Calla-positive acute leukaemia with t(5q;14q) translocation and hypereosinophilia--a unique entity?

A patient with common acute lymphoblastic leukaemia (ALL), hypereosinophilic syndrome and t(5;14) (q31.1;q32.3) translocation is described. Even with intensive treatment only short periods of complete remission were achieved. Recurrence of the leukaemia was always accompanied by the appearance of eosinophilic granulocytes in the blood and in the bone marrow. Although there is no experimental proof we assume that the hypereosinophilic syndrome is causally related to the chromosome aberration. Translocation of the GM-CSF gene from chromosome No. 5 to chromosome No. 14, might have led to the deregulation of the gene by enhancer sequences of the immunoglobulin heavy-chain region on chromosome No. 14, with the consequence of an overproduction of neutrophilic and particularly eosinophilic granulocytes. Furthermore, stimulation of the leukaemic cell clone may have occurred by this translocation. The similarity of the clinical course with cases described in the literature suggests that this condition is a unique entity of ALL.

Prostaglandin-independent protection by furosemide from oliguric ischemic renal failure in conscious rats.

In 38 conscious rats divided into seven groups, acute unilateral ischemic renal failure was induced by 1 hour of complete occlusion of the left renal artery while the contralateral kidney remained intact. Renal excretory function of the left kidney was monitored up to 144 hours after ischemia and revealed a typical course of oliguric renal failure with oligoanuria persisting for more than 48 hours. Urinary osmolality and sodium concentration became plasma isotonic after release of renal artery occlusion and approximated control values on day 6 after ischemia. In nine rats, the i.v. infusion of furosemide before (6 microgram/min/100 g body wt) and after (12 microgram/min/100 g body wt) renal artery occlusion protected the ischemic kidney from oligoanuria with endogenous creatinine clearance of 0.42 +/- 0.11 ml/min/g kidney wt 5 hours after ischemia. Tubular absorption of sodium and water was at least partially preserved 36 hours after ischemia when infusion of furosemide was stopped. The loop diuretic significantly (P less than 0.01) increased total urinary prostaglandin (PG) E2 excretion before and after renal artery occlusion; and 5 hours after ischemia, PGE2 excretion from the ischemic kidney significantly exceeded that from the intact kidney (P less than 0.05). Indomethacin (1 mg/100 g body wt) administered in six animals markedly suppressed control PGE2 excretion (P less than 0.05) as well as the furosemide-induced rise in urinary PG excretion before and after ischemia but did not modify the protective effect of the diuretic in this experimental model. Inhibition of PG synthesis, however, reduced urinary flow rate and sodium and potassium excretion of the contralateral intact kidney and almost completely prevented its compensatory rise in creatinine clearance. The results indicate that mechanisms other than the intrarenal prostaglandin system must be considered to mediate the protective effects of furosemide in acute ischemic renal failure.