FACTORS ALTERING CONCENTRATION OF BLOOD LIPIDS 483 



cholesterol level drops prior to the attack. Cholesterol levels are slightly 

 higher in epileptics than in normal subjects, and the ratios of cholesterol 

 to lipid phosphorus are slightly elevated in the epileptic patients. It is 

 believed that the latter ratio may be correlated with the frequency of epilep- 

 tic seizures. 



m. The Blood Lipids in Infectious Diseases. Most lipids decrease in 

 the serum during the acute stages of febrile infectious diseases. 410 - 795-798 

 Cholesterol is the chief lipid component affected in infectious fevers, while 

 the fatty acids constitute the component which is the least influenced. 

 The hypocholesterolemia resulting during the acute stages of the infec- 

 tion occurs at the onset of the infection and disappears on convales- 

 cence 306 - 410,795,798,799. m f ac ^ as ^ e p a tient recovers, a temporary hyper- 

 cholesterolemia may develop, due to the fact that the normal level is ex- 

 ceeded. 302 ' 796 - 800 Chauffard et a/. 801 report that the decrease in cholesterol is 

 proportional to the intensity of the infection. 



In the group of acute infections, hypocholesterolemia has been found 

 in scarlet fever, 802 in hog cholera, alternating with periods of hypercho- 

 lesterolemia, 803 in colds and similar infections, 283 in typhoid fever, 796 in 

 rats infected with the paratyphoid organism (Salmonella enteritides (dany- 

 szi)) SOi and in pneumonia. 800 - 805 No variation in blood lipids can be effected 

 by artificial fever produced by diathermy or by the administration of 

 phenylethylhydantoin or typhoid vaccine. 798 D'Alessandro 806 found that 

 the blood cholesterol was slightly increased in the tertiary benign and 

 febrile quaternary forms of malaria. 



A number of investigators have reported that a hypocholesterolemia 

 obtains in a variety of chronic infections. 270 - 807 " 809 Thus, lower than nor- 

 mal cholesterol values have been reported in blood serum in the early 



795 H. A. Kipp, J. Biol. Chem., 44, 215-237 (1920). 



796 S. Marino, Arch, farmacol. sper., 55, 1-27 (1933). 



797 I. Rosen, F. Krasnow, and M. A. Lyons, Arch. Dermatol. Syphilol, 27, 383-391 

 (1933). 



798 A. V. Stoesser and I. McQuarrie, Am. J. Diseases Children, 49, 658-671 (1935). 



799 C. Achard, A. Grigaut, A. Le Blanc, and M. David. J. physiol. et path, gen., 26, 

 415^25 (1928). 



800 A. Steiner and K. B. Turner, J. Clin. Invest., 19, 373-377 (1940). 



801 A. Chauffard, G. Laroche, and A. Grigaut, Semaine med., 81, 577-581 (1911). 



802 G. Stern, Z. Kinderheilk., 25, 129-133 (1920). 



803 R. E. Shope, J. Exptl. Med., 51, 179-187 (1930). 



804 W. M. Sperry and V. A. Stoyanoff, J. Biol. Chem., 105, lxxxii (1934). 



805 A. V. Stoesser, Proc. Soc. Exptl. Bwl. Med., 32, 1324-1325 (1935). 



806 R. D'Alessandro, Arch, farmacol. sper., 52, 258-268 (1931). 



807 L. Eichelberger and K. L. McCluskey, Arch. Internal Med., 40, 831-839 (1927). 



808 B. H. Henning, J. Biol. Chem., 53, 167-170 (1922). 



809 S. E. King and M. Bruger, Ann. Internal Med., 8, 1427-1435 (1935). 



