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Idiosyncratic Reactions to Gold Salt Preparations To The Editor: My recent experience with the use of aqueous gold sodium thionlalate (Myochrysine) and oil-based gold thioglucose (Solganol) may be of unusual interest to rheumatologists, especially in view of the recent study reported by Rothermich et al. (Arthritis Rheum 19:132 1-1 327, 1976). A 43 year old woman had active progressive rheumatoid arthritis (RA) that was initially diagnosed in 1974 at another hospital. She was treated with salicylates with partial response, and then gold thiomalate. After her sixth injection an erythematous pruritic rash developed on the face and trunk, and the gold was discontinued. Several weeks later gold thiomalate was reinstituted at a lower dose, but again cutaneous toxicity forced discontinuation. She was seen initially at our clinic in December I974 with clinical, serological, and radiographic evidence of active RA (polyarthritis, subcutaneous nodules, wrist and finger deformities, morning stiffness, anemia, elevated sedimentation rate, high-titer latexfixation test, a strongly positive ANA, osteoporosis. and multiple cortical erosions), Her arthritis proved refractory to therapy with salicylates, prednisone (10 mg/day and then 20 mg/day), and azathioprine (150 mg/day). Penicillamine had to be stopped after 6 weeks of therapy when pruritic erythroderma developed (at a dose of 750 mg/day). Since persistent active disease had not responded satisfactorily to other therapeutic modalities, we elected to give her a trial of gold thioglucose in oil, despite her history of gold intolerance. Prednisone and aspirin were continued. The patient tolerated incremental doses of gold thioglucose without ill effect and was thereafter maintained on weekly doses of 50 mg with remarkable clinical improvement. Within 2 months articular index and morning stiffness had markedly diminished, afternoon fatigue abated, and her hematocrit rose from 3 I % to 39%. No mucocutaneous, hematologic, or renal abnormalities were noted. The major remaining problem was persistent arthritis of the right knee, where pain and swelling markedly limited her activities. She was admitted to the orthopedic service in April 1977 for total replacement of the right knee. The procedure was performed without complication, but due to an oversight she received 50 rng of gold thiomalate instead of her usual dose of gold thioglucose. Within 4 days she had
dkveloped an erythematous pruritic facial rash, and shortly thereafter several painful ulcerations of the lingual and buccal mucosa were noted. Gold therapy was withheld until her discharge 2 weeks later. When seen again as an outpatient, she was suffering from an obvious clinical recrudescence of rheumatoid arthritis with multiple warm, tender joints and enlarging subcutaneous nodules. Cautious reinstitution of gold thioglucose was begun with weekly incremental dosage. Again, clinical remission ensued and has persisted (with decreasing frequency of administration) for 5 months without evidence of gold toxicity. This patient represents an unusual, internally controlled experience. Her ability to tolerate gold thioglucose despite two documented reactions to gold thiomalate is a dramatic illustration that idiosyncratic reactions to gold can vary with the gold salt preparation employed. Clearly other studies are needed in this area. It would certainly be of interest to know whether other physicians have seen similar responses, or the converse, that is, tolerance to gold thiomalate after known toxic reactions to gold thioglucose.
GILBERT L. Ross, M.D. Department of Rheumatology Montefore Hospital and Medical Center Bronx, New York i0467
Arthropathy Associated with Cutaneous Pol yarteritis To the Editor: We read with interest the recent report of Smukler and Schumacher (ARTHRITIS RHEUM20: 1 1 15-1 120, 1977) associating cutaneous polyarteritis with nondestructive inflammatory arthritis of the knees. The two cases described were similar in many respects to a patient we have followed for approximately 3 years, who in addition to having livedo reticularis as a manifestation of cutaneous polyarteritis, has suffered with hecrotizing vasculitis of the toes causing skin discoloration, ulceration, infarction, and gangrene. Pertinent aspects of this case, including evaluation, clinical course, and treatment are summarized below. Case Report. A 58-year-old white male first developed pain and swelliflg of his right knee in 1962. Intermittent synovitis of both knees was noted during the next 6 years, Approximately 9 years ago pain in both
Idiosyncratic Reactions to Gold Salt Preparations To The Editor: My recent experience with the use of aqueous gold sodium thionlalate (Myochrysine) and oil-based gold thioglucose (Solganol) may be of unusual interest to rheumatologists, especially in view of the recent study reported by Rothermich et al. (Arthritis Rheum 19:132 1-1 327, 1976). A 43 year old woman had active progressive rheumatoid arthritis (RA) that was initially diagnosed in 1974 at another hospital. She was treated with salicylates with partial response, and then gold thiomalate. After her sixth injection an erythematous pruritic rash developed on the face and trunk, and the gold was discontinued. Several weeks later gold thiomalate was reinstituted at a lower dose, but again cutaneous toxicity forced discontinuation. She was seen initially at our clinic in December I974 with clinical, serological, and radiographic evidence of active RA (polyarthritis, subcutaneous nodules, wrist and finger deformities, morning stiffness, anemia, elevated sedimentation rate, high-titer latexfixation test, a strongly positive ANA, osteoporosis. and multiple cortical erosions), Her arthritis proved refractory to therapy with salicylates, prednisone (10 mg/day and then 20 mg/day), and azathioprine (150 mg/day). Penicillamine had to be stopped after 6 weeks of therapy when pruritic erythroderma developed (at a dose of 750 mg/day). Since persistent active disease had not responded satisfactorily to other therapeutic modalities, we elected to give her a trial of gold thioglucose in oil, despite her history of gold intolerance. Prednisone and aspirin were continued. The patient tolerated incremental doses of gold thioglucose without ill effect and was thereafter maintained on weekly doses of 50 mg with remarkable clinical improvement. Within 2 months articular index and morning stiffness had markedly diminished, afternoon fatigue abated, and her hematocrit rose from 3 I % to 39%. No mucocutaneous, hematologic, or renal abnormalities were noted. The major remaining problem was persistent arthritis of the right knee, where pain and swelling markedly limited her activities. She was admitted to the orthopedic service in April 1977 for total replacement of the right knee. The procedure was performed without complication, but due to an oversight she received 50 rng of gold thiomalate instead of her usual dose of gold thioglucose. Within 4 days she had
dkveloped an erythematous pruritic facial rash, and shortly thereafter several painful ulcerations of the lingual and buccal mucosa were noted. Gold therapy was withheld until her discharge 2 weeks later. When seen again as an outpatient, she was suffering from an obvious clinical recrudescence of rheumatoid arthritis with multiple warm, tender joints and enlarging subcutaneous nodules. Cautious reinstitution of gold thioglucose was begun with weekly incremental dosage. Again, clinical remission ensued and has persisted (with decreasing frequency of administration) for 5 months without evidence of gold toxicity. This patient represents an unusual, internally controlled experience. Her ability to tolerate gold thioglucose despite two documented reactions to gold thiomalate is a dramatic illustration that idiosyncratic reactions to gold can vary with the gold salt preparation employed. Clearly other studies are needed in this area. It would certainly be of interest to know whether other physicians have seen similar responses, or the converse, that is, tolerance to gold thiomalate after known toxic reactions to gold thioglucose.
GILBERT L. Ross, M.D. Department of Rheumatology Montefore Hospital and Medical Center Bronx, New York i0467
Arthropathy Associated with Cutaneous Pol yarteritis To the Editor: We read with interest the recent report of Smukler and Schumacher (ARTHRITIS RHEUM20: 1 1 15-1 120, 1977) associating cutaneous polyarteritis with nondestructive inflammatory arthritis of the knees. The two cases described were similar in many respects to a patient we have followed for approximately 3 years, who in addition to having livedo reticularis as a manifestation of cutaneous polyarteritis, has suffered with hecrotizing vasculitis of the toes causing skin discoloration, ulceration, infarction, and gangrene. Pertinent aspects of this case, including evaluation, clinical course, and treatment are summarized below. Case Report. A 58-year-old white male first developed pain and swelliflg of his right knee in 1962. Intermittent synovitis of both knees was noted during the next 6 years, Approximately 9 years ago pain in both
