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

Normal human peripheral blood lymphocytes cultured in vitro with lupus sera (LS) were studied for their possible immunoglobulin (Ig) secretion using reverse haemolytic plaque assay (RHPA). Plaque forming cells (PFC) produced in cultures with LS (2,323 +/- 858 PFC/10(6) cultured cells) significantly increased in number compared to the control cultures with normal human serum (206 +/- 43, P less than 0.05). However, the artifactual nature of the PFC formation due to cytophilic Ig in LS subsequently became evident from the kinetic curves, trypsinization or medium change at the end of the culture period, radiation of cells on the first day of culture, or by depletion of nylon wool column-adherent cells from the culture system. These cytophilic Ig were observed in 56% of the sera obtained from untreated lupus patients. Thus, their possible interference with the resultant spurious plaque formation might be difficult to eliminate when performing RHPA in lupus patients.
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PMID:Pseudoplaque formation by cytophilic immunoglobulins in the sera of lupus patients as measured using reverse haemolytic plaque assay. 704 57

Although lupus vulgaris is the most common form of cutaneous tuberculosis seen in Europe, the incidence has steadily declined and it is now rarely seen. We report a case in a 69-year-old lady who presented with a 10-year history of a slowly growing plaque on the left cheek. Skin biopsy confirmed caseating granulomata, and acid-fast bacilli were seen. She was commenced on triple antituberculous therapy with good effect.
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PMID:Lupus vulgaris--a case report. 767 99

In western countries, acute myocardial infarction is the commonest cause of morbidity and mortality [19]. An occlusive coronary thrombus on an ulcerated atherosclerotic plaque in the coronary arteries is the etiological event in more than 90% of patients with Q-wave myocardial infarction [38]. The underlying abnormality in non-Q-wave myocardial infarction is often a ruptured atherosclerotic plaque, which acts as a nidus for the deposition and activation of platelets. In this case, thrombosis occurs, but may not be totally occlusive, or an early spontaneous recanalization may occur. On the other hand, some clinical trials showed that a prolonged treatment with antiplatelet drugs significantly reduces the recurrence of coronary ischemia. Thus, atherosclerosis is a necessary condition for myocardial infarction, but it is not sufficient in that it usually needs the occurrence of thrombosis. However, only 25-30% of these thrombotic events are prevented by the administration of antiplatelets drugs. In recent years, epidemiological studies identified some hemostatic parameters whose abnormalities may help predict the risk of ischemic events: fibrinogen [14], plasminogen activator inhibitor-1 (PAI-1) [3], lipoprotein(a) [46], anticardiolipin antibodies (ACA) and lupus anticoagulant (LA) [10], leukocyte count [34], blood viscosity [34]. Some of these, such as fibronogen and PAI-1 are acute-phase proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma predictors of ischemic complications of atherosclerosis: open issues. 806 Dec 44

A 40-year-old man presented with an ulcerated tumour in a fibrotic plaque on the dorsum of his left foot. Due to severe localized scleroderma, the patient had been treated with azathioprine 10 years earlier. Histopathology of the excised tumour revealed an anaplastic squamous cell carcinoma within a scar of localized scleroderma. The case demonstrates that not only patients with tense scar tissue following burning, congelation, chronic radiodermatitis, lupus vulgaris or lupus erythematosus but also patients who have had localized scleroderma may run a greater risk of developing squamous cell carcinoma. Immunosuppressive therapy has to be discussed as an additional risk factor in our patient. Therefore, narrow clinical follow-up was recommended for early detection of relapse.
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PMID:Squamous cell carcinoma in localized scleroderma following immunosuppressive therapy with azathioprine. 810 25

We describe a patient with subacute cutaneous lupus erythematosus, widespread pruritic papulosquamous plaques, and hypocomplementemia. Skin biopsy specimens revealed liquefaction degeneration and colloid bodies and dyskeratotic cells in basal and suprabasal layers. An immunofluorescence study revealed deposits of IgG, IgM, and C3 at the dermalepidermal junction in a bandlike pattern, and particulate IgG deposition in the basal and suprabasal layers. Treatment with prednisolone (15 mg/day), chloroquine phosphate (200 mg/ day), cyclosporine (5 mg/kg daily), and gold (10 mg/day) failed to reduce pruritic plaque formation, and pulse methylprednisolone therapy led to only a transient remission. Clinical exacerbations correlated with a decrease in complement levels. The disease was successfully controlled with dapsone (75 mg/day) and prednisolone (25 mg/day).
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PMID:Widespread pruritic plaques in a patient with subacute cutaneous lupus erythematosus and hypocomplementemia: response to dapsone therapy. 869 14

The family of antiphospholipid antibodies includes antibodies binding to cardiolipin in serological test for syphilis, antibodies prolonging the clotting time in lupus anticoagulant test, antibodies reacting with plasma phospholipid-binding proteins, such as beta 2-glycoprotein I and prothrombin, and antibodies binding to oxidized low-density lipoprotein (LDL). Antiphospholipid antibodies are traditionally associated with arterial and venous thrombosis in patients with primary or secondary antiphospholipid syndrome. The recent studies, especially those on patients with myocardial infarction, extend the concept of antiphospholipid antibodies, and suggest that they play a role also in atherosclerosis. Based on the clinical studies and immunological findings, it seems that the differences in the specificity of antiphospholipid antibodies may reflect to their pathogenetic mechanisms and, finally, to their clinical consequences. The present review suggests that antibodies to oxidized LDL may not interfere directly with blood coagulation, but seem to have importance in the inflammation of the vessel wall in atherosclerosis and in vasculitis. Instead, antibodies to beta 2-glycoprotein I and to prothrombin show a closer association with thrombosis. It is possible that in the atherosclerotic plaque, the plasma proteins, such as beta 2-glycoprotein I or prothrombin, are bound to the endothelial surface and antibodies to cryptic epitopes revealed in these proteins are induced. These antibodies may contribute to the formation of atherosclerotic thrombosis by changing the balance of haemostasis toward hypercoagulative state.
Lupus 1996 Oct
PMID:Antiphospholipid antibodies and atherosclerosis. 890 78

We identified a group of 24 young (less than 50 years of age) women with isolated, premature atherosclerotic aortoiliac occlusive disease and attempted to identify distinguishing hemostatic characteristics. Most of these patients (62%) presented with acute thromboembolic events (blue toe syndrome, n = 6; macroemboli, n = 6; or aortoiliac thrombosis, n = 3). Aortoiliac reconstruction (aortoiliac endarterectomy, n = 10, aortobifurcation bypass grafts, n = 6; and percutaneous angioplasty, n = 4) was complicated by early thrombosis in 6 of 20 cases (30%), (1 of 10 endarterectomies, 4 of 6 bypass grafts, and 1 of 4 angioplasties). Fresh thrombus overlying an atherosclerotic plaque was a common finding at surgery. This observation and the relatively high incidence of thromboembolic events led us to hypothesize that a characteristic hemostatic profile might underlie the remarkably similar clinical presentations of these women. Levels of antiphospholipid antibodies (anticardiolipin antibodies and lupus anticoagulant), plasminogen activator inhibitor-1, fibrinogen, antithrombin III, protein C, protein S, plasminogen, prothrombin fragment F1 + 2, and D-dimer were determined for these young women and for 21 age-matched white female control subjects without vascular disease and nine white male patients with aortoiliac occlusive disease (mean 61 years, range 43 to 74 years). The incidence of anticardiolipin antibodies was 42% (8 of 19) in the female patients, which was significantly elevated (p = 0.028). The female (62.5%) and male (100%) patients had significantly elevated D-dimer levels (p < 0.001). Deficiencies of antithrombin III, protein C, and protein S were rare. A unique pattern of premature aortoiliac atherosclerosis exists in some young women. Intra-arterial thromboembolic events are common at presentation and complicate surgical management. The role of antiphospholipid antibodies remains uncertain.
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PMID:Young women with advanced aortoiliac occlusive disease: new insights. 898 71

We describe a 56-year-old woman with Mycobacterium avium complex infection of the skin. She presented with a granulomatous plaque studded with pustules and crusts on the cheeks and bridge of the nose. The appearance resembled lupus vulgaris. The lesion responded well to antituberculous treatment within 9 months. An association of Mycobacterium avium complex with squamous cell carcinoma of the cervix is emphasized.
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PMID:Primary cutaneous infection with Mycobacterium avium intracellulare complex resembling lupus vulgaris. 906 47

Lupus erythematosus panniculitis (LEP) is an unusual clinical variant of lupus erythematosus (LE) in which the cutaneous inflammatory reaction occurs primarily in the deeper corium. The common clinical features of LEP includes asymptomatic, firm, sharply defined nodules. The histologic findings are characterized by nonspecific panniculitis composed of lymphoid cells, plasma cells, and histiocytes with varying degrees of necrobiotic changes with fibrinoid deposits. In our case, a 24-year-old male patient visited our clinic with non-tender, hard, plaque-like lesions and overlying erythema on the left zygomatic, nasal, and submandibular area. Histopathologic and direct immunofluorescent findings of the lesion were compatible with LEP. His skin lesions waxed and waned with systemic steroid or hydroxychloroquine therapy. He has responded well to a combination therapy of hydroxychloroquine and quinacrine.
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PMID:Lupus panniculitis treated by a combination therapy of hydroxychloroquine and quinacrine. 935 Jan 2

Atherosclerosis is a process initiated by accumulation of macrophages in distinct areas of endothelial cell damage and uptake of large amounts of lipids. Recently, it has been shown that the immune system plays an active part in the progression of the atherosclerotic plaque although its precise role has not yet been elucidated. Anticardiolipin antibodies (aCL) are generally found in the sera of patients with the antiphospholipid syndrome (APS) and are associated with a prothrombotic state. Several authors have demonstrated that aCL can activate platelets and endothelial cells as well as increase oxidized low density lipoprotein (LDL) uptake by macrophages. In the present study we sought to assess the effect of immunization with aCL (Ab1, leading to the production of mouse aCL-Ab3) on the progression of atherosclerosis. Two groups of 8-weeks old female LDL-receptor knockout mice (n = 13 per group) were immunized with IgG purified from the serum of an APS patient or with normal human IgG, respectively. The aCL immunized mice developed high titres of 'self' aCL (detected using the standard aCL ELISA) as compared with the normal human IgG immunized mice, whereas no differences were noted between both study groups with respect to the serum lipid levels. The extent of fatty streak formation was significantly higher in the aCL immunized mice in comparison with the human IgG injected mice (mean aortic lesion size of 5308 +/- 471 microns2 vs 1027 +/- 184 microns2, respectively, P < 0.01). The immunohistochemical analysis of the atherosclerotic plaques from both mouse groups did not display differences in cellular composition. The results of the study show that mouse aCL induced by immunization with human aCL from an APS patient enhance atherogenesis in LDL-RKO mice and imply that these antibodies may play a role in atherosclerosis development in patients with the APS.
Lupus 1997
PMID:Atherosclerosis in LDL-receptor knockout mice is accelerated by immunization with anticardiolipin antibodies. 941 88


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