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Background. Patients with cirrhosis have a high risk of hepatocellular carcinoma (HCC) but it is unclear how the etiology of liver disease influences tumor development. The authors evaluated hepatitis B and C virus (HBV, HCV) infection in cirrhosis in relation to the risk of HCC. Methods. Two hundred and ninety consecutive cirrhotic patients were followed prospectively with periodic ultrasound examination. At entry, patients were tested for markers of HBV and HCV to assess relation to tumor development during follow‐up. Results. Twenty and five‐tenths percent of patients were hepatitis B surface antigen (HBsAg) positive and 68.9% were positive for HCV antibodies. Previous alcohol abuse was present in 26.2%. During follow‐up (46.3 ± 21.4 months), HCC developed in 32 patients (11.0%) (annual incidence approximately 3%) including 19.6% of HBsAg‐positive patients, 12.2% of HCV antibody positive patients and 14.4% of patients with a history of alcohol abuse. The highest rate of HCC was in patients with dual HBsAg and anti‐HCV positivity with or without previous alcohol abuse, whereas the lowest incidence (0%) was in cases without risk factors. By univariate analysis, age older than 59 years (P < 0.005), longer duration of cirrhosis (P < 0.005), serum alpha‐fetoprotein levels higher than 20 ng/ml (P < 0.05), and dual HBsAg and HCV positivity (P < 0.02) appeared to be associated with HCC. By multivariate analysis, age (P < 0.01), positivity for HBsAg and HCV antibodies (P < 0.05), male sex (P < 0.05), and previous alcohol abuse (P < 0.08) were independently related to tumor appearance. Conclusions. These results, although confirming that male sex and previous alcohol abuse are risk factors for hepatocellular carcinoma in cirrhosis, indicate that concurrent hepatitis B and C virus infection determines the highest risk of developing hepatocellular carcinoma.

The frequency of autoimmune disorders was determined in 373 vitiligo patients and in controls matched for sex, age and race. Vitiligo patients had an increased frequency of clinical autoimmune diseases of thyroid (7.5%), stomach (0.8%), parathyroid (1%), adrenal gland (1.3%). Vitiligo patients, without clinical signs of overt autoimmune diseases, also had a statistically significant increase in the frequency of gastric parietal cell (p < 0.001), thyroid microsomal (p < 0.05) and adrenal autoantibodies (p < 0.05). This increased incidence of autoimmune manifestations was correlated with the duration of vitiligo. Furthermore in 94% of the patients with parietal cell autoantibodies a gastric biopsy showed atrophic gastritis. In addition, in 48% of the patients with thyroid microsomal autoantibodies and in 2 out of 6 patients with adrenal autoantibodies without overt diseases at the beginning of the study, the functional investigation of the target organs during the follow-up allowed the detection of the presence or that of the subsequent development of clinical or subclinical dysfunction.

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Our study, although limited by a relatively short follow-up and small sample size, shows that bilateral oophorectomy for ovarian metastasis from colorectal cancer has a good impact on disease-free and overall survival.

Hepatitis B virus (HBV)-and hepatitis C virus (HCV)-The pathophysiology of liver damage mediated by related liver damage is linked to an increased risk of hepatitis B virus (HBV) and the mechanisms underlyhepatocellular carcinoma, but the mechanisms underly-ing its oncogenic activity have been thoroughly investiing hepatitis C viral activity are not known. We therefore gated in the last 20 years. As for the former, it has compared hepatocellular proliferative activity in become clear that a cell-mediated immune response to chronic C virus-related hepatitis and in liver damage HBV gene products on the cellular membrane of hepaof other etiology. Hepatocyte proliferation rate was in-tocytes is the major cause of liver injury.1 Concerning vestigated in 56 patients with chronic hepatitis using the latter, in addition to the obvious role played by the the Ki67 MIB1 monoclonal antibody in archival material.process of necrosis and regeneration typical of cirrhoAccording to etiology, the patients were subgrouped as sis, the results of various studies point to different follows: HCV (34), HBV (11), Alcohol (4), HCV / Alcohol (4), and Hemochromatosis (3). Proliferation rate was cor-hypotheses: (1) insertional mutagenesis with the modirelated with age, sex, etiology, disease activity, liver iron fication of either sequences coding for oncogenes or stestorage, free-radical production, and glutathione levels roid receptors, 2 or cyclin A gene 3 ; or (2) transactivation, by regression and discriminant analysis. HCV-positive through HBV X gene protein or pre-S/S protein, deleted patients had significantly more MIB1-positive hepato-at the C-terminal, altering host gene expression, and cytes in the periportal area (P õ .011) and in the low-thus ultimately leading to malignant transformation proliferating perivenular area (zones 2 and 3) (P õ .05). of the hepatocyte. evidence has also pointed to the role of iron accumulation in HCV-mediated liver damage, 11 and we have documented an increased liver iron storage, lipid peroxidation, and reduced glutathione (GSH) turnover oncogenesis, and an indirect mechanism is more likely.Received May 22, 1995; accepted February 6, 1996. Whatever the mechanism(s) involved, HCV infection disease activity; liver iron storage; and free-radical pro-

AsTRiAcr Primary intrapulmonary neurogenic tumours are extremely rare. In a series of 1664 patients with pulmonary neoplasms observed during 1967-80 only four such tumours were identified (0.2%). All four patients underwent surgical excision. The histological diagnosis was benign neurilemmoma in three cases and malignant schwannoma in the fourth. The patients with neurilemmoma are alive and well four to 12 years after surgery, but the patient with malignant schwannoma died from metastatic spread of the tumour four months after surgery. No association with von Recklinghausen's disease was observed. Macroscopic and microscopic features generally lead to a correct diagnosis in benign types, but the histological diagnosis of malignant schwannoma may present some difficulties and requires the establishment of a definite origin in a nervous structure, identification of benign neurofibroma in different areas of the same tumour, and a high density of cells with appreciable pleomorphism, with mitosis and atypia. Benign tumours carry a good prognosis with little tendency to recur, but malignant schwannoma has a high invasive tendency and is associated with a low survival rate.