Biomedical subjects

K Tanoue

Publications and source records attributed to K Tanoue.

At least 73 records · Page 4Linked to original sources

PubMed1993

Vascular anatomy of duodenal varices: angiographic and histopathological assessments.

Duodenal varices are a rare occurrence, and the diagnosis and control of related bleeding is problematic. The vascular anatomy of duodenal varices in four patients was examined angiographically. The incidence of these varices was 0.4% in the patients with portal hypertension seen in our clinics from 1982 to 1991. The transparent specimen obtained at autopsy and treated with methyl salicylate and portographies in the remaining three patients revealed that the duodenal varix consisted of a single vessel with afferent and efferent vessels, forming a portasystemic shunt in the retroperitoneum. The varix transversed the duodenum and was present in the submucosal layer of the posterior wall. The afferent vessel was the superior or inferior pancreaticoduodenal vein originating in the portal vein trunk or superior mesenteric vein. The efferent vein drained into the inferior vena cava. In view of these observations, devascularization or percutaneous transhepatic obliteration of the varix would be our first choice of treatment for patients with duodenal varices.

Duodenum↗

PubMed1993

Albumin inhibits hemolysis of erythrocytes induced by ethanolamine oleate during endoscopic injection sclerotherapy.

In attempts to avoid hemolytic nephropathy following injection of 5% ethanolamine oleate during endoscopic injection sclerotherapy for esophageal varices, the relationship between serum levels of albumin and hemolysis induced by ethanolamine oleate was investigated. The rate of hemolysis at various concentrations of ethanolamine oleate and albumin was examined using a spectrophotometer in ten cirrhotic patients and five healthy volunteers (controls). Hemolysis induced by ethanol-amine oleate increased in an ethanolamine oleate concentration-dependent fashion (p < 0.01) but was dose-dependently inhibited by albumin (p < 0.05). The state of liver function was unrelated to the rate of hemolysis. The relationship between hemoglobinuria and serum albumin levels in seventy-nine cirrhotic patients with esophageal varices treated by endoscopic injection sclerotherapy with ethanolamine oleate was also examined. Hemoglobinuria was evident in 20 out of 24 patients (83.8%) in whom the serum albumin level was less than 3.0 g/dl, and in 24 out of 55 (43.6%) in whom it exceeded 3.0 g/dl, the difference being statistically significant (p < 0.01). On the day after endoscopic injection sclerotherapy, creatinine clearance fell from 81.6 +/- 33.8 m/l min to 60.1 +/- 31.4 ml/min in the hemoglobinuria-positive patients (p > 0.01) and two went into acute renal failure. The creatinine clearance ranged from 79.5 +/- 27.9 ml/min to 83.0 +/- 39.9 ml/min in the hemoglobinuria-negative patients (p < 0.1). In the light of this evidence we correct the serum albumin level cut off point to 3.0 g/dl prior to endoscopic injection sclerotherapy in order to maintain renal function.

Aged↗

PubMed1992

Endoscopic injection sclerotherapy for 1,000 patients with esophageal varices: a nine-year prospective study.

We report here the results of endoscopic injection sclerotherapy performed in 1,000 consecutively treated Japanese patients with esophageal varices. This prospective study covered the period from 1982 to 1990. Variceal bleeding was controlled in 215 (97.7%) of 220 patients. Esophageal varices were completely eradicated in 778 patients (77.8%); the mean number of sessions was 4.2. In only 3 of the 778 patients did esophageal varices of the same size recur. Small, dilated, venous vessels that required additional sclerotherapy in follow-up endoscopy at 3-mo intervals appeared in 171 (22.2%) of 778 patients. The cumulative nonbleeding rate at 5 yr was 94.5% in patients in whom the varices had been eradicated. Deaths caused by upper gastrointestinal bleeding accounted for 2.6% of cases, whereas the rates of liver failure and hepatoma were 4.6% and 47.3%, respectively. The 5-yr cumulative survival rate was 54.1% in patients without concomitant hepatoma; it was 12.0% in patients with hepatomas. Multivariate analysis showed that hepatoma, Child classification, indication (acute, elective or prophylactic) and eradication were independent factors that significantly influenced survival time. This study clearly shows that close follow-up with endoscopy and complete eradication lead to significant reduction in bleeding from esophageal varices and reduction of mortality related to this bleeding.

Endoscopy↗

PubMed1992

Immunocytochemical evidence for the translocation of alpha-granule membrane glycoprotein IIb/IIIa (integrin alpha IIb beta 3) of human platelets to the surface membrane during the release reaction.

The localization of glycoprotein (GP) IIb/IIIa (integrin alpha IIb beta 3) in both resting and thrombin-activated platelets was studied immunocytochemically. By the preembedding method where only the GP IIb/IIIa molecules on the surface of platelets were immunostained, the distribution of protein A-colloidal gold label was randomly distributed along the surface membrane of resting platelets at a density of 18.0 +/- 2.7 gold particles/microns of membrane. At 15 s after stimulation by 0.1 U/ml of thrombin in an unstirred platelet suspension, the spheroid-shaped platelets with pseudopodia still had normal numbers of alpha-granules, and the density of gold particles was 19.7 +/- 3.6 particles/microns. At 5 min, the alpha-granules were no longer present because of the release reaction, and the density of gold particles significantly increased (27.0 +/- 3.7 particles/microns; p less than 0.01). In immuno-stained ultra-thin frozen sections, the gold particles were detected not only on the surface membrane, including the open canalicular system (OCS), but also on the alpha-granule membranes of resting platelets. At 30 s after thrombin stimulation the alpha-granules fused with the OCS, resulting in the formation of a swollen OCS, which still had gold particles on its membrane. At 5 min, the gold particles were detected on the membrane of the swollen OCS located near the surface membrane, while very few gold particles were present on the membrane of the OCS in the central part of the platelets. These results demonstrate that alpha-granule membrane GPIIb/IIIa translocates to the surface membrane through the membrane of the OCS.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗

PubMed1992

Normal aggregations of glycoprotein IV (CD36)-deficient platelets from seven healthy Japanese donors.

Since glycoprotein IV (GPIV) has been shown to play an important role in the interaction of platelets with collagen and thrombospondin, the aggregation and secretion of GPIV-deficient platelets were examined. Using a binding assay with monoclonal 125I-OKM5 antibody against CD36 antigen and crossed immunoelectrophoresis of the solubilized platelets against anti-GPIV antibody, the platelets from seven (4.1%) out of 170 healthy Japanese donors were found to be deficient in GPIV. The GPIV-deficient platelets showed normal aggregations in response to collagen as well as ADP, epinephrine, arachidonic acid and thrombin in comparison with GPIV-positive platelets. Polyclonal anti-GPIV antibody aggregated GPIV-positive platelets but not the GPIV-negative ones. The F(ab')2 fragments of the anti-GPIV antibody competitively inhibited the anti-GPIV-induced aggregation, but did not affect the collagen-induced aggregation of GPIV-positive platelets. These results suggest that the deficiency of GPIV does not affect platelet aggregability.

Adenosine Diphosphate↗

PubMed1992

Interaction of platelets and blood vessels--vascular injuries induced by platelet activation in vivo.

We have found that vascular injuries are induced by intravascular aggregation of platelets activated by arachidonic acid (AA) or ADP. The characteristic findings are the appearance of vacuoles in endothelial cells and eventual deendothelialization. In deendothelialized regions, formation of platelet thrombi was observed. The platelets in the thrombi were stained with 2T60, a monoclonal antibody that recognizes activated platelets. The change was more remarkable in the AA-injected animals because AA has a stronger platelet activating effect and a detergent effect on the endothelium. The ADP-injection experiments clarified the role of platelets in vascular injury. These findings suggest that activated platelets play a role in the genesis of vascular injuries, and that their role is related to thrombus formation.

Adenosine Diphosphate↗

PubMed1992

[Platelet structure and function: immunocytochemical localizations of membrane glycoprotein and alpha-granule protein].

The platelet membrane glycoproteins (GPs) are receptors or binding sites for adhesive proteins. GPIb and GPIIb/IIIa complex are major glycoproteins and have important roles, functionally. GPIb plays an essential role in primary hemostasis as receptor for the von Willebrand factor. The GPIIb/IIIa complex acts as the binding site for adhesive proteins on activated platelets and, as such, is essential for platelet aggregation. On the other hand, four adhesive proteins (fibrinogen, fibronectin, thrombospondin and von Willebrand factor), which are present not only in plasma but also in alpha-granules, mediate or modulate the platelet adhesive response. The interaction between these adhesive proteins and platelet membrane GPs are essential for platelet adhesion and aggregation. The present report will focus on the localization of GPIb and GPIIb/IIIa on the platelet surface and that of adhesive proteins in alpha-granules in both resting and activated human platelets.

Blood Platelets↗

PubMed1992

[Detection of circulating activated platelets by anti-GMP-140 monoclonal antibodies].

The clinical significance and detection methods for circulating activated platelets are reviewed. It has been recently demonstrated that three kinds of platelet granules, dense granule, alpha-granule and lysosome, have specific membrane proteins; granulophysin, GMP-140 (PADGEM) and CD63 antigen, respectively, and that these specific granule-membrane proteins become exposed on the surface of the activated platelets. It is believed that detection of circulating activated platelets, using monoclonal antibodies specific to these granule-membrane, may be reliable and diagnostic value in thrombotic and prethrombotic diseases. Preliminary clinical studies using 2T60, a newly developed anti-GMP-140 monoclonal antibody, was presented.

Antibodies, Monoclonal↗

PubMed1992

Splenic hyperkinetic state and splenic artery aneurysm in portal hypertension.

Forty-eight out of six hundred and thirty patients with portal hypertension undergoing a celiac angiography series were diagnosed as cases of splenic artery aneurysm during the period 1977-1988. The case-control study of patients with portal hypertension with splenic artery aneurysms and those without was designed to characterize the angiological features. The splenic arterial flow was assessed by measuring the radii of the splenic arteries on celiac arteriograms. In the portal hypertensive patients with splenic artery aneurysms, the splenic artery was larger (p < 0.05) and the splenic arterial flow greater (p < 0.05), and these patients were in a more hyperkinetic state, than were those with no splenic artery aneurysm. The study suggests that splenic artery aneurysms in cases of portal hypertension may be the consequence of a hyperkinetic state in the spleen.

Adolescent↗

PubMed1992

Comparative effects of 5% ethanolamine oleate versus 5% ethanolamine oleate plus 1% polidocanol for sclerosing esophageal varices.

Sixty-six patients with portal hypertension and esophageal varices due to liver cirrhosis were randomized to receive either 5% ethanolamine oleate (EO) or 5% EO plus 1% polidocanol (EOP) as a sclerosant for endoscopic injection sclerotherapy (EIS). The two groups were well matched with regard to age, sex and the severity of liver disease. In no patient in the two groups was there any major complication, such as esophageal perforation or esophageal bleeding. Eradication of esophageal varices was attained with an average of 4.7 and 4.3 sessions of endoscopic injection sclerotherapy in the ethanolamine oleate and polidocanol groups, respectively. Data on one patient in the ethanolamine oleate group had to be excluded because he left the hospital after 2 sessions of endoscopic injection sclerotherapy. Esophageal ulcers occurred earlier in the polidocanol group (after an average of 2.8 weeks) than in the ethanolamine oleate group (3.8 weeks), the difference being statistically significant (P < 0.01). The rate of occurrence of esophageal stricture requiring more than 2 sessions of bougienage was significantly (P < 0.01) higher in the polidocanol group (16/33, 48%) than in the ethanolamine oleate group (4/32, 12%). This study suggests that the two sclerosants have equal efficacy for treating patients with esophageal varices. With polidocanol there was ulceration and stricture in the distal esophagus.

Drug Combinations↗

PubMed1992

[Platelet aggregations and glycoproteins].

Platelet membrane glycoproteins play important roles in platelet functions. In this symposium, we reported three types of deficiency of platelet membrane glycoproteins; Glanzmann's thrombasthenia, Bernard-Soulier syndrome, GPIV-deficiency and discussed the roles of GPIIb/IIIa, GPIb and GPIV, respectively, in the aggregation of these abnormal platelets. In a patient with Bernard-Soulier syndrome, the abnormality in the patient's GPIb was caused by the double heterozygote from her parents who were unrelated. Roles of GPIV were negligible in platelet aggregation since the GPIV-deficient platelets (Naka-) found in healthy donors showed normal platelet aggregations. We developed two monoclonal antibodies, TM83 and TM60 against GPIIIa and GPIb, respectively, and showed that these antibodies inhibited the function of GPIb and GPIIb/IIIa complex, respectively. We demonstrated that TM83 inhibited an epitope of GPIIIa and/or GPIIb/IIIa complex which changes its conformation due to Ca2+ deprivation and is essential for exposure of the fibrinogen-binding site.

Adult↗

PubMed1992

[A case of myasthenia gravis complicated by cyclic thrombocytopenia].

A 47-year-old woman with myasthenia gravis for last 11 years was admitted because of relapsed muscle weakness, hypermenorrhea and thrombocytopenia. Physical and neurological examinations revealed diplopia, proximal muscle weakness and purpuras on the left arm and bilateral legs. Repeated hematological examinations revealed cyclic fluctuation of platelet counts which spontaneously changed from the nadir levels of 12-27 x 10(3)/microliters to the peak levels of 150-400 x 10(3)/microliters. The platelet count reached a nadir at the onset of menstruation. Platelet-associated IgG (PAIgG) was within normal level when platelet count was at an increasing phase. Survival time of autologous platelets was normal when platelet count was at an increasing phase. Megakaryocytes in the bone marrow were apparently normal at the nadir phase. The patient's serum obtained at the nadir of platelet count significantly suppressed megakaryocyte colony forming unit (Meg-CFU) formation in comparison with that after the stabilization of platelet count, suggesting that this cyclic thrombocytopenia was secondary to cyclic hypoproduction of megakaryocytes caused by a suppressive factor. On the other hand muscle weakness showed no cyclic fluctuation. Administration of 60 mg/day prednisolone stabilized the platelet count at about 280 x 10(3)/microliters, abolished hypermenorrhea and gradually improved muscle weakness. These findings suggested autoimmune mechanism in the production of a Meg-CFU-suppressive factor might be involved in the pathogenesis of thrombocytopenia.

Female↗

PubMed1991

Enhancement by IL-1 beta and IFN-gamma of platelet activation: adhesion to leukocytes via GMP-140/PADGEM protein (CD62).

We have examined the effect of inflammatory cytokines on the platelet activation. IL-1 beta and IFN-gamma were found to enhance the adhesion of thrombin-treated platelets to monocytic leukemia cells (U937), when the adhesion was assayed by platelet-mediated cell agglutination. The agglutination was inhibited by a monoclonal anti-GMP140 antibody or EDTA, suggesting that the enhanced platelet adhesion to the leukemic cells was mediated by GMP140. In addition, these cytokines also increased the release of 5-HT from platelets in the presence of a low concentration of thrombin. These data suggest that platelet functions are regulated by the cytokines and that activated platelets participate in inflammatory process.

Blood Platelets↗

PubMed1991

Superoxide anion hyperproduction by neutrophils in a case of myelodysplastic syndrome. Association with Sweet's syndrome and interstitial pneumonia.

The complication of Sweet's syndrome and interstitial pneumonia occurred in a patient with myelodysplastic syndrome. Superoxide anion production by the patient's neutrophils was considerably higher than that by neutrophils obtained from normal controls after stimulation with opsonized zymosan, phorbol myristate acetate, or myristic acid. Prednisone, which a potent inhibitor of superoxide anion production by neutrophils, dramatically improved the skin and pulmonary lesions, suggesting that they were parts of the same clinical spectrum associated with the superoxide anion hyperproduction.

Dermatitis↗

PubMed1991

Glycoprotein Ib (GPIb)-dependent and GPIb-independent pathways of thrombin-induced platelet activation.

In this study, the question of whether glycoprotein Ib (GPIb) mediates both high and moderate affinity pathways of alpha-thrombin-induced platelet activation was examined. Flow cytometric studies, using a panel of monoclonal antibodies (MoAbs), showed that Serratia marcescens protease treatment removed greater than 97% of the glycocalicin portion of GPIb but did not affect the changes in the expression of GPIX or GMP-140 that were induced by high concentrations of alpha-thrombin (10 nmol/L). However, Serratia treatment almost completely abolished the increase in platelet surface GMP-140 induced by low concentrations of alpha-thrombin (0.5 nmol/L) and diminished the downregulation of platelet surface GPIX by 60.9% +/- 5.6% (mean +/- SEM, n = 3). When present in 20-fold molar excess, an MoAb directed against the alpha-thrombin/von Willebrand factor (vWf) binding domains of GPIb completely blocked the ristocetin-dependent binding of vWf to platelets but inhibited only to about 50% the binding of alpha-thrombin and the activation-dependent binding of vWf. In platelets treated with Serratia marcescens protease to remove GPIb, a concentration of this MoAb 16,000-fold in excess of the maximum possible remaining copies of GPIb failed to inhibit platelet activation by alpha-thrombin. These studies demonstrate that activation of intact platelets by alpha-thrombin proceeds by both GPIb-dependent and GPIb-independent mechanisms.

Antibodies, Monoclonal↗

PubMed1991

Characterization of platelet aggregation induced by the human melanoma cell line HMV-I: roles of heparin, plasma adhesive proteins, and tumor cell membrane proteins.

We investigated the in vitro mechanism of platelet aggregation induced by HMV-I human melanoma cells. HMV-I cells, in the absence of exogenous plasma proteins, induced platelet aggregation, followed by the release reaction. Heparin at an anticoagulant concentration had no effect on the aggregation. Calcium ion was essential for this tumor cell-platelet interaction and could not be replaced by magnesium. Among the adhesive proteins containing RGD sequences that have been reported to enhance experimental metastasis, fibrinogen and thrombospondin significantly enhanced the aggregation induced by HMV-I cells, fibronectin and von Willebrand factor inhibited it, and vitronectin had no effect. To identify the platelet-aggregating factor(s) of the tumor cells, we have developed a monoclonal antibody against HMV-I cells that can inhibit HMV-I cell-induced platelet aggregation. Immunoprecipitation analysis revealed that this antibody recognized an Mr 71,000 membrane protein. These results suggest that the association between the tumor cells and platelets is mediated by the Mr 71,000 membrane protein recognized by this monoclonal antibody.

Antibodies, Monoclonal↗

PubMed1991

High rate of portal thrombosis after splenectomy in patients with esophageal varices and idiopathic portal hypertension.

Data on 126 consecutive patients who were admitted to our clinics from January 1979 to May 1989 were scrutinized to assess changes in portal hemodynamics following splenectomy. Two groups were classified: (1) a group of 106 patients with cirrhosis of the liver and (2) a group of 20 patients with idiopathic portal hypertension (IPH). Portal thrombosis was present in five (25.0%) of the 20 patients with IPH and in two (1.8%) of the 106 patients with cirrhosis of the liver. As seen on celiac arteriography, the mean (+/- SD) diameter of the trunk of the splenic artery and vein was 8.99 +/- 1.55 and 16.2 +/- 3.6 mm, respectively, in patients with IPH, while it was 7.94 +/- 1.28 and 14.2 +/- 3.1 mm, respectively, in patients with cirrhosis of the liver. Changes in portal venous pressure were 78.4 +/- 59.4 mm H2O in patients with IPH and 43.5 +/- 38.7 mm H2O in patients with cirrhosis of the liver. There were no significant differences in the maximum level of thrombocytes in patients with IPH or in those patients with cirrhosis of the liver. These events suggest that portal thrombosis can occur with a significantly higher incidence in patients with IPH than in those patients with cirrhosis of the liver after splenectomy, and a decrease in blood flow in the portal vein may be closely linked to the formation of portal thrombosis after splenectomy in patients with IPH. Preoperative examination of portal hemodynamics must be thorough.

Esophageal and Gastric Varices↗

PubMed1991

Morphological evidence for the association of plasma membrane glycoprotein IIb/IIIa with the membrane skeleton in human platelets.

We examined the association between glycoprotein (GP) IIb/IIIa, a receptor for fibrinogen, and membrane skeletons in both unstimulated and thrombin-activated human platelets. After a treatment with dithiobis succinimidyl propionate (DTSP), a cross-linker, unstimulated and activated platelets were simultaneously extracted and fixed with a fixing solution containing Triton X-100. Also, the localization of GPIIb/IIIa on the plasma membrane was observed by a preembedding staining method of unextracted platelets. In unstimulated platelets, 20-40% of the whole plasma membrane remained in the detergent-extracted samples. Amorphous structures with 10-70 nm in diameters are distributed at 20 to 100-nm intervals on the surface of plasma membrane. Similar structures also were identified in the intact platelets by the immunocytochemical method. By careful inspection, we found that most of the amorphous structures that contained gold particles were connected to the submembrane zone just beneath the plasma membrane. The submembrane zone was identified as the membrane skeleton because actin was detected in the zone. After activation, detergent-insoluble granules were surrounded by dense networks of microfilaments in the central part of platelets. The filaments were identified as actin and became associated with myosin. These results demonstrate that GPIIb/IIIa on the plasma membrane is connected to the membrane skeleton and suggest that, during activation, actin filaments which extend into the cytoplasm from the membrane skeleton increase and form dense networks around Triton-insoluble granules.

Actins↗