Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.1.1.6 (CAD)
 4,420 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to determine the lipoprotein profile of limited cutaneous systemic sclerosis (LcSSc). Fasting lipids were determined in 24 female patients and 24 healthy age-matched and sex-matched controls. Exclusion criteria were conditions that induce an altered lipid profile. Lipoprotein levels of risk were determined in accordance with the National Cholesterol Education Program (NCEP). Significantly lower levels of high-density lipoprotein (HDL) cholesterol (47.6+/-12.4 mg dL(-1) vs. 58.2+/-12.3 mg dL(-1); P=0.003) and total cholesterol (197.0+/-40.7 mg dL(-1) vs. 222.0+/-34.0 mg dL(-1); P=0.02) were observed in LcSSc patients than in controls. The presence of anti-centromere antibodies (ACA) was also associated with lower HDL levels (45.0+/-12.1 mg dL(-1)) compared to ACA-negative patients and controls (50.2+/-12.6 and 58.2+/-12.3 mg dL(-1), respectively, P=0.01). The only clinical variable associated with low HDL levels was pulmonary hypertension (PH) (33.6+/-2.3 mg dL(-1) vs. 49.6+/-11.9 mg dL(-1), P=0.01). No significant correlation was observed among HDL levels and ESR (r=-0.313; P=0.14), CRP (r=-0.296; P=0.16), or BMI (r=-0.263; P=0.21). Remarkably, a higher percentage of risk HDL levels was identified in LcSSc patients (41.6%) than in healthy controls (8.3%) (P=0.02). Our data suggest that LcSSc patients, particularly those who are ACA positive, have an adverse lipid profile characterized by low HDL levels, a known independent risk for CAD in women. The relevance of this finding for the development of atherosclerosis in this disease must be confirmed by epidemiological studies.
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PMID:Lipoprotein profile in limited systemic sclerosis. 1628 68

It has been suggested that spontaneous cervical carotid artery dissection (sCAD) may result from arterial inflammation. Periarterial edema (PAE), occasionally described in the vicinity of the mural hematoma in patients with sCAD, may support this hypothesis. Using cervical high-resolution magnetic resonance imaging, three readers, blinded to the mechanism of carotid artery dissection, searched for PAE, defined as periarterial T2-hyperintensity and T1-hypointensity, in 29 consecutive CAD patients categorized as spontaneous CAD (sCAD, n = 18) or traumatic CAD (tCAD, n = 11; i.e., major head or neck trauma within 2 weeks before the clinical onset). The relationships between PAE, inflammatory biological markers, history of infection and CAD mechanism were explored. Multiple CADs (n = 8) were found only in sCAD patients. Compared with tCAD, patients with sCAD were more likely to have a recent history of infection (OR = 12.5 [(95%)CI = 1.3-119], p = 0.03), PAE (83% vs. 27%; OR = 13.3 [(95%)CI = 2.2-82.0], p = 0.005) and to have elevated CRP (OR = 6.1 [(95%)CI = 1.2-32.1], p = 0.0002) or ESR (OR = 8.8 [(95%)CI = 1.5-50.1], p = 0.002) values. Interobserver agreement was 0.84 or higher for PAE identification. sCAD was associated with PAE and biological inflammation. Our results support the hypothesis of an underlying arterial inflammation in sCAD.
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PMID:High-resolution MR imaging of periarterial edema associated with biological inflammation in spontaneous carotid dissection. 1939 44