香港內科學會 the society of physicians of …november 2015 journal of the society of...

www.soPHYSICIANShk.orgVisit the web site for our monthly CME programmes for doctors

香港內科學會THE SOCIETY OF PHYSICIANS OF HONG KONG

To learn more or to subscribe risk-free,

visit learn.uptodate.com/HongKong15 or call +1-800-998-6374 | +1-781-392-2000.

We interpret the clinical research.

You apply it at the point of care.

is continuously updated based

on the latest medical research to bring you current

evidence-based recommendations.

Our unparalleled team of physicians and

editors places new research in the context

of the existing body of medical knowledge

using their professional expertise and

first-hand clinical experience.

This combination of Evidence & Experience

is invaluable in crafting point-of-care

recommendations trusted by more than

1 million clinicians worldwide.

November 2015 Journal of The Society of Physicians of Hong Kong | 70

71 | Journal of The Society of Physicians of Hong Kong November 2015

00

-4

-8

-12

-16

-20

1

*****

****

**

3 4 6

Week

Placebo + AD (n=148)Quetiapine XR 160mg + AD (n=148)Quetiapine XR 200mg + AD (n=188)

MDD Study 6

00

-4

-8

-12

-16

-20

1 3 4 6

Week

MDD Study 7

******

***** *

* ****Placebo + AD (n=180)

Quetiapine XR 160mg + AD (n=188)Quetiapine XR 200mg + AD (n=181)

LSM change from baseline in MADRS total score


All clinicians know that there are “difficult pneumonias” but there are no formal definitions or criteria

to diagnose or treat them. I would like to define them, for the purpose of this talk, and discuss practical aspects in the man-agement of these cases. Most patients with pneumonia, as defined by sophis-ticated prognostic guides or simpler rules (such as the CURB-65 rule), respond rapidly to oral antibiotic treatment at home. Some patients, for example, those with chronic systemic diseases such as renal, cardiac, respiratory and neurological as well as oncological, are more likely to need hospitalization to stabilize their disease. However, there are patients with non-resolving, recurrent, and progressive

pneumonia despite adequate treatment. The underlying causes of this includes cancer, immunodeficiency, dysphagia and resistant organisms. The treatment of these patients, apart from appropriate antibiotics, needs to include the use of intensive chest physiotherapy, supportive treatment especially nutritional, immu-noglobulins such as Pentaglobin, bron-choscopy, and mechanical ventilation. This presentation will outline some of the practical issues in the diagnosis and treatment of difficult pneumonias.

What are Difficult Pneumonias? How do you Diagnose and Treat Them?

Professor Tsang Wah Tak, Kenneth ( )

MD (Hons, Glasgow), MBChB (Glasgow), MRCP (UK), FRCP (Edinburgh), FRCP (Glasgow), FRCP (London), FHKCP, FHKAM (Med), FCCP, FCP Consultant Physician and Specialist in Respiratory Medicine Honorary Professor, LKS Faculty of Medicine, The University of Hong Kong Honorary Professor, Tung Wah College, Hong Kong Honorary Professor, State Key Respiratory Research Lab, Guangzhou Institute of Respiratory Diseases, Guangzhou Medical College

THE SOCIETY OF PHYSICIANS OF HONG KONGCALL FOR ASSOCIATE MEMBERS

Applicants should be registered medical doctors in good standing, in private practice or public/university service.Fee: For Jan-Dec 2016 HK$300Further information about the Society can be seen on www.SOPHYSICIANSHK.orgEnquires: Tel: 2526 2626

FRCP, FRCPsych, FHKAM (Medicine), FHKAM (Psychiatry), President______________________________________________________________________________________________________________

Reply Slip: £ I wish to apply for Associate Member £ I enclose a cheque of $300 (Jan-Dec 2016)Cheques should be made payable to “The Society of Physicians of Hong Kong Co Ltd“ and posted to: Room 1907, Lane Crawford House, 70 Queen’s Road Central,Hong Kong. Unsuccessful applicants will be refunded.

Name of Doctor (Surname first): _________________________________________________________________________________

Name in Chinese: _____________________________________________________________________________________________

Mailing address: ______________________________________________________________________________________________

______________________________________________________________________________________________________________

Tel: _______________ Fax: _______________ Email: ________________________ Mobile: _____________________________

University: ____________________________________________________ Year of graduation: _____________________________

Current appointment: Private / Public / Retired

Clinic address or Dept: _________________________________________________________________________________________

______________________________________________________________________________________________________________

Hong Kong Medical Council Registration No.: ______________________________________________________________________All applications are subject to admission procedures in accordance with the Constitution of the Society.


Antibiotic Prophylaxis to Prevent Infective Endocarditis

Currently, preoperative antibiotic prophylaxis (PAP) against infective endocarditis (IE) is prescribed

indiscriminately. The latest AHA guideline advises that it be reserved only for patients with the highest-risk medical conditions undergoing high-risk pro-cedures which are likely to result in bacte-raemia with a microbe that is potentially pathogenic for IE.

The following are the highest risk medical conditions:1) Prosthetic heart valves2) History of prior IE3) Selected congenital heart disease:

Unrepaired cyanotic congenital heart disease; completely repaired con-genital heart defects with prosthetic material/device; repaired congenital heart disease with residual defects at the site or adjacent to the site of the prosthetic device

4) Cardiac valvulopathy in a transplanted heart

It should be emphasized that PAP is no longer indicated for acquired aortic stenosis/regurgitation, mitral stenosis/regurgitation, mitral valve prolapse with or without regurgitation, and bicuspid aortic valve. Obstructive hypertrophic cardiomyopathy is also no longer an indication.

The following are the highest-risk procedures:1) Dental procedures that involve manip-

ulation of either gingival tissue or the periapical region of teeth or perfo-ration of the oral mucosa; including routine dental cleaning.

2) Respiratory tract procedures involving incision or biopsy of the respiratory tract mucosa, including tonsillectomy, adenoidectomy, or bronchoscopy with biopsy. Patients who undergo an invasive respiratory tract procedure as part of treatment for an ongoing infection should receive PAP.

3) Genitourinary (GU) and gastroin-testinal (GI) procedures: Routine PAP is not warranted for any GI or GU procedure, even for patients with high-risk cardiac conditions. However, patients with high-risk cardiac conditions and ongoing GI or GU infection warrant PAP.

4) Skin and musculoskeletal infections: Patients with such infections undergoing procedures should receive agents active against staphylococci and beta-hemolytic streptococci.

5) Obstetrical procedures: Routine PAP is not indicated for vaginal or caesarean delivery. It is reasonable to consider AP against IE before vaginal delivery at the time of membrane rupture in select patients with high-risk medical conditions.

Dr Lo Ying Sui, Archie ( )Specialist in Cardiology MD(UChicago)FACC FRCPC FRCPE FRCPG FHKCP FHKAM(Medicine) American Board of Internal Medicine (Cardiovascular Disease) Clinical Associate Professor, Chinese University of HK

Acknowledgment to Sponsors of the 59th Anniversary Scientific Meeting

AstraZeneca Hong Kong Limited

Bristol-Myers Squibb Pharma (HK) Ltd

Chong Lap (HK) Co Ltd

Gilead Science Hong Kong Limited

Merck Sharp & Dohme (Asia) Ltd

Natural-Med Inc. Ltd

Roche Hong Kong Ltd

Takeda Pharmaceuticals (Hong Kong) Limited


Powerful Performance in HIV1–2

Advancing Therapeutics.Improving Lives.Gilead Sciences Hong Kong LimitedRoom 2603, 26th Floor, Hysan Place,500 Hennessy Road, Causeway Bay, Hong KongPhone: +852 3129 2000 Facsimile: +852 2856 2611

The first STR with an Integrase Inhibitorto combine high performance efficacy,

tolerability and dosing convenience of a guidelines-recommended Truvada backbone1–6

Non-inferior virological suppression and tolerability againstATV+RTV + FTC/TDF and EFV/FTC/TDF in phase 3 clinical studies1,2

3

Indication: STRIBILD is indicated as a complete regimen for the treatment of human immunodeficiency virus-1 (HIV-1) infection in adults who are antiretroviral treatment-naïve

®

STR:Single Tablet Regimen; ATV:atazanavir; RTV:ritonavir; FTC:emtricitabine; TDF:tenofovir disoproxil fumarate; EFV:efavirenz

STRIBILD Abbreviated Prescribing InformationPresentation: Green, film-coated tablet containing 150 mg of elvitegravir, 150 mg of cobicistat, 200 mg of emtricitabine and 300 mg of tenofovir disoproxil fumarate (tenofovir DF )I.ndications: As a complete regimen for the treatment of HIV-1 infection in adults who are antiretroviral treatment-naïve. Dosage: One tablet taken orally once daily with food. Renal impairment: Should not be initiated in patients with estimated CrCl < 70 mL per min. As a fixed-dose combination tablet, Stribild should be discontinued if estimated CrCl declines < 50 mL per min during treatment as dose interval adjustment required for emtricitabine and tenofovir DF cannot be achieved. Hepatic Impairment: No dose adjustment is required in patients with mild (Child-Pugh Class A) or moderate (Child-Pugh Class B) hepatic impairment. Not recommended for use in patients with severe hepatic impairment. Contraindications: Coadministration with drugs that are highly dependent on CYP3A for clearance and for which elevated plasma concentrations are associated with serious and/or life-threatening events. These drugs and other contraindicated drugs (which may lead to reduced efficacy of Stribild and possible resistance): Alpha 1-Adrenoreceptor antagonist (alfuzosin); Antimycobacterial (rifampin); Ergot derivatives (dihydroergotamine, ergotamine, methylergonovine); GI motility agent (cisapride); Herbal products (St. John’s wort); HMG-CoA reductase inhibitors (lovastatin, simvastatin); Neuroleptic (pimozide); PDE5 inhibitor (sildenafil when dosed as REVATIO for treatment of PAH); Sedative/hypnotics (triazolam, orally administered midazolam). Warnings and Precautions: Lactic acidosis/Severe hepatomegaly with steatosis (discontinue); HIV-1 and HBV coinfection (severe acute exacerbation of hepatitis B after discontinue); New onset or worsening renal impairment; Use with other antiretroviral products; Decreases in bone mineral density; Fat redistribution; Immune reconstitution syndrome. Side effects: In subjects receiving Stribild in clinical trials: Treatment-emergent adverse drug reactions reported in ≥ 5% of subjects: Diarrhea, nausea, fatigue, headache, abnormal dreams. Laboratory abnormalities reported in ≥ 2 % of subjects: All grades: proteinuria; Grades 3-4: AST >5.0 x ULN; Amylase >2.0 x ULN; Creatinine kinase ≥ 10.0 x ULN; Urine RBC (hematuria) >75 RBC/HPF.

Before prescribing, please consult full prescribing information which is available upon request.STRIBILD and TRUVADA are registered trademarks of Gilead Sciences, Inc., or its related companies.

References: 1. Rockstroh JK, DeJesus E, Henry K, et al. A randomized, double-blind comparsion of coformulated elvitegravir/cobicistat/emtricitabine/tenofovir DFvs ritonavir-boosted atazanavir plus cofomulated emtricitabine and tenofovir DF for initial treatment of HIV-1 infection:analysis of week 96 resutls. J Acquir ImmuneDefic Syndr. 2013;62;483-486. 2. Zolopa A, Sax PE, DeJesus E, et al. A randomized double-blind comparsion of coformulated elvitegravir/cobicistat/embricitabine/tenofovir disoproxil fumarate versus efavirenz/emtricitabine/tenofovir disoproxil fumarate for initial treatment of HIV-1 infection: analysis of week 96 resutls. J Acquir Immune Defic Syndr. 2013;63:96-100. 3. STRIBILD Hong Kong Prescribing Information, HK-MAY13-US-AUG12. 4. British HIV Association (BHIVA). Guidelines for the treatment of HIV-1 postitive adults with antiretroviral therapy. Updated November 2013. 5. European AIDS Clinical Society (EACS). Guidelines for the treatment of HIV-infected adults in Europe. Version 7.0-October 2013. 6. United States Department of Health & Human Services (DHHS). Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescrents. Updated May 2014.

Adverse events should be reported. To report adverse events or safety information, please call (+852) 3129-2000 or email to [email protected]

HK-14-024-02 (2015-01-26)

C

M

Y

CM

MY

CY

CMY

K


Probucol is a potent antioxidant that was found to have anti-atherosclerotic effects in most

animal models and was effective in reducing xanthomas in patients with familial hypercholesterolaemia (FH). In human studies, it reduces high-density lipoprotein cholesterol (HDL-C), but it increases reverse cholesterol transport and the biliary excretion of cholesterol as bile acids.1 When probucol failed to show any effect on the femoral artery

luminal diameter in patients with femoral atherosclerosis in the Probucol Quanti-tative Regression Swedish Trial (PQRST) it was withdrawn from the market in Western countries.2 However, probucol is still used in East Asian countries and there has been a renewed interest in the drug in recent years due to a better under-standing of the relationship between HDL-C and cardiovascular risk. Recent animal studies have demonstrated the anti-atherosclerotic effects of probucol in addition to statins,3 and clinical studies have shown the potential benefits of the combination of probucol with cilostazol in post-stenting restenosis.4 In the Fukuoka AtheroSclerosis Trial (FAST) involving 246 asymptomatic patients with hyper-cholesterolaemia randomized to receive either probucol (500 mg/day), pravastatin (10 mg/day) or diet alone for two years, there was a significant reduction in carotid intima media thickness (IMT) in the groups treated with probucol and pravastatin and a significantly (p=0.0136) lower incidence of cardiac events in the probucol group (2.4%) compared with the control group (13.6%).5 In the Probucol Observational

Study Illuminating Therapeutic Impact on Vascular Events (POSITIVE) study, patients with heterozygous FH were compared retrospectively to those with probucol exposure and those without exposure and, after adjustment for possible confounding factors, multi-variate Cox regression analysis showed probucol significantly (p<0.001) lowered the risk of coronary heart disease in sec-ondary prevention without any obvious safety issues.6 As statin treatment may only reduce the risk of coronary heart disease events by about 30% there is a considerable so-called “residual risk” which represents a target for alternative treatments. Ongoing studies should help to define the role of this old drug in current clinical practice.7

Reference1. Yamamoto, S, H Tanigawa, X Li, et al. Pharmacologic suppression of

hepatic ATP-binding cassette transporter 1 activity in mice reduces high-density lipoprotein cholesterol levels but promotes reverse cholesterol transport. Circulation. 124(12) 2011; 1382-90

2. Walldius, G, U Erikson, AG Olsson, et al. The effect of probucol on femoral atherosclerosis: the Probucol Quantitative Regression Swedish Trial (PQRST). Am J Cardiol. 74(9) 1994; 875-83

3. Keyamura, Y, C Nagano, M Kohashi, et al. Add-on effect of probucol in atherosclerotic, cholesterol-fed rabbits treated with atorvastatin. PLoS One. 9(5) 2014; e96929

Role of Probucol in the Current Treatment of Atherosclerosis and Vascular Disease

Professor Brian Tomlinson ( )

MBBS (London), MD (London), MRCP(UK), FRCP (London), FRCP (Edinburgh), FRCP (Glasgow),FHKCP, FHKAM (Med), FACP, FCP Specialist in Internal Medicine and Clinical Pharmacology, Adjunct Professor, Department of Medicine and Therapeutics The Chinese University of Hong Kong

A complete list of references can be downloaded from www.SOPHYSICIANSHK.org


2015 Update in Diabetes, Endocrinology & Metabolism

2015 has been an exciting year for diabetes mellitus. Since 2008, inter-national regulatory agencies have

requested an evaluation of the long-term cardiovascular (CV) safety profile for new antidiabetic agents. Dipeptidyl peptidase-4 (DPP-4) inhibitors are widely used as antidiabetic agents to improve glycaemic control. The large-scale clinical study TECOS published this year demon-strated that sitagliptin (a DPP-4 inhibitor)

has good long-term safety and does not increase the risk of CV events, including CV death, nonfatal myocardial infarction, nonfatal stroke and hospitalization for unstable angina. The drug has good tol-erability and few other side-effects, espe-cially lower hypoglycaemic events and less weight gain. Sitagliptin is recommended as second-line therapy (in combination with other drugs) after the combination of diet/exercise and metformin fails.

This year a new class of antidi-abetic drug, the SGLT-2 inhibitors, has been launched. These drugs block renal tubular reabsorption of glucose, resulting in lowering of HbA1c, blood pressure and body weight. The efficacy of these drugs is dependent on renal function, and efficacy is reduced in patients who have renal impairment.

Hypercholesterolaemia is a common metabolic problem due to either over-production or excessive absorption of cholesterol. Statins inhibit hepatic LDL-cholesterol synthesis; ezetimibe inhibits intestinal absorption of cholesterol. Ezetimibe has been available for a long time but there have been concerns regarding the

long-term effect on CV risk. The IMPROVE-IT trial published this year demonstrated that patients taking a combination of ezetimibe and simvastatin for a mean of 7 years experienced fewer CVS events than patients treated with simvastatin alone. The results of this study provides reassuring data on ezetimibe long-term safety.

The treatment of osteoporosis has progressed considerably as we have new targets for intervention. Current therapeutic agents include antiresorptive agents such as bisphosphonates, denosumab – a monoclonal antibody against receptor activator of nuclear factor kappa-B ligand (RANKL), the bone forming agent teriparatide, and the uncoupling compound strontium renelate. The new target cathepsin K inhibitor odanacatib has recently been shown to decrease vertebral, non-vertebral, and hip fracture rates and is nearing approval. New bone-forming agents such as romosozumab, an anti-sclerosin antibody, and abaloparatide, a parathyroid hormone-related peptide analog, are currently undergoing clinical evaluation and are demonstrating efficacy together with a favourable safety profile.

Professor Kung Wai Chee, Annie ( )MBBS (HK), MRCP (UK), MD, FHKCP FRCP (Edinburgh), FHKAM (Medicine) FRCP (London), FRCP RCPS (Glasgow) Specialist in Endocrinology Diabetes & Metabolism Honorary Clinical Professor Department of Medicine University of Hong Kong

Rheumatoid Arthritis and Related DisordersRheumatoid arthritis: Revised classification enable early diagnosis

Rheumatoid arthritis (RA) is the most common inflammatory arthritis, with a lifetime prevalence of up to

1% worldwide. Onset can occur at any age, but peaks between 30–50 years. Disability is common and significant.

Growing evidence suggests that early identification and treatment of RA leads to improved outcomes and even improved rates of drug-free remission.

The optimal time to identify and treat RA is not known; however, within 3–6 months of symptoms of inflam-matory arthritis appears to be a good time period for initiation of DMARD therapy.

In 2010, the American College of Rheumatology (ACR) and European League Against Rheumatism (EULAR) collaborated to create a new classifi-cation criteria for RA. These new criteria enable clinicians to diagnose RA earlier in patients who may not meet the 1987 ACR

Dr Yu Ka Lung, Carrel ( )

MBBS, MRCP, FHKAM, FHKCP Specialist in Rheumatology Hong Kong Autoimmune and Rheumatic Diseases Centre


classification criteria. The 2010 criteria does not include presence of rheumatoid nodules or radiographic erosive changes, both of which are less likely in early RA. Symmetric arthritis is also not required in the 2010 criteria, allowing for early asymmetric presentation.

Nonsteroidal anti-inflammatory drugs are used to help reduce arthritis pain and inflammation while disease-modifying antirheumatic drugs (DMARDs) work to modify the course of the disease. Traditional DMARDs include methotrexate, hydroxycholorquine, sulfasalazine, leflunomide, cyclophos-phamide and azathioprine.

The introduction of biologics has rev-olutionized RA treatment. Their success has underlined the key roles of inflam-matory cytokines in the pathogenesis of inflammatory arthritis, particularly tumor necrosis factor-α and interleukin 1 and 6 as well as T cells and B cells. They act more quickly and effectively than conventional DMARDs. Certolizumab, etanercept, adalimumab, infliximab, and golimumab block tumor necrosis factor-alpha. Abatacept blocks the activation of T cells while rituximab blocks B cells. Tocilizumab blocks interleukin-6. A new class of biologics act on JAK pathways. Tofacitinib belongs to this class which can be taken orally.

A substantial and growing research shows that RA outcomes are improved by adopting management strategies in which patients are treated to achieve predefined targets. There is also growing recognition that the most appropriate target is remission. There is evidence that patients with RA who achieve sus-tained remission have less disability, less erosive joint damage, and a better quality of life.

Psoriatic arthritisPsoriatic arthritis (PsA) is a chronic inflam-matory disease which, if left untreated, can result in joint damage,1 disability and increased cardiovascular comorbidity and mortality.2 Approximately 60% of

PsA patients in Hong Kong present with psoriasis before the joint symptoms in PsA.3 Up to 30% of patients with psoriasis will develop PsA. Recognition of signs of PsA, including arthritis, nail dystrophies, dactylitis and enthesitis, is crucial for early diagnosis of PsA.

Dactylitis, or sausage digit, is recognised by the asymmetry of digit size compared with the contralateral side and loss of contour of digit. Swelling and inflammation lies in the subcu-taneous soft tissue, tendon and ligament. Enthesitis is another important feature which is thought to be the primary lesion that underscores diverse skeletal manifestations of PsA.4 Recent studies revealed that the nail bed, finger tendon, enthesis and periosteum of distal phalanx are closely connected anatomically by lamina and connective tissue fiber.5

Early diagnosisEarly diagnosis of PsA is essential for early treatment, which has been shown to reduce inflammation and the potential for comorbidities, prevent further damage and preserve function.6 The CIASsification criteria for Psoriatic ARthritis (CASPAR) are currently used for classification of PsA.7 PsA is diagnosed if there is inflammatory articular disease either in the joint, spine or entheses together with 3 or more points of the fol-lowing:1. Current psoriasis (scores 2 points)2. Personal history of psoriasis (if current

psoriasis is absent)3. Family history of psoriasis (if personal

history of psoriasis or current psoriasis absent)

4. Psoriatic nail dystrophy5. A negative test for rheumatoid factor6. Current dactylitis7. History of dactylitis (if current dactylitis

is absent)8. Radiological evidence of juxta-articular

new bone formation9. These criteria have been validated in

early PsA8 as well as in a Chinese PsA cohort.

New treatmentSynthetic disease-modifying anti-rheumatic drugs (DMARDs) have been used with some success in PsA patients.11-13 The clinical efficacy of biologic therapy, like tumour necrosis factor (TNF) inhibitors in treatment of PsA has been demonstrated.14-16 New treatment include apremilast, a small molecule that specifically inhibits phosphodiesterase 4, and ustekinumab, mAb directed against the p40 subunit of IL-12 and IL-23. The treatment target for PsA is Minimal Disease Activity (MDA), which aims at less than one active joint disease and enthesitis point, minimal psoriasis skin score, low score for patient global assessment and preserved physical function.17-18 Studies have shown that 96% of subjects who achieved MDA at 1 year had no radiographic progression of disease.19 The treat-to-target approach (or tight control approach) targeting MDA in early PsA has shown better 1-year joint and skin outcomes compared to standard treatment approach.19

ConclusionsEarly diagnosis and recognition of the various manifestations enable early treatment. With effective treatment for skin and joint manifestations, strategic and target-orientated approach which aimed at low disease activity, is recom-mended.

References1. Gottlieb A, et al. J Am Acad Derma& 2008;58,851-864. 2. lamnitski A, et al. Ann Rheum Dis 2013,72:211-216. 3. Leung YY, et al. Hong Kong J Dermatol Venereal 2007;15:62-67.4. McGonagle D, et al. Arthritis Rheum 2003;48:896-905.5. McGonagle D, et al. Dermatology 2009;218:97-102.6. American College of Rheumatology Psorlatic Arthritis. 2012. 7. Taylor W, at al. Arthritis Rheum 2006;54:2665-2671 8. Coates LC, et al. Arthritis Rheum 2012;64:3150-3155. 9. Leung YY, or at Rheumatology (Oxford) 2010;49:112-11510. Coates LC, et al. BO Dermatof 2013;168:802-807. 11. Scarpa R, et al. CIO Rheumatol 2008;27:823-B26. 12. Kingsley CH, et at Rheumatology (Oxford) 2012;01:1368-1377. 13. Kaltwasser JP, et al. Arthritis Rheum 2004;50:1939-1950. 14. Gladman DO, et at Arthritis Rheum 2007;56:476-488.15. Cladman DD, et al. Ann Rheum Dis 2007;66163¬168. 16. Antoni CE, et al. Arthritis Rheum 2005;521227-1236. 17. Ritchlin CT, et at Ann Rheum Dis 2009,68:1387-1394. 18. Cossec L, et al. Ann Rheum Dis 2012;7E4-12.19. Coates LC and Helliwell PS. Arthritis Care Res (Hoboken) 2010;62:965-969.


Lymphoma is among the top 10 most common cancers in Hong Kong. Up to 900 new cases are diagnosed

every year. Since it is a systemic disease,

the role for local surgery and irradiation is limited and combination chemotherapy has been the mainstay of therapy since the 1980s. Challenges in treatment include refractory and relapsing cases, as well as treatment toxicity and intolerance. This changed drastically in 1997 with the introduction of B-cell targeted antibody (anti-CD20, rituximab) therapy, which had minimal toxicity and increased cure rate by 30%. The current cure rate of limited stage Hodgkin lymphoma (HL) and non-Hodgkin B-cell lymphomas (NHL) are well above 90%. A recent avalanche of new agents promises further improved survival and reduced toxicity. This is

especially true for relapsing and elderly patients. Some agents are so effective that chemotherapy may no longer be needed. This talk will cover:1. New antibodies and new indications:

eg, alemtuzumab and rituximab main-tenance therapy

2. New chemotherapy-linked antibodies: brentuximab vedotin (anti-CD30 - auristatin)

3. New antibodies against HL/NHL immune-escape: Pembrolizumab

4. New oral B-cell lymphoma enzyme inhibitors: Idelalisib and ibrutinib

5. New use of immuno-modulating agents: Lenalidomide and pomalidomide.

Lymphoma: New Age, New Drugs, New Survival

Dr Au Wing Yan ( )MBBS (HK), MD, MRCP (UK), FHKCP, FHKAM (Medicine), FRCP(Edinburgh)

THE SOCIETY OF PHYSICIANS OF HONG KONG CALL FOR MEMBERS JAN - DEC 2016

MEMBERS Specialists in good standing in private practice in a non-surgical specialty. The fee is $100 per annum. Please send a one page CV to the Secretariat.

MEMBERS (non-voting) Specialist in good standing in a non-surgical specialty in University or Government service. The fee is $100 per annum. Please send a one page CV to the Secretariat. Members (non-voting) enjoy the same privileges as full members except that they may not vote in General Meetings, and they should not hold office as one of the five Executive Committee Members. They are welcome to take an active part in the work of the Journal, and in orga-nizing CME meetings or giving lectures in our CME programme.

ASSOCIATE MEMBERS Registered medical doctors in good standing. The fee is $300 per annum. Please submit application form with your cheque. You may request for an application form from the Secretariat (Tel: 2526 2626) or download a form from the web (see icon Associate members). All Members, Non-voting Members and Associate Members may participate in our CME programmes free of charge or at a nominal fee, receive our Journal and use the website.

Cheques should be paid to: The Society of Physicians of Hong Kong Co Ltd

Please mail to: Room 1907, Lane Crawford House, 70 Queen’s Road Central, Hong Kong.

All applications are subject to the admission procedures of the Society. Unsuccessful applications will be refunded.

Please visit our website: www.SOPHYSICIANSHK.org

Lam Tat Chung Paul ( ) President FRCP, FRCPsych, FHKAM (Medicine), FHKAM (Psychiatry)

JSPHK Abstract book 2015 issue

Page 79 – Role of Probucol in the Current Treatment of Atherosclerosis and Vascular Disease

Professor Brian Tomlinson (湯寧信教授)

References:

1. Yamamoto, S, H Tanigawa, X Li, et al. Pharmacologic suppression of hepatic ATP-binding cassette transporter

1 activity in mice reduces high-density lipoprotein cholesterol levels but promotes reverse cholesterol

transport. Circulation. 124(12) 2011; 1382-90

2. Walldius, G, U Erikson, AG Olsson, et al. The effect of probucol on femoral atherosclerosis: the Probucol

Quantitative Regression Swedish Trial (PQRST). Am J Cardiol. 74(9) 1994; 875-83

3. Keyamura, Y, C Nagano, M Kohashi, et al. Add-on effect of probucol in atherosclerotic, cholesterol-fed rabbits

treated with atorvastatin. PLoS One. 9(5) 2014; e96929

4. Liu, J, M Li, H Lu, et al. Effects of probucol on restenosis after percutaneous coronary intervention: a

systematic review and meta-analysis. PLoS One. 10(4) 2015; e0124021

5. Sawayama, Y, C Shimizu, N Maeda, et al. Effects of probucol and pravastatin on common carotid

atherosclerosis in patients with asymptomatic hypercholesterolemia. Fukuoka Atherosclerosis Trial (FAST). J

Am Coll Cardiol. 39(4) 2002; 610-6

6. Yamashita, S, H Hbujo, H Arai, et al. Long-term probucol treatment prevents secondary cardiovascular events:

a cohort study of patients with heterozygous familial hypercholesterolemia in Japan. J Atheroscler Thromb.

15(6) 2008; 292-303

7. Yamashita, S, D Masuda, and Y Matsuzawa. Did we abandon probucol too soon? Curr Opin Lipidol. 26(4) 2015;

304-16

香港內科學會 the society of physicians of …november 2015 journal of the society of...

Documents