[A case of hepatocellular carcinoma with reduction of primary tumor and disappearance of multiple lung metastasis].

A 56-year-old male had suffered from hepatocellular carcinoma treated by operation, PHoT and TAE since 1994. In December 1995, he had multiple metastases of lung in addition to recurrence of primary hepatic lesions. We discontinued treatment of TAE and decided to administer UFT (400 mg/day) orally as an outpatient. After seven months, the primary hepatic lesions were decreased in size, and metastatic lesions of lung were completely eliminated with reduction of AFP level. Generally, hepatocellular carcinoma with metastasis is refractory to treatment. However, this result suggests that UFT is one of the effective treatments for such advanced cases as having lung metastasis.

Macrolipasemia in Crohn's disease.

A 38-year-old male patient who had been treated for Crohn's disease was found to have serum lipase activity that was persistently increased approximately 10-fold above the normal upper limit. He was diagnosed with chronic pancreatitis based on slightly elevated elastase-1 level and retrograde pancreatography showing slight dilatation of the main pancreatic duct. Therefore, the hyperlipasemia was thought to be due to pancreatitis. However, the serum amylase and trypsin was not increased at any time, and no serious findings suggestive of pancreatitis were detected on morphologic examination. Thus, there were discrepancies between the serum lipase activity and other laboratory and clinical findings. Exclusion chromatography of the patient's serum suggested macromolecular lipase, and further immunologic testing including affinity chromatography, enzyme-linked immunosorbent assay, and immunoprecipitation assay showed that serum lipase was bound to immunoglobulin Gkappa. Therefore, the hyperlipasemia was caused by immunoglobulin-linked lipase, termed "macrolipasemia." Macrolipasemia has rarely been reported, and this is the first reported case of macrolipasemia accompanied by Crohn's disease.

Ulcerative colitis complicated by gastroduodenal lesions.

A case of ulcerative colitis complicated with gastric and duodenal lesions is reported. The patient was a 17-year-old male who was admitted with bloody diarrhea and abdominal pain. Based on the endoscopic and histological findings of the colon, a diagnosis of ulcerative colitis was made. Upper gastrointestinal endoscopy showed multiple erosions and granular changes in the antral greater curvature of the stomach and descending portion of the duodenum. Histological examination of the stomach and duodenum revealed marked inflammatory cell infiltration and crypt abscesses. Clinically, the gastric and duodenal lesions did not respond to antiulcer drugs, but were alleviated by steroid. It was concluded that the pathogenesis of the gastric and duodenal lesions in this patient was similar to that of the colonic lesions of ulcerative colitis.

Serum levels of interleukin-1 beta and interleukin-6 in patients with chronic pancreatitis.

To investigate the role played by cytokines in chronic pancreatitis, we examined serum levels of interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) by radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA) in 33 patients with definitively diagnosed chronic pancreatitis. All the patients, who had received either no treatment or only digestive enzyme products for their chronic pancreatitis, had significantly elevated serum IL-1 beta levels (38.5 +/- 28.8 pg/ml, mean +/- SD), compared to normal controls (16.0 +/- 6.7 pg/ml; P < 0.01); however they showed no changes in serum IL-6 levels. Changes in IL-1 beta and IL-6 serum levels were not correlated with the etiological features of pancreatitis or with complications due to liver diseases. Serum IL-1 beta and IL-6 levels were also not correlated with the activity of any pancreatic enzymes in blood or urine. However, in the patients with chronic pancreatitis, serum IL-6 levels were correlated with C-reactive protein (CRP), whereas serum IL-1 beta levels were not correlated with CRP or with erythrocyte sedimentation rate. These results suggest that serum IL-1 beta is involved in the progression and reduction of chronic inflammation of the pancreas, and that the serum IL-1 beta level may be useful as a marker for chronic pancreatitis.

[Effects of 16,16-dimethyl prostaglandin E2 on pancreatic exocrine function in vivo and in vitro in rat experiments].

The effects of exogenous and endogenous prostaglandin on rat pancreatic exocrine function were investigated in vivo and in vitro. Under stimulation by endogenous CCK or exogenous caerulein, protein output was significantly reduced by intravenous drip infusion of 16,16-dimethyl prostaglandin E2 (DMPGE2), and under stimulation by exogenous secretin, volume and bicarbonate output were markedly reduced by DMPGE2. Amylase release from isolated pancreatic acini was significantly reduced by DMPGE2 under stimulation by 10(-11)-3 x 10(-11) M CCK-8, and was not influenced by DMPGE2 under stimulation by secretin or by indomethacin under stimulation by caerulein. Basal amylase release was not influenced by DMPGE2 or indomethacin. Basal cellular cyclic AMP and cyclic GMP contents were not influenced by DMPGE2, and elevated cyclic GMP content under stimulation by caerulein was significantly reduced by DMPGE2. These findings suggest that pancreatic enzyme secretion is reduced by DMPGE2 under stimulation by physiological or pharmacological concentration of CCK, and one of which mechanism is direct effect of DMPGE2 on pancreatic acini, may be coupling with phosphatidylinositol breakdown system and without cyclic AMP.

[Effect of KSG-504, a new synthetic cholecystokinin receptor antagonist on ethionine-induced acute pancreatitis in rats].

KSG-504, a new synthetic cholecystokinin (CCK) receptor antagonist derived from proglumide, has superior selectivity and affinity to CCK-A receptors. We have investigated the effect of KSG-504 on ethionine-induced acute pancreatitis in rats and the influence of endogenous CCK on evolution of pancreatitis and regeneration of pancreatic acinar cells. Reduction of pancreatic proteins and digestive enzyme contents was dose-dependently prevented by subcutaneous administration of KSG-504. The inhibition of evolution of pancreatitis was demonstrated histologically in KSG-504 treated rats. The effect of KSG-504 on pancreatic regeneration was evaluated by bromodeoxyuridine labeling index (B.L.I.) of acinar cells. There was no significant difference of B.L.I. between KSG-504 treated and non-treated rats. These results suggest that KSG-504 has a beneficial effect on ethionine-induced acute pancreatitis by blockade of endogenous CCK.