Asthma Treatment in Adults

Asthma treatment in adults.

Introduction 

During the nineteenth and early twentieth centuries, people tried a wide range of treatments including opium, morphine, caffeine and iodine to alleviate their asthma. They tried inhaling fumes from burning preparations of stramonium (derived from the hallucinogenic Jimson weed, also called thorn apple), lobelia, potash and tobacco. They even tried cauterizing (burning) the inside of their nasal passage. Some of these treatments might have helped their asthma: for example, caffeine is a chemical relative of theophylline, a drug for asthma used today. But many supposed remedies – inhaling tobacco, for example – probably made asthma worse.

The wide range of ‘asthma treatments’ underscores how difficult managing asthma was before doctors started using theophylline in 1922. Salbutamol, which remains a mainstay of treatment, reached the market in 1968. A variety of bronchodilators and anti-inflammatory drugs followed, delivered by a wide range of devices. Pharmaceutical companies continue to develop new treatments for asthma, COPD and other respiratory diseases.

This wide choice of asthma treatments and devices means that you can probably find the right combination of drugs and devices that controls your symptoms. Properly used, combining a bronchodilator (‘reliever’) and an anti-inflammatory (‘preventer’) controls most cases of asthma. And older people, despite their lower lung function, find that bronchodilators and corticosteroids produce similar improvements in airways obstruction, quality of life, psychological status and disease severity as in younger people.

In this article, we’ll look at some of the most widely used drugs and devices used to treat asthma in the UK.  This article aims to aid your discussions with GPs and asthma nurses as you work together to determine the right treatment for you.

The aims of asthma treatment

Asthma treatment aims to let you live as normal a life as possible. More specifically, doctors try to meet four aims:

  1. to minimize symptoms, including nocturnal and exercise-induced symptoms;  
  2. to prevent exacerbations, and therefore minimize your need to use ‘rescue’ bronchodilators to alleviate asthma attacks;   
  3. to achieve the best possible lung function – ideally to within 80 per cent of your best or predicted value.   
  4. to minimize side effects.

Attaining these asthma treatment goals sometimes proves more difficult in elderly asthmatics than in children or younger adults. For example, many elderly patients show some irreversible airway obstruction. So, attaining near normal lung function may be impossible or require doses of drugs that are likely to cause unacceptable side effects. On the other hand, GPs, asthma nurses and elderly asthmatics need to ensure that adults with asthma are not unnecessarily restricting their lifestyles to accommodate their symptoms.

It may be worth agreeing individual goals for you with your doctor or nurse – especially as doctors and nurses may have a different view as to what constitutes a ‘good’ outcome. Healthcare professionals may focus more on symptoms, while you may want to spend more time in the garden, return to work or run the London marathon. So, you need to discuss how these treatment goals can help you achieve your ambition. Minimizing exercise-induced symptoms may need more intensive therapy if you are planning to run the marathon than if you want to want to play with your kids or grandchildren in the park.

To look at the treatment goals from another angle, if you can answer yes to one or more of the following questions, you may have poorly controlled asthma and you should see your doctor or asthma nurse to review your asthma medication:

  • Have you experienced difficulties sleeping because of asthma, including cough? 
  • Have new asthma symptoms (cough, wheeze, chest tightness or breathlessness) emerged?   
  • Have your usual symptoms become more severe during the day?
  • Has asthma interfered with your usual activities around the home, at work or college?   
  • Are you using more than 10 or 12 puffs of bronchodilator a day – around two canisters a month?

Age and the response to asthma treatment

Despite the wide range of treatments, poor control remains common. Cazzoletti and colleagues found that only 15 per cent of adults who used inhaled corticosteroids during the year before the trial showed well-controlled asthma. Clatworthy and co-workers found that 38 per cent of UK patients aged between 18 and 94 years showed poorly controlled asthma. Indeed, age itself seems to make poor asthma control more likely: every additional year of age increased the chances of having poorly controlled asthma by 1 per cent. That may not sound much. But it soon adds up. Several factors drive the increased risk of poor control as you get older. For example: 

  • People with adult-onset asthma may need to take higher doses of medication to maintain normal lung function, partly because their lungs are less responsive than those of younger asthmatics. 
  • Many adults with asthma show some degree of irreversible airway obstruction, following airway remodelling caused by inflammation and, possibly, repeated cycles of bronchoconstriction.
  • Lung function seems to decline more rapidly in adults with asthma than people of the same age without asthma, again possibly because of airway remodelling.
  • Older people tend to feel their symptoms are more severe than younger people do, even if their lung function tests are similar.
  • Many adults may not admit that symptoms limit their activity, for example because they feel that limitations are an inevitable part of asthma or ageing. So, asthma nurses and doctors may overestimate the control produced by current treatment.

The principles of treatment

Asthma management takes, broadly, a two-pronged approach. First, inhaled corticosteroids and other anti-inflammatory drugs suppress the underlying inflammation. However, steroids dampen inflammation too slowly to relieve attacks rapidly. So, second, bronchodilators open constricted airways and alleviate exacerbations. But bronchodilators do not reduce inflammation.

Treating asthma during pregnancy

The British Guideline remarks that ‘the risk of harm to the foetus from severe or chronically under-treated asthma outweighs any small risk from the medications used to control asthma’. For example, a large UK study found no increased risk of major congenital malformations in children born to women who used asthma treatments in the year before or during pregnancy.

You can use short-acting (relievers) and long-acting bronchodilators as normal during your pregnancy, the British Guideline remarks. Neither drug appears to increase the risk of major congenital malformations or other problems during pregnancy, or complications during labour and delivery. Similarly, inhaled steroids (preventers) do not seem to increase the risk of major congenital malformations or other complications. Indeed, inhaled anti-inflammatory drugs reduce the risk of suffering an exacerbation during pregnancy. As we’ve seen, poorly controlled asthma increases the risk of complications for mothers and babies. So, you can use inhaled steroids as usual during pregnancy. Later in this article, we’ll look at the specific issues surrounding oral steroids in pregnancy.

In other words, most asthmatics need both a preventer (steroid or another anti-inflammatory) and a reliever (bronchodilator). Obviously, it’s important that you don’t get them confused. Read the patient information leaflet that came with the inhaler (you can obtain information about most drugs at: www.medicines.org.uk) and, if you don’t understand something or have a question, speak to your pharmacist, doctor or asthma nurse. It’s especially important that you know how to use your inhaler correctly – as we’ll see later, mistakes are common.

In the UK, doctors and nurses follow a stepped approach to treatment as laid out in the British Guideline on the Management of Asthma. Doctors and nurses start treatment at the level most likely to minimize symptoms and normalize lung function, then move up to the next step if your asthma remains inadequately controlled. Once your asthma is well controlled for several months, treatment moves down a step. On the other hand, if asthma worsens, treatment can move up a step.

Self-management programmes and action plans

Self-management programmes and action plans based on the British Guideline put you in control of your asthma. The programmes and action plans are individualized to each patient’s abilities, circumstances and understanding. Some people want as much control over their disease and treatment as possible and are willing to monitor their symptoms and peak flow rigorously. Other people would rather take a more passive role. So, it’s important to be honest with your doctor or asthma nurse about how much responsibility you want. Your medical team can then develop an action plan that meets your needs.

Most self-management programmes include education about asthma and its treatment. They’ll also allow you to recognize declining control based on symptoms, peak flow or both. Most summarize action to take if asthma deteriorates, including when to:

  • seek emergency help;
  • increase the dose of inhaled steroids;  
  • start oral steroids.

In the latter case, the doctor may provide you with an emergency course of steroid tablets.

Travelling with asthma

It is worth reviewing both your action plan and your treatment before you travel – especially overseas. It’s better to be safe than sorry. Ensure you know when to increase your inhaled steroid dose or start oral steroids: your GP or asthma nurse won’t be on the end of the phone. Make sure you also have: 

  • spare asthma medications (preventer and relievers);
  • a short course of oral steroid (discuss taking some with you, even if you don’t usually have them at home); 
  • adequate health insurance;
  • information about local emergency and other health services in your destination;
  • discussed travel vaccinations.

Flying will not affect inhalers, which you should carry and store in your hand luggage.

Receptors: unlocking your asthma

Numerous chemicals pass messages around your body: 

  • Hormones (such as oestrogen, testosterone and corticosteroids) carry signals between organs, such as a gland and a fat cell or muscle. 
  • Mediators carry messages between cells that activate or inhibit the immune system.
  • Neurotransmitters pass messages between nerves as well as between nerves and muscles. For example, the neurotransmitter noradrenaline causes the muscles around your airways to relax, and another neurotransmitter, acetylcholine, causes the same muscles to contract.

Many of these messengers bind to specific proteins, called receptors. Most receptors are on the surface of the cells where the receptor acts. However, some hormones and steroidal drugs used to treat inflammation bind to receptors inside the cell. Taking a brief look at receptors helps you understand how your asthma drugs act.

Imagine an immune cell or a muscle cell surrounding the airway as a car. The receptor is the ignition lock. The messenger – such as an inflammatory mediator, noradrenaline or acetylcholine – is the key. When the key fits into a lock, the engine starts. And when the messenger binds to the receptor, part of the cell’s internal machine switches on. So, the mediator triggers inflammation or noradrenaline induces bronchodilatation. But the effect is specific: your key only starts your car. And the message only switches on those processes controlled by the receptor. Noradrenaline doesn’t bind to the receptor for acetylcholine, for example.

Now imagine you have a skeleton key. It also fits the ignition lock and switches on the engine. Some drugs – such as certain bronchodilators – act like a skeleton key. The receptor can’t distinguish the drug (called an agonist) from the normal mediator. Both switch on the cell’s machinery. So, a beta-agonist (a bronchodilator) has the same action as noradrenaline. 

Imagine you have another key. It fits the ignition lock, but won’t turn so the car won’t start. But while this key is in the lock, you can’t get the right key in. Some drugs for asthma, such as leukotriene receptor antagonists, bind to the receptor but don’t activate the internal machine (called antagonists). However, antagonists stop leukotrienes (an inflammatory mediator) from binding and promoting inflammation. So, inflammation subsides. Beta-blockers can trigger asthma. They antagonize the same receptors that beta-agonist bronchodilators activate – and so have the opposite effect and close the airways.

Anti-inflammatory drugs for asthma

Even when you don’t suffer symptoms, the inflammation that causes asthma usually remains, lurking in your lungs waiting to flare into an exacerbation. As this inflammation is chronic, you need to take your anti-inflammatory even when you feel symptom-free. Nevertheless, your doctor or asthma nurse should assess your symptoms regularly and adjust the dose of anti-inflammatory to the minimum that maintains control of your symptoms and meets the other treatment goals. This reduces the risk of side effects. Several drugs dampen asthmatic inflammation, of which steroids are the most commonly used.

Steroids

In 1930, American researchers isolated a substance, which they called cortin, from the adrenal glands (these lie on top of the kidneys). The researchers discovered that cortin contained a cocktail of hormones – corticosteroids – that have several important biological actions:  

  • controlling the metabolism of carbohydrates, such as starch and sugar;  
  • regulating the balance of minerals and electrolytes (salts) in the blood; 
  • regulating the amount of fluid in the body;
  • reducing inflammation.

Anabolic steroids and corticosteroids

Steroids are a very large group of natural and synthetic chemicals – including corticosteroids as well as the sex hormones oestrogen, progestogen and testosterone – that produce a wide range of distinct actions. One group, called mineralocorticoids, control the body’s use of minerals and electrolytes. Another group, glucocorticoids, regulate the levels of glucose in the blood. Importantly, the corticosteroids used to reduce allergic inflammation produce different effects from those produced by the ‘anabolic’ steroids abused by some weight-lifters, athletes and body-builders. Anabolic steroids are chemical relatives of testosterone, and are used medically to increase muscle mass and enhance physical performance.

So, you won’t start putting on muscle or develop other side effects linked to anabolic steroids if you take corticosteroids for asthma.

Doctors soon realized that corticosteroids could treat inflammatory diseases, so pharmaceutical companies developed synthetic steroids that reduced inflammation but produced fewer unwanted effects than the natural hormones on, for example, carbohydrate metabolism and fluid balance. Today, low-dose inhaled corticosteroids are the mainstay of asthma treatment in adults as well as children.

How corticosteroids work

As mentioned on earlier, corticosteroids cross the membrane that surrounds each cell and bind to a specific receptor. Rather like sticking two Lego bricks together, the steroid and receptor form a ‘complex’. This complex moves to the nucleus, which is the cell’s ‘control centre’. Here, the complex binds to DNA, which contains your genetic code.

You can think of your genetic code as an instruction manual on 46 chromosomes that contains all the information needed to make you. Each gene is an instruction to make a particular protein, such as a receptor, an enzyme or a protein that maintains the body’s or cell’s structure.

Almost every cell (mature red blood cells are a notable exception)contains all the DNA needed to make your entire body. (That’s why you can clone an entire animal from a single cell.) But you don’t need the alveoli genes to make toenails. And a particular cell doesn’t need all the genes all the time. It may need some genes only when the cell needs to repair damage or divide. So, cells switch genes on and off as needed.

The steroid–receptor complex also switches certain specific genes on or off, which changes the balance of proteins produced by the cell. In particular, corticosteroids reduce production of inflammatory mediators by several types of white blood cell linked to asthma, including T cells, eosinophils and mast cells. These genetic (also called genomic) effects take several hours to emerge. Steroids also decrease the blood flow to the airways within a few minutes, which is far too quickly for steroids to change the balance of proteins in the cell by influencing genes. However, these ‘non-genomic’ actions are probably less important than corticosteroid’s influence on gene expression in reducing the inflammation that underlies asthma.

Inhaled corticosteroids

Regularly using inhaled corticosteroids alleviates asthma symptoms, reduces the risk of exacerbations and improves lung function and quality of life. Lazarus and colleagues comment that inhaled beclomethasone usually increases FEV1 by between 5 and 20 per cent, depending on the severity of the asthma and the extent of irreversible remodelling. So, according to the British Guidelines on the Management of Asthma, the following groups of adults should probably use inhaled steroids: 

  • those who use inhaled bronchodilators three times a week or more;
  • those who suffer symptoms three times a week or more;
  • those who wake one or more nights a week experiencing asthmatic symptoms.

Asthma treatment starts at a dose appropriate to the severity – often 400 mcg beclomethasone dipropionate (the most widely used inhaled steroid) per day or its equivalent (see Tables 1 and 2; a microgram [µg or mcg] is one millionth of a gram). Many adults with mild asthma find that 400 mcg a day controls their asthma. However, some people need up to 2,000 mcg beclomethasone dipropionate (or the equivalent) a day. The risk of side effects rises as the dose increases, so doctors or asthma nurses should determine the lowest dose of inhaled steroid that ensures you meet your treatment goals. 

Table 1 Examples of low-, medium- and high-dose inhaled steroids
Steroid name Daily dose (mcg): low Daily dose (mcg): medium Daily dose (mcg): high
Beclomethasone dipropionate – CFC 200-500 500-1,000 1,000-2,000
Beclomethasone dipropionate – HFA 100-250 250-500 500-1,000
Budesonide 200-400 400-800 800-1,600
Ciclesonide 100-200 200-400 400-1,600
Fluticasone 100-250 250-500 500-1,000

Source: Based on Balter and colleagues

Table 2 Examples of the equivalent doses of inhaled steroid
Steroid Example of brands/inhaler Equivalent dose
Beclomethasone (also spelt beclometasone) Clenil modulite   400 mcg
  Clickhaler   
  Aerobec Autohaler  
  Asmabec Clickhaler  
  Becodisks  
  Easyhaler  
  Pulvinal  
  Filair  
  Qvar  200-300 mcg
  Fostair 200 mcg
Budesonide  Turbohaler 400 mcg
  Metered-dose inhaler  
  Easyhaler  
  Novolizer  
  Symbicort (with formoterol)  
Fluticasone Metered-dose inhaler (HFA) 200 mcg
  Accuhaler  
  Seretide (with salmeterol)  
Mometasone Asmanex 200 mcg
Ciclesonide Alvesco 200-300 mcg

Source: Based on the British Guidelines on the Management of Asthma.

There are several steroids for asthma, administered using various delivery devices. The British Guidelines on the Management of Asthma notes that beclomethasone dipropionate and budesonide show similar efficacy, although the potency may vary depending on the delivery device. For example, a device that creates a fine mist of very small particles will deliver a greater proportion of the dose deep into the lung than one producing larger particles.

That’s why the dose of beclomethasone differs depending on whether the inhaler uses chlorofluorocarbons (CFCs) or hydrofluoroalkane (HFA) as a propellant. As CFCs damage the ozone layer, asthma devices increasingly use HFA. However, steroid particles in the HFA devices are smaller than in CFC-propelled inhalers, so the dose from some inhalers is lower.

Fluticasone and mometasone are more potent than beclomethasone and budesonide: indeed, fluticasone and mometasone need half the dose to produce the same anti-inflammatory effect. People usually, but not always, inhale these steroids twice daily. However, many asthma patients can take another steroid called ciclesonide once daily. Inhaling 160 mcg ciclesonide once daily often controls asthma. But, as with all steroids, the dose is tailored to the severity of your symptoms. In severe asthma, 320 mcg ciclesonide twice daily may reduce the frequency of exacerbations, whereas some can control their asthma with just 80 mcg once daily.

Side effects of inhaled steroids

Inhaled steroids are, generally, relatively safe and less hazardous to your health than poorly controlled asthma. Nevertheless, inhaled steroids can cause several adverse events. For example, according to the British Guideline, in adults doses of less than 800 mcg beclometasone dipropionate per day (or equivalent) can cause oral thrush (oral candidiasis) and dysphonia:  

  • Oral candidiasis: Oral candidiasis (thrush in the mouth) is the most common fungal infection among humans. Between 20 and 75 per cent of humans carry members of the candida family in our mouths, Akpan and Morgan point out. Our immune systems usually prevent the fungi from spreading and causing symptoms. However, inhaled steroids can suppress the mouth’s immune defences. This allows candida to grow, forming white patches around the gums, palates and tongue. Indeed, up to one in 20 people taking inhaled corticosteroids develop oral candidiasis. You can reduce the risk by rinsing and spitting after inhaling the steroid or by using a spacer. 
  • Dysphonia: Dysphonia refers to changes in your voice’s ability to make sounds. Almost everyone has suffered laryngitis (inflammation of the voice box) following an infection – it can make your voice sound hoarse, weak, harsh or rough. (Think of the last time you had a ‘frog in your throat’.) And between 2 and 6 per cent of people taking inhaled steroids develop dysphonia. Higher doses of inhaled steroids are especially likely to cause dysphonia.
Skin side effects

Steroids can ‘thin the skin’ (atrophy) by removing protein. They can also produce red or purple discolorations, called purpura, caused by blood vessels leaking near the skin’s surface. Because of this skin thinning, inhaled steroids may mean you bruise easily, especially if you’re older, taking higher doses of steroid or using long-term treatment.

The forearms and lower legs seem to be especially prone to steroid-related bruising. This pattern led some researchers to suggest that ultraviolet light interacted with the steroid to cause skin atrophy. Using moisturizers and protecting your skin from sunlight (e.g. with sunscreen) may help protect against bruising.

Steroids can also trigger a sudden outbreak of acne in adults, typically those aged 35 to 75 years. The acne tends to be worse on the trunk than on other parts of the body. In other cases, inhaled steroids taken long term can cause fine downy hair to appear on the sides of the face, upper lip and chin (hirsutism). Skin thinning, acne and hirsutism are more common with oral than inhaled steroids. Nevertheless, these side effects occur occasionally in people taking inhaled steroids, especially at high doses.

Diabetes

Doctors realized many years ago that oral steroids potentially trigger diabetes. However, more recent studies suggest that inhaled steroids, especially at high doses, may also cause diabetes. For example, Suissa and collaborators followed 388,584 adults using inhaled corticosteroids for asthma or COPD for, on average, 5.5 years. Over this time, inhaled corticosteroids increased the risk of developing diabetes by 34 per cent. Inhaled corticosteroids also increased the likelihood that people with diabetes would progress from oral hypoglycaemic (blood-sugar lowering) agents to insulin (suggesting that their diabetes got worse) by 34 per cent.

The risk rose progressively with increasing steroid doses. Compared to people not using inhaled corticosteroids, the risk of developing diabetes for the first time increased from 18 per cent with low-dose steroids (less than 500 mcg fluticasone or equivalent daily) to 30 per cent with moderate doses (500–1000 mcg or equivalent daily). The increased risk reached 64 per cent with high doses (at least 1,000 mcg fluticasone or equivalent daily). Similarly, the risk of progressing from oral hypoglycaemic agents to insulin increased from 8 per cent with low doses to 30 and 54 per cent with moderate and high doses respectively.

Other serious side-effects of steroid therapies for asthma

Other serious side effects – including changes in bone density, cataracts and glaucoma – occur in less than 1 per cent of people using inhaled steroids. Again, these side effects generally emerge only at higher doses, during prolonged treatment or both, and are much more common with oral than inhaled steroids. For example, when doctors analysed the scientific studies, beclometasone dipropionate did not seem to influence bone density at doses up to 1,000 mcg. (Bone density measures the strength of your skeleton. Low density means a weak skeleton and therefore a greater risk of suffering a broken bone.)

When to increase your dose of steroid

If you don’t meet the goals of treatment or experience an exacerbation, your GP or asthma nurse might suggest that you increase your dose of steroid or add another drug to your daily treatment. But before you increase your dose of steroid or start a new drug, there are certain checks you and your healthcare professionals should make: 

  • Have you taken your existing drugs as prescribed? Clatworthy and colleagues found that poor adherence to inhaled steroids increased the risk of poor asthma control by 35 per cent. 
  • Is your inhaler technique correct? (We’ll return to this later in the article.)
  • As far as possible, have you eliminated or treated trigger factors, such as smoking, allergens and rhinitis (e.g. hay fever)? Clatworthy and colleagues found that rhinitis increased the risk of poorly controlled asthma almost five-fold, and smoking around four-fold. Even in people with mild asthma, Lazarus and co-authors comment, smoking blunts the response to inhaled corticosteroids. So, people who smoke may need higher doses of inhaled steroids than non-smokers. 
  • Do you need to check whether the diagnosis is correct or whether you’ve developed a concurrent disease that reduces the effectiveness of treatment? For example, anti-inflammatory therapy may have a less marked benefit in people with both asthma and COPD compared to those with asthma alone.

In most patients, doubling the dose of inhaled corticosteroids does not halve the severity of asthma symptoms. The severity may decline by only a third or a quarter, for example. (Researchers describe this as a flat dose-response curve.) However, some patients benefit more than others from higher doses of inhaled corticosteroids. Unfortunately, doctors cannot tell who will benefit from higher doses in advance so, rather than increasing the dose of steroid, your GP or nurse may suggest adding in another drug (usually a long-acting bronchodilator). But if 800 mcg beclometasone dipropionate a day or equivalent plus a long-acting bronchodilator or another add-in therapy still fails to control your symptoms adequately, the British Guideline on the Management of Asthma suggests increasing the steroid dose to up to 2,000 mcg a day.

Oral steroids as an asthma treatment

Inhaled steroids control most cases of asthma. However, if your asthma remains difficult to control, or you suffer a severe exacerbation or show a potentially dangerous decline in lung function, your doctor may prescribe a course of steroid tablets, usually prednisolone, generally lasting a week or two. Very few asthma patients take oral steroids regularly.

The dose delivered by oral steroids is much higher than the inhaled counterparts, so oral steroids are highly effective at controlling the inflammation underlying asthma and can be lifesavers. However, the risk of developing side effects is much greater with oral than inhaled steroids. Some side effects emerge rapidly, such as mood changes (like feeling anxious, irritable, depressed or ‘high’) and stomach problems. Others – such as weakness or a rounder face – take several weeks or months, or a number of courses, to emerge. Elderly asthmatics may be especially prone to these side effects, as they often metabolize (break down) steroids less rapidly than younger patients.

The British Guideline on the Management of Asthma notes that those taking steroid tablets long term (for example, for more than three months) or requiring frequent courses (such as three to four or more times a year) are at risk of potentially serious side effects. So, doctors or nurses should regularly check:   

  • blood pressure and cholesterol levels, to monitor the risk of heart disease; 
  • levels of sugar in urine or blood, to check for diabetes;
  • bone mineral density, to watch for osteoporosis (brittle bone disease);
  • eyes, for cataracts (clouding of the lens).

Many of the common side effects with oral steroids (which we’ll discuss in a moment) are dose-related. We’ve already discussed some of these side effects (such as skin thinning, acne and hirsutism) with inhaled steroids, but the risk is markedly higher with oral steroids.

Furthermore, your body can adapt to oral steroids. So, stopping long-term treatment abruptly can trigger withdrawal reactions, including muscle and joint pain, conjunctivitis, fever, weight loss, runny nose and painful, itchy skin lumps. You should always seek advice from a doctor or asthma nurse before stopping, or reducing the dose of, oral steroids.

Oral steroids and infections

If you have never suffered from chicken pox or shingles, you need to stay away from people with these infections. Oral steroids suppress the immune response. As a result, Varicella zoster virus, which is responsible for chicken pox and shingles, can cause serious complications (including pneumonia) and even prove fatal in people taking oral steroids. If you encounter anyone suffering from chicken pox or shingles you should see your GP immediately. Long-term treatment with oral steroids can exacerbate other diseases or lead to unusual symptoms. So, if you feel unwell it is especially important to seek your doctor’s advice.

Osteoporosis and bone loss

Approximately three million people in the UK have osteoporosis, which causes more than 230,000 fractured bones every year. Osteoporosis is common in post-menopausal women. However, steroids can cause osteoporosis as well as exacerbating the ‘natural’ age-related decline in skeletal strength. Oral steroids can also cause muscle wasting and weakness – especially in the back, hips, ribs and arms – and unusual tiredness. These changes may increase the risk of a fall – and, therefore, the risk that you will break a bone, especially if your skeleton is already brittle.

Despite appearances, your skeleton isn’t inert. The stresses and strains of daily life create numerous tiny cracks in your bones, which would eventually undermine your skeleton’s strength. To prevent this, a group of cells called osteoclasts break down old bone by creating microscopic pits on the skeleton’s surface. Another group of cells, the osteoblasts, fill in the pits with new bone. This maintains your skeleton’s strength (bone mineral density, to use the technical term). However, oral steroids seem to reduce bone mineral density by, for example, reducing the amount of calcium absorbed from the diet, suppressing the formation of osteoblasts and killing osteoclasts.

Taking 5 mg prednisolone or more (or equivalent) each day decreases bone mineral density and therefore increases fracture risk, irrespective of age or sex. For example, after taking oral steroids for three to six months your risk of suffering a broken hip almost doubles. Meanwhile, the chance of experiencing a vertebral (spinal) fracture almost trebles and the risk of breaking a forearm rises by around 10 per cent.

The risk of suffering a fracture declines after you stop taking oral steroids. Dore remarks that around two years after stopping oral steroids, the risk of suffering a fracture is the about the same as that in someone who has never taken these drugs. In general, inhaled steroids do not affect bone, although high doses (more than 2,000 μg/day beclomethasone or equivalent) taken for several years may cause osteoporosis.

To reduce the risk of fracture, you should take the lowest dose of inhaled and oral steroid that controls your asthma symptoms, for the shortest possible time. (But because of the risk of provoking an asthma attack or suffering withdrawal symptoms, don’t stop taking your steroid or change the dose without talking to your doctor or nurse first.) Dore also suggests protecting your skeleton with exercise and ensuring you get enough calcium (1,000 to 1,500 mg per day) and vitamin D (800 to 1,000 IU per day), which may mean taking a supplement; a pint of milk contains about 750 mg of calcium, for example. Doctors can prescribe medicines that treat osteoporosis.

Cataracts and other eye problems

The transparent lens at the front of your eye focuses light on the sensitive retina that lines the rear of your eyeball. Cataracts are cloudy patches in the lens. As cataracts reduce the amount of light that reaches the retina, your vision may become blurred or cloudy. Eventually, untreated cataracts can cause blindness.

Even in people who are not taking steroids, cataracts become increasingly common with advancing age. Indeed, at least half of all people over the age of 65 years in the UK have some cataract in one or both eyes. But inhaled and oral steroids seem to increase the risk of developing cataracts, in part, Gibson and colleagues remark, by disrupting the normal turnover of cells that keeps the lens clear. In addition, oral steroids can cause glaucoma. Again, this can, if untreated, damage the nerves that carry signals from the retina to the brain, leading to loss of vision.

All adults should have their eyes checked regularly; an eye test can detect diseases such as glaucoma and cataracts before they affect your vision. But regular checks are especially important for people taking oral steroids.

Skin problems and hormonal changes

As mentioned earlier, steroids remove protein from the skin, causing skin thinning, reddish or purple ‘stretch marks’ (striae) in the skin, unusual bruising and wounds that won’t heal. Steroids can also alter the production of hormones by the body, such as suppressing the adrenal gland. The changes to hormone levels can increase the amount of fat in the face and shoulders – known as ‘moon face’ and ‘buffalo hump’ respectively. Women taking oral steroids may find their periods become irregular or stop.

While these side effects are unpleasant, you need to remember that oral steroids could save your life. So, make sure you follow your regular treatment course, monitor your symptoms and tackle any trigger factors. This should reduce the likelihood that you’ll need a course of oral steroids. But if and when you do need oral steroids, you should take them as prescribed. You might want to discuss the risks and benefits with your doctor or asthma nurse before you need to resort to the tablets.

Oral steroids during pregnancy

In general, steroid tablets do not appear to cause birth defects. However, some studies suggest that oral steroids may slightly increase the risk of cleft palate or lips, especially if used during the first trimester. The British Guideline comments that the association between steroid tablets and oral clefts is ‘not definite and even if it is real, the benefit to the mother and the fetus of steroids for treating a life threatening disease justify the use of steroids in pregnancy’.

Some studies suggest that expectant mothers who take steroid tablets are more likely to develop pregnancy-induced hypertension (pre-eclampsia) or premature labour, while the growth of the developing baby may be impaired. In one study, oral steroids reduced the length of pregnancy by, on average, about 15 days. In many cases, however, severe asthma – which can also cause these problems – makes it difficult to tease cause from effect.

The British Guideline notes that pregnant women with severe asthma should use steroid tablets as and when they’re required. Doctors and asthma nurses should fully discuss the reasons why, for most women who need oral steroids, the benefits outweigh the risks. So, if you’re worried about the risk, speak to your doctor or asthma nurse.

Non-steroid anti-inflammatories for asthma

Sodium cromoglicate and nedocromil

Healers in the Middle East have traditionally used the plant khella (Ammi visnaga) – a member of the same botanical family as carrots, celery and parsnip – to treat renal colic (pain in and around the kidneys, often caused by stones). The dried flower stalks made useful toothpicks. Between the 1940s and 1960s, researchers prepared thousands of chemical variations on khella’s active ingredients. Doctors started using one of these – sodium cromoglicate – in 1967 to treat asthma. Sodium cromoglicate (also spelt cromoglycate) and a related drug called nedocromil stabilize mast cells, making these important immune cells less likely to release their stores of inflammatory mediators.

However, as they work on only a single type of cell, sodium cromoglicate and nedocromil are generally less effective than inhaled steroids at controlling asthma. Furthermore, most studies assessing sodium cromoglicate and nedocromil treated younger patients suffering from allergic asthma rather than older adults with intrinsic asthma. Nevertheless, sodium cromoglicate and nedocromil can be valuable treatments for people who cannot or won’t take inhaled steroids or for some cases of exercise-induced asthma.

Leukotriene receptor antagonists

In 1938, scientists found that injecting cobra venom into the lungs of guinea pigs triggers bronchoconstriction. At the time, biologists believed that histamine caused bronchoconstriction. But antihistamines did not block the venom’s effect, suggesting another substance was responsible. In 1979, researchers finally discovered that mast cells released the ‘mystery mediators’ – a group of three related chemicals called leukotrienes.

Since then, biologists have identified several types of leukotriene. One group of these mediators, produced by several inflammatory cells (including eosinophils, basophils and mast cells), is called the cysteinyl leukotrienes and contributes to asthma in several ways: 

  • by increasing the permeability (leakiness) of, and dilating, blood vessels in the lung;
  • by contracting the rings of muscle surrounding the airways, causing bronchoconstriction;
  • by increasing mucus secretion and impairing mucociliary clearance.

Indeed, levels of cysteinyl leukotrienes in the lung rise as asthma becomes more severe.

The link between these mediators and asthma suggests that leukotriene receptor antagonists (such as montelukast and zafirlukast) may be a logical approach to controlling asthmatic inflammation. As a rule of thumb, leukotriene receptor antagonists produce a similar improvement in lung function and bronchial hyper-responsiveness as 400 mcg beclomethasone. However, Nyenhuis and colleagues point out, older adults may produce less cysteinyl leukotrienes than younger people. This may undermine the effectiveness of leukotriene receptor antagonists in older people. So, doctors and nurses tend to add leukotriene receptor antagonists to inhaled corticosteroids. The combination controls inflammation more effectively than either drug used alone.

Certain people seem to benefit particularly from using a leukotriene receptor antagonist:

  • those with marked inflammation in their upper airways (for example, caused by allergic rhinitis or nasal polyps);
  • people with aspirin-sensitive asthma;
  • people who experience marked exercise-induced bronchoconstriction;  
  • people who experience problems using inhalers – montelukast and zafirlukast are tablets.

Nevertheless, doctors can’t predict with certainty who will benefit more from adding a leukotriene receptor antagonist rather than a long-acting beta-agonist to the steroid, so your doctor or nurse will probably offer you a trial with leukotriene receptor antagonist. If symptoms haven’t improved after between four and six weeks’ treatment, it’s worth discussing an alternative. Patients commonly switch from a leukotriene receptor antagonist to a long-acting beta-agonist, or vice versa, if the initial choice does not adequately control symptoms.

Theophylline

Theophylline is a member of a family of chemicals – called xanthenes – that includes caffeine. Indeed, tea contains small amounts of theophylline, the first modern asthma drug. Doctors started treating asthma with theophylline in 1922.

Theophylline, which is a tablet rather than inhaled, relaxes the muscles surrounding the airways and therefore acts as a bronchodilator and asthma therapy. It also loosens bronchial mucus, which unblocks the airways, and inhibits T-lymphocytes, a type of white blood cell involved in allergic asthma. However, theophylline is not an especially potent anti-inflammatory, at least compared to inhaled steroids.

Theophylline works by blocking an enzyme, phosphodiesterase. A complex array of chemical networks carries messages around the inside of our cells. One of phosphodiesterase’s actions is to control the duration of these messages. Different cells use different types of phosphodiesterases. Many inflammatory cells produce a type called phosphodiesterase 4 (PDE4). Theophylline is relatively non-selective, acting on several types of phosphodiesterase. But drugs targeting PDE4 selectively are now used to treat COPD and, in the Far East, asthma.

Unfortunately, a relatively small difference separates the dose of theophylline that alleviates asthma and that causing unacceptable side effects, such as abdominal pain, diarrhoea, headache, rapid heartbeat (tachycardia), palpitations and abnormal heart rhythm (arrhythmias), insomnia, nausea, nervousness, tremor, vomiting and liver disease. Indeed, in some patients the beneficial and ‘toxic’ doses overlap, and older people seem to be particularly sensitive to theophylline’s side effects.

This risk of side effects means that the dose of theophylline needs to be carefully tailored for each person. In many cases, this means regular blood tests to measure levels of the drug, especially as numerous factors can influence the way the body breaks down (metabolizes) theophylline. For example, smoking and heavy alcohol use can lower levels, reducing theophylline’s efficacy. Viral infections, heart failure and liver disease can increase levels, potentially causing side effects.

Numerous drugs that you may take for a concurrent condition can also influence theophylline levels. For instance, cimetidine (used to treat indigestion and stomach ulcers) and the antibiotics ciprofloxacin and erythromycin can reduce theophylline’s breakdown by enzymes in the liver, causing blood levels to rise to toxic concentrations. This means that you must make sure your doctor and pharmacist know you’re taking theophylline when you are prescribed a new drug or buy a medicine over the counter. You should also tell your doctor or pharmacist if you are using herbal medicines or another complementary therapy. Again, some of these can interact with theophylline (or, for that matter, several other drugs used to treat other ailments).

Finally, different brands may release different doses of theophylline. Check that the pharmacist gives you the exact brand that you have been prescribed. You should change brand only after discussing the switch with your doctor or asthma nurse. Because of these problems, doctors tend to use theophylline only when long-acting beta-agonist and leukotriene receptor antagonists have failed to adequately control symptoms.

Omalizumab

Antibodies are exquisitely sensitive, able to pick the proverbial molecular needle from the surrounding cellular haystack. So, researchers can use antibodies to tease apart the pathways that lead to asthma or other diseases: the antibody can switch off a particular protein, for example. This specific action also means that antibodies can treat serious diseases such as cancer, arthritis and other inflammatory diseases, including asthma. You can also set an antibody to catch an antibody. Omalizumab is an antibody that stops IgE from binding to its receptors on mast cells and basophils, so preventing the release of inflammatory mediators triggered by the allergen.

Omalizumab is added to the current asthma treatment of adults and adolescents (12 years and older) who have unstable severe asthma despite optimized standard therapy. You receive shots of omalizumab every two to four weeks. Doctors prescribe omalizumab only when you’ve received full trial of, and have complied with, inhaled high-dose corticosteroids, long-acting beta-agonists and, when appropriate, leukotriene receptor antagonists, theophylline, oral corticosteroids, bronchodilator tablets and smoking cessation. Furthermore, doctors need to confirm that you produce IgE to a perennial allergen, and to establish that this has caused the unstable disease. By ‘unstable’, doctors mean, for example, that you have:    

  • experienced at least two severe exacerbations of asthma that required hospital admission within the previous year;
  • suffered at least three severe exacerbations within the previous year, at least one of which required hospital admission, and a further two that required treatment or monitoring in addition to the usual care, in an A&E department.

Omalizumab’s most common adverse events, NICE notes, are bruising, redness and pain at the injection site. However, omalizumab can also cause severe allergic reactions (anaphylaxis), such as bronchospasm, hypotension (dangerously low blood pressure), syncope (fainting), urticaria (a skin reaction also called ‘hives’) and angioedema (serious swelling) of the throat or tongue. Anaphylaxis can occur after the first dose but has been known to develop after a year’s treatment. Because of the risk of anaphylaxis, omalizumab is administered only under a doctor’s or nurse’s supervision and you’ll be monitored carefully. Patients who don’t show an adequate response after 16 weeks’ treatment don’t receive further courses.

The last resort

As a last resort asthma treatment, specialists may try a short course of potent immunosuppressants, such as methotrexate, ciclosporin (also spelt cyclosporine) and oral gold. These drugs are more commonly used to treat other inflammatory conditions – doctors prescribe methotrexate and oral gold for rheumatoid arthritis, for example, and ciclosporin, among other uses, prevents the body from rejecting transplanted organs. While immunosuppressants decrease a person’s need to take oral steroids long term, they have potentially serious side effects. Fortunately, few patients need to take these drugs of last resort.

Bronchodilators in treating asthma

Bronchodilators relax the ring of muscle surrounding the airways, so the airway opens (dilates). Two types of bronchodilators are used to treat asthma: 

  • Short-acting bronchodilators (‘relievers’) ease breathlessness during asthma attacks and can prevent exercise-induced symptoms. 
  • Long-acting bronchodilators (sometimes called long-acting beta-agonists) are taken in addition to anti-inflammatory drugs if you don’t meet your treatment goals with inhaled steroids alone.

Bronchodilators do not reduce the inflammation that underlies asthma, so you still need to take your anti-inflammatory regularly.

Short-acting bronchodilators

Short-acting bronchodilators (‘relievers’) – such as salbutamol and terbutaline – stimulate beta-receptors in the ring of muscle that surrounds the airways. So, they’re also called beta-agonists or β2-agonists. (They act on one specific subtype – the beta2-receptor.) Several different inhalers can deliver short-acting beta-agonists, including Accuhaler, Clickhaler and Turbohaler, so you should be able to find one that you can use. (We’ll look at the different types of inhaler later in the article.)

The dilation of bronchi produced by short-acting beta-agonists peaks within 15 minutes and lasts between four and six hours. This pattern of activity makes short-acting beta-agonists highly effective at treating asthma attacks as well as preventing exercise-induced exacerbations. Indeed, according to the British Guideline on the Management of Asthma, people who experience asthma symptoms even occasionally should receive a short-acting beta-agonist.

As asthma attacks can be unpredictable, you should make sure that you always carry your bronchodilator with you. However, don’t overrely on the reliever: overuse may disguise the severity of the underlying disease. It’s a bit like papering over the cracks on a wall. Sooner or later the inflammation will break through, possibly triggering a severe attack.

Keeping a note of how much you use short-acting bronchodilators can help you track whether your asthma is well controlled. If it is, you’ll probably have little need to resort to short-acting bronchodilators. On the other hand, using two or more canisters of beta-agonists per month, or taking more than 10–12 puffs per day, may suggest that your asthma is poorly controlled – and you may be at risk of suffering a fatal or near-fatal attack. So, ask your doctor or asthma nurse to review your treatment.

Few people develop short-acting beta-agonists’ side effects – which include tremor, palpitations and muscle cramps – unless they use high doses. If you feel that your short-acting inhaler is producing side effects, you should speak to your asthma nurse or GP. Suffering side effects may suggest that you’re using too much beta-agonist and you need to change the dose of anti-inflammatory.

Long-acting beta2-agonists

As we’ve seen, drugs such as salbutamol dilate bronchi for between four and six hours. Another group of drugs, the long-acting beta2-agonists (LABA), keep the bronchi open for at least 12 hours. So, if you take them twice daily, LABAs keep the airways open throughout the day and night. Despite their effectiveness, you must always take LABAs alongside, and not instead of, anti-inflammatory drugs.

If low-dose inhaled corticosteroids don’t control your symptoms adequately, your doctor or nurse may suggest combination therapy with a LABA. According to the British Guideline, several studies suggest that adding a LABA to low-dose inhaled corticosteroids (200–800 mcg beclometasone dipropionate a day or equivalent) reduces the number of exacerbations, decreases the need for reliever medication, alleviates nocturnal symptoms and improves quality of life more effectively than doubling the steroid dose.

However, not everyone’s symptoms improve adequately after starting a LABA – some respond better to a leukotriene receptor antagonist. Your doctor or asthma nurse may suggest that you try the LABA and see whether your symptoms improve. The length of a trial depends on your main symptom: a trial lasting days or weeks may be enough to assess if nocturnal awakenings improve, while preventing exacerbations or decreasing the use of oral steroids may require weeks or months.

Currently, doctors can chose between two LABAs, formoterol and salmeterol, which work in slightly different ways. In general, drugs act by binding to a relatively small region on the receptor called the active site. This is rather like the keyhole in a large lock. Salmeterol has a ‘head’ that binds to the active site and relaxes the muscle. A long tail flows behind the head, and the end of this tail sticks to another part of the receptor – equivalent to the metal plate surrounding the keyhole. Conventional beta-agonists ‘drift away’ from the active site after binding (one reason why they’re short-acting). However, the tail means that salmeterol’s head continually ‘bounces’ in and out of contact with the active site. This keeps the receptor stimulated and the airways open.

Formoterol acts in a different way. The drug deposits in the fatty membrane that surrounds each cell in the lung. When drug levels in the surrounding tissue fall, formoterol leaches from the membrane and stimulates the receptor. Formoterol works more rapidly than salmeterol, dilating airways within one to three minutes while salmeterol’s maximum effects take around 20 minutes to emerge. This allows some people to use formoterol to alleviate asthma attacks – but talk it over with your GP or asthma nurse first.

Salmeterol mildly inhibits the release of inflammatory mediators from mast cells, but this is not effective enough to replace other anti-inflammatory drugs. So, you should only use LABAs if you are already taking inhaled corticosteroids. Indeed, LABAs are now available combined with steroids in a single inhaler. There’s no difference in efficacy compared to using two inhalers, each containing a single drug. But the single inhaler guarantees that you don’t forget to take the inhaled steroid with the LABA.

Oral beta-agonists

Apart from inhaling bronchodilators, you can take beta-agonists as tablets, capsules or syrups to treat asthma. For example, the body breaks bambuterol down to release the active ingredient, terbutaline. Other oral bronchodilator formulations contain salbutamol. The tablets slowly release the beta-agonist, producing sustained bronchodilatation. You’ll need to take your steroid as regularly as you would with an inhaled LABA.

Short-acting oral formulations – such as terbutaline and salbutamol syrups and immediate-release tablets – offer a ‘reliever’ for people unable to use an inhaler (perhaps because they are physically impaired). However, oral beta-agonists often produce more side effects than their inhaled counterparts.

Antimuscarinics

Two sets of nerves control the muscles that surround the airways. Adrenergic nerves act through beta-receptors to dilate the airways when your body needs more oxygen. However, you don’t need your airways fully open all the time: airways also need to constrict to protect your delicate lungs from damage from cold air, pollution and so on. Branches from another nerve – the vagus – contract airways by releasing a transmitter called acetylcholine that binds to muscarinic receptors. So, if you block (antagonize) acetylcholine, the airways will open. Another group of bronchodilators, the antimuscarinics (such as ipratropium), work in this way. They bind to, but don’t activate, muscarinic receptors. But as they’ve stuck to the receptor, acetylcholine cannot bind – which produces bronchodilatation.

Antimuscarinics (also called anticholinergics) act more slowly than beta-agonists, taking about an hour to reach the maximum bronchodilation. The bronchodilatation lasts for around four to six hours. This slow onset makes antimuscarinics less effective than beta-agonists for exacerbations, which need rapid relief. Indeed, most people with asthma find the bronchodilatation produced by antimuscarinics is less marked than that following beta-agonists. On the other hand, antimuscarinics may be less likely to cause tremor and arrhythmias than beta-agonists and may be useful if people have certain cardiovascular conditions. They are also widely used to treat COPD. Some people with asthma who also develop COPD tend to use high bronchodilator doses, and these people may benefit from using ipratropium relatively early in their course of treatment.

Stepping down asthma treatment

As we’ve seen, your GP or asthma nurse will advise you to increase the dose and number of drugs until your symptoms are well controlled and you’ve reached your treatment goals. However, the symptoms of asthma usually wax and wane – if, for example, exposure to the allergen changes or your fitness level improves. Furthermore, once the underlying inflammation is well controlled, you need lower doses of steroid to keep your asthma at bay.

As a result, the British Guidelines on the Management of Asthma emphasizes the importance of stepping down therapy once asthma has been well controlled for a reasonable time. However, the Guideline notes, the step-down stage is ‘often not implemented’ – in other words, doctors and asthma nurses move patients up the steps but don’t reduce the intensity of treatment as readily. So, some patients are over-treated, leaving them at risk of unnecessary side effects.

The Guideline suggests that adults who have reached their treatment goals and whose asthma has remained stable for at least three months could decrease their dose of inhaled steroid by approximately 25–50 per cent. If you feel your asthma has been stable for three months or more, talk to your doctor or asthma nurse about reducing your dose.

You’ll need to monitor your lung function and symptoms carefully. Overall, you should aim to use the lowest possible dose of inhaled steroid that adequately controls your symptoms. Nevertheless, you may need to be prepared (for instance, using a self-management plan) to step up treatment again if or when symptoms re-emerge.

Inhaler devices

Numerous inhalers can deliver anti-inflammatories and bronchodilators, so you should be able to find a device that suits you and that you can use without making critical mistakes.

Unfortunately several factors may hinder adults’ ability to use inhalers, including poor vision, loss of fine motor control and weak inhalation. In one study, Gibson and co-authors remark, 10–15 per cent of people aged 20 to 40 years made a mistake using their dry powder inhaler (DPI) that affected the amount of drug they inhaled. The proportion making a mistake increased to 40 and 60 per cent among those aged more than 60 and 80 years respectively.

The technique varies between inhalers, so always read the educational materials in the pack carefully and – importantly – ask your doctor or nurse to demonstrate. (You can check the patient information at .) You can also find videos showing how to use some inhalers on the net, including on Asthma UK’s site. Your doctor or nurse should regularly check your inhaler technique: it’s easy to slip into bad habits. If this hasn’t been done for a while, you could ask a healthcare professional to make sure your technique remains adequate.

Certainly, training seems to increase the likelihood you’ll use the inhaler correctly. Brocklebank and colleagues reviewed studies examining how well people used their inhaler. They found that between 23 and 43 per cent of patients got all steps correct when using a metered dose inhaler (MDI; see next section). Between 55 and 57 per cent of those using a spacer with an MDI performed all the steps correctly, compared to 53–59 per cent with a DPI. After training, 63 per cent of those using MDIs and 65 per cent of those using DPIs performed all the steps correctly.

Metered dose inhalers

Metered dose inhalers (MDIs), which reached the market in 1956, remain the most widely used device in asthma treatment and management. Basically, you press on the canister that contains the drug (‘actuation’) while breathing in slowly and steadily. You need to continue to breathe in after the inhaler has delivered the drug payload to make sure the medicine reaches as much of your airways as possible. You should then hold your breath for ten seconds.

While many people can use MDIs, these have certain limitations. For example, some people find timing the inhalation while spraying the medication difficult, although the newer MDIs that use HFA as a propellant are often easier to use than the older CFC-driven devices.

Furthermore, some of propellant remains in the MDI canister after you have used all the drug, so it can also be difficult to know when you need to replace your inhaler. You could note when you should replace your inhaler in your diary. (This is especially important with steroids. After all, you’ll soon know if the bronchodilator doesn’t improve your breathlessness during an attack.) Check the insert for the number of doses, then divide by the number of puffs each day; or ask your GP, asthma nurse or pharmacist for advice on when you should ask for a repeat prescription.

Only between 10 and 20 per cent of the dose of drug inhaled from an MDI reaches the lower airways. The rest deposits in the mouth and throat and is swallowed. The drug moves from the gut into blood vessels supplying the liver, which then breaks down most of the steroid or beta-agonist that you absorb in this way. Only a tiny amount of the drug you swallow reaches the general circulation. Nevertheless, even this small amount can cause side effects, especially if you take large doses.

Breath-actuated inhalers and dry powder inhalers

Most people can learn to use MDIs, but those who have trouble inhaling from an MDI may find alternative devices easier to use. Often, these newer inhalers include a counter or let you see when you’re reaching the end of the drug supply.

Breath-actuated inhalers (such as the Autohaler and the Easibreathe) do away with the need to co-ordinate actuation and inhalation. The valve on the inhaler opens only when you inhale. But you still need to breathe in slowly and deeply, as well as hold your breath after the device delivers the drug.

Dry powder inhalers (such as the Turbohaler, Diskhaler, Accuhaler and Clickhaler) don’t use a propellant. The force of the airflow as you inhale releases the powered drug, so you don’t need to co-ordinate actuation and inspiration. However, you need to be able to generate an adequate airflow when you breathe in. In many cases, you may need to generate more inspiratory force than with an MDI. And some (but not all) DPIs need manual dexterity to use, making them less suitable for some elderly people and other adults with weaknesses due to nerve or muscle problems, or suffering from arthritis and other physical impairments.

Spacers

Spacers increase the amount of drug that reaches the airways, make MDIs easier to use, and so improve effectiveness and reduce the risk of side effects. For example:

  • Large-volume spacers (e.g. Volumatic and Aerochamber) roughly double the amount of steroid that reaches the lower airway compared to an MDI used alone. Indeed, using a spacer may mean that you can use a lower total dose of steroid. 
  • Spacers reduce the amount of steroid deposited in the back of the mouth and throat, which reduces the risk of dysphonia and oral candidiasis.
  • Spacers can help reduce the need to co-ordinate actuation (pressing the inhaler) and inhalation when using an MDI.

You place the MDI in one end of the spacer and breathe through the mouthpiece. A one-way valve closes when you exhale. The distance results in a plume of fine particles and makes co-ordinating actuation and inhalation easier. You should clean the spacer monthly in detergent and ask your doctor or asthma nurse for a replacement every year.

Nebulizers

Nebulizers force oxygen or compressed air through a small hole. This creates a change in pressure that draws the drug solution into the airstream. The airstream strikes a small sphere, forming an aerosol of small particles carrying the drug, which you inhale using a mask or mouthpiece. Larger droplets hit the wall and fall back into the solution.

Nebulizers effectively deliver high doses of bronchodilator during an acute asthma attack. Some people keep nebulizers at home if, for example, they suffer regular serious exacerbations. But you still need to take your anti-inflammatory regularly, and don’t delay seeking urgent medical advice during severe acute asthma attacks.

Nebulizers can also deliver steroids. However, properly used DPIs and MDIs used with a spacer deliver a greater proportion of the drug into the airway than nebulizers. As a result, nebulizers tend to be used to deliver steroids only if people can’t use conventional inhalers.

Anne’s asthma – and her arthritis

Anne – a 68-year-old retired teacher – finds her asthma is getting worse; she’s waking up on more nights and feels breathless after walking her dog. But she’s more worried about the pain in her hands. Over the last year or so, osteoarthritis made it increasingly difficult for her to knit and write. She’s even beginning to have trouble turning the key in the door. Anne’s asthma isn’t aspirin-sensitive and she’s taking NSAIDs to alleviate her discomfort. However, she sometimes has trouble pushing the pill out from the packet.

One afternoon, Anne suffers a severe asthma attack. After a night in hospital, she and the asthma nurse try to uncover why the attack occurred – Anne’s asthma is usually well controlled. Anne admits that she’s experienced problems actuating her MDI: she just can’t seem to push hard enough. In addition, while her self-management plan suggests taking prednisolone tablets when her peak flow falls below 50 per cent of the predicted level, she cannot open the bottle’s childproof cap. The asthma nurse switches to a DPI and the pharmacist provides both her asthma and arthritis medication in easy-to-open bottles.

Physical problems using inhalers

Some people with arthritis in their hands or difficulty holding certain inhalers find that devices called the Haleraid or Turboaid help.

  • The Haleraid fits on to certain MDIs and allows you to apply pressure with the palm of your hand to activate the canister.
  • The Turboaid fits on to the breath-actuated Turbohalers.

To top of asthma treatment for adults

Ask your doctor, pharmacist or asthma nurse for further advice about your asthma treatment.