Disease relevance of PAOD1

• Peripheral arterial occlusive disease (PAOD) results from atherosclerosis of large and medium peripheral arteries, as well as the aorta, and has many risk factors, including smoking, diabetes, hypertension, and hyperlipidemia [1].
• This suggests that, although PAOD and other vascular diseases share risk factors, genetic factors specific to subtypes of vascular disease may exist [1].
• DATA EXTRACTION: The correlation of fibrinogen levels on the subsequent incidence of myocardial infarction, stroke, and peripheral arterial occlusive disease was assessed and the causality of the association was analyzed [2].
• BACKGROUND: Intermittent claudication due to peripheral arterial occlusive disease (PAOD) is a common cause of pain and disability in the middle-aged [3].
• The presence of PAOD was defined as > or = 1 stenosis with > or = 50% narrowing, and the extent was defined as the total of > or = 50% lesions in the iliac, femoral, popliteal, and crural beds [4].

Psychiatry related information on PAOD1

• Interventions that have proven effective in the prevention and treatment of PAOD in the general population, such as smoking cessation, preventive foot care, and exercise, have not been systematically applied to ESRD patients [5].
• METHODS: We examined 17 mild chronic PAOD patients, including 2 cases of vascular dementia [6].
• Longitudinal studies are required to determine whether dietary modification can reduce the incidence of PAOD in the population [7].
• CONCLUSION: Progressive decrements in free-living daily physical activity with greater levels of smoking exposure in PAOD patients are primarily due to smoking-related impairments in ambulatory function and peripheral circulation [8].
• Peripheral arterial occlusive disease: clinical data for decision making. Introduction [9].

High impact information on PAOD1

• We designate this locus as "PAOD1." Subtracting 35 patients with a history of stroke increased the LOD score to 4.93 [1].
• PAOD often coexists with coronary artery disease and cerebrovascular disease [1].
• Localization of a gene for peripheral arterial occlusive disease to chromosome 1p31 [1].
• CONCLUSIONS: In PAOD patients, there is a progressive reduction in urinary nitrate and cGMP excretion rates, which may be caused in part by accumulation of ADMA, an endogenous inhibitor of NO synthase [10].
• Plasma L-arginine concentrations were not significantly different between the groups, but ADMA concentrations were elevated in PAOD patients (young control subjects, 1.25+/-0.11; elderly control subjects, 1.01+/-0.05 micromol/L; IIb, 2.62+/-0.24; III, 3.06+/-0.48; and IV, 3.49+/-0.26 micromol/L; P<.05 for PAOD versus control subjects) [10].

Chemical compound and disease context of PAOD1

• Restoring vascular nitric oxide formation by L-arginine improves the symptoms of intermittent claudication in patients with peripheral arterial occlusive disease [11].
• We compared the total costs of treatment in patients treated after minor cerebral ischaemia in the Stroke Prevention in Reversible Ischemia Trial (SPIRIT) and in patients treated because of peripheral arterial occlusive disease in the Dutch Bypass Oral anticoagulants or Aspirin Trial (BOA) [12].
• PURPOSE: This study evaluated the effects of cilostazol on walking distances in patients with intermittent claudication (IC) caused by peripheral arterial occlusive disease [13].
• Body mass index, preexistent peripheral arterial occlusive disease, presence of septic shock, and norepinephrine requirements were significantly higher in patients developing ISL [14].
• Intravenous argatroban infusion therapy is widely used for the restoration of peripheral microcirculation in patients with peripheral arterial obstructive disease (PAOD) [15].

Biological context of PAOD1

• In the logistic model, LDL cholesterol, triglycerides, smoking, and systolic blood pressure were selected as independent predictors of PAOD presence [4].
• Effects of oxygen inhalation on skin microcirculation in patients with peripheral arterial occlusive disease [16].
• Inhalation of 40% oxygen induces a vasoconstriction in the skin microcirculation of toes of the normal subjects and patients with moderate PAOD but induces an increase of the skin microcirculation in patients with severe PAOD [16].
• The management of patients with peripheral arterial occlusive disease (PAD) has to be planned in the context of natural history, epidemiology, and apparent risk factors that predict deterioration [17].
• CONCLUSIONS: Restoring NO formation and endothelium-dependent vasodilation by L-arginine improves the clinical symptoms of intermittent claudication in patients with peripheral arterial occlusive disease [11].

Anatomical context of PAOD1

• CONCLUSIONS: Screening tools that are effective in screening for lower-limb PAOD in the nondiabetic population are less efficacious in diabetes, particularly in the presence of detectable peripheral neuropathy [18].
• Sixty patients had symptoms of transient ischemic carotid artery disease, and 63 patients with peripheral arterial occlusive disease served as controls [19].
• Therapeutical potential of blood-derived progenitor cells in patients with peripheral arterial occlusive disease and critical limb ischaemia [20].
• CONCLUSION: Antibiotic concentrations are reduced significantly in ischemic lesions compared to those of healthy adipose tissue in patients with peripheral arterial occlusive disease [21].
• Serum hepatocyte growth factor in patients with peripheral arterial occlusive disease [22].

Associations of PAOD1 with chemical compounds

• Nine of 14 patients were still in stage IIa of peripheral arterial occlusive disease 1 year after PGE1 therapy [23].
• Intensive vascular training in stage IIb of peripheral arterial occlusive disease. The additive effects of intravenous prostaglandin E1 or intravenous pentoxifylline during training [23].
• In PAOD patients, there was a significant, progressive reduction of urinary nitrate (IIb, 138.4+/-11.9; III, 128.6+/-11.3; and IV, 91.9+/-8.0 micromol/mmol creatinine; P<.05) and cGMP (IIb, 139.9+/-25.2; III, 115.6+/-13.1; and IV, 76.9+/-7.9 nmol/mmol creatinine; P<.05) excretion rates related to the Fontaine stage of PAOD [10].
• Age, smoking, and blood glucose were selected by the discriminant analysis as independent predictors of the extent of PAOD [4].
• CONCLUSIONS: From this large case-control study, it is concluded that the presence of PAOD is predicted by parameters of LDL, triglyceride, and HDL2 metabolism, whereas the extent of PAOD is related to HDL3 and nonlipid risk factors [4].

Other interactions of PAOD1

• The purpose of this study was to investigate the relationship between CCR5 Delta 32 deletion mutation and AAA, peripheral arterial occlusive disease (PAOD), and carotid stenosis [24].
• Plasma adrenomedullin concentration is increased in patients with peripheral arterial occlusive disease associated with vascular inflammation [25].
• A simplified procedure for intra-arterial thrombolysis with tissue-type plasminogen activator in peripheral arterial occlusive disease: primary and long-term results [26].
• C242T polymorphism of the p22 phox gene is not associated with peripheral arterial occlusive disease [27].
• Thrombolytic therapy with use of alteplase (rt-PA) in peripheral arterial occlusive disease: review of the clinical literature. The Advisory Panel [28].

Analytical, diagnostic and therapeutic context of PAOD1

• MR angiography is a noninvasive technique with greater sensitivity than conventional contrast arteriography for detecting distal runoff vessels in patients with peripheral arterial occlusive disease [29].
• METHODS AND RESULTS: This study comprised 102 patients with peripheral arterial occlusive disease (PAOD) referred for elective percutaneous transluminal angioplasty and 100 age-matched control subjects with normal coronary and peripheral angiograms [4].
• Vascular training with drug therapy in peripheral arterial occlusive disease [30].
• Chelation therapy for peripheral arterial occlusive disease: a systematic review [31].
• Quantitative evaluation of the Doppler ultrasonogram permits obtaining detailed functional information on the degree of arterial flow impairment in patients with peripheral arterial occlusive disease [32].

References