SAT0382 THE SAME BUT DIFFERENT? ANALYSIS OF A COHORT OF PATIENTS WITH LATE ONSET ANKYLOSING SPONDYLITIS

Abstract

Background:Ankylosing spondylitis(AS) has long been described as presenting in the third decade of life with the onset rarely occurring over the age of 45 years old. Previous research has shown there are small numbers of patients being diagnosed with AS later in life. These studies have been limited to small numbers limiting the ability to detect patterns in disease. The Ankylosing Spondylitis Registry of Ireland (ASRI) is an epidemiological data source on patients with AS in Ireland. Large registries, such as this, are an opportunity to further study this subtype in large numbers with greater power to detect differences between late and typical onset.Objectives:The purpose of this study was to examine late onset AS in a large, well characterized cohort.Methods:Patient registered in ASRI were analysed on the basis of their age of symptom onset using IBM SPSS version 26. Patients were divided into two groups with an age over 45 years old at symptoms onset categorized at late onset. Mean BASMI, BASFI, BASDAI, HAQ, and ASQoL scores were compared between the two groups and tested for statistical significance using an independent two tailed t-test. Further analysis looking at differences in gender, HLA B27 status, sacroiliitis on MRI, medication use and extra-articular manifestations(EAMs) was also performed using a chi-squared test for independence.Results:A total of 851 patients with AS were included in the analysis. Of these patients 659(77.4%) were males, with 192(22.6%) females, mean age of 45.8 years and mean disease duration of 19.4 years (means: ASQoL 6.52, HAQ 0.54, BASDAI 4.03, BASFI 3.7, BASMI 4.03). Patient population was made up of 797 patients(93.7%) categorized as typical onset, 54 patients(6.3%) categorized as late onset(table 1). Males had a higher rate of late onset AS than females, but this did not reach significance (6.8% vs 4.7%, p=0.19). Patients with late onset AS were noted to have higher BASFI (5.53 vs 3.58, p<0.01), HAQ (0.75 vs 0.53, p<0.01) and ASQoL scores (7.68 vs 6.44, p<0.01). Late onset patients also had lower rates of HLA-B27 positivity (76.5% vs 91.2%, p<0.01). No significant difference was detected in BASDAI or BASMI scores. No difference was detected between groups regarding rates EAMs. The late onset AS patients were noted to have lower rates of biologic therapy use (50% vs 72%, p<0.01). No significant difference was detected in rates of NSAID use.Table 1.Onset < 45 years (n=797)Late Onset (n=54)pvalueMales (n=659)93.2% (614)6.8% (83.3)0.19Females (n=192)23% (183)16.6% (9)HLA B27+ (n=580)90.5% (554)76.5% (26)<0.01Enthesitis (n=146)16.9% (135)20.4% (11)0.45Dactylitis (n=54)6% (48)11.1% (6)0.21Arthritis (n=256)29.7% (237)35.2% (19)0.4MRI Sacroiliitis (n=384)45.3% (361)42.6% (23)0.69Bilateral sacroiliits (n=668)79% (628)74% (40)0.07BASDAI4.024.190.6BASFI3.585.53<0.01BASMI3.964.970.12HAQ0.530.75<0.01ASQoL6.447.68<0.01Uveitis28.5% (227)24.1% (13)0.07IBD9.9% (79)14.8% (8)0.32Psoriasis16.4% (131)18.5% (10)0.54Smokers (ever)57.3% (457)64.8% (35)0.01Alcohol consumption (ever)82% (654)75.9% (41)0.53Biologic tx69.1% (551)48.1% (26)<0.01NSAID tx54.2% (432)61.1% (33)0.2Figure 1.Conclusion:This analysis shows that late onset AS does occur in up to 6.3% of patients with AS. Patients with late onset disease were noted to have similar patterns of disease, EAMs and radiological findings consistent with current classification criteria for AS. Less patients with late onset disease were HLA-B27 positive, the reason for this is unknow. These patients had worse functional outcomes, which could reflect the older age of symptom onset. It is notable that patients with late onset AS are being treated with less biologic agents, and have a slightly higher rate of NSAID usage. Additional registry studies into this subgroup would help to understand these variations in medication usage and prescribing practices.Disclosure of Interests:Sinead Maguire Grant/research support from: ASRI is supported by funding from Pfizer, AbbVie and UCB, Phil Gallagher: None declared, Finbar Barry O’Shea Grant/research support from: ASRI is supported by funding from Pfizer, AbbVie and UCB