Histopathologically were examined polyps of fifteen cases, diagnosed as Peutz-Jegherssyndrome. Similar hsitological pictures were shown on the polyps in each segment of thegastointestinal tract. In gastric lesions, foveolar epithelial hyperplasia is predominant and foveolae are frequentlyelongated and cystically dilated. In those of the small intestine were seen three kind of cells, such as columnar absorbing cells, goblet cells and Paneth cells. Lieberkiihn's glands don'tappear to be involved. Paneth cells are noted rather at the bottom of the crypts. In thecolon, goblet cell hyperplasia is dominant. Concerning malignant transformation of Peutz-eghers polyps, no malignancies wereseen in gastric ones. Distinctive cancerization was observed in a polyp of a case, and penetrationof glands into the wall, from submucosa to the subserosa, was noted in polyps of six cases, in the small intestine. In those of the colon no malignant degeneration was observed. It may be possible histologically to distinguish polyps in Peutz-Jeghers syndrome fromother forms of gastrointestinal polyposis.
To investigate the contribution of aggressive factors to the development of acute gastroduodenallesions, serum gastrin level was determined sarially by redioimmunoassay in patientswith head injury (54 cases). Gastric acid output was also measured in 14 patients amongthem. The level of serum gastrin was higher in patients with head injury than in healthysubjects, those with burn (20 cases) or other trauma (15 cases). This high level of serum gastrinwas observed transiently in patients who had gastric hemorrhagic erosins found by urgentendoscopy. No abnormal level of serum gastrin was found in patients accompanying withgastric ulcers. Hyperacidity was seen only in one of seven patients with acute gastroduodenallesions, although it was observed in one-third of cases with head injury. These results suggestthat hypergastrinemia and hyperacidity might not have an important role in the developmentof the acute gastroduodenal lesions.
It was studied what influence bile acids (CDCA, LCA) has and what effect the additionof lecithin to bile acids has on the formation of gallstone in hamsters bred with the diet of highglucose but lacking unsaturated fatty acid. The occurrence rate of gallstone was 75% in thecontrol group, 44% in CDCA (0.05%) administration group, 67% in CDCA (0.1%) administrationgroup, 72% in LCA (0.1%) administration group, 33% in lecithin administrationgroup, 20% in CDCA (0.05%) +lecithin administration group, 27% in CDCA (0.1%) +lecithin administration group. CDCA produced a dose-dependent difference in the occurrence rate of gallstone. Formationof gallstone was inhibited to some extent by 0.05% CDCA but was not inhibited by 0.1%CDCA. Lecithin used alone produced a higher inhibitory effect on gallstone formationthan CDCA used alone. Addition of lecithin to CDCA, regardless of the dose of CDCA, significantly decreased the occurrence rate with clear potentiation of the inhibitory effectof CDCA on gallstone formation. Also, improvement of cholesterol solubility in bile compositionwas observed in the group of CDCA+lecithin. These suggest the usefulness of theconcomitant use of CDCA and lecithin.
Chronic alcohoics were classified into the following 5 groups according to the histopathologicalfidings of the liver: 1 minimal changes, 2 fatty liver, 3 hepatic fibrosis, 4 acute alcoholichepatitis and 5 cirrhosis of the liver. HBs-Ag, and-HBs and anti-HBc in sera of these patients were assayed by immunoadherencehemagglutination method and passive hemagglutination method. The prevalence of HBV associated antigen and antibody in cirrhotic patients was obviouslyhigher than in other gorups. It was suggested from this fact that HBV infection might havesome role in the development of cirrhosis of the liver at least in some cases with chronic alcoholism. However, there were some cases positive for HBV associated antigen and antibody, whose histological fingings showed liver injuries typical for alcohol-induced features. A case with acute alcoholic hepatitis was reported. He had a high anti-HBs titer in serumon several determinations, and his liver revealed numerous Mallory bodies and diffuse intracytoplasmicHBs-Ag simultaneously.
Ursodeoxycholic acid (UDCA), 7-β hydroxy epimer of chenodeoxycholic acid.(CDCA), has been used as a choleretica for 20 years in Japan. Recent report showing increased formationof UDCA in patients treated with CDCA may suggest that UDCA has similar effectto CDCA on bile cholesterol unsaturation. This paper describes the clinical value of UDCAfor the treatment of gallstones. Seventy-eight patients (22 men and 56 women) who have radiolucent or radiopaquegallstones in functioning gallbladder were studied. UDCA, supplied in tablets (Ursosan®), was given orally 450 mg/day for an average of 6.7 months. The diappearance or reduction of gallstone size or number or both (dissolving effect) was recognized in 29 of 78 patients (37%). In case of rediolucent stones, dissolving effectwas evaluated in 19 of 43 patients (44%). Diarrhea, troublesame side-effect reported in CDCAtreatment, was only occasionally observed in 4 patients. No other abnormalities was encounteredduring UDCA treatment. Although the descrimination between CDCA and UDCA in the gallstone dissolutionefficacy remains to be determined, our own results may indicate that UDCA offer a usefultreatment for cholesterol gallstones in functioning gallbladder.
Pancreatic endocrine function with respect to the alpha cell was investigated in patientswith various liver diseases and in normal controls. The results obtained were as follows: 1. Basic plasma glucagon and insulin levels and the molar ratios between glucagonand insulin in fasting state were significantly higher in the disease group than those in normalcontrol. 2. Insulin-induced hypoglycemia caused a significantly higher increase of plasma glucagonin the disease group compared with those in normal control. 3. Responses in increases of plasma glucagon and insulin levels after adminstration ofarginine were also significantly higher in the disease group. 4. Decrease of plasma glucagon after administration of glucose orally was seemed moregradually in the disease group keeping significantly higher levels than those in normal controland, in contrast, increase of plasma insulin was observed markedly in the disease group afterthe glucose administration. In conclusion, it was conjectured that the glucose intolerance was attributed to the significantelevation of plasma glucagon in patients with liver disease, in connectionwith the changesof plasma insulin, especially of molar ratio between glucagon and insulin.
The effect of exchange transfusion was assessed in comparison with other treatments in35 patients with fulminant hepatitis, of which were treated with exchange transfusion andthe others treated with a conservative therapy. After the exchange transfusion therapy, 4 out of 10 (40%) recovered fully. In contrast, only 1 out of 25 (4%) recovered with a conservative therapy. Recovery of consciousnessoccurred in 60% of the patients treated by exchange transfusion and in 12% of those treatedby the conservative therapy. Prolongation of life was also obtained in the patients treatedwith exchange transfusion. However, exchange transfusion therapy was not an absolute one, because it proved ineffectivein the patients of older ages, patients with very severe hepatocellular damage (unconjugatedbilirubin>40% of the total bilirubin, prothronbin time>40 sec.), or patients aftera duration of more than two weeks from the onset of illness. One patient died of cerebral edema, although his liver was found to have regenerativeactivities at autopsy. From these data, it was suggested that exchange transfusion in the treatment of fulminathepatitis should be the first choice in the patients of relatively young ages, or when hepatocellulardamage is not so severe. The survival rate might increase if complications were prevented.
Recently we came across two cases of high plasma ICG retention and normal BSP. Histologyof both cases showed chronic hepatitis (inactive form). On electronmicroscopy incase 1, modification of mitochondria, increase of “lipofuscin-like” lysozome and lipid dropletswere observed. We also found mild plasma ICG retention in father and a brother of case 1, and so didhigh plasma ICG retention and normal BSP in two sisters and a brother of case 2. Laboratoryfindings showed low grade bilirubinemia (total Bil. 3.5, direct Bil. 1.8) in case 1, and not remarkableabnormality n other cases except high plasma ICG retention. Using column chromatography containing Sephadex G-200 and preparative ultracentrifugalflotation method, we obtained three distinct peaks on the ICG curve and these threepeaks corresponded to 19S, 7S and 4S protein peaks in control group. Ist ICG peak boundto VLDL and LDL, and 2nd ICG peak bound to HDL. In chronic liver disease 2nd ICG peak (HDL) transfered to heavier protein, stillmorethis transfer rate correlated well to plasma ICG retention (r=-0.703, p<0.001). In these5 cases, 3 cases showed increase in 1st ICG peak, on the other hand 2 cases showed transferenceof 2nd ICG peak to heavier protein. From these results it suggested that this discrepancy was congenital or constitutional, and thc abnormality of serum lopoprotein was one of a cause of this discrepancy.