484 V. BLOOD LIPIDS 



acute phases of syphilis, 797,810 leprosy, 270 in the terminal stages of tubercu- 

 losis, 809 in the active stages of rheumatic fever, 811 and also in rheumatic heart 

 disease associated with cardiac failure. 811 - 812 The blood carotene is reduced 

 in various forms of leprosy, and the serum vitamin level is low in lepra 

 nervorum. It is possible that slightly higher than normal cholesterol 

 values obtain in filariasis 813 ; apparently this also occurs in cerebrospinal 

 syphilis. 797 



The decrease in blood cholesterol in infections occurs at the expense of 

 the cholesterol ester, with the result that the ratio, free cholesterol: total 

 cholesterol rises. 800,805 ' 814 The feeding of cholesterol to animals has been 

 shown to increase their resistance to infection. 815 Tunnicliff 816 also re- 

 ported that the addition of small doses of cholesterol doubled the opsonic 

 and cytophagic indices of blood as determined by both in vitro and in vivo 

 tests, while stronger concentrations had the opposite effect. 



Lipids other than cholesterol have been shown to remain constant or to 

 decrease in fever. 817 ^ 819 Phospholipids are reduced on the onset of fever, 

 and increase during convalescence. 796,799,820 Bing and Heckscher 610 and 

 Bonniger 585 reported that fatty acids are increased in pneumonia, although 

 the opposite results were noted in six cases reported by Stoesser and Mc- 

 Quarrie. 798 



n. The Blood Lipids in Cancer. The reports on the effect of cancer 

 on the blood lipids of patients with cancer and on experimental animals 

 suffering from cancer are quite conflicting. Thus, Mattick and Buch- 

 wald 821,822 found that the cholesterol was higher in plasma than in whole 

 blood in most cases of cancer, while the opposite situation usually obtained 

 in normal subjects. A plasma hypercholesterolemia was usually found. 

 On the other hand, the results of Downes and Pack 823 and of Denis 410 



8io y. Feraru and F. M. Offenkrantz, Am. J. Syphilis, Gonorrhea, Venereal Diseases, 

 21, 267-281 (1937). 



811 F. M. Offenkrantz, Am. J. Diseases Children, 56, 67-82 (1938). 



812 C. A. Poindexter and M. Bruger, Arch. Internal Med., 61, 714-719 (1938). 

 8,3 T. C. Boyd and A. C. Roy, Indian J. Med. Research, 17, 949-953 (1930). 

 814 A. V. Stoesser, Proc. Soc. Exptl. Biol. Med., 43, 168-170 (1940). 



818 E. Leupold and L. Bogendorfer, Deut. Arch. klin. Med., 140, 28-38 (1922). 



816 R. Tunnicliff, /. Infectious Diseases, S3, 285-288 (1923). 



817 H. Hamano, Proc. Imp. Acad. (Tokyo), 7, 80-81 (1931). . 



818 E. M. Boyd, J. H. Orr, and G. B. Reed, Proc. Soc. Exptl. Biol. Med., 35, 479^82 

 (1936). 



819 W. Raab, Z. ges. exptl. Med., 89, 616-621 (1933). 



820 1. McOuarrie and A. V. Stoesser, Proc. Soc. Exptl. Biol. Med., 29, 1281-1283 

 (1932). 



821 W. L. Mattick and K. W. Buchwald, J. Cancer Research, 12, 236-245 (1928). 



822 W. L. Mattick and K. W. Buchwald, J. Cancer Research, 13, 157-166 (1929). 



823 H. R. Downes and G. T. Pack, Am. J. Cancer, 16, 290-296 (1932). 



