LETTERS Figure 1. Pemio-like reaction Unusual pernio-like reaction to sulindac To the Editor: I wish to report an unusual pernio-like reaction to sulindac (Clinoril) that should be of interest to rheumatologists, since the reaction may resemble certain cryophenomena seen in vasculitic and connective tissue disorders. A 48-year-old man began to have arthralgias in shoulders, wrists, and small joints of the hands and feet in late 1978. Results of an examination were normal, as were sedimentation rate, rheumatoid factor, and antinuclear antibody tests. Despite trials of salicylates and naproxen, he developed progressive morning stiffness, fatigue, and definite synovitis of several metatarsophalangeal joints. In January 1979, he was placed on sulindac 200 mg twice a day. Ten days later he reported painful tips of the second and third toes bilaterally. He reported no unusual cold exposure, other than normal Minnesota winter living. He was receiving no other medications, had no previous similar episodes, and had no history of diabetes, claudication, Raynaud’s phenomenon, or upper extremity symptoms. Examination revealed changes as shown in Figure 1, consisting of swelling, purple discoloration, red papules, and desquamation of the distal aspects of several toes. Complete blood count, cold agglutinins, cryoglobulins, cryofibrinogens, sedimentation rate, and serologic test for syphilis were all either normal or negative. Sulindac was discontinued, and the lesions resolved over 2 weeks. During the next year, he developed typical seronegative rheumatoid arthritis. He used a number of 1215 other antiinflammatory drugs without any similar reaction. In November 1980, he took 3 doses of 200 mg of sulindac out of curiosity. Within 24 hours he developed identical reactions in several toes. Again, there was no associated unusual cold exposure. The changes resolved in 1 week without residua. The manufacturers of sulindac are aware of reports of similar reactions in 2 women who developed Raynaud-like changes in the hands after brief exposure to sulindac (S. L. Kasdin, personal communication). My patient’s reaction was not Raynaud’s-like but rather resembled pernio, or “chilblains” (Herman EW, Kezis JS, Silvers DN: A distinctive variant of pernio. Arch Dermatol 1 17:26-28, 1981). Physicians should be aware of this reaction in patients on Clinoril, particularly patients in whom such “cryophenomena” might cause diagnostic confusion. JAMESL. REINERTSEN, MD Department of Rheumatology St. Louis Park Medical Center 5000 West Thirty-Ninth Street Minneapolis, MN 55416 Intravenous administration of colchicine To the Editor: The intravenous administration of colchicine is an accepted therapeutic modality for patients with gouty arthritis (1,2). In addition, recent reports suggest that intravenous colchicine may be the treatment of choice in acute pseudogout (3,4). Our rheumatology service saw an alcoholic patient who presented with acute gouty arthritis. Since the patient had gastritis, we felt that it would be prudent to avoid oral administration of colchicine or nonsteroidal antiinflammatory agents which might irritate the gastrointestinal tract. Intravenous colchicine appeared to be the appropriate alternative. Colchicine solution is extremely caustic (sodium hydroxide may be added to adjust the pH). Accidental extravasation of the solution may cause severe local irritation and tissue necrosis (5). Thus, it has been standard practice to dilute the solution prior to injection (6) and often, to administer it through an established intravenous line. To our surprise, a resident physician directed our attention to the current product labeling for injectable colchicine which states that “colchicine injection should not be diluted with or injected into intravenous tubing containing 0.9% sodium chloride, 5% LETTERS 1216 dextrose injection or any other fluid which would even slightly change the pH of the colchicine solution since this may cause precipitation.” Because this is a revision of previous package labeling, we directed inquiries to the Eli Lilly Company, the only pharmaceutical concern currently supplying colchicine for intravenous use. We were informed that this change resulted from communications to them from physicians who had noted precipitates in solutions following dilution of colchicine with dextrose or saline. As a consequence, the company restudied batches of injectable colchicine produced over the last several years but to date has been unable to identify a specific contaminant. Using normal saline as diluent, they have not found significant precipitation. It has been decided to shorten the “out-date’’ time to 4 years, and we have been informed that future product inserts will state that if the solution of colchicine is to be diluted, 0.9% Sodium Chloride Solution USP XX be used, while recommending against the use of 5% dextrose solution or any solution containing a bacteriostatic agent (7). Physicians should, of course, discard any solution in which a precipitate is noted. Precipitate is best seen by holding a solution against a dark background with light directed at the solution from the side. In any event, it would be judicious to use an intravenous system equipped with a final filter when giving diluted colchicine. DAVID J. NASHEL, MD Chief, Rheumatology Section Veterans Administration Medical Center 50 Irving Street, N W Washington, DC 20422 1. McCarty DJ: Pathogenesis and treatment of crystal-induced inflammation, Arthritis and Allied Conditions. Edited by DJ McCarty. Philadelphia, Lea & Febiger, 1979, p 1257 2. Kelley WN: Gout and related disorders of purine metabolism, Textbook of Rheumatology. Vol. 2. Edited by WN Kelley, ED Harris, S Ruddy, CB Sledge. Philadelphia, WB Saunders, 1981, p 1421 3. Tabatabia MR,Cummings NA: Intravenous colchicine in the treatment of acute pseudogout. Arthritis Rheum 23:370-374, 1980 4. Spilberg I, McLain D, Simchowitz L, Berney S: Colchicine and pseudogout. Arthritis Rheum 23: 1062-1063, 1980 5 . Wallace SL: The treatment of gout. Arthritis Rheum 15:317-323, 1972 6. Wyngaarden JB, Kelley WN: Gout and Hyperuricemia. New York, Grune and Stratton, 1976, pp 466471 7. Dyke R: Eli Lilly Company, personal communication Table 1. Incidence of HLA-B27 in J R A patients Onset. No. patients B27+ 96 6 11 14 - - 1 8 50 Males and females A P 0 I Males only A P 0 *A - acute onset; P = polyarticular, 0 = oligoarticular. On the heterogeneity of HLA association in juvenile rheumatoid arthritis To the Editor: In response to a recent article entitled “Heterogeneity of HLA Associations in Systemic Onset Juvenile Rheumatoid Arthritis” by Glass and Litvin (I), we would like to contribute some information about the presence of different HLA antigens in the various subgroups of juvenile rheumatoid arthritis (JRA). The results described in this letter were already discussed at our Rheumatology Congress in 1978 (2). Our experience was based on the typing of 31 JRA patients, 6 with the acute onset form, 11 with the polyarticular form, and 14 with oligoarticular form. Diagnosis conformed to American Rheumatism Association criteria (3); most antisera used for HLA typing have been accepted by the international workshop. B27 antigen was present in 27% of patients of the entire group. Its incidence rose to 85% in males with oligoarticular form and tended to be higher in patients older than 10 (Table 1). Bw35 incidence was higher in patients with the acute form ( 5 of 6) as shown in Table 2. We did not take into account this result, however, because of the small number of subjects and the high incidence of this antigen in our control group (32.09%).At the present time, our cases have almost doubled, and Bw35 is present in 6W0 of the patients with acute onset JRA (4); therefore, our previous report about the incidence of B27 in the oligoarticular form is substantially confirmed (5). Table 2. Acute onset J R A
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