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Biomedical subjects

Shinichiro Uchiyama

Publications and source records attributed to Shinichiro Uchiyama.

At least 19 recordsLinked to original sources

Arterial hypertension in patients with left primary hemifacial spasm is associated with neurovascular compression of the left rostral ventrolateral medulla.

The aim of the study was to clarify the relationship between neurovascular compression of the rostral ventrolateral medulla and arterial hypertension in patients with primary hemifacial spasm. We enrolled 82 patients with primary hemifacial spasm and 82 age- and sex-matched magnetic resonance imaging (MRI) controls of the posterior cranial fossa. Neurovascular compression of the rostral ventrolateral medulla was assessed by MRI, and its association with arterial hypertension was investigated. No significant differences were found in prevalence of arterial hypertension between patients with primary hemifacial spasm and control subjects (39.0 vs. 29.3%, p=0.19). Thirty-two percent of the patients with left primary hemifacial spasm (n=44) and 47% of the patients with right primary hemifacial spasm (n=38) were hypertensive. Neurovascular compression of the left rostral ventrolateral medulla was observed in 86% of those with left (ipsilateral) primary hemifacial spasm with arterial hypertension (n=14) and 33% of those with left (ipsilateral) primary hemifacial spasm without (n=30). The association between neurovascular compression of the left rostral ventrolateral medulla and arterial hypertension was significant in patients with left (ipsilateral) primary hemifacial spasm (p=0.0012), but not in patients with right (contralateral) primary hemifacial spasm (p=0.18). Neurovascular compression of the left rostral ventrolateral medulla was more frequently observed in hypertensive patients with left primary hemifacial spasm, and neurovascular compression of the left rostral ventrolateral medulla correlated with arterial hypertension in these patients. These results are of potential clinical importance for the treatment of primary hemifacial spasm with arterial hypertension.

Adult↗

Synergistic effect of cilostazol and dipyridamole mediated by adenosine on shear-induced platelet aggregation.

INTRODUCTION: The Cilostazol Stroke Prevention Study found that cilostazol, a phosphodiesterase 3 inhibitor, can reduce the risk of subsequent stroke in Japanese patients with cerebral infarction. Here, we measured the effects of cilostazol in vitro on shear-induced platelet aggregation, an important mechanism of thrombosis at arterial bifurcations or stenotic lesions. We also evaluated the influences of intrinsic adenosine on the ability of cilostazol to inhibit shear-induced platelet aggregation by investigating the effect of dipyridamole, an inhibitor of cellular adenosine reuptake, in combination with cilostazol in vitro. MATERIALS AND METHODS: We measured platelet aggregation induced by a shear rate of 10,800 s(-1) in whole blood and in platelet-rich plasma from healthy volunteers using a cone-plate streaming chamber. RESULTS: Both cilostazol and adenosine dose-dependently inhibited shear-induced platelet aggregation in platelet-rich plasma samples. Adding a low concentration of adenosine (0.3 microM) did not inhibit shear-induced platelet aggregation, but significantly enhanced the inhibitory effect of cilostazol in platelet-rich plasma. Dipyridamole dose-dependently inhibited shear-induced platelet aggregation in whole blood and significantly enhanced the inhibitory effect of cilostazol on shear-induced platelet aggregation, but did not affect shear-induced platelet aggregation in platelet-rich plasma. The inhibitory effects of cilostazol combined with dipyridamole in whole blood were almost completely reversed by adenosine deaminase. CONCLUSIONS: Dipyridamole appears to synergistically enhance the inhibitory effect of cilostazol on shear-induced platelet aggregation by maintaining high plasma levels of adenosine.

Adenosine↗

New modalities and aspects of antiplatelet therapy for stroke prevention.

Antiplatelet therapy is indicated for secondary prevention of ischaemic stroke. The first-line antiplatelet agent is aspirin. The effect of aspirin is, however, very limited, and this limited effect of aspirin is argued with termed 'aspirin resistance'. Strategies against aspirin resistance may include alternative use of other antiplatelet agents, combination of aspirin with other antiplatelet agents and investigation into molecular targets to develop novel antiplatelet agents. Progress in antiplatelet therapy should be directed at further reducing the risk of ischaemic events including ischaemic stroke without increasing the risk of haemorrhagic events including haemorrhagic stroke.

Aspirin↗

Pharmacoeconomic analysis of cilostazol for the secondary prevention of cerebral infarction.

BACKGROUND: The antiplatelet agent, cilostazol, is known to reduce the risk of subsequent cerebral infarction. However, the cost effectiveness of such treatment in comparison to aspirin has not been studied. METHODS AND RESULTS: A Markov model was developed to calculate the health outcomes and associated costs for 65-year-old patients with cerebral infarction who were treated with 200 mg/day cilostazol or 81 mg/day aspirin. Cilostazol was more effective, but also more expensive than aspirin. Cilostazol would extend quality-adjusted life years (QALY) by 0.64, while increasing life-time costs by approximately Yen 1.1 million. The incremental cost-effectiveness ratio of cilostazol in comparison with aspirin was estimated to be Yen 1.8 million per QALY. CONCLUSIONS: The use of cilostazol to prevent recurrence of cerebral infarction appears to be cost effective.

Aged↗

[Cerebral infarction].

Diabetes mellitus is the second major risk factor for ischemic stroke. Recent increase in atherothrombotic stroke appears to be related with recent increasing of diabetes. Diabetes is, however, a risk factor not only for atherothrombotic stroke but also for lacunar stroke because there is no difference in prevalence of diabetes between atherothrombotic and lacunar strokes. Diabetes can be a risk factor for cardioembolic stroke as well because the major cause of cardioembolic stroke is atrial fibrillation, and diabetes is a risk factor for stroke in patients with atrial fibrillation. Acute ischemic stroke should be classified into above three subtypes according to the brain and artery imaging as well as cardiac sources of embolism. In hyper-acute patients within 3 hours of onset and without early ischemic signs on CT or ischemic lesions less than one third of the hemisphere on magnetic resonance diffusion-weighted imaging, thrombolytic therapy with alteplase is indicated. In acute stroke patients later than 3 hours of onset, argatroban, heparin, and ozagrel are indicated for atherothrombotic, cardioembolic, and lacunar stroke, respectively. For stroke prevention, total management is required by simultaneous treatments for all risk factors existed. In secondary prevention for stroke, in addition to the more strict control of risk factors antithrombotic therapy is required, that is, antiplatelet therapy is indicated for non-cardioembolic stroke, and anticoagulant therapy is indicated for cardioembolic stroke.

Anticoagulants↗

Low-dose aspirin for prevention of stroke in low-risk patients with atrial fibrillation: Japan Atrial Fibrillation Stroke Trial.

BACKGROUND AND PURPOSE: Although the efficacy of anticoagulant therapy for primary prevention of stroke in patients with nonvalvular atrial fibrillation (NVAF) has been established, efficacy of antiplatelet therapy for low-risk patients is disputable in Japanese patients because of the frequent hemorrhagic complications. We examined the efficacy and safety of aspirin therapy in Japanese patients with NVAF in a prospective randomized multicenter trial. METHODS: Patients with NVAF were randomized to an aspirin group (aspirin at 150 to 200 mg per day) or a control group without antiplatelet or anticoagulant therapy. Primary end points included cardiovascular death, symptomatic brain infarction, or transient ischemic attack. RESULTS: A total of 426 patients were randomized to aspirin group and 445 to no treatment. The trial was stopped earlier because there were 27 primary end point events (3.1% per year; 95% CI, 2.1% to 4.6% per year) in the aspirin group versus 23 (2.4% per year; 95% CI, 1.5% to 3.5% per year) in the control group, suggesting a low possibility of superiority of the aspirin treatment for prevention of the primary end point. In addition, treatment with aspirin caused a marginally increased risk of major bleeding (7 patients; 1.6%) compared with the control group (2 patients; 0.4%; Fisher exact test P=0.101). CONCLUSIONS: For prevention of stroke in patients with NVAF, aspirin at 150 to 200 mg per day does not seem to be either effective or safe. Further prospective studies are needed to determine the best preventive therapy for cerebrovascular events in Japanese patients with NVAF.

Aged↗

Clinical characteristics of stroke patients with antiphospholipid antibodies.

BACKGROUND: Antiphospholipid syndrome is important as a cause of ischemic stroke, although clinical characteristics of the syndrome are not well documented. METHODS: We analyzed differences in clinical characteristics between 40 antiphospholipid-antibody (aPL)-positive and 40 aPL-negative stroke patients. RESULTS: Stroke patients with aPL were significantly younger and were more likely to be women in comparison with stroke patients without aPL. Valvular heart disease, neurological complications and hematological disorders were more frequent in the aPL-positive group. The mean value of thrombin-antithrombin III complex was significantly lower in the aPL-positive group. Cerebral infarctions in the carotid system were less and large-artery lesions more frequent in the aPL-positive patients. CONCLUSIONS: Stroke patients with aPL have clinical characteristics distinct from stroke patients without aPL.

Acute Disease↗

Effect of remnant-like particle on shear-induced platelet activation and its inhibition by antiplatelet agents.

Remnant-like particles (RLPs) have been reported to promote atherosclerosis and to have effects on platelet function. We studied the effects of RLP on shear-induced platelet activation and their inhibition by antiplatelet agents in vitro. RLP were separated using two monoclonal antibodies, anti apo B-100 and anti apo A-I. These RLP fractions were added to whole blood (WB) or platelet-rich plasma (PRP) in serial dilution of 1, 10 or 100 microg RLP triglyceride (TG) per ml of total sample volume. These samples were incubated, and then stimulated with a high shear stress of 108 dyn/cm(2). Shear-induced platelet aggregation (SIPA) was calculated from the percentage of single platelet loss. P-selectin expression on platelet surface and platelet-derived microparticle (PMP) generation were measured before and after stimulation with shear stress using flow cytometer. SIPA was significantly enhanced by RLP in WB but not in PRP. This enhancing effect was not dose-dependent and was greatest at 10 microg TG/ml. P-selectin expression induced by shear stress was only enhanced by RLP at a concentration of 100 microg TG/ml in both WB and PRP, while generation of PMP induced by shear stress was only enhanced by RLP at a concentration of 100 microg TG/ml in WB. Aspirin inhibited only the enhancement of SIPA by RLPs, while cilostazol inhibited the enhancement of not only SIPA but also p-selectin expression and PMP generation by RLPs.

Antibodies, Monoclonal↗

[Bucillamine-induced dermatomyositis-like clinical features in a patient with rheumatoid arthritis].

A 78 year-old woman was admitted to our hospital because of subacutely progressive dysarthria, dysphagia, proximally dominant muscle weakness and erythema in the neck and back. She was diagnosed as having rheumatoid arthritis (RA) at the age of 60 and treated with bucillamine (BUC) for 8 years. Laboratory tests included a rheumatoid factor of 1,472U/ml. Serum creatine kinase level was slightly elevated. The activated T cells in the peripheral blood were markedly increased. Needle EMG demonstrated myogenic changes. The magnetic resonance image of the left upper arm showed diffuse muscle atrophy and inflammatory changes in the triceps muscle. The muscle biopsy revealed perivascular inflammatory cell infiltraton and type II fiber atrophy. A biopsy from the skin showed mild perivascular inflammatory cell infiltraton. According to the results of these findings, she was thought to have dermatomyositis due to BUC. After withdrawal of BUC followed by the administration of prednisolone 1mg/kg, her symptoms improved and activated T cells in the peripheral blood were decreased. In Japan, BUC is widely accepted as an effective drug in the treatment of RA, even though it is known to induce some autoimmune diseases. However, the mechanism of the development of autoimmune disease is unclear. We considered that the long-term use of bucillamine could trigger an autoimmune response such as an increase in activated T cells and the development of dermatomyositis-like clinical features in our patient. In conclusion, when RA patients treated with BUC show a clinical picture compatible with dermatomyositis, its causative relationship has to be considered.

Aged↗

[Multiple cerebral white matter lesions following head trauma with eyeball contusion].

We reported a 36-year-old man with multiple cerebral white matter lesions following head trauma with eyeball contusion. He had suffered from optic neuritis on non-injured side after one and half months from the head trauma. Brain MRI revealed multiple cerebral white matter lesions and lumbar puncture disclosed an elevated level of protein of the cerebrospinal fluid after two and half months from the head trauma. He was treated with steroid pulse therapy and resulted in an improvement of his visual acuity and a remarkable decrease of multiple cerebral white matter lesions. There has been a controversy concerning the causal relationship between trauma and multiple sclerosis (MS). In this case, MS-like multiple cerebral white matter lesions are considered to be relevant to the head trauma.

Adult↗

[Spinal epidural abscess with persistent increase in cerebrospinal fluid protein: a case study].

A 67-year-old man under hemodialysis treatment developed neck stiffness, fever and conscious disturbances. The patient was infected with Methicilin-resistant Staphylococcus aureus (MRSA) sepsis caused by an infection on a dialysis shunt. On admission, he was diagnosed with bacterial meningoencephalitis and underwent a series of antibiotic chemotherapies. The treatment brought cell count in the cerebrospinal fluid to a subnormal level but his clinical status did not improve. The patient continued to have high level of cerebrospinal fluid protein (898 mg/dl). Cervical MRI demonstrated two abscesses deep in the neck as well as in the epidural region of the cervical spinal cord, from C2 to C5 vertebral levels. Based on these findings, spinal epidural abscess (SEA) was diagnosed. Intensive antibiotic chemotherapy especially targeted for MRSA could eradicate abscesses and improve clinical status. However, persistent high protein level in the cerebrospinal fluid could suggest SEA.

Aged↗

[Myelopathy in patients with antiphospholipid antibodies: clinical features, pathogenesis, and review of literature].

We report 5 patients with anti-cardiolipin IgM-positive myelopathy. The lengths of spinal lesions were over two vertebral segments in 4 patients. Four cases showed subacute onset, and 2 out of these 4 cases had inflammatory changes in cerebrospinal fluid (CSF), and all of their symptoms improved. However, in one patient who showed an acute onset and normal findings of CSF, neurological symptoms did not improve. Three patients fulfilled the diagnostic criteria of primary antiphospholipid antibody syndrome. As for the pathophysiology of myelitis associated with antiphospholipid antibodies (aPL), it is suggested that vascular thrombosis affecting the blood cord barrier promotes an inflammatory changes. The heterogeneous CFS findings seem to reflect the difference in the intensity of inflammation. Both vascular thrombosis and inflammatory process should be considered as pathogenesis of these patients. Alone or combination therapy of steroids and anticoagulants might be effective in patients of myelopathy associated with APS.

Adult↗