The differential diagnosis of acute hepatitis involves the separation of (1) acute damage of the hepatic parenchyma from other diseases simulating it, especially in the absence of jaundice, and (2) the different forms of acute parenchymal disease from one another. The latter may be either inflammatory or degenerative in nature. In the liver more so than in any other parenchymal organ, these two basic pathologic phenomena can be differentiated only with extreme difficulty. For practical reasons it is, therefore, preferred to call acute parenchymal disease of the liver "hepatitis." The identification of acute hepatitis without jaundice has become important in view of the recently described infectious form1which is demonstrated by laboratory procedures, such as determination of sulfobromophthalein sodium retention, cephalin-cholesterol flocculation, thymol turbidity and elevated excretion of urinary urobilinogen. In some instances pathologic changes have been found in biopsy specimens. Damage to the liver without jaundice due to
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Hans Pópper (1948) studied this question.
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