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Decreased activity of the multidrug resistance P-glycoprotein in acquired aplastic anaemia: possible pathophysiologic

R T Calado1, A B Garcia, R P Falcão

  • 1Department of Clinical Medicine, School of Medicine of Ribeirão Preto, University of São Paulo, Brazil.

Insights

Multidrug resistance mechanisms, specifically P-glycoprotein function, are impaired in aplastic anemia (AA) patients, even in remission. This reduced P-glycoprotein activity may increase susceptibility to drug-induced injury in hematopoietic cells.

Area of Science:

  • Hematology
  • Cellular Biology
  • Pharmacology

Background:

  • Acquired aplastic anemia (AA) involves potential impairments in multidrug resistance (MDR) mechanisms.
  • Understanding MDR function is crucial for comprehending AA pathophysiology and treatment responses.

Purpose of the Study:

  • To investigate the function of P-glycoprotein (P-gp) and multidrug resistance-associated protein (MRP) in lymphocytes of AA patients.
  • To determine if MDR mechanisms are altered in AA, even after disease remission.

Main Methods:

  • Assessed P-gp function using rhodamine 123 (Rh123) efflux in T cells, B cells, and NK cells.
  • Evaluated MRP function via daunorubicin (DNR) efflux in peripheral blood lymphocytes.
  • Compared efflux activity between AA patients and healthy controls.

Main Results:

  • A significant decrease in Rh123 efflux was observed in T cells from AA patients compared to controls.
  • This reduced P-gp activity in T cells persisted even in patients with AA in remission.
  • Rh123 efflux in B and NK cells, and DNR efflux in lymphocytes, remained unchanged.

Conclusions:

  • P-glycoprotein activity is decreased in T cells of aplastic anemia patients, both during active disease and remission.
  • Impaired P-gp function may contribute to the pathophysiology of AA by increasing hematopoietic cell susceptibility to drug-induced injury.

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