The serum total trypsin inhibitor, stable trypsin inhibitor and trypsin binding protein were determined in 58 normal subjects, 4 cases of acute pancreatitis, 27 cases of chronic pancreatitis, 6 cases of pancreatic carcinoma and 88 cases of other diseases and the clinical significance in pancreatic diseases were examined. The TTI does not originate only in the trypsin departure phenomenon in the pancreas but rises with tissue destruction and inflammatory processes. TTI rises markedly soon after onset of acute pancreatitis and gradually declines with the subsidence of the acute attack. In chronic pancreatitis, a level close to normal is maintained but in cases with pronounced decline in exocrine function, a trend for low levels is observed. The TTI is higher in the exacrebation then remission states of chronic pancreatitis. TBP was low in proportion to the severity of the symptoms in all the cases of acute pancreatitis. Low levels, however, were not found in chronic pancreatitis and other nonpancreatic diseases and the low level was specific for acute inflammatory changes in the pancreas.
In order to investigate diagnostic values of the pancreatogram in chronic pancreatitis, micropancreatographies and their histological analyses were performed on 75 necropsy specimens, including 17 cases of chronic pancreatitis, 22 cases of pancreatic fibrosis, 5 cases of pancreatic fibrosis with focal pancreatitis, 9 cases of carcinomatous lesion of pancreas and 22 cases of normal pancreas. The histological changes of the pancreatic ducts were closely related to those of the parenchyma, and hyperplasia and metaplasia of the ductal epithelium were observed in a high incidence in chronic pancreatitis. The irregular and rigid outline of the main duct observed radiologically in 15 cases of chronic pancreatitis, was closely related to ductal hyperplasia. Dilatation or narrowing with irregular and rigid outline were frequently observed in chronic pancreatitis, although 5 cases of chronic pancreatitis (30% of total) showed no dilatation or narrowing. Severe degree of narrowing of the main duct was seen in the pancreatogram of both chronic pancreatitis and carcinomatous lesion. However, radiological obstruction of the main duct was the characteristic finding in carcinomatous lesion. The relations between the radiological findings of the branches of the pancreatic ducts and their pathological changes were also studied. In chronic pancreatitis, decreases in the numbers of the small branches and cystic dilatations of the branches due to fibrosis, or ductal hyperplasia and metaplasia were frequently observed.
Five year and ten year survival rates of liver cirrhosis diagnosed with peritoneoscopies and liver biopsies were studied. We have followed up a total of 313 cases classified by our peritoneoscopic patterns. This consists of 147 cases in the code number (ban-chi, in Japanese) 100 or 200 (grossly smooth surface and histologically acute hepatitis, chronic hepatitis and those with mild portal fibrosis and/or fatty metamorphosis), 70 cases in the code number 300 (grossly mesh-work pattern without nodules found and histologically precirrhotic stage, chronic hepatitis and liver cirrhosis of the early stage), 66 cases in the code number 400 (moundshaped nodules with histologically liver cirrhosis) and 30 cases in the code number 500 (semispherical nodules with histologically liver cirrhosis). Those cases in the code numbers 100 and 200 have been followed up for at least 10 years and those in the code numbers 300, 400 and 500 have been for at least 5 years since the first examinations. The 5-year survival rates of liver cirrhosis (those in the code numbers 400 and 500) between ages of 20 to 29 and 30 to 39 at the first examination were as high as 80.0% and 89.5% respectively, whereas that of the 4th and 5th decades showed as low as 58.8% and 50.0% respectively. According to calculations using the life table method, the life expectancy of the patients became shorter as the code numbers became greater. Five-year survival rates of the code numbers in 100 and 200, 300, 400 and 500 were 96.6%, 95.6%, 72.3% and 53.3% respectively, and those after 10 years were 95.9%, 70.0%, 37.9% and 24.0% respectively. In the code numbers 100 and 200 one out of 6 fatal cases (16.7%) was dead by a liver cirrhosis, in the code number 300 12 out of 13 (92.3%) were dead by liver diseases (10 cases by liver cirrhosis and 2 cases by liver cancer), in the code number 400 25 out of 27 (92.6%, 22 cases by liver cirrhosis and 3 cases by liver cancer) and in the code number 500 16 out of 19 (84.2%, all liver cirrhosis). Therefore, the code numbers in three digits according to our peritoneoscopic classifications on the liver surface patterns will predict outcome of the patients with viral hepatitis and liver cirrhosis, sufficiently.
Diagnostic values of urinary amylase, expressed as hourly amylase secretion for consecutive 7 days, were evaluated in 92 healthy persons and 858 patients with gastrointestinal disorders, including hepatobiliary and pancreatic diseases. Hyperamylasuria was defined by the frequencies and absolute values of abnormal amylase elevation and it was observed very often in the patients with pancreatic cancer, chronic pancreatitis and choledocholithiasis. But even in the patients with gastric cancer, acute hepatitis and biliary dyskinesia, hyperamylasuria were detected at the rate of 20-30 per cent. Portal cirrhosis, on the other hand, showed very low value of urinary amylase. Comparing hyperamylasuria and normoamylasuria with the data of pancreozymin secretin test, abnormal findings were detected more often in the cases with normoamylasuria. This is thought to reveal the differet significance between both examinations. Even though pancreozymin secretin test is most reliable test for detecting the abnormal function of the exocrine pancreas, urinary amylase reflects well the clinical course of pancreatic impairments by catching the active changes of the pancreatic lesions. The determination of urinary amylase at least for 5-7 days is considered to be a screening test for detecting slight impairment of the exocrine pancreas.