Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic sclerosis is a complex, progressive autoimmune disease. The origin is, so far, unknown and it is characterized by immunological and endothelial damage followed by fibrosis. Interaction between the host genetic backgrounds with environmental factors is thought to turn out an abnormal immune response characterized by clonal expansion of Th2 repertoire, upregulation of pro-fibrotic cytokines and dysregulated B cells. Specific autoantibodies profiles are associated with clinical subtypes of the diseases. Endothelial activation is an early feature with damage of the vasocontrictive and vasodilation response. Finally, persistent tissue ischemia and abnormal immune response produce myofibroblast proliferation andoverproduction of extracellular matrix proteins and fibrosis.
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PMID:[Etiopathogenesis. New concepts]. 2179 88

Takayasu's arteritis (TA) is a chronic vasculitis of unknown etiology. Celiac disease (CD) is an autoimmune disease caused by the ingestion of gluten. TA and CD have been associated with many other autoimmune conditions. However, only five cases with this association have been reported. In this series, three patients with TA and CD were included; all were female, 21, 30 and 54 years old. TA clinical manifestations preceded CD diagnosis in all patients. Aortic arch branches were affected in all of them. Serologic markers were positive and a small intestine biopsy showed typical findings of CD in the three patients. Special attention should be given to this possible association because these entities may be asymptomatic; the recognition of new disease variants modifies treatment, and sometimes CD constitutes a differential diagnosis of mesenteric ischemia.
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PMID:[Celiac disease in 3 patients with Takayasu's arteritis]. 2179 27

Sclerosing mesenteritis is a rare inflammatory disease of the bowel mesentery. It produces tumor-like masses of the mesentery composed of varying degrees of fibrosis, chronic inflammation, and fat necrosis. It has been described variously as fibrosing mesenteritis, retractile mesenteritis, mesenteric Weber Christian disease, and systemic nodular panniculitis. The etiology and pathogenesis of the disease are as yet unknown, but autoimmune disorder, previous abdominal surgery, trauma, and ischemia could play a role. The clinical features include abdominal pain, vomiting, diarrhea, and constipation. Occasionally, patients with this condition may present with bowel obstruction. Rarely, It can be associated with other idiopathic inflammatory disorders such as retroperitoneal fibrosis, sclerosing cholangitis, and orbital pseudotumors. We report a case of idiopathic sclerosing mesenteritis with retroperitoneal fibrosis in a 58-year-old man.
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PMID:[A case of idiopathic sclerosing mesenteritis with retroperitoneal fibrosis]. 2204 24

Posterior reversible encephalopathy syndrome (PRES) is a clinical syndrome of encephalopathy, headache, visual disturbance, and seizures. In most cases, symptoms present acutely or subacutely in the setting of accelerated hypertension, eclampsia, autoimmune disease, immunosuppressive treatment, or cancer chemotherapy. One essential feature of PRES is the presence of reversible cerebral vasogenic edema that has a predominantly posterior distribution on brain imaging. Atypical imaging features are commonly described, including involvement of the anterior brain or brainstem and the coexistence of ischemia or hemorrhage. In most cases, both clinical and radiological findings are reversible, although permanent imaging abnormalities and residual neurological sequelae can be seen in a minority of patients. The syndrome is thought to be caused by a breakdown of the blood-brain barrier and an extravasation of the intravascular fluid. Treatment of hypertension and seizures, and withdrawal of causative agents are the mainstays of therapy in PRES.
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PMID:Posterior reversible encephalopathy syndrome: clinicoradiological spectrum and therapeutic strategies. 2240 96

Thromboangiitis obliterans (TAO) is a segmental inflammatory occlusive disorder that affects small- and medium-sized arteries, and arm and leg veins of young smokers. Several different diagnostic criteria have been offered for the diagnosis of TAO. Clinically, it manifests as migratory thrombophlebitis or signs of arterial insufficiency in the extremities. It is characterized by highly cellular and inflammatory occlusive thrombi, primarily of the distal extremities. Thromboses are often occlusive and sometimes display moderate, nonspecific inflammatory infiltrate, consisting mostly of polymorphonuclear leukocytes, mononuclear cells and rare multinuclear giant cells. The immune system appears to play a critical role in the etiology of TAO. However, knowledge about immunological aspects involved in the progression of vascular tissue inflammation, and consequently, the evolution of this disease, is still limited. There are several studies that suggest the involvement of genetic factors and results have shown increasing levels of antiendothelial cell antibodies in patients with active disease. Vasodilation is impaired in patients with TAO. TAO disorder may actually be an autoimmune disorder, probably initiated by an unknown antigen in the vascular endothelium, possibly a component of nicotine. There are various therapies available for treatment of TAO, but the major and indispensable measure is smoking cessation. Except for discontinuation of tobacco use, no forms of therapy are definitive. Sympathectomy, cilostazol and prostaglandin analogues (prostacyclin or prostaglandin E) have been used in specific conditions. Recently, therapeutic angiogenesis with autologous transplantation of bone marrow mononuclear cells has been studied in patients with critical limb ischemia.
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PMID:Etiopathogenesis, clinical diagnosis and treatment of thromboangiitis obliterans - current practices. 2247 11

Sclerosing mesenteritis is a rare benign disease originated from the mesenteries. It can be related to autoimmune disease, vasculitis, ischemia, infection, trauma and operation, but most of cases are idiopathic. The overall prognosis of sclerosing mesenteritis is usually good with benign, course. However, no consensus of treatment has yet been established. We report a case of spontaneous partial regression of sclerosing mesenteritis presented as a huge mass and diagnosed by finding of contrast enhanced abdominal computed tomography and percutaneous ultrasonography guided needle biopsy.
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PMID:[Spontaneous regression of sclerosing mesenteritis presenting as a huge mass]. 2254 31

Cardiovascular disease is a complex disorder involving multiple pathophysiological processes, several of which involve activation of toll-like receptors (TLRs) of the innate immune system. As sentinels of innate immunity TLRs are nonclonally germline-encoded molecular pattern recognition receptors that recognize exogenous as well as tissue-derived molecular dangers signals promoting inflammation. In addition to their expression in immune cells, TLRs are found in other tissues and cell types including cardiomyocytes, endothelial and vascular smooth muscle cells. TLRs are differentially regulated in various cell types by several cardiovascular risk factors such as hypercholesterolemia, hyperlipidemia, and hyperglycemia and may represent a key mechanism linking chronic inflammation, cardiovascular disease progression, and activation of the immune system. Modulation of TLR signaling by specific TLR agonists or antagonists, alone or in combination, may be a useful therapeutic approach to treat various cardiovascular inflammatory conditions such as atherosclerosis, peripheral arterial disease, secondary microvascular complications of diabetes, autoimmune disease, and ischemia reperfusion injury. In this paper we discuss recent developments and current evidence for the role of TLR in cardiovascular disease as well as the therapeutic potential of various compounds on inhibition of TLR-mediated inflammatory responses.
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PMID:The Emerging Role of TLR and Innate Immunity in Cardiovascular Disease. 2257 89

Activation of adenosine A2A receptors (A2AR) reduces inflammation by generally inhibiting the activation of pro-inflammatory cells, decreasing endothelial adhesion molecule expression and reducing the release of proinflammatory cytokine mediators. Numerous preclinical studies using selective A2AR agonists, antagonists, A2AR knockout as well as chimeric mice have suggested the therapeutic potential of A2AR agonists for the treatment of ischemia reperfusion injury (IRI) and autoimmune diseases. This review summarizes the immunosuppressive actions of A2AR agonists in murine IRI models of liver, kidney, heart, lung and CNS, and gives details on the cellular effects of A2AR activation in neutrophils, macrophages, dendritic cells, natural killer cells, NKT cells, T effector cells and CD4+CD25+FoxP3+ T regulatory cells. This is discussed in the context of cytokine mediators involved in inflammatory cascades. Whilst the role of adenosine receptor agonists in various models of autoimmune disease has been well-documented, very little information is available regarding the role of A2AR activation in type 1 diabetes mellitus (T1DM). An overview of the pathogenesis of T1DM as well as early islet graft rejection in the immediate peri-transplantation period offers insight regarding the use of A2AR agonists as a beneficial intervention in clinical islet transplantation, promoting islet graft survival, minimizing early islet loss and reducing the number of islets required for successful transplantation, thereby increasing the availability of this procedure to a greater number of recipients. In summary, the use of A2AR agonists as a clinical intervention in IRI and as an adjunct to clinical immunesuppressive regimen in islet transplantation is highlighted.
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PMID:The immunosuppressive role of adenosine A2A receptors in ischemia reperfusion injury and islet transplantation. 2293 47

An 82-year-old woman presented with oedema and extensive necrotic ulcerative lesions on the back side of her lower limbs, emerging after the second cycle of chemotherapy consisting of Gemcitabine for metastatic pancreatic cancer. The absence of any convincing argument in favor of cardiovascular or autoimmune disease led us to attribute the onset of skin necrosis to chemotherapy administration. Although skin ischemia has also been described as a paraneoplastic syndrome, in this case we could observe a temporal and causal relationship to Gemcitabine infusion. Recently, this drug has been associated with important vascular side effects; its vascular toxicity is in fact higher than previously estimated. To our knowledge, careful attention should be reserved to neoplastic patients candidated to Gemcitabine administration, especially if previously affected by arterial vascular disease, venous thromboembolism, or collagenoses.
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PMID:Gemcitabine-induced extensive skin necrosis. 2330 62

Experience suggests that African Americans may express autoimmune disease differently than other racial groups. In the context of systemic sclerosis (scleroderma), we sought to determine whether race was related to a more adverse expression of disease. Between January 1, 1990, and December 31, 2009, a total of 409 African American and 1808 white patients with scleroderma were evaluated at a single university medical center. While the distribution by sex was virtually identical in both groups, at 82% female, African American patients presented to the center at a younger mean age than white patients (47 vs. 53 yr; p < 0.001). Two-thirds of white patients manifested the limited cutaneous subset of disease, whereas the majority of African American patients manifested the diffuse cutaneous subset (p < 0.001). The proportion seropositive for anticentromere antibody was nearly 3-fold greater among white patients, at 34%, compared to African American patients (12%; p < 0.001). Nearly a third of African American (31%) patients had autoantibodies to topoisomerase, compared to 19% of white patients (p = 0.001). Notably, African American patients experienced an increase in prevalence of cardiac (adjusted odds ratio [OR], 1.6; 95% confidence interval [CI], 1.3-2.2), renal (OR, 1.6; 95% CI, 1.2-2.1), digital ischemia (OR, 1.5; 95% CI, 1.4-2.2), muscle (OR, 1.7; 95% CI, 1.3-2.3), and restrictive lung (OR, 6.9; 95% CI, 5.1-9.4) disease. Overall, 700 (32%) patients died (159 African American; 541 white). The cumulative incidence of mortality at 10 years was 43% among African American patients compared to 35% among white patients (log-rank p = 0.0011). Compared to white patients, African American patients experienced an 80% increase in risk of mortality (relative risk [RR], 1.8; 95% CI, 1.4-2.2), after adjustment for age at disease onset and disease duration. Further adjustment by sex, disease subtype, and scleroderma-specific autoantibody status, and for the socioeconomic measures of educational attainment and health insurance status, diminished these risk estimates (RR, 1.3; 95% CI, 1.0-1.6). The heightened risk of mortality persisted in strata defined by age at disease onset, diffuse cutaneous disease, anticentromere seropositivity, decade of care at the center, and among women. These findings support the notion that race is related to a distinct phenotypic profile in scleroderma, and a more unfavorable prognosis among African Americans, warranting heightened diagnostic evaluation and vigilant care of these patients. Further, we provide a chronologic review of the literature regarding race, organ system involvement, and mortality in scleroderma; we furnish synopses of relevant reports, and summarize findings.
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PMID:Race and association with disease manifestations and mortality in scleroderma: a 20-year experience at the Johns Hopkins Scleroderma Center and review of the literature. 2379 8


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