We recently examined the clinicopathological and immunohistochemical features of four cases of primary hepatic carcinoma with sarcomatoid elements. Three of the four patients had associated ordinary hepatocellular carcinoma (HCC) and one had a sarcomatoid carcinoma with no apparent elements of HCC. The presenting symptoms were high fever and hypochondralgia in three patients, and right hypochondralgia without a high fever in one. The preoperative diagnoses were liver abscess in two patients, HCC in one, and cholangioma in one. Preoperative imaging showed necrotic change or abscess formation in the tumors. The sarcomatous elements showed a positive reaction to vimentin in three patients, but the ordinary HCC cells did not. Macroscopically, the tumors appeared as a single nodule with pericapsular growth. The prognoses of these patients were poor due to the early development of intrahepatic or distal metastases. We conclude that symptoms such as a high fever or hypochondralgia are characteristics of these tumors and that they may be histogenetically derived from a dedifferentiation of HCC, although no elements of HCC were found in one of our cases.

Weanalyzed the clinicopathological features and therapy in 19 patients with kidney disease accompanied by hepatitis C viral infection, including 12 patients with mesangial proliferative glomerulonephritis (including eight with IgA nephropathy), six with membranoproliferative glomerulonephritis (MPGN),and one with membranousnephropathy. Persistent hematuria and/ or proteinuria (10 patients) was the most commonfinding, followed by nephrotic syndrome (8 patients). Cryoglobulinemia was detected in six of 19 patients examined (four of six patients with MPGN).Analysis of hepatitis C virus (HCV)-RNAgenotype in 13 patients revealed that nine of them had type II genotype. All four patients with MPGN, who had serum positive for HCV-RNA, had type II genotype. Five patients were treated with interferon-a (IFN-a) without a demonstrable effect on renal impairment, whereas five of ll patients treated with steroids showed improvement of the renal impairment. During the course of steroid therapy, the serum titer of HCV-RNA decreased in 5 of7 patients. These observations suggest that HCVinfection may be associated with several forms ofglomerulonephritis. Type II HGV-RNA mayhave a strong association with MPGN in Japan. Steroid therapy is not contraindicated in patients with HCV-associated nephropathy if they are resistant to IFN-a treatment.

Inhibition of hepatocarcinogenesis is a crucial issue in treating chronic hepatitis C patients, especially those who do not respond completely to interferon therapy. Interferon has been reported to reduce the incidence of hepatocellular carcinoma (HCC) not only in sustained virological responders but also in transient biochemical responders. However, the incidence of HCC increases in 5 years or more after interferon therapy in transient biochemical responders. The aim of this study is to assess whether interferon retreatment reduces the incidence of HCC in chronic hepatitis C patients in whom hepatitis C virus was not eradicated during initial interferon therapy. We enrolled 309 patients who were not sustained virological responders after initial interferon treatment consisting of a total dose of more than 250 megaunits of interferon and were followed for more than 2 years after treatment. Ninety-nine patients received interferon retreatment and 210 did not. Two courses of interferon therapy were administered in 84, three courses in 14 and five courses in one. The incidence of HCC was compared between patients with retreatment and those without. In the clinical characteristics, retreated patients were younger and followed up for a longer time period. The cumulative incidence of HCC was significantly lower in retreated patients. In multivariate analysis, patients' age (P=0.018) and the number of courses of interferon therapy (P=0.022) were independently associated with HCC incidence. These results suggest that interferon retreatment reduces or delays the incidence of HCC in chronic hepatitis C patients who did not completely respond to initial therapy.

No abstract

temperature was 36.6°C. There were no abnormal tubular acidosis; respiratory arrest; tubulo-interstitial signs observed in the lungs, heart and abdomen. Blood nephritis gas analysis revealed that pH was 7.278, PaCO 2 was 33.3 Torr, PaO 2 was 161.9 Torr, HCO 3 − was 15.2 mmol/l, base excess was −10.4 mmol/l under oxygen inhalation at 2 1/min. Laboratory data were respectively. Thyroid and microsome tests were Correspondence and offprint requests to: Hiroshi Ohtani, MD, Third normal. Thyroid functions were normal. Plasma renin