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J J Fleming

Publications and source records attributed to J J Fleming.

12 recordsLinked to original sources
PubMed1985

Pharmacokinetics and beta-blocking effects of timolol in poor and extensive metabolizers of debrisoquin.

We studied the pharmacokinetics and beta-blocking effects of a single, oral 20 mg dose of timolol in six poor metabolizers (PMs) and six extensive metabolizers (EMs) of debrisoquin. The plasma timolol concentration was significantly higher in PMs than in EMs. There was a fourfold difference in mean AUC (1590 +/- 1133 vs. 394 +/- 239 ng X hr/ml; P less than 0.01) and a twofold difference in mean t1/2 (7.5 +/- 3 vs. 3.7 +/- 1.7 hours; P less than 0.01), reflecting differences in oral clearance (13.1 +/- 7.8 vs. 48.5 +/- 23.2 L/hr; P less than 0.01). The degree of beta-blockade was greater in PMs than in EMs at 12 hours (30.9% vs. 18.2%; P less than 0.05) and at 24 hours (28.3% vs. 13.1%; P less than 0.05). In the group as a whole the metabolic ratio correlated positively with both kinetic data and beta-blockade, but some overlap was observed. Hence timolol metabolism appears to be subject to debrisoquin-type polymorphism, which results in interphenotypic variation in plasma concentration and beta-blocking effect.

Absorption↗
PubMed1984

Comparison of tubular proteinuria, using sodium dodecyl sulphate polyacrylamide gel electrophoresis, in patients during methotrexate or aminoglycoside treatment or with cadmium or Balkan nephropathy.

The pattern of proteinuria found in patients during the administration of methotrexate (MTX) or aminoglycosides (AG) and in cadmium or Balkan nephropathy was investigated using the technique of sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE). As renal tubular dysfunction increased, measured by the urinary concentration of 4 low molecular mass (LMr) proteins, SDS-PAGE bands appeared in the following order of molecular mass (Mr): 59, 44, 31, then below 31 000. The presence of bands less than 31 000 was not an early indicator of drug-induced renal damage. Tubular proteinuria could be monitored more easily by the serum and urinary measurement of any one of the LMr proteins: alpha-1-microglobulin (alpha 1m), retinol-binding protein (RBP), beta-2-microglobulin (beta 2m), except alpha-1-acid glycoprotein (AGP), than by SDS-PAGE.

Adult↗
PubMed1980

Renal tubular damage without glomerular damage after cytotoxic drugs and aminoglycosides.

Cytotoxic agents and aminoglycosides when given for a maximum of eleven days damaged the renal tubules as indicated by an increased urinary beta 2-microglobulin (beta 2-m), N-acetyl-beta-D-glucosaminidase (NAG) and total protein. Methotrexate (MTX) caused the greatest changes among the cytotoxic agents studied. Prophylactic doses of aminoglycosides in surgical patients also caused tubuloproteinuria. The tubular damage was greatest when aminoglycosides were given to treat septicaemia complicating haematological malignancies in patients who had previously had cytotoxic drugs. However, even in these patients there was no evidence of glomerular failure or increased glomerular permeability seven days after beginning chemotherapy.

Acetylglucosaminidase↗
PubMed1972

Fat embolism.

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Embolism, Fat↗
PubMedDate not supplied

Increased urinary beta 2-microglobulin after cancer chemotherapy.

The serum and urinary concentrations of beta 2-microglobulin (beta 2-m) and creatinine and the urinary concentration of albumin and IgG were measured in 14 patients with hematologic malignancies before and during chemotherapy. There was a transient increase in urinary beta 2-m in nine of the 14 patients during chemotherapy. All of the nine patients but only one of the other five patients had had recent multiple chemotherapy. The urinary beta 2-m increased in 24 courses of chemotherapy given to these nine patients and was already abnormal before 13 of these courses. The increase in urinary beta 2-m was not associated with an increase in serum beta 2-m or a significant increase in urinary albumin or IgG excretion. These results suggest that chemotherapy causes a marked transient tubular proteinuria, particularly in patients who have had previous chemotherapy.

Adolescent↗