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)

Patients presenting with Raynaud's phenomenon pose differential diagnostic problems. The question is whether the discolorations are a symptom of the benign primary type or a symptom of an underlying disease, mostly a connective tissue disease or an atherosclerotic occlusive disease, both having major prognostic implications. To evaluate whether Raynaud patients can be classified properly in the above-mentioned categories on clinical grounds we evaluated 225 patients using a checklist dealing with signs and symptoms supposed to be specific for primary Raynaud's phenomenon or the two major types of the secondary form. Complaints that started before the age of 20, reactive hyperaemia at the end of an attack and discolorations of the earlobes and the nose have a high predictive value for primary Raynaud's phenomenon. Trophic skin disturbances are rare in the latter but are rather specific for connective tissue diseases. In the case of arterial obstructive disease, the feet are always involved and risk factors associated with atherosclerosis are often present, whereas this type is specifically encountered in men in whom the complaints started over the age of 50 [corrected], and in whom signs of atherosclerotic vessel wall disease were seen elsewhere. In conclusion, in most patients who present with a Raynaud's phenomenon a complete history and physical examination are sufficient for a correct diagnosis. Supplementation with determination of anti-nuclear antibodies, measurements of the capillary perfusion and of the finger skin systolic pressure completes the diagnostic classification.
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PMID:The diagnostic value of clinical signs and symptoms in patients with Raynaud's phenomenon. A cross-sectional study. 207 8

Arterial occlusive disease of the upper extremity is most often due to posttraumatic occlusion of the ulnar artery. An embolic source of the ischemia should be considered most strongly when sudden ischemia or vasospasm is associated with atrial fibrillation or follows a myocardial infarction. Connective tissue disorders and several arteridities are infrequent causes of upper-extremity occlusive disease and can usually be detected by a thorough peripheral vascular examination and blood studies. Atherosclerosis of the upper extremity is usually localized to the region of the subclavian artery and can present as a subclavian steal syndrome or arm ischemia. Finally, upper-extremity venous occlusive disease occurs in association with the hypercoagulable state, venous endothelial injury, or arises in otherwise healthy patients because of venous impingement in the thoracic outlet.
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PMID:Occlusive vascular disorders of the upper extremity. 844 72

Pseudoxanthoma elasticum (PXE) is a rare inherited connective tissue disorder which is characterized by elastic tissue degeneration involving the skin, eyes and arteries. We describe the case of a hypercholesterolemic 25 year-old woman with typical genetic dominant form of PXE revealed by distal limb artery involvement after a pregnancy. In young adults with arterial disease, a non atheromatous cause should always be sought for, even if risk factors for atherosclerosis are present.
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PMID:[Pseudoxanthoma elasticum: a rare cause of leg artery diseases in young adults]. 912 Mar 74

Cell surface adhesion molecule expression is likely to be important in inflammation, atherosclerosis and cancer, and soluble forms of many of these molecules are present in plasma. We measured levels of the soluble form of platelet endothelial cell adhesion molecule-1 (sPECAM) by ELISA in the serum of 77 patients with frank atherosclerosis, 69 patients with inflammatory connective tissue disease, and 39 patients with cancer. Each group of patients was controlled by an equal number of age- and sex-matched healthy subjects. There was no difference between sPECAM in patients with atherosclerosis and their matched controls or between patients with connective tissue disease and their controls. However, sPECAM levels were lower (16.6 +/- 5.0 ng/ml, mean +/- SD) in patients with cancer than in their controls (21.1 +/- 4.4 ng/ml, P < 0.001). No differences were found in sPECAM levels between the major subgroups of each type of disease, or as a result of factors such as age, sex or smoking in the controls. In contrast to levels of many other soluble adhesion molecules, levels of sPECAM are not altered in inflammatory or atherosclerotic vascular disease and therefore appear to have little relevance in these conditions. However, there may be significant differences in sPECAM levels in patients with low levels in cancer. Additional investigations are therefore justified.
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PMID:Soluble platelet endothelial cell adhesion molecule-1 (sPECAM-1) in inflammatory vascular disease, atherosclerotic vascular disease, and in cancer. 960 25

Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease marked by immune-complex mediated lesions in small blood vessels of various organs, especially the kidneys, although other factors may also be implicated in the pathogenesis of the disease. This article focuses on the role of lipids in the progression of glomerular, vascular and tubulo-interstitial lesions in two patients with lupus nephritis associated with pronounced hyper- and dyslipidemia. The pathogenesis of progressive glomerulosclerosis in both patients appears to be multifactorial. In addition to immune complex mediated lupus glomerulonephritis, progressively active in the first patient, severe nephrotic-range persistent proteinuria, arterial hypertension associated with hyperfiltration and hyperperfusion injuries and, to a minor extent, hyper- and dyslipidemia were observed. Immunological and non-immunological factors were shown to contribute to the development of tubulo-interstitial lesions. In both patients, in addition to local immune deposits, prominent tubulo-interstitial lipid deposits were probably causally related to both hyperlipidemia and the increased permeability of the glomerular filtration barrier. Tubular lesions were highlighted by intracytoplasmic lipid droplets as well as small cleft-like spaces found to be impacted in the tubular lumina. They were seen to penetrate tubular epithelial cells and eventually lodge in the interstitium, surrounded by mononuclear cell infiltrates and foam cells. In both patients, hypertensive angiopathy and extraglomerular vascular immune deposits were demonstrated. In addition, in the second patient, arteriolar and small arterial hyaline was found at the age of 28 years to be full of lipids and calcium precipitates, suggesting a peripheral atherosclerosis-like process which never occurs as a natural age-related condition. In conclusion, all parts of the nephron may be involved in the pathogenetic process causally related or influenced by hyper- or dyslipidemia. Associated either with endothelial cell injury and consequent insudation of lipids in the vascular walls, glomerular filtration barrier injury with hyperfiltration, or tubulo-interstitial lipid deposition, the mechanism of tissue damage by lipids in all parts of the nephron shares similarities with the pathogenesis of systemic atherosclerosis.
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PMID:Role of lipids in the progression of renal disease in systemic lupus erythematosus patients. 1102 Sep 63

Large increases in mortality related to premature atherosclerosis with coronary artery disease and stroke have been reported in patients with systemic lupus erythematosus (SLE), antiphospholipid syndrome (APLS), or rheumatoid arthritis (RA). Studies found relative risks of 5 for myocardial infarction, 6 to 10 for stroke in SLE patients, and 3.6 for cardiovascular deaths in RA patients. The main risk factors for atherosclerosis included not only the classic factors identified in epidemiological studies such as the Framingham study (advanced age, high cholesterol levels, hypertension, diabetes mellitus, and obesity), but also prolonged glucocorticoid therapy, long duration of SLE, postmenopausal status, and heart failure. SLE per se is an independent risk factor. The current pathogenic hypothesis for atherosclerosis involves an inflammatory response (erythrocyte sedimentation rate, C-reactive protein, and fibrin), autoantibodies, immune complexes (containing antibodies to phospholipids, to oxidized LDLs, and to endothelial cells), cytokine-producing activated T cells, and bacterial or viral infections responsible for an immune response against heat shock proteins (endogenous HSP60 and its equivalent, bacterial HSP65). Early risk factor intervention and effective control of inflammation should be incorporated into the management of connective tissue disease with the goal of protecting patients against atherosclerosis.
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PMID:Atherosclerosis and connective tissue diseases. 1295 20

Systemic lupus erythematosus (SLE) is a connective tissue disease characterized by the formation of autoantibodies and immune complexes. The heart and lungs are among the organ systems commonly affected in SLE. Pericarditis, premature coronary atherosclerosis, pleuritis and pulmonary infections are the most prevalent cardiopulmonary manifestations. Other rare associations include myocarditis, coronary arteritis, acute lupus pneumonitis/pulmonary haemorrhage, acute reversible hypoxaemia and 'shrinking lung' syndrome. Current imaging modalities may provide earlier detection of subclinical disease, which may aid in preventing these potentially fatal complications. The response to treatment varies, depending on the presentation of disease. In this chapter we address the frequency, diagnosis and monitoring, and treatment regimens of cardiac and pulmonary involvement in patients with SLE.
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PMID:How to manage patients with cardiopulmonary disease? 1204 50

Although frequently asymptomatic, homozygous C2 deficiency (C2D) is known to be associated with severe infections and rheumatic disease. We describe the clinical findings in 40 persons with C2D from 33 families identified in Sweden over 25 years. Medical records covering 96% of the accumulated person-years were reviewed, giving a mean observation time of 39 years (range, 1-77 yr). Severe infection was the predominant clinical manifestation in the cohort: 23 patients had a past history of invasive infections, mainly septicemia or meningitis caused by Streptococcus pneumoniae, and 12 patients had repeated infections of this kind. Nineteen patients had at least 1 episode of pneumonia, and recurrent pneumonia was documented in 10 patients. Repeated infections occurred mainly during infancy and childhood. Systemic lupus erythematosus was found in 10 patients. Another 7 patients had undifferentiated connective tissue disease (n = 4) or vasculitis (n = 3). We found no correlation between susceptibility to invasive infection and rheumatologic disease. Cardiovascular disease occurred at a high rate, with a total of 10 acute myocardial infarctions and 5 cerebrovascular episodes in 6 patients. Causes of death among the C2D patients were infection (n = 5), acute myocardial infarction (n = 3), and cancer (n = 1). We suggest that severe infection may be the principal clinical manifestation of C2D. We also provide novel evidence for a possible role of C2D in the development of atherosclerosis consistent with findings in mannan-binding deficiency and experimental C3 deficiency. In addition, we confirm the well-known association between C2D and systemic lupus erythematosus.
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PMID:Hereditary C2 deficiency in Sweden: frequent occurrence of invasive infection, atherosclerosis, and rheumatic disease. 1564 97

Connective tissue diseases (CTD) lead to a high prevalence of common cardiac manifestations (pericarditis and myocarditis) and of ischemic coronary events with a considerable increase in cardiac mortality related to premature atherosclerosis. Although there are several techniques able to detect cardiac involvement in CTD patients, the most useful and non-invasive technique is echocardiographic exam which is able to detect not only valvular abnormalities, pericardial diseases and pulmonary hypertension but also left ventricular (LV) systolic or diastolic (regional or global) wall motion dysfunction. It is also well known that transesophageal echocardiography (TEE) can better identify cardiac abnormalities, vegetations and embolic sources. Symptomatic patients with positive stress echocardiographic exam or dipyridamole thallium imaging test should be referred for possible cardiac catheterization, especially if a large ischemic territory is involved. Until now, the echocardiographic evaluation of coronary artery tree consisted of assessing regional and global left ventricular systolic and diastolic function at rest and during pharmacological stress test. Recently, a new echocardiographic noninvasive method that allows direct assessment of coronary flow velocity in the mid-distal portion of left anterior descending artery (LAD) has been developed and validated. Advanced ultrasound technology (high-frequency broadband transducer with second harmonic capability) has now made possible a direct arterial visualization and measurement of coronary artery flow in left anterior descending in CTD patients with the assessment of coronary flow reserve (CFR).
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PMID:The role of echocardiographic techniques in connective tissue diseases. 1582 3

Vasculitis is considered to be secondary when it arises either in the context of a pre-existing connective tissue disease, as a result of direct infection with a limited range of organisms, especially viruses, or when it arises in response to exposure to a number of medications. Rheumatoid vasculitis is probably the most widely recognised form of secondary vasculitis, and in this article we review the incidence, clinical features and management of this condition. Infections may either trigger or cause some types of vasculitis. Drug therapy is a common cause of limited forms of vasculitis and may enhance our understanding of the mechanism of these diseases. The premature development of atherosclerosis in patients with existing connective tissue diseases or indeed primary vasculitis has been recognised for some time, and the underlying mechanisms are currently being studied. An appreciation of the complex and varied pathophysiology of secondary vasculitis may further our understanding of primary vasculitis.
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PMID:How to diagnose and treat secondary forms of vasculitis. 1585 99


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