Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present here three cases of systemic Lupus Erythematosus which fulfilled the diagnostic criteria of the American Rheumatism Association. These three cases also had Chorea. This kind of association is not frequent and the cases here described are the last three of 32 published until now. We discusse in this paper the significance of the Chorea Syndrome and the probable causes originating it.
Arch Inst Cardiol Mex
PMID:[Lupus erythematosus and chorea (report of 3 cases)]. 43 58

We describe the clinical course and the postmortem cardiac findings in a 12 year old girl with systemic lupus erythematosus, complete heart block, renal failure and hyperkalemia. The conduction system was examined by serial section. The sinoatrial and atrioventricular nodes were found to be almost completely replaced by granulation tissue; we believe that this finding is related to the systemic lupus. The hyperkalemia is not considered to be the cause of the block, since the block persisted despite the lowering of the blood potassium level and the morphologic findings in this case are not found in hyperkalemia.
Am J Cardiol 1975 Feb
PMID:Conduction system in systemic lupus erythematosus with atrioventricular block. 111 91

Three patients, 24, 24 and 25 years of age, with systemic lupus erythematosus had signs of myocardial infarction. Two had serial electrocardiographic changes indicative of infarction without any cardiac symptoms. The third patient had clinical evidence of an acute massive myocardial infarction, which was proved at autopsy to be due to coronary atherosclerosis. This case is presented in detail and the association between systemic lupus erythematosus and myocardial infarction is reviewed. It is postulated that the relation between lupus erythematosus and coronary atherosclerosis is more than coincidental.
Am J Cardiol 1975 Feb
PMID:Myocardial infarction due to coronary atherosclerosis in three young adults with systemic lupus erythematosus. 111 92

A rare case of constrictive pericarditis in procainamide-induced lupus erythematosus syndrome is reported. After 6 months of procainamids therapy fever, pleuritic chest pain, arthralgia and muscle soreness developed in a 47 year old man. These symptoms were soon followed by the onset of acute pericarditis and rapidly accumulating massive pericardial effusion. After withdrawal of procainamide therapy and administration of corticosteroids in large doses, there was marked subjective improvement and rapid reduction in pericardial effusion. However, constrictive pericarditis with massive leg edema and ascites developed 6 weeks after admission as corticosteroid therapy was gradually discontinued. These manifestations subsided after pericardiectomy was performed.
Am J Cardiol 1975 Dec
PMID:Constrictive pericarditis in procainamide-induced lupus erythematosus syndrome. 119 52

Anticardiolipin antibodies (acLa) are associated with a thrombotic tendency (often involving cerebral ischemic events), are frequently present with systemic lupus erythematosus and have been found together with cardiac valve abnormalities. Previous studies evaluated patients characterized by the presence of acLa or lupus, precluding assessment of the frequency of acLa in those with valvular disease. This study aims to establish the prevalence of acLa in patients with valve disease in the absence of lupus and, furthermore, to determine the influence of acLa on the risk of cerebral events in valve disease. Eighty-seven consecutive patients with mitral or aortic regurgitation, or both, prospectively underwent enzyme-linked immunosorbent assay testing for immunoglobulin G (IgG) and M acLa, as did 24 normal subjects. AcLa values greater than or equal to 3 SD above the normal mean were considered "positive." Prior cerebral events were defined retrospectively. Of 87 patients with valvular disease, 26 had positive IgG acLa levels compared with 0 of 24 normal subjects (p less than 0.01). AcLa values did not vary with valve disease etiology. Focal cerebral events had occurred in 8 patients and were embolic or probably embolic in 7, including 7 of 26 IgG acLa-positive and 1 of 60 IgG acLa-negative patients (p less than 0.001). In the absence of lupus, IgG acLa is highly prevalent among patients with aortic or mitral regurgitation, or both; this association may indicate a relatively high risk for cerebral emboli.
Am J Cardiol 1992 Oct 01
PMID:Prevalence of anticardiolipin antibody in isolated mitral or aortic regurgitation, or both, and possible relation to cerebral ischemic events. 152 45

Over the last 10 years, our knowledge of immunologically mediated processes involving the myocardium appears to have made quantum leaps. New and important disease entities such as AIDS have appeared and the cardiologist now becomes an important member of the "AIDS team." Our understanding of "older diseases" such as sarcoidosis, Lyme disease, systemic lupus and other connective tissue syndromes has significantly increased. The concept of high-dose steroid therapy for these processes may, in fact, turn out to be futile and more selective, as less dangerous immunosuppression is being introduced. This concept has significantly advanced in the field of cardiac transplantation where immunosuppression has now been usurped by specific immunotherapy aimed at selective aspects of the immune sequence. New and exciting concepts will emerge from the molecular biology laboratory that will have direct bearing on the management of patients with cardiovascular disorders. This information explosion will force the cardiovascular physician to become more in tune with the world of immunology and molecular biology. Many obvious, significant problems remain, such as accelerated atherosclerosis in the transplant patient and the role of myocarditis in the patient with heart failure. However, it will truly be an exciting decade in which to work and watch the unraveling of these mysteries and hopefully, the study of today's problems will give way to solutions and a clearer understanding of the heart as a target of immune injury.
Curr Probl Cardiol 1991 Jun
PMID:The heart as a target organ of immune injury. 191 12

Early in the course of studies of the Spanish toxic oil syndrome it was recognized that vascular lesions were a major problem, most logically attributable to endothelial damage by the toxic oil. However, most clinical attention has been directed to the pulmonary complications and the evolution into a scleroderma-like illness later. In this study of 11 victims of the toxic oil syndrome careful postmortem studies of the coronary arteries and conduction system and neural structures of the heart demonstrated major injury to all those components of the heart. Obliterative fibrosis of the sinus node in four cases resembled findings in fatal scleroderma heart disease, and in eight the cardiac lesions resembled those of lupus erythematosus. The more impressive pathologic features involved the coronary arteries and neural structures, which were abnormal in every heart. The arterial disease included widespread focal fibromuscular dysplasia, but there was also an unusual myointimal proliferative degeneration of both small and large coronary arteries in five patients, four of whom were young women. In two hearts, portions of the inner wall of the sinus node artery had actually detached and embolized downstream. Coronary arteritis was rarely found. Inflammatory and noninflammatory degeneration of cardiac nerves was widespread. Fatty infiltration, fibrosis and degeneration were present in the coronary chemoreceptor. In most respects these cardiac abnormalities resemble those described in the eosinophilia-myalgia syndrome caused by an altered form of L-tryptophan. In both diseases there is good reason to anticipate more clinical cardiac difficulties than have so far been reported, and even more basis for future concern, especially relative to coronary disease and cardiac electrical instability.
J Am Coll Cardiol 1991 Nov 01
PMID:Cardiac abnormalities in the toxic oil syndrome, with comparative observations on the eosinophilia-myalgia syndrome. 191 15

A 36 year-old male patient developed acute pulmonary edema due acute mitral insufficiency as early manifestation of systemic lupus erythematosus. The patient was treated with supportive measures, oxygen, furosemide, and isosorbide dinitrate. He was started on prednisone 60 mg daily 14 days later, after the diagnosis of lupus was established. The patients is asymptomatic with mitral systolic murmur 5 months after hospital discharge.
Arq Bras Cardiol 1990 Sep
PMID:[Acute pulmonary edema as an early manifestation of systemic lupus erythematosus]. 209 26

A young patient with systemic lupus erythematosus was admitted to our hospital because of acute myocardial infarction, and treated by thrombolysis. Coronary angiography revealed a significant stenosis of the left anterior descending artery, together with an intraluminal thrombus. Clotting studies demonstrated an anticoagulant factor suggestive of lupus erythematosus. We conclude that thrombolytic therapy can be useful in patients with systemic lupus erythematosus who present with acute myocardial infarction, although some caution is needed in treatment.
Int J Cardiol 1990 Nov
PMID:Thrombolytic therapy for a patient with systemic lupus erythematosus and acute myocardial infarction. 226 45

Myocardial infarction has rarely been reported in patients with systemic lupus erythematosus but may develop late in the disease usually as a result of severe and accelerated atherosclerosis or coronary arteritis. A 32-year-old man with untreated and unrecognized systemic lupus erythematosus, in the absence of conventional coronary risk factors (except family predisposition) and definite extracardiac manifestations of systemic lupus erythematosus had a silent myocardial infarction early in the course of the disease. A coronary arteriogram revealed multiple stenosis of the left anterior descending artery and critical stenosis of the right coronary artery. It is our belief that lupus vasculitis is a likely contributing factor in the development of obstructive coronary disease in this patient.
G Ital Cardiol 1990 Jan
PMID:[Silent myocardial infarct as a main manifestation of systemic lupus erythematosus]. 232 60


1 2 3 4 5 6 7 8 Next >>