To the Editor.—
In their recent article
in the Archives (139:978-980,1979), Dr
Lawson and his colleagues suggest
that hypokalemia is unusually frequent in patients with acute myeloblastic leukemia (AML). At present,
the most common form of therapy for
this disease includes daunorubicin
hydrochloride, thioguanine, and cytarabine. None of these drugs is associated with abnormal potassium metabolism or affects renal function.1 On
the other hand, most patients with
AML are treated with broad-spectrum
antibiotics for febrile episodes occurring during the period of granulocytopenia that follows chemotherapy.
Carbenicillin disodium and amphotericin B are among the antibiotics frequently used when severe infections
develop. Both substances are associated with hypokalemia, caused by
increased sodium load and metabolic
alkalosis in the case of carbenicillin,2
and distal renal tubular lesions in the
case of amphotericin B.3 Before theorizing the existence of an idiopathic
mechanism for hypokalemia in AML,
I believe the authors should indicate
whether