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)

A 26-year-old male who had been diagnosed as pulmonary tuberculosis three years ago with an antituberculous chemotherapy of only two months, complained of tiredness, exertional dyspnea and fever since a month ago. Bloody sputum, bloody stool and hematuria have developed three days before admission. Petechiae over the body trunk and lower extremities were observed on admission. Peripheral blood examination revealed lymphocytopenia (672/microliters), low hemoglobin content (6.2 g/dl), thrombocytopenia (3,000/microliters), elevated FDP (36.2 micrograms/ml) and D-dimer (25.0 micrograms/ml) values. Chest radiograph showed a massive pleural effusion in the right hemithorax, bilateral pulmonary infiltrates and a cavity on CT scan. Together with positive acid-fast bacilli in sputum, diagnoses of relapsed pulmonary tuberculosis, tuberculous pleurisy associated with DIC (disseminated intravascular coagulation) were made. Left hydronephrosis which was presumed to be a consequence of infundibulum stenosis due to renal tuberculosis, was detected by abdominal ultrasonography. Treatment with antituberculous drugs and protease inhibitors were started with thoracic tube drainage. DIC condition was improved by the 20th hospital day and sputum culture turned to be negative after the 4th week, however, fever up to 38 degrees C continued until the end of the 7th week and a D-dimer which is a representative marker for secondary fibrinolysis, continuously showed a high level up to the 10th week of hospitalization. The patient was uneventful during the three months follow up period after discharge. DIC is a well known complication of sepsis including miliary tuberculosis, whereas it is rarely associated with cavitary tuberculosis and no case of prolonged elevation of D-dimer have been reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of pulmonary, pleural, and renal tuberculosis associated with DIC and a prolonged increase in D-dimer]. 804 Oct 60

We measured various coagulable factors and molecular markers in plasma and serum in the disease group including DIC, DIC suspect, thrombosis, acute myocardial infarction, angina pectoris, sepsis, malignant tumor and type II diabetes and the healthy subject group, and surmised the intravascular coagulative-fibrinolytic activity in each disease group compared with the healthy group. Additionally we selected parameters useful for early detection of the pre-thrombotic state and hypercoagulable state. As a result, of the parameters for the coagulative system, those considered useful were the assay of soluble fibrin monomer complexes using the synthetic substrate (FM.Oita), assay of soluble fibrin monomer complexes using HPLC(SFMC.Oita) and thrombin-anti-thrombin III complex (TAT) in this order. Of the parameters for the fibrinolytic system, those considered useful were FDP assay using ELISA (FDP.Oita) and plasmin-alpha 2 plasmin inhibitor complex (PIC). This FDP.Oita had a considerably high detection sensitivity compared with the FDP assay (Diayatron Co.) using the latex photometric immunoassay which has been commercially available. When measurement was made with plasma and serum in the subject disease group as the sample by the high sensitivity assays mentioned above, it was made clear that both the coagulative activity and fibrinolytic activity are increased, albeit with some differences in intensity, in all the disease groups compared with the healthy group. In order for the hypercoagulable state and pre-thrombotic state to be detected, it is important to know the balance between the coagulative activity and fibrinolytic activity. According to the results of the present experiment, a significant directly proportional correlation was recognized between FM.Oita and FDP.Oita and between TAT and FDP.Oita. Therefore, examination of these ratios will be a more detailed indicator of coagulative-fibrinolytic activity than the TAT/PIC ratio, PAI-1/TPA ratio and ATIII/alpha 2 PI ratio hitherto in use. If useful molecular markers such as FM.Oita are measured over time in various cases and these data are compiled and analyzed statistically, it will not be long before the criteria for the hypercoagulable state and pre-thrombotic state are established.
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PMID:[Molecular marker for detecting hypercoagulable state]. 810 79

C1-Inhibitor (Berinert, C1 INH), a 104 kDa protein, inhibits complement components (C1 esterase) as well as enzymes of the contact phase of coagulation (Factor XII, Factor XI) and kallikrein, thus regulating kinin generation. C1 INH is used for the treatment of the hereditary angioneurotic edema. This paper will give a survey about the evidence in recent literature concerning the potential efficacy of the compound on other diseases associated with shock, capillary leakage and inflammation as well. In our own experiments we evaluated whether the compound could influence acute inflammatory reactions or the severe systemic inflammatory response syndrome (SIRS) as a consequence of an experimental septic shock. To prevent the sepsis-induced DIC we co-infused the thrombin inhibitors AT III or rec. hirudin in combination with C1 INH. Coinfusion of C1-inhibitor (50-200 U/kg x h) with either rec. hirudin or AT III significantly improved survival rate compared to thrombin inhibitor alone.
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PMID:Influence of C1-inhibitor on inflammation, edema and shock. 817 80

Inflammation and coagulopathies are currently thought to play a role in the pathogenesis and pathophysiology of many forms of critical illness, particularly sepsis, multiple organ dysfunction, DIC, and reperfusion injury. Because much of the new pharmacologic research and therapy focuses on inflammation and coagulation mechanisms, it is imperative for the critical care nurse to have a basic understanding of these two complex mechanisms to intelligently and safely administer these drugs and to increase his or her understanding of the disease process and its manifestations. This article will provide an overview of the significant features of inflammation and coagulation and their close relationship. Major clinical syndromes affecting the critical care population will then be described relative to these inflammatory and coagulation events.
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PMID:Mediators of coagulation and inflammation: relationship and clinical significance. 821 38

In the development of sepsis DIC is a common complication. Several studies presented in this paper show a coincidence between the development of DIC and depletion of Antithrombin III, a serine protease inhibitor which inhibits a large scale of activated clotting factors. It seems very probable that substitution therapy should be of benefit in the treatment of sepsis-related DIC and may improve the outcome of septic patients. Physiological and clinical findings are put together to clarify the basic rationale for running clinical trials and future studies.
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PMID:AT III in septicemia with DIC. 822 35

The pathophysiology of sepsis and septic shock is extremely complex and ultimately involves every physiological pathway. The initiating event is the entrance of endotoxin or similar substances into the blood which initiates the release of multiple mediators. These are designed to react locally and to protect the organism. Their constant release, however, sets in motion up- and down regulations, ultimately resulting in "metabolic anarchy". Tumor necrosis factor alpha and other cytokines trigger several systems, especially coagulation to yield DIC, and the complement system. Many treatment modalities have been developed, most recently those which substitute inhibitors of various systems. Antithrombin III concentrates and potentially protein C concentrates are designed to arrest DIC. C1-esterase inhibitor concentrates should intercept the activation of the complement system and the contact phase of coagulation and its relationship to kinin generation. Even newer approaches entail antibodies to tumor necrosis factor alpha or endotoxin itself. The complex process of sepsis will undoubtedly require a multifaceted therapeutic approach.
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PMID:Perspectives for the future. 822 36

A 75-year-old female was admitted to our hospital because of fever and hypotension. The peripheral blood showed 400 leukocytes/microliters with 13,000/microliters platelets. Bone marrow puncture revealed that NCC stood at 14,000 with 50.0% blasts. The surface characters of the blasts were CD13+, CD33+, and HLA-DR+, and blood culture tests were positive. Coagulation tests revealed DIC. Based on the foregoing results, hypoplastic leukemia was diagnosed accompanied by sepsis and DIC, and was placed on the concomitant administration of a combination of low dose Ara-C and M-CSF. After 14 days of Ara-C administration and 26 days of M-CSF, her clinical symptoms improved, with the peripheral blood showing a WBC of 2,800/microliters and platelet count of 111,000/microliters. The percentage of myeloblasts decreased to 7.0%. After the administration of Ara-C was suspended for 2 weeks, another course of low dose Ara-C plus M-CSF administration was carried out and the patient achieved full remission. M-CSF stimulates not only the production of monocytes but increases the number of neutrophils and platelets through monocytes. It is also expected that tumoricidal activity may be realized by the activation of monocytes. In this patients, the concomitant administration of M-CSF and low dose Ara-C was remarkably effective in treating hypoplastic leukemia with severe complication. This result suggests that M-CSF will be useful for the treatment of leukemia.
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PMID:[Hypoplastic leukemia which achieved remission with administration of M-CSF along with low dose ara-C]. 831 38

Biochemical observations during clinical sepsis using functional and immunological measurements of enzymes, cofactors and inhibitors of the kallikrein-kinin system indicate that activation of these proteases occur during hypotensive gram-negative septicemia and adult respiratory distress syndrome. Using animal models of septicemia, we demonstrated that protease inhibitors or neutralizing monoclonal antibodies to proteins of the contact system inhibit or prevent the formation of kallikrein and the decrease in kininogen. In addition, the irreversible phase of hypotension can be prevented and survival prolonged. Thus, bradykinin is one of the important mediators of hypotension. In contrast, the contact system plays little role in the associated DIC. In cardiopulmonary bypass, the formation of kallikrein leads to neutrophil degranulation and release of elastase. Selective inhibitors of kallikrein not only block its activation but play a predominant role in inhibiting elastase release.
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PMID:Factor XII activation and inhibition in inflammation. 835 19

The patient, a 70-year-old man, diagnosed as having left pneumothorax and hydrothorax, was admitted and had a thoracic drain inserted. The evacuation of stool was noted from 3 days after insertion. With the abscess in the left thoracic cavity shown on emergency CT, a diagnosis of perforation of the digestive tract in the left thoracic cavity was made and emergency operation was performed. On the basis of the intraoperative findings, the case was diagnosed as adult Bochdalek hernia with intrathoracic colon perforation, and repair of hernia and colostomy were done by laparotomy and thoracotomy. However, the patient died of DIC and sepsis 5 days after operation. Two cases of adult Bochdalek hernia complicated with spontaneous pneumothorax have hitherto been report. However, there has been no reported case which had adult Bochdalek hernia complicated with pneumothorax considered due to intrathoracic colon perforation as in this case. So this case was considered very rare and worthy of reporting.
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PMID:[A case of intrathoracic colon perforation due to adult Bochdalek hernia]. 836 Nov 13

During the 19-month study period, 48 (2 per cent) of the 2177 neonates admitted to the neonatal intensive care unit (NICU) yielded Pseudomonas aeruginosa growths in blood cultures. All these neonates had clinical and haematological evidences of sepsis. Prominent clinical features included sclerema, violaceus necrotic patches, necrotizing enterocolitis (NEC), conjugated hyperbilirubinaemia, and DIC. Over all mortality was 23 per cent, distinctly higher in premature neonates with RDS. The mean gestational age and birth weights (+/- SD) of these neonates were 36.42 (+/- 2.73) weeks and 2173.34 (+/- 567.33) g, respectively. Approximately half of the total cases had low birth weight. Other adverse perinatal events before the development of sepsis included birth asphyxia (60 per cent), neonatal resuscitation (67 per cent), meconium aspiration syndrome (29 per cent), hyaline membrane disease (8 per cent), prolonged hospitalization (44 per cent), closed incubator care (17 per cent), prolonged intravenous fluids (42 per cent), repeated blood sampling (63 per cent), and umbilical catheterization (4 per cent). Analysis of the trend of Pseudomonas sepsis in our NICU revealed six definite outbreaks (more than two cases) interspersed with occasional (one or two) cases. Six study months, however, remained free of Pseudomonas sepsis. Index case was demonstrable on seven occasions. Bacteriological surveillance of the NICU after onset of initial case/cases revealed statistically significant colonization of resuscitation equipment, baby placement sites, and various cleansing solutions by the same bacterial species (P < 0.05). It is possible that Pseudomonas was introduced to our NICU from transfer admissions from other hospitals since on four occasions index case was the one transferred from outside.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiology of Pseudomonas aeruginosa infections in a neonatal intensive care unit. 844 85


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