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for R F positivity. In most instances, the R F titers were low, ranging from 1 :80 to 1 : 160 in the latex fixation test (positive > 1:40) or 1.32 to 1:256 in the SSCA test (positive > 1 :8). We regard these findings as preliminary. Larger numbers of patients and confirmation by other investigators definitely are needed before this apparent association can be accepted. We hope others will examine sera from gouty patients for R F activity. This welcome and somewhat unanticipated exchange may stimulate such studies.
FRANKLIN KOZIN,M.D. J. MCCARTY,M.D. DANIEL Division of Rheumatology The Medical College of Wisconsin Milwaukee County General Hospital 8700 W . Wisconsin Avenue Milwaukee, Wisconsin 53226
REFERENCES I . Eisman J, Fan PT: Rheumatoid factor in patients with gout. Arthritis Rheum 20:1147, 1977 2. Kozin F, McCarty DJ: Protein adsorption to monosodium urate, calcium pyrophosphate dihydrate, and silica crystals: relationship to pathogenesis of crystal-induced inflammation. Arthritis Rheum 19:433-438, 1976 3. Kozin F, Ginsberg MH, McCarty DJ: Protein adsorption: a possible mechanism of crystal-induced inflammation in gout (abstr) J Clin Chem Clin Biochem 14:303, 1976 4. Wallace S, Robinson H. Masi AT, et al: Preliminary criteria for the classification of the acute arthritis of primary gout. Arthritis Rheum 202395-900. 1977 5 . McCarty DJ: Diagnostic mimicry in arthritis-patterns of joint involvement associated with calcium pyrophosphate dihydrate crystal deposits. Bull Rheum Dis 25:804-809, 1974- 1975 6. Howell FA, Chamberlain MA, Perry RA, Torrigiani G, Roitt IM: IgG antiglobulin levels in patients with psoriatic arthropathy, ankylosing spondylitis, and gout. Ann Rheum Dis 31:129-131, 1972
Zinc Sulfate and Penicillamine To the Editor: Whitehouse et al. warn that zinc sulfate and penicillamine should not be tried together in patients with rheumatoid arthritis ( I ) . They are entirely correct. Besides possibly causing greater toxicity, as these authors caution, zinc in modest (5 mg) supplements may render oral penicillamine less effective against rheumatoid synovitis (2).
I n my paper, “Oral Zinc Sulphate in Rheumatoid Arthritis” (3), I reasoned that the beneficial effects of penicillamine might be mediated through the profound effect of this agent on the metabolism of zinc. My question, which remains open, was whether an apparently less toxic agent (zinc sulfate) may be as beneficial as a more toxic agent (penicillamine). I did not suggest that the two should be used together. Nevertheless, a few physicians have so interpreted the paper and have tried zinc and penicillamine concurrently. The warning of W hitehouse el al. is thus both timely and appropriate. PETERA. SIMKIN, M.D. Division of Rheumatology RG-20 University of Washington Seattle, Washington 981 95
REFERENCES I . Whitehouse, MW, Hanley WS, Field L A potential hazard: toxicity of zinc with penicillamine. Arthritis Rheum 20: 1035, 1977 2. Mery C, Delrieu F, Ghozian R, et al: Controlled trial of DPenicillamine in rheumatoid arthritis: dose effect and the role of zinc. Scand J Rheumatology 5:241-247, 1976 3. Simkin, PA: Oral zinc sulphate in rheumatoid arthritis. Lancet 2539-542, 1976
Ruptured Popliteal Cyst and Thrombophlebitis To the Editor: A ruptured popliteal (Baker’s) cyst clinically resembles calf thrombophlebitis (1-3). We would like to briefly report a patient who was found to have both an arthrogram-proved ruptured popliteal cyst and phlebogram-proved thrombophlebitis simultaneously in the same leg. This 69-year-old man was hospitalized complaining of pain, swelling, and tenderness of his right calf of 6 days’ duration. He had history of recurrent effusions in his right knee, and there was radiological evidence of osteoarthritis of that knee. He denied any history of pain or swelling of other joints. The right calf was swollen and tender, and Homan’s sign was positive. The diagnosis of thrombophlebitis was made and later confirmed by a positive right leg phlebogram. He developed hemarthrosis in his right knee a day after the start of heparin therapy for thrombophlebitis. An underlying ruptured popliteal cyst on the right side was suspected, and it was confirmed by an arthrogram.
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The anticoagulant therapy was cautiously resumed because the thrombus was extending to the femoral vein up to the mid-thigh, and it was felt that the risk of a potentially fatal pulmonary embolism outweighed the risk of recurrence of hemarthrosis and resultant morbidity. He responded quite well to the treatment, and a repeat phlebogram 18 days later showed almost complete resolution of the thrombus. Spontaneous hemarthrosis in a normal joint during heparin therapy is very rare, and only one such case has been reported (4). Hemarthrosis and cystic hematoma have been described in patients with popliteal cyst who were given anticoagulant therapy for suspected deep vein thrombosis, though phlebograms were not obtained to confirm the diagnosis (1, 2). However, we are not aware of any previous report of an association of arthrogram-proved ruptured popliteal cyst with phlebogram-proved thrombophlebitis. We believe that our patient had a ruptured popliteal cyst as the primary event. He then confined himself to bed with a painful swollen leg for 6 days before seeking medical help, and this immobility led secondarily to the development of thrombophlebitis. The hemarthrosis occurred because of the effect of heparin on the ruptured popliteal cyst. This case demonstrates that the occurrence of knee joint hemarthrosis in a patient on anticoagulant therapy for “thrombophlebitis” of the same leg should suggest the diagnosis of a ruptured popliteal cyst. This may even be true in a patient with phlebogram-proved thrombophlebitis, as was the case in our patient who probably developed thrombophlebitis secondarily to rupture of the popiteal cyst. MUHAMMAD A. KHAN,M.D.,M.R.C.P. CARLOS GANUZA, M.D. Division of Rheumatology Department of Medicine Cleveland Metropolitan General Hospital Cleveland, Ohio 441 09
REFERENCES Good AE: Rheumatoid arthritis, Baker’s cyst and “thrombophlebitis.” Arthritis Rheum 756-64. 1964 Tait GBW. Bach F, Dixon A St J: Acute synovial rupture: further observations. Ann Rheum Dis 24:273-277, 1965 Schmidt MC, Workman JB, Barth WF: Dissection or rupture of a popliteal cyst: a syndrome mimicking thrombophlebitis in rheumatic disease. Arch Intern Med 1341694-698. 1974 Katz AL, Alepa FP: Hemarthrosis secondary to heparin therapy. Arthritis Rheum 19:966, 1976
Myocardial Infarction After a Gold-induced Nitritoid Reaction To the Editor: The recent report by Gottlieb and Brown ( I ) documenting a myocardial infarction after a gold-induced nitritoid reaction prompted us to review the records of a patient first evaluated in 1970. A 62-year-old woman with a 20-year history of rheumatoid arthritis was seen for continuation of gold therapy that had been initiated elsewhere. The patient had no history of cardiovascular disease, and synovitis had been well controlled with salicylates and monthly gold sodium thiomalate (GST). On October 17, 1972, after having been on GST without evidence of toxicity for 4 years, the patient had a mild nitritoid reaction following a 50-mg injection. One month later, GST was administered and no vasomotor reaction occurred. On December 13, 1972, shortly after a 50-mg injection of GST, the patient complained of dizziness, and a transient malar flush was noted. Several hours later she reported vague chest discomfort with nausea and vomiting. The next morning she was hospitalized with a dense left hemiparesis. An electrocardiogram showed changes of an anterior wall myocardial infarction. Twenty-four hours later the patient suffered a cardiac arrest, and efforts at resuscitation were unsuccessful. An autopsy revealed acute anteroseptal myocardial infarction, occlusion of the left anterior descending branch of the left coronary artery, and massive infarction of the right cerebral hemisphere. We assumed that hypotension associated with the nitritoid reaction precipitated the myocardial infarct. Mural thrombus formation with embolization in all likelihood led to the cerebral infarct. Whether there was a direct causal relationship between the gold-induced vasomotor reaction and subsequent events remains speculative. We agree with Gottlieb and Brown, however, that aurothioglucose is the safer gold formulation in patients who might have underlying cardiovascular disease.
K . HARRIS, M.D. BENJAMIN Section of Rheumatology Good Samaritan Hospital Phoenix, Arizona REFERENCES I . Gottlieb NL, Brown HE Jr: Acute myocardial infarction following gold sodium thiomalate induced vasomotor (nitritoid) reaction. Arthritis Rheum 20: 1026-1028, 1977
for R F positivity. In most instances, the R F titers were low, ranging from 1 :80 to 1 : 160 in the latex fixation test (positive > 1:40) or 1.32 to 1:256 in the SSCA test (positive > 1 :8). We regard these findings as preliminary. Larger numbers of patients and confirmation by other investigators definitely are needed before this apparent association can be accepted. We hope others will examine sera from gouty patients for R F activity. This welcome and somewhat unanticipated exchange may stimulate such studies.
FRANKLIN KOZIN,M.D. J. MCCARTY,M.D. DANIEL Division of Rheumatology The Medical College of Wisconsin Milwaukee County General Hospital 8700 W . Wisconsin Avenue Milwaukee, Wisconsin 53226
REFERENCES I . Eisman J, Fan PT: Rheumatoid factor in patients with gout. Arthritis Rheum 20:1147, 1977 2. Kozin F, McCarty DJ: Protein adsorption to monosodium urate, calcium pyrophosphate dihydrate, and silica crystals: relationship to pathogenesis of crystal-induced inflammation. Arthritis Rheum 19:433-438, 1976 3. Kozin F, Ginsberg MH, McCarty DJ: Protein adsorption: a possible mechanism of crystal-induced inflammation in gout (abstr) J Clin Chem Clin Biochem 14:303, 1976 4. Wallace S, Robinson H. Masi AT, et al: Preliminary criteria for the classification of the acute arthritis of primary gout. Arthritis Rheum 202395-900. 1977 5 . McCarty DJ: Diagnostic mimicry in arthritis-patterns of joint involvement associated with calcium pyrophosphate dihydrate crystal deposits. Bull Rheum Dis 25:804-809, 1974- 1975 6. Howell FA, Chamberlain MA, Perry RA, Torrigiani G, Roitt IM: IgG antiglobulin levels in patients with psoriatic arthropathy, ankylosing spondylitis, and gout. Ann Rheum Dis 31:129-131, 1972
Zinc Sulfate and Penicillamine To the Editor: Whitehouse et al. warn that zinc sulfate and penicillamine should not be tried together in patients with rheumatoid arthritis ( I ) . They are entirely correct. Besides possibly causing greater toxicity, as these authors caution, zinc in modest (5 mg) supplements may render oral penicillamine less effective against rheumatoid synovitis (2).
I n my paper, “Oral Zinc Sulphate in Rheumatoid Arthritis” (3), I reasoned that the beneficial effects of penicillamine might be mediated through the profound effect of this agent on the metabolism of zinc. My question, which remains open, was whether an apparently less toxic agent (zinc sulfate) may be as beneficial as a more toxic agent (penicillamine). I did not suggest that the two should be used together. Nevertheless, a few physicians have so interpreted the paper and have tried zinc and penicillamine concurrently. The warning of W hitehouse el al. is thus both timely and appropriate. PETERA. SIMKIN, M.D. Division of Rheumatology RG-20 University of Washington Seattle, Washington 981 95
REFERENCES I . Whitehouse, MW, Hanley WS, Field L A potential hazard: toxicity of zinc with penicillamine. Arthritis Rheum 20: 1035, 1977 2. Mery C, Delrieu F, Ghozian R, et al: Controlled trial of DPenicillamine in rheumatoid arthritis: dose effect and the role of zinc. Scand J Rheumatology 5:241-247, 1976 3. Simkin, PA: Oral zinc sulphate in rheumatoid arthritis. Lancet 2539-542, 1976
Ruptured Popliteal Cyst and Thrombophlebitis To the Editor: A ruptured popliteal (Baker’s) cyst clinically resembles calf thrombophlebitis (1-3). We would like to briefly report a patient who was found to have both an arthrogram-proved ruptured popliteal cyst and phlebogram-proved thrombophlebitis simultaneously in the same leg. This 69-year-old man was hospitalized complaining of pain, swelling, and tenderness of his right calf of 6 days’ duration. He had history of recurrent effusions in his right knee, and there was radiological evidence of osteoarthritis of that knee. He denied any history of pain or swelling of other joints. The right calf was swollen and tender, and Homan’s sign was positive. The diagnosis of thrombophlebitis was made and later confirmed by a positive right leg phlebogram. He developed hemarthrosis in his right knee a day after the start of heparin therapy for thrombophlebitis. An underlying ruptured popliteal cyst on the right side was suspected, and it was confirmed by an arthrogram.
1561
The anticoagulant therapy was cautiously resumed because the thrombus was extending to the femoral vein up to the mid-thigh, and it was felt that the risk of a potentially fatal pulmonary embolism outweighed the risk of recurrence of hemarthrosis and resultant morbidity. He responded quite well to the treatment, and a repeat phlebogram 18 days later showed almost complete resolution of the thrombus. Spontaneous hemarthrosis in a normal joint during heparin therapy is very rare, and only one such case has been reported (4). Hemarthrosis and cystic hematoma have been described in patients with popliteal cyst who were given anticoagulant therapy for suspected deep vein thrombosis, though phlebograms were not obtained to confirm the diagnosis (1, 2). However, we are not aware of any previous report of an association of arthrogram-proved ruptured popliteal cyst with phlebogram-proved thrombophlebitis. We believe that our patient had a ruptured popliteal cyst as the primary event. He then confined himself to bed with a painful swollen leg for 6 days before seeking medical help, and this immobility led secondarily to the development of thrombophlebitis. The hemarthrosis occurred because of the effect of heparin on the ruptured popliteal cyst. This case demonstrates that the occurrence of knee joint hemarthrosis in a patient on anticoagulant therapy for “thrombophlebitis” of the same leg should suggest the diagnosis of a ruptured popliteal cyst. This may even be true in a patient with phlebogram-proved thrombophlebitis, as was the case in our patient who probably developed thrombophlebitis secondarily to rupture of the popiteal cyst. MUHAMMAD A. KHAN,M.D.,M.R.C.P. CARLOS GANUZA, M.D. Division of Rheumatology Department of Medicine Cleveland Metropolitan General Hospital Cleveland, Ohio 441 09
REFERENCES Good AE: Rheumatoid arthritis, Baker’s cyst and “thrombophlebitis.” Arthritis Rheum 756-64. 1964 Tait GBW. Bach F, Dixon A St J: Acute synovial rupture: further observations. Ann Rheum Dis 24:273-277, 1965 Schmidt MC, Workman JB, Barth WF: Dissection or rupture of a popliteal cyst: a syndrome mimicking thrombophlebitis in rheumatic disease. Arch Intern Med 1341694-698. 1974 Katz AL, Alepa FP: Hemarthrosis secondary to heparin therapy. Arthritis Rheum 19:966, 1976
Myocardial Infarction After a Gold-induced Nitritoid Reaction To the Editor: The recent report by Gottlieb and Brown ( I ) documenting a myocardial infarction after a gold-induced nitritoid reaction prompted us to review the records of a patient first evaluated in 1970. A 62-year-old woman with a 20-year history of rheumatoid arthritis was seen for continuation of gold therapy that had been initiated elsewhere. The patient had no history of cardiovascular disease, and synovitis had been well controlled with salicylates and monthly gold sodium thiomalate (GST). On October 17, 1972, after having been on GST without evidence of toxicity for 4 years, the patient had a mild nitritoid reaction following a 50-mg injection. One month later, GST was administered and no vasomotor reaction occurred. On December 13, 1972, shortly after a 50-mg injection of GST, the patient complained of dizziness, and a transient malar flush was noted. Several hours later she reported vague chest discomfort with nausea and vomiting. The next morning she was hospitalized with a dense left hemiparesis. An electrocardiogram showed changes of an anterior wall myocardial infarction. Twenty-four hours later the patient suffered a cardiac arrest, and efforts at resuscitation were unsuccessful. An autopsy revealed acute anteroseptal myocardial infarction, occlusion of the left anterior descending branch of the left coronary artery, and massive infarction of the right cerebral hemisphere. We assumed that hypotension associated with the nitritoid reaction precipitated the myocardial infarct. Mural thrombus formation with embolization in all likelihood led to the cerebral infarct. Whether there was a direct causal relationship between the gold-induced vasomotor reaction and subsequent events remains speculative. We agree with Gottlieb and Brown, however, that aurothioglucose is the safer gold formulation in patients who might have underlying cardiovascular disease.
K . HARRIS, M.D. BENJAMIN Section of Rheumatology Good Samaritan Hospital Phoenix, Arizona REFERENCES I . Gottlieb NL, Brown HE Jr: Acute myocardial infarction following gold sodium thiomalate induced vasomotor (nitritoid) reaction. Arthritis Rheum 20: 1026-1028, 1977
