Quinlan, CT; (2015) Cardiovascular Morbidity in Juvenile-Onset Systemic Lupus Erythematosus. Doctoral thesis , UCL (University College London).

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Abstract

Cardiovascular disease (CVD) is a leading cause of mortality in adults with systemic lupus erythematosus (SLE). As children with conditions such as chronic kidney disease have been shown to have a risk of CVD similar to their adult counterparts, clinicians have become concerned that paediatric patients with SLE are at increased risk of CVD. The aim of this project was to examine the vascular phenotype of a British paediatric population with SLE and gain mechanistic insights into this process. Structural changes in vessels were measured using carotid intima media thickness (cIMT) and function was assessed using pulse wave velocity (PWV). These findings were compared with clinical information, traditional cardiovascular risk factors, disease activity, medications and adipokine activity. 45 children were recruited to the study and compared to historical controls previously studied in our centre. Children with SLE had higher cIMT than controls (0.45 V 0.37mm, p<0.0001) but no difference in PWV (5.27 v 5.34m/s, p=0.77. The increase in cIMT is most marked in patients with hypertension, those on higher doses of prednisolone and those of Afro-Caribbean descent. No significant association was found between increased cIMT and biopsy-proven nephritis, disease activity, age, family history of CVD or physical activity score. Patients with JSLE had increased serum leptin levels (15.5 V 7.56ng/ml, p=0.024). There were slightly higher adiponectin levels in patients than controls (14.2 V 12.4ug/L, p=0.49). Patients with proteinuria had higher leptin (35.5 V 18.8ng/ml) and adiponectin (21.9 V 10.5ug/ml, p=0.03) levels, and cIMT increased with leptin and adiponectin levels. This cohort of children with JSLE show structural changes in their vessels indicative of early CVD but with adaptive changes resulting in normal functional scans. In contrast to adult data this group displays an early increase in serum adiponectin suggesting a possible early protective mechanism, which may be overwhelmed in later disease.

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