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Giant cell arteritis in Mediterranean countriesComment on the article by Salvarani et al.

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LETTERS
1249
The disease duration in our patients was between 2
and 26 years (mean 8.1 years), and all of them showed a
rapid progression before starting MTX. In this particular
group of patients, the severity of the disease was independent of the duration. This does not necessarily apply to an
average population of RA patients.
While our study does not demonstrate a superiority
of MTX over parenteral gold, it does show that clinically
effective treatment with MTX may slow down joint destruction in RA patients whose disease was previously not
sufficiently responsive to parenteral gold treatment. A
double-blind prospective study comparing intramuscular
doses of MTX (15 mg/week) and gold sodium thiomalate (50
mg/week) in early RA did not show significant differences
between the drugs after I year (4).
R. Rau, MD, PhD
Evangelisches Fachkrankenhaus
Ratingen, Germany
I . Nordstrom DM, West SG, Andersen PA, Sharp JT: Pulse methotrexate therapy in rheumatoid arthritis: a controlled prospective
roentgenographic study. Ann Intern Med 107:7974301, 1987
2. Larsen A, Thoen J: Hand radiography of 200 patients with
rheumatoid arthritis repeated after an interval of one year. Scand
J Rheumatol 16:395401, 1987
3. Sharp JT, Wolfe F, Mitchell DM, Bloch DA: The progression of
erosion and joint space narrowing scores in rheumatoid arthritis
during the first twenty-five years of disease. Arthritis Rheum
34:660-668, 1991
4. Menninger H , Rau R, Herborn G. Karger T, Elhardt D: One year
data in a blind randomised trial of methotrexate and gold sodium
thiomalate in active early rheumatoid arthritis (abstract). Arthritis Rheum 34 (suppl 9):S36. 1991
Giant cell arteritis in Mediterranean countries:
comment on the article by Salvarani et al
To the Editor:
We read with interest the article by Salvarani et al
concerning giant cell (temporal) arteritis (GCA) in Italy (1).
We recently investigated the incidence of biopsy-proven
GCA from 1981 to 1990, in an area of northwestern Spain (2).
The average annual incidence rate of biopsy-proven GCA
was 6/100,000 population 50 or older, but if we had considered all patients diagnosed with GCA, i.e., those with a
positive biopsy result plus those diagnosed by clinical criteria alone (3), the annual incidence would be 6.6/100,000 age
50 or older, which is very similar to the rate in Italy reported
by Salvarani and colleagues. The similarity in these findings
may be related to genetic factors.
We raise two issues for consideration by Salvarani et
al: First, they had previously published an article in which
the annual incidence of GCA was reported to be 8.8/100,000
(4). and in their later article ( I ) , the reported incidence was
lower (6.9/100,000). In contrast, we observed a progressive
increase of the annual incidence, which is similar to findings
in other studies (5).
The second issue is that, in the study by Salvarani
and colleagues, only 46.5% of the patients had biopsyproven disease. Ninety percent of our patients had a positive
biopsy result, which is slightly lower than the percentage
found in a study in Olmsted County, Minnesota ( 5 ) . We
believe these differences may be explained by the fact that
Salvarani et al obtained artery specimens that were of
insufficient size; we usually obtain biopsy specimens at least
3 cm in length.
It has been proposed that, in patients with a negative
biopsy result, determination of factor VIII-von Willebrand
factor antigen might be of some help in supporting the
diagnosis of GCA (6). although others have considered this
to be of limited value (7). However, despite the segmented
nature of the lesions in the arterial wall of patients with
GCA, we are in favor of pathologic confirmation, since these
patients, in the majority of cases, will require treatment with
corticosteroids for long periods of time.
Finally, similar to the findings reported by others
(8,9), we have recently observed that treatment with low
doses of immunosuppressive drugs may be useful in enabling
reduction of the steroid dosage and decreasing the frequency
of steroid relapses of GCA.
Miguel A. GonzBlez-Gay, MD
Maria D. Alonso, MD
Juan J. Agiiero, MD
Mercedes Bal, MD
Benjamin FernBndez-Camblor, MD
Amalia SBnchez-Andrade, MD
Hospital Xeral Lirgo
Lugo. Spain
I . Salvarani C, Macchioni P, Zizzi F, Mantovani W, Rossi F, Castri
C, Capozzoli N , Baricchi R. Boiardi L, Chiaravalloti F. Portioli
I: Epidemiologic and immunogenetic aspects of polymyalgia
rheumatica and giant cell arteritis in Northern Italy. Arthritis
Rheum 34:351-356, 1991
2. GonzAlez-Gay MA, Alonso MD, Agiiero JJ, Bal M, FernBndezCamblor B, SAnchez-Andrade A: Temporal arteritis in a northwestern area of Spain: study of 57 biopsy proven patients. J
Rheumatol 19:277-280. 1992
3. Huston KA, Hunder GG,Lie JT, Kennedy RH, Elveback LR:
Temporal arteritis: a 25-year epidemiologic, clinical, and pathologic study. Ann Intern Med 88:162-167, 1978
4. Salvarani C, Macchioni PL, Tartoni PL, Rossi F, Baricchi R,
Castri C, Chiaravalloti F, Portioli I: Polymyalgia rheumatica and
giant cell arteritis: a 5-year epidemiologic and clinical study in
Reggio Emilia, Italy. Clin Exp Rheumatol 5:205-215, 1987
5 . Machado EBV, Michet CJ, Ballard DJ, Hunder GG, Beard CM,
Chu C-P, O'Fallon M: Trends in incidence and clinical presentation of temporal arteritis in Olmsted County, Minnesota, 19501985. Arthritis Rheum 31:745-749, 1988
6. Persellin ST, Daniels TM, Rings LJ, Kazmier FJ, Bowie EJW,
Hunder GG: Factor VIII-von Willebrand factor in giant cell
arteritis and polymyalgia rheumatica. Mayo Clin Proc 60:457462, 1985
7. Nordborg E, Anderson R, Tengborn L, EdCn S, Bengtsson BA:
Von Willebrand factor antigen and plasminogen activator inhibitor in giant cell arteritis. Ann Rheum Dis 50:316-320, 1991
8. DeSilva M, Hazleman BL: Azathioprine in giant cell arteritid
polymyalgia rheumatica: a double-blind study. Ann Rheum Dis
45:136-138, 1986
9. Krall PL, Mazanec DJ, Wilke WS: Methotrexate for corticoster-
oid-resistant polymyalgia rheumatica and giant cell arteritis.
Cleve Clin J Med 56:253-257, 1989
LETTERS
1250
To the Editor:
After carefully reading the letter by GonzBlez-Gay et
al, we offer the following response. The findings in their
epidemiologic study in an area of northwestern Spain from
1981 to 1990 confirm the low incidence of GCA in Mediterranean countries (1,2). The highest incidence rates of GCA
have been reported in northern Europe (3,4) and in Minnesota (5,6), in 2 populations of the same ethnic background. A
lower incidence has been observed in Italy (l), Israel (2),
Spain, and in North American blacks in Tennessee (7).
Interestingly, in parallel, a lower frequency of the DR4 gene
has been reported in North American blacks (5.7%) and in
Mediterranean populations (8.2% in Italy, 10.4% in Spain,
7.0% in Ashkenazi Jews in Israel), compared with Scandinavian and North American whites (15.0% and 15.8%,
respectively) (8). It is likely that genetic factors may influence the risk of GCA in different populations, even if some
additional influence of environmental factors cannot be
excluded.
In our epidemiologic study we also, using the Armitage test for linear trend (9), examined trends in GCA
incidence by sex, evaluating incidence rates over the time
periods 1980-1982, 1983-1985, and 19861988 (data not
reported in the article). We observed a statistically significant reduction in total GCA incidence (P < 0.01) during the
9-year study period, and a significant decrease in incidence
was also noted in the separate groups of men and women ( P
< 0.01 for both groups). The statistical analysis of our data
was limited by the small number of patients identified over
short periods of time.
A reduced awareness of the diagnosis of GCA might
explain the reduction in incidence rates over time. This is
unlikely, however, since in the last few years of our study
period, awareness increased because physicians at the Reggio Emilia Hospital (in particular, in the Departments of
Rheumatology, Internal Medicine, Ophthalmology, and
Neurology) and private practitioners were involved in our
epidemiologic study and were therefore trained in GCA
diagnosis. Our data may therefore indicate a real decline in
the incidence of GCA in Reggio Emilia over the 9-year study
period. Machado et a1 (6) also observed a declining incidence
of GCA in men during the period 1970-1985, in Olmsted
County, Minnesota.
We reported a positive temporal artery biopsy result
in only 46% of our GCA patients who had clinical evidence
of GCA. As outlined in our article, we believe this low
incidence of temporal artery biopsy positivity could be
explained by the low mean length of the biopsy specimens
analyzed. Noltorp and Svensson (4) also reported a histologic diagnosis of GCA in only 50% of their patients who
had the clinical features of the disease. The mean length of
the biopsy specimens in their study (0.6 cm) was very similar
to that in ours (0.5 cm), and contrasted with the larger
specimens obtained in the Olmsted County study (10) and
by GonzBlez-Gay and colleagues (5.4 cm and 3 cm, respectively).
We believe the criteria used in our study for a
diagnosis of probable GCA ( 5 ) were sufficiently selective for
diagnosis. In none of our patients was the diagnosis of GCA
modified during the followup period (mean duration 64
months), making possible errors in the diagnosis unlikely.
We agree with GonzBlez-Gay et a1 that temporal artery
biopsy should be carried out in all patients with suspected
GCA. However, from a practical point of view, the biopsy
result in a patient with clinical evidence of “classic” GCA
would not alter the decision to initiate steroid therapy.
Carlo Salvarani, MD
Pierluigi Macchioni, MD
Luigi Boiardi, MD
Lorenzo Lodi, MD
Italo Portioli, MD
Rheumatology Unit, USL N9
Reggio Emilia, Italy
1. Salvarani C, Macchioni PL. Zizzi F, Mantovani W, Rossi F,
2.
3.
4.
5.
6.
7.
8.
9.
10.
Castri C, Capozzoli N, Baricchi R, Boiardi L, Chiaravalloti F,
Portioli I: Epidemiologic and immunogenetic aspects of polymyalgia rheumatica and giant cell arteritis in Northern Italy.
Arthritis Rheum 34:351-356, 1991
Friedman G, Friedman B, Benbassat J: Epidemiology of temporal arteritis in Israel. Isr J Med Sci 18:241-244, 1982
Bengtsson B-A, Malmvall B-E: The epidemiology of giant cell
arteritis including temporal arteritis and polymyalgia rheumatica: incidences of different clinical presentations and eye complications. Arthritis Rheum 24:899-904, 1981
Noltorp S, Svensson B: High incidence of polymyalgia rheumatica and giant cell arteritis in a Swedish community. Clin Exp
Rheumatol 9:351-355, 1991
Huston KA, Hunder GG, Lie JT, Kennedy RH, Elveback LR:
Temporal arteritis: a 25-year epidemiologic, clinical, and pathologic study. Ann Intern Med 88:162-167, 1978
Machado EBV, Michet CJ, Ballard DJ, Hunder GG, Beard CM,
Chu CP, O’Fallon M: Trends in incidence and clinical presentation of temporal arteritis in Olmsted County, Minnesota,
195G198.5. Arthritis Rheum 31:745-749, 1988
Smith CA, Fidler WJ, Pinals RS: The epidemiology of giant cell
arteritis: report of a ten-year study in Shelby County, Tennessee. Arthritis Rheum 26:1214-1219. 1983
Piazza A, Olivetti E, Griffo RM, Rendine S , Amoroso A,
Barbanti M, Caruso C, Conighi C, Conte R, Favoino B,
Galliano L, Luciani G, Magri D, Martinetti M, Mattiuz PL,
Menicucci A, Misefari V , Moro L. Purpura M, Savi M: The
distribution of HLA antigens in Italy. Gene Geography 3: 141164, 1989
Armitage P: Tests for linear trends in proportions and frequencies. Biometrics I1:375-386, 1955
Hall S , Lie JT, Kurland LT, Persellin S, O’Brien PC, Hunder
GG: The therapeutic impact of temporal artery biopsy. Lancet
11:1217-1222, 1983
Interactions between antibodies and chondrocytes
To the Editor:
A recent article in Arthritis and Rheumatism by Drs.
Takagi and Jasin (1) concerns idiotype-specific interaction
between anticollagen antibodies and the membranes of chondrocytes from bovine articular cartilage. The interaction is
potentially important in the pathogenesis of collagen autoimmunity, since there was enhancement of chondrocyte
metalloprotease secretion following exposure to cytokines
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