Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic infection with Aspergillus fumigatus is an opportunistic disease that affects mainly immunocompromised hosts and is associated with a high mortality rate. We report a case of A. fumigatus endocarditis after an episode of thrombotic thrombocytopenic purpura. Diagnosis was established after sudden rupture of posterior papillary muscle of the normal native mitral valve. Soon after mitral valve replacement, Aspergillus endocarditis recurred, associated with multiple peripheral emboli, which necessitated a second operation.
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PMID:Aspergillus endocarditis in a native valve after amphotericin B treatment. 1546 17

Endogenous generation of nitric oxide (NO) plays an important role in the regulation of cardiovascular and inflammatory responses. This mediator is synthesized by a family of enzymes collectively known as NO synthase. Several isoforms of this enzyme have been identified and can be grouped as constitutive or inducible. Increased production of NO is reported in several inflammatory disorders, such as sepsis, arthritis, thrombotic thrombocytopenic purpura (TTP), and antiphospholipid syndrome. In addition, NO upregulates cyclo-oxygenase-2 and synthesis of several other inflammatory cytokines. Inflammation and thrombotic complications are usually associated with malignancy. Earlier reports indicate the upregulation of tumor necrosis factor-alpha (TNF-alpha), C-reactive protein (CRP), and tissue factor (TF) in patients with malignancy. To determine the relationship between inflammatory cytokines and NO in cancer patients with hypercoagulable states, baseline plasma samples from 160 patients with confirmed malignancy and hypercoagulable state were analyzed for NO levels. A chemical method based on a chemiluminescent reaction between NO and ozone using a highly sensitive gas phase NO analyzer was used. CRP, TF, and TNF-alpha were measured using enzyme-linked immunosorbent assay methods. Of the 160 patients who were plasma tested, the baseline NO levels ranged from 13.7 to 98.6 microM (63.1+/-15.9 microM, mean+/-SD) in contrast to age-matched control, which ranged from 9.1 to 34.6 microM (19.8+/-6.2 microM, mean+/-SD, n=138). Cancer patients also showed marked variations in the NO levels. Eighteen of 60 cancer patients exhibited greater than 60 microM NO levels. The CRP, TNF-alpha and TF were also significantly elevated. A correlation between CRP (r(2)=0.73) and NO levels was noted in cancer patients with hypercoagulable state. These data suggest that the pathogenesis associated with malignancy/hypercoagulable state is associated with an inflammatory component. In addition, the observed hemodynamic changes in some of the cancer patients may be due to increased NO production.
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PMID:Blood levels of nitric oxide, C-reactive protein, and tumor necrosis factor-alpha are upregulated in patients with malignancy-associated hypercoagulable state: pathophysiologic implications. 1549 22

Deficiency of ADAMTS13 is found in patients with thrombotic thrombocytopenic purpura (TTP), and the genetic defects in the ADAMTS13 gene or the autoantibody against ADAMTS13 is thought to be responsible for the development of TTP. The clinical correlation and mechanisms of secondary ADAMTS13 deficiency in other disease states were investigated. In addition to TTP, ADAMTS13 levels were severely decreased in patients with sepsis-induced disseminated intravascular coagulation (DIC). The incidence of acute renal failure and serum creatinine levels in patients with ADAMTS13 activity levels lower than 20% (incidence, 41.2%; creatinine, 160 +/- 150 microM [1.81 +/- 1.70 mg/dL]) (P < .05) were significantly higher than they were in patients with ADAMTS13 activity levels higher than 20% (incidence, 15.4%; creatinine, 84 +/- 67 microM [0.95 +/- 0.76 mg/dL]) (P < .01). Additionally, unusually large von Willebrand factor multimers were detected in 26 (51.0%) of 51 patients with ADAMTS13 activity levels lower than 20%. Lower molecular weight forms of ADAMTS13 were found in the plasma of patients with sepsis-induced DIC, suggesting that the deficiency of ADAMTS13 was partially caused by its cleavage by proteases in addition to decreased synthesis in the liver. These data suggested that severe secondary ADAMTS13 deficiency can be associated with sepsis-induced DIC and may contribute to the development of renal failure.
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PMID:Severe secondary deficiency of von Willebrand factor-cleaving protease (ADAMTS13) in patients with sepsis-induced disseminated intravascular coagulation: its correlation with development of renal failure. 1618 76

Salmonella species may cause wide spectrum of infections changing from enterocolitis to sepsis. However, Salmonella meningitis in adults is a rare but important clinical condition with a high mortality rate. In this report, a 71 years old male patient with Salmonella enteritidis meningitis who was followed-up with the diagnosis of immune thrombocytopenic purpura and had been administered azothioprin and prednisolone, has been presented and similar cases in the literature have been reviewed. The cerebrospinal fluid culture yielded S. enteritidis, and the isolate was intermediate susceptible to ampicillin, susceptible to cefotaxime, trimethoprim-sulphametoxasole, ciprofloxacin and chloramphenicol. Our patient was successfully treated with ceftriaxone (2 x 2 gr i.v.) and discharged with total cure.
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PMID:[Salmonella enteritidis: an unusual meningitis agent in an adult patient]. 1654 53

Thrombotic microangiopathic hemolytic anemias include thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS) and pregnancy associated thrombotic microangiopathy (TMA). Eight adult patients (four males and four females) with TMA who were treated between 2003 and 2004 at the Hospital Italiano de Buenos Aires were reviewed. The average age was 40. Clinical diagnosis of TMA was made on admission in four patients. During their stay in hospital, 4 patients developed HUS characteristics, three as TTP and one presented pregnancy associated TMA. All of them revealed thrombocytopenia and microangiophatic hemolytic anemia. Renal impairment was the third most frequent characteristic at presentation. The patients with TTP revealed the most severe condition. All patients received daily plasma exchange. Immunosuppressants were also used. Four patients recovered completely, 2 passed away, one remains with renal impairment and requires hemodialysis, and a colectomy was performed on one of them. The TMA syndromes are occlusive disorders associated to platelet microvascular thrombi. Systemic and renal circulations are primarily affected. TTP/HUS might represent an overlapping spectrum of idiopathic or secondary disease. Prompt recognition and treatment are vital, because high mortality occurs due to these disorders. Among the differential diagnosis of TMA we can refer to sepsis, neoplasms, systemic vasculitis, eclampsia and others. The mainstay treatments are daily plasma exchange and infusion with fresh frozen plasma. Improving the management of these diseases is required considering their high morbidity and mortality.
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PMID:[Thrombotic microangiopathy in adults]. 1697 62

Thrombotic thrombocytopenic purpura (TTP) has been associated with scleroderma renal crises (SRC) in the past. However such reports markedly diminished after the onset of ACE inhibitor use. Recently, reports again have surfaced that describe scleroderma patients presenting with clinical evidence of TTP. We describe a 50-year-old female with longstanding limited cutaneous scleroderma who presented with hematochezia and thrombocytopenia along with other findings suggesting TTP. A colon biopsy revealed thrombi within the lumen. Her course was complicated by renal failure and hypertension that did not respond to ACE inhibitor therapy alone. She improved after a course of plasma exchange. She was discharged home only to return 2 months later with grand mal seizures and hypertension. During her course she developed adult respiratory distress syndrome. She again responded to plasma exchange and she was discharged home. She has remained stable for 2 years. This report emphasizes the importance of fully evaluating patients with longstanding limited cutaneous scleroderma who present with renal failure, hypertension, and thrombocytopenia in association with multiorgan complications. All possible etiologies, including SRC, TTP, vasculitis, and sepsis should be considered. Tissue biopsies (in this case, a colon biopsy revealed thrombi within the vessel lumen) may prove beneficial in assisting with the diagnosis. For such patients who fail treatment with ACE inhibitors, plasma exchange may be considered.
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PMID:Thrombotic thrombocytopenia purpura in a patient with systemic sclerosis. 1703 6

Microparticles (MP) derived from vascular endothelium or circulating blood cells circulate in the peripheral blood. They originate from blebbing and shedding from cell membrane surfaces in physiological and pathological conditions and are present in low concentrations in normal plasma. Increased levels are generated by a number of mechanisms including platelet activation, direct vascular endothelial damage, thrombin activity on the cell surface, C5b-9 activation, and PF4-heparin-antibody interaction. Several techniques are currently used to study the generation and nature of circulating microparticles. In particular, the genesis and role of microparticles, derived from platelets, endothelial cells and monocytes, in sepsis (especially meningococcal-induced), heparin-induced thrombocytopenia (HIT), thrombotic thrombocytopenic purpura (TTP), aplastic anaemia, paroxysmal nocturnal haemoglobinuria (PNH) and sickle cell disease (SCD) have been well studied, and provide important insights into the underlying diseases. A defect in the ability to form microparticles leads to the severe bleeding disorder of Scott syndrome, which in turn provides a revealing insight into the physiology of coagulation. In addition the complex role of microparticles in vascular and cardiovascular diseases is an area of immense interest, that promises to yield important advances into diagnosis and therapy.
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PMID:Circulating microparticles: pathophysiology and clinical implications. 1711 1

Several case reports have suggested an association between infections and thrombotic thrombocytopenic purpura (TTP). In Case 1, a 37-year-old female presented with TTP 6 times over 7 years, requiring 242 therapeutic plasma exchanges (TPE), for a per-course range of 4-57 TPE (median 48), and treatment durations of 4-241 days (median 71 days), largely on account of multiple exacerbations (range 0-3, median 3). Twelve of 17 (71%) of her presentations or exacerbations were associated with suspected infections, with confirmation in 9 episodes. These included pulmonary TB, CMV pneumonitis, mucocutaneous HSV, ventilator-associated or urinary tract-associated gram-negative sepsis, central line-associated staphylococcal bacteremia, and cellulitis. Except for TB, all infections occurred after splenectomy, which had been performed on day 33 of presentation 1. In Case 2, a 24-year-old female presented with TTP 3 times over 15 months. Her courses were managed with brief courses of TPE (5-11 treatments per course, median 5). Suppressed ADAMTS13 levels due to inhibitors were confirmed twice. Presentation 1 was antedated by atypical community acquired pneumonia. Presentation 3 (and possibly 2) followed prolonged, progressive, antibiotic-refractory periodontal infections ultimately requiring exodontic surgery. Our cases add to a literature that suggests that infection may be associated with exacerbations or relapses of TTP in some patients. Our patients demonstrated repeated TTP exacerbations in association with different infectious agents. A better understanding of the possible relationship between infection and clinical expression of TTP might lead to improved treatment decisions for patients with this complex illness.
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PMID:Do infections provoke exacerbations and relapses of thrombotic thrombocytopenic purpura? 1728 17

Thrombotic thrombocytopenic purpura (TTP) describes syndromes with multiple etiologies, some of which are rapidly fatal without plasma exchange treatment. Although there have been advances in understanding the pathogenesis of TTP, evaluation and management remain difficult because there are no specific diagnostic criteria, as TTP can be clinically similar to other acute disorders, such as sepsis, disseminated malignancy, malignant hypertension, and preeclampsia, and because urgent treatment is required. An unexpected observation of anemia and thrombocytopenia should trigger consideration of TTP; evidence that the anemia is due to microangiopathic hemolysis, suggested by the presence of red cell fragmentation on the blood smear, supports the diagnosis. When the diagnostic criteria of microangiopathic hemolytic anemia and thrombocytopenia without an apparent alternative etiology are fulfilled, plasma exchange treatment is appropriate. However, plasma exchange has risks for severe complications and death; therefore, this management decision must be balanced against the confidence in the diagnosis. With plasma exchange treatment, approximately 80% of patients survive, in contrast to only 10% in the era prior to the availability of plasma exchange. The continuing mortality from TTP, the risks of plasma exchange treatment, and the potential for recurrent episodes of TTP are clinical challenges that remain to be solved.
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PMID:Evaluation and management of patients with thrombotic thrombocytopenic purpura. 1745 28

We reported a Japanese first case of thrombotic thrombocytopenic purpura (TTP) induced by clopidogrel, a newly developed antithrombotic drug, marketed in May 2006 in Japan. This 80 years old woman developed cerebral infarction and suffered from Broca's aphasia and right hemiparesis. Clopidogrel was started on Day 6 after the onset. On Day 10, four days after the administration of clopidogrel, two egg-sized purpura with marked decrease in platelet count was found. The purpura extended over the entire body in next few days. Despite total seven times of plasma exchange, platelet count did not normalize. Twenty four days after the onset of TTP, the patient developed central catheter infection and died of sepsis. TTP will become a lethal side effect of clopidogrel, when diagnosis and treatment are late. Because it is assumed that the mechanism of clopidogrel induced TTP differs from that of ticlopidine, we should establish firm treatment urgently.
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PMID:[Case of thrombotic thrombocytopenic purpura associated with clopidogrel]. 1893 79


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