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 relatively high incidence of heart failure is noted among patients with systemic lupus erythematosus (SLE) without clearly defined clinical causes. To evaluate left ventricular performance in patients with SLE without evidence of cardiovascular disease, noninvasive measurement of the systolic time intervals was carried out. Simultaneous recording of the electrocardiogram, phonocardiogram and carotid arterial pulsation were obtained in 25 patients with systemic lupus erythematosus and compared with 22 normal subjects. The patients with SLE had a shorter left ventricular ejection time (P less than 0.05), a longer pre-ejection period (P less than 0.02) and an increased ratio of pre-ejection period/left ventricular ejection time (P less than 0.005). These abnormalities on ventricular function were independent of age, duration of the disease, hypertension, renal involvement, anemia, immunologic activity and corticosteroid treatment. Several etiologic possibilities are discussed and the clinical usefulness of this method to detect and follow-up the cardiac dysfunction in systemic lupus erythematosus is emphasized.
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PMID:Myocardial involvement in systemic lupus erythematosus. A noninvasive study of left ventricular function. 69 53

The medical records of patients presenting to the Hammersmith Hospital hypertension clinic between 1971 and 1981 were examined to determine presenting clinical data, treatment regimes, and both cardiovascular and non cardiovascular mortality and morbidity. When compared with 1004 patients receiving treatment other than hydralazine 310 patients on hydralazine had a significantly higher risk of developing renal disease (RR = 2.71) in men, and severe weight loss in women (RR = 3.06). Renal disease risk also tended to be high in women on hydralazine (RR = 1.95) compared with all other treatments, but this was not statistically significant and could be explained by poorer renal function and significantly higher untreated blood pressure in the hydralazine treated group at presentation. The 422 patients who were treated with methyldopa but not hydralazine had similar risk factors for cardiovascular disease compared with a group of 167 who received hydralazine but not methyldopa. Comparisons of event rates failed to find significant differences in morbidity or mortality between these two groups. The age adjusted male mortality was 14/1000 patient years on hydralazine and 12/1000 on methyldopa and 13/1000 and 6/1000 years for women respectively. There was no evidence of an increased risk of either renal disease (RR = 0.3 in men, RR = 0.3 in women) on hydralazine or weight loss (RR = 0.7 in men, RR = 1.6 in women), with similar presenting data. Systemic lupus erythematosus was a rare complication (2 of 314) of treatment with hydralazine.
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PMID:Risk of serious morbidity associated with hydralazine versus methyldopa treatment in hypertensive patients. 205 Jan 66

The prevalence of SLE has increased throughout the world, due in part to the recognition of milder forms. Significant renal disease is now less common but late cardiovascular disease is being reported more often. The latter was previously attributed to steroid therapy, but we believe that the thrombotic tendency associated with antiphospholipid antibodies provides a significant contribution. Infection still ranks high in the mortality statistics in SLE, despite the move to more conservative treatment.
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PMID:Survival in systemic lupus erythematosus. 328 90

Because no systematic analysis of drug fever has been done, there has been no means for testing the validity of published characterizations of this clinical entity. We reviewed the clinical characteristics of 51 episodes of drug fever in 45 patients hospitalized at two Dallas hospitals between 1959 and 1986, and 97 episodes reported in the English literature between 1966 and 1986. Unlike characterizations found in textbooks and review articles, we found relative bradycardia in a minority of cases reviewed; little risk associated with rechallenge unless underlying cardiovascular disease was present; no characteristic fever pattern; a highly variable lag time between the initiation of the offending agent and the onset of fever; an infrequent association with either rash or eosinophilia; and no apparent association of drug fever with systemic lupus erythematosus, atopy, female sex, or advanced age.
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PMID:Drug fever: a critical appraisal of conventional concepts. An analysis of 51 episodes in two Dallas hospitals and 97 episodes reported in the English literature. 356 71

Antinuclear antibodies (ANA) can be induced by some drugs used in the treatment of cardiovascular disease. The reported frequency with which these antibodies are detected in patients varies widely. This variation results from a number of factors. The sensitivity of the ANA assay is influenced by the selection of substrates, the concentration of antisera and characteristics of the detection systems such as ultraviolet microscopes or electrophoretic apparatus. The incidence of ANA also varies with age and sex of the patient, being more common in older people and in females. Identification of a drug suspected of producing ANA demands a careful evaluation of the data with precisely standardised laboratory procedures and comparison of data with appropriate control groups of untreated and treated patients. Cardiovascular drugs associated with increased ANA incidence can be considered in two categories: A) A few drugs induce ANA in most patients if therapy is continued for long enough at high enough dosage. Many of these patients develop systemic lupus erythematosus like-syndromes. This group includes procainamide, hydrallazine at high doses and practolol. B) A further group of drugs produces ANA in 20 to 30% of patients, few if any, of whom develop SLE. Methyldopa and acebutolol are clearly in this category, while there is some evidence that labetolol, guanethidine and hydrallazine at low doses may also be implicated. Some very preliminary evidence suggests those patients on the beta-adrenoceptor blocking drugs atenolol, metoprolol and exprenolol exhibit a mildly increased incidence of ANA, but there is no evidence to suggest associated SLE. Only patients who develop ANA while on treatment with category A drugs require careful monitoring for SLE.
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PMID:Antinuclear antibodies and cardiovascular drugs. 610 97

Neuropathologic examination of an autopsy series of 54 patients of various types of CVD revealed a very high frequency of pathologic changes both in brain parenchyma (in 81%) and vessels (in 78%). A broad but continuous spectrum of primary vascular alterations was observed, ranging from fibrinoid deposits in intact or necrotizing vessel walls to fibrohyalinosis and endothelial proliferations. In acute SLE showing LE cells within brain tissues, immune complex deposits were observed for the first time in brain vessels, in addition to similar deposits in the plexus chorioideus and in hematoxylin bodies. Secondary complications are frequently affecting the brain in CVD; they are mainly sequels of systemic atherosclerosis, hypertension, thromboemboli from SLE endocarditis, cardiac, hepatic or renal dysfunctions, or infections and should be clinically differentiated from primary brain involvement in CVD to ensure the appropriate therapeutic measures.
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PMID:Brain pathology in the collagen vascular diseases. 611 36

Among early life SLE mice, the male F1 hybrids of NZW X BXSB crosses are unique by their much earlier onset of glomerulonephritis (GN) (evident by 2 1/2 months of age), progressive hypertension, and high frequency of degenerative cardiovascular disease (CVD) with myocardial infarcts. In contrast, their female counterparts and the other kinds of SLE mice have later onset of GN, minimal hypertension, and lower incidence of CVD. The etiopathogenesis of these F1 males' disease was investigated by reciprocally transferring syngeneic lymphoid cells into lethally irradiated F1 male and female mice. As a result, female recipients of male lymphoid cells developed accelerated GN, hypertension, and severe CVD, but the male recipients of female lymphoid cells (at comparable ages) had delayed SLE, remained normotensive, and were spared coronary or myocardial damage. These findings strongly indicate that the hypertension and CVD of these F1 males originate from immunologic abnormalities rather than from other nonlymphoid factors.
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PMID:Transfer of renovascular hypertension and coronary heart disease by lymphoid cells from SLE-prone mice. 671 79

Estrogen replacement therapy has been demonstrated to shift the lipoprotein profile toward a less atherogenic one with concomitant increases in HDL and reductions in LDL cholesterol and serum triglycerides. Estrogen, however, has also been implicated in playing a significant role in autoimmune disease and may be involved with disease incidence and progression. The MRL/lpr mouse strain represents an autoimmune disease model with features resembling systemic lupus erythematosus including high-titer autoantibodies, glomerulonephritis, and vasculitis. In the present study, the effects of estrogen treatment on serum lipoprotein profiles were investigated by fast protein liquid chromatography in female MRL/lpr mice, in the MRL/++ strain with a milder form of disease, and in control Balb/c mice. Treatment of MRL/lpr mice for periods of 1 week or longer with pharmacologic doses of estrogen resulted in a significant increase in the amount of cholesterol carried on LDL particles. The up to eightfold increase in LDL cholesterol was less significant in the MRL/++ or Balb/c mice. Maximal increases were observed at 1 to 2 mg/kg of estrogen agonists, and the effect on LDL cholesterol increases was inhibited by tamoxifen. The HDL-to-LDL shift in cholesterol observed in estrogen-treated autoimmune mice correlated with an increase in apolipoprotein E, primarily on larger HDL particles. In addition to the increase in LDL cholesterol, hormonal treatment also resulted in a shift in triglycerides from the VLDL to the LDL fraction in both normal and autoimmune mice. These results suggest that pharmacologic doses of estrogen may contribute to cardiovascular disease progression by shifting the relative distribution of cholesterol from HDL to LDL in this murine model of lupus.
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PMID:Estrogen-induced alterations in lipoprotein metabolism in autoimmune MRL/lpr mice. 758 27

Cardiovascular disease is one of the main causes of morbidity and mortality in patients with systemic lupus erythematosus (SLE). The observation that the disease may affect all cardiac tissues, although frequently in a subclinical fashion, has come to attention only recently after the introduction of non-invasive sensitive cardiac imaging technology in clinical practice. We review the current perspective of this topic, placing special emphasis on what is known and what is not known regarding cardiac disease in the pediatric population with SLE. Our current lack of information calls for the initiation of collaborative research in this area.
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PMID:Cardiac function in systemic lupus erythematosus. 756 94

Descriptive and analytic clinical research investigations dealing with systemic lupus erythematosus have focused on disease manifestations involving the heart, kidneys, and central nervous system, the complications of corticosteroid therapy, particularly cardiovascular and peripheral vascular disease, and outcomes of pregnancy. Studies exploring prognostic factors in patients with lupus nephritis as well as risk factors for the development of cardiovascular disease emphasize the importance of control of comorbid conditions, particularly hypertension and hyperlipidemia, in preventing poor outcomes in patients with systemic lupus erythematosus. The effectiveness of parenterally administered pulse cyclophosphamide has been demonstrated in patients with severe central nervous system involvement, and the effectiveness of plasmapheresis in patients with thrombotic thrombocytopenic purpura was reviewed.
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PMID:Clinical features of systemic lupus erythematosus. 839 8


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