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HLA specificities and psoriatic arthritis.

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LETTERS
1389
azathioprine. Arthritis Rheum 24: 1453-1454, 1981). Hypotension and oliguria developed in 2 of their patients suffering
from severe inflammatory arthritis, when the drug was
administered to them a second time. Leukocytosis was
present, and serum creatinine rose. Both patients had previously experienced a hypersensitivity reaction with fever and
leukocytosis in response to azathioprine.
We have observed a patient with quite similar clinical
and laboratory features. In 1979 a 27-year-old man was
diagnosed as having systemic lupus erythematosus. Symptoms were well controlled by corticosteroids (methylprednisolone 60 mgiday). A trial of azathioprine treatment (1.5 mgl
kg/day) caused gastrointestinal upset (nausea and vomiting)
that disappeared shortly after the patient stopped taking this
drug.
During a 2-year followup, the dose of methylprednisolone was maintained at 8-12 mg/day. In July 1981 because
of osteonecrosis of the right femoral head, we again tried
azathioprine (50 mg/day) for the patient. After 4 days,
general malaise and gastrointestinal trouble abruptly reappeared; within a few hours, angioneurotic edema, hypotension (80155 mmHg), and oliguria were evident. The serum
creatinine rose from 1.2 to 5 . 2 mg/dl; uric acid rose to 9.1 mg/
dl; and blood urea nitrogen rose to 47 mg/dl. The central
venous pressure (CVP) was 2.5 cm H20.
Hemodynamic acute renal failure was diagnosed.
With the prompt withdrawal of azathioprine and intravenous
administration of hydrocortisone and fluids, the symptoms
disappeared. Renal function returned to normal during the
next 6 days. CVP increased to 8 cm HzO.
In this case and those reported by Keystone and
Schabas, hypotension and oliguria are shown to be rare but
serious side efects of azathioprine therapy. Although the
cause of this reaction is unknown, it is probably a manifestation of hypersensitivity to the drug or one of its metabolites.
In a recent review azathioprine is included among the drugs
responsible for immunologically mediated toxic acute interstitial nephritis (Kleinknecht D, Kanfer A, Morel-Maroger
L, Mery JPh: Immunologically mediated drug-induced acute
renal failure. Contr Nephrol 10:42-52, 1978).
From our experience, we suggest that symptoms
such as fever, chills, skin rash, and minor gastrointestinal
disorders (vomiting, nausea, or diarrhea) can be indicative of
hypersensitivity to azathioprine. For patients who experience these symptoms when taking azathioprine, the physician should stop the treatment and should not attempt
further azathioprine therapy.
Francesco Trotta
German0 Menegale
Orazio Fiocchi
Division of Rheumatology
Division of Nephrology
St. Anne Hospital
44100 Ferrara, Italy
HLA specificities and psoriatic arthritis
To the Editor:
The existence of an association between HLA specificities and psoriatic arthritis has been widely investigated
(1,2), but most studies have been limited to patients and
controls. The few family studies have been limited to relatives already known to have these diseases.
In our recent personal survey of 113 families of
psoriatic probands (3), we attempted to determine the clinical and genetic relationship between psoriasis and psoriatic
arthropathy. We found that 1) history alone identifies affected relatives in 20% of the families, but direct examination
reveals affected relatives in 68% of the families and 2)
psoriasis, psoriatic arthropathy, or both are found in the
families of probands with either psoriasis or psoriatic arthropathy, but the distribution is different in each generation.
Family studies including HLA typing are certainly
needed to provide more information on these relationships.
Claudio Cervini, MD
Walter Grassi, MD
School of Medicine
University of Ancona, Italy
1 . Lambert JR, Wright V , Rajah SM, Moll JMH: Histocompatibility
antigens in psoriatic arthritis. Ann Rheum Dis 35:526, 1976
2. Buchanan R, Kraag G, Rosenthal D, Siangal DP: HLA antigens
and psoriatic arthritis, Transplant Proc 9: 1873, 1977
3. Cervini C, Grassi W, Milani-Comparetti M: Psoriasi ed artropatie: osservazioni genealogiche. Ann Reumatol 12: 18, 1979
Methodology errors in fibrositis study
To the Editor:
In a recent issue of Arthritis and Rheumatism, Payne
et a1 ( I ) reported a study of psychologic disturbances in
patients with fibrositis. I congratulate you for your wisdom
in publishing studies of such a prevailing problem as soft
tissue rheumatism, and the authors of this article for having
ventured into this dark quarter of rheumatic diseases.
In a spirit of the search for truth, I would point out a
methodological error in the study. A control group for this
condition cannot be considered without considering the
issue of pain per se. To control fibrositis in the typical cases
of inflammatory rheumatism is to ignore what little we have
learned about pain as a quantifiable clinical manifestation.
The authors might see this if they were to do further
parametric analyses of their controls versus fibrositis patients. For example, they may find that the mean MMPI
scores of their rheumatoid arthritis patients who have equal
suffering scores on the McGill questionnaire will be the same
as the mean MMPI scores of those with fibrositis.
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