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)

A total of 104 patients with scleroderma were examined. Anticardiolipin antibodies were detected in 37.5 per cent of the patients with systemic scleroderma and in 3 per cent of healthy individuals; they were more often detected in 46.8 per cent of the patients with diffuse affections of the skin, atherosclerosis, Raynaud's syndrome accompanied by ulcero-necrotic affections of the skin as compared to patients with restricted affections of the skin (sclerodactylia and focal scleroderma)--29.8 per cent. No significant changes in the frequency of detecting a rheumatic factor, antibodies to Scl-70 were revealed in subgroups of patients with scleroderma, positive and negative anticardiolipin antibodies. Of the greatest interest is a significant difference in levels of C-reactive protein which were high in half of the patients with anticardiolipin antibodies. Anticentromere antibodies were detected twice as more often in patients without anticardiolipin antibodies that corresponded to systemic sclerodermia with minimum involvement of the skin into the pathological process. It is suggested that ulcero-necrotic affection of the skin in systemic sclerodermia is associated with C-reactive protein but it is not of an immunocomplex nature.
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PMID:[Anti-cardiolipin antibodies and other immunological disorders in patients with systemic scleroderma]. 209 88

Ketanserin is the archetype of a new class of cardiovascular drugs, the 5HT2 (S2) serotonergic receptor antagonists. In humans, ketanserin inhibits serotonin-induced vasoconstriction and platelet activation. In addition, it reduces platelet hyperactivity, blood viscosity and total serum cholesterol. The antihypertensive effect of ketanserin is more pronounced in older people, in whom it decreases blood pressure gradually to normal levels. It lowers systemic vascular resistance resulting in a reduction of pre- and afterload. It improves vascular compliance and reduces left ventricular hypertrophy. Ketanserin improves the microcirculation of the skin, in particular capillary blood flow. Placebo-controlled studies have established that ketanserin prevents amputations in patients with atherosclerosis, enhances ulcer healing in patients with scleroderma and reduces the frequency and duration of attacks in patients with Raynaud's disease. In a placebo-controlled trial the on-treatment analysis of 3071 patients with intermittent claudication (the PACK-trial) showed a 23% reduction of severe cardiovascular events with ketanserin, suggesting that ketanserin may prevent complications of atherosclerosis. The accumulated clinical evidence indicates that serotonergic antagonism opens new perspectives in the treatment of cardiovascular disease. Current clinical research with ketanserin further explores its potential as a vascular protective agent.
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PMID:Ketanserin: a novel cardiovascular drug. 213 Sep 34

An 80-year-old white man presented with gangrenous lesions involving several distal phalanges of his left hand and an elevated erythrocyte sedimentation rate (ESR). Temporal artery biopsy showed patchy destruction of the internal elastic lamina by mononuclear cell infiltration, consistent with the diagnosis of temporal arteritis. After amputation of gangrenous lesions, he was discharged taking prednisone (60 mg/day). Twelve months after discharge there was no recurrence of ischemic manifestations and ESR was normal. Association of digital gangrene and elevated ESR should alert the clinician toward this diagnosis once other diseases such as atherosclerosis, scleroderma, lupus erythematosus, periarteritis nodosa have been ruled out.
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PMID:Temporal arteritis revealed by upper limb gangrene. 271 2

Inflammation is frequently associated with changes in the surrounding connective tissue. Inflammatory mononuclear cells (MNC) produce biologically active molecules, cytokines (CK), which may regulate the growth and function of connective tissue fibroblasts. In this article, we review the characteristics of lymphocyte and monocyte CK which appear to be involved in regulating fibroblast recruitment, proliferation, and matrix synthesis. Whereas these MNC products are important in normal physiologic wound healing, an imbalance of these CK may lead to pathophysiologic fibrosis and/or destruction of connective tissue components. Clinical states associated with MNC-mediated connective tissue pathology include scleroderma, rheumatoid arthritis, diffuse pulmonary idiopathic fibrosis, sarcoidosis and atherosclerosis. Characterization of the molecular pathways linking inflammatory mononuclear cells and fibrosis may provide avenues for therapeutic intervention.
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PMID:Cytokines and fibrosis. 353 33

In this review, the cardiac lesions which develop in association with the various collagen-vascular diseases are described. In rheumatoid arthritis, the most frequent lesions are: fibrous obliterative pericarditis, with pericardial deposits of calcium, fibrin, cholesterol, and rheumatoid granulomas; granulomatous or nonspecific myocarditis; valvulitis, vasculitis, and amyloid deposits. In ankylosing spondylitis, the lesions involve mainly the valves (aortic and mitral valves) and the aorta. In systemic lupus erythematosus, the predominant cardiovascular lesions are: pericarditis, Libman-Sacks endocarditis, nonspecific myocarditis, vasculitis with fibrinoid necrosis, and acceleration of atherosclerosis. In scleroderma, the main cardiac lesion is fibrosis with only scanty inflammatory cells; pericarditis and nonbacterial thrombotic endocarditis also occur. In dermatomyositis/polymyositis, fibrous or fibrinous pericarditis can occur, as well as myocarditis with infiltrates of lymphocytes and plasma cells and with degeneration and necrosis of myocytes; valvulitis is uncommon except when the disease is related to mucinous adenocarcinoma. In polyarteritis nodosa, various stages of necrotizing vasculitis involve all layers of the arterial walls; foci of myocardial necrosis of various sizes can occur in association with these lesions; cardiac hypertrophy related to hypertension and pericarditis related to uremia, may also be found. In Wegener's granulomatosis, pericarditis, inflammatory infiltrates, necrotizing granulomas, and vasculitis have been observed in the heart.
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PMID:Cardiovascular lesions in collagen-vascular diseases. 391 76

A unifying concept that excessive proliferation of cells and turnover of cellular matrix contribute significantly to the pathogenesis of several diseases, including cancer, atherosclerosis, rheumatoid arthritis, psoriasis, idiopathic pulmonary fibrosis, scleroderma and cirrhosis of the liver, is presented. As corollaries to this concept, the following topics are considered: (1) the role of polypeptide hormones and hormone-like mediators in the initiation, promotion and maintenance of proliferative responses; (2) alterations in collagen metabolism and collagenase activity; (3) the role of proteinases; (4) the potential use of inhibitors of proteinases for prevention of disease; and (5) the potential use of inhibitors of proliferative polypeptide hormones for prevention of disease. As specific proteolytic and proliferative biochemical mechanisms which contribute to the pathogenesis of disease become identified, there is a unique opportunity to develop new pharmacologic methods of prevention.
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PMID:Proliferative diseases. 626 92

We evaluated left ventricular function in 10 scleroderma patients with signs and symptoms suggestive of congestive heart failure. M-mode and two-dimensional echocardiography demonstrated normal to increased systolic function in all patients. The presence of pulmonary venous congestion on the chest radiograph was not useful in assessing left ventricular systolic function. Five of nine patients with normal to increased left ventricular ejection fraction (LVEF) had increased cardiothoracic ratios and increased pulmonary vascular markings. Left ventricular hypertrophy was associated with a worse New York Heart Association functional class, more pulmonary vascular congestion, and greater left atrial size. In the presence of normal systolic function and ventricular hypertrophy, diminished left ventricular diastolic compliance may account for the cardiac dysfunction in these patients. Cold pressor testing induced peripheral Raynaud's phenomenon in nine of nine patients; however, no ST segment changes or chest pain was provoked. In seven of nine patients there was no abnormal fall in LVEF. The mechanism for the fall in ejection fraction seen in two patients may be related to an increase in afterload or myocardial ischemia secondary to coronary atherosclerosis. We found little to suggest that a myocardial Raynaud's phenomenon affects left ventricular perfusion or systolic function. Clinical signs and symptoms of congestive failure as well as chest radiographs are poor indicators of impaired systolic function in scleroderma patients. Based on these findings, it appears that evaluation of left ventricular systolic function should include echocardiographic or angiographic study before such patients are treated for heart failure with inotropic agents.
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PMID:Left ventricular function at rest and during Raynaud's phenomenon in patients with scleroderma. 650 43

We utilized a standardized in vitro method which employs transmission electron microscopy to monitor the degree of surface activation (cytoplasmic spreading) and amount of aggregation displayed by platelet populations from 314 patients with one of five distinct rheumatic diseases and from 72 normal subjects. The percentage of patients in each group whose platelet populations were hyperactive was as follows: polymyalgia rheumatica, 75 percent; scleroderma, 65 percent; primary gout, 61 percent; rheumatoid arthritis, 57 percent; and degenerative joint disease, 40 percent. Pair-wise contrasts performed after an analysis of variance suggest the following differences and similarities: (1) the mean differential platelet count of the normal subjects differed from that in each disease state; (2) the platelet responsivity in patients with degenerative joint disease most closely resembled that in normal subjects; (3) the platelet response in polymyalgia rheumatica plus temporal arteritis was the most abnormal; and (4) platelet response in scleroderma, rheumatoid arthritis, and gout closely resembled each other. The increased platelet response in vitro may reflect the in vivo presence of disease-related "risk factors" (hyperuricemia, immune complexes, and atherosclerosis). Those patients with "triggered" platelet populations may be appropriate candidates for antiplatelet therapy.
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PMID:A comparative study of platelet reactivity in arthritis. 694 59

Embolic disease is often overlooked as a cause of digital ischemia. Unilateral symptoms, in particular, should suggest the possibility of emboli arising from the subclavian or more distal upper extremity vessels. Emboli may originate in the subclavian artery as the result of atherosclerosis at its origin or arterial injury secondary to thoracic outlet compression. Arteriography can be useful in the identification of upper extremity emboli and their source, and should include studies of the aortic arch, proximal subclavian artery, and digital arteries. Retrograde subclavian injections may be required to adequately demonstrate the origin of the subclavian artery. Magnification technique is often essential in differentiating small digital artery emboli from primary arterial diseases, such as Buerger disease or scleroderma.
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PMID:Digital ischemia: angiographic differentiation of embolism from primary arterial disease. 697 89

Raynaud's syndrome manifests as a progressive color change of the fingers in response to cold, vibration or stress; the digits first turn white, then blue and finally red. The condition is called Raynaud's disease when it is a benign, primary condition. When it is secondary to another disease, such as lupus, scleroderma or atherosclerosis, it is termed Raynaud's phenomenon. Laboratory tests, i.e., complete blood count, chemistry screen, antinuclear antibody, lupus erythematous test and rheumatoid factor, should be used to seek underlying diseases before the symptoms are manifest. Other tests should be selected as indicated by the history and physical. There are many adjustments in lifestyle and working conditions that the patient can use to minimize the symptoms of Raynaud's syndrome. The primary care provider has an important role in teaching patients to protect their hands from the effects of cold, stress, nicotine and vibration. Adaptive devices and protective clothing minimize the symptoms of Raynaud's syndrome.
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PMID:The diagnostic puzzle and management challenge of Raynaud's syndrome. 845 39


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