There still is quite a lot of uncertainty about palindromic rheumatism,
but it’s an accepted diagnosis and is classified in ICD-10 as M12.3. It is a
form of episodic inflammatory arthritis. One or even multiple joints swell, may
be red, and are painful - and then go back to normal. Unlike other forms of
arthritis palindromic rheumatism doesn’t damage the joints permanently. Some
scientists say that half the patients develop rheumatoid arthritis, but that’s
a rough estimation as we lack longitudinal data to confirm this number. Time
intervals between attacks vary a lot.
The term palindromic rheumatism was coined in 1941 by P.S. Hench and E.F.
Rosenberg. The description is purely clinical as then rheumatoid factor (RF) or
even ACPA [anticitrullinated protein antibody] weren’t known or waited for lab
tests to be developed. They used palindromic as the symptoms appear and
disappear in a similar way.
The cause is still unknown. It is uncertain, if it is a condition, which
might lead to what we call early arthritis nowadays and/or rheumatoid
arthritis.
Apart from clinical examination lab tests and X-rays are used to rule out
rheumatoid arthritis, but there is no test, which could be used to diagnose
palindromic arthritis. If ACPA or RF are present, rheumatoid arthritis might
develop later. Sometimes palindromic rheumatism is the first presentation of M.
Whipple. The rheumatologist diagnoses
palindromic rheumatism by the patient’s history and his finding of acute
arthritis. And he has to rule out other forms of arthritis like gout (or the
ones already mentioned).
Therapy should focus on treating acute attacks. The mainstays for this
are NSAIDs. Sometimes antimalarials are prescribed, but robust data for this indication
doesn’t exist.
G. Salvador and colleagues asked if palindromic rheumatism could be a an
abortive form of rheumatoid arthritis in a study (1). They looked at 63
patients with palindromic rheumatism: 33 were defined as pure or persistent and
30 as associated palindromic rheumatism. They concluded: “Anti‐CCP [ACPA] and, to a lesser extent, AKA [antikeratin
antibodies], were found in a high proportion of patients with PR [palindromic
rheumatism], suggesting that this syndrome is an abortive form of RA
[rheumatoid arthritis]. The predictive value of these antibodies in PR, as
markers of progression to an established RA, remains uncertain.” I think these
findings are very valuable, but the conclusion is premature as there might be
an admission bias.
S. Cabrera-Villalba and colleagues looked at subclinical synovitis in
patients with palindromic rheumatism in the
intercritical period (2). The study used ultrasound and clinical examination. The
authors concluded: “Some differences emerged in the clinical phenotype of PR [palindromic rheumatism] according to ACPA [anticitrullinated
protein antibody] status. Most patients with PR do not have US [ultrasound] subclinical
synovitis in the intercritical period, even those who are ACPA-positive.”
Y. Emad and colleagues studies, if hand joint involvement and positive ACPA
[anticitrullinated protein antibodies] in palindromic
rheumatism predict development of rheumatoid arthritis after one year of
follow-up (3). The authors concluded: “Early hand joint involvement and
positive anti-CCP at disease onset are good predictors for progression to RA in
this domain.” Interestingly they had already treated 43 patients with
hydroxychloroquine, and the authors think that this had led to remission. Really?
The study can’t tell and it muddies the outcome of the original study. Cabrera-Villalba
and colleagues voiced their concerns in a letter to the editor (4). CRP levels
were high or measurements were made in mg/l and quoted in mg/dl. I think that
CRP levels were high, but that patients rather belong to an early arthritis
cohort than to a palindromic rheumatism in intercritical
period cohort.
R. Sanmartí and colleagues published: “Palindromic
rheumatism with positive anticitrullinated peptide/protein antibodies is
not synonymous with rheumatoid arthritis. A longterm followup study.” In
results we read: “Seventy-one patients (54 women/17 men) with a PR diagnosis
were included. Serum ACPA were positive in 52.1%. After a mean followup of 7.6
± 4.7 years since the first ACPA measurement, 24 patients (33.8%) progressed to
chronic disease: 22% RA, 5.6% systemic lupus erythematosus, and 5.6% other
diseases. […] Progression to RA was more frequently seen in ACPA-positive than
in ACPA-negative patients (29.7% vs 14.7%), but the difference was not
significant. […]”. The authors concluded: “ACPA are frequently found in the
sera of patients with PR, and a significant proportion of these patients do not
progress to RA in the long term.”
To sum it up, palindromic rheumatism still is a challenging diagnosis. We
have to make clear distinctions between palindromic
rheumatism and early arthritis. I would like to see these patients regularly to
make sure that they don’t progress to rheumatoid arthritis.
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