Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Systemic Lupus International Collaborating Clinics/American College of Rheumatology (ACR) Damage Index (SDI) is an accepted instrument to ascertain damage. It has been shown to vary among different SLE populations. The aim of this study was to assess SDI score, pattern and factors related to damage in Brazilian SLE outpatients. The SDI was obtained in 105 patients with a median age of 41 (5-95%, 19-61.7) years and a median SLE duration of 127 (17.6-345.9) months. Patients had a median SDI of 2 (0-8) and 81.9% had some damage (SDI > 0). Damage was associated with a higher number of ACR criteria for SLE in multivariate analysis (OR = 2.32, 95%CI = 1.23-4.37, P = 0.009). Antiphospholipid syndrome (APS) (OR = 9.82, 95%CI = 2.74-35.23, P < 0.001), methylprednisolone pulses (OR = 3.91, 95%CI = 1.19-12.81, P = 0.024), age (OR = 1.70, 95%CI = 1.02-1.13, P = 0.011) and prednisone use duration (OR = 1.01, 95%CI = 1.002-1.02, P = 0.020) were related to severe damage (SDI > or = 4). Hypertension was associated with renal, cardiac and atherosclerotic damage, as cyclophosphamide pulses were with premature menopause. In conclusion, damage was very frequent in Brazilian SLE patients, mainly due to skin involvement, compared to other SLE populations. The presence of APS was the major independent contributor to the development of severe damage. Arterial hypertension was identified as a common risk factor for renal, cardiac and atherosclerotic damage.
Lupus 2003
PMID:Rate, pattern and factors related to damage in Brazilian systemic lupus erythematosus patients. 1459 30

Headache is a common feature in patients with systemic lupus erythematosus (SLE) and represents a significant source of patient discomfort. The exact prevalence of headache in SLE is unknown. The results of different studies widely vary, most likely due to the use of different classification for headache and the lack of controls in most studies. The relationship between headache and SLE is also unclear since it is difficult to determine which degree and type of headaches can be explained on the basis of chronic illness, or as part of the disease spectrum of SLE. No pathogenic mechanism has so far been described that can fully explain headache induced by SLE. The role of circulating cytokines, vascular injury, neuronal damage or antiphospholipid antibodies (aPL) in the development of headache in SLE patients is also a matter of debate. Other concomitant causes such as infection or hypertension should be excluded before assuming that headache is a feature of SLE activity. Therapeutic approach of headache SLE-related remains empirical and based on clinical experience.
Lupus 2003
PMID:Headache and systemic lupus erythematosus. 1471 15

There is a wide variation in the natural history of systemic lupus erythematosus (SLE) among different ethnic and geographical groups. Studies in Arabs are few and those in North Africans and especially in the Tunisian population do not exist. This study aims to demonstrate the demographic, clinical and laboratory characteristics of SLE Tunisian patients and to identify those at high risk for renal and neuropsychiatric involvements. One hundred patients with SLE (American College of Rheumatology criteria), seen at the Department of Internal Medicine of the University Hospital La Rabta in Tunisia over a 15-year period (1987 to 2001) were retrospectively enrolled. There were 92 women and eight men with an average age at the onset of disease of 32 years. Nineteen patients were aged over 50 years at the moment of SLE diagnosis (late-onset SLE). Of the patients, 78% had articular involvement, 53% photosensitivity and 63% malar rash. Serositis occurred in 45 patients of whom 16 had pericarditis and 29 had pleuritis. Nephritis was diagnosed in 43% of the cases and consisted always of glomerular nephritis, in three cases of which tubulointerstitial lesions were also observed. Comparison of patients with and without renal involvement showed that lupus nephritis was significantly associated with pericarditis (P = 0.03), arterial blood hypertension (P < 0.0001), cryoglobulinemia (P = 0.07) and antiphospholipid syndrome (P = 0.03). The SLEDAI at SLE diagnosis was significantly higher for lupus nephritis patients. Twelve patients with lupus nephritis died compared with three patients in the remaining group (P < 0.0001). Neuropsychiatric manifestations were observed in 25% of the cases. The mean age at SLE onset was significantly lower, the mean SLEDAI at SLE diagnosis and the mortality were significantly higher in the neuropsychiatric group than in the remaining group. Immunological features included antinuclear antibodies (100%), anti-DNA antibodies (56%), anti-Sm antibodies (61%), anticardiolipin antibodies (62%), anti-beta2GP1 (13%) anti-Rnp (23%) and hypocomplementemia (48%). The frequencies of pulmonary hypertension (25 versus 2%, P < 0.00001) and vascular thrombosis (25 versus 2%, P < 0.00001) were significantly higher in patients with positive anti beta2GP1 antibodies. The five-year survival rate in our series was 86%. The most frequent causes of death were active SLE and infections.
Lupus 2004
PMID:Systemic lupus erythematosus in Tunisia: demographic and clinical analysis of 100 patients. 1575 24

Antiphospholipid (aPL) antibodies entailing anticardiolipin (aCL) and anti-beta2 glycoprotein I (anti-beta2GPI) antibodies may be involved in a number of vascular diseases including coronary artery diseases (CAD) or stroke. Here we assessed the presence of aPL antibodies in acute coronary syndrome (ACS). The frequency of anti-beta2GPI antibodies was significantly higher (14.4%) in ACS in comparison to control healthy subjects (2%). In addition, serum concentrations of anti-beta2GPI antibodies were also increased in ACS. Anti-beta2GPI antibodies of the IgA isotype might be the most relevant for the onset and outcome of ACS. Regarding subclasses of ACS, anti-beta2GPI IgA antibodies were elevated in unstable angina (UA) and myocardial infarction with ST elevation (STEMI), but not in myocardial infarction without ST elevation (NSTEMI). The involvement of anti-beta2GPI antibodies in ACS was more pronounced in men than women, and in younger rather than older patients. Finally, anti-beta2GPI antibodies in ACS were associated with previous stroke, but not with hypertension or previous myocardial infarction. Thus, anti-beta2GPI antibodies may be involved in the thrombotic events underlying ACS.
Lupus 2004
PMID:Antiphospholipid antibodies in acute coronary syndrome. 1530 68

Twelve systemic lupus erythematosus (SLE) patients with mild to moderate disease activity (SLEDAI of > or = 6 and on prednisolone < 0.5 mg/kg/day) were included in a prospective, randomized, double-blind, placebo-controlled pilot study for 24 weeks. Six were randomized to receive oral leflunomide and six received placebo. Primary outcome of this study included the mean change of SLEDAI at 24 weeks. Secondary outcomes included the changes in proteinuria, complement levels, anti ds-DNA binding, and prednisolone dosage. The mean age of the 12 patients was 41+/-9 years, and the mean disease duration was 8.5+/-5.8 years. All were female except one patient. The disease activity of both groups of patients decreased significantly after six months of treatment (14.7+/-6.0 to 3.7+/-2.3 in leflunomide group, P = 0.028, and 9.7+/-3.4 to 5.2+/-4.1 in placebo group, P = 0.027). Reduction in the SLEDAI from baseline to 24 weeks was significantly greater in the leflunomide group than the placebo group (11.0+/-6.1 in the leflunomide group and 4.5+/-2.4 in the placebo group respectively, P = 0.026). Minor adverse events included transient elevation in ALT, hypertension and transient leucopenia. In summary, leflunomide was more effective than placebo in treating SLE patients with mild to moderate disease activity and was safe and well-tolerated.
Lupus 2004
PMID:Double-blind, randomized, placebo-controlled pilot study of leflunomide in systemic lupus erythematosus. 1546 90

Hypertension is a common manifestation of antiphospholipid syndrome (APS). Antiphospholipid antibodies (aPL) have been described in patients with hypertension secondary to renal artery stenosis (RAS). Twenty-six patients with RAS and 25 patients with severe essential hypertension (diastolic blood pressure > 110 mmHg or > or = 3 hypertensive drugs) were studied and compared to 61 age- and sex-matched healthy subjects. Serum samples were tested for lupus anticoagulant (LA), anticardiolipin (aCL) IgG and IgM, antiprothrombin (aPT) IgG and IgM, anti-beta2glycoprotein 1 (abeta2GP1) IgG and IgM. aPL were negative in all patients with RAS. Two patients with essential hypertension had positive aPL (8%) (LA in one patient confirmed in a second assay and abeta2GP1-IgG in the other patient confirmed one year later together with aCL IgG positivity). Among healthy subjects, one case (1.6%) was found to be positive for LA, aCL IgM, abeta2GP1 IgM, aPT IgG, aPT IgM. In conclusion, the association between RAS and aPL seems to be casual rather than an expression of an elective thrombotic localization ofAPS. The positive finding of aPL in 8% of patients with essential hypertension, a frequency higher than that of the control population, deserves further studies in larger series to better explore the relationship between aPL and hypertension.
Lupus 2004
PMID:Antiphospholipid antibodies and hypertension. 1554 May 8

The American College of Rheumatology renal criteria require re-evaluation to incorporate recent advances in the classification of glomerulonephritidies. Renal biopsy is now common and safely performed by experienced nephrologists in community as well as academic settings. The optimal criterion is renal histopathology findings of an immune complex mediated glomerulonephritis as interpreted by an experienced pathologist employing accepted criteria. Renal biopsies should be analysed by routine histopathology, immunofluorescent and electron microscopy. Rating of activity and chronicity should be noted. Secondary criteria for patients unable to undergo renal biopsy includes a combination of findings. These include proteinuria, hypocomplementemia, elevated anti-dsDNA antibodies and an active urine sediment. Proteinuria is a nonspecific finding and, most importantly, can be associated with a number of comorbidities including diabetes, hypertension and atherosclerotic disease. Persistent proteinuria > 0.5 g per day or a spot protein to creatine ratio of > 0.5 should be accompanied by an additional feature supporting active lupus such as positive serologies (hypocomplementemia and/or elevated anti-dsDNA antibodies) and/or active urinary sediment. Similarly, active urinary sediment should be accompanied by the additional criterion of proteinuria to meet renal criteria. Decline in renal function is not a reliable criterion given the numerous medications, comorbidities and other clinical circumstances which may result in this feature.
Lupus 2004
PMID:Review of ACR renal criteria in systemic lupus erythematosus. 1558 Sep 82

Cardiovascular disease is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Antiphospholipid syndrome (APS) is one of the most important causes of thrombosis in SLE. In addition, an association between hyperhomocysteinemia and increased cardiovascular risk has also been reported. Our aim is to analyse the association of thrombosis with plasma total homocysteine (ptHcy), antiphospholipid antibodies (aPL) and other vascular risk factors in SLE patients. Fasting plasma levels of ptHcy, vitamin B12, folate, total cholesterol and creatinine were measured in 117 SLE patients. Clinical and immunological data were obtained from our prospective computerized database. aPL-positivity was defined according to Sapporo criteria. There was no association between aPL and ptHcy. ptHcy was higher in patients with arterial (median 13.02 versus 10.16 micromol/L, P = 0.010) but not venous thrombosis. In the subgroup analysis, this association was only seen in aPL-negative patients. In logistic regression, aPL (OR 6.60, 95% CI 1.86-23.34) and ptHcy (OR 1.10, 95% CI 1.01-1.19) were independently associated with arterial thrombosis. However, when hypertension, smoking and plasma total cholesterol were added to the model, only aPL (OR 7.38, 95% CI 2.02-26.91) and hypertension (OR 7.70, 95% CI 2.33-25.39), but not ptHcy, remained independently related to arterial events. aPL was the only variable independently related to venous thrombosis (OR 7.68, 95% CI 1.60-36.86). ptHcy concentrations are higher in SLE patients with arterial thrombosis. No interaction between homocysteine and aPL was found. Raised ptHcy may be a marker of increased vascular risk in aPL-negative SLE patients. The role of homocysteine as a marker of vascular risk may depend on the presence of traditional risk factors, although a modest intrinsic effect cannot be entirely excluded.
Lupus 2004
PMID:Homocysteine, antiphospholipid antibodies and risk of thrombosis in patients with systemic lupus erythematosus. 1564 48

Renal thrombotic manifestations have been reported since the earliest descriptions of the antiphospholipid (Hughes) syndrome (APS). The spectrum of clinical features associated with antiphospholipid nephropathy continues to widen. This review will highlight recent developments such as the prevalence of hypertension, livedo reticularis and renal artery stenosis as well as the ultrastructural changes seen in antiphospholipid nephropathy. The increasing risks of renal transplantation in antiphospholipid antibody positive patients is also discussed leading some authors to question whether these patients should undergo transplantation at all.
Lupus 2005
PMID:Renal manifestations of the antiphospholipid syndrome. 1573 87

Optimal care of lupus nephritis patients should include the treatment of proteinuria and hypertension, other measures to delay the progression of chronic kidney disease, the vigorous management of cardiovascular risk factors and finally, the treatment of advanced chronic kidney disease and its consequences. These topics are briefly reviewed in the present paper, with particular emphasis on the recent progresses in antiproteinuric treatment.
Lupus 2005
PMID:Optimal care of lupus nephritis patients. 1573 92


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