NEWSLETTER Supporting the
Derbyshire Health Community
Volume 8: Issue 12 March 2010
Further in this issue Page 2 Oral morphine and equivalent doses to other oral opioids
Page 3 Generic prescribing in epilepsy
FSRH statement on antiepileptic drugs and contraception
Page 4 Withdrawal of sibutramine
Orlistat safety update
Page 5 Tight glycaemic control and car crashes
Blood glucose lowering and mortality
Page 6 Management of osteoporosis
Page 7 Bad medicine: osteoporosis. SSRIs and GI bleeding
Page 8 Anticholinergics in COPD. ICS in COPD
The Joint Area Prescribing Committee (JAPC) is a countywide group covering NHS Derbyshire County and NHS
Derby. It provides recommendations on drugs and medicines management issues.
RED drugs are those where prescribing responsibility lies with a hospital consultant or a specialist. AMBER drugs
are those that are initiated within a hospital/specialist setting but are suitable for shared care with a GP under a
shared care agreement. GREEN drugs are regarded as suitable for primary care prescribing. BROWN drugs are
those that JAPC does not recommend for use, except in exceptional circumstances, due to lack of data on safety,
effectiveness, and/or cost-effectiveness.
The most recent updates are in the table below; the full list is available at
The guidelines, formulary chapters, newsletters, etc can also be found via this link.
Drug Date considered Decision
Epiduo topical gel March 2010 BROWN
Erfa thyroid March 2010 BROWN
Eslicarbazepine March 2010 BROWN
Febuxostat March 2010 GREEN (2nd line use only)
Prasugrel March 2010 RED
Further to the article in the January PACE Newsletter, JAPC has once again discussed the appropriate use of
prasugrel. JAPC has decided on the basis of the best balance of risks and benefits, and of cost-effectiveness and
affordability, that if prasugrel is chosen in ACS instead of clopidogrel, then it is to be used for one month only
(supplied by the hospital) and then switched to clopidogrel for the remainder of the appropriate time period in
primary care (see JAPC clopidogrel guidance). In line with this, prasugrel has been designated as a RED drug.
The only exception to this is if a patient has demonstrated intolerance to clopidogrel.
The following guidelines and shared care agreements have recently been ratified by JAPC:
Heart failure guideline (updated) Acamprosate shared care
Lithium shared care (updated) (updated)
Acetylcholinesterase inhibitors shared care (updated) Buccal midazolam shared
Cabergoline and quinagolide for hyperprolactinaemia shared care care (updated)
Management of ADHD in adults shared care LMWH shared care (updated)
The Newsletter is produced by Peter Burrill - Specialist Pharmaceutical Adviser for Public Health
Oral morphine and equivalent doses to other oral opioids
Morphine is generally the strong opioid of choice and a common question is how to convert a dose of another
opioid to morphine or vice versa. Other opioids may be preferred, for example, if a patient obtains insufficient pain
relief with morphine and/or is suffering severe adverse effects. However, switching to an alternative opioid is only
one approach to managing opioid adverse effects. Other strategies include:
Reducing the dose of opioid (and possibly adding non-opioid or adjuvant analgesics).
Symptomatic management of the adverse effect(s).
Switching the route of administration.
If the strategies above have not worked, or are impractical, then a decision to convert to an alternative opioid may
be taken, preferably with advice from a palliative care or pain team1.
A document from UK Medicines Information provides advice on equivalent doses of oral morphine to other oral
opioids when used as analgesics in adult palliative care1. I enclose the table presented but would recommend
reading the entire document.
Approximate equivalent potencies of oral opioids to oral morphine
Converting from another oral opioid to oral morphine:
Multiply the total daily dose of oral opioid by its potency equivalence to determine the equivalent total daily
dose of oral morphine.
Converting from oral morphine to another oral opioid:
Divide the total daily dose of oral morphine by the potency equivalence for the oral opioid which you are
Oral Drug Duration of Potency Notes
action (hours) equivalence to
release (oral to oral)
Buprenorphine 6-8 80 - 100 Manufacturer states formal dose equivalence study
(sublingual) never undertaken. Only one source suggests a
conversion so this should be used with care.
Codeine 3-6 0.08 - 0.15 Codeine is metabolised to morphine.
Dihydrocodeine 3-6 0.1
Hydromorphone 4-5 3.5 - 10 Some sources suggest a potency equivalence of 5
when converting from morphine to hydromorphone,
but only 3.5 - 4 if switching from hydromorphone to
morphine. The manufacturer states an approximate
potency equivalence of 5 - 10.
Morphine 3-6 1
Oxycodone 3-6 1.3 - 2 Note high oral bioavailability compared to morphine.
Manufacturer advises a potency equivalence of 2.
Pethidine 2-4 0.1 - 0.125 Unsuitable for long-term analgesia.
Tramadol 4-6 0.1 - 0.2 Manufacturer advises a potency equivalence of 0.1 -
Equivalent potencies are only approximate and can be unpredictable. When converting from one opioid
to another, it is often appropriate to use a lower dose than the suggested equivalence above. Close
monitoring for side effects and efficacy is mandatory, especially at higher doses.
Converting from morphine m/r 15mg bd to oral oxycodone:
Total daily dose of morphine is 30mg.
From table, oxycodone potency equivalence = 1.3 - 2
Divide 30mg/1.3 = 23mg and 30mg/2 = 15mg.
Therefore the approximate equivalent total daily dose of oral oxycodone is 15 - 23mg in divided doses.
1. UKMi Q&A 42.4
Generic prescribing in epilepsy
Is generic prescribing a reasonable option for anticonvulsant drugs, especially when used to manage epilepsy?
Following the publication of a DTB article1 that did not find firm evidence that generic prescribing in epilepsy
causes problems and conflicting advice from national bodies, this has been discussed and debated at JAPC. We
sought the opinions of the neurologists at Chesterfield/Sheffield and Derby/Nottingham. They broadly supported
the stance that routine branded prescribing of anticonvulsant drugs in epilepsy is not necessary.
“The opinion of the Epilepsy Service group at STH NHS FT is that we broadly support generic prescribing as a
cost-effective use of resources. There is insufficient data to suggest that generic prescribing adversely influences
the overall quality of care in the vast majority of cases. However, in individual cases there may be a point in brand
A paper from UKMi2 entitled „Which medicines are not suitable for generic prescribing in primary care?‟, advises
that the only anticonvulsants with potential problems are phenytoin and carbamazepine. The BNF gives the same
advice. The UKMi document states that for lamotrigine, the generic and branded products are bioequivalent.
JAPC concluded that the UKMi and BNF advice is sensible and recommends that anticonvulsants are
prescribed generically, except for phenytoin and carbamazepine, which should be prescribed as a brand
when used for epilepsy.
1. DTB 2009; 47 (12): 141-4
2. UKMi Q&A 247.1
FSRH statement on antiepileptic drugs and contraception
The Clinical Effectiveness Unit of the Faculty of Sexual & Reproductive Healthcare has issued a statement on the
concomitant use of antiepileptic drugs (AEDs) and contraception (January 2010). This is the summary. Full
document available here.
What We Already Know
- Epilepsy itself is a condition for which there are no restrictions on the use of contraceptive methods, but
restrictions may apply if certain antiepileptic drugs (AEDs) are used.
- AEDs that induce liver enzymes may reduce the contraceptive efficacy of combined contraceptive methods,
progestogen-only pills and progestogen-only implants.
- AEDs that induce liver enzymes do not reduce the efficacy of depot medroxyprogesterone acetate (DMPA), the
levonorgestrel-releasing intrauterine system or non-hormonal methods
- Combined hormonal contraception (CHC) increases the clearance of lamotrigine and reduces serum
- Women using lamotrigine should be advised that seizure frequency may increase when initiating CHC, and that
lamotrigine side effects may increase in the pill-free interval or when discontinuing CHC.
What This Statement Adds
- There is evidence that progestogen-only methods do not affect lamotrigine levels.
- Lamotrigine levels are not reduced by CHC when lamotrigine is given in conjunction with sodium valproate.
- CHC may increase the clearance of sodium valproate. The clinical significance of this interaction is unknown.
- Long-term treatment with carbamazepine, phenytoin, primidone and sodium valproate is associated with loss of
bone mineral density (BMD) and fracture. Whether concomitant use of DMPA leads to further loss of BMD or
increases the risk of fracture is unclear.
Withdrawal of sibutramine
As reported in last month‟s newsletter, sibutramine has been withdrawn from the market in Europe because of
safety concerns. This is yet another example where evidence of a disease-orientated outcome, in this case weight
loss, has not led to the expected benefits in patient-orientated outcomes i.e. reduction in cardiovascular disease.
We have been misled. As funding in the NHS is reduced in real terms over the next few years, in order to obtain
maximum health gain from a limited pot, shouldn‟t we invest only in drugs with positive patient-orientated outcome
evidence? We need to ask the question „will this make people live longer or better, and by how much?‟
An editorial in the BMJ has discussed the plight of sibutramine1. The author states „The odds were always stacked
against sibutramine, because cardiovascular risk is embedded in its mechanism of action.‟ One has to wonder
then how it was ever granted a licence. He goes on to say „None of the other manufacturers of anti-obesity drugs
signed up for such a long term study of efficacy and safety; with its patent now expired, orlistat, the last man
standing, will never be put to this crucial test.‟ So we will never see any patient-orientated outcome evidence for
He concludes „One of the safest bets in medicine is that obesity is here to stay. The fate of sibutramine reminds us
how little anti-obesity drugs have had to offer - at best, a reduction of a few per cent in the total burden of excess
weight carried until death. With energy homoeostasis so deeply enmeshed in physiology, it has always seemed
unlikely that a magic bullet could ever switch off food intake without hitting something vital.‟
Reconsider if you are thinking of simply switching patients on sibutramine to orlistat. Take the chance to review
them inline with the recently launched adult obesity pathway.
1. BMJ 2010; 340: 377-8
Orlistat safety update
The MHRA has provided an update on the safety of orlistat.1 Orlistat is available in Europe as 120mg capsules
under the brand name Xenical, and as 60mg capsules under the brand name of alli, for weight loss in combination
with a reduced-calorie, lower-fat diet. Xenical has been licensed since 1998 and is available as a prescription-
only medicine; alli was licensed in January 2009 and is available without a prescription under the supervision of a
alli: updated safety information
A recent Europe-wide review of the safety information for alli has led to a number of updates, which bring the
product information in line with that for Xenical. Pharmacists should be aware of this information so that they can
appropriately advise consumers who wish to buy alli or discuss its use.
Patients with kidney disease should consult a doctor before starting alli because use of orlistat could rarely
(>1/10,000 to <1/1000) lead to hyperoxaluria and oxalate nephropathy.
Interaction with levothyroxine
Patients who are taking levothyroxine should consult a doctor before starting alli because reduced control of
hypothyroidism may occur when alli and levothyroxine are taken at the same time. This could be due to
decreased absorption of iodine salts or levothyroxine (or both). These medicines may need to be taken at
different times to reduce the risk of interaction, and the dose of levothyroxine may need to be adjusted.
Interaction with antiepileptic drugs
Patients who are taking an antiepileptic drug should consult a doctor before starting alli because loss of seizure
control has been reported during concomitant treatment with orlistat and antiepileptic drugs such as sodium
valproate and lamotrigine. Orlistat may decrease the absorption of antiepileptic drugs, leading to loss of seizure
control. During concomitant treatment, patients should be monitored for possible changes in the frequency and
severity of convulsions. If this occurs, consideration could be given to administering orlistat and antiepileptic
drugs at different times.
Pancreatitis has also been added as an undesirable effect of alli treatment after reports in a number of patients
alli: reports of counterfeit capsules in the USA
We are aware that consumers may be at risk after reports in the USA of counterfeit alli that contained sibutramine
rather than orlistat. Although the counterfeit product has not been found in the UK, it is still potentially available to
UK customers via the internet. Consumers should not buy medicines from unregulated websites.
Review of hepatotoxicity with orlistat
In July 2009, there was a Europe-wide review of a possible association between orlistat and serious hepatic
reactions. The review included non-clinical, clinical trial, and post-marketing safety data provided by the licence
holders and a review of suspected adverse reaction reports submitted to the MHRA. Data from the licence
holders have also been submitted to the US Food and Drug Administration, which is also conducting a review.
The European review concluded that there is insufficient evidence to show that Xenical or alli are associated with
more serious liver disorders than those already listed in the product information, and that no further action was
recommended at this time.
The current product information for Xenical and alli contains a warning that hepatitis, cholelithiasis, and increased
transaminases and alkaline phosphatase are possible side effects, and that patients who experience symptoms
such as yellowing of the skin and eyes, itching, stomach pain, and liver tenderness should stop taking the
capsules and tell their doctor.
The MHRA, together with European regulatory authorities, will continue to monitor all adverse reactions
associated with orlistat. Suspected adverse reactions can be reported to them via the Yellow Card Scheme (see
www.yellowcard.gov.uk) and they welcome reports direct from patients.
1. Drug Safety Update Volume 3, Issue 7, February 2010
Tight glycaemic control and car crashes
A Canadian case-control study has found an association between low HbA1c and risk of car crashes in people with
diabetes.1 They found a relative increase in risk of crash of about 26% for every 1% (11mmol/mol) lower HbA1c.
Risk of crash was about four times greater in people with a history of severe hypoglycaemia requiring outside
The authors state “Our findings join a growing and contentious literature correlating low HbA1c values with adverse
consequences in adults with diabetes mellitus. For example, three recent randomised trials found that intensive
treatment regimens led to both lower HbA1c values and an increased incidence of severe hypoglycaemia among
The NPC advises2 “While this study has several limitations, and association does not necessarily mean causation,
they provide another consideration in agreeing HbA1c targets with individuals alongside patient preferences, the
balance of likely benefits and harms, and the burden of extra medication.”
1. PLoS Med 6 (12): e1000192. December 2009
Blood glucose lowering and mortality
A large retrospective cohort study (using the UK GPRD) of patients with type 2 diabetes receiving intensive
glucose control treatment suggests that the risk of all-cause mortality increases above and below an HbA1c level
of about 7.5% (59mmol/mol). Intensifying treatment with insulin was associated with a greater risk of these events
than intensifying treatment with oral hypoglycaemic agents.1
The study identified that a mean HbA1c level of about 7.5% was associated with the lowest risk of all-cause
mortality, and that an increase above or a decrease below this level was associated with a greater risk. This
relationship was apparent regardless of whether treatment was intensified with insulin or with oral hypoglycaemic
agents. However, with insulin treatment the risk of all-cause mortality was greater. Also the range of HbA1c over
which there was no statistically significant difference from 7.5% was narrower with insulin (about 7.5% to 8.9%)
than that seen with oral hypoglycaemic therapy (about 6.9% to 9.4%).
In those treated with combined oral therapy, all-cause mortality varied little between HbA1c values of 7 to 9, being
lowest at 7.5. Go as low as 6.4 and it jumps to higher than at 9.4. In those treated with insulin, the 7.5 target is
even more important; if you go any lower, mortality gets higher, even at 7.2, which is worse than being at 9. The
authors state that diabetes guidelines might need revision to include a definition of an HbA1c minimum value (but
not locally – see later). The accompanying editorial2 concludes that this study does provide a rationale for an
HbA1c threshold of 7.5%, corresponding to the lowest death rate and lowest event rate for large-vessel disease.
The NPC advises3 “Health professionals may wish to consider the implications of the present study in their
discussion with patients about risks and benefits of intensifying drug treatment and setting of individual HbA1c
targets, especially if considering an HbA1c target below 7.5%. The study suggests that any benefits of glucose
lowering below this level (e.g. a reduction in microvascular events) could be offset by an increased risk of death
and cardiovascular events, especially if insulin is used.”
A letter in the BMJ4 states that this observational evidence, though not definitive in its own right, is consistent with
the interventional evidence suggesting a possibility of harm from lowering glycated haemoglobin below 7% in
patients with established type 2 diabetes. The authors say that the QoF target of less than 7 % should be
abandoned – “We in the UK should follow the lead of the National Committee on Quality Assurance in the United
States and suspend this target. We cannot risk harm by incentives that encourage practice patterns which the
evidence does not support and which may even compromise patient safety.”
Here is the relevant extract from the JAPC guidance on glucose control in type 2 diabetes (June 2009):
What targets should I set for patients with type 2 diabetes?
When setting a target HbA1c:
involve the person with diabetes in decisions about their individual HbA1c target level, which may differ
from a 7.0 or 7.5% target for people with type 2 diabetes in general.
remember what you are trying to achieve. Is it symptom control, hypoglycaemia avoidance and avoidance
of hospital admission? Or are you trying to prevent complications? Set the HbA1c target in collaboration
with the patient accordingly.
encourage the person to maintain their individual target unless the resulting side effects (including
hypoglycaemia) or their efforts to achieve this impair their quality of life.
offer therapy (lifestyle and medication) to help achieve and maintain the HbA1c target level.
inform a person with a higher HbA1c that any reduction in HbA1c towards the agreed target is
advantageous to future health.
avoid pursuing highly intensive management to levels of 6.5% (unless easily achieved e.g. by metformin or
diet alone). Very tight control may increase the risk of sudden death, particularly if control is tightened
quickly over a period of months in subjects with other risk factors of CV disease.
Local guidelines suggest a target of 7.5%.
Structured education for people with diabetes is integral to their care. This is particularly important at
diagnosis and with any change in medication.
1. Lancet 2010; 375:481-9
2. Lancet 2010; 375:438-40
4. BMJ 2010; 340: c985
Management of osteoporosis
The NPC has produced a useful review of the management of osteoporosis in post-menopausal women.1 It
highlights that low BMD should be thought of as a risk factor for fracture, in much the same way that high blood
pressure and high cholesterol are risk factors for a stroke or myocardial infarction. BMD measurement is a
relatively poor predictor of fracture and there is a large overlap between the BMDs of those people who sustain a
fracture and those who do not. The test does not accurately identify those who will go on to have a fracture.
Therefore, widespread population BMD measurement is not appropriate. NICE specifically states that its
guidance on primary prevention of osteoporotic fractures in postmenopausal women does not imply that a
dedicated screening programme should be created. Instead it refers to opportunistic identification of women who
may be appropriate for referral for scanning or for treatment.
When discussing the NICE recommendations on drug treatment the article states “The cost-effectiveness of
interventions depends on the absolute level of fracture risk, the costs related to each fracture as well as the
efficacy of the various treatments and their costs. Although the recommendations of NICE may appear complex,
they present a stepwise approach to management, which places interventions with the most robust evidence of
clinical effectiveness and highest levels of cost-effectiveness as first-line choices. For individual patients who
cannot take, use, or tolerate particular treatments, alternatives are available. However, these alternatives are
sometimes subject to additional criteria because their increased cost means that the fracture risk needs to be
higher in order to maintain cost-effectiveness.”
“Generally, patients must have lower BMD measurements, or more risk factors, to be eligible for treatment with
risedronate or etidronate. This is due to the higher cost of these second-line treatment options, which means it is
necessary to identify higher-risk people in order for treatment to remain cost-effective. This approach also means
that a woman not meeting NICE criteria for second-line use of risedronate or etidronate, who cannot take, use or
tolerate alendronate, would not be recommended to use any other therapy beyond a calcium and vitamin D
1. MeReC Bulletin Volume 20, Number 01, January 2010
Bad medicine: osteoporosis
This short article1 by Des Spence is a „must read‟. He makes some very valid points:
The truth is that osteoporosis is not a disease but merely a risk factor for fracture, particularly of the hip.
Age over 80 is by far the single greatest risk. Also, there is an assumption that effective “treatment” exists.
There is limited evidence of the effectiveness of the widely prescribed bisphosphonates in the primary
prevention of hip fracture in people with no history of fracture, even in highly selective study populations of
elderly people. For secondary prevention the small reduction in hip fracture is again in highly selected
On closer inspection this research carries the scars of big pharma, with relative risk reductions, non-clinical
outcomes, and composite end points. I can find no mortality data and not even convincing evidence of
reduced back pain. The treatment paradox of managing medical risk – that the individual patient is
unlikely to benefit personally from treatment – is not even acknowledged.
The term osteoporosis is an age dependent concept; primary prevention is questionable in all but the most
frail; and “osteopenia” should be struck from the medical lexicon. The wanton promotion of osteoporosis
and treatment of the young is bad medicine, and that is even before we consider the drugs‟ side effects.
1. BMJ 2010; 340: 320
SSRIs and GI bleeding
Yet another study has shown an association between SSRI use and serious upper gastrointestinal bleeding
(UGB). This Danish population-based case-control study was conducted to evaluate whether use of these agents
is a cause of clinically important bleeding.1 The study involved 3652 cases with a first discharge diagnosis of
serious UGB from 1995 to 2006 who were matched (age and sex) with 36,502 controls. Data on drug exposure
and medical history were retrieved from a prescription database and the patient register, and a case-crossover
design controlled for confounders.
The following adjusted odds ratio (OR) were reported:
UGB among current, recent, and past users of SSRIs: 1.67 (95% CI, 1.46 to 1.92), 1.88 (1.42 to 2.5), and
1.22 (1.07 to 1.39).
Concurrent use of SSRI and NSAIDs: 8.0 (4.8 to 13).
Concurrent use of NSAID, aspirin, and SSRI: 28 (7.6 to 103).
UGB in the case crossover analysis: 2.8 (2.2 to 3.6).
The adjusted OR for tricyclic antidepressant was 1.15 (0.89 to 1.47)
Users of proton pump inhibitors: 0.96 (0.50 to 1.82).
The researchers conclude that “use of SSRI was associated with UGB, consistent with its antiplatelet effects.
SSRIs should be prescribed with caution for patients at high risk for UGB.”
1. Clin Gastro Hep 2009; 7:1314-21
Anticholinergics in COPD
The inhaled anticholinergics ipratropium and tiotropium are the recommended first-line short-acting and long-
acting bronchodilators, respectively, for people with COPD (see the JAPC COPD guideline). Tiotropium provides
at least 24 hour improvement in airflow and hyperinflation and clinical trials have consistently shown that these
physiological effects translate into improvements in lung function, exercise tolerance, and health related quality of
life, in addition to fewer exacerbations, including those requiring hospitalisation. No other drug for COPD provides
all these benefits.
In the past queries have been raised about the cardiovascular safety of the inhaled anticholinergics. Two recently
published studies have attempted to address this issue. One concentrated on tiotropium1 and the authors
concluded “Tiotropium was associated with a reduction in the risk of all-cause mortality, CV mortality, and CV
events.” However, most of the studies in the review are short term (1 month to 1 year) and most of the data on CV
events and death rates are from the 4-year UPLIFT study (see PACE Newsletter of December 2008). Mortality
and CV events were not the primary endpoints in UPLIFT. The primary endpoint was rate of decline in FEV1 and
this was what the power calculation was based on. It is unlikely to have been powered for mortality and although
encouraging, the mortality benefit may not be definitive.
The second study looked at CV risk with ipratropium2. The authors found that exposure to ipratropium within the
past 6 months was associated with a 29% higher relative risk of a CV event compared with no exposure.
However, this was a cohort study and cohort studies cannot prove cause and effect and are prone to bias.
Importantly, the authors did not have data on several important CV risk factors such as smoking status,
hypertension, hyperlipidaemia, diabetes, and BMI. The study only concentrated on an adverse event and did not
evaluate potential benefits associated with ipratropium. So it gives us no idea of the overall risk/benefit ratio. As
the accompanying editorial3 states, the apparent difference in safety data between short- and long-acting
anticholinergics are not easily explained and there seems no reasonable explanation based on the pharmacology
that short-acting anticholinergics would affect the CV system differently than long-acting drugs.
JAPC has discussed these studies. Based on current usage, switching from ipratropium to tiotropium would cost
Derbyshire County PCT over £950,000 per year and Derby City PCT about £350,000 per year. JAPC
recommends that this does not happen. The algorithm for drug use in COPD (see PACE Newsletter of November
2009) still stands i.e. ipratropium is still the first bronchodilator option to be tried, when „as required‟ salbutamol is
1. CHEST 2010; 137: 20-30 2. CHEST 2010; 137: 13-19 3. CHEST 2010; 137: 1-3
Inhaled corticosteroids in COPD
The November 2009 issue of this newsletter highlighted a systematic review that was undertaken to assess the
safety and effectiveness of the use of the combination of a long-acting beta2-agonist (LABA) with inhaled
corticosteroid (ICS) compared with LABA monotherapy in the management of COPD. The conclusion was that
combination therapy with LABA/ICS presents a result of borderline statistical and limited clinical significance
compared with LABA monotherapy. Moreover, combination therapy offers no significant additional survival benefit
and increased the risk of serious adverse events.
A new systematic review has analysed studies that have reported the effectiveness of ICS vs placebo in
preventing COPD exacerbations1. As stated in the introduction “Given the possible morbidity associated with the
use of ICS, it is important to re-evaluate the benefit of ICS, especially with its claim of reducing exacerbations.”
Eleven studies with a total of 8,164 patients were included in the analysis.
The use of ICS was associated with a small relative risk reduction of 18% in exacerbations (RR 0.82 [95% CI 0.73
to 0.92]). An individual would have to be experiencing six exacerbations per year to show a meaningful reduction
i.e. a reduction of one exacerbation from 6 to 5. The authors concluded “There is only modest benefit of ICS in
preventing exacerbations, which is not related to the level of baseline lung function on metaregression analysis.
The benefits of ICS in preventing COPD exacerbations thus seem to be overstated.”
Are ICS overused in your COPD patients?
1. CHEST 2010; 137: 318-25