The morphological classification of acute and chronic viral hepatitis has been subject of considerable controversy. Main problems in nomenclature have arisen from the confusion of pathologically defined lesions with purely clinical designations. The classification used in this article is based on a number of recent reviews in which a certain measure of agreement has been reached between clinicians and histopathologists. As a general rule, in acute forms of hepatitis diffuse lobular changes predominate over portal lesions while chronic hepatitis is characterized by conspicuous alterations of portal (and periportal) areas. This report will merely summarize main diagnostic features of the different forms of viral hepatitis. For more detailed information the reader is referred to several leading articles discussing in detail morphology, and putting emphasis on pathogenesis. An exact "staging" of viral hepatitis by histologic criteria is an important tool in the evaluation of prognosis, indication and control of therapy as well as for comparison with immunologic findings.

Eleven patients with Dubin-Johnson syndrome (DJS) were studied clinicopathologically. In three patients with DJS, concomitant chronic hepatitis was observed. They showed long-standing jaundice with the symptoms of general fatigue and anorexia. Laboratory tests revealed mild hypertransaminasemia, elevated serum bilirubin (over 5.0 mg/dl) and a high level of serum Bromsulphalein (BSP) retention at 45 min (above 18%). Two patients complicated with chronic hepatitis showed a rather slow secondary rise in the BSP excretion curve in comparison with the patients who had no complication. One patient accompanied with the most severe fibrosis showed no secondary rise in the BSP excretion curve. After the treatment of the patient with phenobarbital, however, a secondary rise in the BSP excretion curve appeared and the serum BSP level was also significantly decreased at all points on the BSP excretion curve. Histological examination of the liver revealed the decreased number of the Dubin-Johnson pigments in the patients complicated with chronic hepatitis. Laparoscopically, a patient with a chronic aggressive hepatitis showed a dark gray decololization of the liver surface and another patient with a chronic aggressive hepatitis showed a black color of the liver surface with partial nodule formation.

Gilbert's syndrome is typically associated with a deficiency in hepatic bilirubin UDP-glucuronosyltransferase activity (B-GTA). The overproduction of bilirubin that is often found in this condition could be a fortuitous coincidence that leads to the unmasking of the disease, which otherwise often remains latent. Some cases of chronic unconjugated hyperbilirubinaemia could, however, be related to a defect in hepatic uptake, as reflected by alterations in BSP kinetics. Severe deficiencies of hepatic B-GTA exist in all types of Crigler-Najjar disease. An increased proportion of bilirubin monoglucuronide is always found in bile when a B-GTA deficiency is present. This observation strongly suggests a common biochemical defect in Gilbert's syndrome and in Crigler-Najjar disease, and thus renders the suggestion that the latter condition may be separated into two groups somewhat inappropriate. There is, however, no doubt that further knowledge of the conjugating enzyme, or enzymes, is required: such information may lead to the characterisation of several types of enzymic defects. Whereas little is new as far as the Dubin-Johnson syndrome is concerned, Rotor's syndrome can no longer be considered to be a variant of the former. The transport defect which is involved in most cases of Rotor's syndrome, if not in all, is an impairment of hepatic storage, thus distinguishing it from the impairment of excretion which is involved in the Dubin-Johnson syndrome. The distinct patterns of urinary coproporphyrin excretion, which were recently reported in Dubin-Johnson and Rotor's syndromes, offer additional evidence for a clear differentiation between these two entities.