A histopathological study was carried out on 27 patients with chronic inflammatory liver disease and clinical and/or biochemical evidence of cholestasis who had either mitochondrial antibodies against mitochondrial antigen fractions of 1.19 density ("PBC antigen"; 14 cases) or of 1.13 density ("CAH-PBC mixed-type antigen"; 13 cases). For comparison, the liver biopsies of 17 patients with chronic-aggressive hepatitis (CAH) and antinuclear and/or anti-smooth muscle antibodies but without cholestasis and mitochondrial antibodies, were evaluated. The 14 patients with mitochondrial antibodies against the PBC antigen showed the typical histological features of primary biliary cirrhosis (PBC). The 13 patients with mitochondrial antibodies against the CAH-PBC mixed-type antigen had heterogenous liver alterations. In 11 cases highly active CAH and/or active postnecrotic cirrhosis (AC) were found both with augmented ductular proliferation. Some of these cases showed distinct criteria of PBC as early bile duct lesions or absence of regular bile ducts. The liver histology of one case corresponded to classical PBC; another case to chronic persistent hepatitis. The CAH-patients without cholestasis and mitochondrial antibodies only occasionally showed bile duct proliferation. In conclusion, a high correlation was found between mitochondrial antibodies against the CAH-PBC mixed-type antigen and highly active CAH or early AC with augmented ductular proliferation. This represents an overlapping of CAH and PBC. In contrast, the cases with antibodies reacting to the PBC antigen showed the slowly progressive liver changes of typical PBC.
The laparoscopic photographs of 38 cases of primary biliary cirrhosis with high titres of mitochondrial antibodies were reviewed. The quality of laparoscopic photography is now so high that it proved possible to use these photographs as the basis of a system of laparoscopic staging. By analogy with the system of histological classification, the disease was divided into four stages. Laparoscopy provides an alternative approach to the diagnosis of primary biliary cirrhosis, which should be based on clinical, biochemical, immunological and morphological data. However, by laparoscopy alone it is improssible to separate pure primary biliary cirrhosis from its mixed forms with chronic active hepatitis.
Over a period of 18 months the development of hepatitis after intake of oxyphenisatin, a laxative, was established in 14 patients by re-exposure to the drug. The characteristic feature was nonspecific upper abdominal pain up to colic-like pain, lact of appetite, nausea or vomiting, and pruritus. The biochemical changes were those of chronic hepatitis with varying severity of biliary stasis and abnormal immunofluorescence. On re-exposure there was a particularly remarkable rise in GLDH activity. The histological picture showed acute inflammatory changes in the biliary passages on re-exposure, while the liver cells were clearly involved only secondarily. At a latter point the histological picture became non-specific. At laparoscopy there were different stages of minor periportal hepatic fibrosis to marked postnecrotic liver scars with portal hypertension and decompensation. Early diagnosis is difficult but crucial to the patient's fate, because this form of hepatitis regresses completely after oxyphenisatin has been stopped. Laxatives containing this drug should be withdrawn from the market.
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