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Remitting seronegative symmetrical synovitis with pitting oedema/polymyalgia rheumatica after infection with Mycoplasma pneumoniae
  1. M Matsuda,
  2. Y Shimojima,
  3. T Gono,
  4. W Ishii,
  5. K Kaneko,
  6. M Yazaki,
  7. S-i Ikeda
  1. Third Department of Medicine, Shinshu University School of Medicine, Matsumoto, Japan
  1. Correspondence to:
    Dr M Matsuda
    Third Department of Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan;

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Remitting seronegative symmetrical synovitis with pitting oedema (RS3PE) is similar to polymyalgia rheumatica (PMR) in that it shows arthralgia attributable to tenosynovitis and muscle pain, occurring most commonly in the elderly, and shows a good response to corticosteroid treatment.1–,4 The aetiologies of RS3PE and PMR are still unknown, but they are sometimes associated with neoplastic, other rheumatic, or infectious diseases.5,6

Here, we report clinical findings in four patients with RS3PE or PMR, or both, after infection with Mycoplasma pneumoniae. Increases in inflammatory reactions were seen in all patients, and the final diagnoses were RS3PE alone in patients 1 and 4, RS3PE associated with PMR in patient 2, and PMR alone in patient 3 (table 1).7,8 None of the patients had a headache or blurred vision suggestive of associated temporal arteritis. Recent infection with M pneumoniae was confirmed in all patients by the presence of IgM antibody to this agent in the serum and the results of serial serological studies with or without a positive cold agglutination test. Serum IgM levels were within the normal limits in all patients, and none showed positive results for serological tests for other infectious agents or autoantibodies such as rheumatoid factor or antinuclear antibody. All patients were treated successfully with oral prednisolone, but two relapsed during the tapering of this drug.

Table 1

 Patient characteristics

There are three possible characteristics of RS3PE/PMR after infection with M pneumoniae. The first is the presence of common cold-like symptoms preceding RS3PE/PMR. Two of the four patients showed common cold-like symptoms, and antibiotics were given to patient No 1 because chest radiography demonstrated bilateral pleural effusion due to active infection with M pneumoniae. The extremely high C reactive protein level with an almost normal erythrocyte sedimentation rate in patient 1 may have reflected previous infection with this agent.

The second characteristic is the frequent occurrence of relapse. RS3PE usually shows a good response to corticosteroid treatment, and is generally unlikely to relapse during tapering of drug treatment.1–,4 However, relapse occurred soon after the start of tapering of oral prednisolone in two patients (Nos 1 (fig 1) and 2) in the present study.

Figure 1

 Patient 1 has oedema in both hands and feet, particularly in the latter (A), but this symptom quickly improved after starting oral prednisolone (B).

The third characteristic is a broad spectrum of clinical phenotype. Patients 1, 2, and 4 had oedema in the hands and feet, which is typical of RS3PE, while patient 3 had muscle pain alone, suggestive of PMR. Patient 2 was diagnosed as having RS3PE associated with PMR at the onset of disease, but at relapse the patient had PMR symptoms alone. A possible explanation for these findings is that RS3PE and PMR may be classifiable as the same disease entity with their symptoms of multiple tenosynovitis, and many transitional forms have clinical features of both disorders.1,2 The clinical phenotypes manifested after infection with M pneumoniae may be dependent on the host-disease relationship.

Several lines of evidence suggest that Mycoplasma species can cause rheumatic disorders. Previous exposure to Mycoplasma species is commonly confirmed by immunoblotting in patients with rheumatoid arthritis or juvenile rheumatoid arthritis, but polymerase chain reaction showed no detectable DNA of these agents in the synovial fluid or tissue.9 A prospective epidemiological study in Denmark indicated that the incidence of PMR varied in parallel with epidemics of M pneumoniae infection.10 These findings indirectly suggest that Mycoplasma species may be related to the development of rheumatic disorders, and the present cases represent important direct evidence of the involvement of M pneumoniae in the aetiology of RS3PE/PMR. Further studies in larger numbers of patients are necessary to clarify the pathogenetic mechanism of RS3PE/PMR after infection with this agent.