Prof.KathrynTan Hong Kong, China

Prof.KathrynTan
Kathryn Tan is Sir David Todd Professor in Medicine at the University of Hong Kong, and Honorary Consultant of the Department of Medicine at Queen Mary Hospital. She is past president of the Hong Kong Society of Endocrinology, Metabolism and Reproduction, a founding executive board member of the Asian Association for the Study of Diabetes, and council member of the Hong Kong Atherosclerosis Society. Her main academic research interests range from basic to clinical sciences in lipidology and diabetes. She is currently Senior Editor of the journal Endocrine Connections and Associate Editor of the Journal of Diabetes Investigation.

21 MARCH

Time Session
08:30
10:00
[Symposium] Dyslipidemia
New Development in Dyslipidemia Management
  • Lipoprotein(a): What Endocrinologists Need to Know
    Kathryn TanHong Kong, China Speaker Lipoprotein(a): What Endocrinologists Need to KnowLipoprotein(a) [Lp(a)] is a cholesterol-rich LDL-like particle with apolipoprotein(a) covalently linked to apolipoprotein B100 via a disulfide bond. Lp(a) is synthesized within the liver and there is a general inverse correlation between Lp(a) isoform size and plasma Lp(a) concentrations. About 90% of plasma Lp(a) concentration is genetically determined and plasma levels can modestly rise after menopause in women, and in conditions like hypothyroidism, nephrotic syndrome. It has been shown that elevated Lp(a) is an independent risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis. Although Lp(a) concentration does vary with ethnicity, relationships between Lp(a) concentration and ASCVD risk remain similar across different ethnic groups. Elevated Lp(a) is considered a cardiovascular risk-enhancing or amplification factor, and recent guidelines and consensus have increasingly recommended universal screening for Lp(a). There are as yet, no approved therapies for elevated Lp(a). Current management focuses on intensifying control of concurrent risk factors, particularly LDL-C, to reduce ASCVD risk. Amongst existing lipid-lowering drugs, only proprotein convertase subtilisin/kexin type 9 inhibitors can lower Lp(a) levels modestly. Emerging RNA-based and small-molecule therapeutics are under development and are showing promising Lp(a)-lowering effects up to 80-90%. Ongoing phase 3 cardiovascular outcomes trials will determine whether effectively lowering Lp(a) can translate to cardiovascular benefit.
  • Autologous Implantation of Genetically Modified Adipocytes Expressing LCAT for the Treatment of Familial LCAT Deficiency
    Masayuki KurodaJapan Speaker Autologous Implantation of Genetically Modified Adipocytes Expressing LCAT for the Treatment of Familial LCAT Deficiency
  • Novel and Future Lipid-Lowering Therapy
    Sung Hee ChoiKorea Speaker Novel and Future Lipid-Lowering Therapy
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