We investigated the relation of arterial stiffness, considered an independent predictor of cardiovascular events, to cardiovascular risk factors in a population-based study of 1023 subjects. An Arterial Stiffness Index (ASI) was developed to evaluate arterial stiffness based on an analysis of the pulse wave amplitude pattern acquired from measurements of brachial blood pressure. In control subjects (n = 266) without any major risk factors, the ASI was 46 ± ± ± ± ± 11, and increased with age (r = 0.346). The ASI was significantly higher in women ranging from 50 to 54 years of age than in age-matched men. The ASI rose in correlation with the number of risk factors. Subjects with two risk factors showed a significantly higher ASI than those without any risk factors (54 ± ± ± ± ± 26 vs. 46 ± ± ± ± ± 11). The ASI was significantly increased in diabetic subjects with hypertension in comparison to those without hypertension. Furthermore, hyperlipidemic subjects with hypertension showed significantly higher values than those without hypertension. ASI could be a useful predictor of cardiovascular events in hypertensive subjects with multiple risk factors. J Atheroscler Thromb, 2005; 12: 175-180.

A case of Goodpasture's syndrome with anti-myeloperoxidase (MPO) antibodies is reported. Histological examination revealed crescentic glomerulonephritis and alveolar hemorrhage with linear deposition of IgG along the glomerular capillary walls and alveolar capillary walls by immunofluorescence microscopy. Not only anti-glomerular basement membrane (GBM) antibodies but also anti-MPO antibodies, an anti-neutrophil cytoplasmic antibody, were simul taneously detected in the serum. Although it is generally accepted that crescentic glomerulo nephritis in Goodpasture's syndrome is mediated by anti-GBM antibodies, this case suggested that anti-MPO antibodies might also participate in the pathogenesis of crescentic glomerulo nephritis and probably alveolar hemorrhage of Goodpasture's syndrome, especially with vasculitis.

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Summary: In order to elucidate the role of neutrophils in the pathogenesis of MPO‐specific anti‐neutrophil cytoplasmic antibody (MPO‐ANCA) related glomerulonephritis (GN), MPO release, beta‐glucuronidase (BGL) release, superoxide anion (O2−) production from the neutrophils of patients with MPO‐ANCA related GN were measured. the effect of plasma on MPO release from neutrophils was also studied in patients with MPO‐ANCA related GN. Neutrophils and plasma were obtained from patients with MPO‐ANCA related GN, GN unrelated to MPO‐ANCA and healthy controls. MPO release from the neutrophils of patients with MPO‐ANCA related GN was higher than that of controls significantly. This was also higher than that in patients with GN unrelated to MPG‐ANCA, but this was not statistically significant. Superoxide anion production from neutrophils of patients with MPO‐ANCA related GN was significantly higher than that in patients with GN unrelated MPO‐ANCA, However, BGL release was not significantly different among three groups. Furthermore, MPO release and O2− production increased in parallel with clinical activity of MPO‐ANCA related GN. Neutrophils of patients with MPO‐ANCA related GN showed to be significantly more sensitive to FMLP on MPO release than those in the other two groups. However, plasma from MPO‐ANCA related GN increased the sensitivity to FMLP on MPO release, but not BGL release, in neutrophils obtained from healthy controls, whereas it suppressed MPO release from neutrophils with MPO‐ANCA related GN. This suggests that in patients with MPO‐ANCA related GN MPO can be highly released from activated neutrophils and that the plasma of patients with MPO‐ANCA contains factor(s) which modulate reactivity of neutrophils.

encies, these drugs are frequently implicated in cases of deliberate selfpoisoning. Serious or fatal tricyclic antidepressant intoxication is not un¬ common.16 As in the present case,