{ "chinesename
谭丽珊
title
Prof.
surname
Tam
givenname
LS
photo
../images/people/lstam.png
education
MBChB (CUHK), MRCP (UK), FHKCP, FHKAM (Medicine), MD (CUHK), FRCP (Glasg, Lond, Edin)
post
Professor, Department of Medicine & Therapeutics
Faculty of Medicine, The Chinese University of Hong Kong
Honorary Consultant, Hospital Authority
researcherid
K-4980-2014
expertise
Rheumatology
interest
Inflammation and glucocorticoid induced osteoporosis, premature atherosclerosis in patients with rheumatic diseases and innate immunity in the pathogenesis of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).
tel
(852) 3505 3128
email
lstam@cuhk.edu.hk
research
Regarding the role of inflammation and glucocorticoid induced osteoporosis (GIOP) in patients with rheumatic diseases; we have reported that 20% of SLE patients sustained a fragility fracture and 30% of those patients with fracture had normal bone mineral density (BMD). In order to look for a more sensitive predictor of fracture, we evaluated the volumetric bone density (vBMD), strength and architecture of SLE patients on glucocorticoids (GC) with a novel technology, high-resolution peripheral quantitative computed tomography (HR-pQCT) and found that cortical vBMD can discriminate patients with and without fracture while areal BMD cannot. In a case-control study, we confirmed that bone geometry, vBMD, microarchitecture and bone strength at peripheral site are significantly deteriorated in SLE patients with or without GC therapy, most dramatic at the cortical compartment compared with healthy controls. Disease per se (cumulative inflammatory burden) or in combination with GC therapy plays an important role in the bone mass loss and bone quality deterioration in SLE patients. To further assess the effect of inflammation and bone loss, we applied HR-pQCT in patients with RA, and found that deterioration in density and microstructure in male and female RA patients involved both cortical and trabecular compartments, again affecting predominantly the cortical compartment, manifested as increased cortical porosity.
Regarding the role of inflammation in accelerating premature atherosclerosis in patients with rheumatic diseases, we have reported that cumulative inflammatory burden is associated with arterial stiffness in psoriatic arthritis (PsA), and effective suppression of inflammation using anti-TNF plus methotrexate was more effective than methotrexate alone in preventing the progression of arterial stiffness in patients with early RA. Similarly, in patients with ankylosing spondylitis (AS), the use of TNF-α blockers was more effective than placebo in preventing the progression of arterial stiffness. Based on longitudinal studies in patients with early RA and PsA, soluble receptor of advance glycation end product (sRAGE) and interleukin-33 (IL-33) was found to be associated with the progress of arterial stiffness in patients with early RA and PsA respectively.
With regards to the role of innate immunity in the pathogenesis of SLE, we found that aberrant activation of pathogen recognition (PRR) pathways by endogenous or exogenous molecules triggers the initation and/or perpetuation of autoimmune responses, for example NOD2 may participate in the pathogenesis of lupus via the recognition of MDP and induction of proinflammatory effects. Over-expression of RAGE may also amplify the pro-inflammatory effects of danger associated molecular patterns (DAMPs) such as HMGB1, while sRAGE may serve as a decoy receptor to suppress inflammation in patients with lupus nephritis. Upregulated HMGB1 may act alone or in combine with TLR9 ligand through the phosphorylation of p38 MAPK and NF-κB to promote inflammation in lupus. On the other hand, the immune evasion strategy via avoidance of stimulation and downregulation of PRRs may promote establishment of persistent infection. TLR inhibitor (hydroxychloroquine) and prednisolone may down-regulate protein levels of TLRs 7 and 9 in lupus patients, thereby decreasing the innate immune response against HPV infection.
Our group is currently conducting 2 studies evaluating the effect of treat-to-target strategies aiming at remission on arterial stiffness and subclinical atherosclerosis in patients with early RA and PsA, and whether bone microstructure assessed by HR-pQCT can discriminate GIOP patients with and without fracture independent of areal BMD. We are also studying the role of two novel cytokines, namely IL-35 and IL-36 in the pathogenesis of SLE and RA.

selected
publication
Tam LS, Chan AYK, Chan PKS, AR Chang, Li EK. Higher prevalence of squamous intraepithelial lesion in systemic lupus erythematosus - association with human papillomavirus infection. Arthritis Rheum 2004;50:3619-3625." },{ "publication
Tam LS, Li EK, Wong CK, Lam CW, Li WC, Szeto CC. Safety and efficacy of leflunomide in the treatment of lupus nephritis refractory or intolerant to traditional immunosuppressive therapy: an open label trial. Ann Rheum Dis 2006;65:417-8." },{ "publication
Li EK, Tam LS, Wong CK, Li WC, Lam CW, Wachtel-Galor S, Benzie IFF, Bao YX, Leung PC, Tomlinson B. Safety and efficacy of ganoderma lucidum (lingzhi) and san miao san supplementation in patients with rheumatoid arthritis: a double-blind, randomized, placebo-controlled pilot trial. Arthritis Rheum 2007;57:1143-1150." },{ "publication
Tam LS, Shang Q, Li EK; Tomlinson B, Chu T, Li M, Leung YY, Kwok LW, Wong KC, Li TK, Yu T, Zhu YE, Kun EW, Yip G, Yu CM. Subclinical Carotid Atherosclerosis in Patients with Psoriatic Arthritis. Arthritis Rheum 2008; 59:1322–1331." },{ "publication
Li EK, Zhu TY, Hung VY, Kwok AW, Lee VW, Lee KK, Griffith JF, Li M, Wong KC, Leung PC, Qin L and Tam LS. Ibandronate increases cortical bone density in patients with systemic lupus erythematosus on long-term glucocorticoid. Arthritis Res Ther 2010;12:R198 (22 October 2010)." },{ "publication
Tam LS, Gu J, Yu D. Pathogenesis of ankylosing spondylitis. Nat Rev Rheumatol 2010 2010 Jul;6(7):399-405." },{ "publication
Tam LS, Li EK, Shang Q, Tomlinson B, Li M, Leung YY, Kuan WP, Kwok LW, Li TK, Zhu TY, Kun EW, Yip G, Yu CM. TNF-? blockade is associated with sustained regression of carotid intima-media thickness for patients with active psoriatic arthritis-a 2-year pilot study. Ann Rheum Dis 2011;70:705-706." },{ "publication
Yu SL, Chan PK, Wong CK, Szeto CC, Ho SC, So K, Yu MM, Yim SF, Cheung TH, Wong MC, Cheung JL, Yeung AC, Li EK, Tam LS. Antagonist-mediated down-regulation of toll-like receptors increases the prevalence of human papillomavirus infection in Systemic Lupus Erythematosus. Arthritis Res Ther 2012:18;14(2):R80." },{ "publication
Zhu TY, Griffith JF, Qin L, Hung VW, Fong TN, Au SK, Tang XL, Kwok AW, Leung PC, Li EK, Tam LS. Structure and strength of the distal radius in femalepatients with rheumatoid arthritis: A case-control study. J Bon Miner Res 2013;28:794-806." },{ "publication
Zhu TY, Griffith, JF, Qin L, Hung VW, Fong TN, Au SK, Li M, Lam YY, Wong CK, Kwok AW, Leung PC, Li EK, Tam LS. Alterations of bone density, microstructure and strength of the distal radius in male patients with rheumatoid arthritis: A case-control study with HR-pQCT. J Bone Miner Res 2014; 29:2118-29." }]}