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:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report on a 32-year old female patient with primary antiphospholipid syndrome (PAPS) and several thromboembolic events despite stable doses of oral anticoagulation, good patient compliance and maintained INR values of >3. Over the preceding 3 years the patient had presented a wide spectrum of manifestations of APS, including recurrent venous and arterial thromboses, cardiac, gynecological (HELLP syndrome), neurological involvements, livedo reticularis, a mild thrombocytopenia and the most feared manifestation of the catastrophic antiphospholipid syndrome (CAPS). Life-threatening bilateral subdural bleeding occurred while she was anticoagulated. The clinical features appeared to be refractory to oral anticoagulation with phenprocoumon. They were life threatening on each occasion and she developed repetitive episodes of organ damage with cardiac insufficiency (NYHA III), pulmonary hypertension and other residual defects. Even during heparinization recurrent thromboembolism supervened as well as livedo reticularis of the extremities. Lupus anticoagulants (LAC), anticardiolipin (aCL) antibodies and anti-beta(2)-glycoprotein-1 (beta(2)GPI) titers were all markedly elevated. This case report shows that recurrent episodes of thrombosis can occur despite seemingly adequate anticoagulation in patients with CAPS.
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PMID:Recurrent life-threatening thromboembolism and catastrophic antiphospholipid syndrome in a patient despite sufficient oral anticoagulation. 1516 58

Heparin-induced thrombocytopenia (HIT) type II is an acquired thrombophylic state and life-threatening immune complication of a heparin treatment mainly clinically manifested by marked thrombocytopenia, frequently by arterial and venous thrombosis, and sometimes by skin changes. Functional assay as heparin aggregation test and 14C-serotonin release assays are used in diagnostics as well as antigen assays of which detection tests for heparin-platelet factor 4 antibodies are most frequently used. Considering the fact that there is no single reliable assays for HIT II detection available, sometimes it is necessary to combine both of the above-mentioned types of assays. We present the case of a 57-year-old patient with an acute anterior myocardial infarction with cardiac insufficiency of III and IV degree according to Killip, recurrent ventricular fibrillation and diabetes mellitus type II developing thrombocytopenia to 37 x 10(9)/l accompanied with typical skin changes. The diagnosis was confirmed by the heparin aggregation test. The second patient aged 70 undergoing the treatment for anteroseptal myocardial infarction and reinfarction of the inferior wall complicated by a cardiogenic shock and acute right bundle branch block developed thrombocytopenia 59 x 10(9)/l on the third day of the heparin therapy, with the remark that he had received a heparin therapy during the first infarction as well. Antibodies against heparin-platelet factor 4 were detected by particle gel ID-HPF4 immuno-assay. In both patients, the disease had a lethal outcome despite all then available therapeutic measures applied. Further on we discuss advantages of certain types of tests, a therapy doctrine, need for urgent therapeutic measures, inclusive of the administration of antithrombins, avoidance of harmful procedures like low-molecular-weight heparins administration and prophylactic platelet transfusion as well as preventive measures.
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PMID:[Thrombocytopenia induced by type II heparin and myocardial infarct: 2 case reports]. 1522 63

A 74 year old man was admitted to the hospital for purpura. The history revealed coronary heart disease. Bypass surgery had been performed 18 months ago. Furosemide had recently been prescribed for cardiac insufficiency and the patient had taken the drug intermittently over two weeks. Laboratory analysis showed severe thrombocytopenia. Despite immediate treatment with intravenous prednisolone and platelet transfusions the patient succumbed to cerebral hemorrhage. Autopsy confirmed a diffuse hemorrhagic diathesis and a cellular response of the bone marrow typical for an acute immune reaction. The start of the purpura nine to ten days after the first dose of furosemide, the exclusion of other possible causes for purpura and the focal proliferation of T-lymphocytes in the bone marrow render it highly probable, that furosemide was responsible for the fatal thrombocytopenia. Furosemide is discussed to have a potential for autoimmunological untoward effects due to its sulfonamide structure. Few case reports describe vasculitic and allergic phenomena. The generation of antibodies against thrombocytes and the depression of megakaryocytic function are thought to be involved. Our patient had been treated with furosemide during the bypass surgery 18 months before the development of purpura. A sensitization to furosemide probably took place at that time.
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PMID:[Fatal untoward effect of furosemide: immunocytopenic purpura and cerebral hemorrhage]. 1546 82

(1) Heparin prophylaxis for medical inpatients who are confined to bed is controversial, because there are no reliable comparative data. Prophylaxis only seems justified for some patients at high risk of pulmonary embolism who have no risk factors for bleeding. (2) The licence of dalteparin, a low-molecular-weight heparin (LMWH), has been extended in France to cover prophylaxis of deep venous thrombosis in patients confined to bed for heart failure, acute respiratory failure, acute infections or acute rheumatological conditions who have at least one other risk factor for venous thromboembolism. (3) Evaluation data in this setting include a placebo-controlled trial but no trials versus unfractionated heparin or enoxaparin (another LMWH already available for this use). (4) The PREVENT trial included 3681 patients matching the characteristics described in the licence. They were randomised to receive (double-blind) daily subcutaneous injections of dalteparin (5000 IU) or placebo for 14 days. There was no difference between the groups in the following outcomes: death, pulmonary embolism and venous thrombosis (incidence below 1% in the placebo group). The results based on an endpoint combining clinical outcomes and phlebographic abnormalities favoured dalteparin. (5) Few data are available on the adverse events occurring in this trial. In other clinical situations, dalteparin has the same adverse effects as other LMWH (thrombocytopenia, hyperkalemia, etc.). (6) In practice, for medical inpatients who are confined to bed, where the thromboembolic risk is low, dalteparin offers no tangible advantages over unfractionated heparin or enoxaparin. The optimal dose for preventing symptomatic thromboembolism and minimising the bleeding risk is unknown.
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PMID:Dalteparin: new indication. Prophylaxis in medical patients: no advance. 1575 Nov 68

We report a case of thrombotic thrombocytopenic purpura (TTP) with a positive Coombs' test. A 59-year-old female was admitted to our hospital in February, 1997 with symptoms of heart failure. Ultrasound cardiography showed moderate pericardiac effusion and she was diagnosed as having pericarditis. After admission she had anorexia and her urine volume was reduced. Laboratory tests showed anemia and thrombocytopenia. Her Coombs' test result was positive. Her renal function gradually worsened and her conscious level was reduced. We diagnosed her as TTP and judged that she needed hemodialysis. We performed plasma exchange and started steroid therapy. The renal biopsy was compatible with TTP. After treatment, her level of consciousness improved, but her renal function did not improve. On the 51st hospital day she fell into acute respiratory distress syndrome (ARDS) and entered ICU. We considered ARDS caused by infection and continued treatment, but she died of shock and lactate acidosis. Activity of von Willebrand factor-cleaving protease in our case was 15% before the first PE, and 25 % just before death. A case of TTP without collagen disease usually shows a negative Coombs' test result. We think that this was a rare case in which autoimmune hemolytic anemia was supervened with TTP.
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PMID:[Case of thrombotic thrombocytopenic purpura with a positive Coomb test]. 1597 91

A woman aged middle thirties presented with common cold-like symptoms, and was hospitalized due to hypotension and tachycardia. Echocardiography revealed pericardial effusion and preserved left ventricular fractional shortening (28%). Cardiac index, pulmonary capillary wedge and right atrial pressure were 1.8 l/min/m2, 15 and 13 mmHg, respectively. After drainage of pericardial effusion, cardiac index increased to 3.4 l/min/m2. On the fifth hospital day, left ventricular dysfunction developed (fractional shortening: 16%, cardiac index: 1.5 l/min/m2, pulmonary capillary wedge pressure: 18 mmHg, right atrial pressure: 12 mmHg), so percutaneous cardiopulmonary support was introduced. However, the heart failed in asystole and the cavity was occupied by massive thrombus, probably related to heparin-induced thrombocytopenia. This case of fulminant myocarditis passed through various clinical features of heart failure. She died on the 12th hospital day.
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PMID:[Fulminant myocarditis causing severe left heart failure and massive thrombus formation following cardiac tamponade: a case report]. 1609 28

A 62-year-old man with a history of coronary artery disease and coronary artery bypass graft, chronic heart failure, and peripheral vascular disease required percutaneous coronary intervention (PCI) after progression of shortness of breath and fatigue over 2 years. Four hours after the procedure, the patient developed hematemesis and was found to be thrombocytopenic. The thrombocytopenia was presumed to be due to the abciximab infusion the patient received during and shortly after the PCI. Further review of the patient's medical history revealed that a similar episode had occurred 11 years earlier. At that time, he was enrolled in a clinical trial comparing tirofiban and heparin in patients with unstable angina; he developed profound thrombocytopenia within 24 hours of randomization. After the study unblinding, investigators discovered that the patient received tirofiban, which was thought to be the cause of his thrombocytopenia. Both abciximab and tirofiban are glycoprotein IIb-IIIa inhibitors, and thrombocytopenia induced by this class of drugs is a serious and potentially life-threatening adverse reaction. The mechanism is not well understood but has been described as immune mediated with both ligand-mimetic agents (tirofiban and eptifibatide) and abciximab. Our patient's situation was unusual in that he developed thrombocytopenia from a ligand-mimetic agent and subsequently had a similar reaction to abciximab. To our knowledge, this case report is the first documentation of thrombocytopenia associated with both tirofiban and abciximab in a single patient, and suggests that care should be given in administering glycoprotein IIb-IIIa inhibitors of either type to patients with a history of thrombocytopenia due to one of these agents.
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PMID:Abciximab-associated thrombocytopenia after previous tirofiban-related thrombocytopenia. 1650 24

The exponential increase in the numbers of percutaneous coronary interventions (PCIs) has led to many clinicians having to care for post-PCI patients. We review the management of early problems seen in post-PCI patients, such as vascular access site complications, contrast nephropathy, drug-induced thrombocytopaenia and chest pain. The management of possible restenosis and the use of stress testing are discussed. The complications from dual antiplatelet therapy are addressed. The prognosis of the post-PCI patient, the implications of co-existent heart failure and the newer technologies of implantable defibrillator and cardiac resynchronisation therapy are reviewed. We conclude by emphasising the importance of secondary prevention by risk factor modification as well as the communication between the clinician and the cardiologist.
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PMID:A review of the management of patients after percutaneous coronary intervention. 1670 Aug 59

Autoimmune hemolytic anemia (AIHA) is a well-known complication of chronic lymphocytic leukemia (CLL). In recent years the anti-CD20 monoclonal antibody rituximab has been used for the therapy of steroid-refractory AIHA and autoimmune thrombocytopenia, either idiopathic or in association with CLL. We report the results of rituximab treatment for 14 patients suffering from CLL-associated AIHA. They developed a direct antiglobulin test positive AIHA at a mean time of 47 months (range 0-135 months) from the diagnosis of CLL. In 3 cases AIHA was diagnosed at the same time as CLL. Only 1 patient had fludarabine-related AIHA. All patients received steroids as first-line treatment. At a mean time of 46 days (range 1-210 days) from the diagnosis of AIHA all patients received rituximab at a dosage of 375 mg/m(2)/weekly for 4 weeks. All patients except 3 (2 died of cardiac failure or sepsis soon after the third cycle and 1 HCV-positive patient experienced a rise in serum amino transferases) completed the scheduled four programmed cycles. First injection side effects of rituximab were minimal. All but 2 patients showed an increase in hemoglobin levels in response to rituximab (mean value 3.6 g/dl; range 0.7-10 g/dl) and a reduction in the absolute lymphocyte count and lymph nodes and spleen volume. Nine patients required packed red cell transfusions before starting rituximab; 5 no longer needed transfusions just after the second cycle and another patient after the fourth cycle. Three patients (22%) were considered to fully respond and 7 (50%) only responded partially. At a mean follow-up of 17 months, 8 patients were still alive, 6 of them transfusion-free. Our results prove that the anti-CD20 monoclonal antibody is an effective and well-tolerated alternative treatment for CLL-associated AIHA.
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PMID:Rituximab therapy for chronic lymphocytic leukemia-associated autoimmune hemolytic anemia. 1682 16

We experienced two cases of heparin-induced thrombocytopenia (HIT) which occurred during unfractionated heparin treatment. The first patient was a 72-year-old man, who was admitted to our hospital because of sudden onset dyspnea in January 2000. He was diagnosed as having a pulmonary embolism and heparin was started. Nine days later, progressive embolization of the pulmonary artery and femoral vein was found and thrombocytopenia (platelet count 20 x 10(9)/l) was observed 14 days after that. Cessation of heparin and administration of argatroban resulted in progressive normalization of the platelet count. The second patient was a 62-year-old woman, who was admitted to our hospital in April 2001, with the chief complaint of sudden onset dyspnea. She was diagnosed as having acute left-sided heart failure and heparin was started. Fifteen 15 days later, thrombocytopenia (platelet count 17 x 10(9)/l) was observed. Cessation of heparin resulted in normalization of the platelet count. Both cases were positive for anti-heparin-platelet factor 4 (PF4) antibody. Here we report on the clinical course of two cases of HIT with a review of the literature.
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PMID:[Two cases of heparin-induced thrombocytopenia (HIT) and a review of the literature]. 1698 15


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