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Biomedical subjects

K Kario

Publications and source records attributed to K Kario.

176 records · Page 10Linked to original sources

[Serum uric acid and factor VII hyperactivity in the elderly].

To study the relationship between serum uric acid, lipid fractions, and coagulation factor VII (FVII) in the elderly, we measured FVII coagulation activity (FVIIc). FVII antigen (FVIIag), in 138 normal subjects without alcohol intake ranging in age from 60 to 98 years. We also measured blood lipid fractions including apolipoprotein A-I, A-II, B, E, and serum cholinesterase activity (ChE). Serum uric acid levels significantly correlated with FVIIc (p less than 0.01) and FVIIag levels (p less than 0.05) as well as with tryglycerides, VLDL, LDL, total cholesterol, and ChE in elderly men, but not in women. However, multiple regression analysis showed these correlations in elderly men were not significant, after excluding the effect of triglycerides and VLDL. These results also suggest that elevation of uric acid may be a coronary risk factor in elderly men through high FVII levels.

Aged↗

[Plasma factor VII levels in disseminated intravascular coagulation].

To evaluate the activation of the extrinsic pathway of coagulation in disseminated intravascular coagulation (DIC), plasma factor VII coagulant activity (FVIIc) and antigen levels (FVIIag) were measured in 81 blood samples obtained from the 56 patients with DIC together with various hemostatic parameters. Plasma FVIIc (77 +/- 40%, range: 11-200%) and FVIIag (76 +/- 43%, range: 16-175%) were significantly lower in DIC subjects than in age-matched controls (FVIIc: 128 +/- 28%, FVII: 128 +/- 31%, p less than 0.01) and correlated significantly with both the antithrombin III and plasminogen activities (p less than 0.001). These results indicated that a decrease in factor VII levels is due to the consumption. However, there were several exceptions which showed elevated factor VII levels. This seems to be due to enhanced liver synthesis of factor VII compensating for the consumption. The level of tPA-PAI-I complex, a marker of pathologic endothelial stimulation, was negatively correlated with FVIIag (r = 0.45, p less than 0.05). Thus, the more the endothelium is pathologically stimulated, the more the extrinsic pathway is activated in DIC. The FVIIc/FVIIag ratio, an index of activation of factor VII zymogen, correlated with FDP and fibrin monomer levels (p less than 0.01). There were no correlations between the thrombin-antithrombin III complex. D-dimer, and alpha 2 antiplasmin-plasmin complex levels and factor VII levels. Considering the underlying diseases. the FVIIc and FVIIag levels were markedly lower in liver cirrhosis, but not significantly different in other diseases.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens↗

[Fibrin monomer assay].

Quantitative assay for fibrin monomer was done by use of a chromogenic substrate (S-2390, Coa set fibrin monomer). Samples from DIC prone patients with the underlying disease were assayed and classified into four groups. The pre DIC group showed higher FM values than the control with no laboratory coagulation abnormality, although the FDP . D-dimer showed no significant rise. FM assay is a useful marker for the detection of early coagulopathy in DIC. Administration of the AT III concentrate in the case of low level of plasma ATIII, thrombin . antithrombin complex I (TAT) caused a significant transient rise. The clinical course of DIC by TAT is often affected by the fluctuation of ATIII level in plasma, the usefulness of FM is that it reflects the real thrombin generation in DIC.

Biomarkers↗

[Thrombin.antithrombin III complex].

Increase of TAT is reflected by the generation of thrombin in hypercoagulable state. TAT might increase in DIC characterized by the formation of disseminated micro-thrombosis. DIC was classified into three groups according to the results of screening tests (FDP, platelet count, fibrinogen, prothrombin time). TAT values significantly increased in the stage of pre-DIC compared with the control group consisting of DIC prone underlying disease. Pre-DIC was easily detected by an increase of TAT during the clinical course. Management of high TAT began with the use of an anticoagulant such as heparin under the condition of sufficient ATIII level. The lowering effect of TAT was easily obtained by the anticoagulant. In ATIII-deficient DIC, the high TAT reduced with the substitution of ATIII concentrate, though a transient increase of TAT was found during the administration of ATIII. To reduce the high TAT under the deficient state of ATIII, MD805, a synthetic thrombin inhibitor, was introduced to avoid further consumption of ATIII. The TAT was decreased by the use of MD805 without administration of ATIII. MD805 could be used as an effective anticoagulant in high TAT due to DIC under an ATIII-deficient state. Although the TAT improved with an adequate anticoagulation in DIC, spontaneous bleeding sometimes appeared as a complication associated with the high level of alpha 2 plasmin inhibitor plasmin complex. In this case, the combined use of tranexamic acid relieved the bleeding.

Antithrombin III↗

Phyllodes tumor of the breast: a clinicopathologic study of 34 cases.

Thirty-four cases of phyllodes tumor of the breast were studied to evaluate the clinical and pathological features, which correlate with local recurrence. Histologically, local recurrence correlated with the finding of more than ten mitotic figures per ten high-power fields, marked cellularity, prominent nuclear pleomorphism, and stromal overgrowth. Older patients and patients with larger tumors had a higher probability of local recurrence. Stromal overgrowth correlated with the other histological parameters, with rapid tumor growth, a tumor diameter of over 10 cm, and with local recurrence. It was thus considered to be a histological indicator of the malignant potential of phyllodes tumor of the breast.

Adolescent↗

Infected abdominal aortic aneurysm due to Salmonella: CT evaluation.

Two cases of infected abdominal aortic aneurysm (IAAA) caused by salmonella are reported and the computed tomography (CT) features are discussed and compared with the pathologic findings. Additionally, a review of the literature was performed. A well-enhanced para-aortic mass (PAM) beyond the calcified intima of the abdominal aorta on the CT, which was initially considered to represent a leakage from the infected aneurysm, was observed in 5 of the 6 reported cases (including ours) and identified as a pseudoaneurysm. In one case, multiple gas collections within the PAM were demonstrated for the first time in IAAA due to salmonella.

Aged↗

Characteristics of heparin-induced platelet aggregates in chronic hemodialysis with long-term heparin use.

This study investigated the usefulness of a new platelet aggregometer with a laser-scattering method for detection of heparin-induced small platelet aggregates in chronic hemodialysis patients. Using this device, small platelet aggregates (particle size 9--25 microm) were detectable, but these aggregates could not be detected using a conventional light transmittance aggregometer. The laser-scattering intensity of the small aggregates was increased with an increasing dosage of heparin as agonist. These aggregates were disaggregated by heparin neutralization with protamine sulfate. Induction of small platelet aggregates by heparin was inhibited by preincubation with nafamostat mesilate, a synthetic protease inhibitor, and cilostazol, a platelet phosphodiesterase inhibitor, but not by the therapeutic doses of aspirin or argatroban, a selective thrombin inhibitor. The dialysis patients with long-term heparin use could be divided into two groups: responders to heparin, who formed small aggregates with a scattering intensity over 0.51 x 10(5) V after addition of 0.5 IU/ml of heparin obtained from normal platelet-rich plasma without inductor, and nonresponders, who showed an intensity under 0.51 x 10(5) V. The rate of heparin responders among dialysis patients was significantly higher than the rate among normal subjects. Heparin-induced small aggregates were detected in 13 (36.1%) of 36 normal subjects with no history of heparin infusion and in 37 (62.7%) of 59 dialysis patients who received heparin anticoagulation during each dialysis session. Dialysis patients with coronary heart disease did not have a significantly higher rate of heparin responders than patients without complications. There was no significant difference in the positivity rate between cases complicated by diabetes and those without diabetes. In patients who had more than 2 episodes of thrombotic occlusions of an arteriovenous fistula, the rate of responders and the enhancement of scattering intensity of small aggregates by heparin were significantly increased compared with these in patients without occlusions during the preceding 2 years. Moreover, dialysis patients with a positive heparin response showed a marked increase in scattering intensity of small aggregates after heparin infusion in each dialysis session. Determination of the response to heparin prior to heparin use in dialysis patients with repeated thromboembolic complication may be useful in choosing anticoagulant regimens.

Aged↗

Anticoagulation with nafamostat mesilate, a synthetic protease inhibitor, in hemodialysis patients with a bleeding risk.

Nafamostat mesilate (FUT) is a synthetic serine protease inhibitor with a short half-life that is used during hemodialysis (HD) in patients with a high risk of bleeding because it does not prolong the systemic coagulation time. To evaluate whether or not FUT is able to effectively prevent clot formation in the extracorporeal circuit without increasing systemic bleeding, HD using FUT was carried out for 33 sessions in 12 patients with a high risk of bleeding. FUT was continuously infused during HD at 20-40 mg/h to maintain a 2-fold prolongation of activated partial thromboplastin time (APTT) at the dialyzer outlet on the venous side of the circuit. No APTT prolongation was observed on the arterial side of the circuit before FUT infusion, and none of the patients showed increased bleeding during or after HD. However, clots formed in the arterial chamber (30.3%), the dialyzer (36.6%), and the venous chamber (15.1%). In 2 of the 12 patients, HD was discontinued due to clot formation despite sufficient prolongation of APTT. The mean levels of the thrombin-antithrombin III complex and prothrombin activation fragment 1 + 2 in the circuit gradually increased on both the arterial and venous sides during HD using FUT, and protein C activity decreased. No significant changes in these parameters occurred during heparin HD in the same patients after the bleeding episode had resolved. Despite sufficient prolongation of APTT in the circuit, FUT was less effective in suppressing thrombin generation when compared to heparin.(ABSTRACT TRUNCATED AT 250 WORDS)

Anticoagulants↗

Extrinsic coagulation factors and tissue factor pathway inhibitor in end-stage chronic renal failure.

The relationship between extrinsic coagulation factors, tissue factor pathway inhibitor (TFPI) and activated factor XII (FXIIa) was examined in 71 patients with end-stage chronic renal failure. They had chronic stable uremia due to regular hemodialysis. The patients were divided into two age- and sex-matched groups with and without diabetes mellitus. As extrinsic coagulation parameters, FVIIa and FVII antigen (FVIIag), tissue factor antigen and TFPI (the activity and antigen) were measured. FXIIa was measured as a marker of contact activation, and thrombin generation was evaluated using the two markers thrombin-antithrombin III complex and prothrombin fragment 1 + 2. In both hemodialysis groups with and without diabetes, significant elevations of FXIIa, FVIIa and tissue factor, with high levels of TFPI, were found. Thus, hyperactivation of the coagulation system was in part compensated by TFPI, and a significant increase in FXIIa could not directly affect FVIIa hyperactivation. No differences of these parameters, except for FVIIag and fragment 1 + 2, were found between the groups with and without diabetes. It is suggested that the long-term hemodialysis might have masked any differences due to the underlying disease in these two subgroups.

Aged↗

A case of xanthinuria: a study on the metabolism of pyrazinamide and allopurinol.

A 74-year-old female was diagnosed as having xanthinuria by measurement of the uric acid level in plasma, purine bases in urine and activity of xanthine oxidase in the duodenal mucosa. The determination of the urinary excretion of purine bases in her family demonstrated a slightly increased urinary excretion of oxypurines in her younger brother, suggesting that he was a heterozygote. The pyrazinamide-loading test and allopurinol-loading test demonstrated that she could neither metabolize pyrazinoic acid into 5-hydroxypyrazinoic acid nor allopurinol into oxypurinol, although there was a slight metabolizing of prazinamide into 5-hydroxypyrazinamide. This suggested that she belonged to the subgroup which can neither metabolize pyrazinamide into 5-hydroxypyrazinamide, pyrazinoic acid into 5-hydroxypyrazinoic acid nor allopurinol into oxypurinol.

Aged↗