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Rheumatology 2001; 40: 1420-1422
© 2001 British Society for Rheumatology
Letters to the Editor |
Takayasu's arteritis associated with rheumatoid arthritis: a case report and review of the literature
. Zubaro
lu
Division of Rheumatology, Department of Internal Medicine,
1Department of Radiology, Medical Faculty, University of Osmangazi, 26480 Eski
ehir, Turkey
SIR, Takayasu's arteritis (TA) is a necrotizing and obliterative segmental panarteritis of unknown aetiology, which attacks the aortic arch and its major branches [1, 2]. Autoimmunity is thought to play an important role, and cases associated with various autoimmune disorders have already been reported [3, 4]. Here, a case of rheumatoid arthritis (RA) which developed into TA is presented and English literature is reviewed briefly.
A 36-yr-old woman with pain and swelling in both knees, elbows, and the small joints in her hands was admitted to a local hospital in March 1998. She was diagnosed as having RA. Sulphasalazine was administered (2 g/day). On finding that sulphasalazine was not sufficiently effective after a 6-month period of treatment, methotrexate was also added to her treatment (7.5 mg/week). Her articular symptoms resolved in time. In March 2000 the patient was referred to our hospital with an exacerbation of RA as well as dizziness, neck pain and headaches.
Upon examination, she was found to have both swelling and tenderness in her peripheral joints, as well as a 30° loss of extension in both elbows. Neither pulses nor blood pressure were detectable in the right arm. Bruits were audible over both subclavian arteries. Laboratory results were as follows: haemoglobin 9.6 g/dl with a normochromic and normocytic red cell morphology, platelets 666000/mm3, erythrocyte sedimentation rate (ESR) 119 mm/h, C-reactive protein 16.2 mg/dl. Rheumatoid factor (RF) level was 281 IU/ml (normal <10). Serum chemistry and urine analysis were normal. Antinuclear antibodies (ANA), anti-DNA, anti-Ro, -La, -Sm, RNP, Scl-70, cytoplasmic pattern antineutrophil cytoplasmic antibodies (c-ANCA), perinuclear (p-ANCA), protein C, S and anti-thrombin III were negative or within normal limits. Immunoglobulin G, M, anti-cardiolipin antibodies and Veneral Disease Research Laboratory test were all negative. The HLA serological typing was: HLA-A 24, 32; B 13, 44; DR 1, 4; DQ7 (Q3). A radiograph revealed peri-articular soft-tissue swelling and erosive changes in both hands, with a bilateral narrowing of the knee joints. Aortography showed a complete occlusion in both left and right subclavian arteries (Fig. 1
).
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RA and TA were both diagnosed on the basis of already valid criteria for these diseases [5, 6]. Oral administration of prednisolone (50 mg/day) was added to the aforementioned treatment. Within 3 months, the dizziness and headaches disappeared and the right radial pulse was again detectable, albeit weakly. Her blood pressure on the right arm was 90/50 mmHg. ESR decreased to 20 mm/h.
TA is a rare pathology associated with other autoimmune diseases, such as systemic lupus erythematosus [3] and systemic sclerosis [4]. Our patient is one of several cases developing TA after arthritic signs and symptoms (Table 1) [7–9, 11–15]. Only Rush et al. [10] have reported a case in which a patient developed TA before RA.
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We found 19 other cases, together with the present patient, of RA associated with TA in the English literature. These were composed of 14 females and six males, with a mean age of 48±14.6 yr (range 16–74) at the time of RA diagnosis. The mean age at the time of TA diagnosis was 55.5±15 yr (range 20–82), which was higher than isolated TA [2]. The average time elapsing between the onset of RA and the development of TA was 7.5 yr. Twelve of the cases were not diagnosed until post-autopsy [9, 12, 13]. The death of seven of these patients was directly attributed to vasculitis. Most of the patients had a positive RF and subcutaneous nodules were detected (Table 1
). A study of 107 cases of TA, the aim of which was to correlate RA and TA, found that whilst there was a weak positive RF in some patients with arthralgias, there was no correlation between the presence of arthritis and a positive RF [2]. Likewise, in a study of 84 patients with TA, 12 had a history of arthralgia. Only one of them had a frank synovitis with a positive RF [1]. On the other hand, in a study of 32 North American patients with TA, arthralgia and synovitis were present in 56 and 22% of patients, respectively [16]. Sato et al. [17] from Brazil showed that arthralgias or arthritis were present in 26% of patients with TA. Such a clinical difference regarding arthritis and arthralgias in the course of TA may be attributable to a genetic background, as polymorphic HLA genes and their combinations may have had a role in modulating the clinical findings.
Inflammation of the small- and medium-sized arteries in the extremities may be seen in RA. Aortitis and aortic root changes were previously reported in patients with RA [9, 14]. Although clinically evident aortic incompetence is rarely seen in patients with RA during their lifetime, necropsy data suggested that aortitis and aortic valvulitis may be seen in up to 15% of cases [13]. RA that causes aortitis is almost always a severe, seropositive and nodular disease, associated with extra-articular vasculitic manifestations [13].
Despite the fact that the exact nature of the relationship between RA and TA is unknown, we can speculate that the development of these two diseases in our patient might be a complication of the chronic inflammatory disease and a non-specific arterial response to a generalized inflammatory process in the presence of a genetic background predisposing to both RA and TA. We also make the suggestion that all patients with RA be monitored carefully for the development of an occlusive arterial involvement.
We wish to thank K. Marsden and S. Kiliçaslan for the linguistic corrections to this manuscript.
Notes
Correspondence to: C. Korkmaz, Vinelik mah, Alifuat Güven Cad, Akasya sok 11/11, 26020 Eskiehir, Turkey. 
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