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)

Twenty-seven ill neonates with enterovirus infections were studied to learn if enterovirus infection can be distinguished from neonatal sepsis. Enterovirus infection was associated with the summer-fall season (93%), recent maternal illness (59%), absence of other perinatal problems (81%), and findings of fever (93%), viral meningitis (62%), diarrhea (81%), and rash (41%). Four children developed thrombocytopenia and three necrotizing enterocolitis. Three children died, all with Coxsackie B virus infections that likely were acquired in utero. Although no single feature is pathognomonic, this constellation of epidemiologic and clinical findings, coupled with negative bacterial cultures, should suggest the possibility of neonatal enterovirus infection.
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PMID:Enterovirus infections in neonates. 97 29

Disseminated intravascular coagulation (DIC) is a syndrome of deposition of platelet-fibrin thrombi in the microcirculation, with consumption of platelets and clotting factors and possible clinical features of bleeding or thrombosis or both. It may be produced by activation of coagulation, platelet aggregation or endothelial damage. It is not a primary disease, but a common and important complication of many serious illnesses, especially sepsis, carcinoma and obstetrical accidents. Shock and acidosis are frequent precipitating factors, and vitamin K deficiency is a common complicating factor. DIC usually produces no clinical features, but it may give rise to bleeding, ischemic organ damage or shock. Although its clinical contribution is often difficult to separate from that due to the underlying disease, DIC remains the commonest cause of a generalized bleeding tendency in acutely sick patients. Laboratory confirmation consists of the demonstration of thrombocytopenia, coagulation impairment, hypofibrinogenamia, raised levels of fibrin degradation products, and positive results of para-coagulation tests. The most important therapeutic measure is control of the underlying disease, but replacement therapy and heparin may be required, especially if bleeding is significant and the process is not acute and self-limited.
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PMID:Disseminated intravascular coagulation. 107 54

Between August 1985 and June 1986, 49 previously untreated patients with locally advanced or metastatic non-small-cell lung cancer (NSCLC) were treated with the combination of cisplatin 80 mg/m2 i.v. on day 1, vindesine 3 mg/m2 i.v. on days 1 and 8, and mitomycin-C 8 mg/m2 i.v. on day 1 (MVP), repeating after an interval of 4 weeks, and thereafter every 6 weeks. The median age for all patients was 62 years, with a range of 21 to 77 years. All patients had a performance status of 0, 1, or 2 (ECOG scale) and measurable disease. Histologic types included squamous cell carcinoma (22 patients), adenocarcinoma (22 patients), and large-cell carcinoma (6 patients). Forty-eight patients were evaluable for response. Out of 48 patients, one (2%) achieved a complete response and 24 patients (50%) achieved a partial response, resulting in an overall response rate of 52% (95% confidence interval, 38-68%). The response rates were 52% for squamous cell carcinoma, 45% for adenocarcinoma, and 80% for large-cell carcinoma, respectively. The median duration of response was 4.2 months and the median duration of survival for all patients was 10.6 months. The major toxicity was myelosuppression. Leukopenia and thrombocytopenia of grade 3 or 4 occurred in 85% and 33%, respectively. One patient died of sepsis associated with leukopenia. Other toxicities were manageable and reversible. In conclusion, the MVP regimen was active and tolerable in patients with advanced NSCLC. Prospective randomized study comparing the MVP regimen with the two-drug combination of vindesine and cisplatin is warranted.
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PMID:Mitomycin C, vindesine, and cisplatin in advanced non-small-cell lung cancer. A phase II study. 131 68

We administered one course of 2-chlorodeoxyadenosine (2CdA) at 4 mg/m2 daily for 7 days by continuous intravenous infusion to 46 patients with hairy cell leukemia. Complete remissions occurred in 36 patients (78%; 95% confidence limits, 63% to 89%), partial remissions in five (11%), and a minor response in one. One patient died of candida sepsis 3 weeks after beginning treatment and three patients were clearly resistant to therapy. These three either had morphologically atypical hairy cells, less than 20% of which expressed Ig light chain on the cell surface, or had failed prior treatment with deoxycoformycin and interferon-alpha. At a median of 37 weeks since discontinuation of therapy, recurrent thrombocytopenia has developed in one patient, whose marrow remains normal, while a bone marrow relapse has occurred in another patient, whose blood counts remain normal. Treatment produced a greater than 50% decrease in neutrophil count in 26 patients, which lasted 3 to 4 weeks and was associated with an increased incidence of febrile episodes. These episodes occurred in 21 patients but were associated with documented infection in only four patients. Decreases in the number of CD4+ lymphocytes appeared to occur regularly after treatment and have persisted for a median of 18 weeks without obvious clinical significance. Although years of follow-up will be needed, our results confirm Piro et al's observation (N Engl J Med 322: 1117, 1990) that 2CdA appears to be highly effective in the treatment of hairy cell leukemia.
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PMID:Treatment of hairy cell leukemia with 2-chlorodeoxyadenosine (2-CdA). 134 77

Newborns are predisposed to neutropenia and thrombocytopenia during bacterial sepsis. The presence of peripheral cytopenias during overwhelming infection may be secondary to decreased hematopoietic growth factor production during states of increased demand. We therefore examined circulating levels of granulocyte-colony stimulating factor (G-CSF) and IL-3, production of G-CSF and IL-3 from unstimulated and stimulated mononuclear cells (MNC), expression of G-CSF and IL-3 genes during unstimulated and stimulated conditions, and equilibrium and binding of G-CSF receptors on mature effector peripheral blood cells of adults and neonates. Serum from cord and adult peripheral blood contained negligible amounts of both G-CSF (less than or equal to 50 pg/mL) and IL-3 (less than or equal to 5 pg/mL). Constitutive supernatant levels of G-CSF and IL-3 from cord and adult unstimulated MNC were also undetectable. However, there was a significant difference in G-CSF and IL-3 production from stimulated cord and adult MNC. Supernatants from stimulated adult MNC had significantly more G-CSF (p less than 0.007) and IL-3 (p less than 0.02). Additionally, Northern blot hybridization and densitometry of autoradiographs demonstrated significantly more G-CSF and IL-3 mRNA transcripts from adult than from cord MNC. Lastly, affinity, binding, and number of G-CSF receptors on cord and adult peripheral effector cells were equal. These data suggest that, during states of increased demand, cord MNC produce less G-CSF and IL-3 than do adult MNC and have an associated reduction in their respective mRNA transcripts. These findings may have implications in the pathogenesis of neonatal cytopenias during states of increased demand, such as sepsis.
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PMID:Decreased G-CSF and IL-3 production and gene expression from mononuclear cells of newborn infants. 137 59

Twenty-six patients with advanced renal cell carcinoma were treated with suramin administered by continuous infusion, with dosing determined by a nomogram. One patient achieved a partial response and five patients achieved a minor response or had stable disease for > 3 months. Toxicities included an immune-mediated thrombocytopenia in one patient and Staphylococcus sepsis that was not associated with neutropenia in five patients. Pharmacokinetic parameters were determined by the ADAPT II MAP-Bayesian parameter estimation program. Patient data were fit using a two-compartment open model and first-order rate elimination. This showed a wide interpatient variation in time to target level (median, 13.8 days), volume of distribution (median, 15.2 liters/m2), and t1/2-beta (median, 20.6 days). The patients who achieved a partial response, minor response, or stable disease had a slower elimination rate of suramin, compared to patients with progressive disease. Tumor specimens were obtained prior to therapy and were analyzed for the production of five different growth factor-specific RNA transcripts. These included transforming growth factor alpha, acidic fibroblast growth factor, basic fibroblast growth factor, and platelet-derived growth factor types A and B. No difference in the pattern of growth factor expression was seen in tumors of responding and nonresponding patients. Suramin does not have significant antitumor activity in renal cell carcinoma. The wide variability in pharmacokinetics suggests that individual dosing should be used in future trials of suramin for treatment for other malignancies. Pertinent corollary studies of tumor biology and clinical pharmacology should be included whenever possible in clinical trials in patients with renal cell carcinoma.
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PMID:Phase II trial of suramin in patients with advanced renal cell carcinoma: treatment results, pharmacokinetics, and tumor growth factor expression. 139 2

The Wiskott-Aldrich syndrome is an uncommon X-linked recessive disease characterized by eczema, thrombocytopenia, and immunodeficiency. The clinical features begin early in life and include recurrent infections, bleeding, and severe eczema. Unless the condition is treated by bone marrow transplantation, the prognosis of Wiskott-Aldrich syndrome is grave, and premature death caused by sepsis, hemorrhage, or lymphoreticular malignancy is common. Although the biochemical defect responsible for the syndrome is not known, recent investigations with restriction fragment length polymorphisms have mapped the Wiskott-Aldrich syndrome locus to the proximal portion of the short arm of the human X chromosome (Xp11). The isolation of these DNA markers makes feasible both carrier detection and prenatal diagnosis of Wiskott-Aldrich syndrome and provides an important adjunct to the management of Wiskott-Aldrich syndrome for patients and their families. These genetic data, in conjunction with the recent identification of a specific O-glycosylation defect in lymphocytes from patients with Wiskott-Aldrich syndrome, present an opportunity for the eventual isolation of the Wiskott-Aldrich syndrome gene and identification of the underlying cellular defect. We review the clinical and laboratory features of this syndrome and summarize the new molecular and biochemical approaches that can be used in diagnosis, genetic counseling, and treatment.
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PMID:Wiskott-Aldrich syndrome: new molecular and biochemical insights. 140 1

Thirty-four women with metastatic breast cancer were treated at the National Cancer Institute of the National Institutes of Health, with a regimen of leucovorin (L), 500 mg/m2 i.v. over 30 min, followed in 1 h by 5-fluorouracil (5-FU), 375 mg/m2 i.v. bolus on days 1-5, and carboplatin (CBDCA), 50-100 mg/m2 i.v. bolus on days 2-4, every 28 days. All patients had received previous combination chemotherapy with at least one regimen (29 patients with 5-FU-containing regimens). CBDCA, 100 mg/m2 on days 2-4, resulted in grade 4 neutropenia in 10 out of 11 patients associated with sepsis in all 10 patients. CBDCA, 75 mg/m2 (seven patients) and 50 mg/m2 (15 patients), resulted in grade 4 neutropenia in six and eight patients, and neutropenic sepsis in five and two cases, respectively. Grade 4 thrombocytopenia occurred in 10, five and two patients receiving 100, 75 and 50 mg/m2 of CBDCA, respectively. Other toxicities included grade 3/4 mucositis in 18 patients and grade 3/4 diarrhea in 10 patients. Twenty nine patients were evaluable for response, with one pathologic complete response (3%), two partial responses (6%), 18 stable disease (53%) and eight (24%) progressive disease. Sites of response included bone, viscera and soft tissue. The median time from entry on study to progression, for responders, was 15 months. When platinum-DNA adduct formation in peripheral white blood cells was analyzed in 27 patients at 24 h after drug administration, a significant correlation between adduct level and CBDCA cumulative dose was found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapy of patients with metastatic breast cancer with 5-fluorouracil, leucovorin and carboplatin. 145 Apr 39

Thirty patients with relapsed pediatric solid tumors received high-dose carboplatin and etoposide with autologous marrow support in a dose-escalation trial. These patients had received extensive prior treatment, which included both cisplatin and etoposide in 25 cases. Six patient cohorts received carboplatin in doses of 1200-2100 mg/m2 and etoposide in doses of 960-1500 mg/m2. All courses were associated with severe neutropenia and thrombocytopenia. The median times from bone marrow infusion to granulocyte recovery (> 0.5 x 10(9)/l) and platelet recovery (> 50 x 10(9)/l) were 33 and 28 days, respectively, with similar findings for all dosage levels. The frequency of non-hematologic toxicities was generally low, although hyponatremia (Na+ < 129 mEq/l) was seen in one-third of the courses. Hepatoxicity was dose-limiting and was significantly associated with the cumulative prior cisplatin dose (p = 0.006). There were four toxic deaths (CNS hemorrhage, alfa-streptococcal sepsis, Candida sepsis, and enterocolitis). Eleven patients received a second course of therapy; toxicity profiles and times to hematologic recovery were similar for the two courses. Clinical responses were observed at all dosage levels. Eleven of 26 evaluable patients achieved a clinical response (one complete, 10 partial). The majority of responses were in patients with neuroblastoma (six of 16) or Hodgkin's disease (two of three). For phase II clinical trials, we recommend dosages of 2100 mg/m2 of carboplatin and 1500 mg/m2 of etoposide for children with prior cumulative cisplatin exposure < 960 mg/m2. This carboplatin dose represents a three- to four-fold increase over pediatric doses tolerated without bone marrow support.
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PMID:Escalating sequential high-dose carboplatin and etoposide with autologous marrow support in children with relapsed solid tumors. 146 10

During 1983-1988, hospitalizations of patients with a diagnosis of human immunodeficiency virus (HIV) infection increased from 1.3 to 33.7 per 100,000 persons. We used the National Hospital Discharge Survey, which is based on a representative sample of discharges from nonfederal short-stay hospitals, to describe illnesses among hospitalized patients with HIV infection. Of 222,200 such hospitalizations during 1983-1988, most occurred among persons who were 25-44 years of age (79%), white (66%), and male (90%). Among men 25-44 years of age, HIV admissions increased from 8.5 to 148.6 per 100,000 persons during 1983-1988; among black men 25-44 years of age, HIV hospitalizations increased from 43.1 to 387.4 per 100,000 persons. Among women, hospitalizations increased 3.4-fold. Frequently listed illnesses in the Centers for Disease Control (CDC) AIDS case definition were Pneumocystis carinii pneumonia (30%), candidiasis (20%), and Kaposi's sarcoma (13%). Other frequently listed illnesses included infections (39%) such as pneumonia, sepsis, and urinary tract infections; blood dyscrasias (30%) such as anemia, thrombocytopenia, and agranulocytosis; metabolic (17%), gastrointestinal (16%), and respiratory disorders (12%); and drug abuse (9%). These data provide a minimum estimate of HIV hospitalizations because for some patients HIV infection may not be specified on the discharge record. HIV hospitalizations are increasing markedly and are associated with a broad spectrum of severe morbidity.
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PMID:Increasing impact of HIV infection on hospitalizations in the United States, 1983-1988. 156 Mar 47


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