Spotlight Cardiology This month December 2007

December 2007
This month
n Spotlight
Resistant depression: pharmacological treatment and maintenance
n Cardiology
A 45-year-old man with a large waist circumference
n Dermatology
Nail with dusky red lines
A 20-month-old male brought for evaluation after his parents observed a ‘shaking fit’
n Infectious
A 22-year-old female complaining of burning with urination
HKMA CME Bulletin 持續醫學進修專訊
Spotlight: Resistant depression: pharmacological treatment and maintenance 5
Cardiology: A 45-year-old man with a large waist circumference
Dermatology: Nail with dusky red lines
CNS Medicine: A 20-month-old male brought for evaluation after his parents
observed a ‘shaking fit’
Infectious Disease: A 22-year-old female complaining of burning with urination 14
Answer Sheet 18
International Calendar 22
CME Calendar 23
The Hong Kong Medical Association is dedicated to providing a coordinated CME programme for all members of the medical profession.
Under the HKMA CME Programme, a CME registration process has been created to document the CME efforts of doctors and to provide
special CME avenues. The Association strives to foster a vibrant environment of CME throughout the medical profession. Both members
as well as non-members of the Association are welcome to join us. You may contact the HKMA Secretariat for details of the programme.
HKMA CME Bulletin – MONTHLY SELF-STUDY SERIES to help you grow!
Please read the following articles and answer the questions. Participants in the HKMA CME Programme will be awarded credit points
under the Programme for returning the completed answer sheet via fax (28650943) or by mail to the HKMA Secretariat on or before 15
January 2008. Answers to questions will be provided in the next issue of the HKMA CME Bulletin. (Questions may also be answered online at
請細閱本期文章,並利用答題紙完成自我評估測驗,於 2008 年 1 月 15 日前,將已填妥之答題紙傳真(號碼:2865 0943 )或寄回本會秘書處,
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org 完成自我評估測驗。)
Elsevier (Singapore) Pte. Ltd
Michelle Wong | Tel: 2965 1300
Email: [email protected]
HKMA December 2007
CME Bulletin & Online
Editorial Board
It has been a few months since the launch
of our new CME Bulletin and CME Online.
With our new layout and interface and
restructuring of the contents, the areas
covered are increasing and in general the
bulletin is well received by our members.
Chief Editor 總編輯:
Dr. WONG Bun Lap, Bernard 黃品立醫生
Board Members 委員會成員:
While most of our colleagues are dealing
with organic or structural diseases, psychiatric
or mental illnesses have become much more
prevalent than in the past. Among them, anxiety states and depression
are two common entities that most family physicians encounter. In this
issue, we shall study in depth the cognitive vulnerability to depression
and its pharmacological treatment. Epilepsy, although not a mental illness
by itself, is also a serious problem that affects the central nervous system.
Patients with epilepsy, due to its associated disability and social stigmata and
inconvenience, are often depressive. Two articles on depression are available
in this issue. On the other hand, metabolic syndrome is also a commonly
encountered problem in modern society. This month’s cardiology section
looks into this important topic. Finally, we also look at some aspects of
sexually transmitted diseases.
We hope that with time, more and more members will find our bulletin
an indispensable companion to their lifelong professional career.
Dr. LI Siu Lung, Steven
Co-chairman, CME Committee
Dr. CHAN Man Kam
Dr. CHAN Yee Shing, Alvin
Dr. CHENG Chi Man
Dr. CHEUNG Hon Ming
Dr. CHU Kin Wah
Dr. CHIU Shing Ping, James
Dr. CHOI Kin, Gabriel
蔡 堅醫生
Dr. CHOW Pak Chin
Dr. FONG Chung Yan, Gardian
Dr. FUNG Yee Leung, Wilson
Dr. HO Chung Ping, MH
Dr. HO Hung Kwong, Duncan
Dr. KONG Kam Fu, James
Dr. KWOK Ka Ki
Dr. LAM Tzit Yuen, David
Dr. LEUNG Chi Chiu
Dr. LI Siu Lung, Steven
Dr. LI Sum Wo, MH
Dr. POON Tak Lun
Dr. SHIH Tai Cho, Louis
Dr. TSE Hung Hing
Dr. WONG Shou Pang, Alexander 王壽鵬醫生
Dr. YEUNG Chiu Fat, Henry
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© Elsevier (Singapore) Pte Ltd. 2007
ISSN: 1793-5393
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HKMA December 2007
Resistant depression: pharmacological
treatment and maintenance
Complete this course
and earn
Dr. LAM Tat Chung, Paul
FRCP, FHKAM(Medicine), FHKAM(Psychiatry)
Private Specialist; Hon. Clinical Assistant Professor, HKU
Email: [email protected]
Unipolar major depressive disorder is a common
illness. For men, the lifetime risk is 12% and for women,
21%. In the Global Burden of Disease Study [1, 2],
unipolar depression was the fourth leading cause of
temporary and permanent disability in 1990; for the
year 2020, it is projected to be second only to ischaemic
heart disease as a cause of illness burden worldwide.
Depression can also increase the morbidity of physical
illness. Among middle-aged women, the presence of
depression increases the adjusted risk of dying from heart
disease by 50%.
Pharmacological treatment of depression has
advanced over recent years. Nowadays it is a relatively
simple matter for internists and family doctors to initiate
treatment with medications that are fairly effective and
quite safe. This may bring about 50% of patients into
remission. However, the remaining patients will need
further measures for treatment to be effective. It is for this
latter group of patients that there is a serious shortage of
evidence-based information or consensus about the best
way to proceed. Often, one has to depend on evidence
from small, open trial series, anecdotal reports, personal
experience, etc. Many more high-quality studies need to
be done to address this very important issue. The recent
STAR*D trials (Sequenced Treatment Alternatives to
Relieve Depression) conducted under the US National
Institute of Mental Health have contributed to our
further understanding of the condition. It is important in
that over 4,000 patients were involved and double-blind
methods were adopted [3].
When faced with a case of difficult-to-treat depression,
the doctor must first review the following issues:
1. Diagnosis
Bipolar depression requires different treatment
strategies. Psychotic depression should be identified
and appropriately treated. One could be dealing
with a case of schizophrenia, personality disorder or
adjustment disorder.
2. Psychiatric co-morbidity
Dr ug addiction or alcoholism are frequent
aggravating or perpetuating factors. Anxiety disorder
or obsessive compulsive disorder may be conditions
that interfere with treatment results.
3. Medical co-morbidity, e.g. thyroid or other
endocrine disorders, occult cancers, neurodegenerative disorders, systemic lupus erythematosus, etc.
4. Effect of other medications, e.g. interferon, steroids.
5. Adequacy of dose of antidepressants and compliance
with medication.
Having reviewed and dealt with the above, the doctor
can proceed with alternative pharmacological strategies
to deal with the non-responsive patient.
A. Increase the dose of medication
If the initial medication has produced a weak response,
e.g. 25% symptom reduction after 4 weeks and the
drug is well tolerated, it is often useful to raise the
dose, initially to twice the standard dose and then
perhaps to three times for a selective serotonin reuptake
inhibitor (SSRI). In one study by Fava et al [4], raising
the dose of fluoxetine (Prozac) was more effective
than adding lithium or desipramine. However, dose
increase may be less well tolerated and more risky
for tricyclic antidepressants (TCAs), and a smaller
magnitude of increment at a slower pace and with close
observation of side effects is required. Dose increase is of
particular interest in the case of venlafaxine, a serotonin
norepinephrine reuptake inhibitor (SNRI). Venlafaxine
has been shown to have greater efficacy than SSRIs at
doses of 150 mg and above [5, 6]. Remission rates in
patients with major depressive disorder were significantly
higher with venlafaxine than with SSRIs [7], and are
dose-related [8]. Venlafaxine XL in doses up to 450–
600 mg daily has been used to treat very resistant cases
of depression with good efficacy and tolerability [9].
Raising the dose has the advantage that we will
HKMA December 2007
Definitions of Remission and
Response to Treatment
(with remission)
Partial Response
Fava M and Davidson KG, Psychiatr Clin North Am. 1996; 19(2): 179–200
% Reduction of symptoms is measured by standard rating scales
already have learned the side effects of a particular drug
on a particular patient, and avoids the introduction of
a new drug with new side effects. The problem of drugdrug interaction in polypharmacy is also avoided.
B. Switch to another antidepressant of the same class
Drugs within the same class have different properties. So,
it is possible to use a second drug of the same class when
patients respond poorly to the first drug. A response
rate of up to 50% may be possible. In the STAR*D
trial mentioned above, patients who do not respond to
citalopram (Cipram) have a 26.6% chance of responding
to sertraline (Zoloft). The advantage of this strategy
is that the side effects of the second drug are more
predictable, and no wash-out period for the first drug
is required. The first drug can be abruptly discontinued
and the second drug started on full dose. However, it
is generally felt that switching to a different class of
antidepressant will yield better overall results.
C. Switch to another antidepressant of a different class
This strategy benefits about 50% of non-responders to
the first medication. There are theoretical advantages in
that a different neurotransmitter system is tackled, or dual
mechanisms are involved, as in the case of SNRIs. Several
studies support switching from an SSRI to venlafaxine
[10-14], with response rates of up to 70%. Cases of
severe, melancholic depression are more responsive to
venlafaxine. Mirtazapine, monoamine oxidase inhibitors
(MAOIs), tricyclics and bupropion are other alternatives.
In switching to a different class of antidepressants, it
is necessary to taper the first drug gradually, say over 2
weeks, and to increase the dose of the new drug slowly,
paying particular attention to drug–drug interaction. In
cases involving MAOIs, it is necessary to have a wash-out
period of 2 weeks before the new drug is started. SSRIs
can be switched to venlafaxine immediately.
MAOIs are currently not available in Hong Kong.
An alternative may be to use a reversible inhibitor of
monoamine oxidase A (RIMA, e.g. moclobemide),
for which no dietary restriction is required. A new
transdermal form of selegiline, a MAO-B inhibitor, has
been successfully developed as an effective antidepressant
for use in the US.
D. Combination of antidepressants
Fluoxetine plus desipramine, a TCA with noradrenaline reuptake inhibition properties, was found
to be superior to either drug alone [15, 16].
Most SSRI drugs, with the exception of
citalopram and escitalopram, inhibit cytochrome
P450 liver enzymes and decrease the degradation
of TCAs. Hence the dose of TCAs needs to be
carefully monitored, perhaps employing 50% of
the standard dose to avoid dangerous side effects,
e.g. cardiotoxicity.
2) SSRI + norepinephrine reuptake inhibitors (NRIs)
SSRI plus reboxetine has shown some efficacy;
however, another NRI, atomoxetine (Strattera),
was not effective in a large double-blind trial
3) SSRI + trazodone (Trittico) or nefezodone (Serzone)
The two latter drugs are 5HT2 receptor blockers,
thus an alternative pathway is invoked. The
combination is effective in small open trials. However, nefezodone has fallen out of favour due to
4) Other combinations
In the STAR*D Trial, bupropion added to
citalopram resulted in a 29.7% remission in patients
Common Terms
Acute phase — start of treatment until remission (3–6 months)
Continuation phase — continuation of medication when patient is in the early stage of remission (about 6 months)
Maintenance phase — further continuation of medication for high-risk cases (indefinite)
Response :50–75% reduction of symptoms
Remission :More than 75% reduction of symptoms, near full recovery of functional capacity
Relapse :Deterioration after initial response
Recurrence:Onset of new episode after full recovery
HKMA December 2007
non-responsive to citalopram. Bupropion acts via
the noradrenergic and dopaminergic systems and
thus theoretically may have an advantage when
added to an SSRI.
SSRI + mianserin (Tolvon) or mirtazapine
(Remeron) has the theoretical advantage of
utilizing two classes of drugs with different
mechanisms of action. Mianserin and mirtazapine
are presynaptic alpha-2 noradrenergic blockers.
The combination was found to be effective in
three double-blind studies [17-19]. In the study
by Carpenter et al, mirtazapine added to an SSRI
was shown to increase the response rate from
20% (placebo) to 65% in SSRI non-responsive
Mirtazapine + venlafaxine was given to a group
of highly resistant patients in the 4th level of the
STAR*D Trial, i.e. patients who had not responded
adequately to treatment in three prior prospective
medication trials. The remission rate was 13.7%,
which was not statistically different from 6.9% for
monotherapy with tranylcypromine, a MAOI.
E. Augmentation
This strategy refers to adding a drug that is not an
1) Lithium augmentation has been used for over 40
years. It was found to be highly effective in older
studies. However, more recent studies have been rather
disappointing [20-22]. The reason might be that older
studies done in 1970–1990 did not exclude cases of
bipolar depression, which respond better to lithium
treatment. In the STAR*D Trial, which recruited only
patients with unipolar depression, patients who failed
to respond to two levels of treatment were randomized
to receive lithium or T3 augmentation. The remission
rate was 15.9% for lithium versus 24.7% for T3.
Overall clinical experience shows that about 20% of
patients are intolerant to the side effects of lithium,
which include polyuria, polydipsia and tremor. Blood
level has to be monitored to a target lithium level of
0.8–1 mmol/L.
2) Thyroid augmentation of TCAs offers better
evidence than it does with the newer antidepressants.
T3 in doses of 25–50 µg daily is preferred to T4,
but T4 has also been found to be effective in some
studies [23]. Super-physiological doses (400–
500 µg/day) of T4 have been used in an open study
to treat patients who are severely resistant to therapy.
The antidepressant effect was excellent with 50% of
patients responding well. Tolerance was good [24].
3) Buspirone augmentation of SSRIs
Buspirone is a 5HT1A partial agonist. There are
two placebo-controlled studies which showed effects
similar to placebo, but in one of the studies it was
effective for patients with severe depression [25, 26].
In the STAR*D trial, the remission rate for buspirone
augmentation (10–30 mg bd) for patients failing to
respond to citalopram was 30%.
4) Pindolol is a β-blocker and a 5HT1A antagonist.
It is used at 2.5 mg tds. Clinically it is observed to
accelerate response to SSRIs. However, in controlled
trials it was shown to be ineffective in the treatment
of resistant depression.
5) Dopaminergic agonist augmentation
Pergolide 0.25–2 mg/day, amantadine 100–200
mg bid, pramipexol 0.125–1 mg tid, and ropinirole
0.5–1.75 mg tid have been found to be useful in some
patients, supported by open trials.
6) Stimulants
Methylphenidate (Ritalin), dextroamphetamine
(Dexedrine) and modafinil (Provigil) were effective
in some open trials. These drugs have a rapid onset
of action, but the therapeutic effect may be transient.
They also have the problem of increasing anxiety and
irritability, and the risk of abuse.
7) Atypical antipsychotics are supported by small
open trials. Olanzapine, risperidone, aripiprazole,
ziprasidone and quetiapine have been used. They
are particularly useful for patients with agitation and
psychotic depression [27].
8) Anticonvulsants
Lamotrigine, gabapentin, carbamazepine, valproate
and topiramate have been tried with variable success,
but are not supported by good controlled trials.
9) Benzodiazepines
Lormetazepam (Loramet) has been shown to
augment TCAs [28] and clonazapam (Rivotril)
augments fluoxetine [29]. They have the added
advantage of controlling anxiety symptoms.
10)Health foods
Eicosapentaenoic acid (EPA) at a dose of 1 g (not 2 g or
3 g) daily has been found to be effective in augmentation.
Methylfolate and S-adenosyl methionine (SAMe) are
methyl donors that promote neurotransmitter synthesis.
They are effective for augmentation of SSRIs in small
open trials. Double-blind controlled trials are underway.
HKMA December 2007
Other treatment methods such as psychotherapy,
electroconvulsive therapy, repetitive transcranial
magnetic stimulation, vagus nerve stimulation, and deep
brain stimulation are outside the scope of discussion of
this paper.
Maintenance treatment
Major depressive disorder is a recurrent illness. There
is a 85% risk of recurrence within 15 years following
recovery from an index episode. Among patients who
have remained well for 5 years, the risk of recurrence is
58% [30]. The risk of recurrence increases over time and
with each subsequent episode [31]. As the number of
recurrences increases, depressive episodes tend to become
more frequent, last longer, and symptoms become more
resistant and severe [32]. The length of time before
treatment and the severity of residual symptoms are
proportional to the likelihood of recurrence [33]. Thus,
vigorous treatment to full remission and continued
treatment to prevent relapse and recurrence are important
targets in the management of major depressive disorder.
It has been recognized that antidepressants that
are effective in the acute treatment phase should
be continued on full dose in the continuation and
maintenance phase to prevent relapse and recurrence.
Patients who continued to take active antidepressant
therapy had less than half of the risk (18% vs 41%) of
patients switched to placebo [34]. The continuation
phase should last for 6 months to 1 year [35]. Patients
at higher risk should receive maintenance treatment.
This include patients with very severe episodes, suicidal
history, multiple and prolonged episodes, strong family
history and patients with resistant or residual symptoms.
However, the ideal period of maintenance treatment is
ill-defined. One retrospective study examined the rates
of relapse/recurrence during maintenance therapy and
found that, in slightly over 2 years, the breakthrough
episodes for venlafaxine and TCAs were 3.7% compared
to 14.1% for SSRIs [36].
High-quality maintenance studies extending for
more than 1 year on SSRIs and newer antidepressants
are scarce. The Prevention of Recurrent Episodes of
Depression with Venlafaxine for Two years (PREVENT)
study was published in August 2007 [37]. In this study,
1,096 outpatients with unipolar major depressive
disorder were recruited. Patients who entered the trial
had at least three episodes of major depression, two of
which had occurred in the previous 5 years. Responders
to venlafaxine at week 10 entered a continuation phase
for 6 months, after which responders were randomized
to receive venlafaxine or placebo for two 12-month
periods. Results of the 2-year maintenance study showed
the cumulative probability of preventing a relapse was
HKMA December 2007
72% for the venlafaxine treatment group and 53%
for the placebo group. Put in another way, three of
four patients on treatment remained well compared
with only half of the patients remaining well in the
placebo group. This is the only large scale double-blind
placebo controlled study to date of an SSRI or newer
antidepressant spanning 2 years that yielded a positive
result, and is an important contribution to our current
state of knowledge in the area.
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the Contribution of Risk Factors: Global Burden of Disease
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2. Idem. Alternative Projection of Mortality and Disability by
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3. Ruyh AJ, et al. Depression IV: STAR*D Treatment Trial for
Depression. Am J Psychiatry 2003;160-237.
4. Fava M, et al. Lithium and Tricyclic Augmentation of
Fluoxetine Treatment for Resistant Major Depression: A
Double-blind, Controlled Study. Am J Psychiatry 1994;
5. E i n a r s o n , e t a l . C o m p a r i s o n o f E x t e n d e d - re l e a s e
Venlafaxine, Selective Serotonin Reuptake Inhibitors, and
Tricyclic Antidepressants in the Treatment of Depression:
A Meta-analysis of Randomized Controlled Trials. Clin Ther
6. Smith D, et al. Efficacy and Tolerability of Venlafaxine
Compared with Selective Serotonin Reuptake Inhibitors
and Other Antidepressants: A Meta-analysis. Br J Psychiatry
7. Thase ME, et al. Remission Rates During Treatment with
Venlafaxine or Selective Serotonin Reuptake Inhibitors. Br J
Psychiatry 2001;178:234-41.
8. Rudolph RL. Achieving Remission from Depression
with Velafaxine and Venlafaxine Extended Release: A
Literature Review of Comparative Studies with Selective
Serotonin Reuptake Inhibitors. Acta Psychiatr Scand Suppl
9. Mbaya P. Safety and Efficacy of High Dose of Venlafaxine
X L i n t re a t m e n t re s i s t a n t m a j o r d e p re s s i o n . H u m
Psychopharmacol 2002;17(7):335-9.
10. Nierenberg AA, et al. Venlafaxine for Treatment-resistant
Unipolar Depression. J Clin Psychopharmacol 1994;14:
11. De Montigny C, et al. Venlafaxine in Treatment-resistant
Major Depression: A Canadian Multicenter, Open-label Trial.
J Clin Psychopharmacol 1999;19:401-6.
12. Mitchell PB, et al. Efficacy of Venlafaxine and Predictors
of Response in a Prospective Open-label Study of
Patients with Treatment-resistant Major Depression. J Clin
Psychopharmacol 2000;20(4): 483-7.
13.Saiz-Ruiz J, et al. Efficacy of Venlafaxine in Major Depression
Resistant to Selective Serotonin Reuptake Inhibitors. Prog
Neuropsychopharmacol Biol Psychiatry 2002:26(6):1129-34.
14.Poirier MF, Boyer P. Venlafaxine and Paroxetine in
Treatment-resistant Depression: Double-blind, Randomized
Comparison. Br J Psychiatry 1999;175:12-6.
15.Nelson JC, et al. A Preliminary, Open Study of the
Combination of Fluoxentine and Desipramine for Rapid
Treatment of Major Depression. Arch Gen Psychiatry
16.N e l s o n J C , e t a l . C o m b i n i n g N o re p i n e p h r i n e a n d
Serotonin Reuptake Inhibition Mechanisms for Treatment
of Depression: A Double-blind, Randomized Study. Biol
Psychiatry 2004;55:296-300.
17.Maes M, et al. Pindolol and Mianserin Augment the
Antidepressant Activity of Fluoxetin in Hospitalized Major
Depressed Patients, Including Those with Treatment
Resistance. J Clin Psychopharmacol 1999;19:177-82.
18.Ferreri M, et al. Benefits from Mianserin Augmentation of
Fluoxetin in Patients with Major Depression Non-responders
to Fluoxetin Alone. Acta Psychiatr Scand 2001;103:66-72.
19.Carpenter LL, et al. A Double-blind, Placebo-contolled
Study of Antidepressant Augmentation with Mirtazapine.
Biol Psychiatry 2002;51(2):183-8.
20.Nierenberg AA, et al. Lithium Augmentation of Nortriptyline
for Subjects Resistant to Multiple Antidepressants. J Clin
Psychopharmacol 2003;23(1):92-5.
21.Fava M, et al. Double-blind Study of High-dose Fluoxetine
Versus Lithium or Desipramine Augmentation of Fluoxetine
in Partial Responders and Nonresponders to Fluoxetine. J
Clin Psychopharmacol 2002;22(4):379-87.
22.Januel D, et al. Multicenter Double-blind Randomized
Parallel-group Clinical Trial of Efficacy of the Combination
Clomipramine(150 mg/day) Plus Lithium Carbonate (750
mg/day) Versus Clomipramine (150 mg/day) Plus Placebo in
the Treatment of Unipolar Major Depression. J Affect Disord
23.Lojko D, et al. L-thyroxine Augmentation of Serotonergic
Anti-depressants in female patients with refractory
depression. J Affect Disord 2007.
24.Bauer M, et al. Treatment of Refractory Depression
with High Dose Thyroxin. Neuropsychopharmacology
25.Lauden M, et al. A Randomized, Double-blind, Placebocontrolled Trial of Buspirone in Combination with an SSRI
in Patients with Treatment-refractory Depression. J Clin
Psychiatry 1998;59(12):664-8.
26.Appelberg BG, et al. Patients with Severe Depression May
Benefit from Buspirone Augmentation of Selective Serotonin
Reuptake Inhibitors: Results From a Placebo-controlled,
Randomized, Double-blind, Placebo Wash-in Study. J Clin
Psychiatry 2001;62(6):448-52.
27.Shelton RC, et al. A Novel Augmentation Strategy for
Treating Resistant Major Depression. Am J Psychiatry
28.Nolen WA, et al. Hypnotics as Concurrent Medication in
Depression. A Placebo-controlled, Double-blind Comparison
of Flunitrazepam and Lormetazepam in Patients with Major
Depression, Treated with a (Tri)cyclic Antidepressant. J
Affect Disord 1993; 28(3):179-88.
29.Smith WT, et al. Short-term Augmentation of Fluoxetine
with Clonazepam in the Treatment of Depression: A Doubleblind Study. Am J Psychiatry 1998;155(10):1339-45.
30.Muller TI, et al. Recurrence After Recovery From Major
Depressive Disorder During 15 Years of Observational
Follow-up. Am J Psychiatry 1999;156:1000-6.
31.Solomon DA, et al. Multiple Recurrences of Major
Depressive Disorder. Am J Psychiatry 2000;157:229-33.
32.Greden JF. Physical Symptoms of Depression: Unmet Needs.
J Clin Psychiatry 2003;64(suppl 7):5-11.
33.Judd LL, et al. Does incomplete recovery from first lifetime
major depressive episode herald a chronic course of illness?
Am J Psychiatry 2000;157:1501-4.
34.Geldes JR, et al. Relapse Prevention with Anti-depressant
Drug Treatment in Depressive Disorder: A Systematic
Review. Lancet 2003;361:653-61.
35.Practice Guideline for the Treatment of Patients with
Major Depressive Disorder (Revision) American Psychiatric
Association. Am J Psychiatry 2000;157:4 April Supplement.
36.Shelton C, et al. Venlafaxine XR Demonstrates Higher Rates
of Sustained Remission Compared to Fluoxetine, Paroxetine
or Placebo. Int Clin Psychopharmacol 2005;20:233-8.
37.Keller MB, et al. The Prevention of Recurrent Episodes of
Depression with Venlafaxine for Two Years (Prevent) Study:
Outcomes from the 2-Year and Combined Maintenance
Phases. J Clin Psychiatry 2007;68:1246-56.
Further Reading
Thase ME. Preventing Relapse and Recurrence of
Depression: A Brief Review of Therapeutic Options.
CNS Spectr 2006;11:12 (Suppl 15); December.
Answer these on page 18 or
make an online submission at:
Please indicate whether the following questions are true or false
1. Drug abuse including alcoholism is a common cause of
treatment resistance in depression.
8. In the maintenance phase, the same dose of
antidepressants should be used as in the acute phase.
2. High-dose venlafaxine is effective for the treatment of
resistant depression.
9. In the PREVENT study, patients had at least three
episodes of depression.
3. Most SSRIs raise the blood levels of TCAs, hence the
dose of TCA has to be reduced when the combination
is used.
10.Venlafaxine in a 2-year maintenance study was shown
to be effective in the prevention of relapse in patients
with major depressive disorder.
4. Transdermal selegiline is an effective antidepressant.
5. The evidence is better with T3 augmentation of TCAs
than of SSRIs.
6. DHA at a dose of 1 g daily is useful for augmentation
treatment of depression.
7. Major depressive disorder is a recurrent illness with
high relapse rate.
Clinical management of type 2 diabetes
1. True
2. True 3. True
4. True
5. True
6. False 7. True 8. False 9. False 10. True
HKMA December 2007
A 45-year-old man with a large waist
A 45-year-old man went for a routine health check.
His body mass index (BMI) was 32 and his waist
circumference was 110 cm. His blood pressure was
142/93 mmHg. His fasting glucose level, triglyceride
level, HDL cholesterol and LDL cholesterol levels
were 8 mmol/L, 12.8 mmol/L, 0.8 mmol/L and 4.2
mmol/L, respectively.
The content of the Office Cardiology Series is provided by:
Dr. LI Siu Lung, Steven
F.H.K.A.M. (Med), F.R.C.P. (Glasg), F.R.C.P. (Edin), F.R.C.P. (Lond), Specialist in Cardiology
Dr. WONG Shou Pang, Alexander
F.R.C.P., F.H.K.A.M.(Med.), F.H.K.C.P., Specialist in Cardiology
Answer these on page 18 or
make an online submission at:
Please answer TRUE or FALSE
1. His metabolic profile is abnormal.
2. He has metabolic syndrome.
3. He needs dietary therapy and, failing that, drug
therapy to control his metabolic derangements.
4. He is at risk of pancreatitis.
November ANSWERS
A 38-year-old man presented with a few days’ history of
increasing shortness of breath and chest discomfort on
exertion. He has diabetes newly diagnosed this year and was
on metformin 500 mg bd. Physical examination revealed no
evidence of heart failure but the oxygen saturation was only
90% in room air. There was no pitting oedema but the left
lower limb was mildly swollen. Chest X-ray showed normal
heart size with clear lung fields. Electrocardiography (ECG)
showed mild T inversion lead III. Troponin-I was elevated
to 0.23 ng/ml. Echocardiogram was done, which showed
normal left ventricular size and function with no regional
wall motion abnormalities. However, the right ventricle was
dilated with moderate tricuspid regurgitation and pulmonary
1. What is your diagnosis?
2. What would be your next investigation?
3. What would be the treatment of choice if your diagnosis is confirmed?
4. What long-term treatment would he need?
1. The likely diagnosis is pulmonary embolism due to deep vein thrombosis (DVT) of his
left lower limb.
2. The next investigation should be computed tomography (CT) of the thorax with contrast,
followed by a Doppler study of his left lower limb. In this patient, thoracic CT confirmed
massive bilateral pulmonary embolism. Doppler study showed deep vein thrombosis of
the left popliteal vein. In patients presenting with shortness of breath, hypoxemia and
lower limb swelling, DVT with pulmonary embolism is the first diagnosis to be ruled out.
Sometimes in mild-to-moderate pulmonary embolism, a transthoracic echocardiogram
may not show any specific sign; thus, thoracic CT remains a more sensitive investigation
for this purpose.
3. In general, anticoagulation with intravenous (IV) heparin is the initial drug of choice for
pulmonary embolism. In view of the significant right ventricular stress and hypoxemia in
this case, thrombolytic therapy was given. IV t-PA 100 mg followed by IV heparin infusion
for 1 day was given. Oral anticoagulation with warfarin was then started with subcutaneous
low molecular weight heparin injection given before international normalized ratio (INR)
reached the therapeutic level. Clinical response was dramatic with rapid improvement of
his symptoms and oxygen saturation the next day. Echocardiogram repeated on day 5
showed complete resolution of his right ventricular strain and pulmonary hypertension.
His was discharged on day 6 when his INR reached 2.0.
Fig. 1. Bilateral pulmonary
embolism, axial view.
4. He needs anticoagulation with warfarin for 3–6 months.
Fig. 2. Bilateral pulmonary
embolism, coronal view.
HKMA December 2007
Nail with dusky red lines
BOTH Dermatology and
Cardiology courses and earn
A 35-year-old gentleman had noticed an abnormality
on his left index fingernail for 6 months. It was
asymptomatic and there was no definite history of
trauma. His past health was good. On inspection,
there were several thin dusky red lines on his
fingernail. The longest one measured about 5 mm
in length. There was also onycholysis affecting the
middle fingernail. Other fingernails and toenails
were normal. Physical examination including the
cardiovascular system was otherwise unremarkable.
He worried about tinea unguium.
Answer these on page 18 or
make an online submission at:
Please answer ALL questions
1. What is the clinical sign shown on his nail?
2. What is the underlying pathophysiology?
3. Is it commonly associated with significant heart
The content of the Dermatology Series is provided by:
Dr. CHAN Loi Yuen, Dr. TANG Yuk Ming, William, Dr. MAK Kam Har &
Dr. CHOW Ka Yuen.
4. What are the possible causes?
5.Does the patient have tinea unguium?
Specialists in Dermatology & Venereology
november ANSWERS
A 28-year-old gentleman presented with a 1-year
history of slowly extending linear depression on
his forehead, over the left side to the midline. The
lesion gradually extended downward from the
frontal hairline region to the eyebrow edge. There
was no preceding history of trauma or redness,
and the lesion is asymptomatic. He has used an
over-the-counter topical cream on the area, but no
appreciable improvement was noted.
1. What are the clinical diagnosis and possible differential diagnoses?
2. What investigation(s) will you perform for this gentleman?
3. What local complications can occur from this condition?
4. What treatments can be offered to the patient?
5. What is the prognosis of the condition?
1. The clinical diagnosis is linear morphea, which is a subtype of localized
scleroderma. It is a rare connective tissue disease affecting mainly the
skin and subcutaneous tissue, and less commonly the underlying muscle,
fascia and bone. Physical examination should be performed to exclude
generalized involvement which may suggest systemic scleroderma.
Differential diagnoses include acrodermatitis chronica atrophicans,
lichen sclerosus et atrophicus, and eosinophilic fasciitis.
2. Linear morphea can be diagnosed clinically. In case of doubt, a diag- nostic biopsy can be performed.
3. Extension to the scalp (en coup de sabre) or eyebrow can lead to
scarring alopecia. Hemiatrophy of the face can occur with involvement
of the underlying bony structure. Involvement over joint regions may
lead to joint contractures, deformities, and severe limb atrophy.
4. Morphea is difficult to treat. Topical treatment including topical or
intralesional steroid, topical calcipotriol, topical imiquimod and topical
tacrolimus are used as a first-line treatment. Second-line therapies
include psoralen-UVA or UVA1 therapy. With severe disabling morphea,
systemic treatment with methotrexate or cyclosporin may be tried.
Surgical treatment with implant may improve the cosmetic result.
5. Morphea can be progressive, but the condition can become inactive
spontaneously even without intervention. Once fibrosis has set in, no
medical treatment is helpful and surgery may be considered to correct
the defect. However, morphea will not progress to systemic sclerosis.
HKMA December 2007
CNS MediCIne
A 20-month-old male brought for evaluation
after his parents observed a ‘shaking fit’
Complete this course
and earn
A 20-month-old child was brought to the emergency department by his parents because he had had a
“shaking fit.” They were not sure how long the episode had lasted, but they guessed it was < 2 or 3 minutes
and had occurred about 30 minutes before presentation. During the episode, the child had not appeared
to be aware of his parents calling to him, and all his limbs were shaking. The parents could not say whether
he was incontinent, as he still wore diapers. He had not had any similar episodes and had been in good
general health. The parents had noticed that he had been congested with a runny nose that had started 1–2
days earlier, and he had had a low-grade fever (99.5°F) during the afternoon before presentation. The child
was up to date on his immunizations, with the most recent having been administered at 18 months of age.
He had had normal development and growth. The parents could not recall anything unusual to suggest that
the child had ingested medications or anything toxic. His mother reported that her younger brother had
seizures with a high fever as an infant. There was no other history of seizures. On examination, the child was
mildly irritable but alert and had a temperature of 39°C (102°F). His right tympanic membrane was bright
red and bulging. The child had clear rhinorrhoea. His lungs and throat were clear, and he had mild anterior
cervical adenopathy. His reflexes were normal, and his neurological examination results were normal with no
focal signs. He had no meningeal signs and no rash.
On the basis of shaking lasting only a few minutes and
the history of new-onset febrile illness, it is likely that
the child experienced a febrile seizure. However, fainting
and hard, shaking chills also may cause a child to shake
vigorously, and parents may confuse these movements
with a seizure. From this history, it appears that the child
was not conscious during the episode, a factor that lends
support to fainting or a seizure as possible explanations.
The presence of a fever of recent origin also suggests a
febrile seizure.
Although the circumstances suggest febrile seizure,
other possible causes of seizure should be considered.
Seizures can result from some vaccines (e.g. measles,
mumps, and rubella vaccine) and may occur up to a
week and a half after administration. In addition, seizures
may result from encephalitis or meningitis, and the
child should be carefully evaluated for these conditions
because young children may have atypical signs and
symptoms with meningitis. The seizure could also be
the first manifestation of a neurological abnormality
or seizure disorder or could be the result of metabolic
disorders, drug ingestion, or other toxic ingestion.
A simple febrile seizure is defined as a generalized
seizure that occurs once in a 24-hour period in
association with an acute fever of at least 100°F. Most
occur in children between the ages of 18 months and
2 years, but they can occur in children up to 6 years of
age. If the seizure is focal, prolonged, or repetitive, it is
considered a complex febrile seizure if no other causes
for the seizure are identified.
Some suggested causes for febrile seizures include
an underlying genetically determined susceptibility
combined with the local expression of inflammatory
cytokines, genetic cellular abnormalities (e.g. abnormal
sodium transport), and the neurotropic properties of
HKMA December 2007
viruses. The most consistent risk factor is a family history
of febrile seizures; risk in a sibling of an affected child
has been reported to be 10–45%. The risk also appears
to be higher in children with an underlying neurological
abnormality. Repeated seizures, seizure with a low fever,
and seizure at an older age appear to correlate with an
increased risk of recurrence. In about 2% of children
with febrile seizures, epilepsy develops, and about
13% of children with epilepsy have a history of febrile
The diagnosis of a febrile seizure is made in a child
who presents with a fever and a seizure for which no
other cause can be found. Each child who presents for
the first time with a seizure requires a complete physical
examination and evaluation for the cause of the fever.
Further testing should be done as indicated because the
diagnosis is one of exclusion. In most cases, observation
alone is sufficient for a child >18 months with an initial
seizure and who has an identifiable cause for the fever,
fully normal findings on physical examination, and
no evidence of meningitis or encephalitis. However, a
lumbar puncture (LP) to evaluate for meningitis should
be considered in children between the ages of 12 and
18 months and is recommended (albeit controversially)
in infants younger than 12 months. Cervical rigidity
typically does not develop in children in these age
groups, and they may have very subtle signs associated
with meningitis. Seizures are more typical of meningitis
caused by Hemophilus influenza, and most children are
now immunized against Hemophilus. Findings of an LP
performed early in the course of meningitis may still
be normal, making observation mandatory in any case.
With those considerations, it has been suggested that
observation is more appropriate than automatic LP in
young children.
CNS Medicine
If the neurological examination results are normal and
the seizure lasted only a few minutes and was associated
with a short post-ictal phase, further neurological
evaluation with imaging or electroencephalogram (EEG)
may not be necessary. An EEG may be useful later in the
evaluation but will not be useful in the early post-ictal
phase because results may be transiently abnormal even
after a benign febrile seizure. The recommended EEG
after a complex febrile seizure is not evidence-based,
and it has been suggested that EEG is not necessary
unless the seizures are recurrent or are associated with
developmental abnormalities.
For patients with a history of repeated seizures,
seizures with unusual features (e.g. complex partial
seizure), a long post-ictal phase, a seizure that persisted
beyond 15 minutes, or any physical examination
abnormalities (including developmental abnormalities),
computed tomography or magnetic resonance imaging
of the brain, toxicology as indicated, lumbar puncture,
complete blood count, electrolyte panel, and other tests
as indicated should be done.
No specific seizure treatment is indicated for
an otherwise healthy child who is diagnosed with a
simple or complex febrile seizure that resolves without
sequelae. For children with recurrent febrile seizures, one
intervention to consider is rectal diazepam administered
at the onset of a fever or seizure. Treatment with
diazepam may shorten the duration of the seizure or
lessen the likelihood of additional seizures if the child
is prone to multiple febrile seizures during the onset of
illness, but is associated with adverse effects that may
not justify its use (e.g. prolonged sedation). Prophylactic
medication in a child who does not have a known seizure
disorder is not indicated.
Answer these on page 18 or
make an online submission at:
Please indicate 1 answer to each question
1. Febrile seizures may be caused by an underlying
genetically determined susceptibility or represent a
manifestation of the neurotropic properties of viruses.
a. True
b. False
2. Which statement is FALSE regarding the use of
EEG in paediatric febrile seizure?
a. It may not be necessary if the neurological
examination results are normal
b. It may not be necessary if the seizure lasted only a
few minutes
c. It should be used in the early post-ictal phase when
results are predictably normalized
d. Evidence suggests that EEG is unnecessary
unless seizures are recurrent or associated with
developmental abnormalities
3. Diazepam treatment is
recommended even in otherwise healthy children
diagnosed with a simple or complex febrile seizure that
resolves without sequelae.
a. True
b. False
4. What other possible causes of seizure should be
considered in a child of this age?
a. Recent vaccination (e.g. measles, mumps, rubella vaccine)
b. Encephalitis or meningitis
c. First manifestation of a neurological abnormality or
seizure disorder, or metabolic disorders
d. Drug or other toxic ingestion
e. All of the above
1. a
2. b
3. e
4. b
Current Studies
Association between ABCB1 C3435T polymorphism and drugresistant epilepsy in Han Chinese
P. Kwan et al. / Epilepsy & Behavior / 11 (2007) 112–117
Excerpt: There is accumulating evidence to suggest that overexpression of efflux drug transporters at the blood
–brain barrier, by reducing antiepileptic drug (AED) accumulation in the seizure foci, contributes to drug
resistance in epilepsy. P-glycoprotein, encoded by the ABCB1 gene, is the most studied drug transporter. There
are conflicting data as to whether the CC genotype of the ABCB1 3435C > T polymorphism is associated with
drug resistance in Caucasian patients with epilepsy. We investigated this association in ethnic Chinese.
HKMA December 2007
infectious disease
A 22-year-old female complaining of
burning with urination
Complete this course
and earn
A 22-year-old woman presented to the emergency department complaining of burning with urination. She
had neither fever, abdominal pain, nausea, nor diarrhoea. She had noted no change in vaginal discharge
but had noticed an odour for the past few days. On examination, she had neither abdominal tenderness,
costovertebral angle tenderness, nor abdominal masses. Urinalysis showed a trace of protein but no
blood, no white blood cells, and no nitrites. During the pelvic examination, a slight amount of discharge
with a mild odour was noted. Swab samples from the cervix and the vaginal vault were sent for evaluation.
Numerous infectious causes of urethritis exist. Sexually
transmitted infections, such as Neisseria gonorrhoeae,
Chlamydia trachomatis, Ureaplasma urealyticum, and
Trichomonas vaginalis are commonly found in the
sexually active population. Viral infections can also cause
symptoms. Herpes simplex (both type 1 and type 2) and
human papilloma virus (HPV) can infect the urethra
and periurethral tissues, causing pain. Infection from
Candida albicans also produces local inflammation and
pain. In addition to infection of the urethra, infection of
the bladder is a well-known cause of dysuria.
Numerous non-infectious causes of urethral
inflammation also exist. Uroliths (strictures of the
urethra) and urethral scarring from surgery or injury may
cause symptoms. Systemic inflammatory diseases also
must be considered; these include Reiter's syndrome and
Wegener's granulomatosis.
Another cause of vaginal irritation that occasionally
may cause dysuria is non-specific bacterial vaginitis.
Gardnerella vaginalis is frequently the cause of nonsexually transmitted vaginitis and appears to represent a
change in the vaginal bacterial composition. The usual
Lactobacillus species are replaced with an overgrowth of
anaerobic bacteria. Although local irritation and a slight
discharge may occur, the bacteria do not invade the local
tissue, so it is not considered a true infection. Unusual
causes of dysuria should be considered, including
interstitial cystitis, which also usually increases frequency
and urgency, and urethral transitional cell carcinoma.
If a saline wet mount examination of the vaginal
d i s c h a r g e i s d o n e i m m e d i a t e l y, t r i c h o m o n a d s
may be visible in more than half of the infections.
These organisms are protozoans with 2 cilia and are
approximately the size of white blood cells. If the saline
is kept warm, the cilia may be seen in active motion. A
more sensitive but slower test is a culture. A culture has
more than 95% sensitivity and specificity but has the
disadvantages of delayed diagnosis and much greater cost.
Trichomonas infection is often confused with nonspecific vaginitis. The two often occur together, so the
clue cells that are typical with G. vaginalis may be seen
on wet preparations, even if the trichomonads are not.
In addition, a potassium hydroxide preparation may
produce a fishy odour from G. vaginalis, which may be
mistaken for the odour of Trichomonas infection.
HKMA December 2007
Another test is Affirm VP (Becton, Dickinson and
Company, Franklin Lakes, NJ), which detects the DNA
of T. vaginalis, G. vaginalis, and C. albicans. This test
can be useful if the saline wet mount and potassium
hydroxide mount are equivocal or if a mixed infection
is present. The sensitivity and specificity compare
favourably with culture, but the test may not be available
in all medical centres.
The recommended treatment regimens are metronidazole as 2 g in a single dose or 500 mg twice a day for 7
days. Sexual contacts should be treated, even if they are
Although most patients infected with Trichomonas
are asymptomatic, many experience discomfort, dysuria,
dyspareunia, itching, and scant-to-copious discharge.
In asymptomatic patients, screening or treatment as a
sex partner of an infected patient may be the only way
infection is detected.
Detection is important, because a number of
potential long-term problems are associated with
Trichomonas infection. Female patients are more likely
to develop pelvic inflammatory disease and subsequent
infertility. Infection also appears to be a risk factor for
cervical cancer, even apart from concurrent infection
with HPV. In men, trichomoniasis has been associated
with infertility and chronic prostatitis. And in both
sexes, as with most sexually transmitted infections, there
is an increased susceptibility to HIV.
Treatment of Trichomonas during pregnancy is being
reconsidered. Preterm delivery, premature rupture of
the membranes, and low infant birth weight have been
thought to be associated with infection. However,
because treatment does not seem to benefit these
patients, it is not clear whether the problems are caused
by the infection. The results of some studies suggest that
the treatment — not the infection — is responsible for
complications during pregnancy. Until the relationship
between such problems and trichomoniasis is better
understood, the treatment of pregnant women should be
left to the discretion of specialists.
As with all sexually transmitted infections, patient
counselling about safer sexual practices is necessary,
particularly in teenagers and patients with multiple sex
partners. These persons are at high risk for other sexually
transmitted diseases and recurrent trichomoniasis.
infectious disease
Answer these on page 18 or
make an online submission at:
Please indicate 1 answer to each question
1. Common sexually transmitted infections found in
the sexually active population include:
a. Neisseria gonorrhoeae
b. Chlamydia trachomatis
c. Ureaplasma urealyticum
d. Trichomonas vaginalis
e. All of the above
2. Trichomonads are fungi with two cilia, approximately
the size of white blood cells, and are not actively
mobile under saline wet mount.
a. True
b. False
3. Which of the following is not a potential long-term
problem associated with Trichomonas infection?
a. Increased risk of pelvic inflammatory disease
and subsequent infertility in females
b. Infertility and chronic prostatitis in men
c. Alopecia areata
d. Increased susceptibility to HIV in both sexes
4. Recommended treatment regimens are metronidazole 2 g single dose or 500 mg bid for 7 days, and
should include asymptomatic as well as symptomatic
sexual contacts.
a. True
b. False
ANSWERS TO November 2007
1. b
Current Studies
2. a
3. d
4. b
Global control of sexually transmitted infections
Low N, et al / Lancet / 2006;368:2001–16
Sexually transmitted infections other than HIV are important global health issues. They have, however, been
neglected as a public-health priority and control efforts continue to fail. Sexually transmitted infections, by their
nature, affect individuals, who are part of partnerships and larger sexual networks, and in turn populations.
We propose a framework of individual, partnership, and population levels for examining the effects of sexually
transmitted infections and interventions to control them. At the individual level we have a range of effective
diagnostic tests, treatments, and vaccines. These options are unavailable or inaccessible in many resource-poor
settings, where syndromic management remains the core intervention for individual case management. At the
partnership level, partner notifi cation and antenatal syphilis screening have the potential to prevent infection and
re-infection. Interventions delivered to whole populations, or groups in whom the risks of infection and onward
transmission are very high, have the greatest potential effect. Improvements to the infrastructure of treatment
services can reduce the incidence of syphilis and gonorrhoea or urethritis. Strong evidence for the effectiveness of
most other interventions on population-level outcomes is, however, scarce. Effective action requires a multifaceted
approach including better basic epidemiological and surveillance data, high quality evidence about effectiveness
of individual interventions and programmes, better methods to get effective interventions onto the policy agenda,
and better advocacy and more commitment to get them implemented properly. We must not allow stigma,
prejudice, and moral opposition to obstruct the goals of infectious disease control.
HKMA December 2007
答 題 紙 December 2007
Name 姓名:________________________________________________________
Please return completed answer sheet to the
HKMA Secretariat (Fax: 2865 0943) on or before
15 January 2008 for documentation. However,
if you choose to do the exercises online, you
do not need to return this answer sheet by fax.
HKMA Membership No. or HKMA CME No.
請回答所有問題,並於 2008 年 1 月 15 日前將答題紙
傳真或寄回香港醫學會(傳真號碼:2865 0943 )。
Signature 簽名: ____________________________________________________
HK ID No. 香港身份証號碼:
□□-□□□xxx (x)
Contact Tel No. 聯絡電話:___________________________________________
Please answer ALL questions and write the answers in the
space provided. Both the Cardiology and Dermatology
courses must be completed to earn 0.5 CME point.
The other courses attract 1 CME point each.
HKMA December 2007
HKMA CME Programme 香港醫學會持續進修計劃
CME Lecture – January 2008 進修講課 – 二零零八年一月
VENUE & TIME 地點及時間
10 January 2008 (Thursday)
The HKMA Dr. Li Shu Pui Professional Education Centre
2/F, Chinese Club Building
21-22 Connaught Road Central, Hong Kong
Lecture: 2:00 – 3:00 p.m.
(Light lunch will begin at 1:15 p.m.)
HKMA Structured CME Programme with
HKS&H Year 2008 Session I:
Focus Ultrasound Management of Fibroid
Dr. YUEN Pong Mo
Director, Minimally Invasive Gynaecology, HKS&H
MBChB (CUHK), FHKAM(Obstetrics and Gynaecology),
FHKCOG (HK), FRCOG (UK), Specialist in Obstetrics and
This symposium is co-organized with
Hong Kong Sanatorium & Hospital
Please return the completed Registration Form together with a cheque for the appropriate amount made payable
to “The Hong Kong Medical Association” to 5/F Duke of Windsor Social Service Building, 15 Hennessy Road,
Hong Kong. Each lecture will carry 1 CME point under the MCHK/HKMA CME Programme (unless otherwise
stated). Accreditation from other colleges is pending. (Secretariat Fax No: 2865 0943)
Please be informed that Confirmation Letter of Registration is required. If you have not received any replies,
please do not hesitate to contact us at 2527 8452.
參加者可獲醫務委員會/香港醫學會持續醫學進修計劃積分一分 (除特別註明外)。其他專科學院之學分尚在申請中。
(秘書處傳真號碼:2865 0943)
參加者需持有講課確認通知書出席持續醫學進修講課。假若你沒有收到任何通知,請致電 2527 8452 查詢。
Please register for participation. First come, first served. 名額有限 請早登記
Reply Slip 回條
I would like to register for the following CME lecture(s):
HKMA Structured CME Programme with HKS&H
10 January 2008
HKMA Structured CME Programme with HKS&H Year 2008
Session I: Focus Ultrasound Management of Fibroid
HKMA Member
CME Participants
Please “✔” as appropriate. 請在適用處加上 ✔ 號
I enclose herewith a cheque of
現隨表格附上支票一張作為講課之報名費用:HK$港幣 ______________
Name 姓名:__________________________ Tel No 電話:___________________ Fax No.傳真 :____________________
HKMA Membership No. 會員編號
or HKMA CME No. 或進修號碼:______________________________ Signature 簽名:_____________________________
Data collected will be used and processed for the purposes related to the MCHK/HKMA CME Programme only. All registration fees are not refundable or transferable.
HKMA December 2007
HKMA Structured CME Programme at Kwong Wah Hospital
香港醫學會 ─ 廣華醫院分科進修課程
Jointly organized by
Hong Kong Medical Association
Kwong Wah Hospital
27 January 2008
Radiology & Pathology
1. PETS in Clinical Practice
Dr. FUNG Po Yan, Eliza
Venue moved to:
Lecture Theatre,
G/F, Block M,
Queen Elizabeth Hospital
Associate Consultant, Dept of Radiology, KWH
2. Emerging Zoonotic Infection
Dr. TSE Wing Sze, Cindy
Clinical Microbiologist & Associate Consultant, Dept of Pathology, KWH
24 February 2008
Venue moved to:
Lecture Theatre,
G/F, Block M,
Queen Elizabeth Hospital
Orthopaedics & Traumatology
1. Update in Spinal Surgery
Dr. WONG Kam Kwong
Specialist in Orthopaedics & Traumatology, Dept of O&T, KWH
2. Adult Joint Reconstruction & Replacement
Dr. HUI Wai Kwong
Specialist in Orthopaedics & Traumatology, Dept of O&T, KWH
Lecture Theatre, G/F, Block M, Queen Elizabeth Hospital
伊利沙伯醫院 M 座地下演講廳
2:00–5:00 p.m.
HK$50 per lecture for HKMA Members
HK$80 per lecture for CME Participants
Light snacks and lecture notes will be provided.
Please fill in and return the Registration Form on p.21 together with a cheque for the correct amount made
payable to “The Hong Kong Medical Association” to 5/F Duke of Windsor Social Service Building,
15 Hennessy Road, Hong Kong before the date of the function. Each lecture will carry 3 CME points under
the MCHK/HKMA CME Programme.
書明支付「香港醫學會」。 參加者可獲醫務委員會/香港醫學會持續醫學進修計劃積分三分。
HKMA December 2007
HKMA Structured CME Programme at Queen Elizabeth Hospital
香港醫學會 ─ 伊利沙伯醫院分科進修課程
Jointly organized by
Hong Kong Medical Association
Queen Elizabeth Hospital
6 January 2008
1.Dry Eye – Diagnosis and Management in GP Setting
Dr. WONG Lee, Amy
Assistant Professor, Dept of Ophthalmology & Visual Sciences, CUHK
2. Ocular Complications in Diabetes Mellitus – A GP Perspective
Dr. CHAN Kar Mun, Carmen
Honorary Clinical Assistant Professor, Dept of Ophthalmology & Visual Sciences, CUHK
3.Ocular Infection – A GP Perspective
Dr. CHENG Chi On, Andy
Honorary Clinical Tutor, Dept of Ophthalmology & Visual Sciences, CUHK
Venue moved to:
8A, Training Centre, 8/F.
Administration Building,
Kwong Wah Hospital
3 February 2007
Flexural Dermatosis
Dr. CHENG Tin Sik
Dermatologist i/c, Wanchai Male Social Hygiene Clinic, Social Hygiene Service, PHSB, CHP, DH
6 January 2008
8A, Training Centre, 8/F,
Administration Building, KWH
2008 年 1 月 6 日 廣華醫院行政大樓 8A
3 February 2008
Lecture Theatre, G/F, Block M, QEH
2008 年 2 月 3 日 伊利沙伯醫院 M 座地下演講廳
2:00–5:00 p.m.
HK$50 per lecture for HKMA Members
HK$80 per lecture for CME Participants
醫學會會員 - 每課堂港幣五十元正
持續進修參加者 - 每課堂港幣八十元正
Light snacks and lecture notes will be provided. 敬備茶點及講義
Please register for participation. First come, first served. 名額有限 請早登記
HKMA Structured CME Programme at
QEH/KWH — Registration Form
I would like to register for the following lecture(s) 本人欲參加下列講課:
27 January 2008
HKMA Member
CME Participants
(Non-HKMA member)
Radiology & Pathology
Venue moved to: Lecture Theatre,
G/F. Block M, Queen Elizabeth Hospital
24 February 2008
Orthopaedics & Traumatology
Venue moved to: Lecture Theatre,
G/F. Block M, Queen Elizabeth Hospital
6 January 2008
Venue moved to: 8A, Training Centre, 8/F,
Administration Building, Kwong Wah Hospital
3 February 2008
I enclose herewith a cheque of
Please “✔” as appropriate. 請在適用處加上 ✔ 號
Name 姓名:______________________________________ Tel No. 電話:________________________ Fax No.傳真 : ________________________
HKMA Membership No. 會員編號:
or HKMA CME No. 或進修號碼:_________________________________ Signature 簽名: _________________________________________________
Data collected will be used and processed for the purposes related to the MCHK/HKMA CME Programme only. All registration fees are not refundable or transferable.
HKMA December 2007
World Allergy Congress 2007
Bangkok, Thailand
49th Annual Meeting and Exposition of the
American Society of Hematology
Atlanta, GA
17th International Congress on Parkinson’s
Disease and Related Disorders
Amsterdam, Netherlands
San Antonio Breast Cancer Symposium
San Antonio, TX
The 16th Asian Pacific Congress of Cardiology
Taipei, Taiwan
66th Annual Meeting of the American Academy of
San Antonio, TX, USA
15th International Union Against Sexually Transmitted infections (IUSTI) — Asia Pacific Congress on
Sexually Transmitted Infections and HIV/AIDS
36th Annual International Neurological Society
(INS) Meeting – Neuropsychological Contributions
to Transdisciplinary Research
12th World Congress of Echocardiography and
Vascular Ultrasound
The American Society of Clinical Oncology
Genitourinary Cancers Symposium
San Francisco, CA, USA
Maastricht Exhibition & Congress Centre,
Maastricht, the Netherlands
Paris, France
8th International Conference on New Trends
in Immunosuppression and Immunotherapy
San Diego, CA, USA
Berlin, Germany
5th Mayo Clinic State of the Art Symposium on
Hematologic Malignancies: Hematologic
Malignancies In 2008 — Translating Today’s Clinical
Excellence Into Tomorrow’s Cure
International Symposium on Cardiovascular &
Neurovascular Medicine, in conjunction with
International Heart Failure Symposium – HK 2008
The American College of Radiology Radiation
Therapy Oncology Group
Phoenix, Arizona (JW Marriott Desert Ridge Resort & Spa)
World Congress on Neck Pain
Los Angeles, CA, USA
Papeete, French Polynesia
Asia Pacific International Conference of Travel
Medicine 2008
Melbourne, Australia
The Interface of Medical Illness and Depression:
A Clinical Review for Primary Providers
Las Croabas, Puerto Rico
The American Society of Clinical Oncology
Gastrointestinal Cancers Symposium
MARCH 2008
The 14th World Congress of Anaesthesiologists
Cape Town, South Africa
ECR 2008 – European Congress of Radiology
ACV – Austria Center Vienna, Vienna, Austria
44th Annual Meeting of the Society of Thoracic
Surgeons (STS) 2008
Fort Lauderdale, Florida, USA
Prague, Czech Republic
4th Asian Pacific Congress of Heart Failure:
Heart Failure in 3D Official Heart Failure Meeting
for the Asian Pacific Society of Cardiology
American Academy of Allergy, Asthma and
Immunology (AAAAI) Annual Meeting 2008
Philadelphia, PA, USA
Victoria, Australia
mail to: [email protected]
Seminar on Legal-Medical Issues Asia Pacific
5th Asia Pacific Medical Education Conference
Orlando, FL, USA
Hong Kong Convention and Exhibition Centre
Hilton Waikoloa Village, Waikoloa, Hawaii, USA
EASL Special Conference: Hepatitis B & C Virus
Resistance to Antiviral Therapies
5th EuroNeuro (2008)
Dubai United Arab Emirates
HKMA December 2007
2nd International Conference on Hypertension, Lipids, Diabetes and Stroke Prevention
The 5th Asia-Pacific Conference Against Stroke
Pasic City, Philippines
December 2007
Note: For each issue of the CME Bulletin, we shall try our best to include all the CME activities for the month, which are made known to the Association Secretariat. Members interested in
any of these functions are encouraged to check with the individual Colleges for credit points awarded by the Colleges and with respective organizers for confirmation of the details.
Pharmaceutical advertisements are welcome. For advertising rates and placement details, please contact Michelle Wong at Tel: 2965 1300, Fax: 3764 0374 or email: [email protected]
Your comments to the HKMA CME Bulletin are most welcome. Please send your opinion to Dr. Wong Bun Lap, Bernard, Editor of HKMA CME Bulletin, by fax at 2865 0943 or via e-mail at
[email protected]
Hospital Authority Head Office, Anaesthesiology Dept
9:00 am–12:00 noon
HA–Pamela Youde Nethersole Eastern Hospital, Paediatrics Dept co-joint with Comprehensive Paediatric
Rehabilitation Centre
Lecture Theatre, Hospital Authority Building,
147B Argyle Street, Kowloon
Skindy Liu – Tel: 23006307
4:30–5:30 pm
Patient Safety and Anaesthetic Practice
HA – Hong Kong East Cluster Hong Kong East Cluster Quality & Safety Seminar 2007
Education Programme on Paediatric Rehabilitation –
Nutrition in Autism
Child and Youth Health Link (Ward D6, 6/F, Main Block, PYNEH)
Lecture Theatre, G/F, Multicentre Block B, PYNEH
Lai Pui Shan – Tel: 25956706
9:00 am–1:00 pm
Refresher Course for Health Personnel 2007 —
Management of stroke & related complication
Update management of dyspepsia
2:00–3:00 pm
Lecture Theatre G/F, Wai Oi Block,
Caritas Medical Centre,
111 Wing Hong Street, Shamshuipo, Kowloon
Mr. Dennis Lau – Tel: 2785 7871
2:15-3:45 pm
Lecture Theatre, G/F, Block P, UCH
Ms. Marina Pun – Tel: 3513 4888
E-mail: [email protected]
Assn of Licentiates of Medical Council of HK
1) Situation and Outlook of Infectious Disease in the
Pearl River Delta Region
2) The Research on Cross-border Cooperative System of
Health and Preventing Disease in Zhuhai, Hong Kong
and Macau
HA-PWH-Dept of Clinical Oncology
HK College of Radiologists
1:00–2:00 pm
Hong Kong College of Community Medicine
Research Meeting
6:00–8:00 pm
Centre for Health Protection in Argyle Street/Wu Chung House
Ms. Fanny Kwong – Tel: 2871 8745
8:30–10:00 am
K509, Seminar Room, Professorial Block,
Queen Mary Hospital
Ms. Annie Chow – Tel: 2855 3401
HKU-HKU Family Institute
Certificate Course in Family Therapy (Level 1)
12:45–2:00 pm
Bereavement Service
2:00–3:00 pm
Lecture Theatre, Wai Oi Block G/F, CMC
Dennis Lau – Tel: 2150 7211/ 3408 6252
1) Early detection of Dementia in Family Practice
2) Practical Case Discussion on Diagnosis and Management
1:30–3:30 pm
HA–Sub-Committee in Obstetrics and Gynaecology
Introductory Gynaecological Endoscopic Surgery Workshop
9:00 am-4:30 pm
MAS Training Centre, PYNEH
TC Pun – Tel: 28554261
HA-UCH-Dept of Medicine & Geriatrics
HA-UCH-Dept of Paediatrics & Adolescent Medicine
HA-UCH-Dept of Pathology
12:45–2:00 pm
Multi-media Conference Room, 2/F, Block S,
United Christian Hospital
Tel: 3513 6007
Ms. Karen – Tel: 2871 8777
Update Management of Dyspepsia
HK College of Family Physicians
UCH Infectious Diseases & Microbiology Grand Round
2:30–5:30 pm
Shanghai Room I, Level 8, Langham Place Hotel, Mongkok
Ms. Wendy Yip – Tel: 2855 4487
HA–Caritas Medical Centre, Family Medicine Dept co-joint with HKMA, HKDU, HKCFP
UCH Infectious Diseases & Microbiology Grand Round
Hong Kong Medical Association, 2/F,
Dr Li Shu Pui Professional Education Centre, Central
Ms. Bess Lam – Tel: 2518 5656
12:45–3:30 pm
Central Academic Course Term V
1) Clinical Trials
2) Research Design and Methodology
3) Feedback–Feedback on Term V
2:30–4:30 pm
A.K.C. Surgical Library, 4/F, Clinical Sciences Building, PWH
Tel: 2632 2128
HK College of Psychiatrists
HA-UCH-Dept of Medicine & Geriatrics
HA-UCH-Dept of Paediatrics & Adolecent Medicine
HA-UCH-Dept of Pathology
Certificate Course in Clinical Dermatology
10:00–11:00 am
Certificate Course in Psychological Medicine 2007-08
3/F., A&E Training Centre, Tang Shui Kin Hospital
Ms. Juana Ng – Tel: 2871 8877
HKU-Dept of Family Medicine
Combined Head and Neck Meeting
HKU-Dept of Psychiatry
Lecture Theatre, 3/F, Tang Siu Kin Hospital,
282 Queen’s Road East, Wanchai, HK
Ms. Carmen Cheng – Tel: 2861 1808
Conference Room I, 1/F Shatin Hospital
CHIU Lai-fong – Tel: 2636 7688
E-mail: [email protected]
HA-PWH-Dept of Clinical Oncology
HK College of Radiologists
American Heart Association Advanced Cardiovascular
Life Support (ACLS) Course (2 Days)
Multi-media Conference Room, 2/F, Block S,
United Christian Hospital
Tel: 3513 6007
Lecture Hall, HKU Family Institute, 5/F Tsan Yuk Hospital,
30 Hospital Road, Sai Ying Pun
Ms. Daisy KW Lai – Tel: 2859 5300
Hong Kong College of Emergency Medicine
12:45–2:00 pm
6:40–9:40 pm
HA–Shatin Hosptial, Palliative Medicine Dept co-joint with Bradbury Hospice
Review Meeting in areas related to Public Health Medicine
九龍亞皆老街 147B 號醫院管理局大樓 M/F 演講廳
ALMCHK – Tel: 2327 2869
Mem: $50, Non-Mem: $100
Combined Breast Cancer Meeting
Meeting Room, Dept. of Clinical Oncology, PWH
Tel: 2632 2128
1:00-5:00 pm
HKU-Dept of Obstetrics & Gynaecology
HA-Caritas Medical Centre
Lecture Theatre, Multicentre Block B, PYNEH
Mr Edwin Chow – Tel: 2595 6352
HA – United Christian Hospital
HK College of Family Physicians
Monthly Video Viewing Sessions
1) Understanding Fats Good Vs Bad
2) Latest Treatment of Cardiovascular Disease
2:30–3:30 pm
8/F, Duke of Windsor Social Service Building, Wanchai
Ms. Carmen Cheng – Tel: 2861 1808
HKMA December 2007
持 續 進 修 日 程 JANUARY 2008
HA–Castle Peak Hospital, Psychiatry Dept
Seminar–What is the benefit of having a
HeadStart Program?
Lecture Theatre, Blk D, CPH
Ms. Cherry MAN – Tel: 2456 7855
Joint Clinical Meeting & Didactic Lectures
5:00–7:30 pm
HA-TMH-Dept of Family Medicine
Paediatric Renal Problem
5:30–6:45 pm
3/F Yan Oi GOPC Tuen Mun
Cowin Tang – Tel: 2468 6601
Paediatric Renal Problem
Medical Intervention of Clinical Emergencies (MICE)
Workshop (Identical)
2:00–3:30 pm
Institute of Clinical Simulation, 3/F,
North District Hospital,
9 Po Kin Road Sheung Shui, New Territories
Wong Pui Ying – Tel: 2683 8307
Board of Education Interest Group in Dermatology
Lecture Theatre, G/F, Block M, Queen Elizabeth Hospital
Ms. Gloria – Tel: 2527 8941
8:30 am–1:00 pm
HK College of Family Physicians
Hong Kong Medical Association
HK Council of Social Service
Lecture Theatre, M/F, Hospital Authority Building,
147B Argyle Street, Kowloon
Tel: 2527 8452
Registration Fee: $50
HKMA December 2007
Refresher Course for Health Care Providers 2007/ 2008 —
Management of Peptic Ulcer Disease and GERD in
Primary Care
Training Room II, 1/F, OPD Block, Our Lady of Maryknoll Hospital,
118 Shatin Pass Road, Wong Tai Sin, Kowloon
MS. Clare Tsang – Tel: 2354 2440
Beat Drugs Seminar 2008: Team Approach in the
Community-based Management of Substance Abusers
1:45–5:00 pm
Hong Kong Medical Association
HK College of Family Physicians
HA-Our Lady of Maryknoll Hospital
2:30–4:30 pm
1:30–3:30 pm
5/F, Duke of Windsor Social Service Building, Wanchai
Ms. Carmen Cheng – Tel: 2861 1808
HKMA Structured CME Programme with HKS&H Session 1:
Focus Ultrasound Management of Fibroid
Kidney Disease Management Course 2008
1) The impact of Chronic Kidney Disease and the Kidney
Awareness Program
2) Running a Low Clearance Clinic
Shanghai Room I, Level 8,
Langham Place Hotel, Mongkok
Ms. Wendy Yip – Tel: 2855 4487
Hong Kong Medical Association
Hong Kong Sanatorium & Hospital
HKMA-HKMA Community Network
12:45–3:30 pm
HA-NDH-Institute of Clinical Simulation
(Fee: Please call contact person)
The HKMA Dr. Li Shu Pui Professional Education Centre, 2/F,
Chinese Club Building, 21-22 Connaught Road Central, Hong Kong
Tel: 2861 1979
Mem: $50, Non-Mem: $80
3/F, Yan Oi GOPC, Tuen Mun
Cowin Tang – Tel: 24686601
Certificate Course in Psychological Medicine 2007-08
Basic Life Support Workshop for Health Care Provider
1:15–3:00 pm
5:30–6:45 pm
HKU-Dept of Psychiatry
HA–Our Lady of Maryknoll Hospital co-joint with American Heart Association
Training Room II, 1/F, OPD Block, Our Lady of Maryknoll Hospital,
118 Shatin Pass Road, Wong Tai Sin
Mr. Edward Chow –Tel: 2354 0559
E-mail: [email protected]
HA–Tuen Mun Hospital, Family Medicine Dept
2:00–5:00 pm
8:30 am–2:30 pm
7/F, Block H, Lecture Theatre,
Princess Margaret Hospital
Ms. Juana Ng – Tel: 2871 8877
HKMA Structured CME Programme at QEH 07/08 (X) – Eye
8A, Training Centre, 8/F, Administration Building, Kwong Wah Hosptial
Tel: 2861 1979
Mem: $50, Non-Mem: $80
11:30 am–1:00 pm
Hong Kong College of Emergency Medicine
Hong Kong Medical Association
HA-Queen Elizabeth Hospital
Management of Tuberculosis in Primary Care Settings /
Pituitary Disorders
2:00–5:00 p.m.
九龍亞皆老街 147B 號醫院管理局大樓 M/F 研討室
Fax: 2327 2248
HKU-Dept of Psychiatry
Certificate Course in Psychological Medicine 2007-08
12:45–3:30 pm
Shanghai Room I, Level 8, Langham Place Hotel, Mongkok
Ms. Wendy Yip – Tel: 2855 4487