Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiorgan dysfunction ensuing from severe heatstroke includes hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. We attempted to assess whether human umbilical cord blood-derived CD34+ cell therapy improves survival during experimental heatstroke by attenuating multiorgan dysfunction. Anesthetized rats, immediately after the onset of heatstroke, were divided into 2 major groups and given CD34- or CD34+ cells (1 x 10(5)-5 x 10(5)/mL/kg body weight) i.v. They were exposed to ambient temperature of 43 degrees C to induce heatstroke. Another group of rats were exposed to room temperature (26 degrees C) and used as normothermic controls. Hypotension, hepatic and renal failure (evidenced by increased serum urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase levels in plasma), hypercoagulable state (evidenced by increased prothrombin time, activated partial thromboplastin time, and D-dimer, and decreased platelet count and protein C in plasma), activated inflammation (evidence by increased TNF-alpha levels in serum), and cerebral dysfunction (evidenced by intracranial hypertension, cerebral hypoperfusion and hypoxia, and cerebral ischemia and injury) were monitored. When the CD34- cell-treated or untreated rats underwent heat stress, their survival time values were found to be 19 to 23 min. Resuscitation with CD34+ cells significantly improved survival time (duration, 63-291 min). As compared with normothermic controls, all CD34- cell-treated heatstroke animals displayed hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. However, CD34+ cell therapy significantly caused attenuation of all the above-mentioned heatstroke reactions. In addition, the levels of IL-10 in plasma and glial cell line-derived neurotrophic factors in brain were all significantly increased after CD34+ cell therapy during heatstroke. Our data indicate that CD34+ cell therapy may resuscitate persons who had a heatstroke by reducing multiorgan dysfunction or failure.
 ...
PMID:Human umbilical cord blood-derived CD34+ cells cause attenuation of multiorgan dysfunction during experimental heatstroke. 1750 7

Hyperbaric oxygen has been found to be beneficial in treating heatstroke animals. We attempted to further assess the possible mechanism of therapeutic protection offered by hyperbaric oxygen in experimental heatstroke. Anesthetized rats, immediately after the onset of heatstroke, were randomized into the following groups and given: a) hyperbaric oxygen (100% O(2) at 253 kPa for 1 h); or b) normal air. They were exposed to 43 degrees C temperature to induce heatstroke. When the untreated rats underwent heat stress, their survival time values were found to be 20-24 min. Resuscitation with hyperbaric oxygen increased the survival time to new values of 152-176 min. All untreated heatstroke rats displayed cerebrovascular dysfunction (evidenced by hypotension, intracranial hypertension, and cerebral hypoperfusion, hypoxia, and ischemia), hypercoagulable state (evidenced by increased levels of activated partial thromboplastin time, prothrombin time, and D-dimer, but decreased values of platelet count and protein C in plasma), and tissue ischemia/injury (evidenced by increased levels of creatinine, serum urea nitrogen, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase in plasma, and dihydrobenzoic acid, lipid peroxidation, and oxidized-form glutathione/reduced-form of glutathione ratio in hypothalamus). The cerebrovascular dysfunctions, hypercoagulable state, tissue ischemia/injury, and brain oxidative stress that occurred during heatstroke were all suppressed by hyperbaric oxygen therapy. The current results indicate that hyperbaric oxygen therapy may resuscitate rats that had a heatstroke by decreasing multiple organ dysfunction and brain oxidative stress.
 ...
PMID:Hyperbaric oxygen improves survival in heatstroke rats by reducing multiorgan dysfunction and brain oxidative stress. 1750 57

Asthma control is a key point in patient management. GINA's most recent report emphasises the need to investigate uncontrolled asthma, of which non-compliance with treatment, COPD, smoking, chronic sinusitis, gastroesophageal reflux disease and obesity are the usual causes. The aim of this work is to evaluate the role of pulmonary thromboembolism (PTE) in cases of difficult- -to-treat asthma. We reviewed the case reports of patients with severe persistent asthma followed in our Asthma Outpatients Clinic between 2004 and 2006. We selected the ones that maintained uncontrolled disease despite an optimal therapeutical approach and investigated the causes. In this group (n=254), 28 (11%) had severe persistent asthma and their mean age was 44 +/- SD18 years old. 86% were females. Of these, 57% (n=16) had uncontrolled disease: 35% (n=6) due to non-compliance with treatment; 29% (n=5) pulmonary thrombombolism (scintigraphic confirmation); 12% (n=2) severe rhinosinusitis; 6% (n=1) hypereosinophilic syndrome; 6% (n=1) persistent allergen exposure and 6% (n=1) are still being investigated. Patients with TPE (mean age 56 +/- SD9 years old; 80% females; 80% Caucasians) were diagnosed with asthma as adults (mean age 37 +/- SD14 years old). The mean time until the diagnosis of TPE was 18 +/- SD12 years. Predisposing factors for TPE were venous insufficiency (40%), hypertension (40%) and deficit of functional protein C and S (20%). All these patients received anticoagulant therapy (80% are still medicated). It should be noted that after the beginning of anticoagulants, 40% of the patients achieved control of their asthma and 40% have partially controlled disease. There were no hospital admissions for asthma exacerbations after the beginning of anticoagulation in this group. This study supports the inclusion of TPE in the group of comorbidities to consider while investigating uncontrolled asthma.
 ...
PMID:[Pulmonary embolism and difficult-to-treat asthma]. 1818 29

Inherited thrombophilic disorders are a well-recognized risk factor for systemic thromboembolism. These disorders include deficiencies of anticoagulant proteins such as protein C, protein S, and antithrombin III, abnormalities of factor V and prothrombin resulting from genetic mutations, and hyperhomocysteinemia. Except for hyperhomocysteinemia, which has been associated with both venous and arterial thrombosis, the other heritable disorders primarily cause venous thromboembolism. We have reviewed the association between heritable thrombophilia and the development of thrombosis in the eye. The available literature consists of case-control studies and case reports. Preliminary data suggest a relationship between thrombotic disorders of the eye and the inherited hypercoagulable states. Some reports show a risk of thrombosis with the presence of factor V Leiden and hyperhomocysteinemia but these associations frequently disappear upon multivariate analysis. It is possible that inherited thrombophilia plays a supportive role to well-established risk factors such as hypertension and diabetes. Larger, well-designed studies will be necessary to clearly define the role of inherited thrombophilia in the development of thrombotic disorders of the eye.
 ...
PMID:Inherited thrombophilia and the eye. 1832 Apr 77

Management of acute coronary syndromes, particularly unstable angina, acute myocardial infarction and non-Q-wave myocardial infarction, is one of the most common and costly problems facing modern medicine. Furthermore, the increasing availability of new research and clinical information relevant to the treatment of these conditions means that continuing reappraisal of management strategies is necessary. Accordingly, the Ushuaia conference, Tierra Del Fuego, Argentina, was convened to discuss current approaches and future treatment prospects for patients with these conditions. The conference was comprised of leading Argentinian cardiologists whose primary aim was to formulate consensus recommendations regarding the management of patients with acute coronary syndromes. The first of the major recommendations for the pharmacological management of acute coronary syndromes arising from the Ushuaia Consensus Conference was that aspirin (200 to 500mg initially, then 100 to 325 mg/day) should be administered to all patients except those for whom aspirin is absolutely (or relatively, depending on the clinician's discretion) contraindicated. In such cases, ticlopidine is a suitable alternative. Intravenous nitrates are indicated for patients with angina pain (24 to 48 hours' duration), ECG changes, recurrence of angina, or signs of heart failure; in other cases, oral, transdermal or sublingual nitrates may be administered. Use of beta-blockers is recommended except when absolutely contraindicated or when there is a strong suspicion of vasospasm as a dominant mechanism in angina. Intravenous administration of these agents is preferred in patients with tachycardia, arterial hypertension or angina. Calcium antagonists are generally not recommended as first choice therapy, but can be indicated (preferably using agents that decrease heart rate) when beta-blockers are contraindicated or when there is a strong suspicion of vasospasm as a dominant mechanism in angina. Calcium antagonists are also useful in combination with other drugs in patients with high blood pressure or treatment-refractory recurrent angina. Subcutaneous low molecular weight heparins and intravenous unfractionated heparin provide similar results and are indicated in a number of clinical situations. Emergency videocoronary angiography (VCA) is indicated in patients with persistent clinical and haemodynamic instability, recurrent ischaemia with heart failure, and refractory angina. Patients should also be referred for VCA if they have signs of left ventricular dysfunction, post-acute myocardial infarction angina with ECG changes, or ischaemia during functional studies. Post-VCA treatment will be determined by anatomical findings during VCA. Future prospects in the management of acute coronary syndromes include the development of more accurate prognostic markers and means of stratifying risk, such as sophisticated ECG criteria, serum markers of necrosis (e.g. troponin T and I), markers of thrombosis (e.g. D-dimer and fibrinopeptide A levels), markers of inflammation (e.g. reactive protein C, cell adhesion receptor expression, neopterine), and markers of 'good' prognosis (e.g. interleukin-10). Other pharmacological approaches under investigation include platelet IIb/IIIa receptor antagonists, clopidogrel and hirudin. Novel agents, such as anti-Xa, pentasaccharide, anti-tissue factor compounds, Ib receptor-blocking agents, agents that influence vascular endothelium and control cellular acidosis (e.g. HOE 642), macrolide antibiotics, HLA-DR system blockers and fusion compounds, are also in various stages of investigation or development.
 ...
PMID:Current treatment and future prospects for the management of acute coronary syndromes: consensus recommendations of the 1997 ushuaia conference, tierra del fuego, Argentina. 1837 Apr 92

Portal vein thrombosis secondary to protein C deficiency is a rare finding. Diagnosing a portal vein thrombosis itself is difficult due to nonspecific symptoms such as nausea, vomiting, anorexia, and weight loss. Proving that a protein C deficiency is the cause of a portal vein thrombosis is even more difficult as an extensive and thorough workup is required to rule out malignancies, myeloproliferative disorders, and hypercoaguable states which can all lead to thromboses. Patients require anticoagulation to prevent two dangerous complications of portal vein thrombosis; portal hypertension leading to esophageal varices with massive hemetemesis and extension of thrombus from the portal vein into the mesenteric veins leading to intestinal ischemia and death. In this case report, we present a patient with the complaint of painless jaundice who was found to have an incidental finding of portal vein thrombosis secondary to protein C deficiency. The different etiologies of portal vein thrombosis, along with diagnosis and treatment options will be discussed and highlighted.
 ...
PMID:A rare incidental finding in a case of painless jaundice. 3071 33

Orthostatic stress causes significant plasma shift and raises transmural pressure in lower extremities, resulting in an increase in endothelial activation and plasma proteins concentrations, possibly including coagulation factors. This may lead to activation of the coagulation system during standing. To test this hypothesis, we recruited 18 healthy volunteers (9 females and 9 males; mean age: 25+/-1.2 years; body mass index: 21.7+/-0.5 kg/m(2)). Hemodynamics, plasma shift (extrapolated from sequential hematocrit concentration), plasma proteins, and coagulation tests, including procoagulants; fibrinogen, factor V, and factor VIII activity; prothrombin fragments 1 and 2; and endothelial activation-related factors (tissue factor and von Willebrand factor), as well as protein C global pathway, were determined at rest supine and at 15 minutes, 30 minutes, and 60 minutes of still standing. Thirty minutes of standing caused a decrease in plasma volume by 12.0+/-0.5% and an increase in plasma protein by 13.0+/-0.7%. Fibrinogen, factor V, and factor VIII activity rose by 12.0+/-1.2%, 13.0+/-1.0%, and 40.0+/-6.0% (P<0.002 for all), respectively. Prothrombin fragments 1 and 2 were elevated by 150.0+/-30.0%. Tissue factor and von Willebrand factor increased by 30.0+/-9.0% and 17.4+/-51.0% (P<0.02 for both), respectively. However, protein C assay results decreased from 0.95+/-0.20 to 0.83+/-0.16 (P<0.001). We hereby introduce a novel physiological mechanism, "orthostatic procoagulation," that should be considered during coagulation tests. Furthermore, it could be extrapolated to the pathophysiology of stasis and venous thromboembolism.
Hypertension 2008 Jun
PMID:Orthostatic hypercoagulability: a novel physiological mechanism to activate the coagulation system. 1841 85

An 84-year-old female patient was scheduled to undergo AVR, CABG, and Maze procedure. She had a history of hypertension, cerebral infarction, and branch retinal vein occlusion. Warfarin was administered preoperatively. Before the cardiopulmonary bypass (CPB), heparin 5,000 units was administered. Activated coagulation times (ACTs) before and after CPB were 123 sec and 157 sec, respectively. Additional heparin of 5,000 units extended ACT to 221 seconds, which was not enough for the CPB. Heparin 10,000 units was added, and ACT was 157 sec. AntithrombinIII (ATIII) and platelet counts were 75% and 270,000 mm(-3), respectively. ATIII 1,500 units was administered. ACT and ATIII became 133 sec and 123%, respectively. Because heparin resistance did not respond to ATIII, the operative method was changed to off-pump CABG. A postoperative examination revealed high factor VIII activity of 263%. Other results were as follows: protein C antigen, 40%; protein S antigen, 65%; factor VII, 50%; platelet factor 4, 12%; heparin cofactor II, 104%; von Willebrand factor antigen, 181%; heparin-PF4-IgG antibody, negative; factor VIII inhibitor, negative. The low values of protein C, protein S, and factor VII may have been caused by warfarin. Other values were normal, except for the von Willebrand factor antigen.
 ...
PMID:[Heparin resistance associated with elevated factor VIII]. 1841 8

We carried out clinical-instrumental examination of 456 men aged 40-54 years. First degree arterial hypertension was revealed in 165 men. Left ventricular hypertrophy was found in 48 (30%), increased intima-media thickness (IMT) - in 67 (41%) patients. There was significant medium power relationship between IMT and left ventricular myocardial mass (correlation coefficient 0.41). Formation of left ventricular hypertrophy was related to parameters of 24 hour blood pressure monitoring, arterial hypertension in brothers and sisters, body weight, and duration of obesity. Significant medium power relation was obtained between tension of endothelial system of hemostasis (protein C) and severity of left ventricular hypertrophy (correlation coefficient - 0,3). Age, heredity, low density lipoprotein, cholesterol, uric acid level mattered for IMT increase.
 ...
PMID:[Left ventricular hypertrophy and thickening of common carotid artery wall in men aged 40 - 54 years with I degree arterial hypertension]. 1842 55

Pregnancy is widely authorized in systemic lupus erythematosus (SLE). Fertility is similar in SLE and in the general population although the age of menarche seems higher. Some cases of sterility might be attributed to SLE because of autoimmune ovaritis or antiphospholipid antibodies (aPL). These antibodies might lead to endothelial activation and thrombosis by influencing homeostasis, complement activation, inhibition of protein C and annexin V. They might have a deleterious effect on embryonic implantation by adhesion to the trophoblast, inhibition of invasion and placentation and decreased hCG production. The most important part of sterility seems secondary to the use of cyclophosphamide and might be prevented by acetate leuprolide administration. Maternal morbidity seems correlated to SLE activity (controlled by pregnancy planning), hypertension, preeclampsia, Hemolysis, Elevated Liver Enzymes, Low Platelets (HELLP) syndrome, therapy and aPL. Hydroxychloroquine (HCQ) should be maintained throughout pregnancy. Aspirin is prescribed alone in patients with asymptomatic aPL and in addition to heparin if there is a history of thrombosis or fetal loss with aspirin. Fetal and neonatal morbidity correlate with prematurity, adverse effects or maternal steroid therapy and maternal anti-SSA antibodies with 1 to 2% risk of congenital atrioventricular block. Abnormal obstetrical echography-doppler examination is the best predictor of pregnancy outcome. Abnormal umbilical artery flow on the second trimester echodoppler examination and history of thrombophlebitis predict fetal or neonatal death. Abnormal uterine notch on the second trimester echodoppler examination predicts adverse pregnancy outcome. Except for the preventive therapy of congenital atrioventricular block, modalities of SLE pregnancy monitoring and therapy are now well established.
 ...
PMID:[Pregnancy and systemic lupus erythematosus]. 1869 42


<< Previous 1 2 3 4 5 6 7 8 9 Next >>