1. health and fitness
2. disease

The Lung Association
and Health Professionals
working together can
make a difference in the
respiratory health of Ontarions.
J. Peter Macleod
Chair, Better Breathing 2006 Planning Committee
Respirologist, The Ottawa Hospital
Civic Campus
W I N T E R
2 0 0 5 - 2 0 0 6
Features
In this Issue
V O L U M E
1 8 ,
N U M B E R
1
Idiopathic Pulmonary Fibrosis
Is there light at the end of the tunnel?
Editorial
Idiopathic Pulmonary
Fibrosis . . . . . . . . . . . . .2
Martin R.J. Kolb, MD, PhD, Department of Medicine, Firestone Institute for Respiratory Health
& Department of Pathology and Molecular Medicine, Center for Gene Therapeutics, McMaster
University, Hamilton, Ontario, Canada
Chair’s Letter . . . . . . . .3
Although the total numbers of
INTRODUCTION
patients affected by IPF are not huge, it
Idiopathic pulmonary fibrosis (IPF) is
still is one of the most common forms
certainly not the first differential
of interstitial lung disease. The
diagnosis coming into mind when
incidence of IPF is not precisely
patients in their early sixties report
known, but it is estimated to be in the
mild to moderate exertional dyspnea
range of 15-40 per 100,000(1, 2), and
combined with cough. The nonspecific
approximately 20,000 Canadians are
presentation, initially often perceived
affected. Once diagnosed, the median
as “due to the aging process” by the
MARTIN KOLB
survival is between 2-3 years, placing
patient and not as expression of
IPF in the same category as pulmonary
disease, combined with the progressive
functional deterioration and inefficacy of current malignant disease in regard to prognosis. The
treatment is a major clinical problem. However, past 10 years have considerably enhanced our
recent efforts supported by all major international knowledge about the pathology and the clinical
respiratory societies and several pharmaceutical course of IPF. A few years ago, a new
companies have generated novel and promising classification was put forward and ratified in a
treatment approaches, which will hopefully consensus statement by the American Thoracic
translate into direct benefit for these unfortunate Society and European Respiratory Society
patients in the future.
Continued on page 4
Report of Chair,
Research Advisory
Committee . . . . . . . . . .3
Better Breathing OTS
Conference Program . .7
Coming Up
Non-Invasive Positive
Pressure Ventilation for
Acute Respiratory
Failure: Moving from
Evidence to Practice
Spring/Summer 2006
FIGURE 1
Mission Statement
To Promote Respiratory
Health through Medical
Research and Education.
The OTR can also be viewed
on-line at on.lung.ca/ots/otr.html.
www.on.lung.ca
Classification of idiopathic interstitial pneumonias according to the
2002 ATS/ERS consensus statement(1). Only disorders classified
as usual interstitial pneumonia should be termed “IPF” – after
exclusion of all other causes of interstitial lung disease that may
also reveal this histological subtype.
ONTARIO THORACIC EDITORIAL
REVIEWS
Idiopathic Pulmonary Fibrosis (IPF)
An official publication of the Ontario
Thoracic Society, Medical Section of
the Ontario Lung Association,
573 King Street East,
Toronto, Ontario M5A 4L3
(416) 864-9911 • Fax (416) 864-9916
E-mail: [email protected]
Web Site: www.on.lung.ca
Charles K.N. Chan, MD, FRCPC, FCCP, FACP, Head, Respirology, University Health Network, Mount
Sinai Hospital, Sunnybrook and Women’s College Hospital; Professor of Medicine, University of Toronto
ONTARIO THORACIC SOCIETY
EXECUTIVE COMMITTEE
2005-2006
Dr. Diane Lougheed (Chair)
Dr. John Bertley (Chair-Elect)
Dr. John Fisher
Dr. Mark Inman
Mr. Robert Kelly (Chair, OLA)
Dr. Robin McFadden (OLA Board Rep.)
Dr. Susan Moffatt
Dr. Elizabeth Powell (OMA Rep.)
Dr. Joe Reisman
Dr. Matthew Stanbrook
Dr. Susan Tarlo
Mr. Keith Vrieswyk (OLA Board Member)
Dr. Kenneth Willis (Past Chair)
ONTARIO THORACIC REVIEWS
EDITORIAL BOARD
Dr. Robert Hyland (Editor)
Dr. Diane Lougheed (Chair, OTS)
Dr. James Edney (Ontario Chapter,
College of Family Physicians of Canada)
Mr. Manu Malkani (President & CEO, OLA)
n the current issue of the OTR, Dr.
early on in the illness can be very
Martin Kolb succinctly summarizes
helpful. In such cases, the VAT biopsy
the state of knowledge with regard to a
not only helps in establishing the
challenging lung condition –
diagnosis but also aids in excluding
Idiopathic Pulmonary Fibrosis (IPF).
other conditions such as occupational
All practicing respirologists see
or environmental lung diseases.
patients with IPF regularly. Most of us
are frustrated by our lack of ability to
EMERGING THERAPIES
alter the natural history of this
Traditional immunosuppression therapy
CHARLES K.N. CHAN
condition and frequently are indecisive
is not impressive but, as noted by Dr.
with our diagnostic and therapeutic decisions. Kolb, likely helps some in stabilizing or slowing
However, this condition in most cases is fatal the rate of decline. Immunosuppression is by no
irrespective of what we do. For a select few, lung means the solution and does increase the risk of
transplant offers the hope of long-term survival. opportunistic infections. However, with careful
In a small subset, the condition remains quite patient selection and assessment of responses
stable or “dormant” for years, but most patients using multiple variables like pulmonary function
deteriorate gradually, stepwise or rapidly. tests, standardized walk test distance, one can use
National guidelines are helpful but clearly the conventional therapies for some patients.
lack sound evidence in support of the
Promising therapies derived from our
recommendations. Nevertheless, there has been knowledge of both the cellular and molecular
some improvement over the last ten years.
basis of lung inflammation and repair are still in
rigorous clinical trials. However, there are several
DIAGNOSIS
agents that look promising that may aid us in the
As highlighted in this article, the use of high therapeutic options within the next few years.
resolution computed tomography (HRCT),
In the interim, day to day management of IPF
especially when done in prone plus supine patients should include regular exercise,
positions, together with comparable clinical and preservation of bone, immunization, monitoring
laboratory features are often sufficient in making and treatment for gastroeosphageal reflux
a diagnosis without biopsy.
diseases, aggressive treatment for chest
For those patients who have unusual clinical infections, and surveillance for pulmonary
features and/or atypical HRCT findings, proper thromboembolism when there is acute hypoxic
biopsies from multiple sites via videoscope- decompensation that is not associated with
assisted thoracoscopy (VAT) approach especially apparent worsening of parenchymal diseases.
I
Robert Kelly (Chair, OLA)
Dr. Hedy Ginzberg (Medical Director, OTS)
CORRECTION
Ms. Bernie Voulgaris (OTS Administrator)
We regret that the information which
identified Christopher Licskai as
Respiratory and Critical Care
Association in the Fall 2005 Ontario
Thoracic Reviews was incorrect.
Christopher Licskai is Assistant
Professor of Medicine, University of
Western Ontario, St. Joseph’s Health
Care of London. We apologize for the
error and for the mis-spelling of
Dr. Licskai’s name.
Ms. Corinne Holubiwich (Medical Librarian)
We gratefully acknowledge the
support of our sponsors:
Join the OTS or Renew
Your Membership
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degree and scientists holding a PhD or equivalent degree of
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Associate members do not pay fees and may not vote or hold office
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To join the OTS or to renew your membership for 2006-2007, call
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www.on.lung.ca
2
O NTARIO T HORACIC R EVIEWS W INTER 2005-2006
CHAIR’S LETTER
Diane Lougheed, MD, MSc, FRCPC, Chair, OTS, Associate Professor, Department of Medicine, Queen’s University, Kingston
sincere appreciation to those individuals and groups who
005 was a year of new beginnings in many ways for
have given generously to this pilot program! I encourage
the OTS and the OLA. Under the able leadership of
those of you who are considering this unique donation
Mr. Manu Malkani, President and CEO, the OLA has
opportunity to contact members of the Executive or
undergone reorganization and consolidation of its
Research Advisory Committees if you have any questions
management structure. Out of difficult decisions and
about the fund. John Fisher (Chair, Research Advisory
challenging times I believe will come renewed
Committee) and Hedy Ginzberg deserve special recognition
opportunity for future growth. The OTS Medical Director,
for bringing several years worth of efforts to fruition!
Hedy Ginzberg, and ORCS Director of Administration,
Our education committee, under the able leadership of
Sheila Gordon-Dillane are now voting members of
DIANE LOUGHEED
Susan Tarlo, continues to address our educational
OLA Senior Management Committee – which is a
reflection of the value the OLA places on obtaining and recognizing mandate well. Better Breathing 2005 attendance and evaluations
were once again excellent. Our other annual events including the
input from its member societies now and in years to come.
OTS had several notable achievements in 2005. Research Respiratory Residents’ Symposium, the Job Fair at Better
funding reached a high of $990,000.00. This was largely due to an Breathing, and the Ontario Respirology Residents CanMEDS
additional $90,000 from the OLA and $90,000 in matching funds Workshop were also tremendous successes this year. The Cameron
from GlaxoSmithKlein (the latter for research in obstructive Gray fellowship for 2005-2006 was awarded to Virjanand
airways diseases). As a result, numerous Block Term Grants and 15 Naraine from the University of Toronto.
Thanks to the many OTS members who participated in the
one or 2 year Grants In Aid of up to $50,000 were funded in the
2005/06 competition! We will strive to maintain this level of Ministry of Health and Long-Term Care-funded Asthma Guidelines
funding from the OLA, continually enhance industry partnerships workshops as expert presenters and facilitators. The 3-year program
and explore new funding opportunities. To begin, OTS launched the evaluation results are very positive and as a result the Ministry
“Top it Up” for Respiratory Research Breathe New Life Award, wishes to continue to fund the OLA/OTS for a similar initiative.
toward which OTS members (only) may donate directly to Stay tuned for more opportunities to participate in OLA/OTSrespiratory research. As of December 2005, $20,000 has been sponsored asthma CME events locally!
raised. This is a slower start than we had hoped. I wish to extend
Continued on page 6
2
REPORT OF THE CHAIR
John Fisher, PhD, Chair, Research Advisory Committee; Professor of Medicine, Queen's University, Kingston
national program with the condition that a majority of the
n several occasions I have presented data justifying
provincial thoracic societies participate. Currently, only
increased base funding for OTS research, and
BC, Alberta and Ontario participate in the National CTS
extolled the virtues of the OTS/OLA plan to award multipeer review process and renewed efforts to seek a
year research grants. In 2005/06 OTS received funding
national consensus would perhaps entice more provincial
that translated into a remarkable 35% one-time increase
thoracic societies to contribute funds for national
in the grant-in-aid (GIA) budget. This reflected the OLA
strategy of offering $90k of one-time new research
distribution. One rationale for the OTS condition was
funding if external matching funds were available. Glaxo
that without wider participation, OTS would
Smith Kline (GSK) boldly stepped forward to be the
differentially fund other regions. Perhaps this is the right
JOHN FISHER
“The” corporate sponsor and by doing so acknowledged
thing to do, but consider Ontario’s role in research as
the high impact of OTS research and its importance in a reflected by the distribution of CIHR funds across Canada. Of the
knowledge-based economy. GSK has again demonstrated superior roughly $350 million CIHR funding announced by Federal Health
corporate citizenship by partnering with the OLA for the 2006/07 Minister Ujjal Dosanjh in October 2005, Ontario garnered
grant-in-aid (GIA) competition. This success would not have approximately 40%, followed by Quebec 31%, BC 12% and
occurred without the vision, hard work and enthusiasm of both our Alberta 11%. Other provinces account for the remaining 6% (data
Medical Director, Dr. Hedy Ginzberg and Ms. Renata Rea, from CIHR E-Alert Issue 6). The presence of outstanding research
Professional Communications Manager at GSK. The challenge for in Ontario is clear and at least partially reflects the density of
the OLA and OTS is now to ensure that the increased funding medical schools and research institutes that are associated with the
becomes a permanent component of the progress towards the Ontario population. A CTS/CIHR National grant program will need
adoption of multi-year research grants.
to balance the risk of participation for the OTS and maintain OLA
The question of partnering with CIHR is often suggested as a accountability to its donors. Policies that would consider the
strategy to help achieve multi-year research awards and the national research impact of each region, while relying on a CIHR
potential role of OTS research funding in establishing a National vision that would adopt a funding formula to increase respiratory
grant competition surfaced at the CTS annual meeting in Montreal. research in all regions, will increase the likelihood of success of a
In the past, the OTS has indicated its willingness to participate in a National Research Program.
O
O NTARIO T HORACIC R EVIEWS W INTER 2005-2006
3
Idiopathic Pulmonary Fibrosis...
(figure 1)(1). It is agreed that interstitial
lung disease with unknown cause should
be separated into granulomatous disease
(e.g. sarcoidosis), idiopathic interstitial
pneumonias
(IIP),
and
others
(lymphangioleiomyomatosis, histiocytosis
X etc). Seven different entities belong into
the group of IIP. The most common type is
usual interstitial pneumonia and this is the
only IIP that should be called IPF.
Simplified message: UIP/IPF has the worst
prognosis and is treatment resistant. In
contrast, nonspecific interstitial pneumonia
and desquamative interstitial pneumonia are
associated with better prognosis and more
favorable treatment response. It is still
unclear and matter of ongoing debate, if the
various entities within the group of IIP are
distinct pathologic processes, or reflect
different stages of the same disease(3).
PATHOGENESIS
The prevailing hypothesis that chronic
inflammation and altered immune response
resulting in repeated scarring and
eventually pulmonary fibrosis (“pathway
A” in figure 2) has been challenged of
late(4, 5). There is increasing evidence that
a primary abnormal repair process is the
driving force in IPF and other
fibroproliferative disorders. It is believed
that wound repair mechanisms which are
physiologically initiated after tissue injury
get out of control in the context of
pulmonary fibrosis - independent of
inflammation (“pathway B” in figure 2).
The repair process is altered on different
levels. Epithelial cells undergo apoptosis
and fail to re-populate the alveoli in
response to epithelial injury. In contrast,
Continued from page 1
mesenchymal cells, especially fibroblasts,
show reduced apoptosis, they proliferate
and accumulate forming “fibroblastic foci”
in the lungs(4, 6). In association with these
foci, there is increased synthesis of
extracellular matrix, and reduced matrix
degradation. On a molecular level
numerous cytokines and growth factors
mediating these processes have been
identified, and several of those are target
molecules for novel therapies, e.g. platelet
derived growth factor (PDGF), endothelin,
transforming growth factor beta (TGFb)
and others(7).
The ongoing fibrogenesis in the lung
causes a progressive restrictive lung disease
with impaired diffusing capacity and
hypoxia, eventually causing respiratory
failure.
DIAGNOSTICS
The diagnosis of idiopathic pulmonary
fibrosis requires that all other causes for
interstitial lung disease have been
excluded(2, 8). Clinical symptoms develop
over months to years; they are nonspecific
and include shortness of breath, dry and
mostly
nonproductive
cough
and
occasionally chest tightness. On physical
examination coarse crackles are heard in
both lower zones (“velcro rales”), finger
clubbing is found in a minority of patients.
Clinical signs of cor pulmonale and right
heart failure reflect advanced disease.
Pulmonary function test shows restrictive
pattern with impaired diffusing capacity
and later on decreased pO2 and O2
saturation. High resolution CT of the lungs
shows bibasilar reticular abnormalities,
more subpleural than central, in advanced
FIGURE 2
The pathogenesis of fibroproliferative lung disease can be related to repeated
inflammatory episodes resulting in ongoing scarring (pathway A), or in a fairly
inflammation independent development and progression of fibrotic processes (pathway
B). The prototype of a disease following pathway A would be chronic hypersensitivity
pneumonitis. One of the current hypotheses is that IPF follows pathway B, which would
explain the failure of anti-inflammatory treatment strategies.
4
stages with “honeycombing”, and is very
efficient in providing a fairly accurate
diagnosis. The need for histological
diagnosis by videoscopic assisted lung
biopsy has to be determined individually
but may be required to make a definite
diagnosis(8, 9).
CURRENT TREATMENT
The treatment of IPF is difficult and so far
no efficient therapy has been found(8, 10).
In the past, immunosuppressive agents have
been used based on the assumption that IPF
is an autoimmune inflammatory disease.
Response rates to corticosteroids, either
alone or in combination with azathioprine
or cyclophosphamide are not better than 1530%. Treatment response may be somewhat
higher when disease stabilization is
considered as a positive result (which
probably is reasonable considering IPF is
typically a continuously progressive
disease). However, in “mild defense” of
immunosuppressive drugs a recent editorial
in the American Journal of Respiratory and
Critical Care Medicine mentioned correctly
that no trial has ever investigated these
drugs appropriately in a prospective
randomized and controlled manner, and
thus it may not be justified to completely
rule out a potential role for them(11). The
current recommendation of the ATS/ERS
consensus statement suggests using a
moderately high dose of Prednisone (0.5
mg/kg body weight in combination with
either azathioprine or cyclophosphamide
[2-3 mg/kg body weight])(1, 8).
Other drugs have been used, such as
cyclosporine,
methotrexate
and
penicillamine, and most of this experience
has been published as retrospective studies
or case presentations. None of these drugs
are likely to have marked efficacy(12).
It is important to keep in mind that
patients with IPF are more susceptible to
lower respiratory tract infections, even if
they are not taking immunosuppressive
medication(13, 14). Hence, antibiotic
treatment is often given at an earlier time to
IPF patients although there is no clear
evidence for this practise. It is also
controversial if home oxygen therapy
should only be initiated when the pO2 is
below 55 mmHg on room air or when
pulmonary hypertension is present.
Continued on page 5
O NTARIO T HORACIC R EVIEWS W INTER 2005-2006
Idiopathic Pulmonary Fibrosis...
CURRENT PROSPECTIVE CLINICAL STUDIES
Intense research efforts in the past two
decades have provided several new
treatment approaches and novel drug
compounds. Some drugs are already
approved for clinical use for other
indications, and are now applied to IPF.
Others are being developed and may
proceed to clinical trials in the near future.
INTERFERON GAMMA 1B
Interferon is a pluripotent cytokine playing
a major role in host defense mechanisms. It
has been shown that Interferon gamma can
inhibit collagen synthesis in fibroblasts and
is antifibrotic in different animal models of
disease(15). A study published in 1999
showed that total lung capacity and oxygen
saturation on exertion improved in patients
with progressive IPF after they were treated
with Interferon gamma for 12 months in
combination with prednisone(16). This
observation led to a multi-centre trial with
interferon gamma in IPF which was
published in 2004(17). In this study the
primary endpoint of progression free
survival time (defined as >10% decrease of
predicted FVC, or >5% increase of A-a
gradient) was not different between the
treatment arms. However, there was a
surprising survival advantage for patients
treated with Interferon compared to
placebo. This has led to a new international
study (INSPIRE, Intermune Inc, California)
involving more than 60 study sites with 600
patients, for which recruitment is currently
underway, and which will focus on survival
in patients treated with Interferon over 2
years. It is also noteworthy that a recent
meta-analysis of three published studies has
suggested a survival advantage for patients
treated with interferon gamma 1b(18).
PIRFENIDONE
Pirfenidone is a novel antifibrotic drug
which has been shown to inhibit experimental
lung and kidney fibrosis. It is not an antiinflammatory agent, but interferes with
different biological mechanisms leading to
accumulation of fibroblasts and collagen,
amongst them TGFb(19). In an open label
phase II study it has been shown that
Pirfenidone can stabilize pulmonary
function values after 12 months of
treatment(17). A double-blind placebo
controlled clinical trial conducted in Japan
was recently published, and demonstrated
Continued from page 4
beneficial effects in regard to improvements
in 6 minute walk tests and VC in a subgroup
of less severely impaired patients(20). The
trial was terminated early because patients
in the placebo group had more episodes of
acute exacerbation after 6 months of
treatment compared to the Pirfenidone group.
IMATINIB
Imatinib is a tyrosine kinase inhibitor and
inhibits the receptor of PDGF. The
compound is marketed with the trade name
Gleevec and indicated for treatment of
chronic myeloid leukemia (CML). PDGF is
known to be involved in different
experimental fibroproliferative disorders,
such as asbestos and bleomycin induced
lung fibrosis, and the properties of this
“anti-PDGF” drug suggest that it might be
efficient in IPF as well(21). Some newer
experimental studies demonstrated a
beneficial effect of imatinib in pulmonary
fibrosis(22). The first clinical trial in the
United States has just finished recruiting
patients, and results of this trial are
expected in spring 2006.
Two other studies with drugs interfering
with receptors potentially involved in the
pathogenesis of IPF have completed patient
recruitment. One with bosentan, a
endothelin receptor antagonist used for
treatment of pulmonary hypertension, the
other with etanercept, which is anti-tumor
necrosis factor alpha and used in rheumatoid
arthritis and ankylosing spondylitis. Other
novel compounds interfering with TGFb
and its receptors are under development and
close to Phase I/II clinical trials.
N-ACETYLCYSTEINE
N-acetylcysteine (NAC) is a drug used for
prevention of liver toxicity in acetaminophen
overdose. In Europe NAC is also widely
prescribed as mucolytic agent in patients
with COPD. The drug is a glutathione
precursor and has considerable antioxidant
properties. It has also been shown that NAC
can reduce fibroblast proliferation and
collagen synthesis. Previous studies have
demonstrated that there is a lack of
glutathione in bronchoalveolar lavage fluid
in patients with IPF, and thus it is
reasonable to assume that therapy with
NAC might be beneficial in IPF(23, 24). A
large European study with a total of 182
patients (IFIGENIA) has just been
published in the New England Journal of
O NTARIO T HORACIC R EVIEWS W INTER 2005-2006
Medicine (25). Patients received 600 mg
NAC t.i.d for one year in addition to
prednisone and azathioprine as recommended
by ATS/ERS consensus guidelines. The data
suggest that stabilization of vital capacity
and diffusing capacity is more likely in the
NAC group compared to placebo. Although
statistically significant, it is questionable if
this is clinically meaningful. No significant
difference is reported in regard to mortality.
Further studies need to be done to address
open questions, specifically to investigate if
NAC per se is beneficial or if it facilitates
immunosuppressive therapy by reduction of
side effects.
SUMMARY
IPF is a progressive interstitial lung disease
of unknown origin with nonspecific
presentation and bad clinical outcome. The
current hypothesis of the pathogenesis is
that IPF is more likely caused by pathologic
repair processes and not so much by
immune mediated mechanisms. This has lead
to novel treatment approaches with some
known and some newly developed drug
compounds. Some of those drugs are currently
in prospective multicenter clinical trials.
There is substantial hope that these efforts
will result in a benefit for our patients and
the identification of therapies that are superior
to unsuccessful immunosuppressive strategies.
The pathogenesis of fibroproliferative
lung disease can be related to repeated
inflammatory episodes resulting in ongoing
scarring (pathway A), or in a fairly
inflammation independent development and
progression of fibrotic processes (pathway
B). The prototype of a disease following
pathway A would be chronic hypersensitivity
pneumonitis. One of the current hypotheses
is that IPF follows pathway B, which would
explain the failure of anti-inflammatory
treatment strategies.
References
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5
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lung fibrosis. J Pharmacol Exp Ther. 291(1):367-373.
20. Azuma, A., Nukiwa, T., Tsuboi, E., Suga, M., Abe, S.,
Nakata, K., Taguchi, Y., Nagai, S., Itoh, H., Ohi, M., Sato, A.,
and Kudoh, S. 2005. Double-blind, Placebo-controlled Trial of
Pirfenidone in Patients with Idiopathic Pulmonary Fibrosis. Am.
J. Respir. Crit. Care Med. 171(9):1040-1047.
21. Lasky, J.A., and Brody, A.R. 2000. Interstitial fibrosis and
growth factors. Environ Health Perspect. 108 Suppl 4:751-762.
22. Daniels, C.E., Wilkes, M.C., Edens, M., Kottom, T.J.,
Murphy, S.J., Limper, A.H., and Leof, E.B. 2004. Imatinib
mesylate inhibits the profibrogenic activity of TGF-{beta} and
prevents bleomycin-mediated lung fibrosis. J. Clin. Invest.
114(9):1308-1316.
23. Meyer, A., Buhl, R., Kampf, S., and Magnussen, H. 1995.
Intravenous N-acetylcysteine and lung glutathione of patients
with pulmonary fibrosis and normals. Am J Respir Crit Care
Med. 152(3):1055-1060.
24. Behr, J., Maier, K., Degenkolb, B., Krombach, F., and
Vogelmeier, C. 1997. Antioxidative and clinical effects of highdose N-acetylcysteine in fibrosing alveolitis. Adjunctive therapy to maintenance immunosuppression. Am J Respir Crit
Care Med. 156(6):1897-1901.
25. Domedts et al, N Engl J Med 2005; 353:2229-42
6
Chairs Letter...
Continued from page 3
Our Medical Advisory committee has been busy behind the scenes – advocating on
several important respiratory-related issues. Thanks to the many members who provided
input into the submission to the Ontario Drug Benefits formulary!
2006 is upon us with the promise of another fantastic Better Breathing conference
program next month. You should all by now have received the brochure by mail. If you
haven’t already registered, even a quick glance through the program outlined in this issue
of the OTR is sure to lure you to the provincial meeting. Peter Macleod and the Planning
Committee are to be congratulated for their hard work preparing this year’s meeting! Many
of you will be wondering about the outcome of deliberations regarding the future location
of the meeting. I am pleased to report that OTS Executive made a commitment to actively
assist OLA in raising the funds required to move the conference back to a downtown
location for 2007! Your feedback helped guide this decision – and we trust you will
support the executive if called upon!
This year will bring a number of changes in the composition of our committees. Robin
McFadden will turn over the reins as OTS representative on the OLA Board of Directors
to the OTS Past-Chair (yours truly). He has been our ear-to-the-ground, finger-on-thepulse of activity and our voice within the organization in more ways than one! I do not
think many of us realize the dedication and enthusiasm with which Rob has carried this
torch for more years than I can count. He has been a unifying force for OTS, particularly
when we were without a medical director. Rob, on behalf of all of our membership,
THANK YOU! John Fisher will step down as Chair of the Research Advisory Committee
in June 2006. John has demonstrated outstanding leadership and vision in his 7 year term,
for which we are extremely grateful. The nomination for his successor is Jim Lewis
(voting takes place at the OTS Business meeting at Better Breathing).
Thank you for the opportunity to represent Ontario respirologists as the Chair of OTS!
I have thoroughly enjoyed working with the many esteemed members of our society’s
committees and interacting with OTS members at each opportunity. My job was made
much easier by the fantastic administrative support of Bernie Voulgaris and Hedy
Ginzberg – two truly special individuals we are most fortunate to have under “our”
employ! I look forward to my new role on the OLA Board of Directors and am confident
our new Chairperson, John Bertley, will ably guide our endeavors to improve lung health!
We are pleased to announce the 3rd Annual
Respirology Job Fair
to be held at
The Ontario Thoracic Society Better Breathing 2006 Conference
Doubletree International Plaza Hotel, Toronto
655 Dixon Road, Toronto, On M9W 1J3 (near Pearson Airport), Toronto Room
Friday, February 3, 2006
after the OTS Annual General Meeting
5:00 – 6:00 pm
You will have an opportunity to present information about positions available in your centre to all residents
in the Respirology Programs in Ontario. Tables will be available to set up material if desired. In addition,
the Ontario Respirology Program Directors will be available for discussion of your future manpower needs.
Please RSVP to Bernie Voulgaris, OTS office
416-864-9911 or [email protected] by Friday, January 27th
O NTARIO T HORACIC R EVIEWS W INTER 2005-2006
WE HOPE TO SEE YOU AT BETTER BREATHING! OTS Conference Program
FRIDAY, FEBRUARY 3, 2006
7:00 a.m.
7:30 a.m.
8:15 a.m.
10:00 a.m.
10:45 a.m.
12:15 p.m.
1:45 p.m.
2:45 p.m.
3:15 p.m.
4:30 p.m.
5:00 p.m.
6:15 p.m.
6:45 p.m.
NOVARTIS PHARMACEUTICALS CANADA INC. CLINICAL SYMPOSIUM AND BREAKFAST Pre-registration is required
Speaker: to be announced
Registration
PLENARY SESSION
Welcome Address Mr. Robert Kelly, Chairman, Ontario Lung Association
THEME: RESPIRATORY DISEASE FROM CRADLE TO GRAVE
Chair: Dr. Peter Macleod, OTS Better Breathing 2006 Planning Committee
Childhood and the Development of Respiratory Disease Dr. Malcolm Sears
Palliative Approach to Patients Suffering From Respiratory Disease Dr. Deborah Cook
Refreshment Break with Exhibitors
OTS/ORCS SCIENTIFIC PROGRAM – WHAT’S NEW IN LUNG HEALTH
Co-Chairs: Dr. Diane Lougheed (OTS Chair), Dr. Lisa Cicutto (ORCS Chair)
Gender and Respiratory Health: Fad or Fashion Dr. Anna Day
Clinical Utility of Quantative Sputum Cell Counts in All Airway Diseases Dr. Frederick Hargreave
The Old is New Again: High Flow Nasal Cannula Oxygen Therapy…..Does it really work? Mr. Michael Keim
GENERAL LUNCH OR LUNCH WITH A PROFESSOR
1
GENERAL LUNCH
2
Managing Difficult Sarcoid Patients Dr. Meyer Balter
3
Staying Out of Trouble in Respirology Dr. Meri Bukowskyj, Dr. Robert Rivington
4
The André Péloquin Clinical Case Series Chair: Dr. Steven Bencze
Dr. Harry Birman, Dr. Marcus Newton, Dr. Jacqueline Nemni
AFTERNOON SESSION
THEME: PULMONARY POTPOURRI Chair: Dr. Peter Macleod
Interventional Pulmonology Dr. Kayvan Amjadi
Update on Pulmonary Vasculitis Dr. Christopher Allen
Refreshment Break with Exhibitors
Resident Case Presentations
Chair: Dr. Elizabeth Tullis
Case Presenters: University of Ottawa (Dr. Robert Chernish); Queen’s University (Dr. Farzad Saberi);
University of Western Ontario (Dr. Abdul Gari); University of Toronto: tba
OTS ANNUAL GENERAL MEETING
RESPIROLOGY JOB FAIR
BANQUET (ticketed event)
Banquet Reception
DINNER AND AWARDS PRESENTATIONS
Banquet Entertainment: James Gordon, Canadian singer/songwriter
SATURDAY, FEBRUARY 4, 2006
7:30 a.m.
8:30 a.m.
10:00 a.m.
10:30 a.m.
12:00 noon
1:30 p.m.
BREAKFAST SESSION (ticketed event) A Health Care Provider’s Perspective on Being Critically Ill Courtney Maguire
DEBATES – THEME: CONTROVERSIES IN PUMONARY MEDICINE Chair: Dr. Charles George
All Patients With Sleep Apnea Should be Reported to the Ministry of Transportation-Round II
Pro: Dr. Charles George
Con: Dr. Michael Fitzpatrick
A Formal Incremental Cardiopulmonary Exercise Test Should be Standard Practice
in the Evaluation of Patients with COPD
Pro: Dr. Kieran Killian
Con: Dr. Nha Voduc
REFRESHMENT BREAK
For further information – or to register,
Respiratory Quinolones Should be First Line Therapy of CAP
visit www.on.lung.ca or call
Pro: Dr. Charles Chan
Con: Dr. D. William Cameron
the
OTS office: 416-864-9911 x 254
Allergy Testing in Asthma Patients is a Waste of Time
Pro: Dr. Susan Waserman
Con: Dr. Michael Cyr
THERAPEUTIC UPDATE AND LUNCH SPONSORED BY BOEHRINGER INGELHEIM AND PFIZER Pre-registration is required.
DEFINING DISEASE MODIFICATION Dr. Donald Tashkin
Close of Better Breathing 2006
O NTARIO T HORACIC R EVIEWS W INTER 2005-2006
7
▲
SPIRIVA significantly
reduced dyspnea1,2*§
▲
SPIRIVA maintained full
24-hour bronchodilation with
once daily inhaled dosing1,2*
▲
SPIRIVA significantly
reduced exacerbations
and exacerbationrelated hospitalizations1*¥‡
SPIRIVA is a bronchodilator, indicated for the long term, once daily maintenance treatment of bronchospasm associated with COPD,
includ ing chronic bronchitis and emphysema.2
SPIRIVA is contraindicated in patients with a history of hypersensitivity to atropine or its derivatives, or to the excipient lactose monohydrate.2
SPIRIVA should not be used for the initial treatment of acute episodes of bronchospasm, i.e. rescue therapy.2
The most common adverse reaction was dry mouth. Other adverse reactions reported and consistent with possible anticholinergic effects
included: constipation, increased heart rate, supraventricular tachycardia, atrial fibrillation, blurred vision, glaucoma, urinary difficulty and
urinary retention.2
As with other anticholinergic drugs, SPIRIVA should be used with caution in patients with narrow-angle glaucoma, prostatic hyperplasia, or
bladder-neck obstruction. Patients should be cautioned to avoid getting the drug powder into their eyes. If this occurs, they should consult
a doctor immediately.2
* Results from two 1-year, double-blind, randomized studies of SPIRIVA (n=550, 18 µg once daily) vs placebo (n=371).
Salbutamol prn was allowed throughout the study period. Concomitant use of theophyllines, inhaled steroids, and minimal
doses of oral corticosteroids (equivalent of ≤10 mg prednisone/day) was allowed if doses were stabilized for at least
6 weeks prior to screening.
§ SPIRIVA group (42-47% achieved a TDI focal score of ≥1 unit) vs placebo (29-34%)(p<0.01).
¥ SPIRIVA group (0.76 exacerbations per patient year) vs placebo (0.95)(p=0.045).
‡ SPIRIVA group with 47% reduction (0.086 events per patient per year) vs placebo (0.161)(p=0.019).
SPIRIVA is a registered trademark of Boehringer Ingelheim Ltd.