In order to elucidate the change of gastric emptying in liver cirrhosis, an examination was attempted to measure the half gastric emptying time (T1/2) employing 99mTc-DTPA. The study was performed by analyzing the gastroscintigram and the gastric emptying curve using the nuclear medicine data analyzer (shimazu Scinti Pack 1200). As aresult, a distinctive delay in half T1/2 was recognized in patients with liver cirrhosis, in comparison with the normal subjects. In addition, the delay in T1/2 is more remarkable in cirrhotic patients with esophageal varices and/or gastric varices. Furthermore, cirrhotic patients with erosive gastritis and/or gastric ulcer showed a more distinctive delay than in ones without gastric lesions. In cases in which the T1/2 emptying time exceeds 80 minutes, incidence of gastric lesions was high (80%). From the above observation, the delay in gastric emptying is considered as one of the factors contributing to the high incidence of gastric lesions in liver cirrhosis patients.
Gastric acid secretion stimulated by beef consomme soup was measured in 7 normal controls, 16 gastric ulcer patients and 19 duodenal ulcer patients by intragastric titration to a constant pH 5.5 and 2.5. Serum gastrin was also measured by radioimmunoassay, using Dinabot gastrin kit. The ratios of acid output and integrated gastrin response (IGR) at pH 2.5 vs pH 5.5 were calculated to determine the rate of suppression in acid and gastrin responses at low acid pH. In duodenal ulcer patients, acid response was decreased only by 35%, compared with 45% in normal controls and 48% in gastric ulcer patients. IGR was suppressed by 62% in normal controls and 63% in gastric ulcer patients, whereas the rate of suppression was only 16% in duodenal ulcer patients. These differences were statistically significant. The results suggest that a defect in negative feedback mechanism of gastric acid secretion and gastrin release atlow pH exists in duodenal ulcer patients.
Antibody of forming cells against TNP-SRBC were induced to a simillar extent when the peripheral blood mononuclear cells from normal or patients with primary biliary cirrhosis (PBC) were stimulated in vitro with pokeweed mitogen (PWM). Although these antibody responses were significantly augmented by adding 1×10-6mg/ml-1×10-8mg/ml of estrogen simultaneously with PWM to the mononuclear cells prepared from normal, no such augmentation of antibody response by 1×10-6mg/ml-1× 10-8mg/ml of estrogen were demonstrable in PBC. Furthermore, these antibody responses were augmented by adding 1×10-5mg/ml of estrogen with PWM to the mononuclear cells cultures prepared from patients with PBC. These observations suggest that a factor (or factors) may correlate with the induction of PBC such as a different responsiveness to the concentration of estrogen at least partially.
It is clinically important to distinguish primary liver cancer from metastasis. We sometimes have difficulty in deciding the primary source of the liver cancer by ordinary Papanicolaou and/or Giemsa staining, especially in the case of adenocarcinoma. In order to decide primary source of the liver cancer, cytological examination by amino acid naphthylamidase staining (N-ase staining) was performed in four cases of cholangicarcinoma, various metastatic liver cancers (seven due to gallbladder cancer, one choledochus, five pancreas, 12 stomach and four colon cancers) and these primary lesions, making up 33 cases as sum total. Results are as follows: In all cases of cholangiocarcinoma, cytoplasm was evenly stained as lots of granular dots with red-brown color, but bile canaliculi like structure were not found. In all cases of metastatic liver cancer from choledochal and gallbladder cancer, the stained dots were found in the cytoplasm making a crescent form. In all cases of metastatic liver cancer from pancreatic, gastric and colonic cancer, these staining characteristics were found to be lacking. In all cases of primary lesions of these metastatic liver cancer, the staining was shown same cytologic findings. In conclusion, cytological examination using N-ase staining is valiable to differentiate cholangiocarcinoma from metastatic liver cancer and to differenciate cholangiocarcinoma from metastatic liver cancer of biliary tract cancer.
Using Toxicolor, commercially available kit for the quantitative measurement of endotoxin in the blood, endotoxemia was investigated on various liver diseases and gram-negative septicemia. Toxicolor proved itself to yield nearly 90% of recovery of endotoxin acitivity from plasmas of normal controls and patients. Moreover, its recovery was not influenced by the bilirubin level of the plasmas. In cirrhotic patients, hitherto reportedly having high positive rate of endotoxemia, decompensated cases with ascites only showed endotoxemia with positive rate of 44% and its maximum level of 39pg/ml, a hundredth order of previous reports. In patients with hepatocellular carcinoma, endotoxemia was only present in hepatic failure. In gram-negative septicemia, endotoxin was detected in all cases. Disseminated intravascular coagulation (DIC) complicated the endotoxemia at relatively high concentration, above 50pg/ml.
The present study was undertaken to clarify the functional and/or morphological pancreatic injury in patients with primary biliary cirrhosis (PBC). Clinical observation of the pancreas was done on 22 patients with PBC chiefly on the basis of pancreozyminsecretin (PS) test and endoscopic retrograde pancreatocholangiography (ERCP). In addition, 4 autopsied pancreases from patients with PBC were examined pathologically. PS tests were abnormal in 27% of 15 cases and ERCP were abnormal in 47% of 17 cases. However, these changes remained mild except for one patient. Abnormalities of PS test or ERCP were not correlated with the pathological stages of PBC or the association of sicca complex. In 2 of 4 autopsied pancreases, findings of mild chronic pancreatitis with lymphocytic infiltration were observed. These results suggest that pancreatic injury may occur with considerable frequency in PBC, but this injury is almost always slight.
Lipids and bile acids in both gallbladder bile and gallstone were analyzed by high-performance liquid chromatography. In comparison with the patients with other types of gallstones, those with calcium bilirubinate stones showed markedly lower concentrations of cholesterol, phospholipids, total bile acid and relatively high lithogenic index in their gallbladder bile. Furthermore, in the patients with calcium bilirubinate stones, free bile acids were detected especially in their gallbladder bile. The weight composition of cholesterol, fatty acids and total bile acids in calcium bilirubinate stones were 10.8%, 6, 3% and 5.3%, respectively. Characteristically, in those stones, 36.5% of total bile acids was free form, while it was not detected in other stones with the exception of one case of a black stone. Our experiment suggested that the conjugated bile acid detected in stones were involved into the stones in process of calcium bilirubinate precipitation and aggregation.
Carcinoembryonic antigen (CEA) levels in the bile were measured in 110 patients with gallstone diseases (benign group) and 28 patients with carcinoma of pancreas and biliary system (malignant group). There was no significant difference in average of CEA levels in the bile between two groups, and there was no significant difference in frequency of high CEA levels more than 15ng/ml. The levels of bile CEA had not correlated with that of serum CEA, orbile amylase. CEA levels in the bile tended to become higher when it was extracted with HCLO4, however, it was not shown any elevation in patients with carcinoma. Moreover, the mucosal epithelium of gallbladder was reacted with CEA antigen both in groups of gallbladder disease and carcinoma of gallbladder by histochemical observation using peroxidase-antiperoxidase (PAP) technique. From these results, it was suggested that CEA in the bile had been excreted not only from cancer cells, but also from benign inflammatory mucosa. Therefore, the elevation of CEA levels in the bile which was measured by currently available methods, was not sufficient to distinguish a carcinoma of pancreas and biliary system from other biliary diseases.
In order to ascertain acute gastric mucosal lesions accompanied with acute pancreatitis, we studied the pathophysiology of experimentally induced acute pancreatitis in rats. Experimental acute pancreatitis was induced with ligation of the distal part of the common bile duct. The increase of the values of serum amylase and lipase and histologic findings of pancreas demonstrated the occurrence of acute pancreatitis soon after ligation of the distal part of the common blie duct. At this early stage, there were no marked lesions in the stomach. However, aspirin induced ulcers in acute pancreatitis group were aggravated with statistical significance compared with those of the group of no surgical procedure except laparotomy. Gastric mucosal blood flow and pancreatic blood flow were measured simultaneously with hydrogen gas clearance technique until 4 hours after ligation of the distal part of the common bile duct. Pancreatic blood flow decreased with the development of acute pancreatitis. Moreover, marked decrease of gastric mucosal blood flow was observed. At the time 4 hours after ligation of the distal part of the common bile duct, gastric mucosal blood flow decreased to about 50% compared with the value before ligation. We thought that the fragility of gastric mucosa was based on this marked decrease of gastric mucosal blood flow. Moreover, it was demonstrated that the intravenous administration with 10mg/kg of cimetidine improved the decreased gastric mucosal blood flow associated with experimental acute pancreatitis, and clinical usefulness of this drug was suggested.
The influence of renal function on serum pancreatic secretory trypsin inhibitor (PSTI) concentration was studied by measuring serum PSTI, creatinine and urea nitrogen (BUN) concentrations in 116 patients with chronic renal failure. Serum PSTI concentration determined by radioimmunoassay was compared with serum creatinine and BUN concentrations, and creatinine clearance. Serum PSTI concentration was markedly elevated in patients with chronic renal failure, more so in patients undergoing hemodialysis. Elevated serum levels of PSTI in chronic renal failure were highly correlated with elevation of both serum creatinine and BUN. In addition, inverse correlation between serum PSTI concentartion and creatinine clearance was observed. The simultaneously high serum levels of PSTI and creatinine strongly suggest that clearance of these substances is reduced in pchronic renal atients with failure. These results indicate that renal function is one of factors that influence serum levels of PSTI. Thus, it is important to consider the renal function before assessing the elevated serum PSTI levels in patients with various diseases.