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Lupus acquired immunodeficiency syndrome and antimalarial agents.

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372
LETTERS
The IgG level was normal. The levels of complement components CH50, C3, and C4 were 8.4 unitsiml (normal 30-40),
80.4 mg/dl (normal 60-loo), and 5.0 mg/dl (normal 25-50),
respectively. Urinalysis revealed proteinuria >0.5 gmiday,
without evidence of infection. The patient had a history of
epilepsy. She underwent a rheumatologic examination and
was diagnosed as having SLE that met the American Rheumatism Association criteria (2). Corticosteroid therapy was
then started, which resulted in a marked improvement of her
symptoms. When the patient was readmitted for renal biopsy, which showed mesangioproliferative glomerulonephritis, a peripheral neutrophil was found to have 2 drumsticks.
Results of a buccal mucosal smear and chromosomal analysis of peripheral blood lymphocytes revealed the 47,XXX
karyotype (Figure 1).
Her menstrual cycles were normal. Results of endocrinologic studies during the follicular phase showed a
24-hour urinary estrogen excretion level of 52.6 pg (normal
6.7-54.Og). Plasma concentrations of testosterone, estradiol,
follicle-stimulating hormone, and luteinizing hormone were
35 ng/dl (normal 10-70), 89 pg/ml (normal 19-255), 3.6
mIU/ml (normal 3.1-23.9), and 4.9 mIU/ml (normal 0.915.9,respectively.
The association of SLE and the 47,XXX karotype in
this patient may be coincidental, because there is no evidence that the prevalence of X chromosomal abnormalities
is increased among patients with SLE (3). Nevertheless, the
presence of both Klinefelter’s syndrome, which is frequently
associated with SLE, and an autoimmunity syndrome has
been reported in a patient with the 47,XXX karyotype (4).
The 47,XXX syndrome in association with immunoglobulin
deficiency and epilepsy has also been described ( 5 ) . The
significance of these results and the findings in our patient is
unclear with regard to immunoglobulin regulation; however,
results of both studies are strongly suggestive of an abnormal
contribution of X chromosome or X-linked immune response
mechanisms. Mozes and Fuchs have reported a relationship
between anti-DNA antibody and sex chromosomes in SJL x
DBAR hybrid mice (6). Also, a study by Talal and Steinberg,
using New Zealand black x New Zealand white mice,
showed that sex is a relevant characteristic in SLE (7).
However, additional studies are needed to determine if the
association between SLE and the 47,XXX karyotype is
coincidental.
Shinji Kurosawa, MD
Osamu Kimura, MD
Tomakomai City General Hospital
Tomakomai, Japan
Akira Sagawa, MD
Hokkaido University School of Medicine
Sapporo, Japan
1. Masi AT, Kaslow RA: Sex effects in systemic lupus erythematosus: a clue to pathogenesis. Arthritis Rheum 21:48&484, 1978
2. Tan EM, Cohen AS, Fries JF, Masi AT, McShane DJ, Rothfield
NF, Schaller JG, Talal N, Winchester RJ: The 1982 revised
criteria for the classification of systemic lupus erythematosus.
Arthritis Rheum 25: 1271-1277, 1982
3. Price WH, MacLean N, Littlewood AP: SLE and Klinefelter’s
syndrome. Lancet 12307, 1976
4. Michalak DP, Zacur HA, Rock JA, Woodruff JD: Autoimmunity
in a patient with 47XXX karyotype. Obstet Gynecol62:667-669,
I983
5. Sills JA, Brown J K , Grace E, Wood SM, Barclay GR, Urbaniak
SJ: XXX syndrome associated with immunoglobulin deficiency
and epilepsy. J Pediatr 93:469-471, 1978
6. Mozes E , Fuchs S: Linkage between immune response potential
to DNA and X chromosomes. Nature 249:167-168, 1974
7. Talal N, Steinberg AD: The pathogenesis of autoimmunity in
New Zealand black mice. Curr Top Microbiol Immunol 64:79103. 1974
Lupus, acquired immunodeficiency syndrome, and
antimalarial agents
To the Editor:
Overlapping clinical and serologic features may blur
distinctions when patients present with systemic lupus
erythematosus (SLE) or human immunodeficiency virus
(HIV) infection. Despite this, acquired immunodeficiency
syndrome (AIDS) and SLE tend to be mutually exclusive.
Only 4 reports of their coexistence have appeared; 3 of the 6
patients had congenital AIDS, and SLE developed (1-4).
Kaye ( 5 ) hypothesized that SLE may be protective against
AIDS because of its marked antibody production. Assuming
500,000 Americans have SLE and 150,000 have AIDS, at
least 400 concurrent cases would be expected. This negative
correlation becomes more impressive when one considers
that if 10% of patients with SLE had autoimmune hemolytic
anemia or other complications that required transfusions
(e.g., uremia, surgery) between 1978 and 1983, when the
blood supply was not being screened, up to 50,000 would be
at risk of becoming infected with HIV. However, there is not
a single report of a patient becoming HIV positive.
I wish to bring to the attention of the rheumatologic
community 2 recent reports in the AIDS literature documenting the inhibition of HIV infectivity by chloroquine and
hydroxychloroquine (6,7). These antimalarial drugs block
virus production, because of their interference with terminal
glycosylation in the trans-Golgi network. Since many SLE
patients receive chloroquine or hydroxychloroquine therapy, this could represent a potential protective mechanism.
The interrelationships between lupus and AIDS warrant
closer examination.
Daniel J. Wallace, MD
Cedars-Sinai Medical Center
UCLA School of Medicine
Los Angeles, C A
1. Kopelman RG, Zolla-Panzer S: Association of human immunodeficiency virus infection and autoimmune phenomena. Am J
Med 8432-88, 1988
2. D’Agati VD, Seigle R: Coexistence of AIDS and lupus nephritis:
a case report. Am J Nephrol 10:243-247, 1990
3. Strauss J, Abitbol C, Zilleruelo G, Scott G, Paredes A, Malaga S,
Montane B, Mitchell C, Pardo V: Renal disease in children with
LETTERS
the acquired immunodeficiency syndrome. N Engl J Med 321:
4.
5.
6.
7.
625-630, 1989
Furie R, Kaell A, Patrucci R , Farber B, Kaplan M: Systemic
lupus erythematosus complicated by infection with human immunodeficiency virus (abstract). Arthritis Rheum 3 1 (suppl 4):
S56, 1988
Kaye BR: Rheumatic manifestations of infection with human
immunodeficiency virus. Ann Intern Med 1 I1:158-167, 1989
Tsai WP, Nara PL, Kung HF, Oroszlan S: lnhibition of human
immunodeficiency virus infectivity by chloroquine. AIDS Res
Hum Retroviruses 6:481-489, 1990
Sperber K, Bekesi JG, Stecher V , Mayer L: Hydroxychloroquine inhibits HIV infection in T cells and monocytes (abstract).
FASEB J 4:3301, 1990
Comment on the article by Hernandez-Avila et a1
To the Editor:
Hernandez-Avila and colleagues, in examining the
association of the use of exogenous sex hormones, including
oral contraceptives, with the risk of rheumatoid arthritis
(RA), concluded “. . . that no important relationship exists
between oral contraceptive use and RA” (1). We present an
alternative conclusion based on our own and other recent
work in this area.
First, Hernandez-Avila et a1 state that “analyses of
secular trends in the incidence of RA in Europe have not
shown a declining incidence of this disease among women
paralleling the introduction of oral contraceptives.” We
performed a secondary analysis of data collected during the
Second and Third National Studies of Morbidity Statistics
from General Practice in England and Wales (2). The average annual age-adjusted incidence rate of RA in females
showed a significant reduction of 20% between 1970 and
1972 and between 1981 and 1982. These data did not show a
significant decline in the incidence rate of RA in males during
the same time period. The observations by Silman (3), cited
by the authors, support a continued decline in the incidence
of RA among females in England through the 1980s. In
addition, more recent data on the incidence rate in Seattle,
WA (4), when compared with incidence rates observed in
Rochester, MN in the 1970s (9, also would suggest a
declining incidence of RA in the United States.
Second, we also have performed a meta-analysis of
the analytic epidemiologic studies of the relationship of oral
contraceptive use and RA (6). The principal result of this
meta-analysis, which included the data from the Nurses’
Health Study, as used by Hernandez-Avila et al, was that
there was a small protective effect of oral contraceptive
usage against the development of RA: The pooled odds ratio
was 0.73, with a 95% confidence interval (CI) of 0.61-0.85.
We performed subgroup analysis and found that the average
odds ratio for 6 case-control studies (refs. 3 , 5 , 6 , 2 5 , 27, and
28 in the article by Hernandez-Avila et al) was 0.60 (95% CI
0.48-0.75), whereas that for 3 longitudinal studies (refs. 2
and 26 in the article by Hernandez-Avila et a1 and ref. 7
herein) was not significantly different from unity (i.e., no
protective effect). A further subgroup analysis, wherein
studies were grouped based on type of cases, produced a
pooled odds ratio of 0.49 (95% CI 0.39-0.63) for the 5 studies
373
with hospital- or clinic-derived cases, which was significantly different from that of 0.95 (95% CI 0.78, 1.16) for the
4 studies with population-derived cases. This difference was
unlikely to have been explained by bias due to selection of
controls.
Based on the results of the subgroup analysis, we
suggest that oral contraceptive use may not have a “protective effect” on the development of RA, but rather, may have
a “disease-modifying effect,” preventing the progression to
severe disease by modifying the disease process. Patients
from population-based sources are likely to have milder or
more transient disease than patients from hospital-based
clinics (8-1 1). Furthermore, population-derived patients are
less likely to show an association with HLA-DR4 (12), or to
have a greater-than-expected case-fatality or mortality rate
(5,13,14). Therefore, oral contraceptive use may prevent
only the more severe forms of RA. Support for this hypothesis comes from a recent reanalysis of data from the latest of
the Dutch case-control studies, which demonstrated a stronger protective effect in the most severely affected RA
patients (15).
Further recent evidence of a modest effect of oral
contraceptive use comes from preliminary data from the
large, ongoing, population-based case-control study in Seattle, which suggest that current, but not past, oral contraceptive use is protective against the development of RA (16).
Hernandez-Avila et a1 were not able to “. . . completely
exclude the possibility that . . . current oral contraceptive
use causes a small reduction in the risk of RA.”
To date, at least 9 independent epidemiologic studies
specifically examining the relationship between oral contraceptive use and RA have been published. It is important,
therefore, to view a single study in this context, and attempt
to provide a unifying acceptable explanation for the results.
Oral contraceptive use could have important therapeutic
implications, if it does have a mild disease-modifying effect.
Timothy D. Spector, MD, MSc, MRCP
St. Bartholomew’s Hospital Medical College
London, U K
Marc C . Hochberg, MD, MPH
The Johns Hopkins Medical Institutions
Baltimore, MD
1. Hernandez-Avila M, Liang MH, Willett WC, Stampfer MJ,
Colditz GA, Rosner B, Chang RW, Hennekens CH, Speizer FE:
Exogenous sex hormones and the risk of rheumatoid arthritis.
Arthritis Rheum 33:947-953. 1990
2. Hochberg MC: Changes in the incidence and prevalence of
rheumatoid arthritis in England and Wales, 1970-1982. Semin
Arthritis Rheum 19:294-302, 1989
3. Silman AJ: Recent trends in rheumatoid arthritis. Br J Rheumato1 25:32&336, 1986
4. Dugowson CE, Bley L, Koepsell TD, Nelson JL, Daling JR:
Incidence of rheumatoid arthritis in women (abstract). Arthritis
Rheum 32 (suppl4):S63, 1989
5 . Linos A, Worthington JW, O’Fallon WM, Kurland LT: The
epidemiology of rheumatoid arthritis in Rochester, Minnesota: a
study of its incidence, prevalence and mortality. Am J Epidemiol 11 1:87-98, 1980
6. Spector TD, Hochberg MC: The protective effect of the oral
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