[Horizontal pigmented bandings of the nails with daunorubicin therapy (author's transl)].
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Biomedical subjects
Publications and source records attributed to K Tanoue.
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Prolonged, probably indefinite storage of viable and functional human platelets is now possible by freezing with dimethylsulfoxide (DMSO). These platelets have a nearly normal survival upon reinfusion and are capable of sustained hemostatic effectiveness in thrombocytopenic patients. Adaptation of the freezing technique for large-scale usage has more recently been achieved. The method is mainly based on the following principles: (1) use of plasma for suspension of the platelet concentrate; (2) gradual addition (0.5% every 2 min) of DMSO to a final concentration of 5% and its gradual removal; (3) a slow cooling rate of about 1 degree C per min and rapid thawing (in 1 min); (4) use of a polyolefin plastic bag for freezing; (5) a washing medium of 20% plasma in Hanks' balanced salt solution; (6) final resuspension of the platelets in 50% plasma in Hanks' solution.
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A group of 1127 patients who underwent sclerotherapy for esophageal varices were compared for outcome in terms of age: over and under age 70 years. Esophageal varices were completely eradicated in 81 of 110 patients > 70 years (73.6%) and in 791 of 1017 patients < 70 years (77.8%). Gastrointestinal bleeding after sclerotherapy occurred in 9 patients > 70 years (8.2%) and in 84 of those < 70 years (8.3%). Complications occurred in 16 patients > 70 years (14.5%) and in 141 < 70 years (13.9%). Liver failure and hepatoma accounted for more than 80% of the causes of death in both groups (80.3% versus 83.8%). The 5-year cumulative survival rates in patients with bleeding esophageal varices (bleeders) without hepatoma were 21.8% in those > 70 years and 58.7% in those < 70 years (p < 0.01), the relative survivals being 25.3% versus 66.6%. Patients without hepatoma and treated by prophylactic sclerotherapy accounted for 66.2% of patients > 70 years and 61.7% of those < 70 years, the relative survivals being 75.9% versus 71.9%. As analyzed by the Cox proportional-hazards model, age > 70 years was a prognostic factor in the bleeders (p < 0.01) but not in the nonbleeders. We recommend that elderly patients with esophageal varices be given prophylactic sclerotherapy, as the outcome for these patients is poor once bleeding has occurred.
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The effect of endoscopic injection sclerotherapy (EIS) for esophageal varices on portal hypertensive gastropathy (PHG) was investigated in 137 patients who underwent EIS from July 1987 to March 1990. Two groups, PHG(+) (N = 35) and PHG(-) (N = 102) were distinguished by endoscopic findings obtained before EIS. PHG was classified into four grades by endoscopy scored as 0, 1, 2, or 3. The PHG score significantly worsened after EIS (p < 0.01), and PHG became worse 6 to 9 months after the eradication of varices followed by gradual improvement. Recurrent small veins, which required additional EIS, appeared more frequently in the PHG(+) group (p < 0.05). New gastric varices appeared or gastric varices enlarged after EIS more frequently in the PHG(+) group (7 patients, 20.0%) than in the PHG(-) group (12 patients, 11.8%), but this was not statistically significant. Thus, frequent endoscopy after EIS is needed with special attention directed to development of PHG and gastric varices, especially for patients with PHG prior to treatment.
Fifty cirrhotic patients with esophageal varices underwent endoscopic treatment in a prospective randomized trial carried out to compare variceal ligation with injection sclerotherapy, with respect to safety, efficacy, and complications in the initial session. Twenty-five patients each were treated using endoscopic variceal ligation or endoscopic injection sclerotherapy in the initial session and then only endoscopic injection sclerotherapy for all following sessions. Ligations numbered 4.1 at the initial session. The total number of sessions of endoscopic injection sclerotherapy was 4.0 +/- 1.3 in the endoscopic injection sclerotherapy group compared with 3.6 +/- 1.4 in the endoscopic variceal ligation group. The total volume of the sclerosant used by the end of all the sessions was 23.9 +/- 10.3 ml in the endoscopic variceal ligation group and 39.0 +/- 11.5 ml in the endoscopic injection sclerotherapy group (p < 0.0001). In all patients, complete eradication of the varices was achieved, and at 7 to 15 months follow-up no evidence of recurrence was seen. Adverse effects such as pyrexia, chest pain, and pleural effusion after the initial session were significantly lower in the endoscopic variceal ligation group (p < 0.05), and total bilirubin, serum creatinine, lactate dehydrogenase, and urinary beta 2-microglobulin were significantly increased and PaO2 decreased after endoscopic injection sclerotherapy (p < 0.05). This study shows that endoscopic variceal ligation significantly decreased the adverse effects associated with endoscopic injection sclerotherapy in the initial session, and it is recommended as an alternative to sclerotherapy.
Intravascular platelet aggregation induced by ADP injection into the carotid artery of rabbits caused ipsilateral cerebrovascular injuries. We have observed the details of these in vivo vascular changes under the electron microscope. Intracytoplasmic vacuole (1.0-2.0 micron in diameter) formation and partial deendothelialization followed by platelet thrombus formation were characteristic changes in the middle cerebral artery. These vacuoles did not contain horseradish peroxidase (HRP) which was used as a marker of vascular permeability change. Compared with these phenomenon, increased vesicular (0.05-0.2 micron in diameter) transport was prominent, and vacuole formation was rarely seen in small vessels, namely, capillaries and arterioles in the cortex. Endothelial cell damage seemed to be more prominent in large arteries, but only the smaller vessels show marked extravasation of HRP-reaction product and perivascular edema. Blood levels of TXB2 and 6-keto PGF1 alpha were significantly increased 3 min after the ADP injection and returned to pre-injection levels at 60 min after. These results suggest that vasoactive substances resulting from platelet activation may play an important role in producing cerebrovascular injuries caused by platelet aggregation induced with ADP.