ABSTRACT
We report three patients with acute promyelocytic leukaemia (APL) occurring after treatment for other malignant disorders. One patient had had razoxane (a drug affecting DNA topoisomerase II) for cancer of the colon, and the other two had had treatment for cancer of the breast. Two out of the three patients went into complete remission. We review the published literature on therapy-related acute promyelocytic leukaemia (t-APL) and suggest that it is a genuine clinical entity which may be caused by drugs affecting DNA topoisomerase II, and has a prognosis similar to de novo APL.
Subject(s)
Antineoplastic Agents/adverse effects , Leukemia, Promyelocytic, Acute/chemically induced , Neoplasms, Second Primary/chemically induced , Adult , Aged , Breast Neoplasms/drug therapy , Colonic Neoplasms/drug therapy , DNA Topoisomerases, Type II/drug effects , Female , Humans , Male , Middle Aged , PrognosisABSTRACT
Anaesthetized Brattleboro rats with hereditary diabetes insipidus were infused with vasopressin at three different doses (1.3, 13 or 130 mu./hr) in order to study the effect of the hormone on renal blood flow and its distribution. Radioactive microspheres were used to determine intrarenal blood flow. The plasma vasopressin level during infusion of the lowest dose was calculated to be within the physiological range. At this dose vasopressin was antidiuretic but was without effect on arterial blood pressure or solute excretion, whereas the two higher doses were both pressor and natriuretic. All doses of vasopressin increased renal vascular resistance and decreased renal blood flow. The vasoconstrictor effect of the lowest dose was confined to the outer cortex, whereas the two higher doses affected the entire cortex. In separate experiments, [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid), 2(O-methyl) tyrosine] arginine vasopressin, an antagonist of the vascular action of vasopressin, was administered to anaesthetized Long Evans or Brattleboro rats. In the Long Evans rats the antagonist caused a decrease in renal vascular resistance and a consequent increase in renal blood flow, this effect being restricted to the outer cortex. In Brattleboro rats the antagonist had no effect on renal vascular resistance or renal blood flow. It is concluded that physiological levels of vasopressin influence the distribution of renal blood flow by causing vasoconstriction in the outer region of the renal cortex. Higher levels of the hormone increase vascular resistance throughout the cortex.
