occurred.
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PMID:Platelet receptor glycoprotein IIb/IIIa inhibition with eptifibatide in a patient with thrombocytopenia after treatment with abciximab. 1102 16

Platelet aggregation and activation of coagulation are key events in the development of acute coronary syndromes. Patients with an acute coronary syndrome are at high risk of death or myocardial infarction, and hence there is a strong rationale for the use of antithrombotic agents. Heparin has been shown to reduce the risk of death or myocardial infarction in aspirin-treated patients with acute coronary syndromes, but it has a number of limitations, including the need for regular monitoring and the risk of hemorrhage and thrombocytopenia. Low-molecular-weight heparins offer a number of practical and clinical advantages over unfractionated heparin, such as higher bioavailability and administration by subcutaneous injection. Several low-molecular-weight heparins are available that differ in their biochemical and pharmacologic properties, and it is not possible to predict their clinical efficacy from their pharmacologic profile. The decision regarding the use of a specific low-molecular-weight heparin should be based on the efficacy and safety data available for each product. In clinical trials comparing low-molecular-weight heparin with heparin, only enoxaparin sodium has been shown to reduce the risk of coronary events in patients with non-ST segment elevation acute coronary ischemia.
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PMID:Low-molecular-weight heparins in the treatment of acute coronary syndromes. 1142 95

P-selectin-dependent leukocyte-endothelial cell adhesion has been implicated in the pathogenesis of ischemia/reperfusion (I/R) injury in several vascular beds, including the gut. Because platelet-endothelial (P/E) cell adhesion also occurs in postischemic venules, the possibility exists that the expression of P-selectin on the surface of platelets that are adherent to venular endothelial cells may mediate the leukocyte recruitment elicited by I/R. P-selectin expression [dual radiolabeled monoclonal antibody (MAb) technique] and neutrophil accumulation [myeloperoxidase (MPO) activity] were measured in the postischemic small intestine of untreated rats and rats treated with either antiplatelet serum (APS) or MAbs directed against either P-selectin, GPIIb/IIIa, or fibrinogen. The increases in P-selectin expression and tissue MPO normally elicited by I/R were significantly attenuated in the different treatment groups, suggesting that I/R-induced neutrophil recruitment is a platelet-dependent, P-selectin-mediated process. Intravital microscopy was then employed to examine this process relative to leukocyte-endothelial cell adhesion in postischemic rat mesenteric venules. The recruitment of adherent and emigrated leukocytes after I/R was attenuated by pretreatment with a MAb against, either P-selectin, GPIIb/IIIa, or fibrinogen, as well as an Arg-Gly-Asp peptide. Whereas thrombocytopenia greatly blunted leukocyte emigration, it did not alter the leukocyte adherence response to I/R. These findings suggest that platelet-associated P-selectin contributes to the accumulation of leukocytes in postischemic tissue via a mechanism that alters transendothelial leukocyte migration.
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PMID:Platelets modulate ischemia/reperfusion-induced leukocyte recruitment in the mesenteric circulation. 1170 48

Heparin-induced thrombocytopenia, an increasingly recognized aspect of heparin therapy, occurs in 0.6% to 30% of patients receiving heparin. Approximately 1% of those patients develop the more severe heparin-induced thrombocytopenia II, also called white clot syndrome, in which synchronous venous and arterial thrombi impede blood flow in central vessels. Mortality (as high as 25%) and morbidity are related to the site and extent of thrombi formation. Following vascular surgery, one patient manifested an unusual consequence of heparin-induced thrombocytopenia II when thrombotic blockage of the vessels supplying the bilateral gluteus maximus and minimus muscles resulted in tissue ischemia and death. Supporting the patient through numerous complications and managing the extensive wound healing process required multidisciplinary skills and innovative technology, including use of vacuum-assisted closure therapy, platelet-derived growth factors, parenteral and enteral nutritional support, and spirit-restoring favorite foods. This article describes the patient's life-threatening and long-lasting effects from an allergic reaction to heparin therapy. In addition to information about the diagnosis of heparin-induced thrombocytopenia, this article also describes management of the wound and other aspects of care and comforting that occurred over a 9-month hospitalization.
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PMID:Heparin-induced thrombocytopenia as the cause of gluteus muscle necrosis: a case study describing the benefits of multidisciplinary physical and psychosocial interventions. 1188 19

Pathogenic mechanisms of renal injury by thrombotic microangiopathies present a challenge to the multidisciplinary team caring for a patient with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS). First recognized 77 years ago as a rare disorder characterized by reversible platelet aggregation in the microcirculation causing ischemia in various organs, the prognosis was always fatal. In the past 20 years, due to effective treatment with plasma exchange therapy, there has been a decline in the mortality rate to 10-20%. The classic pentad of symptoms of TPP-HUS include thrombocytopenia, microangiopathic hemolytic anemia, neurologic abnormalities, fever, and renal impairment. Frequency of TTP-HUS appears to be increasing. Due to the urgent need for a diagnosis, sufficient diagnostic criteria for TTP-HUS are currently thrombocytopenia and microangiopathic hemolytic anemia in the absence of another apparent cause. It is imperative to have a solid understanding of the pathophysiology and current standards of practice of TTP-HUS in order to facilitate positive patient outcomes in this unique group of patients.
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PMID:Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome: pathophysiology and management. 1199 52

Thrombotic microangiopathies (TMA) encompass various severe diseases characterized by microangiopathic hemolytic anemia and peripheral thrombocytopenia, associated with fever, neurological signs and renal involvement. Microvascular thrombosis is the typical lesion, and results in tissue ischemia. Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are the two most classical forms. These two entities are clinically and histopathologically closely related. There is a body of evidence suggesting that endothelial cell injury is the initial event in TTP and HUS, and that it may be related to a large number of triggering factors, such as infection, connective tissue disease, drugs, cancer and chemotherapy, transplantation, and pregnancy. Endothelial cell injury enhances the release of ultra large forms of von Willebrand factor (ULvWF) multimers and other prothrombotic agents, such as plasminogen activator inhibitor and platelet activating factor, whereas it decreases the release of prostaglandin-I2, a strong inhibitor of platelet aggregation. Recently however, it has been shown that TTP and HUS were pathophysiologically distinct. Actually, TTP is associated with a deficiency in von Willebrand factor-cleaving protease, an enzyme involved in cleavage of ULvWF into circulating 200 kDa and 350 kDa fragments. This deficiency may be either congenital or acquired, and then related to an IgG inhibitory autoantibody. This protease deficiency may account for the high amounts of plasmatic ULvWF in TTP patients. In HUS, vWF-cleaving protease activity is found normal. HUS encompasses two distinct entities. Epidemic, or diarrhea-associated HUS, is associated with verotoxin or Shiga toxin-associated enterobacteriaceae. These toxins are directly responsible for endothelial cell injury. Sporadic HUS (also termed atypical HUS in children) is closely related to TTP, and shares the same triggering factors. Familial HUS has been associated in some cases with hypocomplementemia and factor H dysfunction, the pathophysiological role of which remains unclear. The study of the different triggering factors and predisposing factors may be useful to define different subsets of TMA, that may be characterized by their course and prognosis.
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PMID:[Pathophysiology of thrombotic microangiopathies: current understanding]. 1221 98

The term thrombotic microangiopathy (TMA) encompasses syndromes of thrombocytopenia, microangiopathic haemolytic anaemia, neurologic deficits, renal dysfunction and variable signs of organ impairment. Childhood cases of TMA with predominant renal failure are usually referred as Haemolytic Uremic Syndrome (HUS), and adult cases with major neurological involvement as Thrombotic Thrombocytopenic Purpura (TTP). Exotoxins, produced in most cases by E. Coli O 157:H7, have been related to diarrhea associated HUS(D + HUS). Anticancer (mitomycin), immunosuppressive drugs (cyclosporin, tacrolimus and OKT3) and as well as some antiplatelet agents (ticlopidine, clopidrogel) have been associated with both HUS and TTP. Defective factor H or vWF protease activity have been found with familiar and recurrent forms. Endothelial damage and dysfunction is most likely the initial event of the pathogenic process that eventually leads to platelet aggregation, microvascular thrombosis and tissue ischemia. TMA may occur de novo in the native kidneys of patients who received a non-kidney transplant or in the transplanted kidney of patients who progressed to ESRD because of a disease other than HUS. Calcineurin inhibitors and vascular rejection are most often involved in these cases. The disease may also recur on the transplanted kidney in patients who progressed to ESRD because of HUS/TTP. The risk of postransplant recurrence is negligible for D + HUS but is close to 100% in familial/recurrent forms associated with low C3 and decreased factor H bioavailability or activity. Withdrawal or treatment of precipitating factors are the most effective approach. Plasma therapy is usually attempted with the rationale to limit the microangiopathic process, but its efficacy for improving graft survival is unproven. The outcome of recurrent forms is almost invariably poor.
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PMID:Thrombotic microangiopathy in renal transplantation. 1222 1


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