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)

The Dialysis Centre at the Lagos University Teaching Hospital became operational in November 1981 and caters for acute haemodialysis, chronic maintenance haemodialysis and continuous arteriovenous haemofiltration. In the past 5 years, over 600 patients had presented out of whom 245 could be accommodated within the realities of available facilities and patients' financial status. Of the 245 patients, 25 were discharged against medical advice and five were transferred to hospitals abroad but did not survive. There were 117 patients in end-stage renal failure (ESRF), 75 males, 42 females, ratio M:F 1.8:1, age range 13-69 years, mean 37.5. There were 51 males and 47 females in acute renal failure (ARF), ratio 1.1:1, age range 13-76 years, mean age 32.3 (Table 1). All patients in ESRF had moderate to severe hypertension (diastolic pressure of greater than or equal to 120 mmHg or 22.1 kPa) and a creatinine clearance of less than or equal to 5 ml/min and about 75% had established cardiac decompensation. Full pertinent investigations were precluded or contra-indicated in most patients in ESRF because of late presentation. In only 13 patients was renal biopsy performed and the pathohistologies were end stage renal disease (8), chronic glomerulonephritis (4) and glomerulosclerosis (1). In ARF the cause of the renal damage was multifactorial in 66.7%, with sepsis being the direct cause of death in 60.0%. The commonest conditions were septicaemia (61.4%), nephrotoxin (17.2%), trauma (31.3%), septic abortion (33.3%) and toxaemia of pregnancy (29.0%) (Table 2). The dialysis associated complications which were encountered included shunt infection (7%), burst membrane (9%), suspected pyrogen reaction (5.6%) and femoral vein perforation (0.9%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Five years experience of haemodialysis at the Lagos University Teaching Hospital--November 1981 to November 1986. 255 Nov 60

Hantaviruses, the causative agents of HFRS, have become more widely recognized. Epidemiologic evidence indicates that these pathogens are distributed worldwide. People who come into close contact with infected rodents in urban, rural and laboratory environments are at particular risk. Transmission to man occurs mainly via the respiratory tract. The epidemiology of the hantaviruses is intimately linked to the ecology of their principal vertebrate hosts. Four distinct viruses are now recognized within the hantavirus genus and that number is likely to increase to six very soon; however, further investigations are necessary. Much more work is still needed before we fully understand the wide spectrum of clinical signs and symptoms of HFRS as well as the pathogenicity of the different viruses in the hantavirus genus of the Bunyaviridae family. HFRS is difficult to diagnose on clinical grounds alone and serological evidence is often needed. A fourfold rise in IgG antibody titer in a 1-week interval, and the presence of the IgM type of antibodies against hantaviruses are good evidence for an acute hantavirus infection. Physicians should be alert for HFRS each time they deal with patients with acute febrile flu-like illness, renal failure of unknown origin and sometimes hepatic dysfunction. Especially the mild form of HFRS is difficult to diagnose. Acute onset, headache, fever, increased serum creatinine, proteinuria and polyuria are signs and symptoms compatible with a mild form of HFRS. Differential diagnosis should be considered for the following diseases in the endemic areas of HFRS: acute renal failure, hemorrhagic scarlet fever, acute abdomen, leptospirosis, scrub typhus, murine typhus, spotted fevers, non-A, non-B hepatitis, Colorado tick fever, septicemia, dengue, heartstroke and DIC. Treatment of HFRS is mainly supportive. Recently, however, treatment of HFRS patients with ribavirin in China and Korea, within 7 days after onset of fever, resulted in a reduced mortality as well as shortened course of illness.
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PMID:Hemorrhagic fever with renal syndrome. 257 14

Interleukin-2 (IL-2)-based immunotherapy is associated with profound reversible cholestasis and hyperbilirubinemia. We performed a nonrandomized retrospective and prospective analysis to determine the incidence, characteristics, clinical course, and nature of the IL-2-induced liver dysfunction in patients with cancer. Patients received IL-2 at a dose of 20,000 to 100,000 units (U)/kg thrice daily for up to 5 days. Fifty-one patients on adjuvant treatment protocols received a mean of 10.18 +/- 2.38 IL-2 doses and 11.67 +/- 4.16 doses were delivered to 210 patients with advanced disease during this period. Retrospective analysis of all patients receiving this therapy revealed increases in the following liver function tests expressed as median, 25th percentile, and 75th percentile (range): bilirubin (mg/dL) 4.5, 2.6, 6.5 (.4 to 38.5); alkaline phosphatase (U/L) 256, 179, 378 (56-1680); SGOT (U/L) 80, 52, 117 (18 to 483); SGPT (U/L) 91, 64, 132 (20-540); prothrombin time 13.4, 12.8, 14.5 (10.8 to 35.4); and albumin (g/dL) values decreased (trough) slightly 3.0, 2.8, 3.2 (2.3 to 3.8). Multiple regression analysis revealed several factors that were significantly associated with the increase in bilirubin when jointly considered (model P2 less than or equal to .001) including total IL-2 dosage, increase in creatinine, alkaline phosphatase, weight, and SGOT. Similar increases were noted in a prospectively evaluated group of 10 patients. A return to normal levels of bilirubin was noted within 5.6 days of stopping IL-2. Fasting serum cholylglycine increased from a mean of 32.3 +/- 1.6 to a peak of 1556.0 +/- 625.0 mg/mL. Although conventional ultrasound examinations were unrevealing, tissue ultrasound examinations revealed a mean scatterer spacing (MSS) increase compared to baseline of .10 +/- .04 (P less than .02) suggesting hepatic edema or an infiltrative process. Further, computerized hepatobiliary nuclear medicine scans revealed a delay in uptake (2.2 +/- 0.5 fold greater) and excretion (8.0 +/- 5.9 fold greater) of technetium-99m labeled disofenin. These findings support the development of profound reversible cholestasis as the primary basis for the elevated bilirubin in patients undergoing IL-2 treatment and may have implications for understanding the jaundice observed in some patients postoperatively as well as that associated with sepsis and other inflammatory disorders. Specifically, the release of IL-2 or the induction of other factors similarly induced by IL-2 may be responsible for these findings. Tissue ultrasound and computerized hepatobiliary scans provide additional noninvasive assessments of liver function and physiology.
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PMID:Interleukin-2 induces profound reversible cholestasis: a detailed analysis in treated cancer patients. 258 24

Recently, the association of granulocytic fragments on blood smear with leukoerythroblastosis in sepsis has been identified in nine patients. Granulocytic fragments were identified by both light and electron microscopy as well as cytochemistry. Leukoerythroblastosis is a poorly defined, uncommon syndrome with leukocytosis, left shift, and nucleated red blood cells (nRBCs) disproportionate to the degree of anemia, which may be associated with leukemia or neoplasia in the bone marrow, acute infection, hemolysis, myelofibrosis, or miscellaneous causes. Here a subgroup with high white blood cells (WBC) and acute infection was studied. The corrected WBC for nine patients was 40 x 10(9) per L with 33 nRBC per 100 WBC; serum C3 and C4 levels before and after the development of leukoerythroblastosis were 0.6 +/- 2 g per L; 0.18 +/- 0.04 g per L pre-leukoerythroblastosis and 0.7 +/- 0.46 g per L; 0.30 +/- 0.27 g per L post-leukoerythroblastosis, respectively, in four patients. The platelet count, prothrombin time (PT), and activated partial prothrombin time (aPTT) were 133 x 10(9) per L, 24.4 sec., and 53.5 sec., respectively, for nine patients. Multiphasic chemistries at the time of leukoerythroblastosis were measured in five patients; abnormal values included calcium of 2.0 +/- 0.4 mmol per L, creatinine of 336 +/- 130 mumol per L, total protein of 45 +/- 17 g per L, albumin of 27 +/- 11 g per L, total bilirubin of 421 +/- 362 mumol per L, uric acid of 499 +/- 264 mumol per L, triglycerides of 4.9 +/- 3.7 mmol per L, and alkaline phosphatase of 3.5 +/- 1.0 mu kat per L.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biochemical values, complement levels, and hemostatic data in septic leukoerythroblastosis. 260 78

A boy, aged 14 1/2 years, presented with Burkitt leukemia. His renal status was normal before treatment. Chemotherapy (SFOP LMB 86 protocol) was begun Oct. 9, 1986. After the first 2 courses of chemotherapy, the patient had Gram negative sepsis treated with cefotaxime, netilmycine, Vancomycin and ornidazole. During sepsis, nephrotic syndrome developed (albumin 25 g/l, non selective proteinuria 15 g/24 h), with moderately high blood pressure, functional renal failure (creatinine 141 mumols/l, U/P urea = 20), polyuria and tubular damage. Kidney ultrasonography was normal. Needle biopsy showed minimal glomerular lesions, acute tubular lesions, and no deposits in immunofluorescence. The nephrotic syndrome disappeared within 3 weeks, with treatment of leukemia. He is at present in complete remission with a follow-up of 25 months.
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PMID:[Nephrotic syndrome and B leukemia]. 262 44

We investigated the role of beta 2-microglobulin as a noninvasive parameter to monitor acute rejection and severe infection in 45 consecutive heart transplant recipients. Endomyocardial biopsy revealed moderate (41 patients) or severe (three patients) rejection in 44 patients. Severe infections of bacterial septicemia (11 patients), bronchopneumonia (two patients), and viral infection (seven patients) were detected by a meticulous schedule of various clinical and laboratory tests. beta 2-Microglobulin levels in serum, generally corrected for serum creatinine, were significantly elevated in patients with infections (median, 6.3 mg/l; range Q10-Q90, 3.47-10.27 mg/l) compared with levels in patients with rejection (p less than 0.0001) or in patients in obviously good condition (p less than 0.0001). At the onset of acute rejection, the median corrected beta 2-microglobulin serum level was 1.56 mg/l (range Q10-Q90, -0.05-3.46 mg/l) and was significantly different from the control group (p less than 0.01). In addition, density function and empirical quantile analyses allowed us to define ranges of beta 2-microglobulin levels that would differentiate between rejection (2.05-3.46 mg/l) and infection (greater than 3.46 mg/l). With these values, sensitivity and specificity were 0.9 and 0.938 for detection of infection and 0.23 and 0.925 for detection of rejection, respectively. By means of beta 2-microglobulin, two cases of infection were misinterpreted as rejection (10%), and four of 44 rejections were mistaken for infections (9%). We conclude that measurements of beta 2-microglobulin may improve the management of heart transplant patients.
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PMID:Beta 2-microglobulin. A reliable parameter for differentiating between graft rejection and severe infection after cardiac transplantation. 268 73

A new reproducible animal model of sepsis was established to investigate interrelationship between disseminated intravascular coagulation (DIC) and multiple organ failure (MOF). Sepsis was induced by injecting fecal suspension into bile duct of rabbits, in which the amount of endotoxin in circulating blood was gradually increased and manifestations of sepsis were confirmed. During 9 hours' observation period, an occurrence of hypercoagulable state leading to DIC was evidenced by the abnormal hemostaseological parameters. Simultaneously the elevation of plasma bilirubin and creatinine levels was observed, indicating the presence of liver and kidney failure, which was confirmed by the histological examination. Thereby, the present sepsis model complicates DIC and MOF with high reproducibility, which is relevant to sepsis seen in clinical patients.
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PMID:Sepsis model with reproducible manifestations of multiple organ failure (MOF) and disseminated intravascular coagulation (DIC). 272 56

A 3-year-old girl is reported on who underwent laparotomy for ileocaecal intussusception elsewhere one week following severe gastroenteritis. Immediately after surgery, she developed haemolytic-uraemic syndrome with haemolytic anaemia, thrombocytopenia, increase of urea and creatinine and anuria as well as subsequent peritonitis, enterocolitis and sepsis. Following relaparotomy with establishment of ileostomy, peritoneal dialysis for several days was carried out for treatment of the haemolytic-uraemic syndrome. This case demonstrates that the haemolytic-uraemic syndrome can be treated effectively by peritoneal dialysis despite fresh bowel anastomoses, and that simultaneously occurring peritonitis can be managed by intraperitoneal administration of antibiotics via dialysis fluid.
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PMID:[Peritoneal dialysis in hemolytic-uremic syndrome following ileocecal resection for invagination in postoperative peritonitis]. 275 Mar 44

This retrospective study was conducted to identify the frequency of cytomegalovirus (CMV) disease in seronegative recipients of donor-specific transfusion (DST) and living-related donor (LRD) kidneys from seropositive donors. A total of 151 LRD transplants (TX) were performed at six transplant centers over a 3-year period. A total of 33 patients were identified as having been seronegative (pre-TX) for CMV, yet they had DST and a TX from a seropositive LRD. Of these patients, 12 (36.4%) seroconverted within the first 6 months post-TX and developed clinical CMV disease. Additional patients seroconverted, but did not have evidence of clinical disease and were not tested further. All TX centers, with the exception of one, had seronegative patients that became ill after receiving a seropositive DST/LRD TX. Six patients manifested their disease as a febrile illness with leukopenia and liver enzyme elevations, four had pneumonitis, and two developed CMV ulcerations of the colon (one of whom died from resultant sepsis). Of the 36 seronegative patients who received seronegative DST/LRD TX none became ill with CMV disease. Of the 72 seropositive patients who received DST/LRD TX, only 2 (2.8%) developed CMV illness (one, seropositive into seropositive, the other, seronegative into seropositive). Of the 33 seronegative patients receiving seropositive DST/LRD TX, 17 received antilymphocyte preparations (ALP), and 8 of these became ill (47.1%). Of 16 patients not receiving ALP, 5 (31.3%) developed clinical CMV illness. Of the 33 patients who were identified as having been seronegative for CMV yet received seropositive DST/LRD TX, the 12 who did develop CMV illness had two graft losses, one death, and a serum creatinine for the remaining 9 patients of 2.3 +/- 1.6 at last follow-up. The remaining 21 patients who developed no illness had a serum creatinine of 1.3 +/- 0.6 with no graft losses at the last follow-up. This evidence suggests that a prospective TX recipient who is seronegative for CMV who receives DST/LRD TX from a seropositive family member has a significant risk for developing morbidity related to clinical CMV illness.
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PMID:Incidence and morbidity of cytomegalovirus disease associated with a seronegative recipient receiving seropositive donor-specific transfusion and living-related donor transplantation. A multicenter evaluation. 282 52

The efficacy of ceftazidime in the treatment of neonatal sepsis was studied in 42 low birthweight premature babies. Forty-nine courses of ceftazidime (25 mg/kg bd, iv or im were administered. In 19 babies, treatment was stopped after 48 h, the remainder were treated for 5 days or more. Six neonates had bacteriological evidence of infection, one other was pyrexial and 29 had radiological evidence compatible with respiratory tract infection. Eight of the study population died. Only one death was attributed to infection which arose 3 days after completion of a 5-day course of ceftazidime. Two babies developed clinical signs of necrotizing enterocolitis (NEC). Clostridium difficile (7) and Cl. perfringens (2) were isolated from 34 post-treatment faecal samples but not from the two babies with NEC. No faecal sample contained Cl. difficile toxin. Post-treatment cultures from 12 neonates yielded ceftazidime-resistant micro-organisms. Ceftazidime therapy was not associated with significant alteration in serum alanine aminotransferase, urea, creatinine, protein or albumin. Four babies had an eosinophilia, three transient and one following two intrauterine transfusions. Coombs' tests were performed on 17 babies. There were no false positives. The abnormal clotting studies observed in one baby were not due to ceftazidime. In a concurrent pharmacokinetic study, the half-life of ceftazidime was 7.4 (SD +/- 4.1) h following iv administration. Other pharmacokinetic values were C max 74 (SD +/- 20) mg l-1 trough concentration 20 (SD +/- 10) mg l-1. Total body clearance ranged from 0.13 to 2.10 ml min-1 per kg and increased with increasing postnatal age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ceftazidime in the treatment of neonatal infection. 286 90


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