Contributions
Abstract: EP1370
Type: ePoster
Abstract Category: Clinical aspects of MS - Epidemiology
Background/Goals: In the general population, interactions between SLE, variation in the 5-HTTLPR polymorphism and depression/anxiety have been observed. We will now examine this in people with MS.
Methods: A population-based cohort of 198 people with MS was followed 6-monthly for 2.5 years. Depression and anxiety symptoms were measured at each review using the Hospital Anxiety and Depression Scale. SLE were assessed retrospectively using a questionnaire based on the Social Readjustment Rating Scale. The 5-HTTLPR polymorphism was genotyped and was categorised into both a bi-allelic (S/S, S/L and L/L) and tri-allelic (LALA vs LASA + LALG vs SASA + SGLG + LGSA) models.
Results: When compared to the L/L allele type, having a S/S allele type was associated with an increased depression score (test for trend (tt): β=0.65, 95%CI=0.09, 1.20, p=0.02) and anxiety score (tt: β =0.80, 95%CI=0.12, 1.48, p=0.02) however this was not replicated under a tri-allelic model (p>0.08).
SLE number in the previous 6 or 12 months or SLE load in the previous 6 months was not associated with depression or anxiety score (p>0.06). However SLE load at 12 months was associated with depression, mainly driven by the highest category (tt: β =0.39, 95%CI=0.08, 0.71, p=0.02).
No interaction between SLE, variation in the 5-HTTLPR polymorphism and anxiety was found. We found some evidence of interaction between SLE load at 12 months, 5-HTTLPR and depression when assessing both allelic models (p=0.01).
Conclusion: In line with the general population, we found an interaction between SLE, variation in the 5-HTTLPR polymorphism and depression in people with MS. No interaction was observed with anxiety.
Disclosure: Authors have no relevant disclosures.
Abstract: EP1370
Type: ePoster
Abstract Category: Clinical aspects of MS - Epidemiology
Background/Goals: In the general population, interactions between SLE, variation in the 5-HTTLPR polymorphism and depression/anxiety have been observed. We will now examine this in people with MS.
Methods: A population-based cohort of 198 people with MS was followed 6-monthly for 2.5 years. Depression and anxiety symptoms were measured at each review using the Hospital Anxiety and Depression Scale. SLE were assessed retrospectively using a questionnaire based on the Social Readjustment Rating Scale. The 5-HTTLPR polymorphism was genotyped and was categorised into both a bi-allelic (S/S, S/L and L/L) and tri-allelic (LALA vs LASA + LALG vs SASA + SGLG + LGSA) models.
Results: When compared to the L/L allele type, having a S/S allele type was associated with an increased depression score (test for trend (tt): β=0.65, 95%CI=0.09, 1.20, p=0.02) and anxiety score (tt: β =0.80, 95%CI=0.12, 1.48, p=0.02) however this was not replicated under a tri-allelic model (p>0.08).
SLE number in the previous 6 or 12 months or SLE load in the previous 6 months was not associated with depression or anxiety score (p>0.06). However SLE load at 12 months was associated with depression, mainly driven by the highest category (tt: β =0.39, 95%CI=0.08, 0.71, p=0.02).
No interaction between SLE, variation in the 5-HTTLPR polymorphism and anxiety was found. We found some evidence of interaction between SLE load at 12 months, 5-HTTLPR and depression when assessing both allelic models (p=0.01).
Conclusion: In line with the general population, we found an interaction between SLE, variation in the 5-HTTLPR polymorphism and depression in people with MS. No interaction was observed with anxiety.
Disclosure: Authors have no relevant disclosures.