Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The atheroembolic disease, often non recognized and fatal in the elderly, is a complication of atherosclerosis characterized by obstruction of multiple small arteries by cholesterol crystals. It may occur spontaneously or after aortic wall trauma, latter usually following angiography or cardiovascular surgery, and the use of anticoagulants. Renal failure, livedo reticularis and acrocyanosis of the lower extremities have been frequently described. In some cases the clinical picture may resembling a vasculitis. The diagnosis can be confirmed by skin, muscle or kidney biopsy. In practice, the treatment is symptomatic. The most effective measure is prevention.
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PMID:[Atheroembolic disease (cholesterol crystal embolism)]. 923 4

A 37-year-old man sought medical advice because of an 8-year history of a slowly progressive dementing illness with no clinically apparent discrete strokelike episodes. Cognitive functioning was markedly, globally impaired without lateralizing or localizing features. Widespread livedo reticularis led to a diagnosis of Sneddon's syndrome. Antiphospholipid antibodies and lupus anticoagulant were negative. Magnetic resonance imaging showed widespread cerebral atrophy, cortical and subcortical cerebral infarcts, and extensive periventricular white matter abnormalities. Cerebral angiography revealed diffuse medium- and small-vessel occlusive disease, with numerous collaterals in the mid and distal circulation but no evidence of atherosclerosis or vasculitis. No other cause of a dementing illness was found. We postulate that our patient's dementia was due to the cumulative effects of multiple cerebral infarcts.
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PMID:Gradually progressive dementia without discrete cerebrovascular events in a patient with Sneddon's syndrome. 1059 61

Antiphospholipid Syndrome (APS) was first described by Hughes and sometimes called as Hughes syndrome. Recent studies revealed that the antigen to anticardiolipin antibody (aCL) is not cardiolipin itself but co-factor beta 2-GPI which expresses its epitope when it combines cardiolipin or gets oxidized. Lupus Anticoagulant is now possibly considered as anti-prothrombin antibody. Livedo including Snedden syndrome, pulmonary hypertension and skin ulcer became considered as the part of symptoms of this disease. In ISAPA 1998, it is reported from several laboratories that IgA aCL is also pathogenic to thrombosis as well as IgG aCL. Atherosclerosis is also accelerated by aCL. Catastrophic APS is rare but fatal, reported 3 cases in Japan and 50 cases in the world.
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PMID:[Antiphospholipid syndrome]. 1007 9

The aim of this study was to examine potential links between antiOxLDL antibodies and the clinical and biological features of secondary antiphospholipid syndrome (II APLS) associated with systemic lupus erythematosus (SLE). A cohort study was done of 98 SLE patients followed-up for 1 y, including 18 with definite II APLS and 13 patients with definite primary APLS (I APLS). IgG anticardiolipin, IgG anti beta2 GPI, lupus anticoagulant, VDRL and IgG antiOxLDL were measured in all 98 study subjects. High antiOxLDL titers were found in seven (39%) of the 18 patients with II APLS vs 10 (12.5%) of the 80 patients without APLS (P < 0.01; OR = 4.45; 95% CI = 1.4-14.1) and none of the 13 patients with I APLS (P < 0.02). The mean antiOxLDL titer was not significantly higher in the SLE patients with than without II APLS (P > 0.05). A high antiOxLDL titer was correlated with deep venous thrombosis (P < 0.01; OR = 5.77; 95% CI = 0.54-61) but not with arterial thrombosis (P > 0.05; OR = 1; 95% CI = 0.29-3.09), thrombocytopenia, central nervous system involvement, livedo reticularis, or a positive Coombs test. The antiOxLDL antibody titer was correlated with the IgG anticardiolipin antibody titer (r = 0.235; P = 0.02) and with the IgG anti-beta2 GPI antibody titer (r = 0.224; P = 0.026). AntiOxLDL elevation was found in 17% of SLE patients and was significantly associated with II APLS and venous thrombosis. We found no evidence suggesting that antiOxLDL may be associated with atherosclerosis.
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PMID:Anti-oxidized low-density-lipoprotein (OxLDL) antibodies in systemic lupus erythematosus with and without antiphospholipid syndrome. 1140 65

The multiple cholesterol emboli syndrome (MCES) is a rare, multi-organ disease than can occur spontaneously or after arterial or cardiac catheterization, arteriography, angioplasty, cardiovascular surgery, oral or intravenous anticoagulation, systemic fibrinolysis and cardiorespiratory resuscitation, predominantly in male subjects with disseminated atherosclerosis over the age of 60 years. Clinical signs of MCES vary considerably depending on the organs involved, but the signs most frequently encountered are renal failure, skin lesions (livedo reticularis, purple toc, ulcers, etc) and transient eosinophilia. Optimal treatment of this syndrome is controversial and is often symptomatic. However, the most effective measure remains prevention based on identification of high-risk patients, treatment with platelet antiaggregants and careful handling of catheters. This syndrome has a serious prognosis in the majority of cases. In this article, the authors describe a case of MCES. After thoracic aortography, this 73-years-old patient presented typical clinical sign of MCES (angina, cerebrovascular accident, bilateral blindness, transient renal failure and splenic infarction). The clinical course was favourable in response to heparin therapy and splenectomy and caudal pancreatectomy. Histology confirmed the presence of cholesterol emboli in the lumen of splenic arterioles. Except in the case of severe bleeding diathesis, the authors recommend early heparin therapy for MCES caused by catheterization, angioplasty or cardiovascular surgery. However, complementary studies must be performed to more clearly define the effects of heparin on MCES.
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PMID:[Multiple cholesterol emboli syndrome: beneficial effects of early heparin therapy. A case report]. 1255 63

Diffuse atherosclerosis entails a 15-30% risk of plaques on renal arteries (ARAS), with a correlation with coronary atherosclerosis. Ischemia induces generation of angiotensin II (Ang II) that maintains sufficient hydrostatic pressure within the tuft to preserve the GFR. Ang II inhibition suppresses this protective mechanism. In fact, any antihypertensive drug may lead to reaching a "critical perfusion pressure". ARAS should be suspected in case of renal asymmetry. It should also be envisaged in case of "flash pulmonary edemas". Ultrasonography and renal tomography show aortic calcifications and often the outline of an abdominal aortic aneurysm. Tomodensitometry may detect large aorto-renal plaques. Spiral scanner tomography represents a progress, in terms of renal artery imaging and of renal cortical atrophy. Magnetic resonance imaging is less accurate but avoids iodine toxicity. The best noninvasive method is pulsed echo-doppler. It is particularly useful for evaluating stenoses progression. Some stenoses progress to renal atrophy and renal artery thrombosis, whereas others follow a stable course. Pulsed Doppler helps predict whether revascularization will improve renal function, according to the resistance index. Renal arteriography entails a high risk of cholesterol crystal embolism. However, it is the obligatory first step for angioplasty and stent positioning, indicated when the kidney is not atrophic. The indication for revascularization essentially depends on evaluation of the benefits vs risks of angioplasty or surgery. Some publications underscore the frequent stability of renal function and the fact that, revascularized or not, most patients will shortly die of myocardial infarction. Renal cholesterol crystal embolism (CCE) is a severe condition, which occurs when large arteries undergo surgery, aortography or interventional radiology. Anticoagulants are a frequent cause of CCE. CCE may also occur spontaneously, resulting in slowly progressive renal insufficiency. Migration of crystals in small caliber intrarenal arteries induces obstruction, followed by an inflammatory reaction. The clinical picture resembles angiitis, with laboratory evidence of inflammation along with high eosinophil counts and hypocomplementemia. Diagnosis rests on: 1) a iatrogenic event in a patient with an atherosclerotic background; 2) examination of the skin disclosing purple toes, small necrotic lesions and livedo of the lower limbs. Crystals may also be found by funduscopy. Skin or muscle biopsy are contributive in showing crystals and help avoid renal biopsy; 3) other localizations involve the mesenteric circulation and the central nervous system. Until recently, the prognosis was considered disastrous. However, a recently published treatment schedule proved efficient in reducing mortality. A last issue regarding the relationships between atherosclerosis and the kidney deserves mention. In an autopsy-based study it was shown that atherosclerosis per se is accompanied by an increase in the glomerular surface area along with a greater proportion of obsolescent glomeruli by comparison with matched controls. Finally, it should be recalled that atherogenic hyperlipidemia usually aggravates the course of any renal disease, including ARAS. Treatment with statins is indicated in all forms of atherosclerotic renal disease.
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PMID:[Atherosclerosis and the kidney]. 1689 85

Antiphospholipid antibodies (aPL) are an heterogeneous group of circulating immunoglobulins arising in a wide range of infectious and autoimmune diseases. Since the early 80s, the interest on anticardiolipin antibodies (aCL) has exponentially increased due to their association with thrombosis. The antiphospholipid syndrome (APS) was defined as a clinical disorder characterized by thrombosis and pregnancy morbidity associated to the persistent presence of aCL and/or lupus anticoagulant (LA). Thrombosis is the major manifestation in patients with aPL, but the spectrum of symptoms and signs associated with aPL has considerably broadened, and other manifestations such as thrombocytopenia, non-thrombotic neurological syndromes, psychiatric manifestations, livedo reticularis, skin ulcers, haemolytic anemia, pulmonary hypertension, cardiac valve abnormality and atherosclerosis have also been related to the presence of those antibodies. Numerous mechanisms have been proposed to explain the thrombotic tendency of patients with aPL, but the pathogenesis seems to be multifactorial.
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PMID:Antiphospholipid antibodies: lessons from the bench. 1738 59

In 1983, a detailed clinical description of a new syndrome was published. This prothrombotic syndrome was initially called the anticardiolipin syndrome and subsequently the antiphospholipid syndrome (APS), or Hughes Syndrome. Almost uniquely, it results in arterial as well as venous thrombosis and is marked by the presence of circulating antiphospholipid antibodies. Clinical features are protean, ranging from peripheral deep vein thrombosis (DVT) to involvement of internal organs such as the liver, kidneys, and adrenals. Likewise, arterial thrombosis can result in life-threatening infarction of organs such as the heart. The nervous system is frequently affected, with migraine, memory loss, balance disorders, stroke, and atypical multiple sclerosis being prominent. Other features include recurrent miscarriage, thrombocytopenia, and livedo reticularis. More recent observations have included ischemic bone fractures, renal and celiac artery stenosis, and a possible tendency toward accelerated atherosclerosis. The condition is seen in patients with lupus, but, significantly, occurs without associated lupus ("primary" APS)-indeed, increasing clinical recognition of Hughes Syndrome suggests that this condition will overtake lupus in prevalence. Treatment at present is by anticoagulation. The mechanisms for thrombosis are being worked out; it has been suggested that in some situations (e.g., pregnancy loss), an inflammatory component as well as thrombosis may play a part.
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PMID:Hughes Syndrome: the antiphospholipid syndrome--a clinical overview. 1742 56

A 55-year-old man was hospitalized for endovascular stent placement in both right common iliac and femoral arteries for relief of claudication symptoms due to peripheral vascular disease. Angiography demonstrated diffuse atherosclerosis of the infrarenal aorta and severe stenosis of the right common iliac and right femoral arteries. Physical examination showed diminished but palpable peripheral pulses. Uncomplicated stent placement was done in the right common iliac and right femoral arteries via a left femoral artery approach resulting in improved pedal pulses. Over the next 36 hours, the patient developed severe bilateral lower extremity pain followed by extensive livedo reticularis over lower extremities, elevated creatine kinase levels, myoglobinuria, and a rise in serum creatinine to 1.5 mg/dL (133 micromol/L). Pedal pulses continued to be palpable. This was followed by bilateral lower extremity compartment syndrome, requiring fasciotomies. Myoglobinuria cleared with hydration and creatinine kinase levels returned to normal; however, the patient ultimately developed gangrene of both lower extremities. Bilateral below the knee amputations were performed and histopathology showed wide spread cholesterol crystals in arterioles and small and medium sized arteries in skin and muscle of both lower extremities. This case emphasizes the potential for major complications of cholesterol embolism associated with even uncomplicated vascular procedures performed for treatment of peripheral vascular disease.
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PMID:Catastrophic cholesterol crystal embolization after endovascular stent placement for peripheral vascular disease. 1848 Jun 61

The antiphospholipid syndrome is an autoimmune disease characterised by recurrent arterial or venous thrombosis, pregnancy morbidity and the persistence of positive antiphospholipid antibodies. Many other clinical manifestations may occur including heart valve disease, livedo reticularis, thrombocytopenia and neurological manifestations such as migraine and seizures. We review a number of other manifestations including stenotic lesions, coronary artery disease and accelerated atherosclerosis, skeletal disorders and the concept of seronegative antiphospholipid syndrome.
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PMID:Antiphospholipid (Hughes) syndrome: beyond pregnancy morbidity and thrombosis. 1945 15


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