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Sustained remission of rheumatoid arthritis following hypersensitivity reaction.

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further method of relieving pain and stiffness in patients with
AS. Because AS takes decades to develop fully, a multidisciplinary effort to control the natural evolution of AS, with
an intensive remedial exercise program and a suitable antiinflammatory agent, should include TENS as a therapeutic
adjunct. It is hoped that others will perform similar studies of
a larger number of patients in order to obtain confirmation of
the present data.
Gabriele Gemignani, MD
Ignazio Olivieri, MD
Giusta Ruju, MD
Giampiero Pasero, MD
University of Pisa
Pisa, Italy
Nienhuis RLF, Hoekstra AJ: Transcutaneous electronic nerve
stimulation in ankylosing spondylitis (letter). Arthritis Rheum
27: 1074-1075, 1984
Bennett PH, Burch TA: New York symposium on population
studies in the rheumatic diseases: new diagnostic criteria. Bull
Rheum Dis 17:453458, 1967
Mannheimer J , Lampe G: Clinical Transcutaneous Electrical
Nerve Stimulation. Philadelphia, FA Davis, 1984
Langley GB, Sheppeard H , Johnson M, Wigley RD: The analgesic effects of transcutaneous electrical nerve stimulation and
placebo in chronic pain patients. Rheumatol Int 4:119-123, 1984
Sustained remission of rheumatoid arthritis following
hypersensitivity reaction
To the Editor:
Rheumatoid arthritis (RA) is a chronic inflammatory
disease of unknown etiology. Immunologic abnormalities,
including type IV hypersensitivity response abnormalities,
have been described in RA (1). It is widely believed that the
tissue damage is caused by the type I11 immune response
The possible association of atopy with RA has been
investigated in several studies, but it has been concluded
that the prevalence of atopy is not increased among patients
with RA (2,4). The type I hypersensitivity response in RA
patients has not, however, been closely studied. Some
investigators have found abnormalities in serum IgE (low or
high levels) in patients with RA (43). It has been reported
that patients with dermatitis from gold treatment experience
remission or near remission of their RA (6); this is believed
to be possibly related to an immunologic response to the
gold. In addition, we have observed incomplete remission in
2 patients with RA and 1 with Behcet’s disease, after
anaphylactic reaction. In 1 of these patients, the reaction
was manifested by severe urticaria.
In spite of these reports, however, a clear relationship between RA or other rheumatic conditions and type I
hypersensitivity reaction has not been demonstrated. Because generalized anaphylaxis occurs only rarely in patients
with RA, little is known about the effects of anaphylaxis on
the RA disease course. We describe herein a patient with RA
who had sustained remission after generalized anaphylaxis
and anaphylactic shock.
The patient, a 45-year-old man, had erosive RA since
1969. He had been treated with steroids, various nonsteroidal antiinflammatory drugs, and D-penicillamine; all provided only temporary or limited benefit. Clinical examination in 1969 revealed swelling, stiffness, and pain bilaterally
in the second metacarpophalangeal joints, the proximal
interphalangeal joints, and the metatarsophalangeal joints.
Synovitis of the right elbow and both knees was noted.
Motion was painful and restricted in most major joints such
as the shoulders, elbows, and hips. There were nodules over
several joints and extensor tendons.
The results of laboratory investigations were as
follows: hemoglobin 1 1 gm/dl, white blood cell (WBC) count
10,000/mm3, erythrocyte sedimentation rate (ESR) 65 mm/
hour, C-reactive protein 7 mg/dl, strongly positive rheumatoid factor (RF; measured qualitatively), serum IgG 1,450
mg/dl (normal 5661,373). No tests were performed for the
presence of cryoglobulins or circulating immune complexes.
A node was removed from the patient’s right elbow, and
pathologic examination revealed features consistent with
rheumatoid nodule.
In March 1979, the patient was admitted to our
hospital with fever, cough, and shortness of breath of 1-week
duration. On physical examination, rhonchi were heard in
the left lower lung area. The WBC count on admission was
27,400/mm3, with 98% polymorphonuclear leukocytes.
Chest radiography demonstrated inflammation of the left
lower lobe, with minimal effusion on the same side. There
was no allergic reaction documented in his medical history.
Intravenous semisynthetic penicillin was started, but, on the
third day of hospitalization, anaphylactic reaction and shock
occurred. He was hospitalized and resuscitated immediately, using adrenaline and methylprednisolone (total of 500
mg intravenously).
He remained in the hospital for 1 week more, without
any medication except antihistamines. He was then discharged and was followed up as an outpatient by our staff.
After 3 months, he was RF negative, with an ESR of 15
mm/hour. All therapy for RA was discontinued. By the
second year after the anaphylactic episode, he had no
nodules or clinical signs or symptoms that might be related
to RA. We have followed his case for 1 1 years, during which
time he has remained asymptomatic.
It is believed that pharmacologically active amines
which are released in increased levels during the type I
hypersensitivity reaction (i.e., histamine, slow-reacting substance of anaphylaxis, eosinophil chemotactic factoranaphylaxis, serotonin, heparin, kinins, and prostaglandins)
can cause some symptoms resembling RA (2-5). But the
sustained remission after generalized anaphylaxis and anaphylactic shock in our patient leads us to believe that these
mediators might play a preventive role in the immunologic
mechanism of RA. It is doubtful that the 500-mg dose of
methylprednisolone received by our patient had a role in the
remission (2,7).
The hypothesis that anaphylaxis could affect the
regulation of autoantibody production in RA is unproven,
but this case leads us to believe that anaphylaxis might play
a preventive role in some patients. We hope further studies
of the mechanisms involved will be conducted, to explain the
relationship between RA and the type I hypersensitivity
Tansu K. Arasil, MD
Safiye Tuncer, MD
Mehmet Tosun, MD
University of Ankara
Ibn-i Sina Central University Hospital
Ankara, Turkey
1. Emery P, Panayi GS, Symmons D, Brown G: Mechanisms of
depressed delayed type hypersensitivity in rheumatoid arthritis:
the role of protein energy malnutrition. Ann Rheum Dis 43:430434, 1984
2. O’Driscoll BR, Milburn HJ, Kemeny DM, Cochrane GM, Panayi
GS: Atopy and rheumatoid arthritis. Clin Allergy 15547-553,
3. Walport MJ, Parke AL, Hughes GRV: Food and the connective
tissue diseases. Clin Immunol Allergy 2: 113-120, 1982
4. Peskett SA, Platts-Mills TAE, Ansell BM, Stearnes GN: Incidence of atopy in rheumatic disease. J Rheumatol 8:321-324,
5 . Grennan DM, Palmar OG: Serum IgE concentration in rheumatoid arthritis: lack of correlation with gold toxicity. Br Med J
2~1477-1478, 1979
6. Cecil RL: Discussion. Ann Rheum Dis 15:395, 1956
7. Byron MA, Kirwan JR: Corticosteroids in rheumatoid arthritis:
is a trial of their disease modifying potential feasible? Ann Rheum
Dis 46:171-173, 1986
The findings of radiographs of the affected joints and of the
sacroiliac joints were normal.
Laboratory investigation revealed the following: hemoglobin 13.2 gm/dl, white blood cell count 4.2 x 106/liter
(58% lymphocytes), erythrocyte sedimentation rate 39 mm/
hour, serum IgG 25 gm/liter, serum IgA 4.2 gm/liter, serum
IgM 3.1 gm/liter, creatine phosphokinase 470 IU (normal
<170). Normal or negative results were found on tests for
serum creatinine concentration, liver function, rheumatoid
factor, antinuclear antibodies, antimitochondrial antibodies,
and anti-striated muscle antibodies. Anti-smooth muscle
antibodies were present at a titer of 1:lOO. HLA-B27 was
negative. The CD4 lymphocyte count was 670/mm3. The
urogenital tract was clinically normal, and cultures for
Mycoplasma and Chlamydia were negative. The patient was
treated with nonsteroidal antiinflammatory drugs, and her
symptoms resolved within 1 month.
As in most rheumatic manifestations occurring in
HIV-1-infected individuals, it is not possible to confirm a
direct pathogenetic role of the virus. Our patient’s symptoms
did not fulfill diagnostic criteria for Reiter’s syndrome (4),
which is a common rheumatic manifestation of HIV-1 infection. However, monarticular or oligoarticular arthritis with
normal radiographic findings, with a mean duration of 1
month, has been reported in HIV- I-infected HLA-B27
negative individuals (5). Our observations suggest that
HIV-2 might also be responsible for such manifestations.
Marie-Christophe Boissier, MD, PhD
Hhpital Avicenne
Universitk Paris Nord
Bobigny, France
Jean-Jacques Lefrere, MD
Institut National de Transfusion Sanguine
Paris, France
Pierre Dreyfus, MD
Hhpital Avicenne
Universitk Paris Nord
Bobigny, France
Rheumatic manifestations in a patient with human
immunodeficiency virus type 2 infection
To the Editor:
Espinoza et a1 have recently reviewed the various
rheumatic manifestations linked to human immunodeficiency virus (HIV) infection (1). To date, all reported
rheumatic manifestations have occurred in association with
HIV type 1. We report herein the occurrence of inflammatory talalgia in an individual infected with HIV-2, which
suggests that this virus can also be associated with rheumatic
The patient, a 26-year-old woman, was a native of
Cape Verde who had been living in France since the age of
20. She was asymptomatic but had been diagnosed as being
HIV-2 seropositive, as a result of routine screening of
donated blood (begun in France in August 1985). The enzyme-linked immunosorbent assay result was positive, and
specific Western blotting showed a typical pattern of HIV-2
infection (2). No coinfection with HIV-1 was noted. She had
stage I1 HIV infection according to the Centers for Disease
Control classification (3).
Twenty months after this diagnosis, she developed
tricipital myalgias and severe pain in her heels, which was
present both during the day and at night, but was accentuated upon walking or ascending stairs. Physical examination
revealed only pain and tenderness upon application of pressure to the Achilles tendons and triceps. The tenderness was
greatest in the area of the triceps insertion on the calcaneum.
1. Espinoza LR, Aguilar JL, Berman A, Gutierrez F, Vasey FB,
Germain BF: Rheumatic manifestations associated with human
immunodeficiency virus infection. Arthritis Rheum 32: 16151622, 1989
Clavel F, Guetard D, Brun-Vezinet F , Chamaret S, Rey MA,
Santos-Ferreira MO, Laurent AG, Dauguet C, Katlama C, Rouzioux C , Klatzman I), Champalimaud JL, Montagnier L: Isolation
of new human retrovirus from a West African with AIDS.
Science 233:343-346, 1986
Centers for Disease Control: Classification for human T-lymphotropic virus type III/lymphadenopathy-associatedvirus infection.
MMWR 35:334-339, 1986
Willkens RF, Arnett FC, Bitter T, Calin A, Fisher L, Ford DK,
Good AE, Masi AT: Reiter’s syndrome: evaluation of preliminary criteria for definite disease. Arthritis Rheum 24:844-849,
Berman A, Espinoza LR, Diaz JD, Aguilar JL, Roland0 T, Vasey
FB, Germain BF, Lockey RF: Rheumatic manifestations of
human immunodeficiency virus infection. Am J Med 85:5944,
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reaction, following, arthritis, sustained, rheumatoid, hypersensitivity, remission
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