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Remitting seronegative symmetrical synovitis with pitting oedema (RS3PE) as recurrence of aborted PMR
  1. M A CIMMINO
  1. Clinica Reumatologica, DIMI
  2. Università di Genova, Italy
  3. Sezione di Diagnostica per Immagini, DIMES
  4. Università di Genova, Italy
    1. E SILVESTRI,
    2. G GARLASCHI
    1. Clinica Reumatologica, DIMI
    2. Università di Genova, Italy
    3. Sezione di Diagnostica per Immagini, DIMES
    4. Università di Genova, Italy

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      A comparison of clinical and laboratory findings in patients with RS3PE alone, PMR alone, and RS3PE associated with PMR has been recently published by Cantini et al.1 Their results suggest that the three conditions might represent a continuum, with PMR, a more severe condition, at one end and, RS3PE alone, at the other. PMR has a longer duration, is more commonly associated with systemic symptoms, requires higher doses of steroids for a longer time, and shows more relapses and recurrences. Although Cantini et alemphasised the similarities between PMR and RS3PE, they concluded that RS3PE alone is a separate entity. Other studies by the same group of authors have shown that RS3PE may be a feature of different diseases, such as spondyloarthropathies, psoriatic arthritis, rheumatoid arthritis (RA), acute sarcoidosis, and neoplasms.2 Whether RS3PE is a distinct syndrome or a clinical feature of different inflammatory diseases is still unknown.

      We have recently followed up a patient, whose disease course might help in interpreting the relation between PMR and RS3PE. This 76 year old man had a sudden onset of pain and stiffness in the shoulder and pelvic girdles in September 1997. Two days afterwards, he was seen by his general practitioner, who prescribed intramuscular betamethasone (4 mg daily for six days). A few days after completion of treatment, the patient was seen by one of us. At this time, physical examination was completely normal. In particular, no joint pain could be elicited and there were no signs of arthritis or tenosynovitis. His clinical history was unremarkable except for mild hypertension. Routine laboratory examinations performed before the onset of the disease, in January 1997, were normal with an erythrocyte sedimentation rate (ESR) of 1 mm/1st h. No further treatment was given and it was suggested that the patient called us if his symptoms recurred.

      At the end of October, the patient again complained of joint pain and was admitted to our unit. At physical examination, there was pain at movement of the wrists and dorsal hand swelling with pitting oedema. There were no skin lesions compatible with psoriasis and no personal or family history of psoriasis. ESR was 38 mm/1st h and C reactive protein 12 mg/l (normal <5 mg/l). IgM rheumatoid factor, antinuclear antibodies, and a panel of antiviral antibodies were negative. Radiograms of hands and sacroiliac joints were normal. Magnetic resonance imaging (MRI) of the hands was performed by a dedicated extremity 0.2 T system (Artoscan, Esaote, Genova, Italy). Sequences included axial and coronal T1 weighted gradient echo and short τ inversion recovery (STIR). Section thickness was 3.5 mm, interslice gap was 0.3 mm, and the field of view was 11 cm. Tenosynovitis of the flexor and extensor tendons was seen in both hands, with mild synovitis in the left wrist (fig 1). A diagnosis of RS3PE was made and treatment with prednisone 5 mg/day and indometacin 50 mg at night was started. The signs and symptoms resolved completely after one week. Treatment was stopped after three months. Recently (June 2000), the patient is completely well with no recurrences of his disease.

      Figure 1

      Dorsal hand swelling, mild synovitis, tenosynovitis of the extensor carpi ulnaris (arrow) and of the flexor tendons (arrowhead). Axial STIR image of the left wrist (TR/TE 1840/30; TI=85; NEX=1; matrix=180 × 180).

      This case report suggests that RS3PE may be the only clinical sign of recurrence in a patient with PMR. With the exception of the indexes of inflammation, which were not tested at disease onset, our patient fulfilled all the commonly accepted criteria for PMR.3Clinical features and MRI imaging of the recurrent disease were typical of RS3PE . It is tempting to speculate that early treatment of PMR might have aborted disease by downgrading the inflammatory response. If this is true, recurrence might have occurred at a more localised level of inflammation, represented by RS3PE. Two patients with PMR described by Healey had three subsequent episodes responsive to steroids, with typical signs of PMR, RS3PE, and seronegative RA.4 In their series of RS3PE, Olivé et al studied two patients with PMR before RS3PE.5 However, no precise description of the clinical features of these patients was given. These data confirm the view that PMR and RS3PE may be different manifestations of the same disease.

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