A Case of Pancreatic Cancer With Liver Metastasis Which Responded to Chemotherapy

A case of pancreatic cancer with liver metastasis is reported,in which chemotherapy had a marked effect, with the responsesclearly documented. The patient was a 59-year-old male who experienced epigastricpain in February 1985, upper gastrointestinal X-ray examinationrevealing extragastric compression by the pancreas. He visitedthe National Cancer Center Hospital, Tokyo, in April 1985 andthe diagnosis of pancreatic cancer with liver metastasis wasmade using the imaging procedures of ultrasonography, computedtomograph scanning and endoscopic retrograde cholangiopancreatographyas well as by biochemical and serological tests. At the timea 5 cm tumor was palpable in the middle upper abdomen. The patient was treated with Cis-diaminedichloro platinum, tegafur,and 5-fluorouracil, successively, and the abdominal tumor graduallydiminished, finally becoming impalpable. The response was evaluatedas one of partial responses (PR) by ultrasonography, and theimprovement substantiated by computed tomography and tumor markers.     

Toxicity and Metabolism of Trimethylarsine in Mice and Hamsters

Toxicity and Metabolism of Trimethylaisinc in Mice and Hamsters.YAMAUCHI, H., KAISE, T., TAKAHASHI, K., AND YAMAMURA, Y. (1990).Fundam. Appl. Toxicol. 14, 399–407. Trimethylarsine (TM-As)proved to be an arsenic compound of low toxicity, with a poLD50 of 7870 mg/kg in mice. A single po dose of 10 mg/kg ofTM-As caused no hemolysis, but a single po dose of 750 mg/kginduced mild, transient hemolysis in hamsters. TM-As was veryrapidly eliminated into the urine, with a biological half-lifeof 3.7 hr. TM-As was oxidized In vivo to form trimethylarsineoxide (TMAO) and excreted as such into the urine. TM-As wasnever demethylated In vivo. A mechanism was demonstrated bywhich a part of TM-As was eliminated directly into the expiredair. We drew a conclusion that TM-As is far less toxic thanarsine, most probably due to its In vivo conversion to TMAO.c 1990 Society of Toxicology.     

Response to interferon in chronic hepatitis C due to mixed genotype infection

We examined the response to interferon (IFN) in patients with chronic hepatitis C (CHC) due to two different genotypes of hepatitis C virus (HCV) infection. Among 64 CHC patients studied, one (2%) had HCV-RNA genotype I, 36 (56%) had genotype II, 19 (30%) had genotype III, 2 (3%) had genotype IV and 6 (9%) had both genotypes II and III. There was no significant difference in age, sex, history of blood transfusion and liver histology among patients with genotypes II, III and II + III. The HCV-RNA titre of genotype II patients was significantly higher than that of genotype III patients (P < 0.05). However, there was no significant difference in the HCV-RNA titre between genotype II + III and the other groups. The complete response rate achieved with IFN therapy was significantly higher in genotype III patients (74%) than in genotype II patients (17%; P < 0.01). Of the six patients with genotype II + III, a complete response to IFN was only achieved by two patients (33%), both of whom had a low HCV-RNA titre (≦ 10^4,5 copies/mL) and HCV serotype 2. The remaining four patients had HCV serotype 1 and three of the patients had a high HCV-RNA titre (≧ 10⁵ copies/mL). The HCV genotype III was lost in two patients after IFN therapy. These data suggest that HCV-RNA titre and HCV serotype are important factors for predicting the efficacy of IFN therapy in patients with mixed genotype infection and show direct evidence of higher susceptibility towards CHC of patients with genotype III than genotype II.     

Type la glycogen storage disease with focal nodular hyperplasia in siblings

Glycogen storage disease type I (GSD-I) is an inherited disorder that is due to a glucose-6-phosphatase (G6Pase) deficiency. There have been recent reports of hepatocellular tumors in adults with this disease. Hepatic adenoma is the most common tumor described but others, including hepatocellular carcinomas, hepatoblastomas, and focal nodular hyperplasia (FNH) have been reported. FNH of the liver is a rare benign lesion that has been reported in eight patients with GSD-I. Three of these eight patients, in addition to the patient in our study, had been treated with portacaval shunts. When these patients were compared with patients who had not received such treatment, it appeared that the portacaval shunts may have induced the development of FNH and may have been associated with earlier complications. FNH is a benign tumor that may coexist with adjacent fibrolamillar carcinomas and/or adenomas and requires careful follow-up.     

Activation of Complement System by Streptococcal Preparation OK-432 (Picibanil) in Patients with Malignancy

A streptococcal preparation, OK-432 (Picibanil), was administeredto two patients with gastric carcinoma and two with chronicmyelogenous leukemia. All the patients revealed an increasinglevel of serum complements CH50, C4 and C3, as well as FactorB by 40 days of the therapy. Fixation of C4, C3 and Factor Bappeared in the gastric carcinoma tissue and on the leukemiccell surface determined by fluorescent antibody technique, indicatingthat OK-432 might play a role as an immunopotentiator via thecomplement system.     

Characteristic Laparoscopic Findings of Chronic Hepatitis C: A Comparison with Hepatitis B.

Abstract: We performed laparoscopy on 72 patients with chronic hepatitis C (CH-C) to elucidate its morphological features and characteristics relating to its progressive clinical course. We then compared these findings with those of 188 patients with chronic hepatitis B (CH-B). The frequency of reddish hepatic markings was almost the same in the patients with CH-B (21%) and the patients with CH-C (24%). In the patients with CH-B, reddish markings were present more frequently in the subjects with sublobular hepatic necrosis (34%) than in those without it (5%, p<0.01), but in CH-C the difference was not significant. Reddish markings were more even in the patients with CH-B with respect to form, size and distribution, whereas those in the patients with CH-C were more uneven. Prenodular patchy markings were present more frequently in the patients with CH-B (14%) than in the patients with CH-C (6%, p<0. 05). These findings suggested that the progression of hepatic necrosis was more variable in different parts of the liver, and that the regeneration of hepatocytes was less active in the patients with CH-C, compared with the patients with CH-B.     

Subclass restriction of immunoglobulin G in liver cirrhosis

The serum immunoglobulin G (IgG) subclasses were determined in 41 patients with liver cirrhosis (LC) and in 15 normal controls. In 19 cases of LC and in 6 normal controls, the IgG subclasses were also determined in lymphocyte culture supernatants. The determinations were performed by enzyme immunoassay. It was found that the absolute mean IgG1 and IgG3 levels were increased in all LC due to various causes. The mean IgG1 increase was most pronounced in post-hepatitic LC, and the mean percentage of IgG1 to total IgG was also increased in this type of LC in comparison with the normal controls and the other types of LC. The IgG3 fraction was significantly increased in primary biliary cirrhosis (PBC). In alcoholic LC, all IgG subclasses were increased significantly in comparison with normal controls. In lymphocyte culture supernatants from PBC patients, the mean IgG1 and IgG3 levels were increased in supernatants from unstimulated cultures, and the mean IgG1, IgG3, and IgG4 were increased after pokeweed mitogen (PWM) stimulation. In post-hepatitic LC, the mean IgG4 level was increased in both unstimulated culture supernatants and after PWM stimulation. In alcoholic LC, the mean IgG4 level was increased in unstimulated culture supernatants, whereas the mean IgG1 level was increased after PWM stimulation. These findings showed that LC of differing aetiologies exhibited different profiles of IgG subclasses. This may be related to the different aetiological agents and the pathogenesis of the different types of LC.     

CASE REPORT: Haemothorax due to hepatocellular carcinoma rupture successfully controlled by transcatheter arterial embolization

A 64-year-old man was admitted to our hospital with multiple hepatocellular carcinoma (HCC) lesions in the liver and lung. On the seventh hospital day, a chest radiograph showed a marked increase in right pleural effusion. A thoracentesis revealed a haemothorax. Despite repeated pleural taps and blood transfusions, the patient's clinical status worsened and he developed severe dyspnoea. An inferior phrenic arteriography on the 19th hospital day showed a tumour growing over the diaphragm into the right thoracic cavity, suggesting a tumour rupture. A transcatheter arterial embolization (TAE) of the inferior phrenic artery successfully controlled the bleeding and improved the haemothorax. There was no rebleeding; however, the patient died of advanced HCC 3 months later. To our knowledge, this is the first case of a haemothorax secondary to a ruptured HCC that was treated successfully with TAE.     

Regurgitation of bile acids in rat liver under bile drainage: quantitative analysis by taurine or ursodeoxycholate loading test

Abstract In rats with an interrupted enterohepatic circulation of bile acids, levels of serum taurine-conjugated bile acids were increased significantly 3 h after intravenous administration of taurine. Similarly, serum taurine- or glycine-conjugated ursodeoxycholic acid (UDCA) was increased significantly 2 h after UDCA administration. These findings suggested that the administered taurine or UDCA was taken up into hepatocytes and utilized to form conjugated bile acids, which were thereafter regurgitated into the systemic circulation from the liver. The proportion of regurgitated taurine-conjugated bile acids relative to total serum bile acids measured by taurine loading (30%) almost coincided with that of regurgitated taurine- or glycine-conjugated UDCA relative to total serum bile acids measured by UDCA loading (31.6%). Thus, the present study showed conclusively that at least 30% of serum bile acids are derived from newly conjugated bile acids that are regurgitated from the liver in rats with bile fistula.