Pulmonary abnormalities caused by interferon with or without herbal drug: CT and radiographic findings.
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Biomedical subjects
Publications and source records attributed to T Kamisako.
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A 58-year-old Japanese man was admitted to our hospital with appendicitis and marked unconjugated hyperbilirubinemia (11.6 mg/dl). The jaundice worsened following appendectomy, and the direct-reacting bilirubin increased, probably due to the ceftizoxime administered postoperatively. Bilirubin diglucuronide was the main component of the serum direct-reacting bilirubin (51%) in serum measured by liquid chromatography. Because the discontinuation of ceftizoxime did not markedly improve the jaundice, epomediol, 200 mg tid, was administered orally. There was a marked decrease of serum bilirubin with an increase in the delta bilirubin/(conjugated bilirubin + delta bilirubin) ratio. After improvement of jaundice to below the pre-surgical level (4.4 mg/dl), we analyzed the duodenal bile for bilirubin fractions; those showed a marked reduction in bilirubin diglucuronide and a marked increase in bilirubin monoglucuronide, which was consistent with type II Crigler-Najjar syndrome. A marked increase of bilirubin diglucuronide in serum of this patient during cholestasis suggests that bilirubin conjugation proceeds in this syndrome when excretion of conjugated bilirubin decreases.
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To elucidate the possible implication of hepatic blood supply to the occurrence of hepatolithiasis, the rat superior mesenteric vein, which drains blood from the intestine, or the splenic vein, which drains from the spleen, was occluded for 30 minutes. Changes in the hepatic oxygen saturation index, intrahepatic uridine diphosphate-glucuronic acid concentration, bile flow, and the excretion of bilirubin as well as its fraction, along with bile acid in bile before and after the procedure, were observed. In association with superior mesenteric vein occlusion, oxygen saturation index, hepatic uridine diphosphate-glucuronic acid concentration, bile flow, bile acid concentration in bile, and percentage of biliary bilirubin diglucuronide were all decreased. Incubation of bile under sterile conditions from rats with occluded superior mesenteric veins resulted in precipitation of mainly calcium salt of fatty acid. In contrast, splenic vein occlusion caused no changes except for a decrease in biliary bilirubin concentration. Incubation of bile from rats with occluded splenic veins did not induce precipitation. From these findings it can be concluded that blood flow in the superior mesenteric vein is the primary source of oxygen supply to the rat liver and that this vein plays an important role in maintaining bile flow, bile acid excretion, and bilirubin conjugation and in preventing the precipitation of bile (possibly preventing hepatolithiasis).
To determine the effect of UDP-glucuronic acid (UDPGA) depletion on bilirubin metabolism, salicylamide (SAM, which is metabolized primarily through glucuronidation, was administered to rats at a dose of 2 mmol/kg, and biliary bilirubin excretion and the proportion of bilirubin glucuronides were determined. At 15 min after administration of SAM, the UDPGA level in the liver was markedly decreased. Although the total biliary excretion of bilirubin showed no change, the bilirubin diglucuronide level in the 0- to 30-min period after SAM administration was significantly lower (36.9 +/- 4.3%) than that of the untreated control group during the same period (47.5 +/- 1.7%; P less than .01). The biliary bilirubin monoglucuronide (BMG) level in the 0- to 30-min period was significantly increased, compared with the control group. The C8-BMG/C12-BMG ratio in the 0- to 30-min period was significantly higher than that of the control group. At 150 min after SAM administration, there was an increase in the UDPGA level in the liver accompanied by an increase in bilirubin diglucuronide and a decrease in BMG. These results indicate that changes in UDPGA in the liver due to SAM administration influence the bilirubin composition of the bile.
A 45 year old Japanese man with alcoholic hepatitis developed thrombocytopenia together with an increase in the level of platelet-associated immunoglobulin G (PAIgG). Bone marrow aspiration revealed a normal nucleated cell count and a slight increase of megakaryocytes. After abstinence from alcohol, laboratory and symptomatic improvement occurred in association with a prompt increase in the platelet count and a corresponding decrease of PAIgG. These findings suggest that PAIgG may have been involved in the development of thrombocytopenia in this patient.
We report two cases of early gastric cancer with distant metastases (stage IV). At our institute 1428 cases of primary gastric cancer were resected between 1980 and 1997; 536 were diagnosed as early gastric cancer based on the resected specimens (304 cases of mucosal cancer, Tis--TNM classification--and 232 of submucosal cancer, T1). 528 of these 536 cases were classified as histological stage I, six as stage II, none as stage III and two as stage IV. The incidence of stage IV early gastric cancer was 0.14% of all gastric cancers and 0.37% of the early gastric cancers. The two patients with stage IV early gastric cancer were women. Both tumors were defined as early cancer because they were confined to the submucosa. One was a type 0 IIc + III early cancer, histologically classifiable as a small, moderately differentiated adenocarcinoma (tub2 according to the Japanese Classification of Gastric Carcinoma, G2; TNM classification: ICD-O C16), size 10 x 8 mm; the other was a surface spreading type 0 IIc, classifiable as a signet-ring cell carcinoma (sig, G3), size 50 x 35 mm. Stage IV factors were N3 in the first and ovarian metastasis (Krukenberg tumor) in the second case.