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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute venous thromboembolism (VTE) is a serious and potentially fatal disorder, which often complicates the course of hospitalized patients, but may also affect ambulatory and otherwise healthy people. While the introduction of thromboprophylactic measures has most likely affected the present occurrence of postoperative VTE, there is an increasing awareness of the importance of medical conditions in determining thromboembolic events. Among the conditions that predispose patients to VTE are increasing age, cancer and its treatment, prolonged immobility, stroke or paralysis, previous VTE, congestive heart failure,acute infection, pregnancy or puerperium, dehydration, hormonal treatment, varicose veins, long air travel, acute inflammatory bowel disease, rheumatologic disease, and nephrotic syndrome. Other factors that have recently been associated with an increased risk of VTE disorders include persistent elevation of D-dimer and atherosclerotic disease. Recognition of the incidence and clinical importance of thrombosis will most likely encourage more widespread use of antithrombotic prophylaxis in medical patients.
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PMID:Acquired risk factors of venous thromboembolism in medical patients. 1685 57

Both ischemic stroke and peripheral arterial thromboembolism have been described as extraintestinal complications of inflammatory bowel disease. Here, we present the first case with direct cooccurrence of ischemic stroke and peripheral thromboembolism in a 39-year-old patient with Crohn's disease. A pathophysiological model explaining this cooccurrence as well as the significance of prothrombotic risk factors ("hypercoaguable state") in the setting of inflammatory bowel disease and stroke are discussed.
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PMID:Ischemic stroke and peripheral arterial thromboembolism in a patient with Crohn's disease: a case presentation. 1790 58

Two maternal-fetal case presentations illustrate the possible association of active maternal ulcerative colitis during pregnancy and fetal brain injury resulting in long-term neurological sequelae. Thromboembolic complications may occur in the fetus based on similar mechanisms for stroke in children and adults with active inflammatory bowel disease. Identification of thrombophilia in the pregnant woman with active ulcerative colitis may better explain a pathophysiologic mechanism for long-term neurological morbidity in offspring.
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PMID:Maternal ulcerative colitis and fetal brain injury: long-term neurologic outcome. 1800 59

Leukotrienes (LTs) are powerful proinflammatory lipid mediators that may play a central role in cardiovascular diseases, including arteriosclerosis, myocardial infarction, and stroke. Owing to restricted expression of 5-lipoxygenase (5-LO), the enzyme required for their synthesis, LTs are almost exclusively produced by myeloid cells. Here, we report that human cytomegalovirus (HCMV) infection of human vascular smooth muscle cells (SMCs) increases 5-LO mRNA levels by up to 170-fold in a dose- and time-dependent manner. Infected cells expressed 5-LO protein, as shown by immunohistochemistry, enabling them to synthesize bioactive LTB(4). HCMV-infected vascular SMCs expressing 5-LO protein were readily detected in tissue samples from CMV-infected patients with inflammatory bowel disease or AIDS. Thus, pathogen-induced LT production in HCMV-infected tissues may contribute to local inflammation, consistent with the ability of HCMV to control cellular and immunological functions. HCMV-induced LT biosynthesis in SMCs offers a molecular mechanism to explain HCMV-induced pathogenesis in inflammatory diseases.
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PMID:Human CMV infection induces 5-lipoxygenase expression and leukotriene B4 production in vascular smooth muscle cells. 1818 Mar 7

Inflammatory bowel disease has been linked to cerebrovascular lesions, but the mechanisms of these vascular complications and their frequency among children with inflammatory bowel disease are unclear. We present 4 children with inflammatory bowel disease who developed ischemic or hemorrhagic stroke or cerebral sinovenous thrombosis. All 4 patients were female; 3 had Crohn's disease and 1 had indeterminate colitis. All of the patients had additional risk factors for thrombosis including thrombocytosis, severe dehydration attributable to an inflammatory bowel disease exacerbation, and, in 2 instances, genetically mediated coagulation defects. It is believed that the occurrence of thrombotic complications in individuals with inflammatory bowel disease is attributable to multifactorial causes. The current literature on cerebrovascular complications and treatment in the setting of pediatric inflammatory bowel disease is reviewed.
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PMID:Inflammatory bowel disease and cerebrovascular arterial and venous thromboembolic events in 4 pediatric patients: a case series and review of the literature. 1818 42

Thrombosis is a recognised complication of inflammatory bowel disease (IBD), in particular venous thrombosis. Arterial thrombosis, especially stroke is rare. There is a paucity of information regarding stroke in IBD and its management. The authors describe two cases of stroke in patients with IBD during periods of increased disease activity. The literature regarding this devastating complication and the procoagulant state that exists in IBD are reviewed.
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PMID:Stroke in inflammatory bowel disease: a report of two cases and review of the literature. 1835 77

Chondroitin sulphate (CS) is a natural glycosaminoglycan present in the extracellular matrix and is formed by the 1-3 linkage of D-glucuronic acid to N-acetylgalactosamine. In chondrocytes, CS diminishes interleukin-1 beta(IL-1beta)-induced increases in p38 mitogen-activated protein kinase (p38MAPK) and signal-regulated kinase 1/2 (Erk1/2) phosphorylation, and decreases nuclear factor-kappaB (NF-kappaB) nuclear translocation and as a consequence, reduces the formation of pro-inflammatory cytokines, IL-1beta and TNF-alpha, and pro-inflammatory enzymes, such as phospholipase A2 (PLA2), cyclooxygenase 2 (COX-2) and nitric oxide synthase-2 (NOS-2). The mechanism of action of CS explains its beneficial effect on the cartilage, synovial membrane and subchondral bone. On the other hand, in vivo, CS given orally prevents hepatic NF-kappaB nuclear translocation, suggesting that systemic CS may elicit an anti-inflammatory effect in many tissues besides the articulation. There is preliminary evidence showing that in human beings, CS may be of benefit in other diseases where inflammation is an essential marker, such as psoriasis and atherosclerosis. The review of the literature suggest that CS might also be of interest for the treatment of other diseases with an inflammatory and/or autoimmune character, such as inflammatory bowel disease, degenerative diseases of the central nervous system and stroke, multiple sclerosis and other autoimmune diseases.
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PMID:Immunomodulatory and anti-inflammatory effects of chondroitin sulphate. 1952 43

Alterations in expression of protein C (PC) pathway components have been identified in patients with active inflammatory disease states. While the PC pathway plays a pivotal role in regulating coagulation and fibrinolysis, activated PC (aPC) also exhibits cytoprotective properties. For example, PC-deficient mice challenged in septic/endotoxemic models exhibit phenotypes that include hypotension, disseminated intravascular coagulation, elevated inflammatory mediators, neutrophil adhesion to the microvascular endothelium, and loss of protective endothelial and epithelial cell barriers. Further, inflammatory bowel disease has been correlated with diminished endothelial PC receptor and thrombomodulin levels in the intestinal mucosa. Downregulated expression of the cofactor, protein S, as well as PC, is also associated with ischemic stroke. Studies to elucidate further the structural elements that differentiate the various functions of PC will serve to identify novel therapeutic approaches toward regulating these and other diseases.
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PMID:The protein C pathway and pathologic processes. 1963 Jul 87

Pyruvate is an important metabolic intermediate, and also is an effective scavenger of hydrogen peroxide and other reactive oxygen species (ROS). Pharmacological administration of pyruvate has been shown to improve organ function in animal models of oxidant-mediated cellular injury. However, pyruvate is relatively unstable in aqueous solutions, which could limit the therapeutic potential of this compound. Ethyl pyruvate (EP), a simple derivative of pyruvic acid, is also an ROS scavenger, but seems to exert pharmacological effects, such as suppression of inflammation, which are at least quantitatively different and in some instances are qualitatively distinct from those exerted by pyruvate anion. Treatment with EP has been shown to improve survival and/or ameliorate organ dysfunction in a wide variety of pre-clinical models of acute illnesses, such as severe sepsis, acute pancreatitis and stroke. Using other animal models, some studies have demonstrated that more prolonged treatment with EP can ameliorate inflammatory bowel disease or slow the rate of growth of malignant tumors. In a clinical trial of patients undergoing cardiac surgery, treatment with EP was shown to be safe, but it failed to improve outcome. The true therapeutic potential of EP and related compounds remains to be elucidated. In this review, some of the biochemical mechanisms, which might be responsible for the pharmacological effects of EP, are discussed.
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PMID:The biochemical basis for the anti-inflammatory and cytoprotective actions of ethyl pyruvate and related compounds. 2023 Aug

Research in the last two decades has transformed the way hydrogen sulphide (H2S) is perceived from a noxious gas to a gaso-transmitter with a vast potential in pharmacotherapy. H2S is synthesized in various body-systems using the enzymes cystathionine beta-synthase and cystathionine gamma-lyase; either of these being the predominat enzyme in a particular system. H2S may be one of the physiological modulators of blood pressure in humans. The gas relaxes the vascular smooth muscle cells by opening up K(ATP) channels. Moreover, it suppresses the proliferation of vascular smooth muscle cells. H2S may also be contributing in the protection afforded by ischaemia-preconditioning. Testosterone is thought to be responsible for the higher central nervous system level of H2S in males. In the central nervous system, H2S is implicated in Alzheimer's disease, epilepsy, stroke and Down's syndrome. Insulin secretion is associated with a decrease in the H2S levels. Raised H2S is detrimental in acute pancreatitis as well as in septic shock. Recently, H2S-releasing derivatives of certain drugs have shown promise in protection against gastric ulcer and in inflammatory bowel disease. The beneficial effects of certain sulphur containing herbs like ginseng and garlic may be mediated via H2S. In future, development of specific drugs modulating H2S levels may prove beneficial in varied disorders.
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PMID:Gaso-transmitter hydrogen sulphide: potential new target in pharmacotherapy. 2111 45


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