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Our study suggests that TACE through extrahepatic collaterals is possible with high success rates, and is also relatively safe.

The purpose of this study was to evaluate the clinical course of main bile duct stricture at the hepatic hilum after transcatheter arterial chemoembolization (TACE) for hepatocellular carcinoma (HCC). Among 446 consecutive patients with HCC treated by TACE, main bile duct stricture developed in 18 (4.0%). All imaging and laboratory data, treatment course, and outcomes were retrospectively analyzed. All patients had 1 to 2 tumors measuring 10 to 100 mm in diameter (mean ± SD 24.5 ± 5.4 mm) near the hepatic hilum fed by the caudate arterial branch (A1) and/or medial segmental artery (A4) of the liver. During the TACE procedure that caused bile duct injury, A1 was embolized in 8, A4 was embolized in 5, and both were embolized in 5 patients. Nine patients (50.0%) had a history of TACE in either A1 or A4. Iodized oil accumulation in the bile duct wall was seen in all patients on computed tomography obtained 1 week later. Bile duct dilatation caused by main bile duct stricture developed in both lobes (n = 9), in the right lobe (n = 3), in the left lobe (n = 4), in segment (S) 2 (n = 1), and in S3 (n = 1). Serum levels of alkaline phosphatase and γ-glutamyltranspeptidase increased in 13 patients. Biloma requiring drainage developed in 2 patients; jaundice developed in 4 patients; and metallic stents were placed in 3 patients. Complications after additional TACE sessions, including biloma (n = 3) and/or jaundice (n = 5), occurred in 7 patients and were treated by additional intervention, including metallic stent placement in 2 patients. After initial TACE of A1 and/or A4, 8 patients (44.4%), including 5 with uncontrollable jaundice or cholangitis, died at 37.9 ± 34.9 months after TACE, and 10 (55.6%) have survived for 38.4 ± 37.9 months. Selective TACE of A1 and/or A4 carries a risk of main bile duct stricture at the hepatic hilum. Biloma and jaundice are serious complications associated with bile duct strictures.

Background: In patients with chronic liver disease (CLD), glycated haemoglobin (HbA 1C ) levels have been shown to be apparently lower than real values, whereas serum glycated albumin (GA) levels are apparently higher. The present study was aimed to examine whether both glycaemic indices are influenced by hepatic function. Methods: Subjects consisted of 82 patients with CLD. Various indicators for hepatic function as well as HbA 1C and GA were also measured. Estimated HbA 1C values were calculated from the mean plasma glucose levels. Two hundred and two type 2 diabetic patients without CLD were studied as controls. Results: Although GA was strongly correlated with HbA 1C in patients with CLD as well as diabetic patients, GA levels in patients with CLD were relatively higher than those in diabetic patients. In patients with estimated HbA 1C 5.8%, GA levels significantly increased but HbA 1C levels decreased as a function of decreasing hepaplastin test (HPT). The ratio of GA/HbA 1C (G/H ratio) increased as a function of decreasing HPT. In patients with estimated HbA 1C .5.8%, in contrast, GA levels were independent of HPT levels. In the patients with CLD, GA and HbA 1C were associated with mean plasma glucose levels and some indicators for hepatic function. The multivariate analysis revealed a significant association of G/H ratio with HPT, cholinesterase and direct bilirubin. The G/H ratio was not associated with the mean plasma glucose but with HPT and cholinesterase levels. Conclusions: The G/H ratio correlates with hepatic function but not with plasma glucose levels. Therefore, CLD should be suspected for diabetic patients with an elevated G/H ratio.

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