The outcome of 30 consecutive patients with active aortic prosthetic valve endocarditis and root abscesses treated by the technique of homograft aortic root replacement with reimplantation of the coronary arteries is detailed. The principles of this technique are the removal of all abscesses and infected areas likely to drain into the infected mediastinum, excision of infected tissues down to healthy noninfected tissue and replacement with an antibiotic-impregnated homograft aortic root. All patients had evidence of progressive cardiac failure and ongoing sepsis. Mean patient age (+/- SD) at the time of operation was 42 +/- 18 years. The mean number of previous aortic valve replacements per patient was 1.6 +/- 0.7; 14 patients (47%) had undergone greater than or equal to 2 previous replacements. At operation, aortic root abscesses were found in all patients; abscess extension to adjacent structures and partial valve dehiscence had occurred in 23. In-hospital death occurred in 9 (30%) of the 30 patients. The 21 hospital survivors have been followed up for a mean of 66 +/- 42 months (range 9 to 144). Overall, 17 (81%) of the 21 hospital survivors have remained free of major adverse events (recurrence of endocarditis, need for reoperation or death). The results of our study suggest that homograft aortic root replacement should be considered favorably in the treatment of patients with aortic prosthetic valve endocarditis and root abscesses.

Reactivity toward soluble recall antigens (Candida albicans, cytomegalovirus, herpes simplex, streptokinase-streptodornase, and influenza) was determined in cultures of peripheral blood mononuclear cells from 41 rheumatoid arthritis patients (with clinically active as well as inactive disease) and from 28 controls. In the group with clinically active rheumatoid arthritis we found an increased incidence of "anergy," defined as nonreactivity to three or more antigens. In an attempt to explain this decreased antigen reactivity, the latter was correlated with peripheral blood lymphocyte subsets, as defined by two-color immunofluorescence with a panel of eight monoclonal antibodies. We found a significantly lower number of memory T4 cells (CD4+CD45RA-) and a significantly higher number of the CD3-CD57+ (nonspecific suppressor) cells and of CD3-CD56+/CD16+ (natural killer) cells in anergic RA patients. In the total group of rheumatoid arthritis patients, the antigen reactivity correlated positively with the percentage of memory T4 cells. Antigen reactivity was negatively correlated with the percentage of CD3-CD57+ cells and of the CD3- natural killer cells in peripheral blood. Our data suggest that a decrease in memory T4 cells and an increase in nonspecific suppressor cells may contribute to the impaired cellular immune function in peripheral blood of rheumatoid arthritis patients.

Objective. To assess the role of T lymphocyte sensitization in the etiology of side effects of gold therapy in patients with rheumatoid arthritis (RA). Methods. Lymphocyte proliferation induced by gold(III) and gold(I) salts was measured in 53 subjects: 30 RA patients with gold‐induced side effects (17 with dermatitis, 9 with proteinuria, 3 with hematologic complications, and 1 with colitis), 9 RA patients without side effects despite prolonged chrysotherapy, 4 RA patients who had never received gold, and 10 healthy controls. Peripheral blood lymphocytes were cultured with the different gold salts and proliferation was measured by 3H‐thymidine incorporation. Results. Thirteen of the 17 RA patients who developed gold‐induced dermatitis showed significant T lymphocyte proliferation in response to gold(III) salts, and this proliferation could be completely blocked by monoclonal antibodies directed at the HLA—DR molecule. Such proliferative responses were not seen in patients with other gold‐induced side effects, in patients who had never received gold, or in healthy controls. Only 1 of 9 patients who had not developed side effects despite long‐term maintenance chrysotherapy showed significant lymphocyte activation with gold(III) salts. Lymphocyte proliferation could not be induced with gold(I) salts or with other metal salts. Conclusion. Patients with RA who develop dermatitis following treatment with sodium aurothiomalate [gold(I)] have T cells which proliferate in an HLA—DR—restricted manner in response to HAuCl4 [gold(III)]. We believe this observation can lead to more accurate diagnosis and treatment of side effects, which currently limit the use of one of the most effective antirheumatic drugs.

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Objective. To report the findings of a 10-year followup of patients enrolled in a randomized trial of total lymphoid irradiation (TLI) versus chemotherapy for rheumatoid arthritis (RA). Methods.A retrospective analysis of the charts of 19 patients who had been included in a randomized trial comparing TLI and chemotherapy for the treatment of RA.Results. Ten years after the start of the trial, a higher number of TLI-treated patients had died (7 of lo), compared with patients who had received chemotherapy (2 of 9). In addition, 3 of the TLI-treated patients developed B cell-related malignancies, whereas no such malignancies developed in the control group.Conclusion. TLI was associated with a lessfavorable long-term outcome than chemotherapy. These data stress the importance of careful long-term followup in experimental trials of immunosuppressive agents.