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)

Large increases in mortality related to premature atherosclerosis with coronary artery disease and stroke have been reported during the last few years in patients with systemic lupus erythematosus (SLE). Studies found relative risks of 5 to 7 for myocardial infarction in SLE patients. The traditional risk factors fail to fully account for accelerated atherosclerosis in SLE and APS, in addition prolonged glucocorticoid therapy and long duration of SLE seem to be of importance. The disease SLE per se is an independent risk factor. The current pathogenic hypothesis for atherosclerosis involves an inflammatory response, autoantibodies, immune complexes (containing antibodies to phospholipids, to oxidized LDLs, and to endothelial cells), CD40/CD40 ligand interactions, and bacterial or viral infections responsible for an immune response. The determination of classic and new risk factors, together with specific autoantibody titers and the use of Doppler carotid ultrasound, are useful methods to detect early atherosclerosis. Therapeutic strategies, including early risk factor intervention and effective control of inflammation, are essential to reduce morbidity and mortality and should be incorporated into the management of connective tissue disease with the goal of protecting patients against atherosclerosis.
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PMID:[Accelerated atherosclerosis in rheumatic systemic diseases as an example of systemic lupus erythematosus--what is the consequence?]. 1590 83

Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease with complex pathogenesis, various clinical presentation and chronic course with relapses. Mode of treatment depends on the disease activity and kind of internal organ involvement. In most cases clinical remission could be obtained after antimalarials, nonsteroidal anti-inflammatory drugs, corticosteroids, and photoprotection use. Despite the approved antimalarials therapeutic value, the mechanisms by which they provide benefit in lupus, patients are not fully understood. Literature data indicate that they can influence lipid metabolism. The aim of the performed study was the objective evaluation of the influence of 3-month chloroquine treatment (Arechin, 250 mg/day) on lipid metabolism and selected laboratory parameters. In 34 patients with SLE clinical and laboratory evaluation was performed twice, before and after 3-month treatment. After 3 months significantly lower total cholesterol level was observed (mean value 184.91 mg%, 165.26 mg%, p < 0.001). Also LDL level was evidently lowered (111.27 mg%, 99.25 mg%). Similar tendency was noticed in triglycerides, which level after 3 months decreased from the average 152.38 mg% to 104.97 mg%, p < 0.001. Moreover the lowering of sedimentation rate, increasing hemoglobin level and lengthening coagulation time was perceived. The results of the study indicate the influence of chloroquine on decreasing of the disease activity, its anti-inflammatory properties and mainly the drug impact on lipid metabolism. Not only does antimalarials treatment reduce the risk of atherosclerosis development but it also minimizes corticosteroids side effects, which are considered to be the basic medication in lupus patients.
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PMID:[Chloroquine influence on lipid metabolism and selected laboratory parameters]. 1654 17

"It is quite useless to argue the questions concerning the development of intimal scleroses if we study and discuss the late stages of the disease alone. If we wish to gain insight into the complex question of arterio-sclerosis we must attempt to follow the lesion from its earliest beginning" (Klotz and Manning, J Path Bact 1911: 16; 211-20). Over thirty years ago Boneu and colleagues published a report of raised levels of plasma von Willebrand factor (vWf) in patients with arteritis, diabetes and sepsis. They concluded that raised levels of this molecule indicate endothelial damage, and may possibly be a contributory factor in thrombosis in arterial disease. The former aspect of this conclusion is now accepted, and numerous studies on the risk factors for atherosclerosis provide mechanisms for this damage. Other studies have demonstrated raised levels in cancer and in connective tissue disease. Numerous long-term follow-up studies have also demonstrated that increased vWf predicts major cardiovascular end points. However, the link between these studies, and the latter aspect of Boneu's conclusion, that raised vWf contributes to thrombosis is, although attractive, nevertheless unproven. Despite this, vWf remains the most important plasma marker of endothelial damage/dysfunction and as such attracts clinical attention.
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PMID:Plasma von Willebrand factor, thrombosis, and the endothelium: the first 30 years. 1654 61

Vulvar hematomas occur rarely outside the obstetric population but may present after other trauma to the pelvis or perineum. Spontaneous rupture of the internal iliac artery is described mostly in the presence of an aneurysm, with atherosclerosis, connective tissue disease, infection, and trauma as causative factors. It most often presents with abdominal pain and neurologic or urologic symptoms. We present an unusual case of a spontaneous rupture of the internal iliac artery that presented as a vulvar hematoma in a nulliparous woman that was successfully treated with selective arterial embolization and surgical evacuation. The literature is reviewed and management options discussed.
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PMID:Vulvar hematoma secondary to spontaneous rupture of the internal iliac artery: clinical review. 1948 25

Connective tissue diseases are associated with increased morbidity and mortality related to a higher rate of cardiovascular events and higher prevalence of subclinical atherosclerosis. Atherosclerosis is now considered a multifactorial process where autoimmunity and chronic inflammation play an important pathogenic role. In systemic autoimmune rheumatic diseases in general, and in systemic lupus erythematosus in particular, atherosclerosis cannot be explained by traditional cardiovascular risk factors alone. Cellular and humoral mechanisms, together with specific factors associated with the disease itself and/or its treatments, have been advocated to explain the acceleration of arterial wall organic damage in these patients. Endothelial dysfunction, carotid intima-media thickness and plaque evaluations provide accurate detection of atherosclerotic process at a preclinical stage, before appearance of clinical disease, allowing preventive measure introduction with the aim to modify the cardiovascular risk in subjects with systemic autoimmune rheumatic diseases.
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PMID:Accelerated atherosclerosis in systemic lupus erythematosus and other connective tissue diseases. 2047 58

Systemic sclerosis (SSc) is a connective tissue disease characterised by widespread vascular lesions and fibrosis of the skin and internal organs. Cardiac involvement is recognised as a poor prognostic factor when clinically evident. Primary myocardial involvement is common in SSc. Increasing evidence strongly suggests that myocardial involvement is related to repeated focal ischaemia leading to myocardial fibrosis with irreversible lesions. Reproducible data have shown that this relates to microcirculation impairment with abnormal vasoreactivity, with or without associated structural vascular abnormalities. Consistently, atherosclerosis and macrovascular coronary lesions do not seem to be increased in SSc. Myocardial involvement leads to abnormal systolic and diastolic left ventricular dysfunction and right ventricular dysfunction. Sensitive and quantitative methods have demonstrated the ability of vasodilators, including calcium channel blockers and angiotensin converting enzyme inhibitors, to improve both perfusion and function abnormalities further emphasising the critical role of microcirculation impairment. Recent quantitative methods such as tissue Doppler echocardiography and magnetic resonance imaging have underlined these results.
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PMID:Primary myocardial involvement in systemic sclerosis: evidence for a microvascular origin. 2105 May 45

Pseudoxanthoma elasticum (PXE) is a generalized connective tissue disorder in which there is calcification of elastic fibers within arteries, eyes, and skin. Characteristic features include yellow-orange papular skin lesions, angioid streaks radiating out from the optic discs, and arterial calcification. The prevalence in the general population varies widely from 1/70,000 to 1/160,000. PXE has an autosomal recessive inheritance pattern and results from mutations in the ATP-binding cassette transporter C6 (ABCC6) that has been mapped to 16p13.1. Over 300 loss-of-function mutations have been identified. Individuals with PXE may come to forensic attention because of sudden death involving accelerated coronary atherosclerosis with acute myocardial ischemia, systemic hypertension, mitral valve prolapse, restrictive cardiomyopathy, gastrointestinal hemorrhage, and cerebral ischemia or hemorrhage. Because of the heritable nature of the disease, family counseling and screening are in order when previously unsuspected cases are encountered at autopsy.
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PMID:Pseudoxanthoma elasticum and sudden death. 2121 Aug 5

Systemic lupus erythematosus is an autoimmune connective tissue disorder that affects multiple organs. While the clinical manifestations may vary in intensity over time and be associated with chronic disease, occasional cases occur where sudden and unexpected death has occurred. Cardiovascular disease is common, with accelerated atherosclerosis, intravascular thrombosis associated with antiphospholipid syndrome, and hypertensive cardiomegaly. Vasculitis with superimposed thrombosis may result in critical reduction in blood to vital organs, such as the heart and brain with infarction. Mesenteric ischemia may be caused by vasculitis, thrombosis, and accelerated atherosclerosis and may result in lethal intestinal infarction. Other diverse causes of sudden death include myocarditis, epilepsy, pulmonary hypertension, pulmonary thromboembolism, and sepsis. The autopsy evaluation of such cases requires careful examination of all organs with extensive histological sampling to include blood vessels, and microbiological sampling for bacteria, viruses, and fungi.
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PMID:Lethal manifestations of systemic lupus erythematosus in a forensic context. 2130 76

Although mammography is primarily used for the detection of breast cancer, it can occasionally reveal breast abnormalities related to extramammary disease. Cardiovascular diseases such as congestive heart failure and central venous obstruction may manifest as venous engorgement and breast edema at mammography. Pathologic arterial calcifications seen at mammography can indicate an underlying risk factor for accelerated atherosclerosis such as chronic renal failure. Connective tissue diseases including rheumatoid arthritis, systemic lupus erythematosus, dermatomyositis-polymyositis, and systemic scleroderma typically manifest with bilateral axillary lymphadenopathy, and stromal calcifications are also seen in the latter three disease processes. Some diseases such as neurofibromatosis type 1 and filariasis may manifest with pathognomonic findings at mammography, whereas other systemic diseases such as Wegener granulomatosis, sarcoidosis, and amyloidosis can manifest as nonspecific breast masses that are indistinguishable from breast cancer and usually require tissue biopsy for confirmation. Knowledge of the imaging characteristics of various systemic diseases affecting the breast will aid the radiologist in differentiating systemic disease from suspect breast lesions, thereby helping ensure appropriate follow-up. Furthermore, recognition of systemic diseases such as Cowden syndrome that are associated with an increased risk of breast cancer will allow the radiologist to recommend appropriate surveillance.
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PMID:Mammographic signs of systemic disease. 2176 40

Pseudoxanthoma elasticum is a rare, inherited connective tissue disorder associated with coronary and peripheral arterial disease and accelerated atherosclerosis in medium sized arteries. We describe 110-month symptom-free survival in a patient with pseudoxanthoma elasticum who underwent coronary bypass using the left internal mammary artery at 56 years of age. The vessel was evaluated pre-operatively with angiography to determine suitability, and he has not required further investigation or intervention due to lack of symptoms.
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PMID:Evaluation of arterial grafts prior to coronary bypass in pseudoxanthoma elasticum. 2190 98


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