Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to examine mortality rates related to cerebrovascular disease in systemic lupus erythematosus (SLE) compared to the general population. Our sample was a multisite Canadian SLE cohort (10 centres, n = 2688 patients). Deaths due to cerebrovascular disease were ascertained by vital statistics registry linkage using ICD diagnostic codes. Standardized mortality ratio (SMR, ratio of deaths observed to expected) estimates were calculated. The total SMR for death due to cerebrovascular disease was 2.0 (95% confidence interval [CI] 1.0, 3.7). When considering specific types of events, the category with the greatest increased risk was that of ill-defined cerebrovascular events (SMR 44.9 95% CI 9.3, 131.3) and other cerebrovascular disease (SMR 8.4, 95% CI 2.3, 21.6). Deaths due to cerebral infarctions appeared to be less common than hemorrhages and other types of cerebrovascular events. Our data suggest an increase in mortality related to cerebrovascular disease in SLE patients compared to the general population. The large increase in ill-defined cerebrovascular events may represent cases of cerebral vasculitis or other rare forms of nervous system disease; alternately, it may reflect diagnostic uncertainty regarding the etiology of some clinical presentations in SLE patients. The suggestion that more deaths are attributed to cerebral hemorrhage, as opposed to infarction, indicates that inherent or iatrogenic factors (eg, thrombocytopenia or anticoagulation) may be important. In view of the paucity of large-scale studies of mortality attributed to neuropsychiatric outcomes in SLE, our findings highlight the need for additional research in large SLE cohorts.
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PMID:Mortality related to cerebrovascular disease in systemic lupus erythematosus. 1721 87

Giant cell arteritis (GCA) is a systemic vasculitis associated with severe complications such as loss of vision and, rarely, scalp necrosis. We present a patient with GCA who had bilateral scalp necrosis and an erythrocyte sedimentation rate of only 21 mm after the first hour. Therapy with systemic steroids, which were slowly tapered over 1 year, led to secondary wound healing without recurrence. As there are no systematic reviews on the occurrence of scalp necrosis in patients with GCA, we performed a literature research and meta-analysis and discovered 78 cases published between 1946 and 2007. Analysis of the data revealed that GCA with scalp necrosis is associated with a higher incidence of vision loss (32%) and other visual defects (37.3%) than GCA without scalp necrosis (visual disturbances in up to 20%). GCA with scalp necrosis is also associated with an increased mortality (standard mortality ratio [SMR], 4.2) in contrast to GCA without scalp necrosis, which has no significantly higher mortality than age-matched controls (SMR 0.8-1.034). In patients with scalp necrosis, the diagnosis of GCA was made about 1 month later than in patients without scalp necrosis, and scalp necrosis was never reported to occur after onset of therapy with glucocorticoids. Thus, for reasons beyond potential loss of vision, physicians should be alert for symptoms of GCA as only timely diagnosis and immediate therapy may prevent serious complications and increased mortality.
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PMID:Scalp necrosis in giant cell arteritis: case report and review of the relevance of this cutaneous sign of large-vessel vasculitis. 2063 4