LETTERS

graphy revealed that the shin mass was an anterior dissec- tion of the popliteal cyst (Figure 1).

Antibiotic therapy (fusidic acid and cephalexin) was started, and a surgical drainage procedure with wide de- bridement was performed, along with a synovectomy of the left extensor tendons.

The anterior dissection of a popliteal cyst is unusual (2); O’Dell found only 1 other case in the English literature (3). Possibly, additional cases of this complication have occurred but have not been published.

The diagnosis was not difficult in our patient because we were aware of the presence of a popliteal cyst. The infection may have caused rapid enlargement of the anterior dissection (4). A septic hematogenous spread from a chronic infection of the olecranon bursitis must be suspected. We don’t think the previous synoviorthesis of the cyst could have caused the infection, since it was performed much

Figure 1. Cystogram showing the anterior dissection of the popliteal cyst.

earlier, and we are not aware of osmic acid synoviorthesis ever having led to septic complication (5).

If clinical examination leads to an unconfirmed suspi- cion of popliteal cyst as the cause of a shin mass, puncture and cystogram can easily be performed to verify the diagno- sis.

A. Thevenon, MD P. Hardouin, MD B. Duquesnoy, MD H6pital de lu Charit6 Lille, France

I . O’Dell JR, Andersen PA, Hollister JR, West SG: Anterior tibia1 mass: an unusual complication of popliteal cysts. Arthritis Rheum 27:113-115, 1984

2. Hench PK, Smith JL: Atypical syndromes associated with syno- vial cysts of the knee (abstract). Arthritis Rheum 12:302-303, 1969

3. Jayson MIV, Dixon AS: Valvular mechanisms in juxta-articular cysts. Ann Rheum Dis 29:415-420, 1970

4. Stewart IM, Swinson DR, Hardinge K: Pyogenic arthritis pre- senting as a ruptured popliteal cyst. Ann Rheum Dis 38: 181-182, 1979

5. Delcambre B, DeFrance D, Douchy P, Robert d’Eshougues J: Les synoviortheses B I’acide osmique dans le traitement de la maladie rhumatoi‘de: remarques et bilan de 5 annkes d’utilisation. Lille Mtd 21:813-820, 1976

Comment on article by Brenner et al

To the Editor: Brenner et al recently reported that T-enriched pe-

ripheral blood mononuclear cells (PBMC) from patients with Reiter’s syndrome responded better to formalin-treated Yer- sinia enterocolitica serotype 3 (Ye3) than did similarly enriched cells from HLA-B27 positive controls (Brenner MB, Kobayashi S, Weisenhutter CW, Huberman AK, Bales P, Yu DTY: In vitro T lymphocyte proliferative response to Yersinia enterocolitica in Reiter’s syndrome: lack of re- sponse in other HLA-B27 positive individuals. Arthritis Rheum 27:250-257. 1984). This difference was not seen if non-enriched PBMC were used, nor was it seen if heat-killed Ye3 were used. They suggested that this represented a disease-specific response to a Ye3 antigen present on forma- lin-killed but not heat-killed organisms, and that the re- sponse was detectable only by the T-enriched populations.

An examination of the data reveals an alternative interpretation. Lymphocyte response was assessed in the conventional way by the incorporation of tritiated thymidine into proliferating lymphocytes. The results were expressed as average counts per minute of stimulated cells, minus background. Although stated to be consistently less than 4,000 cpm, this latter figure is not provided for individual groups.

Even without knowledge of the actual background levels, it can be seen from Table 1 that all subjects responded

LETTERS 479

22 7 Table 1. Response of peripheral blood mononuclear cells (PBMC) to heat- and formalin-killed Yersinia enterocolitica serotype 3 (Ye3)

Counts per minute of cultured cells from:

Reiter’s B27+ Antigen Cells used Datients controls

Ye3 formalin PBMC 28,531 29,943 Ye3 formalin T-enriched PBMC 27,409 5,414 Ye3 heat T-enriched PBMC 21,888 15,383

to both heat- and formalin-killed Ye3 antigens, with a significant elevation of cpm.

However, when lymphocytes depleted of non-T cells were studied, Reiter’s patients maintained their response to formalin-killed Yrrsinia, while the response of the controls was reduced by the procedure. This emphasis is different from that of Brenner et al.

The change in response in the B27 positive control subjects remains an interesting finding, but may have more to do with qualities of antigen-presenting cells in the 2 groups. We agree that the response is likely to reflect exposure to a cross-reacting antigen on a locally prevalent organism, but we remain unconvinced that the evidence clearly demonstrates a difference in sensitivity between the 2 groups of subjects to a specific Yrrsinia antigen.

Stephen Aaron, FRCP(C) University of Alberta Edmonton, Alberta Canuciu

Tender point count

To the Editor: Since Smythe first proposed it as a diagnostic sign in

1972 ( I ) , the “tender point count” has been an essential criterion for fibrositis diagnosis in studies published on the disorder (2-6). Although Smythe originally required 12 of 14 possible tender areas for diagnosis, other investigators have required less; as few as 4 tender points have been accepted as meeting the tender point criterion (2,3).

Although the presence of tender points is uncommon in a healthy, young population ( 2 ) , there are no published data concerning the frequency of tender points in patients with rheumatic disease in whom joint disease could be associated with musculoskeletal tenderness.

To investigate the frequency of tender points in a rheumatic disease population, 980 consecutive patients at- tending a private practice rheumatic disease clinic were examined by the same physician for tenderness in the 14 areas suggested by Smythe, using his methodology (7). Sixty-eight percent (669 of 980) had no tender points. This group included 165 of 248 patients with definite or classic rheumatoid arthritis (66.6%) and 128 of 185 patients with

0 R.A. Patients

A 0 .A Patients

W All Other Patients

20

4

2

NUMBER OF TENDER POINTS

Figure 1. The tender point count in 980 consecutive rheumatic disease patients. RA = rheumatoid arthritis; OA = osteoarthritis.

peripheral joint osteoarthritis (69.2%). Four or more tender points were found in 19-21s of patients, and only 11-12rlO had 7 or more tender points. A tender point count of 12 or greater was unusual (Figure I ) . There was no statistically significant difference in the proportion or distribution of tender points among the disease groups, as shown in Figure I . These data suggest that, except in fibrositis patients, a high number of tender points is uncommon. Thus, the identifi- cation of multiple tender points in patients with musculoskel- etal pain suggests the possibility of the diagnosis offibrositis.

Frederick Wolfe, MD University uf Kansas School of’ Mr.dic,ini. Wichitcr, KS

1. Smythe HA: Nonarticular rheumatism and fibrositis, Arthritis and Allied Conditions. Edited by DJ McCarty. Philadelphia, Lea & Febiger, 1972, pp 874-884

2. Yunus M , Masi AT, Calabro J J , Miller KA, Feigenbaum SL: Primary fibromyalgia (fibrositis): clinical study of 50 patients with matched normal controls. Semin Arthritis Rheum 1 I : 151- 171, 1981

3. Payne TC, Leavitt F, Garron DC, Katz RS. Golden HE, Glick- man PB, Vanderplate C: Fibrositis and psychogenic disturbance. Arthritis Rheum 25:213-217, 1982

4. Campbell SM, Clark S, Tindall EA, Forehand ME. Bennett RM: Clinical characteristics of fibrositis. Arthritis Rheum 26317-824. I983

5. Wolfe F, Cathey M: Prevalence of primary and secondary fibrositis. J Rheumatol 10:965-968, 1983

6 . Wolfe F, Cathey M, Kleinheksel S, Amos S, Hoffman R, Young D, Hawley D: Psychological status in primary fibrositis and fibrcisitis associated with rheumatoid arthritis. J Rheumatol I I :SOO-SOS, 1984

7. Smythe HA: Fibrositis and other diffuse musculoskeletal syn- dromes, Textbook of Rheumatology. Edited by WN Kelley, ED Harris Jr , S Ruddy. CB Sledge. Philadelphia. WB Saunders. 1980, 485-493