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had gone into spontaneous clinical remission 5 years ago, but she also had the group’s highest ESR (30 mm/hour). Control of her disease by suppressor T cells might be suggested, but her cells did not seem to bear the Ia marker (the percentage of OK1 1 + cells was not elevated), although the increase of expression of Ia antigens has been shown to be on the OKT 8+ subset (4).

These data indicate the importance of complete clinical, biologic, and therapeutic information to accurately define the clinical status of RA patients. We believe that a thorough study of patients in clinical remission would further the understanding of the biologic dysfunction that occurs in RA. Moreover, the use of other biologic parameters may help to define more precisely future subgroups of RA patients in clinical remission.

G. Faure Hbpital Necker Puris, France and Luhoratoire d’lmrnunologie FacultP de MPdecine Vandoeuvre-Les-Nuncy, France M. F. Kahn Hbpitul Bichut Paris, France M. A. Bach J. F. Bach Hbpitul Necker Paris, France

Pinals RS, Masi AT, Larsen RA: Preliminary criteria for clinical remission in rheumatoid arthritis. Arthritis Rheum 24: 1308-1315, 1981 Ropes MW, Bennett GA, Cobb S, Jacox R, Jessar RA: 1958 revision of diagnostic criteria for rheumatoid arthritis. Bull Rheum Dis 9:175-176, 1958 Faure G , Bach MA, Bene MC, Kahn MF, Bach JF, Gaucher A: Etude des sous-populations lymphocytaires T au cours des rhumatismes inflammatoires chroniques. Rev Rhum 49:439-445, 1982 Burrnester GR, Yu DTY, Irani AM, Kunkel HG, Winchester RJ: la+ T cells in synovial fluid and tissues of patients with rheuma- toid arthritis. Arthritis Rheum 24: 1370-1376, 1981

Colchicine and arthropathy of Behqet’s disease

To the Editor: In your February 1982 issue, Frayha reported a

patient with marked synovial pleocytosis who responded dramatically to colchicine therapy, and he encouraged the use of that drug for the arthropathy of Behqet’s disease (Frayha RA: Arthropathy of Behqet’s disease with marked

synovial pleocytosis responsive to colchicine. Arthritis Rheum 25:235-236, 1982). In a similar case, we treated a patient with colchicine; there was no clinical benefit, al- though the cellular population of synovial fluid was greatly changed.

For 5 years our patient, a 35-year-old white man, has had definite Behqet’s disease with recurrent aphthous sto- matitis and genital ulcers, arthritis of the knees, and cutane- ous hyperreactivity to pricking. During an episode of febrile arthritis of the right knee, 35 ml of cloudy yellow synovial fluid was aspirated. The fluid exhibited a “fair” mucin test; specific gravity was 1,030 and total protein was 5.28 gm%. Total white blood count was 70,000/mm3 with 90% polymor- phonuclear leukocytes. Synovial sugar was normal; results of bacteriologic tests and polarized microscopic study for crystals were negative. Colchicine therapy (2 mgiday orally) was started.

In spite of a slight improvement at the start of therapy, severe signs of phlogosis persisted with marked swelling and reappearance of abundant fluid. Two weeks after the start of colchicine treatment, arthrocentesis was again performed. Surprisingly, the synovial fluid had only a few mononuclear cells, while specific gravity and protein were at the same high levels as before.

For our patient, the colchicine treatment had a biologic effect (disappearance of polymorphonuclear leuko- cytes from synovial fluid) but did not produce any clinical benefits. We conclude that the enhanced chemotaxis of leukocytes is not the only cause of synovitis in Behqet’s disease and that trials with other drugs-such as de Mer- ieux’s study of levamisole (de Merieux P, Spitler LE, Paulus HE: Treatment of Behqet’s syndrome with levamisole. Ar- thritis Rheum 24:64-70, 1981)-are justified.

Venceslao Fossaluzza Ospedule Civile S. Muriu della Misericordiu 33100 Udine, Ituly

Colchicine and pseudogout

To the Editor: In a letter to the editor (Spiliotis TE: Colchicine and

chronic pseudogout. Arthritis Rheum 24:862, 198 I ) , Spiliotis described a case in which small oral doses of colchicine were used to treat a patient with chronic pseudogout accompanied by frequent acute-subacute attacks. Colchicine was effective both in treatment of the chronic synovitis and in prevention of the acute-subacute attacks.

We, too, have used oral colchicine in the treatment of pseudogout, as we reported to the Twelfth Spanish Rheumatology Conference in May 1978. In that report we described the use of oral colchicine for the prophylaxis of acute attacks of pseudogout in 12 patients suffering from this

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condition, who presented with acute attacks (average 9.3) the year before the study. Each patient was treated exclu- sively with oral colchicine (1 mg daily) for 1 year. The result was an evident decline of acute attacks in these patients (average 2.4, P < 0.05). This suggests that colchicine can have a prophylactic effect in the acute inflammation of pseudogout.

Tomas Gonzalez Marian Gantes Hospital General y Clinic0 de Tenerife Facultud de Medicinu de La Laguna Cunary Islands, Spain

Thrombocytopenia in Sjogren’s syndrome

To the Editor: Recently we reported a patient with Sjogren’s syn-

drome, thrombocytopenia, and paraproteinemia, and we stressed the rarity of thrombocytopenia in this syndrome ( I ) . We now report another patient with a similar disease course.

A 45-year-old woman was referred to us because of thrombocytopenia found on routine examination. She had a history of back pain some years earlier but had been treated only with analgesics.

On admission, no liver, spleen, or lymph nodes were palpable. Laboratory data were as follows: erythrocyte sedimentation rate (ESR) 15 mmihour (Westergren); hemo- globin 13.7 gm/liter; hematocrit 41%; white blood cell count (WBC) 5,400 x IO‘lliter, with a normal differential count; platelet count 70 x lO’/Iiter. Results of blood chemistry tests, urinalysis, and serologic tests (including lupus erythe- matosus preparation, complement levels, and antinuclear factor) were within normal limits. Cryoglobulin was not found; serum protein electrophoresis showed a mild hetero- genic hypergammaglobulinemia, but no paraprotein. Be- cause the patient complained of dryness in the mouth, a Schirmer’s test was performed; the results showed a partial positive reaction. Bone marrow examination showed an increase in immature megakaryocytes and mild lymphoplas- mocytosis; because of this finding, chronic immune throm- bocytopenic purpura could not be excluded.

No treatment was given to the patient, but her progress was followed in the outpatient clinic. One year after the first examination, dryness in the mouth and eyes was more severe. Results of the laboratory tests were as follows: ESR 40 mm/hour; hemoglobin 12.7 gm/liter; hematocrit 37%; WBC 5,200 x 106/liter with normal differential count; plate- lets 70 X 109/liter. Results of blood chemistry tests (including kidney and liver tests) and protein studies remained within normal limits. Leukocyte and thromboagglutinin test results were negative, as were the results of direct immunofluores- cence tests for platelet IgG. C3 was 85 mgiml (earlier it had been 123 mg/ml); C4 was 15 mg/ml (earlier it had been 24.5 mg/ml); and total hemolytic activity was 25% of normal. The Schirmer test results were positive for both eyes (earlier they had been positive for only one eye).

To confirm the diagnosis of Sjogren’s syndrome, we performed a labial biopsy. No immunoglobulins were detect- ed by direct immunofluorescence on frozen sections. The histology showed foci of lymphocytic infiltrate in the sali- vary glands, which is consistent with Sjogren’s syndrome grade 4 (2).

In summary, thrombocytopenia can occur in Sjo- gren’s syndrome (1,3) and, as in this patient, can even precede the complete picture of the syndrome.

Alain Berrebi, MD Motti Shtalrid, MD Monica Talmor, MSc Eljakim Vorst, BSc Kaplan Hospital Rehovot, Israel

1. Berrebi A, Schattner A: Sjogren’s syndrome with IgG kappa paraprotein and thrombocytopenia. Arthritis Rheum 24: 145 1- 1452, 1981

2. Chisholm DM, Mason DK: Labial salivary gland biopsy in Sjogren’s disease. J Clin Pathol 2 I :656-660. 1968

3. Whaley K, Webb J , McAvoy BA: Sjiigren’s syndrome. 11. Clinical associations and immunological phenomena. Q J Med 42:513-548, 1973

Rarity of nephropathy in ankylosing spondylitis

To the Editor: In a recent article, Jennette et al (1) suggested that

IgA nephropathy may be associated with seronegative spon- dylarthropathies. They questioned whether this apparent link could be a general one demonstrable at low frequency or a local phenomenon caused by a regional environmental stimulus. The former possibility, as they suggest, seems unlikely since there have been several studies performed that have looked repeatedly at renal function in ankylosing spondylitis.

In one such investigation, a pharmacologic study (21, 30 patients with ankylosing spondylitis were seen on nine occasions during a 6-month period. In a more specific investigation of renal glomerular function (3), a different series of 38 consecutive patients was evaluated with urinaly- sis and formal study of glomerular function. In none of these 68 patients was there an episode of microscopic hematuria. If a nephropathy occurs in ankylosing spondylitis, it appears to be extraordinarily rare.

Andrei Calin, MD, MRCP Stunford University Medical Center Stanford, C A

1 . Jennette JC, Ferguson AL, Moore MA, Freeman DG: IgA nephropathy associated with seronegative spondylarthropathies. Arthritis Rheum 25: 144-149, 1982

2. Calin A, Britton M: Sulindac in ankylosing spondylitis: double blind evaluation of sulindac and indomethacin. JAMA 242: 1885- 1886, 1979

3. Calin A: Renal glomerular function in ankylosing spondylitis. Scand J Rheumatol 4:241-242, 1975