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Marked synovial sensitivity to pricking in Behqet's syndrome.

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7. Leca AP, Crouzet J, Attali P. et al: InterZt de la recherche
du groupe HLA W27 pour le diagnostic des forrnes frustes
ou atypiques de la spondylarthrite ankylosante sans
signes radiologiques visibles. Ann Med Int 125:755-759,
8. Calin A. Fries JK: Striking prevalence of ankylosing
spondylitis in healthy W27 positive males and females. N
Engl J Med 293:835-839, 1975
9. Thorel JB, Cavelier B, Bonneau JC, et al: Etude d’une
population porteuse de I’antigene HLA 827 comparee a
celle d’une population temoin non 927 a la recherche de
la spondylarthrite ankylosante. Rev Rhum 45:275-282,
10. Brewerton D A , Hart FD. Nickolls A, et al: Ankylosing
spondylitis and HLA-B27. Lancet 1:904-905, 1973
I I . Schlosstein L. Terasaki PI, Bluestone A, et al: High association of an HLA antigen W27 with ankylosing spondylitis. N Engl J Med 288:704, 1973
Marked synovial sensitivity to pricking in
Behqet’s syndrome
To the Editor:
In Behqet’s syndrome a marked skin sensitivity
to pricking with a sterile needle or to injection of saline
has been observed (1). The skin puncture test is considered to be specific of the syndrome by some and has
been used as a guide in therapy (2). The case recorded
below suggests that synovial membrane also is abnormally sensitive to pricking in Behqet’s syndrome.
A 37-year-old man was admitted to the Institute
of Rheumatology of the University of Rome in February 1979 with oral and scrotal ulcers, erythema nodosum, painless swelling of the proximal interphalangeal
joint of the third finger of the right hand. He reported a
5-year history of acute episodes of monafthralgia or
monarthritis involving one knee, one shoulder, and the
left elbow of 2 to 10 days’ duration and recurring intermittently two or three times a year. No eye lesion was
detected. Physical examination of the viscera did not reveal any abnormality. Routine laboratory studies were
found to be normal or negative. HLA typing disclosed
the following antigens: Al, A29, BS, B7, Bw4, and Bw6.
X-rays showed no abnormality in the chest, knee, shoulders, or sacroiliac joints. No bony changes were seen in
the hands. The skin puncture test was positive.
In June 1978 he had been referred to another hospital with oral and scrotal ulcers, erythema nodosum, and
arthritis of the left knee. At that time arthrocentesis was
carried out without symptomatic relief, but marked exacerbation of the swelling and pain of the knee joint oc-
curred. Articular symptoms subsided after 3 days apparently because of the oral administration of prednisolone.
In February 1979 synovial biopsy of the completely asymptomatic left knee was camed out using the
Polley-Bickel needle. Within 24 hours the knee became markedly swollen with moderate stiffness and pain.
Two days later, knee aspiration yielded 50 ml of slightly
bloody and sterile fluid which contained 7,200 white
cells/mm’ with 66% neutrophils. Twenty milligrams of
triamcinolone hexacetonide suspension were injected
into the joint with definite improvement. The patient
was discharged. Two months later he complained of
pain and swelling of the right knee. He was seen with
this symptom only at the outpatient department and arthrocentesis of the right knee was carried out using a 18
gauge needle. Synovial fluid, removed as completely as
possible from the joint, was opalescent with decreased
viscosity. It contained 5,000 nucleated cells/mm3 with
79% neutrophils. The following day the joint was
markedly swollen with particularly severe pain. Rapid
relief in two days occurred after the oral administration
of methylprednisolone (8 mg daily).
The case presented above satisfied the criteria for
“definite” Behqet’s syndrome (3). A synovial inflammatory reaction with marked joint swelling was observed
on three different occasions within 24 hours after needle
biopsy or joint aspiration. In one case a sterile synovial
fluid was obtained, and in all cases this synovitis subsided after oral or intraarticular administration of corticosteroids. This needle-induced synovitis suggests that
not only the skin but also the synovial membrane is abnormally sensitive to pricking or trauma in Behqet’s
syndrome. If confirmed by other reports, needle-induced synovitis may be a useful sign to alert the physician to the possibility of a Behqet’s syndrome when the
arthritis precedes the triad manifestations (4).
Institute of Rheumarology
University of Rome
Rome, Italy
I . Nazzaro P: Cutaneous manifestations of Behqet’s disease:
clinical and histopathological findings, International Symposium on Behqet’s Disease, Rome, 1966. Vol. I . Basel/
New York, Karger, pp 15-41, 1966
2. Fellner M, Kantor I: Behqet’s syndrome: skin puncture test
as a guide in therapy. N Y J Med 64:1760-1761, 1964
3. Mason RM, Barnes CG: Behqet’s syndrome with arthritis.
Ann Rheum Dis 289-103, 1969
4. Strachan RW, Wigzell FW: Polyarthritis in Behqet’s multiple symptom complex. Ann Rheum Dis 22:26-35, 1963
Clinical experience-NSAID
To rhe Editor:
“Clinical experience” has been defined by at
least one physician as “the art of making the same mistake over and over again.” This definition has merit,
and as a country doctor practicing rheumatology in the
backwoods of Maine, I tend to attribute most unusual
experiences to anecdote or chance.
Nonetheless, my experience with salicylates
and the other nonsteroidal antiinflammatory drugs
(NSAID) greatly varies with most of the recent literature. For example, Dr. Edward Huskisson (a rheumatologic “giant” whom I would approach with only the
greatest respect and would argue against with only the
greatest temerity) writes “Proprionic acid derivatives
are now the first line treatment for symptom relief in
rheumatic diseases. The message that aspirin is the first
line treatment of rheumatoid arthritis is so much part of
their dogma that one would imagine it was handed to
rheumatologists on tablets of stone. It is no longer true.
There are now drugs which are just as effective but with
strikingly fewer side effects” (1).
Now, my experience does agree with Dr. Huskisson in as much as all forms of regular soluble aspirin, in
the doses required to achieve antiinflammatory blood
salicylate levels, seem to cause a significant incidence of
gastric symptoms and/or bleeding. Buffered compounds
are only slightly better tolerated in these doses. On the
other hand, I think that enteric coated aspirin is much
better tolerated, causes much less blood loss, and
achieves equally effective salicylate levels. Although the
cost of enteric coated forms is high for aspirin, it is very
inexpensive when compared to the other NSAID. Following salicylate levels is useful and also offers an advantage over the NSAID. (It has been my experience
that generic brands may be less reliable in their site or
degree of dissolution, and therefore I use the Lilly or
Smith, Kline and French brands.)
Most studies comparing NSAID to aspirin have
prejudiced their results against aspirin by using soluble
forms and/or fixed doses, and not following salicylate
levels to be sure antiinflammatory levels have been
Drawing by Joseph Fams; 0 1978 The New Yorker Magazine, Inc.
achieved. 1 have filled a wastecan with such reports and
suggest that other readers do the same.
Therefore, I do not think that the proponents of
the NSAID as the first line of antiinflammatory therapy
have proved their case. Well made enteric coated forms
of aspirin are far less expensive, more easily monitored,
perhaps equally effective, better defined in terms of recognition of toxicity when given over long periods of
time, and tolerated well enough to suggest that they remain the prescription of first choice. Indeed, my opinions have been more graphically expressed by Joseph
Farris’ drawing in The New Yorker magazine.
Bangor, Maine 04401
I. Huskisson EC: Nonsteroidal antiinflammatory analgesics:
basic clinical pharmacology and therapeutic use. Curr
Therapeutics 19:43-57, 1978
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