Clinical features of stroke mimics in the emergency department.

AIM: To clarify the features of stroke mimics. METHODS: We retrospectively investigated stroke mimic cases among the suspected stroke cases examined at our emergency department, over the past 9 years, during the tissue-type plasminogen activator treatment time window. RESULTS: Of 1,557 suspected acute stroke cases examined at the emergency department, 137 (8.8%) were stroke mimics. The most common causes were symptomatic epilepsy (28 cases, 20.4%), neuropathy-like symptoms (21 cases, 15.3%), and hypoglycemia (15 cases, 10.9%). Outcomes were survival to hospital discharge for 91.2% and death for 8.8% of the cases. Clinical results were significantly different between stroke mimics and the stroke group for low systolic blood pressure, low National Institutes of Health Stroke Scale score on initial treatment, history of diabetes, and no history of arrhythmia. On multivariate analysis, distinguishing factors for stroke mimics include systolic blood pressure ≤ 140 mmHg, National Institutes of Health Stroke Scale score ≤ 5 points, history of diabetes, and no history of arrhythmia. CONCLUSIONS: Frequency of stroke mimics in cases of acute stroke suspected cases is 8.8%, and the most common cause is epilepsy. In order to distinguish stroke mimics, it is useful to understand common diseases presenting as stroke mimics and evaluate clinical features different from stroke by medical interview or nerve examination.

Leukocytapheresis for ulcerative colitis: a comparative study of anticoagulant (nafamostat mesilate vs. dalteparin sodium) for reducing clinical complications.

Leukocytapheresis (LCAP) is a therapeutic strategy for extra corporeal immunomodulation that has been used to treat several immunological disorders, including ulcerative colitis (UC), with encouraging results, inducing remission in steroid-resistant patients. However, we have experienced some complications during or after LCAP therapy. Common adverse effects include fever, chills, nausea, vomiting, and hypotension. One of the reasons for these adverse effects might be the use of nafamostat mesilate (NM) as an anticoagulant. In the present study, 75 patients with UC were divided into two groups, an NM group and a dalteparin sodium (DS) group. The clinical efficacy of these treatments, improvement after treatment, changes in leukocyte differential count, and adverse effects after LCAP therapy were then compared. The clinical efficacy, improvement after treatment, and changes in leukocyte classification were not significantly different between the two groups, while some adverse effects were observed in the NM group but not in the DS group. In conclusion, LCAP therapy is a useful therapy for patients with moderate to severe UC who fail to respond to glucocorticoid therapy, however, a safe anticoagulant should be used to avoid its related adverse effects.

Effect of adrenomedullin administration on acetic acid-induced colitis in rats.

Adrenomedullin (AM) administered intracolonically ameliorated the severity of acetic acid-induced colonic ulceration in rats. Ulcers were induced by subserosal injection of acetic acid into the colon. AM-treated group was administered 0.25-1.0 microg of AM in 0.5 ml of saline intracolonically once a day; the control group received only saline. AM administration dose-dependently and significantly reduced the size of the ulcerative lesions, the associated edema, and the infiltration of the affected area by inflammatory cells. AM also reduced tissue levels of interleukin-6, but not interferon-gamma. AM reduces the severity of acetic acid-induced colitis in rats, probably by inhibiting the production and/or release of Th-2 cell-derived factors such as interleukin-6.

Cerebral sinus thrombosis associated with severe active ulcerative colitis.

A 19-year-old man with severe active ulcerative colitis was admitted to our hospital where he was prescribed 80 mg prednisolone and underwent leukocytapheresis (LCAP). Two weeks after initiating therapy, his symptoms had not recovered. We administered cyclosporin via continuous intravenous infusion for 12 days. Although his clinical symptoms improved, he complained of severe headache. Immediate plain computed tomography (CT) and magnetic resonance imaging angiography (MRA) revealed extensive thrombosis in the superior sagittal sinus and right transverse sinus. We treated this condition with the anticoagulant agent, heparin, which prevents and can treat venous thrombosis. We report an occurrence of cerebral sinus thrombosis accompanying ulcerative colitis, where active anticoagulant therapy was useful.

Direct measurement of glycine-extended adrenomedullin in plasma and tissue using an ultrasensitive immune complex transfer enzyme immunoassay in rats.

The mature form of the vasodilator peptide adrenomedullin (AM-m) is synthesized from a glycine-extended precursor (AM-Gly) by enzymatic amidation. We have developed a highly sensitive enzyme immunoassay (Immune Complex Transfer Enzyme Immunoassay; ICTEIA) that enables us to measure levels of AM-Gly in plasma and tissue directly. The detection limit of this assay is 1 amol/assay, and the intra- and inter-assay precision are 4.5-14.1% and 9.9-20.5%, respectively. Dilution curves for plasma samples showed good linearity, and the analytical recovery was 107-116.6%. Using ICTEIA, we determined that the plasma concentration of immunoreactive AM-Gly is substantially higher than that of AM-m (5.22 +/- 2.56 vs. 1.21 +/- 0.79 fmol/ml). In contrast, levels of AM-Gly were much lower than those of AM-m in the lung, heart, kidney, adrenal gland and liver. We also evaluated AM-Gly and AM-m levels in rats in a morbid state induced by intraperitoneal administration of lipopolysaccharide (LPS). In most tissues, levels of AM-m and AM-Gly were both increased by LPS; however, AM-Gly/AM-m ratios were not significantly affected, which suggests that AM-Gly is rapidly converted to AM-m in tissue.

Protein-losing gastropathy associated with autoimmune disease: successful treatment with prednisolone.

We report a patient with protein-losing gastropathy probably associated with autoimmune disease, in whom prednisolone treatment was highly effective. A 45-year-old woman was admitted to our hospital with edema of the face and lower extremities. Blood examination revealed hypoproteinemia, hypoalbuminemia, and hypercholesteremia. Renal biopsy revealed no definite findings of lupus nephritis, including vasculitis. A diagnosis of protein-losing gastropathy was made on the basis of increased alpha1-antitrypsin clearance and 99mTc-labeled human serum albumin scintigram showing abnormal radioactivity in the stomach. Endoscopic gastric biopsies revealed nonspecific inflammation, but marked intramural edema. Based on a slight elevation of antinuclear antibody level, autoimmune disease was suspected to be involved in this patient. Administration of prednisolone, as a diagnostic therapy, alleviated the hypoproteinemia, hypoalbuminemia, and hypercholesteremia. These findings suggest that an autoimmune mechanism could have been involved in this case of protein-losing gastropathy.