PURPOSE: In many other countries, based on research, recombinant tissue plasminogen activator (r-tPA) has been approved for the treatment of acute ischemic strokes. However, in Korea, little research has been done till now, in spite of using r-tPA widely. We sought to assess the feasibility and the efficacy of treatment and to evaluate the prognosis and complications at the violation of using r-tPA. Our study was compared with other previous studies. METHODS: A retrospective review is presented of 25 the cases of patients with acute ischemic stroke treated with rtPA according to the National Institutes of Neurological Disorders and Strokes (NINDS) protocol. We classified the groups by protocol violation (time, blood pressure, and computed tomography). We then analyzed neurologic outcomes by using the National Institutes of Health Strokes Scale (NIHSS) and complications based on whether or not intracerebral hemorrhage (ICH) had occurred. RESULTS: Of the 25 patients (mean age: 57 males: 19), 6 had time violation (onset time > 180 min), 4 had blood-pressure violation (systolic BP > 185 mmHg), 5 had CT violation (low density at initial CT). The NIHSS score improved in 64% of all patients after 24 hours. However, improvement was lower in the case of deviation present than it was in the case of deviation absent (time, blood pressure, and CT, respectively, 20%, 50%, and 40%; p-value respectively 0.0274, 0.8350, and 0.4125). ICH occurred in 6 cases, but in cases of deviation present, ICH occurred at a greater frequency. CONCLUSION: Our safety and feasibility of outcome compared favorably with NINDS and other previous studies. In addition, we confirmed that the presence of protocol deviation was associated a poor outcome.
Academies and Institutes ; Blood Pressure ; Cerebral Hemorrhage ; Humans ; Korea ; Male ; National Institute of Neurological Disorders and Stroke ; National Institutes of Health (U.S.) ; Nervous System Diseases ; Prognosis* ; Retrospective Studies ; Stroke* ; Thrombolytic Therapy ; Tissue Plasminogen Activator

PURPOSE: It is now well recognized that reperfusion of ischemic tissues initiates a complex series of reactions that can paradoxically injure tissues. Apoptosis occurs in select cell populations during morphologic development and during cellular injury, including oxygen radical exposure, ischemia-reperfusion, and sepsis. Thus, in this study, we examined relation of the melatonin effect to the injection time and the dose, and role of melatonin in apoptosis. METHODS: Intestinal ischemia-reperfusion injury was induced in rats by clamping the superior mesenteric artery for 30 minutes. After reperfusion injury for 30 minutes, the experimental group was administered melatonin (10 mg/kg) intraperitoneally and the control group received saline and ethanol. At 30 minutes, 60 minutes, and 90 minutes, 1) pulmonary histological assessments (interstitial PMNs/10HPFs and lung (alveolar) injury score), 2) alveolar microvascular permeability assessments (wet-weignt to dry-weight ratio and lipid peroxidation activity, malondialdehyde, MDA), and 3) western blotting assessments (p53, p21, Bax, and bcl-2) were made. For comparison, long- time (60-minute) reperfusion and double- dosage melatonin (20 mg/kg) were also studied. RESULTS: The lung injury score was 1.00+/-0 in the melatonin group at 90 minutes and 3.28+/-0.30 in the saline group (p<0.01). The number of sequestered neutrophils was significantly higher in the control group at 90 minutes (34.38+/-16.76/10 HPFs) than in the melatonin-treated group (5.63+/-2.73/10 HPFs; p<0.01). In the melatonin group at 90 minutes, the wet-weight to dry-weight ratio was 4.69+/-0.16, and in the saline group, the ratio was 4.78+/-0.17 (p>0.05). A marked difference was found between the ischemia-reperfusion control group and the experimental group at 90 minutes regarding lipid peroxidation activity (Malondialdehyde, 16.45+/-0.19 micrometer vs 10.93+/-0.11 micrometer, p<0.01). In the melatonin group, p21 expressions were found to be much more than in the control group. But, p53, bcl-2, and Bax expressions were found to be in the control group. CONCLUSION: Melatonin injection within 60 min after reperfusion may promote recovery of reperfusion injury, but double-dose melatonin injection was inefficacious. Also, melatonin inhibit apoptosis by p21 expression.
Animals ; Apoptosis ; Blotting, Western ; Capillary Permeability ; Constriction ; Ethanol ; Intestines* ; Lipid Peroxidation ; Lung ; Lung Injury ; Malondialdehyde ; Melatonin* ; Mesenteric Artery, Superior ; Neutrophils ; Oxygen ; Rats ; Reperfusion ; Reperfusion Injury ; Sepsis

Eosinophils are only a small minority of peripheral blood leucocytes and, in normal subjects, most are found in the tissues of the lung and gastrointestinal tract. Peripheral blood eosinophilia is occurred by various causes, allergic diseases, parasite infection, clonal disorder, and drug. Moderate to severe eosinophilia may be caused by the idiopathic hypereosinophilic syndrome (HES), but the commonest cause of eosinophilia worldwide is helminthic infection and, in industrialized nations, atopic disease. Whatever the cause for the eosinophilia, in certain circumstances the eosinophils produce damage to various organs by activation of eosinophils, thrombotic events, release of eosinophil granule contents, and deposition of eosinophil proteins. Clinical manifestations are characterized by thromboembolic events of the involved organ, such as the heart, lungs, or nervous system. To our knowledge, the association between hypereosinophilia and intraabdominal multivessel (portal, splenic and superior mesenteric vein) thrombosis has never previously been reported. Thus, we report a case with portal, splenic and superior mesenteric venous thrombosis simultaneously with disseminated intravascular coagulapathy in the patient with hypereosinophilia.
Developed Countries ; Eosinophilia ; Eosinophils ; Gastrointestinal Tract ; Heart ; Helminths ; Humans ; Hypereosinophilic Syndrome ; Lung ; Mesenteric Veins* ; Necrosis* ; Nervous System ; Parasites ; Portal Vein* ; Splenic Vein* ; Thrombosis* ; Venous Thrombosis