[Etanercept in routine German clinical practice to treat rheumatoid arthritis patients : A one-year observational study on effectiveness, safety and health economics]. / Etanercept in der klinischen Routinebehandlung von Patienten mit rheumatoider Arthritis : Eine einjährige nichtinterventionelle Studie zur Bewertung der Wirksamkeit und Sicherheit.

BACKGROUND: The efficacy and safety of the TNF­α inhibitor etanercept (ETA) as a treatment for rheumatoid arthritis (RA) is well established by randomized controlled trials. The purpose of this study was to evaluate the benefit yielded by ETA within the regular outpatient care. PATIENTS AND METHODS: This prospective non-interventional trial included patients being treated with ETA. Data concerning efficacy, safety and life quality were collected over a period of 52 weeks. Statistical evaluation was done on a solely descriptive level. RESULTS: From 329 specialized medical centres, 4945 patients were enrolled. Of all patients, 94.4% received a co-medication for RA, additionally to their treatment with ETA. At baseline, 22.1% of all patients fulfilled the criteria for functional remission according to the Funktionsfragebogen Hannover (FFbH) questionnaire (95% CI: 21.0-23.3%); at 52 weeks, functional remission rate accounted for 41.1% (last observation carried forward [LOCF], 95% CI: 39.4-42.9%). The disease activity score (DAS) DAS28 declined from 5.4 ± 1.3 (N = 4304) to 3.3 ± 1.4 (as observed; N = 2608). EuroQol EQ-5D, a measurement of health-related life quality issues, indicated an improvement on the visual analogue scale (VAS) from 53.1 ± 21.3 mm (N = 4718) at baseline to 70.0 ± 20.5 mm (as observed; N = 3036). Generally, ETA has been tolerated well. With regard to the safety profile specified by previous studies, no meaningful deviations concerning the nature, frequency or severity of adverse events were detected. CONCLUSION: Based on a large number of patients and in a treatment context that is representative of routine outpatient care in Germany, it was confirmed that patients with RA may benefit from a treatment with ETA.

Experimental heterotopic bone transplant.

We studied the reaction in rats to implants of heterotopic bone in the paravertebral region, using three types of material: bone preserved in alcohol, homologous bone preserved in alcohol associated with autogenous cancellous bone obtained from the iliac crest of the same animal, and isolated autogenous cancellous bone. Thirty rats were operated on, ten in each group. Some were sacrificed after 6, 14 and 21 days. The excised grafts were histologically studied. Animals in the third group showed new bone formation even in the first days, those in the second group presented less intense bone formation and those in the first group showed only traces of new bone tissue in the third week.

Murine systemic autoimmune disease induced by mercuric chloride (HgCl2): Hg-specific helper T-cells react to antigen stored in macrophages.

The adoptive transfer popliteal lymph node assay (PLNA) was used to demonstrate Hg-specific T-cell responses of mice that were continuously treated with HgCl2 by a regimen known to induce a systemic autoimmune disease in H-2s (murine histocompatibility complex, haplotype s) mice, but not H-2d mice. We found that spleen cells of B10.S and A.SW donors (both H-2s) responded anamnestically to HgCl2 by inducing a significant increase in cellularity in the draining PLN of the recipient: In contrast, spleen cells of HgCl2-treated DBA/2 (H-2d) donors failed to induce an increase in PLN cellularity, and spleen cells of B10.D2/n (H-2d) donors induced no changes or even diminished PLN cellularity upon re-encounter with HgCl2. Kinetic studies showed that spleen cells of B10.S donors were stimulatory from day 3 until day 14 of donor HgCl2 treatment and, when purified splenic T-cells were tested, still on day 28, the last point in time tested. The Hg-specific T-cells prepared from HgCl2-treated B10.S mice not only induced an increased cellularity, but also B-cell activation to antibody secretion in the draining PLN of the recipient. Moreover, the Hg-specific donor T-cells transferred could specifically be restimulated by killed peritoneal cells obtained from the same donors or from syngeneic donors previously treated with HgCl2. Interestingly, when killed peritoneal cells were injected as antigen the amount of Hg required for T-cell restimulation was only 1/40 of that required when free HgCl2 was used. Taken together, these results show that an HgCl2 treatment schedule designed to induce systemic autoimmune disease primes Hg-specific T-helper (Th) cells and generates immunogenic material in peritoneal cells to which the T-cells react. The possible contribution to the pathogenesis of HgCl2-induced auto-immune disease of these Hg-specific T-cells and the autoreactive T-cells reported in the literature is discussed.