1992-06 http://hdl.handle.net/10564/1899 2026-04-10T15:40:39Z 2026-04-10T15:40:39Z 奥村, 徹 渡辺, 明彦 澤田, 秀智 中野, 博重 中谷, 勝紀 http://hdl.handle.net/10564/1907 2017-05-29T06:07:52Z 1992-06-29T15:00:00Z

タイトル: 術式別にみた胃切除術後骨代謝障害に関する研究 著者: 奥村, 徹; 渡辺, 明彦; 澤田, 秀智; 中野, 博重; 中谷, 勝紀 抄録: To study the effect of surgical procedures on metabolic bone disease (MBD) after gastrectomy, the incidence of MBD was examined with Microdensitometry in 210 gastrectomized patients. In 97 (46.2%) of 210 patients MBD was found. The incidence in female patients was significantly higher than in males (p<0.01). The incidence did not correlate with the length of time after gastrectomy, age group or primary diseases. In relation to extent of gastrectomy, MBD in patients with total gastrectomy was significantly higher than in those with distal gastrectomy (p<0.05). In relation to reconstructive procedures, MBD in patients with pylorus preserving gastrectomy (PPG) was significantly lower than in those with Birrloth-Ⅰ (B-Ⅰ) or Birrloth-Ⅱ (B-Ⅱ) (p<0.05) ; MBD in patients with pylorus preserving nearly total gastrectomy (PPNTG) was significantly lower than in those with Roux-en-Y (R-Y) or interposition (I.P) (p<0.05). The level of serum alkalinephosphatase in patients with PPG was significantly lower than the level in those with B-Ⅰ or B-Ⅱ (p<0.01). The level of serum calcium in patients with PPNTG was significantly higher than level in those with R-Y or I. P (p<0.05). The calcitonin level in patients with total gastrectomy was significantly higher than the level in patients with distal gastrectomy or subtotal gastrectomy (p<0.05). This study reveals that the incidence was low in the procedure involving a small extent of gastric resection and in reconstructive procedures with pyloric preservation, such as pylorus preserving gastrectomy or pylorus preserving nearly total gastrectomy. It is concluded that metabolic bone disease after gastrectomy is attributable to physical and chemical decrease in digestive and absorptional function influenced by gastrectomy.

1992-06-29T15:00:00Z 榎本, 康博 http://hdl.handle.net/10564/1906 2017-05-29T06:07:51Z 1992-06-29T15:00:00Z

タイトル: IgA腎症とループス腎炎におけるトロンボモジュリン，プロテインC，プロテインCインヒビターの血中・尿中動態およびトロンボモジュリンの糸球体内局在 著者: 榎本, 康博 抄録: The author investigated plasma and urinary levels of thrombomodulin (TM) antigen, protein C (PC) antigen, protein C inhibitor (PCI) activity and intraglomerular localization of TM antigen in IgA nephropathy (IgA-GN) and in lupus nephritis (LN). The subjects enrolled in this study were 40 patients with IgA-GN, 20 patients with LN and 19 healthy volunteers as controls. Plasma and urinary levels of TM and PC antigen were measured by sandwich enzyme immunoassay. Plasma and urinary levels of PCI activity were expressed as inhibition activity for activated PC. Intraglomerular localization of TM antigen was detected by immunohistochemical methods using a polyclonal antibody for human TM. Plasma TM levels in the advanced stage of IgA-GN and in diffuse proliferative LN were significantly higher than those in controls. On the contrary, urinary TM levels in the advanced stage of IgA-GN and in mesangial LN were significantly lower than those in controls. In IgA-GN there were significant positive correlations between the grade of mesangial proliferation and plasma levels of TM, PC or PCI. As for intraglomerular localization of TM, in IgA-GN the staining intensity of TM on endothelial cells of glomerular tufts was decreased according to mesangial proliferation. The staining intensity of TM was higher in mesangial LN than in diffuse proliferative LN. These findings suggest that plasma TM, PC and PCI may be involved in progression of IgA-GN and that intraglomerular TM localization is influenced by the severity of glomerular lesions in IgA-GN as well as LN.

1992-06-29T15:00:00Z 松永, 健司 http://hdl.handle.net/10564/1905 2017-05-29T06:07:51Z 1992-06-29T15:00:00Z

タイトル: 小児腎疾患における尿中安定化フィブリン分解産物(XLFbDP)の動態に関する研究 ：第2報 尿中FDP分画と糸球体内フィブリン/フィブリノーゲン関連抗原(FRA)について 著者: 松永, 健司 抄録: In children with several kinds of renal diseases, fragments of urinary fibrin/fibrinogen degradation products (FDP) and crosslinked fibrin degradation products (XLFbDP) were investigated by autoradiography using western blotting method. Results were compared with distribution and immunological features of intraglomerular fibrin/fibrinogen related antigen (FRA) based on immunohistopathologic method containing monochloroacetic acid (MCA) treatment. In patients with minimal change nephrotic syndrome or membranous nephropathy, crosslinked fibrin (XLFb) was not present in their glomeruli, and urinary FDP were composed of fibrinogen degradation products (FgDP) such as X, Y and D. On the other hand, in cases of proliferative glomerulonephritis such as Henoch-Schönlein purpura nephritis or IgA nephropathy, XLFb was frequently observed along glomerular capillary walls. In these cases, urinary FDP were composed of XLFbDP (D-dimer) together with FgDP. It was concluded that the presence of D-dimer in the urine suggested intraglomerular XLFb, but some part of urinary FDP, especially FgDP, were derived from plasma fibrinogen or FDP.

1992-06-29T15:00:00Z 鞠子, 眞済 田中, 妥永子 橋本, 和子 吉田, 裕慈 高橋, 幸博 吉岡, 章 福井, 弘 竹内, 雅春 http://hdl.handle.net/10564/1904 2017-06-11T23:20:26Z 1992-06-29T15:00:00Z

タイトル: 脾梗塞をおこした先天性Antithrombin Ⅲ(AT Ⅲ)欠乏症Type Ⅰの一家系 著者: 鞠子, 眞済; 田中, 妥永子; 橋本, 和子; 吉田, 裕慈; 高橋, 幸博; 吉岡, 章; 福井, 弘; 竹内, 雅春 抄録: A family with inherited antithrombin Ⅲ (AT Ⅲ) deficiency is reported. The propositus was a 28-year-old male who first suffered from abdominal pain without any trigger at the age of 27. He was admitted to the hospital because of splenomegaly and splenic infarction and diagnosed as having splenic vein thrombosis. At the age of 28, he suffered a recurrence of abdominal pain accompanied by multiple pulmonary infarction. Most physical findings were normal. Laboratory blood count and blood chemistry examination revealed no significant abnormality. A detailed coagulation study revealed that both the activity and antigen of plasma ATⅢ were lower than those of normal adults. The ATⅢ levels of his mother, sisters, brother and niece were also decreased. The results of other coagulation tests such as those for heparin cofactor Ⅱ, Protein C, Protein S, and α₁-antitrypsin were essentially normal. The mobility of the patient's ATⅢ in the heparinized agarose gel on two dimensional crossed immunoelectrophoresis was identical to that of normal controls. These findings indicate that the family members possessed the Type Ⅰ ATⅢ deficiency described by Nagy.

1992-06-29T15:00:00Z