scholarly journals Neutrophil life span in paroxysmal nocturnal hemoglobinuria

Blood ◽  
1977 ◽  
Vol 50 (4) ◽  
pp. 657-662 ◽  
Author(s):  
LH Brubaker ◽  
LJ Essig ◽  
CE Mengel

Abstract We have studied neutrophil intravascular life span in six patients with paroxysmal nocturnal hemoglobinuria (PNH); four had normal neutrophil counts when studied and two were neutropenic. Five patients had enough circulating neutrophils to isolate for tests in vitro. Lysis of labeled neutrophils was greatly increased, compared to that of normal volunteers, when these neutrophils were incubated with acidified fresh serum as a source of active complement plus serum containing antineutrophil antibodies (from three different sources). Despite the in vitro lesion, however, each of these patients had a normal neutrophil intravascular life span as measured by the 32P- diisopropylfluorophosphate technique. One neutropenic patient, who had a normal neutrophil life span, had a shift of cells from the circulating to marginated pool of sufficient degree to cause the neutropenia. A second (severely) neutropenic patient was found to have developed extreme marrow hypoplasia, also explaining the neutropenia. Thus, in contrast to the shortened red cell life span, we have been unable to find a shortened neutrophil life span in PNH.

Blood ◽  
1977 ◽  
Vol 50 (4) ◽  
pp. 657-662 ◽  
Author(s):  
LH Brubaker ◽  
LJ Essig ◽  
CE Mengel

We have studied neutrophil intravascular life span in six patients with paroxysmal nocturnal hemoglobinuria (PNH); four had normal neutrophil counts when studied and two were neutropenic. Five patients had enough circulating neutrophils to isolate for tests in vitro. Lysis of labeled neutrophils was greatly increased, compared to that of normal volunteers, when these neutrophils were incubated with acidified fresh serum as a source of active complement plus serum containing antineutrophil antibodies (from three different sources). Despite the in vitro lesion, however, each of these patients had a normal neutrophil intravascular life span as measured by the 32P- diisopropylfluorophosphate technique. One neutropenic patient, who had a normal neutrophil life span, had a shift of cells from the circulating to marginated pool of sufficient degree to cause the neutropenia. A second (severely) neutropenic patient was found to have developed extreme marrow hypoplasia, also explaining the neutropenia. Thus, in contrast to the shortened red cell life span, we have been unable to find a shortened neutrophil life span in PNH.


Blood ◽  
1961 ◽  
Vol 18 (2) ◽  
pp. 220-224 ◽  
Author(s):  
WILLIAM H. CROSBY ◽  
CALOGERO VULLO ◽  
SERGIO GARRIGA

Abstract Autohemolysis occurs in vitro in the blood of some patients with leukemia and other disseminated neoplastic diseases. It is known that patients with such diseases are frequently anemic and hemolytic disease frequently contributes to the anemia. The present study has demonstrated that the in vitro autohemolytic phenomenon is not necessarily associated with a short red cell life span. This suggests that the abnormality does not damage the red cells while they are in the circulation.


1966 ◽  
Vol 19 (2) ◽  
pp. 471-473 ◽  
Author(s):  
Ward D Noyes ◽  
Hyram Kitchen ◽  
W Jape Taylor

Blood ◽  
1963 ◽  
Vol 21 (1) ◽  
pp. 63-69 ◽  
Author(s):  
MARTIN J. CLINE ◽  
NATHANIEL I. BERLIN

Abstract 1. The erythrocyte Cr51 elution rate was determined in 38 patients with hematologic diseases. 2. In four patients with finite red cell life spans, two exponential Cr51 elution rate constants could be calculated. In the remaining 34 patients, the data were consistent with a single exponential elution rate constant from day 1 to day 30-40 following Cr51 administration. 3. The single elution rate varied from 0.62 to 2.27 per cent per day. 4. In two patients, the chromium elution rates determined on two separate occasions were not significantly different. In a third individual, the chromium elution rate constant was 0.75 per cent per day when the red cell life span was 66 days and 1.07 per cent per day when red cell life span was 79 days.


1957 ◽  
Vol 35 (1) ◽  
pp. 1171-1181
Author(s):  
L. G. Israels ◽  
A. Chutorian ◽  
G. E. Delory ◽  
Esther Israels

Sulphaemoglobinaemia was produced in rabbits by the injection of para-aminopropriophenone and calcium sulphide. The disappearance of this pigment from the blood was used as an index of red cell survival. Sulphaemoglobin disappeared in an exponential fashion, indicating a mean red cell life span of 36 days. The red cells were also tagged with Cr51, and this method of measuring erythrocyte life span yielded values strongly suggesting that sulphaemoglobin in the red cell impairs its viability and leads to random cell destruction. Under these conditions it would seem that the disappearance rate of sulphaemoglobin is not a true measure of red cell survival.


Blood ◽  
1976 ◽  
Vol 47 (6) ◽  
pp. 909-917 ◽  
Author(s):  
TA Lane ◽  
ER Burka

Abstract Red blood cells exposed to cyanate (CNO) in vitro have a concentration- dependent decreased cell survival time associated with an inhibition of the ability of the cell membrane to synthesize lipids. The t1/2 of rabbit erythrocytes exposed to 30 mM or 50 mM cyanate for 1 hr at 37 degrees C is reduced from the normal 24 days to 15 and 9 days, respectively. The cyanate-induced defect in membrane lipid metabolism is irreversible. Carbamylation of membrane proteins and damage to metabolism are minimized by limiting exposure in vitro to 15 mM cyanate at 4 degrees C for 30 min. Cells carbamylated under these conditions do not have a shortened life span. Levels of globin carbamylation of 0.5 moles CNO/mole hemoglobin, shown to be clinically effective in prolonging the life span of sickle erythrocytes, are obtained under these conditions and reach maximal levels after only 30 min of incubation. Carbamylation of blood in CPD anticoagulant is inferior to either ACD or heparin. The findings indicate that adequate carbamylation of sickle erythrocytes with minimal red cell membrane damage can be achieved without significant modification of the standard plasmapheresis procedure utilized by the working blood bank.


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