Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following a renal PTA a 63-year-old man developed a multisystem illness caused by disseminated cholesterol embolism. The clinical manifestations were changing myalgia, peripheral ischaemia, livedo reticularis, episodic hypertension, eosinophilia and rapidly progressive renal insufficiency. The diagnosis was made on the clinical picture and confirmed by skin biopsy. Ultimately, chronic intermittent haemodialysis was necessary. There is no specific treatment available for this disease. It is possible that this complication occurs more frequently, but often remains subclinical.
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PMID:[Terminal kidney insufficiency caused by disseminated cholesterol emboli as a complication of intra-arterial manipulation]. 252 70

The two patients described in this article are among the first to have been diagnosed with extensive bowel infarction as a result of cholesterol embolization following cardiac catheterization. The presence of acute hypertension, renal insufficiency, livedo reticularis, and gangrenous skin changes are characteristic manifestations of the multiple cholesterol emboli syndrome. Additionally, gastrointestinal symptoms and melena may herald ischemia and infarction of the alimentary tract. Anticoagulation and thrombolytic therapy are relatively contraindicated in this syndrome and may, in fact, be a precipitating cause. The prognosis is usually poor; however, survival is possible with aggressive medical and surgical therapy, despite extensive infarction of the gastrointestinal tract and other organs. Prevention remains the most critical aspect of management of this potentially catastrophic illness.
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PMID:Multiple cholesterol emboli syndrome. Bowel infarction after retrograde angiography. 280 4

Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiovascular manifestations of systemic lupus erythematosus: current perspective. 286 Jun 99

A 51-year-old woman with Sneddon's disease presented with transient right hemifield loss of vision and transient right-sided weakness. Over the preceding decade she had experienced a slow decline in mental function. She also had hypertension, migraine, and a mixed seizure disorder. She had skin changes typical for generalized livedo reticularis but she did not have Raynaud's phenomenon or winter ulcerations. Her disease was not understood until the stroke-related symptoms were associated with the skin abnormalities. We review the neuro-ophthalmic manifestations of Sneddon's disease and add data from our case to the growing body of fact that suggests that Sneddon's disease may be an immunologically mediated vasculopathy.
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PMID:Sneddon's disease presenting with visual loss and dementia. 297 41

Two young women (aged 32 and 25 years) with systemic lupus erythematosus and heart valve lesions in association with antiphospholipid antibodies are presented. In addition to the presence of the 'lupus anticoagulant' and false positive Venereal Disease Research Laboratory (VDRL) tests, both patients had high levels of IgG anticardiolipin antibodies. The first patient additionally had contraceptive induced chorea, chorea gravidarum, seven miscarriages, livedo reticularis, pulmonary embolism, and thrombocytopenia and developed culture negative endocarditis as well as hypertension. The second patient, who had presented with hypertension, developed aortic and mitral regurgitation, suspected myocarditis, manifested transient ischaemic attacks, and responded well to anticoagulation and steroid treatment.
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PMID:Diagnostic and therapeutic problems in two patients with antiphospholipid antibodies, heart valve lesions, and transient ischaemic attacks. 314 42

Milian's white atrophy (1929), linked by English authors with livedoid vasculitis and segmentary hyaline vasculitis, is "the microvascular expression of diseases of variable aetiologies". It can be isolated, without vasculitis (idiopathic or secondary to an inflammatory livedo); the variety with vasculitis, most often observed, stems from loco-regional causes (above all from post-phlebitic venous hypertension) but also from general causes (collagenoses, infections, carcinamatoses). The need for an attempt at a better approach to white atrophy is clear.
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PMID:[The viewpoint of the dermatologist toward white atrophy]. 378 32

This paper presents 3 cases of generalized livedo racemosa and cerebral infarction in female patients ages 27, 39, and 42 years. Livedo racemosa is characterized by a broken, irregular pattern on the skin. It is probably caused by patchy impairment of cutaneous arteriolar circulation, resulting in reflectory venous dilation and stasis of blood. Livedo may accompany diseases such as atherosclerosis, diseases with intravascular occlusion, and collagen disorders, indicating a need for a careful search for an underlying condition. These 3 patients demonstrated several risk factors for atherosclerosis: hypertension (1 patient), oral contraceptive use (2 patients), and smoking (2 patients). The clinical findings in these 3 cases provide support to the theory that a chronic endarteritis obliterans of the small and medium-sized arteries is the underlying cause for the skin and neurologic manifestations in livedo racemosa associated with stroke.
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PMID:Livedo racemosa generalisata and stroke. 402 92

The cases of 3 middle aged women admitted to the hospital because of cerebrovascular accidents in whom examination disclosed idiopathic livedo reticularis are reported. This association has only been described recently, but does not seem fortuitious; some of the clinical manifestations are characteristic but histology is usually nonspecific and the basic abnormality remains unknown. The main problem is prognostic and therapeutic. In an attempt to prevent neurological defects, tobacco and contraception should not be permitted for those women showing widespread livedo acquired reticularis; high blood pressure should be treated systematically. (author's modified)
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PMID:[Livedo reticularis and cerebrovascular accidents]. 673 16

Six cases of suspected multiple cholesterol emboli syndrome were identified by a review of reports contained in the company's records of adverse event reports. Antecedent risk factors in these reports included cardiac catheterization, thrombolytic therapy, translumbar aortography, renal arteriography, subclavian arteriography, abdominal aortography, and heparinization. Unlike the commonly reported subacute presentation, onset occurred during or immediately after catheterization in 5 of the 6 patients reported. Acute renal failure; hypertension; back, leg, and/or abdominal pain; and livedo reticularis were the events most frequently reported. Angiographers should consider multiple cholesterol embolization when multiple organ system dysfunction occurs during or immediately after intraarterial catheterization.
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PMID:Multiple cholesterol emboli syndrome--six cases identified through the spontaneous reporting system. 766 80

Sneddon's syndrome is a rare disease characterised by cerebrovascular ischaemic attacks and generalised livedo. Since previous observations, other symptoms were described: involvement of heart, of kidney, arterial hypertension, complicated obstetric or gynaecologic history in women. Prognosis is highly variable, depending on extent and speed of progression of cerebrovascular changes, which can lead to severe permanent mental deterioration. In livedo, histopathology shows pathological changes of small to medium-sized dermal arteries in a distinct time sequence: an early phase localized in endothelium followed by a late fibrotic phase. No specific laboratory findings are found. Recently some cases were reported in association with antiphospholipids antibodies. The etiopathogeny of Sneddon's syndrome is still unknown and could result from different processes: progression to an autoimmune disease such as lupus erythematosus, primitive endarteritis obliterans, or a new clinical expression of the antiphospholipid antibodies syndrome. At present, none of the therapeutic modalities provides significant improvement.
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PMID:[Sneddon syndrome]. 770 55


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