Exocrine pancreatic function by means of pancreozymin secretin test was investigated in 21 control subjects and in 30 patients with diabetes mellitus. The results obtained were as follows: 1. Significant decreases of volume, maximal bicarbonate concentration and amylase output of pancreatic juice were observed in diabetic patients compared with control subjects. 2. These decreases were related to the condition of diabetic control, duration and complications of diabetes mellitus. 3. Administration of insulin was closely related to the amelioration of amylase output, indicating that insulin would accelerate the synthesis or the secretion of the pancreatic amylase. 4. A significant increase of immunoreactive glucagon, which was known to inhibit the amylase output from the pancreas, was observed in the plasma of diabetic patients. In conclusion, the most important factor of the pancreatic exocrine dysfunction in diabetes mellitus was attributed to a lack of insulin action and in addition a concomitant elevation of plasma glucagon, and an interaction of these hormones were to be considered.
Exocrine pancreatic function with pancreozymin or secretin loading test and changes of insulin and glucagon levels were studied in streptozotocin induced diabetic rats. The results obtained were as follows: 1. A remarkable and significant decrease of amylase output was observed in diabetic rats. An improvement of amylase output was achieved by the administration of insulin. 2. A moderate decrease of immunoreactive insulin(I) level was indicated in diabetic rats, however, immunoreactive glucagon(G) level revealed no changes. The molar ratio in G/I was higher in diabetic rats than in control rats. A significant elevation of glucagon level, on the other hand, was shown after intravenous injection of arginine to diabetic rats. In conclusion, pancreatic exocrine dysfunction observed in streptozotocin induced diabetic rats was also attributed to a diminution of insulin and concomitant elevation of G/I molar ratio. These findings would support the clinical findings indicated previouly.
Little is known about the pathogenesis of pancreatic lithiasis and there has been noreport succeeded in producing pancreatic lithiasis in experimental animals. Incomplete orcomplete obstruction of the pancreatic duct was produced by ligating the duct in adultmongrel dogs and long term observation was made for the purpose of creating experimentalpancreatic lithiasis and elucidating the mechanism of pancreatic calculus formation. Theresults were as follows: 1. Pancreatic lithiasis was obtained in six dogs among 13 experiments observed longerthan six months after incomplete ductal obstruction, the incidence was 46 per cent. Noneof the dogs with complete obstruction developed pancreatic lithiasis. 2. The calculi were analized to be composed principally of calcium carbonate with amixture of calcium phosphate and organic bodies, which was extremely resembled to thehuman pancreatic calculi. 3. The main duct of the pancreas with calculi showed marked tortuous dilatationassociated with stasis of pancreatic juice. 4. Significant degrees of diffuse periductal fibrosis and mucoid alterations of the ductalepithelium were histologically noted after incomplete ductal obstruction. As it is plausible, from the results above, that the calculi were formed by calcium precipitationon inspissated mucus which was produced from the altered ductal epithelium, incompleteand prolonged obstruction of the pancreatic duct is concluded to be an importantfactor for pancreatic calculus formation.
Humoral and cellular immunologic status of 27 patients with protein-losing gastroenteropathywas assessed. In serum immunoglobulins, marked decrease in serum IgG levels wasfound in most of the cases, but serum IgA and IgM levels were varied in each case. Immunofluorescentstudy showed remarkable decrease in population of immunoglobulin-containingcells in the lamina propria of the jejunal mucosa. In delayed hypersensitivity tests, PPDsskin tests or DNCB skin tests were negative in most of the patients. Blastoid transformation ofperipheral lymphocytes induced by PHA was impaired, while populations of peripheral T-cells of the cases had no decrease when compared with those of control. In summary, this study suggests that humoral and cellular immunologic status was remarkablyimpaired in protein-losing gastroenteropathy.
The antibody to hepatitis B core antigen (anti-HBc) titer in sera of 28 asymptomatichepatitis B surface antigen carriers (AsC) and 143 patients with various liver diseases wassurveyed by indirect immunofluorescent technique. The relationship between the anti-HBc titer and the appearance of HBc-Ag in the liver was studied. The anti-HBc titer was low in AsC, compairing to that in chronic liver diseases. Especiallythe highest anti-HBc titer was observed in chronic active hepatitis. The positive casesof HBc- Ag in liver tissue revealed higher anti-HBc titer than the negative cases. No HBc-Ag was found in liver tissue of the cases with anti-HBc titer less than 23. These results suggested that the anti-HBc titer in the serum might be closedly relatedto the injury state of the liver and the active replication of hepatitis B virus in liver.
The purpose of this paper is to discuss the factors which influence the excretion of antibioticsinto the bile juice in the cases with obstructive jaundice. The levels of antibioticssuch as Ampicillin, Carbenicillin, Thiamphenicol, Cephalothin were studied in serum andbile on complete biliary obstruction, incomplete obstruction and after biliary drainagegroup. The results are follows; the rate of biliary excretion of antibiotics in the cases ofobstructive jaundice was affected chiefly by the grade of biliary passage regardless of theamount or sort of antibiotics. In patients with complete bile duct obstruction, Ampicillin, Carbenicillin, Thiamphenicol, Cephalothin were not excreted. And in patients with incomplete bile duct obstruction, excretionof those antibiotics were a little better. However, in patient whose bile duct wasdrained, the excretion of antibiotics was encreted promptly into the bile juice and its concentrationwas moderately. These phenomena were not correlated directly with the degree or duration of jaundice andthe grade of liver damage.
In order to ensure the in vitro diagnosis of drug-induced allergic hepatitis, a microvolumewhole blood culture technique was devised. In a settled experimental condition, clearlymphocyte transformation was observed in the whole blood culture when activated withmitogen, such as PHA or PWM. These were detected with either 3H-thymidine uptakeinto DNA or appearances of lymphoblastoid cells. More over MIF production was alsoconfirmed in this method when lymphocytes taken from the tuberculine-positive individualswere stimulated with PPD. The whole blood culture prepared from 57 patients who developped jaundice or liverinjury during the course of treatment with some drugs have shown the positive lymphocytetransformation to the drug. The causative drugs were 16 cases of antituberculotic drugs, 13 cases of antibiotics, 4cases of sulfa drugs, 4 cases of psycotherapeutic drugs and others. Eosinophilia wasobserved in 35.4% and high level of total bilirubin in serum was detected in 51.2%. Also, in most of patients (85.5%) who showed the positive blastogenesis, high levels oftransaminase (under 500 units) were revealed. Out of 18 cases who showed the positiveresponse, 13 cases were cholestatic type of liver injury. These results suggested the micro volume whole blood culture technique provide a usefulin vitro methodology to detect the drug induced allergic hepatitis because of requiring thevery small amount of blood.
Lymphocyte transformation induced by the stimulation with nuclear membrane fractionsof rat liver was studied using a microvolume peripheral blood cultures obtained from patientswith liver disease. Although no responses were seen in healthy controls, positive responseswere frequently observed in patients with liver disease: 43% in acute hepatitis, 35% inchronic inactive hepatitis, 86% in chronic active hepatitis, 30% in liver cirrhosis and 14% inhepatoma. Many cases which had shown the positive response to the nuclear membrane fractionswere also revealed the positive response against the HBs-antigen, while those of negative caseswere less responsible to the HBs-antigen. Also, correlation between the responsiveness of lymphocytes to the liver specific antigenand to the nuclear membrane fractions was high in patients with liver diseases.
In 2 cases of Japanese schistosomiasis associated with colon carcinoma and with agiant polyp suggesting partially malignant changes of the sigmoid colon, respectively, microscopic counting of the total number of eggs distributed throughout the whole operationmaterials was tried. Thickness of boundary mucosae between cancer lesions and intactparts was measured. Then, constitutions responsible for their mucosal thickness werehistologically investigated. As base on these metrical data, the present study was designedto elucidate collaborative findings of carcinogenesis with eggs. The data obtained hereinlead to the following conclusions: 1) Complete absence of eggs in tumor lesions and their adjacent areas proximal to anus. 2) Numbers of eggs in submucosal layers of whole area approximately equal to those inthe entire wall of rectum. 3) No definite foreign-body reaction on eggs. 4) No intimate relationship between the egg localisation and proliferation of mucosalelements. 5) Various values of thickness and abundant histological aspects in boundary mucosalareas between cancer and intact parts. 6) The mucosal thickness of 6mm. consistently indicated that of carcinoma, themselves. 7) Values, meas. up to 2 or 4mm, were expressed as the summation of the thickness ofintra- and/or sub-mucosal cancer nests, and intact mucosa, with occasional distinct lateralextension. 8) No transitional pictures between carcinoma and intact mucosal constituents inhistology. 9) Scanty numbers of eggs in the boundary areas. 10) Non-specific glandular hyperplasia quite regardless of malignant transformation.