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Abstract Number: 810

Damage Assessment in Takyasu Arteritis Using Takayasu Arteritis Damage Score (TADS)

Debashish Danda1, Ruchika Goel2, Raheesh Ravindran2 and George Joseph3, 1Clinical Immunology& Rheum, Christian Medical College, Vellore Tamilnadu, India, 2Clinical Immunology & Rheumatology, Christian Medical College & Hospital, Vellore, India, Vellore, India, 3Cardiology, Christian Medical College & Hospital, Vellore, India, Vellore, India

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Takayasu arteritis

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Session Information

Title: Vasculitis

Session Type: Abstract Submissions (ACR)

Background/Purpose

Takayasu arteritis (TA) is a prototype large vessel vasculitis. Assessment of disease activity and damage has been challenging in TA due to lack of composite indices and biomarkers. TADS is damage index devised by the Indian Rheumatology Association Vasculitis Group. It consists of 42 items with 8 from cardiovascular system, classified under 7 headings. Only features persistently present for at least the preceding 6 months are scored. Both TADS1 and DEI.TAK2 (Disease Extent Index.TA) are derived from Birmingham vasculitis activity score (BVAS). We aimed to assess damage in TA using TADS, a novel composite clinical index.

Methods: TADS and DEI.TAK were calculated prospectively at baseline visit for incident patients with TA (ACR 1990 classification criteria) from our rheumatology and cardiology clinics between May 2012 and May 2014. TADS of this prospective cohort was compared with that calculated retrospectively for TA patients presenting to us prior to May 2012. SPSS version 16 was used; data was depicted as median (Inter Quartile Range) and Pearson’s correlation coefficient between TADS and selected parameters were done.

Results: A total of 102 consecutive TA patients (80 females, 22 males) with age of 27.5 (20.7- 36) years, disease duration of 27 (9.8- 65.8) months and diagnostic delay of 12 (6-36) months were recruited. Type 5 was the commonest angiographic type (n=60) with DEI.TAK of 9 (7-13) at presentation. Coronaries and pulmonary artery were involved in 18 and 9 patients respectively. Median TADS score at presentation was 6.0 (4-10) with a third of our patients (n=34) having very high damage score (TADS >8). Absent arterial pulse (59%), persistent claudication (59%), hypertension (56%), persistent dyspnea (41%) and cardiac damage (23.5%) contributed to most of the damage as reflected in TADS. Period of delay in diagnosis and age at presentation did not correlate with the damage score (r= – 0.073 and -0.87 respectively).

A marginally lower TADS [6.0 (4-10)] at presentation in the prospective cohort of 102 patients was noted as compared to that [8(4-11)] of the earlier retrospective cohort of 48 patients whose TADS was calculated from hospital records. No other parameter was different between these two cohorts. A follow up of these 48 patients for 36 (24-57) months showed an insignificant rise in TADS to 9(6-12) at the last recorded visit from 8(4-11) at baseline, in spite of treatment with steroids and 2nd line cytotoxic agents in all.

Conclusion: This is the first study using TADS for damage assessment in a large cohort of TA.  Over these years, TA continues to be associated with high damage score right from its initial presentation. Ongoing damage can probably be prevented by aggressive immunosuppression from early disease.


Disclosure:

D. Danda,
None;

R. Goel,
None;

R. Ravindran,
None;

G. Joseph,
None.

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