Hyponatremia in hospitalized patients with the acquired immunodeficiency syndrome (AIDS) and the AIDS-Related complex

1993 ◽  
Vol 94 (2) ◽  
pp. 169-174 ◽  
Author(s):  
Winson W. Tang ◽  
Elaine M. Kaptein ◽  
Eben I. Feinstein ◽  
Shaul G. Massry
1990 ◽  
Vol 322 (19) ◽  
pp. 1333-1340 ◽  
Author(s):  
John S. Lambert ◽  
Mindell Seidlin ◽  
Richard C. Reichman ◽  
Carol S. Plank ◽  
Maura Laverty ◽  
...  

1987 ◽  
Vol 112 (2) ◽  
pp. 259-264 ◽  
Author(s):  
A. Klein ◽  
B. Bruser ◽  
J. B. Robinson ◽  
P. H. Pinkerton ◽  
A. Malkin

ABSTRACT We have observed previously that the rate of cortisol catabolism by lymphocytes (CCL) was indicative of the vulnerability of these cells to cortisol. We attempted to ascertain whether cortisol-sensitive lymphocytes (e.g. thymocytes) metabolize cortisol at a different rate from cortisol-resistant cells and whether lymphocytes in which cortisol catabolism is inhibited become cortisol sensitive. The work was facilitated by the observation that an ethanol extract plasma from patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) had the capacity to inhibit CCL. The capacity of thymocytes to metabolize cortisol was found to be 11 times lower than that of peripheral lymphocytes. Inhibition of CCL with an ethanol extract of plasma from AIDS/ARC patients made the cells vulnerable to cortisol, causing them to die at a rate seven times greater than that of control samples. It is suggested that these findings may have important implications with regard to the nature of lymphocyte depletion in AIDS/ARC patients or in people at risk of developing the syndrome. J. Endocr. (1987) 112, 259–264


1985 ◽  
Vol 147 (4) ◽  
pp. 269-280 ◽  
Author(s):  
Henk-Jan Schuurman ◽  
Philip M. Kluin ◽  
Frits H. J. Gmelig Meijling ◽  
Jan A. M. van Unnik ◽  
Louis Kater

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