Central Surgical Association| Volume 82, ISSUE 4, P495-503, October 1977

Benign hepatocellular tumors

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      This series summarizes all cases diagnosed as benign hepatocellular tumors occurring at the University of Minnesota Hospitals from 1950 to 1976. Excluding hemangiomas, 40 tumors were reviewed and reclassified. Eighteen were diagnosed as focal nodular hyperplasia (FNH), 10 as hepatocellular adenomas (HCS), 11 as bile duct adenomas (BDA), and one as a mesenchymal hamartoma. FNH: The female: male ratio was 8:1, and the mean age was 43 years ±18 (SD). Two patients were symptomatic; of these, one presented with portal hypertension. Treatment consisted of local resection in 12, left hepatectomy in one, and right hepatectomy in two. Eight patients had a history of oral contraceptive or other steroid intake. The tumors occurring after 1964 were larger (p < 0. 05). HCA: The female: male ratio was 4:1, and the mean age was 33 years ±20 (SD). Five tumors were found at necropsy; the other five were symptomatic. Treatment consisted of local resection in one patient, right hepatectomy in two, and left hepatectomy in one. Three patients had a positive history of oral contraceptive intake. There was no statistically significant difference in the size or the incidence of hepatocellular adenomas between the time spans of 1950 to 1963 and 1964 to 1976. BDA: The female: male ratio was 7:4, and the mean age was 57 years ±15 (SD). Only one case was symptomatic and this lesion measured 10 cm. The other BDAs were 1 cm or less in diameter. There is no suggestion that these tumors are associated with use of birth control pills. This series has a lower proportion of symptomatic patients and of patients on oral contraceptives than is suggested by reviewing the literature. From our series we conclude that a causal relationship between use of oral contraceptives, or other steroids, and benign hepatocellular tumors cannot be demonstrated. However, this conclusion does not rule out that oral contraceptives, or other steroids, might have a contributory influence on the initiation of certain of these tumors or on tumor size.
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