Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective analysis of 140 cases with amebic liver abscess (ALA) seen at the AUNL University Hospital was done to see if patients with complications can be identified earlier in order to decrease morbidity and mortality. Sixteen patients (11.4%) presented complications and six patients died (4.2%). Patients with complications presented jaundice, large or multiple abscesses, acute abdomen, liver failure and sepsis more often than patients without complications. Hemoglobin, hematocrit, prothrombin time, total proteins, albumin, LDH, and BUN were more altered in patients who presented complications. The titer of antibodies against E. histolytica was higher in this group of patients. The six patients who died had been operated on. The causes of death were septic shock in two, sepsis in one, peritonitis in one, liver failure in one and colon perforation in one patient. Pleural effusion, jaundice and acute abdomen were seen in three patients, respectively (50%), two cases had multiple abscesses (33.3%), one patient had a ruptured abscess (16.7%). Patients who died exhibited more alterations in six laboratory examinations at admission: partial prothrombin time, total bilirubin, albumin, BUN, LDH, and leukocytes. Clinical data together with the severe alterations in laboratory examinations at admission for patients with ALA should alert the clinician to suspect complications earlier in order to decrease morbidity and mortality.
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PMID:Early detection of complications in amebic liver abscess. 134 Mar 6

This study examines nutritional status and clinical outcomes, including pressure ulcers and death in 40 chronically tube-fed long-term care patients. Anthropometric, biochemical, clinical and dietary data were collected over a 3-month period, with follow-up of mortality at 1 year. Subjects' functional and cognitive status was generally poor. Adequate calories and protein were provided, with sample means exceeding standard means for energy, protein and micronutrients. Still, subjects showed weight loss and severe depletion of lean and fat body mass. Mean serum protein and micronutrient status measures were in the low normal range. Hemoglobin, hematocrit, and serum zinc and carotenoid levels were below normal in a sizable proportion of patients. Pressure ulcers were present in 65% of patients. Weight loss was associated with longer time on tube feeding and more pressure ulcers. Negative correlations with ulcer number were observed for cholesterol, albumin, zinc, retinol, alpha-tocopherol and iron. This study shows that despite administration of apparently adequate formula, micronutrient deficiencies and marasmic malnutrition exist in chronically ill patients. Causes may include the combined effects of chronic disease, sepsis, immobility, and severe neurologic deficits. Clinical outcomes may be expressions of an organism-wide diminution of protein synthesis, the cause of which is unknown. For clinical management, serial measures of weight, albumin, cholesterol, hemoglobin and hematocrit are recommended. Future research must address the many subsets of the population of chronically tube-fed patients.
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PMID:Prolonged tube feeding in long-term care: nutritional status and clinical outcomes. 161 83

Intravenous immunoglobulin (Gammagard 5%), 500 mg/kg, was given over 3 hours to 10 acutely ill infants with proven or suspected sepsis (treatment group) and 10 clinically stable preterm infants less than 1750 gm birthweight as prophylaxis for sepsis (prevention group). No differences were found in heart rate, respiratory rate, mean arterial blood pressure, or urine output in either group during or following the infusion compared with preinfusion values, except for a small but significant decrease in heart rate postinfusion in the prevention group. Likewise, serum glucose, sodium, serum glutamic oxaloacetic transaminase, and osmolality were unchanged 15 minutes and 6 hours following infusion. Urea nitrogen rose a small but significant amount in both groups. Hemoglobin concentration declined a small but significant amount 15 minutes postinfusion in the prevention group, but returned to baseline by 6 hours postinfusion. There were no changes in white blood cell count or platelet counts in either group. These data indicate that intravenous immunoglobulin in the dose given was associated with no adverse effects. Additional studies are warranted to evaluate the efficacy of these preparations in the treatment and prevention of neonatal septicemia.
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PMID:Safety of intravenous immunoglobulin infusion in neonates at risk for sepsis. 212 Nov 51

Because of the spleen's role in host defence and the recognition of overwhelming post-splenectomy sepsis, the current aim of treatment for splenic injuries is to preserve the spleen. A number of hemostatic agents have been used in an effort to control bleeding but have not proved satisfactory. The authors report the results of an experiment using a two-component fibrin seal on injured rabbit spleens. In female rabbits a longitudinal laceration of the entire spleen was made. After 2 1/2 minutes of continuous hemorrhaging, the spleens were either not treated (5 rabbits) or treated by splenectomy suture repair or fibrin-seal repair. Hemoglobin values were measured preoperatively and 3 days postoperatively. The greatest number of deaths within 14 days occurred in the untreated group. There was no difference in death rate between the treated groups; similarly, there was no difference in blood loss or fall in hemoglobin values. Fewer adhesions formed in the fibrin-seal group than in the others (p less than 0.02). Histopathological examination revealed a greater fibrinoblastic response in the spleens treated with fibrin seal than in the other groups. The authors believe that fibrin seal is an effective and safe hemostatic agent applicable to splenic parenchymal injuries, and that it promotes wound healing and suppresses adhesion formation.
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PMID:Preservation of the spleen using human fibrin seal. 245 80

The lethal effects of the fluorinated ether anesthetic, fluroxene, in rats are a consequence of its metabolism, which is catalyzed by cytochrome P-450 to the toxic metabolite 2,2,2-trifluoroethanol (TFE). The anesthetic or TFE (0.21 g/kg) caused decreased white blood cell counts, necrosis of bone marrow and lymphocytes, and decreased small intestine dry weight and was associated with septicemia. To elucidate the mechanism of TFE toxicity in rats we undertook histopathologic, ultrastructural and bacteriologic studies. TFE produced severe edema of intestinal lamina propria and submucosae, dilatation of crypts, loss of surface epithelium, vacuolation and necrosis of intestinal epithelial cells, and infiltration of polymorphonuclear leukocytes into the edematous lamina propria. Intestinal epithelial villi lost their cellular tissue integrity. Coccobacillary organisms were numerous in the ulcerated intestine. Hemolytic E. coli were isolated from intestinal tissue at a two-log increase in concentration relative to controls. Hemograms from TFE-treated rats exhibited marked leukopenia and morphologic differences. The platelets lost their discoid shape, extended pseudopods, and centralizing granules. Hemoglobin precipitation as Heinz bodies and crystalloid structures was observed in TFE-treated rats. Together the data suggest that TFE-induced enteropathy was most probably due to E. coli precipitated from TFE-mediated alterations in the population of small intestinal microbes. The antibiotics erythromycin, active against gram-positive bacteria, and streptomycin, active against gram-negative bacteria, and the antiendotoxin, polymyxin B, were administered to rats prior to TFE in an effort to differentiate between these mechanisms by altering the intestinal bacteria populations. The results indicate that the TFE-induced small intestinal lesions are initiated by the direct focal necrotic effect of TFE or its metabolites on the small intestinal epithelium. The focal coagulation necrosis produced by TFE predisposes the animals to lethal enteritis and systemic bacteremia.
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PMID:2,2,2-Trifluoroethanol-induced enteropathy in rats: chemically or bacterially mediated effects. 332 84

To determine the advantages and complications of splenectomy in the treatment of beta thalassemia, 221 splenectomies for thalassemia performed upon pediatric patients from 1971 to 1982 are evaluated. There were 125 boys and 96 girls with a mean age of 8.2 +/- 2.5 years at the time of the operation. Sixty-one other patients who underwent splenectomy for other diseases served as the controls. Early and late complications after splenectomy are considered with a follow-up study of ten years. Hemoglobin (Hb) value, transfusional quotients and mean of transfused blood previous to surgical treatment are matched with the same parameters evaluated during the follow-up period. The effect of treatment with salicylates and dipyridamole upon the incidence of early complications after operation is analyzed. The postoperative complications in patients with thalassemia were 43.4 versus 3.2 per cent (p less than 0.01) registered in control patients. Late complications occurred with an incidence of 10.7 per cent and were due principally to sepsis. Six patients died of sepsis during the follow-up period, but the mortality rate for sepsis in the patients we studied was significantly lower than that reported by others in 73 instances of splenectomy for beta thalassemia. Blood consumption dropped from 270 +/- 99 to 155 +/- 31 milliliters per kilogram per year postoperatively (p less than 0.01) and Hb levels rose from 9.7 +/- 1.3 to 11.2 +/- 0.7 grams per milliliter. These results suggest that, even though splenectomy for beta thalassemia causes a relevant incidence of complications and fatalities, surgical treatment permits an improvement in the quality of the lives of patients with beta thalassemia and significantly reduces blood consumption. Prophylactic antibiotic therapy can reduce the incidence of sepsis, as was observed in the patients we studied.
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PMID:Indications and results for splenectomy for beta thalassemia in two hundred and twenty-one pediatric patients. 340 27

A prospective study to evaluate the iron dosage needed to restore serum iron levels was performed on patients receiving prolonged total parenteral nutrition (TPN). Intravenous iron intakes of 0, 25, 87.5, and 175 mg/wk were sequentially studied. No untoward responses were seen in 42 patients studied for 2758 patient days. When compared to pre-TPN levels, serum iron levels increased significantly with increasing iron dosage (p less than 0.002). In every single patient at the two highest dosage levels, serum iron levels at 3 wk rose from the pre-TPN level. Hemoglobin, reticulocyte count, transfusion requirement, total iron binding capacity, and red cell indices were not affected by iron dosage. There was no increased incidence of sepsis in patients who received increasing iron dosage. Both the 87.5 and 175 mg/wk iron doses increased serum iron levels from pre-TPN values, but the highest dose increased serum iron levels above the normal range in 80% of patients after 3 wk of administration allowing us to recommend the 87.5 mg/wk dose.
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PMID:Iron supplementation of total parenteral nutrition: a prospective study. 641 64

Hemoglobin SD-Los Angeles is an uncommon sickle hemoglobinopathy. We describe a boy with documented Hb SD-Los Angeles who had experienced acute splenic sequestration, pneumococcal sepsis, aplastic crisis and functional asplenia during his first two years of life. We suggest that children with Hb SD-Los Angeles are at similar risks for the life-threatening complications which characterize sickle cell anemia and should receive the same comprehensive medical care currently recommended for children with Hb SS disease.
Hemoglobin 1984
PMID:Life-threatening complications in a child with hemoglobin SD-Los Angeles disease. 654 33

Your recent lead article on toxic shock and tampons (November 1, p. 1161) prompts me to report a case of pelvic infection and staphylococcal septicemia 8 days after the insertion of a Lippes loop. Pelvic infection is a recognized complication of IUDs; although there have been 2 reports of endocarditis occurring in susceptible patients following the insertion of an IUD, septicemia is rare. A previously healthy 31-year old married woman had a loop inserted at a family planning clinic. 3 days later she developed sweating, vomiting, confusion, and cough and during the following 48 hours became disoriented with hallucinations. She was referred to the hospital with suspected encephalitis and on admission was febrile (38.8 degrees Celsius) and stuporose but responded to simple commands. Blood pressure was 95/60 mmHg but there were no other abnormal signs. Hemoglobin was 12.2 g/dl, white blood count 4.0x109/1 (80% neutrophils), erythrocyte sedimentation rate 70mm in the 1st hour; cerebrospinal fluid normal. Chest x-ray examination revealed patchy consolidation in the upper lobes of both lungs and an electroencephalogram showed bilateral nonspecific abnormality. 3 blood cultures taken on admission yielded penicillin-resistant Staphylococcus aureus. She was treated with high-dose intravenous cloxacillin and 24 hours after starting the antibiotic had improved markedly and the IUD was removed. Culture from the coil and also from a high vaginal swab yielded Staph aureus with a similar antibiogram to that of the organism cultured from the blood. Subsequent recovery was uneventful, although repeat chest x-ray examination showed small abscess cavities in the upper lobes of both lungs. The patient was discharged 4 weeks after admission and serial chest radiographs have confirmed complete resolution of the pneumonia and abscesses. There is little doubt that this patients' septicemia with lung abscess formation and encephalopathy originated in the genital tract. The patient was both toxic and shocked but was different from patients with the recently described toxic shock syndrome in that her blood culture was positive for Staph aureus. The case provides another example of the importance of this organism as a cause of infection associated with the insertion of foreign bodies into or through the vagina.
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PMID:Staphylococcal septicaemia after insertion of an intrauterine contraceptive device. 744 49

In this phase I/II study, 9 patients with myelodysplastic syndromes (MDS) were treated with interleukin-3 (IL-3) followed by granulocyte-macrophage colony-stimulating factor (GM-CSF). Each treatment cycle was 28 days long and administered as follows: 1 microgram/kg/d IL-3 on days 1 through 7 and 3 micrograms/kg/d GM-CSF for days 8 through 21, followed by a 7-day rest period. IL-3 dose escalations were planned, but the dose of GM-CSF was fixed. Three patients had refractory anemia, 4 had refractory anemia with ringed sideroblasts, and 2 had refractory anemia with excess blasts. Six patients were dependent on red blood cell transfusions, 1 on platelet transfusions, and 2 on both. The absolute neutrophil count improved in 7 (77%) patients and the platelet count improved in 3 (33%) patients during therapy. Hemoglobin levels were unchanged. A clinically relevant response was seen in only 1 patient with thrombocytopenia, and he received five cycles of therapy. The neutrophil count decreased in 2 patients and the platelet count decreased in 4 patients during treatment. The toxicity of the treatment was significant. In the first cohort of 3 patients, 1 patient developed supraventricular tachycardia and congestive heart failure. In the second group, 1 patient developed progressive granulocytopenia and died of gram-negative septicemia. Because of the disparate toxicity, 3 more patients were treated at the same dose level. One of these experienced a high fever and bone pain requiring hospitalization. Because of these adverse effects, the IL-3 dose was not escalated and all patients received 1 microgram/kg/d for 7 days. We believe that sequential therapy with IL-3 and GM-CSF at these dose levels causes unacceptable toxicity in patients with MDS. The major toxic events occurred during weeks 4 and 5 after starting treatment and may have been primarily caused by GM-CSF therapy. Although neutrophil counts improve in most patients, the effect on red blood cells and platelets is minimal. At present, this form of therapy remains problematic and appears to have a limited potential in the management of MDS.
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PMID:A phase I/II study of sequential interleukin-3 and granulocyte-macrophage colony-stimulating factor in myelodysplastic syndromes. 828 36


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