The precise nature of the leukocytic reactions during measles still remains a subject concerning which there are surprising differences of opinion. Although it is generally held that a leukocytosis is present during the incubation period, followed as a rule by a leukopenia during the acute febrile stage,1 there is a lack of agreement regarding the changes in the differential count. It was early pointed out by several investigators 2 that the fall in the blood count was due chiefly to a diminution in the number of lymphocytes. Diametrically opposed to this finding, however, have been the reports of a lymphocytosis occurring simultaneously with the rash.3 Moreover, it has been maintained 4 that variations in the number of polymorphonuclear cells principally account for the leukocytosis or the leukopenia observed in the different phases From the Hospital of the Rockefeller Institute for Medical Research.

An increasing amount of evidence has been accumulated (1-3) which indicates that the albumin of the plasma is formed in the liver. The fact that the degree of albumin depression correlates well with the severity of liver involvement in patients with various types of liver disease (4) is strong evidence in favor of such a concept. In view of the significance of the metabolic and oncotic effects of the albumin level of the plasma in determining the course of patients with various types of hypoproteinemla, it would appear to be of special importance to obtain information regarding albumin synthesis in these patients in an attempt to discover possible remediable defects. Direct studies of albumin turnover have yielded some information, but the picture in cirrhosis and nephrosis is often obscured by continued loss of albumin in ascitic fluid or urine. The therapeutic use of concentrated solutions of human albumin has made it even more difficult to determine the rate of production of albumin and to evaluate the changes brought about by such therapy. The use of radioactive and isotope techniques has not as yet been feasible. Two other plasma proteins, fibrinogen and prothrombin, also have been shown to be formed by the liver (5, 6). To this list it is now possible to add a fourth protein appearing in the plasma and synthesized by the liver, namely plasma esterase.The possibility arose that, through a study in various hypoproteinemic states of the other proteins synthesized by the liver and their changes during therapy, information could be obtained regarding the general formation of proteins by the liver which might be applicable to the problem of albumin synthesis.Of the group of liver proteins the plasma esterase lends itself most readily to accurate estimation. In addition, the regeneration of this enzyme can be studied in various pathological states, following its destruction by a parenteral injection of diisopropyl fluorophosphate (DFP). This material is an extremely powerful and specific inhibitor of the esterase group of enzymes. Several observers (7,8) have demonstrated conclusively that these enzymes are irreversibly destroyed beth in ~o and in ~/vo by DFP. Comroe, Todd, and Koelle (8), in connection with their use of this material in patients with myasthenia gravis, studied the regeneration of plasma esterase following its destruction by DFP. Wescoe (9) and Grob (10) have independently applied this technique to the study of patients with liver disease. 325 on