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Navajo Arthritis reconsidered.

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Relationship to HLA-B27
“Navajo arthritis” was described in 1971 as an
acute, self-limited, asymmetric polyarthritis of unknown
etiology seen in Navajo Indian patients. This description
was before published accounts relating HLA-B27 to
certain seronegative arthropathies. Review of 92 cases
of arthritis seen between 1977 through 1979 in adult
Navajo Indians revealed 16 cases of complete Reiter’s
syndrome, 6 cases of incomplete Reiter’s syndrome, and
7 cases of ankylosing spondylitis. The phenotype frequency of HLA-B27 in this Navajo population is 36%
and, of the Reiter’s syndrome and ankylosing spondylitis
patients tested, 85% were found to be HLA-B27 positive. We suggest that “Navajo arthritis” may not be a
unique form of arthritis affecting only the Navajo, but a
variant of either Reiter’s syndrome or ankylosing
In 1971, Muggia, Bennahum, and Williams described 21 cases of an acute, self-limited, asymmetric
polyarthritis of unknown etiology in Navajo patients
(I). The entity was termed “Navajo arthritis” and felt to
be a distinct syndrome. Our recent clinical experience
From the Public Health Service Indian Hospital, Keams
Canyon, Arizona, and the National Institute of Arthritis, Metabolism,
and Digestive Diseases, Epidemiology and Field Studies Branch, 1440
East Indian School Road, Phoenix, Arizona.
Supported in part by the Indian Health Service under provisions of PL 94-437, Title 11, Section 201(d). Additional funds provided by NIAMDD.
Robert G. Rate, MD: Public Health Service Indian Hospital;
Harold G. Morse, MD: Public Health Service Indian Hospital; Mark
D. Bornell, MD: Public Health Service Indian Hospital; Timothy T.
Kuberski, MD: NIAMDD.
Address reprint requests to Dr. T. Kuberski, NIAMDD,
Epidemiology and Field Studies Branch, 1440 East Indian School
Road, Phoenix, Arizona 85014.
Submitted for publication June 2, 1980; accepted in revised
form July 29, 1980.
Arthritis and Rheumatism, Vol. 23, No. 11 (November 1980)
with arthritis in Navajos and the finding of a high frequency of HLA-B27 in this population (2) suggested to
us ,hat the previously reported cases of “Navajo arthritis” may in fact have been HLA-B27-related forms of
arthritis. This report summarizes 3 years experience
with arthritis in Navajos at the Keams Canyon Indian
Hospital (KCIH), a 38-bed hospital located in northeastern Arizona which provides medical care for approximately 6,000 Navajos. The objective of this study
was to examine the arthritides seen by us in Navajo Indians, particularly the proven and probable HLA-B27related forms, and to compare these with the previously
described cases of “Navajo arthritis.”
The charts of all adult ( 2 1 5 years) KCIH Navajo patients with a discharge diagnosis of arthritis during the 3-year
period 1977 through 1979 were reviewed. ’Ihe diagnosis of
rheumatoid arthritis, ankylosing spondylitis, systemic lupus
erythematosus, osteoarthritis, and gout were made using established criteria (3). Gonococcal arthritis was diagnosed in
patients with arthritis from whom Neisseria gonorrhea had
been isolated. The diagnosis of Reiter’s syndrome was considered established when the classic triad of arthritis, conjunctivitis, and urethritis occurred. Incomplete Reiter’s syndrome was based on the presence of arthritis in addition to
either conjunctivitis or urethritis. HLA typing was done using
the microlymphocytotoxicity method (4) at the discretion of
the attending physician. Statistical analysis was done using
the Chi-square test.
The charts of 121 adult Navajo patients with arthritis were reviewed for the 3-year period. Table 1 is
the compilation of our results, compared to those reported by Muggia et al from the Gallup Indian Medical
Table 1. Discharge diagnoses of adult Navajo patients with arthritis
who were seen at Keams Canyon Indian Hospital (KCIH) 1977-79
compared to discharge diagnoses at Gallup Indian Medical Center
(GIMC), 1969
Number of patients
Rheumatic fever
Reiter’s syndrome
Incomplete Reiter’s syndrome
Ankylosing spondylitis
Undetermined origin
Center (GIMC) in 1969. Not included in the data from
KCIH in Table 1 are 21 patients with traumatic arthritis, 5 with septic arthritis, and 3 with arthritis grouped
under collagen vascular disease (these diagnoses were
not reported in the GIMC series). In comparing the two
series, there are significant dserences in the number of
patients seen with arthritis of acute rheumatic fever,
gonococcal arthritis, and osteoarthritis. However, the
most significant difference is between those patients
having HLA-B27 related arthropathies. There were 22
patients with Reiter’s syndrome (complete and incomplete) and 7 with ankylosing spondylitis seen at
KCIH, while only 1 patient with Reiter’s syndrome was
reported from GIMC (P < 0.001). Also significant was
that only 5 of our cases were classified as undetermined
origin, whereas 39 were so classified at GIMC (P <
Of the 22 patients with Reiter’s syndrome seen at
KCIH, 21 were tested for HLA-B27 and 18 (86%) were
positive. Eighty percent (4 of 5) of the ankylosing
spondylitis patients tested for HLA-B27 were positive.
Thus, of those patients tested who had either Reiter’s
syndrome or ankylosing spondylitis, 85% (22 of 26) were
HLA-B27 positive.
A comparison of the various findings observed in
the Reiter’s syndrome, ankylosing spondylitis, and arthritis of undetermined origin patients at KCIH and the
“Navajo arthritis” patients from GIMC is given in
Table 2. Male predominance, similar age range, and
predilection for knee involvement were seen in both
We were able to obtain followup information
and HLA typing on only 1 of our 5 patients with arthritis of undetermined origin. This 27-year-old woman
presented in early 1979 with peripheral arthritis involving her knees and hips. Subsequent to the chart review, she developed signs and symptoms which fulfill
criteria for the diagnosis of ankylosing spondylitis. This
patient was found to be HLA-B27 positive. Interestingly, a diagnosis of Reiter’s syndrome has been
made in her 5-year-old daughter, who is also HLA-B27
positive (5).
Recent observations associating HLA-B27 with
certain forms of arthritis, particularly Reiter’s syndrome
and ankylosing spondylitis (6,7), have expanded knowledge concerning these arthritides. The phenotype frequency of HLA-B27 in the Navajo population served
by the Keams Canyon Indian Hospital has been shown
to be about 36% (2). This is approximately five times the
HLA-B27 frequency for whites (7). The report in 1971
(1) which described “Navajo arthritis” as being a distinct, previously undescribed example of an acute, selflimited arthritis was before the published observations
associating HLA-B27 with certain forms of arthritis
(6,7). Because we had encountered patients who clinically had “Navajo arthritis” and discovered that many
were HLA-B27 positive, we began to examine the hy-
Table 2. Reiter’s syndrome, ankylosing spondylitis, and arthritis of undetermined origin in adult
Navajos, Keams Canyon Indian Hospital, 1977-79, compared to “Navajo arthritis” patients, Gallup
Indian Medical Center, 1969
Form of arthritis
No. of
No. of
men (%)
involvement (70)
27-7 1
15 (68)
3 (43)
4 (80)
22 (65)
21 (100)
Reiter’s syndrome
Ankylosing spondylitis
Undetermined origin
KCIH totals
22 (loo)
7 (100)
3 (60)
32 (94)
Patient with “Navajo arthritis”
reported from GIMC
16 (76)
pothesis that our patients with “Navajo arthritis” might
have been, in many cases, HLA-B27 related arthritis.
The patients reported in 1971 with “Navajo arthritis” (1) were characterized by the “preponderance of
males and the absence of a chronic course, residual deformities, morning stiffness, rheumatoid nodules, lupus
cells or positive tests for rheumatoid factor.” The clinical findings were described as “typically lasting a few
days or several weeks, marked by the rapid onset of
asymmetric distribution of acutely painful, red, swollen
joints with a predilection for the knee. This is followed
by rapid and complete resolution leaving no residual
deformities or clinical symptoms.” Except for the presence of conjunctivitis and/or urethritis, this description
characterizes many of our Reiter’s syndrome patients
and, similarly, could have been observed early in the
course of a few of our ankylosing spondylitis patients.
Except for the uniform self-limited nature (1-3 weeks)
of “Navajo arthritis,” this characterization also is compatible with the description of some incomplete Reiter’s
syndrome patients who are HLA-B27 positive and have
peripheral arthritis with no urethritis or conjunctivitis
(8). The description of “Navajo arthritis” is also consistent with the heterogeneous group of arthritides associated with HLA-B27 termed “reactive arthritis” (9).
Based on our experience, Reiter’s syndrome is comparatively common among the Navajo, as is incomplete
Reiter’s syndrome. Presumably this is related to the
high frequency of HLA-B27 in the Navajo population
served by our hospital.
In the report by Muggia et a1 (1) describing
“Navajo arthritis,” only one patient (1%) with Reiter’s
syndrome was observed in the 99 arthritis patients seen
during 1 year, and 39 (39%) were found to have arthritis
of undetermined origin. In our series of 92 patients with
similar diagnoses seen over 3 years, there were 16 (17%)
cases of Reiter’s syndrome, 6 (7%) incomplete Reiter’s
syndrome, 7 (8%) ankylosing spondylitis, and 5 (5%)
cases of arthritis of undetermined origin. Eighty-five
percent of our Reiter’s syndrome and ankylosing
spondylitis patients tested were found to be HLA-B27
Certainly some of the differences observed in the
various forms of arthritis are due to differences in the
type of patients seen; KCIH is community based,
whereas GIMC is a referral hospital. The patient population differences probably account for the greater number of cases of arthritis associated with rheumatic fever
(in addition to a decreasing incidence) and the fewer
cases of osteoarthritis seen at GIMC. Nevertheless, the
Navajo is a relatively homogeneous American Indian
population (lo), and we have no reason to believe that
the Navajos seen at KCIH differ substantially from
Navajos seen elsewhere. This suggests that a large proportion of the patients described with “Navajo arthritis”
may have been patients with HLA-B27 associated arthritis, particularly incomplete Reiter’s syndrome or
“reactive” arthritis. This hypothesis could be confirmed
(or refuted) only if the 21 cases of “Navajo arthritis”
were evaluated again and HLA typing performed. If
these 21 patients represented a random sampling of our
Navajo population, only 7 or 8 would be expected to be
HLA-B27 positive. If some, or all, of the patients had
Reiter’s syndrome, about 17 or 18 of the 21 would be
expected to be HLA-B27 positive.
With the advantage of new information and
techniques that can be applied to the study of arthritis,
we suggest that “Navajo arthritis” is not a unique form
of arthritis affecting only the Navajo, but probably represents variants of classic Reiter’s syndrome or ankylosing spondylitis.
The authors thank the Navajo and Hopi tribes for
their cooperation in this study; Dr. Peter Bennett for his advice; and Theona Vyvial of Arizona Blood Services for her assistance in the histocompatibility antigen typing. We also appreciate the invaluable help of the staff at the Keams Canyon
Indian Hospital.
The opinions expressed in this paper are those of the
authors and do not necessarily reflect the views of the Indian
Health Service.
1. Muggia AL, Bennahum DA, Williams RC Jr: Navajo arthritis-an unusual, acute, self-limited disease. Arthritis
Rheum 14:348-355, 1971
2. Morse HG, Rate RG, Bonnell MD, Kuberski TT: High
frequency of HLA-B27 and Reiter’s syndrome in Navajo
Iridians. J Rheumatol (in press)
3. Bennett PH, Burch TA: New York symposium on population studies in the rheumatic diseases: new diagnostic
criteria. Bull Rheum Dis 17:453458, 1967
4. Terasaki PI, McClelland JD: Microdroplet assay of human serum cytotoxins. Nature 204:998-1000, 1964
5. Morse HG, Rate RG, Bonnell MD, Kuberski TT: Reiter’s
syndrome in a five-year-old girl. Arthritis Rheum 23:960961, 1980
6. Schlosstein L, Terasaki PI, Bluestone R, Pearson CM:
High association of an HL-A antigen, W27, with ankylosing spondylitis. N Engl J Med 288:704-706, 1973
7. Morris R, Metzger AL, Bluestone R, Terasaki PI: HL-A
W27-ia clue to the diagnosis and pathogenesis of Reiter’s
syndrome. N Engl J Med 290554-556, 1974
8. Arnett FC, McClusky OE, Schacter BZ Lordon RE: Incomplete Reiter’s syndrome: discriminating features and
HL-A W27 in diagnosis. Ann Intern Med 84:8-12, 1976
9. Aho K, Ahvonen P, Lassus A, Severs K, Tiilikainen A:
Yersinia arthritis and related diseases: clinical and i m m u nogenetic implications, Infection and Immunology in the
Rheumatic Diseases. Edited by DC Dumonde. London,
Blackwell Scientific Publications, 1976, pp 341-344
10. Vogt EZ: Navajo, Perspectives in American Indian Culture Change. Edited by EH Spicer. Chicago, The University of Chicago Press, 1961, pp 278-336
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arthritis, reconsidered, navajo
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