Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A thirty-three year-old woman with systemic lupus erythematosus (SLE) suffered from acute myocardial infarction. Prednisolone 20 mg/day was used because the signs of SLE, such as fever and decreased serum C3, levels, became aggravated on the fifth hospital day of acute myocardial infarction. Fatal cardiac rupture occurred on the twenty-second hospital day. At autopsy, extensive myocardial infarction with coronary artery thrombi and diffuse coronary arteritis were revealed. The rare clinical picture of a fatal cardiac rupture in the later phase of acute myocardial infarction and the precise dosage of prednisolone for her SLE are described.
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PMID:Cardiac rupture following acute myocardial infarction in systemic lupus erythematosus: case report. 238 46

To determine whether or not male (NZWXBXSB)F1 [WXB)F1) mice exhibiting a lupus-like syndrome died of acute myocardial infarction (MI), and whether acute MI is directly related to small coronary artery disease, acute and old MIs were examined histologically in 55 dead (WXB)F1 male mice and 30 age-matched, surviving (WXB)F1 male mice used as a control group. In each heart from the 15 dead mice with MI and the five surviving mice without MI, 300 to 400 5-microns-thick serial sections were made; every fourth section was stained. Acute MI was found in 35 (64%) dead mice and in one (3%) survivors, whereas old MI was found in 50 (91%) dead mice and 17 (57%) survivors: a significant difference between the dead and surviving mice. The MIs were numerous, scattered, and small in most mice. Quantitative analysis revealed that the percentage of acute MI and old MI in the left ventricular (LV) wall was 6% +/- 11% and 3% +/- 3% in the dead group, and 0.4% and 2% +/- 3% in the control group. This indicated that recurrent acute MI is a major factor in the death of the mice. Although all the epicardial major coronary arteries of the (WXB)F1 male mice were intact, significant stenoses were noted in the intramyocardial small arteries. The serial sections in the 15 dead mice with MI revealed 1) segmental occlusive thrombi in the infarct-related small coronary artery in 14 of the 20 foci of acute anemic MIs, two of the 18 foci of acute hemorrhagic MIs, and four of the 58 foci of old MIs; and 2) segmental intimal thickenings in the infarct-related small artery in six of the 20 foci of acute anemic MIs, two of the 18 foci of acute hemorrhagic MIs, and 56 of the 58 foci of old MIs. There was no evidence of small coronary artery disease in the surviving mice without MI. The thrombus would result in thickened intima as MI progresses from the acute to the old stage. Because it was established that acute MI of hemorrhagic type follows reperfusion after transient occlusion of the coronary artery, hemorrhagic acute MI with rare incidence of thrombi in this mouse suggests that thrombolysis occurs after occlusion due to thrombus formation. Thus, the pathogenesis of multiple MIs is occlusive thrombi, recanalization in small coronary arteries or both. Some of the mice had dilated cardiomyopathy (DCM)-like features (marked LV dilatation).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:High frequency of spontaneous acute myocardial infarction due to small coronary artery disease in dead (NZWxBXSB)F1 male mice. 259 79

A 26 year old woman with systemic lupus erythematosus, including malar rash, photosensitivity, and arthritis, developed a cerebrovascular accident and acute myocardial infarction. High titres to antinuclear factor, anti-DNA antibodies, positive Venereal Disease Research Laboratory (VDRL) test, and anticardiolipin antibodies were found in her serum. A possible association between the presence of anticardiolipin antibodies and the two major thrombotic events is discussed.
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PMID:Cerebrovascular accident and myocardial infarction associated with anticardiolipin antibodies in a young woman with systemic lupus erythematosus. 263 95

A 26-year-old Papuan woman with systemic lupus erythematosus (SLE) died following an acute myocardial infarction. Coronary arteritis was the likely pathogenesis of her cardiac damage. Some genetic and environmental factors relevant to Papua New Guinea are discussed.
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PMID:Acute myocardial infarction in a young Papuan woman with systemic lupus erythematosus. 281 82

This paper presents epidemiological data on the prevalence of 26 common (i.e., having a lifetime prevalence of more than 1 per 10(4) individuals in the population) multifactorial diseases in Hungary and estimates of detriment associated with them. The detriment is expressed using 3 indicators, namely years of lost life (LL), potentially impaired life (PIL) and actually impaired life (AIL). The total prevalence of these diseases in Hungary has been estimated to be about 6500 per 10(4) individuals in the population. This estimate is in agreement with published data for other parts of the world. On the basis of clinical severity, these diseases have been split into 3 groups, namely (1) very severe (schizophrenia, multiple sclerosis, epilepsy, acute myocardial infarction and related conditions, and systemic lupus erythematosus); (2) moderately severe and/or episodal or seasonal (15 entities including Graves' disease, diabetes mellitus, gout, affective psychoses, essential hypertension, peptic ulcers, asthma, etc.); and (3) less severe than those in the first 2 groups (varicose veins, allergic rhinitis, atopic dermatitis, Scheuermann disease and adolescent idiopathic scoliosis). The essential clinical and genetic aspects of these diseases are briefly discussed. With the exception of epilepsy, none of the diseases included in our list causes mortality between ages 0 and 19. However, they are among the leading causes of death between ages 20 and 69 and thereafter. A sizeable proportion of those with essential hypertension, diabetes mellitus, rheumatoid arthritis, etc. survive to 70 years and beyond, as do those with gout, glaucoma, allergic rhinitis, psoriasis, etc. Overall, about 16% of all deaths that occur in Hungary every year (all age groups) can be attributed to these diseases. The mean number of years of PIL covers a wide range (about 20-40, 12-70 and 40-60 for groups 1, 2 and 3, respectively), the overall mean being about 24 years. However, the nature and degree of impairment and the impact on the life quality of those afflicted differ for the different diseases. Likewise, the mean number of years of AIL (for which the interval between the mean age at premature retirement and mean age at death was used as a rough index) also spans a wide range from 16 to 45, and the overall mean is about 20 years. At the population level, the diseases considered in this paper cause about 2700 years of LL, 96,000 years of PIL and about 5800 years of AIL per 10(4) individuals in the population. Relative to Mendelian diseases as a whole, these multifactorial diseases are associated with much greater detriment (LL: 1.4 X; PIL: 30 X and AIL: 3.9 X).
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PMID:The load of genetic and partially genetic diseases in man. II. Some selected common multifactorial diseases: estimates of population prevalence and of detriment in terms of years of lost and impaired life. 305 77

A 32-year-old white woman presented with angina pectoris and an acute myocardial infarction (MI) complicated by congestive cardiac failure. Other symptoms and results of immunological investigation were highly suggestive of systemic lupus erythematosus (SLE). Thallium-201 scintigraphy confirmed an extensive MI, as initially suspected from an ECG. Cardiac catheterization delineated a poorly contracting left ventricle secondary to MI. Selective coronary angiography showed features suspicious of coronary arteritis involving the left anterior descending and left circumflex coronary arteries. Right ventricular endomyocardial biopsy failed to show any 'small-vessel disease', vasculitis or myocarditis. We suggest that the acute MI was caused by coronary arteritis due to SLE. Overview of the literature indicates that coronary arteritis is not as rare a complication of SLE as previously believed; however, acute MI is most unusual.
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PMID:Systemic lupus erythematosus with coronary vasculitis and massive myocardial infarction. A case report. 371 54

Acute myocardial infarction (AMI) is relatively rare in systemic lupus erythematosus (SLE), although other cardiac complications, such as pericarditis and myocarditis, occur frequently in this disease. A 20-year-old woman with documented SLE experienced a transmural anterior AMI due to thrombi in saccular aneurysms of the left main coronary artery and the proximal portion of the left anterior descending coronary artery. There were also saccular and fusiform aneurysms in the right coronary artery, but thrombi were not observed in them. Aorto-coronary bypass surgery was performed to salvage the viable myocardium and to prevent recurrent myocardial infarction and rupture or infection of these coronary aneurysms. Postoperative coronary angiography revealed a new small saccular aneurysm in the mid-portion of the right coronary artery. During this period, there was no immunological evidence of active SLE. It is important to ascertain whether such coronary aneurysms resulted from atherosclerosis or arteritis, because of the choice of the different therapeutic interventions. In this case, however, it was difficult to determine. It was speculated that these coronary aneurysms arose from an arteritic process, because the saccular aneurysm in the mid-portion of the right coronary artery was formed in less than three months, there were no coronary risk factors, and any microscopic evidence of atherosclerosis was not obtained in the aortic specimen during aortocoronary bypass surgery. Serial coronary angiographic studies are necessary for accurately diagnosing coronary artery disease. Anticoagulant therapy and antiinflammatory medication may be necessary to prevent myocardial infarction in patients with SLE, even if there is no immunological evidence of active SLE.
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PMID:[Myocardial infarction due to thrombi in coronary aneurysms in a young woman with systemic lupus erythematosus]. 378 87

A 19-year-old man with untreated systemic lupus erythematosus had an acute myocardial infarction. A coronary arteriogram five hours after the onset of symptoms revealed total occlusion of the left anterior descending coronary artery. Reperfusion was achieved by coronary thrombolytic therapy with urokinase. Four weeks later, a coronary arteriogram showed only minimal luminal irregularities at the original site of occlusion, where significant reduction in diameter could be induced by ergonovine maleate. This case suggests that coronary arterial involvement in systemic lupus erythematosus may be related to coronary arterial spasm.
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PMID:Acute myocardial infarction associated with systemic lupus erythematosus documented by coronary arteriograms. 400 40

A 41-year-old woman with chronic systemic lupus erythematosus (SLE), uncomplicated by sepsis or other "secondary infection," died of an acute myocardial infarction. All of the available necroscopic material was reviewed to determine whether acid-fast cell wall deficient bacteria (CWDB) could be demonstrated in vivo. Variably acid-fast coccoid forms, suggestive of CWDB, were observed in specially-stained (intensified Kinyoun acid-fast stain) microscopic sections of the heart, lungs, kidney, adrenal glands, brain, connective tissue, and other organs. Acid-fast "hematoxylin bodies" were also observed. The finding of variably acid-fast bacteria in postmortem tissue in SLE may relate to the current finding of variably acid-fast CWDB within the blood stream of "normal" and diseased persons. In addition, the finding of acid-fast bacteria may relate to the previous reports of similar bacteria in scleroderma, pseudoscleroderma, and cutaneous lesions of SLE. The further search for CWDB in necropsied cases of SLE may elucidate the possible pathogenic role, if any, of these microbes in SLE.
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PMID:Variably acid-fast bacteria in a necropsied case of systemic lupus erythematosus with acute myocardial infarction. 620 17

We describe the case of a young woman with systemic lupus erythematosus (SLE) who suffered an acute myocardial infarction (MI). The patient was treated by corticosteroids in addition to the usual management for acute MI. The role of arteritis in producing the infarction is also discussed.
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PMID:Myocardial infarction in a young woman with systemic lupus erythematosus. 696 50


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