Adenosquamous carcinoma of the rectum showing endocrine-cell differentiation: report of a case.

PURPOSE: Previous records of adenosquamous carcinomas with endocrinologic features rarely have been reported. Although the disease behaves in an extremely aggressive manner, chemotherapy after surgery has never been proposed. We used regional chemotherapy for treatment of unresectable liver metastases. METHODS: Hartmann colostomy was performed and 5-fluorouracil was infused into the hepatic artery for 15 weeks after the operation. RESULTS: Multiple liver metastases were present at the initial operation. Three months after the start of the chemotherapy, computed tomography showed that metastatic tumors in the liver had disappeared. The patient survived 18 months after the initial operation. CONCLUSION: This case report describes the first successful treatment with adjuvant regional chemotherapy of a patient who had an adenosquamous carcinoma with endocrine-cell differentiation in the rectum and liver metastases.

[Peripheral 5-FU blood concentration after high-dose injection into the hepatic artery: potential preventive effect on extrahepatic metastatic foci].

To clarify the effect of high-dose 5-FU injection into the hepatic artery (1,000 mg/m2 weekly) on liver metastases of colorectal cancer, the peripheral venous 5-FU concentration was measured in two groups of patients, one which had undergone hepatectomy and the other which had not. The area under the concentration-time curve (AUC) was calculated and the preventive effect of 5-FU on extrahepatic lesions was examined. The peripheral venous 5-FU concentration and AUC were higher in patients who received the drug via the hepatic artery after hepatectomy, and 5-FU was effective for the prevention of extrahepatic lesions as well as against recurrence in the residual liver.

Pelvic nerve grafts restore bladder function in denervated rats.

BACKGROUND: Autonomic nerve preservation techniques for use during surgery for rectal cancer have improved. Nevertheless, in some patients pelvic nerves must be sacrificed to excise all tumor. For these patients, nerve reconstruction at the time of operation by using nerve grafting would be useful. A rat model of this type of nerve reconstruction is described. METHODS: Animals were divided into three groups. In the sham control group, a pelvic exploration was conducted without division of the pelvic nerves. In the nerve ablation group, both pelvic nerves were excised segmentally. In the graft group, both pelvic nerves were excised and genitofemoral nerves were interposed bilaterally. At 2-week intervals postoperatively, animals from each group underwent cystometry under urethane anesthesia and neuronal tracing using fragment C of tetanus toxin for demonstration of axonal transport via regenerated nerves. RESULTS: At 6 weeks postoperatively, 60% of the grafted animals produced rhythmic contractions of the bladder. In neuronal tracing studies at weeks 4 and 6, respectively, 40% and 100% of the nerve-grafted rats had labeled neurons in the sacral parasympathetic nucleus. CONCLUSIONS: These findings suggest that pelvic nerve grafting in rats can successfully restore bladder function after surgical injury. Clinical use of pelvic nerve grafting may be indicated for patients whose pelvic nerves must be sacrificed to excise all tumor.

Protective effects of dibutyryl cyclic AMP on acute hepatic failure in rats.

To study the effect of cyclic AMP on liver dysfunction, dibutyryl cyclic AMP (DBcAMP, 15 mg/kg) was given to rats with acute hepatic failure induced by D-galactosamine (D-Gal; 500 mg/kg) and lipopolysaccharide (i.e., endotoxin) (Et; 0.5 mg/kg). The survival rate was only 7% for rats given D-Gal and Et (control group), while it was 100% for rats given seven doses of DBcAMP, and 53% for rats given two doses. The ALT level was high at 3475 +/- 488 KU in group III, while it was 242 +/- 69 KU in group I, and 376 +/- 49 KU in group II. The hepaplastin test level was decreased at 24 hr in all groups except group I, in which it was high at 55 +/- 11%. The serum tumor necrosis factor (TNF) level was 155 +/- 42 IU/ml in group I, 463 +/- 30 IU/ml in group II, and 1334 +/- 328 IU/ml in group III. The results of the blood biochemistry and liver tissue blood flow studies were better in the DBcAMP-treated groups, and the serum TNF levels were also lower in the treated groups. Histological examination of the liver showed extensive necrosis in the control group, but mild necrosis and inflammatory cell infiltration in the DBcAMP-treated groups. Therefore, treatment with DBcAMP suppressed acute hepatic failure induced by D-Gal and Et, resulting in a significant increase in the survival rate.

[Influence of splenectomy on drug therapy for acute liver failure induced by D-galactosamine and lipopolysaccharide in rats].

We studied protective effects of dibutyryl cyclic AMP (DBcAMP 15 mg/kg i.p.) and OK-432 (5 KE/body), and the role of the spleen on D-galactosamine (D-Gal 500 mg/kg i.p.) and lipopolysaccharide (endotoxin: Et 0.5 mg/kg i.p.) induced acute liver failure. The survival rates were 10% in the control group (D-Gal+Et), 53% in the group I A (DBcAMP was administered at 1 hour before D-Gal administration), 79% in the group I B (Splenectomy was performed at 24 hours before D-Gal administration on the group I A), 87% in the group II A (OK-432 was administered at 24 hours before D-Gal administration), and 64% in the group II B (Splenectomy was performed at 24 hours before D-Gal administration on the group II A). GOT activities and TNF activities were significantly improved in the treatment groups, and in the group I B and group II A, they were more improved than in the group I A and group II B. In conclusion, spleen had the positive effect for OK-432 treatment, and also had the negative effect for DBcAMP treatment on acute liver failure induced by D-Gal and Et.

MRI appearance of thorotrast-induced cholangiocarcinoma in a case of thorotrastosis.

The case of a 71-year-old man with thorotrastosis and a cholangiocarcinoma detected by MRI is presented, and the radiographic appearance of the cholangiocarcinoma is discussed. We concluded that MR is more useful for detecting Thorotrast-induced liver tumors than US and CT, but CT is more useful for the detection of Thorotrast deposits.

[The present status and the future of artificial liver support].

Orthotopic liver transplantation, started by Dr. Starzl in 1963, has already become an well established therapeutic method for the treatment of fulminant hepatic failure especially since the introduction of Cyclosporin A. On the other hand, hemoadsorption using charcoal, PAN membrane hemodialysis and plasma exchange were actively applied for clinical cases with fulminant hepatic failure between 1960 and 1970, but the survival rates were not so improved as expected due to the lack of metabolic functions. Hybrid artificial liver has been therefore investigated experimentally to support metabolic functions by using biomaterials such as isolated hepatocytes. Today many efforts are being made to keep hepatocytes highly viable for a long period of time by calcium alginate entrapment, spheroid formation, or by using biomatrix, some polymers, and microcarriers, etc. In the future, xeno-hepatocytes or so-called super cell will be realized and applied for artificial liver support with the development of gene operation techniques.

[Protective effects of DBcAMP on ischemic liver failure in dogs].

We studied protective effects of Dibutyryl cyclic AMP (DBcAMP) which is a permeable form of cyclic AMP on ischemic liver failure (ischemic time: 90 minutes). Mongrel dogs were used. A portal-systemic bypass was established by inserting a heparinized catheter between the splenic vein and the femoral vein. Acute liver failure was induced by the en bloc clamp of the porta hepatis. In the treated group, 0.1 mg/kg/min (total dose, 300 mg) of DBcAMP was injected intravenously from three hours before the clamp to the end of the experiment. The control group was injected physiological saline. Effects of DBcAMP were evaluated according to survival rates, blood pressure, serum biochemical findings, hepatic blood flow, ATP levels in liver tissues and histological findings. The survival rates were 16% in the control group, and 88% in the treated group. The mean blood pressure after reperfusion was rapidly decreased in the control group while in the treated group, it was maintained nearly 100 mmHg. Serum biochemical findings, hepatic blood flow and tissue ATP levels were significantly improved in the treated group. On histological findings, necrosis with bleeding was observed one day after ischemia in the control group while in the treated group mild chronic ischemic change without necrosis was observed on two weeks after ischemia. In conclusion, ischemic liver failure was apparently protected by the administration of DBcAMP.

[Protective effects of DBcAMP on acute liver failure induced by D-galactosamine in rats].

We studied protective effects of Dibutyryl cyclic AMP (DBcAMP) which is a permeable form of cyclic AMP (cAMP), the intracellular second messenger, on D-galactosamine (D-Gal, 1.5g/kg i.p.) induced acute liver failure. Experimental animals were divided into four groups: Group I; DBcAMP was administered before (7.5mg/kg) and after (7.5mg/kg) D-Gal treatment, group II; only before (15mg/kg) D-Gal treatment, group III; only after (15mg/kg) D-Gal treatment, and group IV; no DBcAMP was administered. Effects of DBcAMP were evaluated according to survival rates, serum biochemical findings and hepaplastin test (HPT), ATP levels in liver tissues, hepatic blood flow, and histological findings. The survival rates after D-Gal treatment were 100% in group I, 90% in group II, 32% in group III and 10% in group IV. The serum biochemical findings, tissue ATP levels and hepatic blood flow were significantly improved in groups I and II compared with that in groups III and IV. The level of HPT in group I was the highest among the experimental groups. On histological findings, inflammatory changes were observed in group I and focal necrosis in group II while liver degeneration with massive necrosis was seen in groups III and IV. In conclusion, acute liver failure induced by D-Gal was apparently protected by the administration of DBcAMP.