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 prospective study the diagnostic value of urinary thromboxane B2 (TXB2) and beta 2-microglobulin (beta MG) in renal allograft rejection was studied in 34 patients after transplantation. Twenty-four episodes of rejection were diagnosed by clinical symptoms. The clinical diagnosis of rejection was confirmed by an increase of urinary TXB2 in 21 (88%) cases. The augmented renal excretion of TXB2 proceded the clinical signs of rejection for 2.0 +/- 0.75 days. The symptoms in the remaining three (12%) cases of supposed allograft rejection without increased urinary TXB2 were caused by non-immunological events (urinary tract infection, acute tubular necrosis). No elevated TXB2 excretion was observed during urinary tract infection, sepsis, and acute tubular necrosis whereas urinary beta MG increased during these events as during transplant rejection. Urinary TXB2 was found to be an early, specific, and sensitive marker of renal allograft rejection with greater reliability than beta MG excretion or clinical signs of rejection.
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PMID:Thromboxane B2 and beta 2-microglobulin as early indicators of renal allograft rejection. 388 70

Beta 2-microglobulin concentrations in cerebrospinal fluid (CSF) were measured in a prospective study on 56 children 0-12 years old. In all the patients with virus meningitis values of beta 2-microglobulin exceeded 3000 micrograms/l (x = 10.825 micrograms/l). The highest value (48.096 micrograms/l) of beta 2-microglobulin in CSF was found in a 13-day-old infant with serious herpes simplex meningitis. The value was 50 times the values in normal children. None of the patients with fever of other origin had values exceeding 3500 micrograms/l, except for one patient with facial nerve paresis and 3 patients with sepsis. Some correlation between the concentrations of beta 2-microglobulin and albumin was found in the diagnostic groups as a whole, while this correlation disappeared when considering each patient individually. The significance of beta 2-microglobulin as a guide in serious infections is discussed.
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PMID:beta 2-Microglobulin in cerebrospinal fluid from children with different diseases. 616 20

Urine protein excretion patterns have been studied in 42 patients with sepsis and compared with that in 21 healthy controls. Patients with sepsis were shown to have highly significant increases in fractional clearances for beta 2-microglobulin, albumin, amylase and immunoglobulin G as compared with the controls. Analysis of the pattern of protein excretion demonstrates that the proteinuria is of the tubular rather than the glomerular type. There was no evidence that administration of aminoglycoside antibiotics contributed to the production of tubular proteinuria, and in particular these drugs did not appear to affect the excretion of beta 2-microglobulin.
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PMID:Patterns of urinary protein excretion in patients with sepsis. 618 21

The nephrotoxicity of gentamicin and amikacin was compared during presumed sepsis in 107 premature neonates. To examine the possibility that nephrotoxicity was directly associated with the clinical conditions of "sepsis," a control group of 26 chloramphenicol-treated newborns was also studied. Two markers of proximal renal tubular injury, N-acetyl-beta-glucosaminidase (NAG) and beta 2-microglobulin, were measured in 6-hr aliquots of urine. Because urine creatinine excretion increased with postconception age, markers were expressed in terms of excretion rate rather than per milligram of creatinine. The NAG excretion rate was significantly higher in gentamicin-treated patients (138 +/- 10 U/min, mean +/- SE) than in amikacin-treated patients (85 +/- 7 U/min) but did not differ between patients treated with amikacin and those treated with chloramphenicol (81 +/- 11 U/min). Excretion of beta 2-microglobulin did not differ among the three patient groups. We conclude that amikacin may be less nephrotoxic than gentamicin in the premature newborn.
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PMID:Aminoglycoside-related nephrotoxicity in the premature newborn. 636 3

Blood serum levels of myoglobin, creatinine, urea, beta 2-microglobulin were measured in 37 patients with the prolonged crush syndrome (PCS) injured during the Yerevan earthquake. A drastic increase of myoglobin level in the blood was observed in all the patients by the moment of hospitalization, this level being the higher, the more severe the injury. If PCS complications developed, such as sepsis or acute renal failure, myoglobin level increased by several tens of times. Effective treatment normalized myoglobin level before discharge from hospital.
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PMID:[Myoglobin concentration in blood: a criterion in the evaluation of muscular tissue injury in patients with prolonged crush syndrome]. 748 97

The potential tubulotoxicity of tobramycin and cefotaxim were assessed in neonates by measuring the urinary level of adenosine deaminase binding protein (ABP) and urinary alpha 1-microglobulin and beta 2-microglobulin. In a prospective study, 33 neonates who received tobramycin and cefotaxim for suspected neonatal sepsis were compared with 48 untreated newborns during the first 10 days of life. The urinary concentrations of ABP and its excretion rates, corrected for body weight and body surface area, were significantly increased from the 1st day of treatment. Urinary alpha 1-microglobulin and beta 2-microglobulin were not elevated under tobramycin and cefotaxim during the first 2 days of treatment. We conclude that ABP may be a sensitive marker for the detection of proximal renal tubular injury during tobramycin and cefotaxim treatments of neonates. The increase in urinary ABP which occurs before an elevation of urinary alpha 1-microglobulin and beta 2-microglobulin may reflect earlier structural than functional alterations. However, since none of the treated infants had signs of electrolyte disorders or glomerular dysfunction, the clinical relevance of ABP measurement should be reevaluated.
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PMID:Urinary excretion of adenosine deaminase binding protein in neonates treated with tobramycin. 757 99

Soluble tumour necrosis factor receptors (sTNF-Rs) play a role as modulators of the biological function of tumour necrosis factor-alpha (TNF-alpha) in an agonist/antagonist pattern. In various pathologic states the production and release of sTNF-Rs may mediate host response and determine the course and outcome of disease by interacting with TNF-alpha and competing with cell surface receptors. The determination of sTNF-Rs in body fluids such as plasma or serum is a new tool to gain information about immune processes and provides valuable insight into a variety of pathological conditions. Regarding its immediate clinical use, sTNF-Rs levels show high accuracy in the follow-up and prognosis of various diseases. In HIV infection and sepsis, sTNF-Rs concentrations strongly correlate with the clinical stage and the progression of disease and can be of predictive value. Determination of sTNF-Rs also gives useful information for monitoring cancer and autoimmune diseases. The information provided is often even superior to that obtained with classical disease markers, probably due to the direct involvement of the "TNF system" in the pathogenetic mechanisms in these patients. The available data imply that the measurement of sTNF-Rs, especially of the sTNF-R 75kD type, is a useful adjunct for quantification of the Th1-type immune response, similar to other immune activation markers such as neopterin and beta 2-microglobulin. Endogenous sTNF-Rs concentrations appear to reflect the activation state of the TNF-alpha/TNF receptor system.
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PMID:Soluble receptors for tumour necrosis factor in clinical laboratory diagnosis. 785 70

Ten patients undergoing long-term renal dialysis for end-stage renal failure developed a destructive, non-infectious spondylarthropathy. All 10 patients had biopsy-proven dialysis-associated spondylarthropathy and subsequent spinal instability secondary to beta 2-microglobulin deposition in the vertebrae, intervertebral disc spaces, and support structures of the spine. Nine patients had cervical spinal instability and one had thoracolumbar spinal instability, with resultant neural compression. In at least one patient, the spinal instability was rapidly progressive. All had received renal dialysis for 34 months or longer (mean 109 months, range 34 to 154 months). Each patient required spinal stabilization (external in seven patients, internal in three). Nine of the 10 patients underwent neural decompression and spinal stabilization and fusion procedures. One patient's neurological condition was worse following surgery due to a postoperative cervical epidural hematoma; in the other nine patients, the presenting symptoms and signs improved. Three of these chronically ill patients did not survive their hospitalization, for a perioperative mortality rate of 30%. Death was due to cardiopulmonary arrest in two patients on Day 5 and 9 postoperatively and to sepsis in the third on Day 14. Of the seven early survivors, two additional patients died: one on Day 59 due to congestive heart failure and the other on Day 273 due to a cerebrovascular accident. Four of five patients who were followed for 8 months or longer (mean 14 months, range 8 to 20 months) had successful neural decompression and spinal stabilization procedures with evidence of stable bone fusion, indicating that these chronically ill, difficult-to-manage patients can be successfully treated. Clinicians who treat patients with renal disease and neurosurgeons who treat spinal disorders should be aware of dialysis-associated spondylarthropathy as a potential cause of degenerative vertebral column instability.
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PMID:Dialysis-associated spondylarthropathy. Report of 10 cases. 815 49

The articular complications observed in dialysed chronic renal failure failures, whose incidence increases with the duration of dialysis, are closely correlated with the development of beta 2-microglobulin amyloidosis, responsible for nerve tunnel syndromes, arthralgia and chronic joint swelling with frequently multiple subchondral cysts on x-rays. Microcrystalline pathology is dominated by apatite deposits, which may also be involved in the pathogenesis of destructive arthropathy. Articular complications with destruction of the large joints or involvement of the first carpometacarpal joint interfere with the functional prognosis. Sepsis must be excluded in cases of destructive cervical spondyloarthropathies. The pathogenesis of destructive arthropathies is probably multifactorial, consisting of apatite and amyloid deposits, secondary hyperparathyroidism and aluminium poisoning.
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PMID:[Rheumatological complications of dialysis]. 833 5

Fifteen patients with stage II, IIIA, and IIIB non-small cell lung cancer (NSCLC) received subcutaneous (s.c.) recombinant, glycosylated, human interferon-beta 1a (Rebif; rHuIFN-beta 1a) on each day of conventionally fractionated radiation therapy (RT) given in 2.0 Gy fractions to 60 Gy in 6 weeks. The rHuIFN-beta 1a was generated in CHO cells by recombinant DNA technology and is identical to natural IFN-beta produced by fibroblasts in primary sequence and glycosylation. Cohorts of three patients each were treated with escalating doses of rHuIFN-beta 1a: 1.5, 3, 6, 12, and 24 MIU/m2 per treatment day. Acute toxicity was assessed according to modified WHO criteria; late toxicity was graded using RTOG late toxicity criteria. The maximum tolerated dose (MTD) of rHuIFN-beta 1a was defined as the dose level immediately below that in which dose-limiting toxicity occurred in > or = two of six patients. Immunomodulatory effects and antigenicity of rHuIFN-beta 1a were assessed by 2-5A synthetase, beta 2-microglobulin, and neopterin levels and by measurement of anti-rHuIFN-beta antibodies, respectively. Fourteen of fifteen patients experienced grades 1-3 acute (early) toxicity (< or = 90 days), which was primarily gastrointestinal: dysphagia/esophagitis (14/15), nausea/vomiting (12/15), anorexia (7/15), and liver transaminasemia (6/15). One of three patients treated with 24 MIU/m2 per treatment day (total rHuIFN-beta 1a dose 672 MIU) died of complications secondary to pneumonia, sepsis, adult respiratory distress syndrome (ARDS), and radiation pneumonitis. Twelve patients were evaluable for late toxicity (> 90 days). Maximum toxicity was grade 0 in five patients, grade 1 in four patients, and grade 5 in one patient (radiation pneumonitis). Clinical responses from the combination were 1/15 CR, 6/15 PR, 6/15 stable disease, and 1/15 progressive disease. The MTD of rHuIFN-beta 1a has been estimated at 12 MIU/m2 per treatment day when given daily during conventional RT to 60 Gy in 6 weeks. Biologic response by rHuIFN-beta 1a alone was reflected by significant and dose-related increases in 2-5A synthetase, beta 2-microglobulin, and neopterin. Radiation therapy alone had no effect on these immune response parameters and did not diminish their augmentation by rHuIFN-beta 1a. There was no association of biologic modulation with clinical response or survival.
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PMID:Recombinant human interferon-beta (rHuIFN-beta) and radiation therapy for inoperable non-small cell lung cancer. 893 64


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