LETTERS 1413

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Shulman LE, Wallace SL: Preliminary criteria for the classifi- cation of systemic lupus erythematosus. Bull Rheum Dis 21:643-648, 1971 Evans DAP: An improved and simplified method of detecting the acetylator phenotype. J Med Genet 6:405407, 1969 Olson W, Miceli J , Weber W: Dose-dependent changes in sulphamethazine kinetics in rapid and slow isoniazid acetyla- tors. Clin Pharmacol Ther 23:204-211, 1978 Varley H: Practical Clinical Biochemistry. Third edition. Lon- don, Heinemann, 1962, p 634

Response to Paolaggi et al: bridging the communications gap

To the Editor: The letter by Paolaggi et a1 suggests that the mea-

surement of the acute-phase reactants orosomucoid and haptoglobin might be useful in the diagnosis and monitoring of giant cell arteritis and polymyalgia rheumatica (Paolaggi JB, Chaouat D, Auquier L: An additional test for the diagnosis and monitoring of giant cell arteritis and polymyal- gia rheumatica [letter]. Arthritis Rheum 28:837-838, 1985). Their original work was published in 1982 in French, and because of the poor communication between the French- and English-speaking rheumatologic worlds, I am afraid it was missed.

I assume it must be for the same reasons, working in reverse, that a similar study, presented in 1981 in the Annals of Rheumatic Diseases (Park JR, Jones JG, Hazelman BL: The relationship of the ESR to acute phase proteins in polymyalgia rheumatica and giant cell arteritis. Ann Rheum Dis 40:493-495, 1981), was overlooked by Paplaggi et al. This study involved 108 patients who had polymyalgia rheumatica and/or giant cell arteritis at various stages. In addition to the erythrocyte sedimentation rate (ESR), orosomucoid level, and haptoglobin level, my colleagues and I measured a,-antitrypsin and C-reactive protein levels in that study. In essence, the results of the 2 studies are in agreement. Unlike the French authors, though, we found the correlation between the various acute-phase reactants and the ESR to be so strong that we concluded, “There was nothing to suggest that any other measurement was superior to the ESR which showed the highest correlation with disease activity. In those occasional cases where the ESR is normal in the presence of acute disease, measurement of the other acute phase reactants may be worthwhile.”

One of the main objectives of the recently approved plan to build a tunnel connecting France to the British Isles is to improve communication between the two nations. Perhaps this should inspire the English- and French- speaking rheumatologic worlds to draw more closely to- gether. Our ignorance of each other’s work on the same topic illustrates that there is certainly a gap to be bridged (or tunnelled under).

Je vous prie d’agreer, Monsieur, l’expression de ma consideration distinguee.

J. G. Jones, MD, FRACP Queen Elizabeth Hospital Rotorua, New Zealand

“Choree fibrillaire de Morvan” followed by Guillain-BarrC syndrome in a patient receiving gold therapy

To the Editor: Neurologic complications and psychiatric alterations

are well-documented adverse reactions to gold therapy (1). Symmetric sensory or sensorimotor neuropathy accounts for the majority of reported cases (2). Some patients develop acute illness: psychiatric manifestations (3), or a cluster of signs and symptoms which Morvan called “choree fibril- laire” (4), or a polyradiculitis resembling Guillain-Barre syndrome (5). In a recent issue of Arthritis and Rheumatism, Roquer et a1 (6) described a case of Miller-Fischer syndrome (Guillain-Barre syndrome with ophthalmoplegia). We ob- served a patient with rheumatoid arthritis (RA) who pre- sented with choree fibrillaire during gold therapy, and Guil- lain-Barre syndrome when gold was restarted 11 months later. To the best of our knowledge, this association of adverse reactions during gold therapy has not been previ- ously reported.

The patient, a 47-year-old woman, had had RA for 6 months and had been receiving gold salts (sodium aurothio- propanol sulfonate [SATPS]) for 2 months when she devel- oped severe pain in the back and in both thighs. The pain was continuous, in spite of symptomatic drug therapy, and the patient complained of feeling depressed. Two weeks later, she presented with erythema and pruritus, so we withdrew gold therapy. The cumulative dosage of metallic gold at that point was 0.26 gm.

The patient was admitted to the Department of Rheumatology , where the following were noted: severe back pain, depression, insomnia, generalized fascicular twitching (though not involving the facial muscles), labile blood pres- sure, tachycardia (120 beatdminute), and excess sweating without fever. No other abnormalities were found on neurologic examination. A diagnosis of choree fibrillaire de Morvan was proposed. The laboratory findings were as follows: erythrocyte sedimentation rate, 12 mm/hour; blood cell count, normal, with an eosinophil count of 243/mm3; positive rheumatoid factor, with a latex fixation titer of 1 : 320; and low-titer antinuclear antibodies. Anti-DNA and anti-extractable nuclear antigen assays were negative. Roentgenogram studies showed erosions of several metacar- pal and metatarsal heads, and narrowing of the third and fourth interphalangeal joints of both hands. The patient improved gradually, but she remained depressed and was transferred to a psychiatry ward. She was discharged in good condition after 2 months, at which time she was taking only nonsteroidal antiinflammatory drugs. Six months later, gold therapy was resumed with a low-dose regimen of SATPS, 0.01 gm/week.

After 3 months and a cumulative metallic gold dose of 0.20 gm, she complained of numbness of the hands and feet. Shortly afterwards, she presented with symmetric ascending motor weakness, areflexia, distal sensory impair- ment, and albumino-cytologic dissociation of the spinal fluid. The protein level was 3.4 gm/100 ml, and the leukocyte count was 2/mm3. A diagnosis of Guillain-Barre syndrome was made. Gold therapy was discontinued, but paralysis spread to her respiratory muscles. The patient was transferred to an