Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A three-drug antibiotic regimen including vancomycin and amikacin has been recommended as effective treatment in clinical settings in which Gram-positive bacteremias are a serious problem. To determine if vancomycin potentiates the tubular proteinuria associated with amikacin therapy, we studied febrile, neutropenic children with leukemia who were treated with either amikacin (800 mg/m2/day) and ticarcillin-clavulanate or with vancomycin (1.2 g/m2/day), amikacin and ticarcillin. Tubular proteinuria was assessed in 14 children by monitoring the excretion of total urinary protein and two other sensitive indicators of nephrotoxicity, the renal tubular enzymes N-acetyl-beta-D-glucosaminidase and alanine aminopeptidase, in sequential 8-hour urine collections during 7 days of antimicrobial therapy. There were no significant differences between the two treatment groups in excretion of the three marker proteins when values were compared on any day of therapy or for the entire 7-day course. Nor did we observe any significant changes in either serum creatinine concentrations or amikacin clearance rates in the larger study group of 101 children from which these patients were drawn. Although amikacin was subclinically nephrotoxic, the addition of vancomycin to amikacin therapy did not enhance clinical or tubular nephrotoxicity in these children.
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PMID:Vancomycin does not enhance amikacin-induced tubular nephrotoxicity in children. 265 16

In clinical chemistry, determination of serum alanine aminopeptidase (AAP) levels has been found to be useful for detecting or confirming biliary obstructions from either intra- or extra-hepatic disorders. In haematology, 'gp150' is a surface-expressed protein molecule, recognised by monoclonal antibodies belonging to the so-called 'Cluster of Differentiation' (CD-) 13, which has independently been found to be a useful marker of myeloid leukaemia in addition to providing potential prognostic value. The current report links these two independent research streams and provides evidence that the hepatobiliary disease marker, serum AAP, predominantly comprises a circulating isoform of 'gp150'. Thus, a (CD-13) monoclonal antibody raised to, and specifically reactive with, cell surface myeloid 'gp150' is able to specifically and almost completely block serum (or plasma) AAP activity otherwise observed in its absence. This holds true for serum (or plasma) derived both from normal individuals or from patients suffering hepatic dysfunction, with or without associated biliary obstruction. In the case of patients with obstructive jaundice, raised levels of AAP are observed, which fall to near normal levels following preincubation with this monoclonal antibody. In addition, data are presented to support the view of varying isoforms of AAP within flowing blood. Finally, preliminary data is provided on AAP activity in cases of leukaemia. These studies should thus prove of use to clinical laboratories investigating the involvement of AAP activity in various pathological processes.
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PMID:The hepatobiliary disease marker serum alanine aminopeptidase predominantly comprises an isoform of the haematological myeloid differentiation antigen and leukaemia marker CD-13/gp150. 790 44