In an effort to implicate immune responses to specificBorrelia burgdorferi proteins that may have a role in chronic Lyme arthritis, we studied the natural history of the antibody response to B. burgdorferi in serial serum samples from 25 patients monitored throughout the course of Lyme disease. In these patients, the immunoglobulin G (IgM) and IgG antibody responses to 10 recombinant B. burgdorferi proteins, determined during early infection, early arthritis, and maximal arthritis, were correlated with the severity and duration of maximal arthritis. The earliest responses were usually to outer surface protein C (OspC), P35, P37, and P41; reactivity with OspE, OspF, P39, and P93 often developed weeks later; and months to years later, 64% of patients had responses to OspA and OspB. During early infection and early arthritis, the levels of IgG antibody to P35 correlated inversely with the subsequent severity or duration of maximal arthritis. In contrast, during periods of maximal arthritis, the levels of IgG antibody to OspA and OspB, especially to a C-terminal epitope of OspA, correlated directly with the severity and duration of arthritis. Thus, the higher the IgG antibody response to P35 earlier in the infection, the milder and briefer the subsequent arthritis, whereas during maximal arthritis, the higher the IgG response to OspA and OspB, the more severe and prolonged the arthritis.
The expression of adhesion molecules in synovium in patients with Lyme arthritis is surely critical in the control of Borrelia burgdorferi infection but may also have pathologic consequences. For example, molecular mimicry between a dominant T-cell epitope of B. burgdorferi outer surface protein A and an adhesion molecule, human lymphocyte function-associated antigen 1 (LFA-1), has been implicated in the pathogenesis of treatment-resistant Lyme arthritis. Using immunohistochemical methods, we examined synovial samples for expression of adhesion molecules in 29 patients with treatment-resistant Lyme arthritis and in 15 patients with rheumatoid arthritis or chronic inflammatory monoarthritis. In Lyme arthritis synovia, endothelial cells showed intense expression of P-selectin and vascular adhesion protein-1 (VAP-1). Expression of LFA-1 was also intense on infiltrating cells, particularly in lymphoid aggregates, and intercellular adhesion molecule-1 (ICAM-1) was markedly expressed on synovial lining and endothelial and infiltrating cells. Moderate expression of vascular cell adhesion molecule-1 (VCAM-1) was seen on synovial lining and endothelial cells, and mild expression of its ligand, very late antigen-4, was apparent in perivascular lymphoid infiltrates. Except for lesser expression of VCAM-1 in Lyme synovia, the levels of expression of these adhesion molecules were similar in the three patient groups. We conclude that certain adhesion molecules, including ICAM-1 and LFA-1, are expressed intensely in the synovia of patients with Lyme arthritis. Upregulation of LFA-1 on lymphocytes in this lesion may be critical in the pathogenesis of treatment-resistant Lyme arthritis.
9. Golstein PE, Deviere J, Cremer M. Acute hepatitis and drug-related lupus induced by minocycline treatment. Am J Gastroenterol. 1997;92:143-146. 10. Singer SJ, Piazza-Hepp TD, Girardi LS, Moledina NR. Lupuslike reaction associated with minocycline. JAMA. 1997;277:295-296. 11. Crosson J, Stillman MT. Minocycline-related lupus erythematosus with associated liver disease. J Am Acad Dermatol. 1997;36(5 More than 44000 new cases of melanoma are detected annually in the United States, and the number is steadily increasing. The majority of patients are treated with surgical excision and may, in addition, undergo sentinel node mapping, lymph node dissection, and adjunctive treatment. The purpose of this study was to develop rational, evidence-based guidelines for following up patients with 1983 American Joint Committee on Cancer stage I (Ͻ1.5 mm thick), II (localized disease Ͼ1.5 mm thick), and III (local nodal or in-transit metastases) melanoma. The study was a retrospective review of charts of 373 patients who were followed up according to the surveillance protocol at the Yale Melanoma Unit, New Haven, Conn, between January 1988 and December 1994. Each patient was followed up for at least 2 years. The surveillance protocol included combined frequent comprehensive examination with extensive patient education. Periodic examinations included history and physical examination; laboratory tests, such as complete blood cell count, liver function tests , and serum lactate dehydrogenase level; and chest x-ray (CXR) (computed tomographic scans were done for patients with stage III melanoma).The collected data included (1) the time between first visit and recurrence; (2) whether the recurrence was detected by the patient or by a physician during a follow-up visit; (3) the method of detection for physician-detected recurrences (ie, history and physical examination, review of systems, complete blood cell count, liver function tests, serum lactate dehydrogenase level, and CXR or other imaging techniques); (4) survival; (5) location of recurrences; and (6) development of second primary melanomas.The results indicated that there were recurrences in 52 (25%) of 210 males and 26 (16%) of 163 females. Of the 373 patients, 78 (21%) had a recurrence. The proportions of patients who developed recurrence were 9 (5%) of 193, 35 (30%) of 117, and 34 (54%) of 63, for patients with stage I, II, and III disease, respectively. The median time to recurrence in patients with stages I, II, and III disease was 22 months (range, 2-61 months), 13 months (range, 2-71 months), and 11 months (range, 2-54 months), respectively. Most patients (n=62, 79%) who developed a recurrence in the follow-up period did so within the first 2 years. Six percent (n=5) of patients developed recur-(REPRINTED) ARCH DERMATOL / VOL 136, SEP 2000
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