Gastrointestinal lymphangioma: endosonographic demonstration and endoscopic removal.
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Biomedical subjects
Publications and source records attributed to K Aoyagi.
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Upper gastrointestinal endoscopy was performed in patients with rheumatoid arthritis (RA) during the period 1989-1991, and biopsy specimens were obtained from the stomach and from the duodenum for examining amyloid deposits. Among 407 patients, gastrointestinal amyloidosis was confirmed in 54 (13.3%). Twenty-two patients were regarded as having slight amyloid deposits, while 32 patients were categorized as having marked amyloid deposits. The incidence of clinical manifestations suggestive of systemic amyloidosis was more frequent in the marked deposits group than in the slight deposits group (47% vs 14%, P<0.05). Among the patients who died of manifestations associated with amyloidosis, the survival period following endoscopy was shorter in the marked deposits group than in the slight deposits group. These findings suggest that gastroduodenal biopsies may be useful for diagnosing secondary amyloidosis and that the degree of amyloid deposits seems to be correlated with the clinical manifestations of RA.
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Angiodysplasia of the small intestine is a rare but important cause of gastrointestinal bleeding. We present a 64-year-old man with repeated melena in whom the diagnosis of multiple angiodysplasia of the jejunum was suggested by angiography. The affected segment of the small intestine, in which reddish patches were detected by intraoperative endoscopy, was removed. The combined technique of injecting a dye and a water-soluble contrast medium into the resected specimen revealed areas of dilated vessels, which were diagnosed histologically as angiodysplasia. This case suggests that angiodysplasia of the small intestine can be recognized clinically before the operation and that the intravascular injection technique is useful in confirming the diagnosis in the resected specimen in vitro. We describe this case in detail and review other cases of small intestinal angiodysplasia reported in the English literature.
A case of a 20 year old Japanese woman who developed thyroid cancer exhibiting unusual cribriform structures while being followed up for familial adenomatous polyposis/Gardner's syndrome is reported. The patient presented with osteomas, pigmented retinal lesions, and adenomas of the duodenum and the papilla of Vater, in addition to numerous adenomatous polyps in the colorectum. On ultrasonography, the thyroid cancer was localised to the right lobe and was identified as an irregular, internal echo tumour with a peripheral hypoechoic zone, measuring 1.8 cm in diameter. Histological examination of the resected tumour showed a concomitance of papillary proliferation and cribriform structures with follicles of varying sizes. These features can be distinguished from sporadic thyroid cancer.
PURPOSE: To characterize the growth and developmental changes of superficial depressed colon cancer by using retrospective radiographic and histologic data. MATERIALS AND METHODS: In a retrospective study, the radiographs in patients with nine superficial depressed and those with 12 elevated (sessile or semipedunculated) colon cancers were analyzed. RESULTS: The initial superficial depressed lesions were 11.7 mm (mean) in diameter and took an average of 32.3 months to double in size. The initial elevated lesions were 15.7 mm (mean) in diameter and took an average of 8.6 months to double in size. The initial size of the former was not statistically significantly different from that of the latter; however, the doubling time of the superficial depressed cancers was statistically significantly slower than that of the elevated cancers. Superficial depressed cancers did not have concomitant adenomatous components, did not develop rapidly into advanced cancer, and did not change greatly from their original configuration; their growth rate was rather slow. Histologically, superficial depressed cancers showed a nonpolypoid growth pattern. CONCLUSION: Superficial depressed cancer develops more slowly than does elevated cancer, and this development follows a nonpolypoid growth pattern.
This study investigated the peroxidative state of renal failure by measuring lipid peroxidation. The generation of lipid peroxides by rat hepatic microsomes was compared between experimental renal failure caused by 7/8 nephrectomy and healthy control animals. The concentrations of BUN at the point of sacrifice were 84.2 +/- 18.4 (mean +/- SD) in nephrectomized and 19.8 +/- 4.3 mg/dl in the control group (p < 0.01, n = 5). Microsomal generation of thiobarbituric acid reactive substance was 31.2 +/- 2.8 in the nephrectomized group and 20.9 +/- 4.9 nmol/incubation/min in the control group. There was a significant difference between the groups (p < 0.01, n = 5). In summary, the generation rate of lipid peroxides in the microsomes obtained from the rats with experimental renal failure was significantly higher than the control. This study confirms an increased peroxidative state, and specifies one of the sites of increased lipid peroxide generation in renal failure.
This study aims to raise the possibility of methylguanidine, a peroxidative product of creatinine, as a measure of the peroxidative state. As a known standard, we measured the inhibitory effect of uremic serum on the NADPH-dependent microsomal lipid peroxidation. This is an established method for evaluating the peroxidative state and is compared to the effect of uremic serum on methylguanidine synthesis. The study shows decreased serum antioxidant activity in hemodialysis patients by both methods, though there is no correlation between them. These results support the use of methylguanidine as a peroxidative marker and suggest a difference in the reactive oxygen species involved in the reactions of methylguanidine synthesis and microsomal lipid peroxidation.
Synthesis of guanidinosuccinic acid (GSA), a uremic toxin, has been suggested to relate to the urea concentration and synthetic rate. Among the urea cycle enzymes, inhibition of argininosuccinate (ASA) lyase by urea has been reported. Argininosuccinate which contains a GSA structure is a candidate of a GSA precursor. We found that another uremic toxin, methylguanidine, is formed from creatinine with reactive oxygen species. Therefore, we investigated in vitro whether GSA is formed from ASA with reactive oxygen species. GSA was measured by HPLC by a post-column-labeling method using 9,10-phenathrequinone. When 1 mmol/l ASA was reacted with the hydroxyl radical-generating system for 5 min at pH 7.4, 9 mumol/l GSA was formed. Dimethylsulfoxide, a hydroxyl radical scavenger, markedly inhibited GSA synthesis. The superoxide radical generated by xanthine and xanthine oxidase reaction also formed 1 mumol/l GSA from 1 mumol/l ASA and the GSA formation was inhibited by superoxide dismutase or catalase almost completely. Addition of FeCl2 to the xanthine/xanthine oxidase reaction further increased GSA synthesis. These results indicate that GSA is formed from ASA by reaction with the hydroxyl radical and the superoxide radical.
The synthesis of guanidinosuccinic acid (GSA) increases in uremics, and GSA is implicated as a uremic toxin. The GSA synthesis increases roughly in proportion to the serum urea level that increases in patients with renal failure. Urea is a specific inhibitor of argininosuccinase, the fourth urea cycle enzyme, and might lead to the increase of argininosuccinate (ASA). We found that GSA is formed from ASA by reactive oxygen species in vitro. In this paper, we investigated GSA synthesis from ASA in isolated rat hepatocytes and the effect of reactive oxygen species on this synthesis. When isolated rat hepatocytes were incubated with 5 mmol/l ASA, GSA was formed linearly with time up to 6 h (16 nmol/g wet liver/6 h). GSA was formed depending on the ASA concentration up to 10 mmol/l. Dimethylsulfoxide, a hydroxyl radical scavenger, inhibited GSA synthesis by 65%. GSA was actively formed when the hepatocytes were incubated with 32 mmol/l urea. The GSA formation in the presence of urea was also inhibited by dimethylsulfoxide, although the inhibition was less marked. FeCl2, that increases the hydroxyl radical generation, increased GSA synthesis. These results indicate that GSA is formed from ASA in isolated hepatocytes. The results also suggest that reactive oxygen species are important for GSA synthesis in the cells.
The pharmacokinetics of tamsulosin hydrochloride in patients with renal impairment were compared with those in healthy volunteers, and the factors that influenced plasma levels of tamsulosin were elucidated. A single oral dose of 0.2 mg of tamsulosin was given and blood and urine samples were obtained for 36 hours after administration. Unbound plasma concentration of tamsulosin was measured by a combination of equilibrium dialysis and liquid chromatography tandem mass spectrometry methods to examine the effect of protein binding on the pharmacokinetics of tamsulosin. Mean values for maximum concentration (Cmax) and area under the concentration-time curve (AUC) of total drug (Cmax,t and AUC1) in patients with renal impairment were 73% and 211% greater, respectively, than those in healthy volunteers. Mean Cmax and AUC of unbound drug (Cmax,u and AUCu), however, were almost the same in the two groups. A high correlation was found between alpha 1-acid glycoprotein (alpha 1-AGP) concentration and AUCt, but no correlation was found between alpha 1-AGP concentration and AUCu,0-36) or between creatinine clearance (ClCR) and AUCu,0-36). These results show that in patients with renal impairment, the pharmacokinetics of tamsulosin are affected by the change in protein binding that is associated with alteration of plasma alpha 1-AGP concentration, but are not largely affected by the decrease in the renal excretion. Although total tamsulosin levels increased as plasma protein binding increased, unbound tamsulosin levels (which are directly associated with the pharmacologic effects) remained unchanged in these patients.
We report on the histochemistry of copper-metallothionein (Cu-MT) in the kidneys of Long Evans Cinnamon (LEC) rats. We used the visualization principle of histochemistry based on the autofluorescence emission from the fluorophore of Cu(+)-thiolate clusters in proteins. Intense autofluorescence signals were observed with a ring at the outer stripe of the outer medulla. Orange fluorescence signals were observed in the nuclei and cytoplasm of proximal straight tubular (PST) cells of segment 3 (S3) at the outer stripe of the outer medulla, and yellow-orange signals were detected in lysosome-like organelles in the proximal convoluted tubule (PCT) cells of segments 1 and 2 (S1 and S2) adjacent to the glomeruli in the cortex. These fluorescent materials were identified as Cu-MT because both signals were quenched by withdrawing Cu+ or by blocking cysteine residues, the distributions of cysteine residues and immunoreactive MT showed identical patterns to the localization of the fluorescence signals, and the fluorescent proteins containing Cu were eluted at the same Kd value of purified Cu-MT by gel filtration chromatography. However, a high level of MT mRNA was detected only in the outer stripe of the outer medulla where the orange fluorescence signals were detected, but not in the cortex. This difference in localization between the protein and the mRNA suggested that synthesis of renal MT occurs do novo in the outer stripe of the outer medulla. The yellow-orange fluorescent Cu-MT located in the lysosomal organelles at S1 and S2 of the PCT cells in the cortex could be Cu-MT of nonrenal origin, i.e., Cu-MT transported from other organs.
Eight rare cases of remnant-stump early gastric cancer (RS-EGC) were investigated, retrospectively. The incidence of RS-EGC was 0.9% (8/845) of all resected early gastric cancers. The macroscopic cancer type was elevated in 75% and mucosal in 88%. All were the differentiated type with no lymph node metastasis. The initial reconstruction involved a Billroth II in 75% of the patients. The RS-EGC was usually found during a periodic endoscopic follow-up. All patients are still alive with no postoperative complications and no cancer recurrence.
We studied retrospectively the clinicopathological features of gastric cancer with duodenal invasion and compared these with those with non-invasion, to investigate the prognostic significance of duodenal invasion. The patients were grouped into two groups of Group A (65 patients) with duodenal invasion and Group B (197 patients) without invasion who underwent gastrectomy for advanced distal gastric carcinoma according to histological findings. In Group A, many were at high age and with symptoms of pyloric stenosis. Group A (91%) had a significantly higher incidence of serosal invasion and infiltration into the pancreas head than did Group B (76%) (p < 0.01). In N3 metastasis, there was a significant difference between Group A (60%) and Group B (36%) (p < 0.01). The five-year-survival rate in Group A was 14.0% and in Group B was 43.3% (p < 0.001). In cases of duodenal invasion, patients with symptoms of pyloric stenosis demonstrated a poorer prognosis than those without. Those with longer than 20 mm invasion had a significantly higher incidence of N3 metastasis than those with less than 10 mm (p < 0.05). Lymphangitic type had longer invasive length to duodenum, and N3 metastasis of the lymphangitic type was frequent comparing to localized type (42%) and invasive type (47%) (p < 0.001) (95%) (p < 0.01). These results showed that duodenal invasion was a significant prognostic factor in cases of distal gastric carcinoma. In the therapeutic strategy for advanced gastric carcinoma with duodenal invasion, it is necessary to perform gastrectomy with regional lymph nodes dissection and with combined resection of adjacent organs.