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Discordance for psoriatic arthropathy in monozygotic twins.

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LETTERS
805
Discordance for psoriatic arthropathy in
monozygotic twins
To the Editor:
Although the etiology of psoriasis and psoriatic
arthropathy remains unknown, a genetic contribution is
suggested by prominent familial occurrence (1,2). Studies of identical twins are of special value in defining the
roles of heredity and environment in the pathogenesis
of disease. In surveys of identical twins with uncomplicated psoriasis, only 7wo of monozygotic twin pairs are
concordant for the disease (3) clearly implicating an environmental triggering factor. In 1969, concordance for
psoriatic arthropathy was reported in 2 monozygotic
members of a set of triplets (4). The proband had psoriasis and spondylitis, his identical brother had psoriasis
and peripheral arthritis, and a third nonidentical
brother had no disease. More recently, discordance for
the related condition ankylosing spondylitis has been
described in monozygotic twins (5). We have observed
67-year-old monozygotic twins, one of whom has psoriasis and severe long-standing peripheral psoriatic arthropathy, while the other remains disease free (Figure
1).
The proband, a 67-year-old white male, presented with a 46-year history of wide-spread psoriasis
and a 40-year history of asymetric oligoarthropathy
progressing to severe destructive changes. Clinically and
radiologically (Figure 2) this is considered to be psoriatic arthropathy. His identical twin brother has remained free of symptoms and on examination had no
evidence of inflammatory skin, joint, or spinal disease.
Pelvic radiographs of both individuals showed normal
sacroiliacjoints. The patients and his twin were HLA-A
and B identical and their lymphocytes were mutually
nonresponsive in mixed lymphocyte culture. Identical
phenotypes for ten red cell antigens, nine red and white
Figure 2. Right hand of 67-year-old monozygotic twin showing destructive disease with characteristic pencil-in-cup deformities, whittling, and distal interphalangealjoint fusion. These changes are typical of psoriatic arthropathy.
HLA-A2,B 17
HLA-B44
Figure 1. Discordance in monozygotic twins for psoriatic arthritis.
Proband (r)developed psoriasis at age 21 and arthritis at age 27.
cell isoenzymes, and three serum gene markers confirmed their monozygotic twin status (6). A detailed inquiry into possible environmental exposure revealed no
specific differences between the two brothers. The patient volunteered a history of trauma to the left knee at
age 27 preceding the onset of chronic arthropathy in
that joint. Thereafter, other joints became involved.
LETTERS
806
Since the patient has had psoriasis and psoriatic
arthropathy for over 40 years and his twin brother has
remained unaffected, it is unlikely that the discordance
results from late disease expression. These subjects provide compelling evidence for the contribution of environmental factors in the pathogenesis of psoriatic arthropathy.
MICHAEL
GOTTLIEB,
MD
ANDRE1 CALIN, MD
Division of Immunology
Department of Medicine
Stanford University School of Medicine
Stanford, California 94305
ROBERTPETERGALE,MD
Division of Hematology- Oncology
Department of Medicine
University of California School of Medicine
Los Angeles, California
REFERENCES
1. Wright V, Moll JMH: Seronegative Polyarthritis. Amsterdam, North Holland Publishing Company, 1976
2. Moll JMH, Wright V: Familial occurrence of psoriatic arthritis. Ann Rheum Dis 32:181-201, 1973
3. Farber EM, Nall ML, Watson W Natural history of psoriasis in 61 twin pairs. Arch Dermatol 109:207-211, 1974
4. Wright V: Psoriatic arthritis, Textbook of the Rheumatic
Diseases. Edited by WSC Copeman. Edinburgh and London, Livingston, 1969
5. Eastmond CJ, Woodrow JC: Discordance for ankylosing
spondylitis in monozygotic twins. Ann Rheum Dis 36:360364, 1977
6. Sparkes MC, Crist ML, Sparkes RS, Gale RP, Feig SA:
Gene markers in human bone marrow transplantation.
Vox Sang 33:202, 1977
Legionnaires’ disease
To the Editor:
Jacoux and Stuard reported an interesting case
of pneumonia in a patient with systemic lupus
erythematosus (Arthritis Rheum 21:975-977, 1978).
While there is substantial circumstantial evidence presented that this patient may have had Legionnaires’ disease, it is entirely misleading to call it such without
more specific data. A negative tissue Gram stain with a
positive silver impregnation stain is not specific enough
to identify an etiologic agent. Specific retrospective diagnosis is possible either by determination of antibody
titers by using stored frozen sera, by direct immunofluorescent staining of formalin preserved lung or of
paraffin blocks.
The question of a cutaneous portal of entry is
purely speculative and should be labeled as such. Basic
information such as results of skin biopsy and Gram
stain of the aspirated fluid are not reported.
In conclusion, it would be unfortunate if naive
readers thought that this case was a well documented
case of Legionnaires’ disease with an unusual portal of
entry.
PAULH. EDELSTEIN,
MD
Associate Investigator
Infectious Disease Section
Wadsworth VA Hospital
Los Angeles, CA
Brucellu abortus arthritis
To the Editor:
Acute Brucella abortus arthritis is an uncommon
disease (1,2). We have reviewed 7 cases of proven Brucella abortus arthritis treated in the Royal Aberdeen
Children’s Hospital between 1961 and 1970.
Only 3 of the 7 cases were asymptomatic. Four
patients complained of intermittent pain in the joints
previously affected. One patient had clinical and radiologic evidence of severe osteoarthrosis in the joints originally affected.
Review of the treatment originally carried out revealed that 3 of the 4 symptomatic patients had been
treated with tetracycline, and the remaining patient was
treated conservatively.
Our findings show the failure to be expected with
tetracycline treatment alone and substantiate the advice
of other reports (2,3) that the acute disease should be
treated with a combination of antibiotics in order to
avoid severejoint damage.
DAVIDJAFFRAY,
MB, FRSCEd
MD, FRCSEd
IANG. MACKENZIE,
A berdeen, Scotland
REFERENCES
1. Adam A, MacDonald A, MacKenzie IG: J Bone Joint Surg
49B: 652-657, 1967
2. Kelly PJ, Martin WJ, Skirger A, Weed LA: JAMA 174
347-353, 1960
3. Glasgow MMS: Br J Surg 63: 283-288,1967
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arthropathy, monozygotic, psoriatic, twin, discordant
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