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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aortic valve calcification is associated with atherosclerosis in the general population. We investigated the prevalence of and associates of aortic valve calcification in systemic lupus erythematosus (SLE). One-hundred and ninety-nine SLE patients enrolled in a clinical trial had aortic valve calcification assessed by helical CT. The patients had a mean age of 44.3 +/- 11.4 years and were 92% female, 61% Caucasian, 34% African-American, 2% Asian and 2% Hispanic. Aortic valve calcification was present in 1.5%, whereas coronary calcium was found in 43% and carotid plaque in 17%. Among cardiovascular risk factors, hs-CRP (P = 0.0592), fibrinogen (P = 0.0507), and lipoprotein(a) (P = 0.0250), were associated with aortic valve calcification. Prednisone use (P = 0.049) and use of methotrexate (P = 0.0174) were also associated with aortic valve calcification. Aortic valve calcification was associated with antiphospholipid antibody positivity (0.0287) (lupus anticoagulant, by dilute Russell viper venom time). It was not associated with coronary calcium or carotid plaque. Aortic valve calcification, although rare in SLE, was associated with some novel cardiovascular risk factors and with a marker of hypercoagulability (lupus anticoagulant). In contrast to the general population, aortic valve calcification in SLE is not associated with subclinical measures of atherosclerosis, such as coronary calcium or carotid plaque.
Lupus 2006
PMID:Aortic valve calcification in systemic lupus erythematosus. 1721 93

There has been a sea change in our understanding of atherosclerosis. We have come a long way from the days where eating too much fat and not getting enough exercise and having the wrong genetic background was thought to be the entire story. A few years ago, the cardiologists began to embrace inflammation as a possible pathogenetic mechanism and from that came high-sensitivity C-reactive protein testing for just about everyone. Chronic systemic inflammation became an area of interest. We have learned that it is more than just corticosteroid use that causes accelerated atherosclerosis in our rheumatoid and lupus patients. Even C-reactive protein may be a pathogenetic player, not only a diagnostic clue. Oxidized phospholipids and the cells that recognize them may be crucial in the evolution of the atherosclerotic plaque. Statins may be useful in suppressing inflammation, not only in suppressing cholesterol levels. And now even cardiologists are thinking about immune mechanisms! A strange world, but the beneficiaries of going through this looking glass will be our patients. A true understanding of this seems to have required a most circuitous route-sometimes you have to leave for a long journey before you can return and really see home for the first time.
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PMID:Basic science for the clinician 44: atherosclerosis: an immunologically mediated (autoimmune?) disease. 1755 86

Tinea corporis classically presents as an erythematous annular plaque with a scaly, centrifugally advancing border. However, sometimes vesicles and pustules are observed. Occasionally, even frank bullae appear secondary to severe inflammation. Diagnostic difficulties arise when atypical manifestations mimic other inflammatory skin diseases, including atopic or seborrheic dermatitis, subacute cutaneous lupus erythematosus, or vesicular diseases. We report five cases of atypical tinea corporis, where the initial clinical diagnosis was different from dermatophytosis. The differential diagnoses and the diagnostic difficulties related to atypical manifestations of fungal infections are discussed. Moreover, our cases emphasise the importance of conventional histological examination, which enables a fast, correct diagnosis.
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PMID:Atypical manifestations of tinea corporis. 1768 Oct 52

Our objectives were to evaluate the oral health and the masticatory system of 48 juvenile systemic lupus erythematosus (JSLE) patients and to compare them with 48 healthy children and adolescents. Demographic data, clinical manifestations and therapies of JSLE were reviewed. The DMFT index (DMFTI), the plaque (PI) and the gingival bleeding (GI) indices, dental relationship, facial profile, clinical dysfunction and mandibular mobility indices were evaluated. The two groups were homogeneous regarding age, gender, Brazilian social-economic class and dental decay index (P > 0.05). Of note, the medians of the PI and the GI were higher in JSLE patients than in controls (61.5 versus 38.10, P = 0.003 and 26.0 versus 15.95, P = 0.014; respectively). Likewise, a linear statistical correlation was evidenced between the JSLE duration and the GI (P = 0.017, r = 0.11), cumulative dose of prednisone and the PI (P = 0.01, r = 0.385) and cumulative dose of prednisone and the GI ( P = 0.001, r = 0.471). The clinical dysfunction and mandibular mobility indices were higher in JSLE patients versus controls (P = 0.002, P = 0.025). Moreover, the median of the mandibular mobility index was higher in JSLE patients who used at least one immunosuppressive than on those who did not use this medication (P = 0.0001). These results suggest that JSLE patients had an inadequate oral hygiene, higher incidence of gingivitis and temporomandibular joint dysfunction.
Lupus 2007
PMID:Oral health and the masticatory system in juvenile systemic lupus erythematosus. 1772 64

The morphological diagnosis of the plaque form of lupus vulgaris was made on the basis of distinct clinical features. An endeavor to supplement this diagnosis was made through laboratory investigations comprising total differential leukocyte count,erythrocyte sedimentation rate (ESR), immunoglobulin M (IgM), and polymerase chain reaction (PCR); the results of which were largely ambiguous. Regimented anti-tubular therapy (ATT) was utilized to arrive at the diagnosis. A perceptible regression of the lesions over the course of 6 weeks was remarkably beneficial to completing the treatment subsequently. ATT seems to bea feasible and well-conceived tool in the diagnosis of lupus vulgaris tuberculosis verrucosa cutis and pediatric scleroderma.
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PMID:Inadequacy of clinical and/or laboratory criteria for the diagnosis of lupus vulgaris, re-infection cutaneous tuberculosis: fallout/implication of 6 weeks of anti-tubular therapy (ATT) as a precise diagnostic supplement to complete the scheduled regimen. 1793 36

A 14-year-old girl presented with a 10-year history of a large crusted plaque over the right thigh for 10 years and small reddish plaque over the left upper back for 3 months. On routine evaluation, she was found to have hematuria. Skin biopsy from the lesion was suggestive of skin tuberculosis (lupus vulgaris), and kidney biopsy showed features of IgA nephropathy (IgAN). Fine-needle aspiration from the inguinal lymph node was consistent with granulomatous disease. The patient has been on anti-tubercular treatment, and the hematuria has subsided.
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PMID:Lupus vulgaris with tubercular lymphadenitis and IgA nephropathy. 1817 53

To determine the frequency of carotid plaque and intima-media thickness (IMT) in patients with systemic lupus erythematosus (SLE) and their association with risk factors in a Brazilian university setting. Carotid plaque and IMT were identified and measured by ultrasonography. Traditional risk factors and lupus-related factors were analysed. One hundred and seventy-two patients (women = 96%, age = 38 +/- 11 years) were evaluated. The frequency of carotid plaque was 9.3%. The median (IR) IMT was 0.60 mm (0.54-0.71 mm). Age, family history (FH) of premature coronary disease, low-density cholesterol (LDL-c) >100 mg/dL, hypertriglyceridemia, diabetes, hypertension, smoking, postmenopause, number of risk factors, Framingham risk score, age at diagnosis, duration of lupus, mucocutaneous manifestations and duration of prednisone use were associated with plaque (P < 0.05), univariate analysis. Nephritis, immunosuppressive therapy, intravenous methylprednisolone and a higher average daily dose of prednisone were associated with the absence of plaque. Independent predictors of plaque were smoking (P = 0.004), LDL-c >100 mg/dL (P = 0.044), Framingham score (P = 0.006) and absence of immunosuppressive therapy (P = 0.032). There was an independent correlation between IMT and age (P < 0.001) and duration of prednisone use (P = 0.020). Subclinical atherosclerosis was associated with traditional risk and SLE-related factors, especially the absence of immunosuppressive therapy. The present study suggests that the levels of LDL-c should be kept under 100mg/dL in lupus.
Lupus 2008 Feb
PMID:Carotid atherosclerotic alterations in systemic lupus erythematosus patients treated at a Brazilian university setting. 1825 Jan 33

The accelerated atherosclerosis that occurs in some patients with systemic lupus erythematosus (SLE) has a complex pathogenesis, including alterations in lipids, inflammation and the immune system. In this article, we review the evidence that peroxidase-related alteration of normal, protective high-density lipoprotein (HDL) converts them to pro-inflammatory HDL (piHDL), characterized by lower content of the cholesterol transport lipoprotein ApoA1 and impaired function of the antioxidant enzyme paroxonase, which prevents oxidation of low-density lipoprotein (LDL). Forty-five per cent of women with SLE have piHDL compared with 20% of patients with rheumatoid arthritis and 4% of healthy controls. The presence of piHDL increases risk for coronary artery events and carotid artery plaque. Another result of lipid oxidation in patients with SLE is generation of highly oxidized LDL and phospholipids (PL), probably stimulating antibodies to OxPL phospholipids. These antibodies along with promoting thrombosis also interfere with deposits of Annexin V onto endothelial cells, which probably promote increased instability of atherosclerotic plaque. Thus, piHDL and anti-OxPL promote plaque formation, plaque instability and thrombosis, accounting for some of the large increase in atherosclerosis and coronary artery events in SLE.
Lupus 2008 May
PMID:Atherosclerosis and systemic lupus erythematosus: the role of altered lipids and of autoantibodies. 1849 Apr 9

Tuberculosis is a major public health problem in both developing and developed countries. Cutaneous Tuberculosis constitutes a minor proportion of extra-pulmonary manifestations of Tuberculosis. Lupus Vulgaris (LV) is one of the clinical variants of Cutaneous Tuberculosis. A case of a large plaque type psoriasiform lesion of lupus vulgaris on the thigh, of 15 years' duration, in an 18-year-old girl is reported. This case highlights the ignorance level among the patients and consequent failure to avail proper anti-tuberculous treatment despite campaign in print and audio visual media.
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PMID:Psoriasiform lupus vulgaris. 1851 27

Ever increasing evidence supports the association between psoriasis and cardiovascular risk. Antiphospholipid antibodies (APAs), which can occur in many autoimmune diseases, are considered prothrombotic and have been associated with atherosclerosis. The aim of this study is to evaluate the prevalence and levels of APAs in psoriasis patients. Fifty patients with moderate to severe plaque psoriasis and 48 healthy subjects were investigated for lupus anticoagulant (LAC) by screening and confirmatory coagulation tests, as well as for antibodies against cardiolipin or beta2-glycoprotein I. Levels of APAs and LAC-related parameters were similar for patients with psoriasis and normal controls (p>0.05). APAs were found in only one psoriatic patient (2%) and in none of the controls. LAC was detected in 2 patients (4%) and in one subject of the control group (2.1%). These results suggest that the prevalence of APAs is not increased in plaque psoriasis as compared to the control group. The increased cardiovascular risk observed in psoriatic patients is therefore likely to be correlated to factors different from APAs.
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PMID:Is there an association between antiphospholipid antibodies and psoriasis? 1884 75


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