Cerebral hemorrhage is one of the most common causes of dysphagia. In many cases, dysphagia gets better once the acute phase has passed. Structural lesions such as thyromegaly, cervical hyperostosis, congenital web, Zenker's diverticulum, neoplasm, radiation fibrosis, and retropharyngeal abscess must be considered as other causes of dysphagia as well. Retropharyngeal abscess seldom occur in adults and if it does so, a search for a prior dental procedure, trauma, head and neck infection is needed. The symptoms may include neck pain, dysphagia, sore throat, and in rare cases, dyspnea accompanied by stridor. We present a case and discuss a patient who had dysphagia and neck pain after a cerebral hemorrhage. Testing revealed a retropharyngeal abscess. The symptoms were successfully treated after the administration of antibiotics.
Adult ; Anti-Bacterial Agents ; Cerebral Hemorrhage ; Craniocerebral Trauma ; Deglutition Disorders ; Dyspnea ; Humans ; Hyperostosis ; Neck ; Neck Pain ; Pharyngitis ; Radiation Pneumonitis ; Respiratory Sounds ; Retropharyngeal Abscess ; Subarachnoid Hemorrhage ; Zenker Diverticulum

We analyzed aquaporin (AQP) expression in the rat spinal cord following an electrical shock (ES) to elucidate the roles of AQP in spinal cord injury (SCI) induced by an electrical burn. In control animals, AQP1 immunoreactivity was observed in the small diameter dorsal horn fibers of laminae I and II and in astrocytes and neurons in the spinal cord. Both AQP4 and AQP9 immunoreactivity were detected in astrocytes. One week after the ES, AQP1 immunoreactivity in dorsal horn fibers was downregulated to 83, 61, and 33% of control levels following a 1-, 4-, or 6-second ES, respectively. However, AQP1 immunoreactivity in ventral horn neurons increased to 1.3-, 1.5-, and 2.4-fold of control levels following a 1-, 4-, or 6-second ES, respectively. AQP4 immunoreactivity was upregulated after an ES in laminae I and II astrocytes in a stimulus-intensity independent manner. Unlike AQP1 and AQP4, AQP9 immunoreactivity was unaffected by the ES. These findings indicate that altered AQP immunoreactivity may be involved in SCI following an ES.
Animals ; Anterior Horn Cells ; Aquaporins ; Astrocytes ; Burns ; Horns ; Neurons ; Rats ; Shock ; Spinal Cord ; Spinal Cord Injuries

BACKGROUND AND OBJECTIVES: Biochemical markers are useful for the prediction of cardiac events in patients with acute coronary syndrome (ACS). The N-terminal fragment of the BNP prohormone (NT-proBNP), which is synthesized by cardiac ventricles in response to increased wall stress, may be a prognostic marker in ACS. The relation between the NT-pro BNP levels on admission and major adverse cardiovascular events (MACEs) were assessed in a cohort of patients with ACS. SUBJECTS AND METHODS: Between October 2002 and April 2004, blood samples for the determination of NT-proBNP level were obtained on admission from 78 patients with ST-elevation myocardial infarction (STEMI), 32 with non-ST elevation MI(NSTEMI) and 66 with unstable angina (UA). Patients were followed concerning MACEs (death, MI, heart failure, stroke and revascularization) for a median of 7 months in median. RESULTS: 22 patients (13%) had events. The mean NT-proBNP level was significantly lower in the event-free survivors than in those with events (1342+/-1598 versus 6129+/-6522 pg/mL, p<0.0001). The optimal cut-off value of the NT-proBNP level using a receiver-operating-characteristic curve was 1445 pg/mL. The unadjusted risk ratio of patients with an NT-proBNP level greater than the threshold was 7.0 (95% confidence interval, 2.6 to 19.0). In a multivariate Cox regression model, including clinical background factors and other biochemical markers, the NT-proBNP level was the most powerful indicator of MACEs (risk ratio, 8.0 [95% confidence interval, 1.7 to 37.1]). The coronary angiographic Gensini score was also a predictor of prognosis in ACS (risk ratio, 3.8 [95% confidence interval, 1.0 to 14.0]). CONCLUSION: A single measurement of the NT-proBNP level on admission appears to be useful as a prognostic factor in the prediction of MACEs in patients after ACS.
Acute Coronary Syndrome* ; Angina, Unstable ; Biomarkers ; Cohort Studies ; Heart Failure ; Heart Ventricles ; Humans ; Myocardial Infarction ; Odds Ratio ; Prognosis ; Stroke ; Survivors

Background: Atherogenic dyslipidemia, which is frequently associated with type 2 diabetes (T2D) and insulin resistance, contributes to the development of vascular complications. Statin therapy is the primary approach to dyslipidemia management in T2D, however, the role of non-statin therapy remains unclear. Ezetimibe reduces cholesterol burden by inhibiting intestinal cholesterol absorption. Fibrates lower triglyceride levels and increase high-density lipoprotein cholesterol (HDL-C) levels via peroxisome proliferator- activated receptor alpha agonism. Therefore, when combined, these drugs effectively lower non-HDL-C levels. Despite this, few clinical trials have specifically targeted non-HDL-C, and the efficacy of triple combination therapies, including statins, ezetimibe, and fibrates, has yet to be determined. Methods: This is a multicenter, prospective, randomized, open-label, active-comparator controlled trial involving 3,958 eligible participants with T2D, cardiovascular risk factors, and elevated non-HDL-C (≥100 mg/dL). Participants, already on moderate-intensity statins, will be randomly assigned to either Ezefeno (ezetimibe/fenofibrate) addition or statin dose-escalation. The primary end point is the development of a composite of major adverse cardiovascular and diabetic microvascular events over 48 months. Conclusion This trial aims to assess whether combining statins, ezetimibe, and fenofibrate is as effective as, or possibly superior to, statin monotherapy intensification in lowering cardiovascular and microvascular disease risk for patients with T2D. This could propose a novel therapeutic approach for managing dyslipidemia in T2D.

Background: Atherogenic dyslipidemia, which is frequently associated with type 2 diabetes (T2D) and insulin resistance, contributes to the development of vascular complications. Statin therapy is the primary approach to dyslipidemia management in T2D, however, the role of non-statin therapy remains unclear. Ezetimibe reduces cholesterol burden by inhibiting intestinal cholesterol absorption. Fibrates lower triglyceride levels and increase high-density lipoprotein cholesterol (HDL-C) levels via peroxisome proliferator- activated receptor alpha agonism. Therefore, when combined, these drugs effectively lower non-HDL-C levels. Despite this, few clinical trials have specifically targeted non-HDL-C, and the efficacy of triple combination therapies, including statins, ezetimibe, and fibrates, has yet to be determined. Methods: This is a multicenter, prospective, randomized, open-label, active-comparator controlled trial involving 3,958 eligible participants with T2D, cardiovascular risk factors, and elevated non-HDL-C (≥100 mg/dL). Participants, already on moderate-intensity statins, will be randomly assigned to either Ezefeno (ezetimibe/fenofibrate) addition or statin dose-escalation. The primary end point is the development of a composite of major adverse cardiovascular and diabetic microvascular events over 48 months. Conclusion This trial aims to assess whether combining statins, ezetimibe, and fenofibrate is as effective as, or possibly superior to, statin monotherapy intensification in lowering cardiovascular and microvascular disease risk for patients with T2D. This could propose a novel therapeutic approach for managing dyslipidemia in T2D.

Background: Atherogenic dyslipidemia, which is frequently associated with type 2 diabetes (T2D) and insulin resistance, contributes to the development of vascular complications. Statin therapy is the primary approach to dyslipidemia management in T2D, however, the role of non-statin therapy remains unclear. Ezetimibe reduces cholesterol burden by inhibiting intestinal cholesterol absorption. Fibrates lower triglyceride levels and increase high-density lipoprotein cholesterol (HDL-C) levels via peroxisome proliferator- activated receptor alpha agonism. Therefore, when combined, these drugs effectively lower non-HDL-C levels. Despite this, few clinical trials have specifically targeted non-HDL-C, and the efficacy of triple combination therapies, including statins, ezetimibe, and fibrates, has yet to be determined. Methods: This is a multicenter, prospective, randomized, open-label, active-comparator controlled trial involving 3,958 eligible participants with T2D, cardiovascular risk factors, and elevated non-HDL-C (≥100 mg/dL). Participants, already on moderate-intensity statins, will be randomly assigned to either Ezefeno (ezetimibe/fenofibrate) addition or statin dose-escalation. The primary end point is the development of a composite of major adverse cardiovascular and diabetic microvascular events over 48 months. Conclusion This trial aims to assess whether combining statins, ezetimibe, and fenofibrate is as effective as, or possibly superior to, statin monotherapy intensification in lowering cardiovascular and microvascular disease risk for patients with T2D. This could propose a novel therapeutic approach for managing dyslipidemia in T2D.

Background: Atherogenic dyslipidemia, which is frequently associated with type 2 diabetes (T2D) and insulin resistance, contributes to the development of vascular complications. Statin therapy is the primary approach to dyslipidemia management in T2D, however, the role of non-statin therapy remains unclear. Ezetimibe reduces cholesterol burden by inhibiting intestinal cholesterol absorption. Fibrates lower triglyceride levels and increase high-density lipoprotein cholesterol (HDL-C) levels via peroxisome proliferator- activated receptor alpha agonism. Therefore, when combined, these drugs effectively lower non-HDL-C levels. Despite this, few clinical trials have specifically targeted non-HDL-C, and the efficacy of triple combination therapies, including statins, ezetimibe, and fibrates, has yet to be determined. Methods: This is a multicenter, prospective, randomized, open-label, active-comparator controlled trial involving 3,958 eligible participants with T2D, cardiovascular risk factors, and elevated non-HDL-C (≥100 mg/dL). Participants, already on moderate-intensity statins, will be randomly assigned to either Ezefeno (ezetimibe/fenofibrate) addition or statin dose-escalation. The primary end point is the development of a composite of major adverse cardiovascular and diabetic microvascular events over 48 months. Conclusion This trial aims to assess whether combining statins, ezetimibe, and fenofibrate is as effective as, or possibly superior to, statin monotherapy intensification in lowering cardiovascular and microvascular disease risk for patients with T2D. This could propose a novel therapeutic approach for managing dyslipidemia in T2D.