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of autoantibodies cytotoxic to lymphocytes, gran- ulocytes, and monocytes. Some of these antibodies were reactive in the cold, whereas others were capable of killing cells at 37°C. In the majority of instances, these antibodies required nonhuman complement to be acti- vated; however, in a few instances (especially in the case of monocytotoxins) cytotoxic activity was observed in the absence of rabbit serum. At the present time we have eluted these cytotoxic antibodies from various cells. We found that some eluates were capable of killing more than one type of cell thus implying an existence of common antigenic determinants. I would like to stress that studies of monocytotoxic antibodies are com- plicated by the fact that the monocytes in part are lysed during the monocytotoxicity assay, thus escaping try- pan-blue staining.

W. PRUZANSKI, M.D., F.R.C.P.(C)., F.A.C.P. Professor of Medicine Director Immunoglobulin Diagnostic & Research Centre University of Toronto Toronto, Canada

Declassification of Arteritis

To the Editor: I was interested in the comments by Dr. Sergent

in the June issue case report of a patient with systemic vasculitis. Since the original classification of arteritis by Zeek et al. ( I ) , it has become apparent that many pa- tients do not satisfy the criteria for any one of the types of described vasculitides. The physician is often left with a poorly defined illness to which he has to ascribe a diagnosis that is neither complete nor satisfactory. In a recent article by Alarc6n-Segovia (2), the author pro- poses a classification by delineating the potential etiol- ogies of the vasculitic syndrome along with their charac- teristic clinical pictures.

In trying to deal with the large number of vari- ables that one might encounter with a vasculitic syn- drome, such as the etiologic associations as defined by Dr. Sergent (cryoglobulinemia, hepatitis-associated an- tigen, or drugs) and the different clinical presentations such as neuropathy, skin ulcers, or renal disease, I would propose a “declassification” of arteritis that is based on the New York Heart Association’s criteria for cardiac disease. For example, a patient such as the one described in the case report would have a diagnosis of vasculitis, etiology unknown; pathoanatomical diagno- sis-necrotizing vasculitis involving the small and me-

dium size arteries; physiologic diagnosis-mono- neuropathy multiplex.

This description of disease would alleviate the confusion arising out of whether the patient has poly- arteritis, the vasculitis associated with rheumatoid ar- thritis, hypersensitivity angiitis or whatever. Addition- ally, a diagnosis could be made based on the available information only.

JOHN G. PATY, JR. M.D. Appalachian Arthritis Foundation & Section of Rheumatology Department of Medicine University of Tennessee Clinical Education Center Chattanooga, Tennessee

I .

2.

REFERENCES Zeek PM: Periarteritis nodosa and other forms of necrotiz- ing arteritis. N Engl J Med 248:764, 1953 Alarc6n-Segovia D: The necrotizing vasculitides. Med Clin N Am 61:241-259, 1977

Clinical Drug Efficacy and in Vitro Inhibition of Lymphocyte Responses in Rheumatoid Arthritis

To the Editor: Mechanisms of antiinflammatory effects of

drugs are not known (1). Among other actions many antirheumatic drugs affected in vitro respon- siveness of normal human peripheral blood lympho- cytes (PBL) (2,3). Also, responses of patients with rheumatoid arthritis (RA) to individual drugs are often unpredictable, We therefore examined possible relationships between in vitro drug effects and sub- sequent clinical responses of patients to those drugs during clinical trials.

Seventeen patients with RA were studied. Pa- tients’ PBL, obtained after drug therapy was dis- continued for more than 48 hours, were placed into short-term cultures with or without mitogens and with or without drugs, as described (2). We deter- mined inhibition of stimulated PBL responses by aspirin (ASA), 80 pg/ml; indomethacin (IND), 350 pg/ml; naproxen (NAP), 300 pg/ml; and sodium meclofenamate (MFA), 175 pg/ml-concentrations approximating 50% inhibitory dosages for normal PBL (2). Degree of i n vitro inhibition was related