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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angioplasty has long been used in the treatment of peripheral arterial occlusive disease with variable long-term results. In this case report, we present a patient with marfanoid features and acute ischemia of the lower extremity. Angioplasty provided us with the means of emergently relieving the acute symptoms. The patient was subsequently found on further work-up to have hyperhomocysteinemia (HC) and appropriate medical therapy was initiated. We conclude that angioplasty should be considered in pediatric patients with acute occlusive limb ischemia, providing excellent immediate results to preserve the limb as well as the time to investigate the underlying causes.
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PMID:Percutaneous balloon angioplasty for the treatment of iliofemoral arterial stenosis resulting from hyperhomocysteinemia in a child. 1274 59

The vascular placental pathology (VPP) is associated with many etiologies. Some are the consequence of a maternal genetic or acquired predisposition. Others are associated with a chronic maternal disease (hypertension, lupus, obesity, diabetes, ...). Finally, some others are associated with placental implantation leading to fetal ischemia (multiple pregnancy, chorioangioma, primiparity, feto-placental hydrops) or to environmental (altitude) or nutritional factors (famine and specific alimentary depressions). We classify these factors into three categories according to the risk level (moderate, significant and elevated). While any of these factors can increase the risk of VPP, no one is sufficiently sensitive or specific in predict inevitable onset of VPP. In most cases VPP results from a combination of two (or more) risk factors. The risk factors of VPP classified as moderate include age (> or = 35 years), increased blood pressure during the second trimester of pregnancy, a new paternity, dietetic factors or environmental factors, smoking and controlled diabetes (class B, C), or inactive systemic diseases. Risk is significantly elevated among obese (BMI > or = 25), primiparous women, women with a past familial history (first degree) of preeclampsia or eclampsia, cocaine use or association of tobacco and caffeine use, increased placental mass (associated with twin pregnancy, fetal hydrops or molar pregnancy), uncontrolled diabetes, lupus, active scleroderma. Risk is considered to be high among patients with chronic hypertension, women with a past history of preeclampsia, diabetes (class D, F, R), patients with active systemic disease or with antiphospholipid antibodies or women with lupus or renal lesions and/or proteinuria as well as chronic kidney disease resulting in proteinuria, hypertension and renal insufficiency. Finally, the risk of VPP is considered to be increased in the presence of acquired thrombophilia. It remains moderate in the presence of isolated genetic thrombophilia, except in forms presenting with multiple genetic mutations or associated with an hyperhomocysteinemia. A "high-risk group" is defined among women with past history of deep venous thromboembolic events outside pregnancy, or with a past history of placental vascular pathology (intra-uterine death, placental abruptio, severe and precocious placental, intra-uterine growth retardation, early and repetitive fetal loss) and who, in addition, present with acquired thrombophilia (antiphospholipid antibodies, thrombocytemia), unique homozygous genetic thrombophilia, amultiple genetic thrombophilia or unique heterozygous genetic thrombophilia associated with hyperhomocysteinemia. Prophylactic treatment of acquired thrombophilia and of the multiple genetic forms or associated with hypercysteinemia is a logical rationale, particularly among women with a past history of placental vascular pathology, or with a past history of venous thromboembolic events. On the contrary, prophylaxis using low-molecular-weight heparin in the event of asymptomatic genetic thrombophilic mutations and for women without a past history of deep venous thromboembolism or vascular placental pathology remains controversial.
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PMID:[Vascular placental pathology in high-risk groups: definition and synopsis]. 1502 87

We are presenting the case of a 63 year-old man with a dural arteriovenous malformation of the transverse sigmoid sinus who developed focal deficits followed by less localized symptoms such a disorientation, lethargy and eventually comatose status. Initial cerebral angiography showed retrograde filling of the cortical and deep cerebral venous system with marked delay in venous empting. Following embolization clinical symptoms completely cleared at the time that control angiography showed retrograde venous flow turning anterograde. Patient's symptoms recurred four months later when there was a relapse of retrograde cerebral venous drainage at the time he developed thrombosis of the superior longitudinal and right transverse sinuses. Sinus thrombosis and thrombosis of the central retinal artery were coincidental with hypercoagulability related to hyperhomocysteinemia. Since control angiography still showed persistence of the AV shunting radical excision of the involved dural sinuses was performed. The final outcome was excellent. The physiopathological mechanism responsible for neurological deficits in our patient most likely was ischemia of venous origin secondary to venous hypertension resulting from retrograde cerebral venous drainage. The clinical and angiographic presentation in few similar cases reported in the literature is reviewed.
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PMID:Unruptured dural arteriovenous malformation of the transverse-sigmoid sinus presenting with focal symptoms and coma. 1555 3

A 51-year-old woman had no known cardiovascular risk factor. She presented with bilateral calf intermittent claudication from February. She was hospitalized in August for acute right leg ischemia without loss of sensorymotor functions, following angiography by one week. She had an occlusion of both superficial femoral arteries and abdominal aorta thrombus, plausible source for embolism. Her condition quickly improved with heparin and iloprost infusion. Since the aortic thrombus was removed on ultrasound, aortic surgery was not performed at this time. Investigations showed hyperhomocysteinemia (25 microg/L after overnight fasting and 115 after methionin load) and decrease in folic acid. This report highlights the occurrence of severe arterial disease in young women with high serum homocysteine levels.
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PMID:[Subacute ischemia of the lower limb revealing hyperhomocysteinemia in a young woman]. 1614 82

Autoimmune or type 1 diabetes mellitus (T1DM), accounts for 90-95% of all cases of diabetes, while type 2 diabetes mellitus (T2DM), characterized by impaired insulin sensitivity and production, accounts for the other 5-10%. Atherosclerotic process starts during childhood and recognize several mechanisms that are activated in response to NOXIUS STIMULI and participate in a complex state which is accepted to be a chronic inflammatory state. T1DM patients, especially those with a non-optimal metabolic control, have a higher risk of developing all macrovascular complications such as myocardial infarction, stroke and silent ischemia. Macrovascular disease is mainly associated with hyperglycemia, dyslipidemia, obesity, hypertension, hypercoagulable state, cigarette smoking, lack of exercise, endothelial dysfunction, hyperhomocysteinemia and vascular wall abnormalities. In this paper we review the importance of traditional and non-traditional risk factors for macrovascular complications in children with T1DM and discuss their role in the pathogenesis of the excess cardiovascular mortality in these patients.
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PMID:Macroangiopathy in adults and children with diabetes: risk factors (part 2). 1711 Dec 97

Ischemia followed by reperfusion is a major cause for renal injury in both native kidney and renal allografts. Hyperhomocysteinemia, a condition of elevated plasma homocysteine (Hcy) level, is associated with cardiovascular diseases. Recent evidence suggests that Hcy, at higher levels, may be harmful to other organs such as the kidney. In this study, we investigated the role of Hcy in ischemia-reperfusion-induced renal injury. The left kidney of a Sprague-Dawley rat was subjected to either 30-min or 1-h ischemia followed by 1- or 24-h reperfusion. Ischemia-reperfusion caused a significant increase in peroxynitrite formation and lipid peroxidation in kidneys, which reflected oxidative stress. The number of apoptotic cells in those kidneys was also markedly increased. Hcy levels were elevated 2.9- and 1.5-fold in kidneys subjected to ischemia alone or ischemia-reperfusion, respectively. Further investigation revealed that elevation of Hcy level in the kidney upon ischemia-reperfusion was due to reduced activity of cystathionine-beta-synthase, a key enzyme in Hcy metabolism. Administration of anti-Hcy antibodies into the kidney not only abolished ischemia-reperfusion-induced oxidative stress and cell death in the kidneys but also restored renal function after 1 h of reperfusion. However, such a protective effect was not sustained after 24 h of reperfusion. In conclusion, ischemia-reperfusion impairs Hcy metabolism in the kidney. Hcy, at elevated levels, is capable of inducing oxidative stress and renal injury. Neutralization of Hcy with antibodies offers transient functional benefit against ischemia-reperfusion-induced oxidative stress and renal injury. These results suggest that Hcy may play a detrimental role in the kidney during ischemia-reperfusion.
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PMID:Detrimental role of homocysteine in renal ischemia-reperfusion injury. 1726 13

Functional changes of the vessel wall--specifically dysfunction of endothelial cells--may precede the formation of frank plaques at the initiation of atherosclerosis. Clinically endothelial function and dysfunction can be measured by angiography or ultrasound techniques. Another possibility is the measurement of circulating markers of endothelial dysfunction in human plasma, such as the endogenous NOS inhibitor ADMA (asymmetric dimethylarginine). In our recent studies we were able to show that ADMA accumulates in the presence of metabolic changes such as hyperhomocysteinemia, insulin resistance and type-2 diabetes, and that these elevations of plasma ADMA correlate well with the amount of endothelial dysfunction and with NO bioavailability. Furthermore ADMA was shown to be dynamically regulated and to play an important patho-physiologic role in myocardial ischemia and reperfusion. Thus, measurements of plasma ADMA in patients could help to screen for manifestations of atherosclerosis. Moreover attempts to reduce plasma and tissue ADMA could potentially play an important role in the treatment of endothelial dysfunction, atherosclerosis, but also of ischemia reperfusion injury.
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PMID:[Asymmetric dimethyl arginine (ADMA): a novel cardiovascular risk factor?]. 1734 60

Peripheral arterial occlusive disease (PAOD) of the lower extremities is becoming more prevalent worldwide. Nonsurgical treatment options provide the foundation for management. Lifestyle and risk factor modification should be emphasized in this patient population because of the associated adverse cardiovascular events. This includes implementation of a regular walking and smoking-cessation programs, aggressive control of hyperlipidemia, hypertension and diabetes mellitus, and treatment of hyperhomocysteinemia. Antiplatelet agents such as aspirin (acetylsalicylic acid) or clopidogrel are not specifically indicated for claudication but these drugs should be used in all patients with PAOD to prevent secondary ischemic events. Currently, cilostazol is the only US FDA approved agent that appears effective for the treatment of claudication symptoms. Several agents have been used with success outside of the US and others are still undergoing testing. Definitive recommendations cannot be made on the use of these drugs until further evaluation is completed. Ongoing research with new strategies for angiogenesis and the use of progenitor cells has yielded encouraging results, particularly for patients with critical limb ischemia and limited options. Advances in endovascular technology over the last several years have greatly enhanced the ability to diagnose and treat specific anatomic lesions that previously would have required open surgical correction. The use of percutaneous transluminal angioplasty and stents in the lower extremities has had considerable success when following specific guidelines such as those set forth by the TransAtlantic Inter-Society Consensus Working Group.
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PMID:Current management of peripheral arterial occlusive disease: a review of pharmacologic agents and other interventions. 1735 66

Our previous study found that hyperhomocysteinemia was strongly associated with central retinal vein occlusion (CRVO) in the Chinese population. The aim of this study is to determine whether MTHFR C677T mutation is an independent risk factor for CRVO in the Chinese population. A matched case-control study was conducted between July 2004 and May 2005. The study cohort consisted of 64 individuals that had been diagnosed with CRVO and 64 healthy controls (matched for age, gender, hypertension, smoking, and drinking habits). None of the cases or controls had a history of diabetes, glaucoma, medication or any other vascular events that might influence plasma homocysteine levels. A cross-sectional analysis among the 64 cases was performed to compare the prevalence of MTHFR C677T mutation among subjects with and without ischemia and subjects aged above 45 and below 45 years. MTHFR C677T mutation was determined by the template-directed dye-terminator incorporation with fluorescence polarization (TDI-FP) method. The result showed that the prevalence of the MTHFR 677 TT genotype did not significantly differ between patients and controls. However, 10 (34.5%) MTHFR C677 TT genotype was found in the ischemic group but only 4 (14.3%) in the nonischemic group (p=0.026). And we found that 6 MTHFR C677 TT genotype patients who have hyperhomocysteinemia in the ischemic group but only 2 in the nonischemic group (p=0.016). It suggests that MTHFR C677T mutation is associated with hyperhomocysteinemia in the ischemic CRVO in the Chinese population. It may contribute to hyperhomocysteinemia and associate with the development of CRVO.
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PMID:MTHFR C677T mutation in central retinal vein occlusion: a case-control study in Chinese population. 1771 79

Abnormal increases of antiphospholipid antibody and plasma homocysteine levels are recently emerging as nonlipidic risk factors for cerebral atherogenesis and thrombosis. Both antiphospholipid antibody and homocysteine share many similar bioeffects in hemostasis, but their interaction is still inconsistent. In this study, we examined the relation between the plasma homocysteine level and lupus anticoagulant, anticardiolipin antibody, and anti-beta2-glycoprotein I antibody in patients with noncardiac cerebral ischemia. Systemic lupus erythrematosus patients were excluded. The results showed a higher frequency of moderate hyperhomocysteinemia in patients with an abnormal increase of lupus anticoagulant only. Neither the serum folate and cobalamin levels nor methylenetetrahydrofolate reductase allele mutation contributes to this result. Accordingly, homocysteine interacts with lupus anticoagulant to promote cerebral atherosclerosis and ischemia. The role of vasculopathic or prothrombotic autoantibody generation in response to specific pathological change such as hyperhomocysteinemia warrants further investigation.
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PMID:Hyperhomocysteinemia relates to the subtype of antiphospholipid antibodies in non-SLE patients. 1791 Nov 91


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