Faculty Bibliography

OBJECTIVE:To investigate the occurrence, clinical correlates, and immunohistochemical phenotype of temporal small-vessel inflammation (TSVI) in temporal artery biopsies from patients presenting with clinical features of giant cell arteritis (GCA). METHODS:We retrospectively reviewed 41 temporal artery biopsy specimens for the presence of inflammatory infiltrates in small vessels external to the temporal artery adventitia (TSVI); 33 had sufficient clinical and pathological data for detailed analysis. Clinical and laboratory features at presentation and corticosteroid treatment patterns of patients with isolated TSVI were compared to those of patients with positive and negative biopsies. The cellular composition of the infiltrates was further characterized by immunohistochemistry. RESULTS:Twenty-three (70%) specimens had evidence of TSVI including 10 with concurrent GCA and 13 (39%) with isolated TSVI. TSVI was found in all positive temporal artery biopsies. The proportion of macrophages and of lymphocyte subpopulations differed between infiltrates observed in TSVI and those of the main temporal artery wall. Initial erythrocyte sedimentation rate (ESR) was similar in the TSVI and positive biopsy groups and was significantly higher than in the negative biopsy group. Patients with isolated TSVI more often had symptoms of polymyalgia rheumatica compared to the positive biopsy group. Patients with TSVI received corticosteroid doses that were intermediate between patients with positive and those with negative biopsies. CONCLUSION/CONCLUSIONS:A significant number of patients with clinical features of GCA demonstrated isolated TSVI. Differences in the clinical presentation and cellular composition suggest that TSVI may represent a subset of GCA and should be considered in the interpretation of temporal artery biopsies and treatment decisions.

Atherosclerotic cardiovascular disease (ASCVD) contributes to morbidity and mortality in systemic lupus erythematosus (SLE). Immunologic derangements may disrupt cholesterol balance in vessel wall monocytes/macrophages and endothelium. We determined whether lupus plasma impacts expression of cholesterol 27-hydroxylase, an anti-atherogenic cholesterol-degrading enzyme that promotes cellular cholesterol efflux, in THP-1 human monocytes and primary human aortic endothelial cells (HAEC). THP-1 monocytes and HAEC were incubated in medium containing SLE patient plasma or apparently healthy control human plasma (CHP). SLE plasma decreased 27-hydroxylase message in THP-1 monocytes by 47 +/- 8% (p < 0.008) and in HAEC by 51 +/- 5.5% (n = 5, p < 0.001). THP-1 macrophages were incubated in 25% lupus plasma or CHP and cholesterol-loaded (50 microg ml(-1) acetylated low density lipoprotein). Lupus plasma more than doubled macrophage foam cell transformation (74 +/- 3% vs. 35 +/- 3% for CHP, n = 3, p < 0.001). Impaired cholesterol homeostasis in SLE provides further evidence of immune involvement in atherogenesis. Strategies to inhibit or reverse arterial cholesterol accumulation may benefit SLE patients

We present the first reported case of a patient with dermatomyositis found to have primary gastric melanoma. The possibility of primary gastric melanoma occurring before, concurrently or after the onset of dermatomyositis is the subject of this case report.

A 21-year-old woman with a history of systemic lupus erythematosus (SLE) presented to the emergency room with a chief complaint of substernal chest pain and palpitations. She had undergone a four-vessel coronary artery bypass graft operation with separate saphenous vein grafts to the left anterior descending (LAD), obtuse marginal (OM) 1 and 2, and distal right coronary arteries (RCA) 8 months prior to admission. The patient underwent angiography of the coronary vessels, which showed severe diffuse disease with a long, 90% narrowing of the vein graft to the LAD and closed vein grafts to OM1 and OM2. The RCA graft showed mild diffuse disease. An intervention was done in which the LAD was stented twice with subsequent TIMI 3 flow. Advances in medical therapy and a better understanding of the disease have contributed to a dramatic improvement in the long-term survival of patients with SLE. However, despite the overall long-term improvement, coronary artery disease remains a major cause of morbidity and mortality with an incidence of approximately nine-fold greater than would be expected for this population