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)

In a pilot clinical trial, treatment of patients with advanced colorectal carcinoma with the combination of fluorouracil (5FU) and recombinant interferon alfa-2a (IFN) resulted in objective tumor regression in 62% of patients. To confirm these findings in a multiinstitutional setting, a phase II clinical trial was initiated by the Eastern Cooperative Oncology Group (ECOG) in 1989. The treatment regimen was identical to that used in the earlier study: 5FU 750 mg/m2/d for 5 days as a continuous infusion followed by weekly outpatient bolus therapy and IFN 9MU subcutaneously beginning day 1 and administered three times per week. Doses were modified for gastrointestinal, hematologic, and neurologic toxicity and for fatigue, similarly to those used in the previous pilot trial. Thirty-eight patients were registered; 36 are evaluable for response (one lost to follow-up and one with nonmeasurable disease). All patients had metastatic or locally recurrent disease beyond the scope of resection; 31 of 38 had liver metastases, and 20 of 38 had two or more sites of involvement. Eight patients had grade 4 toxicities, including sepsis (nonneutropenic) (one), watery diarrhea (two), and granulocytopenia (six). Grade 3 neurologic toxicities were observed in two (5%) patients and included slurred speech and gait disturbance. Objective response was 42% (95% confidence interval [Cl], 27% to 58%), including one clinical complete responder and 14 partial responders. Among the responding patients, the median time to treatment failure was 8 months. Two patients remain on treatment at 10+ and 16+ months: median survival has not been reached. The results of this multiinstitutional trial suggest that the addition of IFN to 5FU enhances the objective response rates achieved in patients with advanced colorectal carcinoma and that the toxicities of this regimen are acceptable.
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PMID:Phase II trial of fluorouracil and recombinant interferon alfa-2a in patients with advanced colorectal carcinoma: an Eastern Cooperative Oncology Group study. 191 31

23 cases of drug-induced blood disorders were reported from 7 hospitals in Chugoku district. These cases were treated between Oct 1982 and Jun 1990. These included 5 cases of anemia, 2 cases of leukopenia, 6 cases of thrombocytopenia, 1 case of anemia and leukopenia, 2 cases of anemia and thrombocytopenia, and 1 case of leukopenia and thrombocytopenia. There was a case of methemoglobinemia due to Sedes-G. A patient of agranulocytosis due to cimetidine died of sepsis. The all other patients recovered. The reported drugs which induced blood disorders were analgesics, anticonvulsant agent, chemotherapeutic agent, antituberculosis agent, and H2 receptor blockade, etc. in order of number. The drugs in 3 cases were definitely thought to be the cause of blood disorders, probably in 18 cases, and possibly in 2 cases.
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PMID:[Cases of drug-induced blood disorders in Chugoku district]. 192 Aug 32

Thirty-six cases of drug-induced blood dyscrasias were collected in Kinki District. They were consisted of 14 agranulocytosis, 9 agranulocytosis with anemia, 7 pancytopenia, 2 anemia (hemolytic anemia and pure red cell aplasia), 2 thrombocytopenia and 2 agranulocytosis with thrombocytopenia. The causative agents were 10 antibiotics, 10 cardiovascular drugs, 5 anti-rheumatic drugs, 3 antithyroid drugs and 3 anticonvulsants. Six patients with advanced age died from sepsis within 14 days after the onset of agranulocytosis.
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PMID:[Drug-induced blood dyscrasia in Kinki district]. 192 Aug 33

Clinical data of 70 patients, treated and observed with myelodysplastic syndrome between 1977 and 1989 were analysed. Two-thirds of the patients belonged to the elder age-group and a mild female predominance was registered. With the application of complex cytochemical-histological and cytogenetical methods, correct diagnosis could be established. The clinical material included patients from different morphologic subtypes: 19 with refractory anaemia (with a longer course of the illness). 20 with sideroblastic anaemia, 26 with chronic myelomonocytic leukaemia and the remaining 5 with refractory anaemia with excess of blasts (a more progressive type of the myelodysplastic syndrome, with a short duration). The mean survival of all patients were 42 months. 45 (69%) died during this period and 12 (18.5%) among them in acute myelogenous leukaemia (mean survival: 16 month). Megakaryoblastic leukaemic transformation was observed in three patients with sideroblastic refractory anaemia. Haemorrhage and infection-sepsis, due to thrombocytopenia and/or granulocytopenia, was fatal in 30 cases. In the treatment of the myelodysplastic syndrome an appropriate supportive therapy (blood transfusion, antibiotics) has a decisive importance. A more aggressive treatment with cytostatic drugs is suggested in the progressive form of the disease of younger patients and in patients with overt acute leukaemia.
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PMID:[The myelodysplastic syndrome]. 206 28

Twenty haemophiliacs (17 CDC group IV and 3 CDC group II) were treated with zidovudine for a median of 37 weeks (range 10-66). Eight (40%) tolerated zidovudine without a dose change. Two patients died and five patients (29%) developed opportunist infections. Haematological toxicity occurred in ten CDC IV patients (59%) but only one case of sepsis occurred in 101 episodes of documented granulocytopenia. Thrombocytopenia responded to treatment with zidovudine in four of five patients. It is concluded that zidovudine is beneficial for symptomatic haemophiliacs and although the haematological toxicity is high, it is mostly asymptomatic, reversible and well tolerated. Two of the three CDC II patients treated with zidovudine progressed to CDC IV, but had low initial T4 lymphocyte counts and were P24 antigen positive.
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PMID:Zidovudine treatment for anti-HIV positive haemophiliacs. 208 77

The mesna, doxorubicin, ifosfamide, dacarbazine regimen produced a 47% response rate (including 10% complete responses) in 105 eligible adults with advanced sarcoma. The major dose-limiting toxicity was granulocytopenia. There was one toxic death from sepsis. Central nervous system and renal toxicity occurred infrequently, perhaps as a result of the continuous-infusion schedule. This regimen is being evaluated further in advanced disease, the adjuvant setting, and in combination with bone marrow colony-stimulating factors.
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PMID:Mesna, doxorubicin, ifosfamide, dacarbazine (MAID) regimen for adults with advanced sarcoma. 211 Mar 85

GBS (Group B Hemolytic Streptococci) cause pulmonary hypertension with associated neutropenia. We investigated whether there is a correlation between the neutropenia of sepsis and GBS-induced pulmonary vasoconstriction, through study of the effects of inhibiting pulmonary vasoconstriction on the neutropenia of GBS in newborn piglets. Fifteen piglets were infused with GBS. After one hour, animals were given either a thromboxane inhibitor (DAZ), a combined cyclooxygenase/lipoxygenase inhibitor, BW755C, or placebo. With GBS infusion, WBC and PMN counts dropped steadily, from similar baselines, to 2250 +/- 570, 3300 +/- 500 and 5400 +/- 1100 cells/mm3 respectively (p less than 0.05; DAZ and BW vs. placebo). PMN's dropped similarly to 710 +/- 320, 2390 + 1240 and 3130 +/- 1050 cells/mm3 respectively (p less than 0.05; DAZ vs. BW and placebo). The drop in WBC's predominantly resulted from proportional decreases in PMN's (DAZ: r = 0.98; BW: r = 0.88; placebo r = 0.93). Compared to GBS alone, DAZ reduced pulmonary vasoconstriction, but exacerbated the granulocytopenia. BW755C similarly reduced pulmonary hypertension: however, it ameliorated the exacerbation of GBS induced neutropenia described above. These data imply that there is no direct correlation between GBS induced granulocytopenia and pulmonary hypertension.
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PMID:Prostanoid inhibition and group B hemolytic streptococci (GBS) induced neutropenia in newborn piglets. 212 31

Doxifluridine, a new fluorouracil analog with a low myelosuppressive effect, has recently been subject to various disease-oriented, Phase II trials. For the present evaluation of drug tolerance, the Phase II data of 114 patients having received 376 doxifluridine cycles has been used. The treatment cycles consisted of 5 daily intravenous injections of 4,000 mg/m2 non-pretreated patients, and 3,000 mg/m2 in pretreated patients. Previous observations showing that doxifluridine is less myelotoxic than fluorouracil have been confirmed. 54% of the patients had no leucopenia (maintaining WBC counts over 3,000/mm3 and 90% had no thrombopenia (platelets not lower than 100,000/mm3) throughout treatment. However, a WHO grade 4 hematologic toxicity was observed in 9 patients, and 2 toxic deaths were related to severe granulocytopenia and sepsis. Digestive tract toxicity was similar and equally frequent as the one observed with fluorouracil: mucositis with oral ulcerations (19%), nausea and vomiting requiring specific treatment (8%) and severe but never hemorrhagic diarrhoea (5%). Neurologic toxicity was frequent, with 20% of patients complaining of somnolence and/or peripheral neuropathy, 7% of impaired consciousness and 1% of WHO grade 4 cerebellar ataxia. Among the 10% of patients with cardiac symptoms, 6% were benign and transient arrhythmias, and 4% were severe, including 1 myocardial infarction, 1 spontaneously reversible cardiac arrest and 2 ventricular fibrillations successfully treated with cardioversion. In spite of its encouraging antitumor activity and its good hematologic tolerance, intravenous doxifluridine, as used in this study, cannot be recommended because of the observed neurologic and cardiac toxicity. Oral doxifluridine is presently under investigation with preliminary results suggesting a lack of neuro- or cardiotoxicity.
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PMID:[Doxifluridine toxicity, a fluorouracil analog with low myelosuppressive effect]. 214 Feb 80

That there are so many models of sepsis and septic shock is tacit evidence that none of them are perfect. Although sepsis presents in many forms clinically, most clinicians would probably agree that virtually all severely septic patients manifest respiratory failure and ventilator dependence. Furthermore, failure of organs other than the lungs typically occurs days to weeks after the onset of the septic process. Although early deaths occur commonly in some situations (e.g., meningococcemia, pneumococcal bacteremia in asplenic individuals, Gram-negative bacteremia in the setting of profound granulocytopenia), most deaths due to sepsis occur after a protracted course in an intensive care unit. Thus, for certain important experiments, there is a need for an animal model of severe chronic sepsis characterized by these features: persistent hypermetabolism, low systemic vascular resistance, respiratory failure severe enough to require mechanical ventilation, late (nonpulmonary) organ system failure, and death. Obviously, creation of such a model will require a major commitment of resources, because it will require, in essence, the creation of an animal intensive care unit. Nevertheless, we believe that progress in sepsis-related research would be substantially facilitated were such a model available. Even without such a model, progress will continue in this field. A wide variety of good animal models are already available to investigators. In the next decade, as new methods, such as the powerful tools of molecular biology, are applied to problems related to the sepsis syndrome, these models will be invaluable in improving our understanding of pathophysiology and in developing new and more effective approaches toward therapy.
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PMID:Laboratory models of sepsis and septic shock. 219 35

The elastase-alpha1-proteinase inhibitor complex (E-alpha 1-PI) is a well known, sensitive indicator of infection. The significance of this parameter was investigated in 12 febrile paediatric-oncological patients. With neutrophil counts greater than 500/microliters infections caused a definitive increase in E-alpha 1-PI serving as an additional diagnostic parameter. E-alpha 1-PI provided no additional information in situations of sepsis with leukopenia and simultaneous agranulocytosis. In patients with metastatic tumours, the assay of E-alpha 1-PI may differentiate between infection-related and tumour-related serological disturbances.
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PMID:[Value of the elastase-alpha 1-proteinase inhibitor complex in pediatric oncologic patients with fever]. 231 98


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