Liver transplantation is an effective treatment for small, unresectable hepatocellular carcinomas in patients with cirrhosis.

RFA is a safe and effective treatment of small HCC in cirrhotics awaiting OLT, although tumor size (>3 cm) and time from treatment (>1 year) predict a high risk of tumor persistence in the targeted nodule. RFA should not be considered an independent therapy for HCC.

No abstract

A series of 132 patients who underwent liver transplantation for primary liver cancer was collected from three different Italian hospitals and studied for recurrence of hepatocellular carcinoma after liver replacement. Twenty-one patients (15.9%) had a neoplastic recurrence after an average follow-up period of 7.8 months after transplantation (range, 1-25 months); 15 (71%) occurred within the first 18 months after transplant and only two recurred later than 2 years. The sites of recurrence were grafted liver (19%), lung (19%), bone (14%), and other (5%). Eight patients (38%) had multiple organ involvement at the onset. After 1, 2, 3, and 4 years the overall survival rates were 62%, 43%, 29%, and 23%, respectively. The tumor factors related to early cancer recurrence after transplantation were diameter of nodules more than 3 cm (P < 0.05), tumor stage not meeting the "Milan criteria" (P < 0.03), and presence of peri-tumoral capsule (P < 0.05); the number of nodules, TNM stage, presence of vascular invasion, alpha-fetoprotein level more than 150 UI/l, pre-transplant chemoembolization and resectability of cancer deposits did not seem to be related to early recurrence. The prognosis differed in the 7 patients with resectable recurrences (57% 4-year survival) and the 14 patients with unresectable disease (14% 4-year survival) (P < 0.02). Better patient selection and new combined medical strategies could reduce the incidence of and mortality from liver cancer recurrence after transplantation. The role of surgical resection of recurrence should be further investigated.

Diabetes mellitus frequently complicates cirrhosis but the pathogenic mechanisms are unknown. To assess the contribution of reduced insulin action and secretion, 24 cirrhotic-diabetic patients waiting for liver transplant because of an unresectable hepatocarcinoma underwent an oral glucose tolerance test (OGTT) to assess the ␤-cell function and an insulin clamp combined with [3-3 H]glucose infusion to measure whole body glucose metabolism before and 2 years after the transplant. Seven cirrhotic nondiabetic patients, 11 patients with chronic uveitis on similar immunosuppressive therapy, and 7 healthy subjects served as control groups. Cirrhotic patients showed a profound insulin resistance, and diabetics in addition also showed increased endogenous glucose production (P Ͻ .05) and insulin deficiency during the OGTT (P Ͻ .05). Liver transplantation normalized endogenous glucose production and insulin sensitivity but failed to cure diabetes in 8 of the 24 patients because a markedly low insulin response during the OGTT. Age, body mass index, family history of diabetes, immunosuppressive drugs, and pathogenesis of cirrhosis did not predict in whom liver transplant was going to cure diabetes. On the contrary, a reduced secretory response characterized the patients in whom the transplant would not be curative. In summary, insulin resistance was a primary event complicating cirrhosis but additional ␤-cell secretory defects were crucial for development of diabetes. Liver transplantation, lessening insulin resistance, cured hepatogenous diabetes in 67% of cirrhotic-diabetic patients; nevertheless 33% were still diabetics because the persistence of a reduced ␤-cell function, which makes these patients eventually eligible for combined islet transplantation. (HEPATOLOGY 2000;31:694-703.)Cirrhotic patients are characterized by impaired glucose metabolism 1 ; 60% to 80% are glucose intolerant and 10% to 15% develop overt diabetes mellitus. [2][3][4] The development of diabetes following liver cirrhosis seems also to be relatively rapid; during a period of 5 years nearly 15% to 20% of cirrhotic patients develop frank hyperglycemia. 5 The high incidence of diabetes among cirrhotic patients was recognized to be secondary to the hepatic disease since 1906 when the term ''hepatogenous diabetes'' was first coined. 6 Diabetes does not affect short-term survival, but it seems to be significantly correlated with poor prognosis in long-term follow-up, the higher mortality rate being mainly caused by an increased risk of hepatocellular failure. 7 The sequence, the relative importance, and the molecular mechanisms of the pathogenic factors are still largely unknown because liver cirrhosis is characterized by heterogeneous clinical pictures related to etiologic and environmental factors, nutritional state, complex physiologic endocrine interactions, and stage and stability of the liver disease. Recently liver transplantation was found to be an effective treatment for small unresectable hepatocellular carcinomas in patients with cirrhosis,...