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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with systemic lupus erythematosus may develop premature atherosclerosis, notably coronary artery disease. A group of 10 patients with peripheral vascular disease presenting with intermittent claudication or gangrene were studied from a group of 563 patients followed prospectively at the Wellesley Hospital Lupus Clinic. These 10 patients were compared with the next lupus clinic patient matched for age and sex, with respect to demographic characteristics and risk factors. The patients and controls did not differ significantly in lupus activity criteria count, partial thromboplastin time, the number with antibody to cardiolipin, number receiving steroids or mean steroid dose, family history of atherosclerosis, hyperlipidaemia, smoking, hypertension or use of oral contraceptives. The risk factors for developing peripheral vascular disease were a longer duration of systemic lupus erythematosus and a longer duration of use of steroids. Eight of the 10 patients had coexistent coronary artery disease or transient ischaemic attack.
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PMID:Peripheral vascular disease in patients with systemic lupus erythematosus. 154 39

Lid tumors appear to invite the physician to make a diagnosis at first glance. This poster displays examples of lid tumors that occur in the context of malignancies, inflammatory and metabolic diseases and phacomatoses. The most frequent primary sites in metastatic eyelid tumors are the breast, the lung and cutaneous melanoma. Because of their comparatively low incidence and variable appearance these lid tumors are, at least in the beginning, often misinterpreted. Careful differential diagnosis may help in avoiding the diagnostic pitfalls of the masquerade syndromes. Lid tumors associated with sarcoidosis, lupus erythematosus discoides, lupus vulgaris, syphilis are briefly mentioned. Xanthelasmas occur more frequently in diabetics than in the normal population. About 5% of patients with xanthelasma suffer from hyperlipidemia. Neurofibromas and cavernous hemangiomas of the lid may accompany von Recklinghausen's and Sturge-Weber's diseases.
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PMID:[Tumorous eyelid changes in systemic diseases]. 161 52

We investigated the anticardiolipin antibody (ACA) in a series of patients with cerebral infarction without systemic lupus erythematosus (SLA). Clinical and laboratory data were assessed from a series of 250 non-SLE patients with cerebral infarction who visited our clinic from 1988 to 1990. The concentration of anticardiolipin IgG antibody was measured by an enzyme-linked immunosorbent assay technique. An elevated ACA level was defined as one which was greater than 3 standard deviations above the mean level for normal controls. We examined the CT findings and risk factors for stroke such as hypertension, diabetes mellitus, hyperlipidemia and cardiac disease. Laboratory data such as the platelet count, the presence of lupus anticoagulant and a biologic false-positive test for syphilis were also investigated. Among the 250 patients with infarction, IgG ACA was detected in 22 (8.8%). There was no significant difference in incidence of ACA between the patients with cerebral thrombosis and those with cerebral embolism. On CT scan, multiple cerebral infarcts were noted in 18 of the 22 patients. As regards the location of the infarct, the cerebral cortex together with the basal ganglia was more common than isolated lesions of the cortex or basal ganglia. Concerning the risk factors for stroke, hypertension was noted in 12, diabetes mellitus in 2, hyperlipidemia in 2 and cardiac disease in 2. Lupus anticoagulant and thrombocytopenia were not detected in any of the cases. A biologic false-positive test for syphilis was observed in one case. Dementia was present in 12 of the 22 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anticardiolipin antibody in cerebral infarction]. 191 23

Between 1974 and 1988, 7 myocardial infarctions occurred in 6 (4 men, 2 women) out of 400 systemic lupus erythematosus patients. Their ages at the onset of lupus ranged from 13 to 44 years (m = 26). Four had renal involvement. Control of lupus in all 6 patients required high-dose steroids (at least 1 mg/kg/d of prednisone). Myocardial infarction occurred 4 to 19 years after the onset of lupus (m = 13). One patient died of cardiogenic shock. When the infarction occurred, only one patient was undergoing a lupus flare, while the disease was quiescent or slightly active in the 5 others. One patient had no risk factors for atheroma but had been taking steroids for 10 years. Among the other 4, one had hypertension, another had hyperlipidemia and 3 were smokers; they had been on steroids for 2, 4, 11 and 13 years. Coronary angiogram showed occlusion in all 4, but atheroma in only 2 patients. Lupus anticoagulant was present in 3 of these 4 patients. The mechanisms responsible for coronary occlusion in lupus patients are probably complex and interwoven. In addition to "classical" factors (i.e., vasculitis or steroid-induced atheroma), other factors, such as antiphospholipid antibodies and/or smoking, may play an important thrombogenic role.
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PMID:[Myocardial infarction in systemic lupus erythematosus. 7 cases in 6 patients]. 228 5

The pathogenesis of avascular necrosis of bone (ANB) was investigated in 111 patients with systemic lupus erythematosus (SLE) (24 with ANB, 87 without ANB); patients' ages, corticosteroid treatment, clinical and laboratory features associated with SLE, and haemostatic profiles were all taken into account. The mean ages of patients with and without ANB at the time of diagnosis of SLE was 24.1 and 31.2 years respectively. The mean maximal daily dose of prednisolone in the group with ANB was 50.8 mg, which was significantly higher than the dose (41.8 mg) in the group without ANB. Disease features of SLE, such as Raynaud's phenomenon, hyperlipidaemia, nephrotic syndrome, hypertension, and disease activity, were not found to be related to ANB. The percentage of patients who had lupus anticoagulant as well as a shorter activated partial thromboplastin time was greater in those with ANB than in those without. Multiple factors may be involved in the pathogenesis of ANB in SLE, and it is suggested that haemostatic abnormalities, which could be influenced by corticosteroids and young ages, play some part in the development of ANB.
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PMID:Avascular necrosis of bone in systemic lupus erythematosus: possible role of haemostatic abnormalities. 250 41

The results are reported of a clinical and laboratory evaluation of the use of a random-access centrifugal analyzer linked to a personal computer in the management of the routine workload of a hemostasis laboratory. Over a three-month period, prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin clotting time (TCT), and derived fibrinogen (Fib) were performed on a total of 929 samples. Included in the study were 448 samples from patients receiving anticoagulants (oral anticoagulants, 228; heparin, 166; heparin and warfarin, 130) and 351 samples from patients requiring coagulation screens (PT, APTT, TCT, Fib). Tests were done in parallel with tilt-tube manual techniques and the results correlated. The correlation coefficients were PT, 0.99; TCT, 0.72; APTT, 0.96; Fib, 0.97. Discrepancies were analyzed and were due to hypofibrinogenemia and hyperlipidemia. The poorer correlation coefficient of TCT was attributable both to lower reproducibility of the manual test and the effect of dysfibrinogenemia or FDPs in liver disease. In no case was an abnormality or diagnosis missed using the centrifugal analyzer. In several cases the increased sensitivity of the analyzer improved the detection of the lupus anticoagulant. The use of automation was accompanied by a major reduction in workload and reagent costs. The machine has been used to assay a wide range of coagulation tests by clot based and chromogenic substrate methods. In conclusion, a programmed centrifugal analyzer is a safe, efficient, and flexible way of automating routine coagulation tests. It widens the reportoire of tests performed in the Hemostasis laboratory by using a machine capable of being used in other areas of pathology.
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PMID:Automation of routine coagulation testing using a random access centrifugal analyzer. 334 69

Conflicting data exist with respect to the existence and clinical manifestations of a hyperlipidemic arthropathy. Reasonable evidence supports the existence of a migratory polyarthritis similar to rheumatic fever in patients homozygous for type II hyperlipidemia. Although similar complaints have been described in patients heterozygous for this condition, findings have been inconsistent among various reports. It is possible that high lipid levels are required to induce rheumatic complaints, and these are found predominantly in homozygous patients. Even so, rheumatic syndromes appear to be more attributable to periarthritis because evidence of inflammatory arthritis is largely lacking. In contrast, Achilles tendinitis appears to be associated with heterozygous type II hyperlipidemia and presumably is based on lipid deposits within the tendon. Gout is an accepted association of type IV hyperlipidemia. In addition, oligoarticular symptoms have been described with type IV hyperlipidemia. However, no consistent clinical entity has emerged. Drugs used in the treatment of hyperlipidemia are associated with a variety of rheumatic problems, including proximal myopathy and lupus-like syndromes. The most commonly implicated drugs are the hydroxymethylglutaryl-coenzyme A reductase inhibitors and the fibric acid derivatives.
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PMID:Rheumatic manifestations of hyperlipidemia and antihyperlipidemia drug therapy. 826 12

Vascular damage in systemic lupus erythematosus (SLE) occurs through vasculitis, premature atherosclerosis, and hypercoagulability (predominantly due to the antiphospholipid antibody syndrome). In the Hopkins Lupus Cohort, a prospective cohort study, the incidence of thrombosis is 2 per 100 person-years of follow-up. Markers of immune-complex mediated injury (high anti-dsDNA and low C3), atherosclerosis (hypertension, hyperlipidemia, homocysteine) and antiphospholipid antibodies (lupus anticoagulant or anticardiolipin) are independent predictors of thrombosis. Hydroxychloroquine use is protective against future thrombosis.
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PMID:Thrombosis and systemic lupus erythematosus: the Hopkins Lupus Cohort perspective. 879 94

Hydroxychloroquine is used by 35% of SLE patients enrolled in the Baltimore Lupus Cohort. Eighty per cent of patients who took hydroxychloroquine at cohort entry remain on it six years later. In addition to its role for disease manifestations of lupus, hydroxychloroquine may be indicated for the prevention of disease or treatment-induced complications, including hyperlipidemia, diabetes mellitus, liver function test elevation and thrombosis.
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PMID:Hydroxychloroquine use in the Baltimore Lupus Cohort: effects on lipids, glucose and thrombosis. 880 5

Both immune and nonimmune mechanisms are operant in lupus nephritis. Recent findings have begun to elucidate fundamental questions in the pathogenesis of the disease. Genetic linkage studies have identified susceptibility loci contributing to nephritis in lupus-prone mice. Polymorphisms of the Fc gamma Rlla gene have been found to correlate with the development of renal disease in black Americans and white Europeans. Genetic factors are important in determining both predisposition to nephritis and outcome (and likely response to therapy). In lupus nephritis, prevention of tissue injury involves effective immunosuppressive therapy and aggressive management of hypertension and hyperlipidemia. Although with intensive immunosuppressive therapy most lupus patients achieve remission, a substantial number of these patients either do not respond, respond partially, or relapse after discontinuation of therapy. Moreover, the toxicity of available immunosuppressive drugs is substantial, suggesting that alternative therapeutic regimens are needed. In the future, other inhibitors of inflammatory, immune, vasoactive, proteolytic, and growth-promoting mediators are likely to play a role in the management of lupus nephritis.
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PMID:Lupus nephritis. 894 44


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