Palindromic Rheumatism

Veena R. Iyer, MD; George L. Cohen, MD


South Med J. 2011;104(2):147-149. 

In This Article


The incidence of PR is relatively equal in each sex, with a female to male ratio that varies between 1.7:1 and 0.55:1.[4] The mean age of onset of PR is about 45 years, with cases reported from the early 20s to the 80s.[4] The joints most commonly affected in PR are the shoulders, knees, wrists, ankles, and small joints of the hand. The hips, elbows, and feet are less often involved; however, PR can affect any joint.[5] Although several joints can be affected at the same time, PR is usually monoarticular. The joint involvement is asymmetric and migratory, and patients frequently complain of very severe pain. An attack of PR begins with slowly worsening joint pain that peaks within a few hours and usually subsides within 48 hours. PR attacks may vary in frequency, from one each day to one per month. Asymptomatic periods between attacks are also variable. Redness and swelling of a joint or swelling near a joint is frequently associated with PR.[6] Constitutional symptoms like fever are absent during presentation. In some cases, transient intracutaneous or subcutaneous nodules on the hands have been described, disappearing within a few days of the attack.[5]

The etiology and pathogenesis of PR is not well understood. When they first described this condition, Hench and Rosenberg suspected a possible allergic origin for the disease.[1] Later investigations have tried to establish allergy to foodstuffs as the trigger for PR.[7,8] Investigators have also found a clinical association between antiphospholipid syndrome and PR.[9]

Laboratory tests in PR are normal, with the exception of raised ESR and C-reactive protein (CRP) levels. White blood cell counts are normal and ANA studies are usually negative. In this patient, the presence of positive ANA and dsDNA suggest the diagnosis of possible SLE. The joint manifestations are typical for PR. A diagnosis of SLE or another related disorder is suspected but cannot be substantiated. Additionally, thyroid disease with thyroid peroxidase (TPO) antibodies, as seen in our patient, is also associated with higher circulating levels of ANA and dsDNA and may explain the elevated titers of these. Radiographic studies are also always normal in PR. Thus, PR can be diagnosed by the typical joint involvement, with normal blood tests and normal x-rays, after ruling out other forms of arthritides.

Several diseases, both common and rare, mimic PR and must be ruled out for definitive diagnosis. PR can be differentiated from RA because of the transient nature and asymmetric distribution of the arthritis, the frequent episodes of swelling adjacent to joints, the general absence of significant constitutional symptoms, and the lack of progression and radiographic changes.[1] Crystal arthropathies, reactive arthritis, other seronegative spondyloarthropathies, intermittent hydrarthrosis, Behcet disease, relapsing polychondritis, sarcoidosis, and Whipple disease are all differential diagnoses of PR.[6]

The further clinical course in patients with PR is one of the following: (1) remission of attacks; (2) recurrent attacks without persistent joint involvement; or (3) development of chronic disease, most commonly RA. There is still some controversy about the existence of PR as a distinct nosological entity versus it being a precursor lesion for RA. Although this controversy remains, only about one-third of PR cases progress to RA.[10] Factors which predict progression include a positive rheumatoid factor (RF) and small joint involvement early in the disease.[10] Additionally, a positive anti-CCP antibody test within the first year of presentation of PR is highly suggestive for progression to RA.[11] Other chronic diseases that have been seen to develop in patients with PR include systemic lupus erythematosus, seronegative spondyloarthropathies, including psoriatic arthritis and rarely, Wegener granulomatosis.[6] In this patient, both RF and anti-CCP were negative which portends a low likelihood of progression.

Acute attacks of PR may respond favorably to nonsteroidal anti-inflammatory drugs (NSAIDs). Several drugs used for the treatment of RA like antimalarials, gold salts, penicillamine, sulfasalazine, methotrexate, and TNF- α inhibitors have been used in PR. It has been difficult to evaluate the utility of these treatments in PR with prospective randomized controlled studies due to its relative rarity and variable clinical presentation. A retrospective study has shown that the use of antimalarials in patients with PR may be associated with a reduction in the risk of developing subsequent RA or other connective tissue disease.[12] Antimalarials are seen to have a role in some patients in preventing attacks or reducing the frequency and intensity of attacks, and hydroxychloroquine was found to be very useful in our patient.

In conclusion, PR should be considered in the differential diagnosis of recurrent attacks of migrating oligoarthritis, presenting without constitutional symptoms when laboratory tests and imaging studies are normal. It is important to identify this condition so that patients may be counseled about the possibility of developing chronic autoimmune conditions, and treated in the appropriate cases.


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