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22.12 — Steroids and Anti-Inflammatories
If you take prednisolone daily for more than about three weeks and then stop it suddenly, your body cannot produce its own cortisol, and you can go into circulatory collapse.
Not from the illness. From the stopping.
That single fact is the most important thing in this chapter, and a large number of people taking steroids have never had it explained to them.
What a steroid actually is
"Steroid" describes a chemical shape, not a function — a four-ring carbon skeleton (Chapter 12.1).
Which is why the word covers three completely different groups of drugs, and why the confusion between them is so persistent:
Corticosteroids — anti-inflammatory drugs, the subject of this chapter.
Anabolic steroids — testosterone derivatives that build muscle.
Sex steroids — oestrogen, progesterone, testosterone (Chapter 15.1).
When a doctor says steroid, they mean the first. When a newspaper says steroid, they usually mean the second. They are not the same drugs and they do not have the same effects.
How corticosteroids work
The body makes cortisol in the adrenal cortex, released in a daily rhythm peaking in the early morning (Chapter 12.4).
Cortisol is a stress hormone in the literal sense: it prepares the body to survive a serious challenge — raising glucose, maintaining blood pressure, and suppressing inflammation so the response does not run away.
Corticosteroid drugs are synthetic versions, at doses far above what the body produces.
The mechanism is genomic, and this explains almost everything about how they behave:
The drug crosses the cell membrane easily, because it is fat-soluble.
It binds a receptor inside the cell.
The complex travels into the nucleus and changes which genes are transcribed (Chapter 2.4) — switching on anti-inflammatory proteins and switching off the genes for inflammatory cytokines.
New proteins must then be made, which takes hours.
So: steroids do not work immediately. This is why they are started early in an asthma attack rather than relied on to relieve it, and why an anaphylaxis reaction is treated with adrenaline first and steroids second (Chapter 23.5).
And it is why the effect persists for a while after the drug is stopped — the changed gene expression takes time to revert.
The common ones
| Drug | Relative strength | Typical use |
|---|---|---|
| Hydrocortisone | 1 | Replacement, emergencies |
| Prednisolone | 4 | Most oral courses |
| Methylprednisolone | 5 | Injection, high dose |
| Dexamethasone | 25 | Brain swelling, croup, COVID |
| Fludrocortisone | Salt-retaining | Adrenal replacement |
Hydrocortisone is essentially identical to cortisol, which is why it is used for replacement.
Prednisolone is the workhorse — 5 mg of prednisolone is roughly equivalent to 20 mg of hydrocortisone.
Dexamethasone is powerful, long-acting and has almost no salt-retaining effect, which is why it is chosen where fluid retention would be a problem.
And dexamethasone earned a place in history in 2020, when the RECOVERY trial found it reduced deaths in severely ill COVID patients requiring oxygen — a cheap, old, widely available drug that turned out to be the first treatment shown to save lives in that illness.
What they are used for
Almost anything driven by inflammation or immune activity:
Asthma and COPD attacks (Chapter 21.1). Autoimmune and rheumatic disease (Chapter 21.5). Inflammatory bowel disease. Allergic reactions and severe skin conditions. Preventing transplant rejection. Some cancers, both as treatment and for symptoms. Brain swelling around a tumour. Adrenal insufficiency, as replacement (Chapter 21.4).
And two time-critical uses worth knowing specifically:
Giant cell arteritis — high-dose steroids the same day, before biopsy, because delay costs sight (Chapter 20.1).
Antenatal steroids — given to a mother in preterm labour, they mature the baby's lungs by accelerating surfactant production and substantially reduce neonatal deaths (Chapter 15.7). One of the highest-impact interventions in obstetrics.
The side effects
And they are extensive, because cortisol receptors are everywhere.
Short courses, under about three weeks:
Increased appetite, insomnia, mood changes — from mild elation to irritability and, occasionally, frank psychosis at high doses. Raised blood glucose. Fluid retention. Indigestion.
Long-term use, and this is where the real burden is:
Weight gain in a characteristic pattern — central, with a rounded face and a fat pad between the shoulders, and thinning of the arms and legs (Chapter 21.4).
Skin thinning, easy bruising, poor wound healing, stretch marks.
Osteoporosis, and it happens fast — most bone loss occurs in the first 3 to 6 months, which is why bone protection is started at the same time as the steroid and not later (Chapter 21.6).
Muscle weakness, particularly the thigh muscles, showing up as difficulty rising from a chair.
Diabetes, or worsening of existing diabetes.
High blood pressure.
Cataracts and glaucoma.
Increased infection risk, and blunted signs of infection, so someone on steroids with a serious infection may not develop a fever. A lower threshold for seeking help is warranted.
Avascular necrosis of the hip — bone death from disrupted blood supply, uncommon and serious.
Stomach ulcers, particularly combined with NSAIDs, which is why gastric protection is added.
Growth suppression in children.
And adrenal suppression, which is the one that has its own section below.
Adrenal suppression
The mechanism is simple feedback (Chapter 12.2).
The pituitary releases ACTH, which tells the adrenal glands to make cortisol. Cortisol feeds back and suppresses ACTH.
Give steroid from outside, and the pituitary sees plenty of cortisol. It stops sending ACTH. The adrenal glands, unstimulated, shrink and become unable to respond.
Stop the drug suddenly and there is nothing — the external supply is gone and the internal one cannot restart for weeks to months.
The result is adrenal crisis: severe weakness, vomiting, abdominal pain, low blood pressure, confusion, collapse. It can be fatal, and it is entirely preventable.
Which produces three rules:
1. Never stop long-term steroids abruptly. Taper.
Courses under about three weeks can usually be stopped directly. Longer courses, repeated courses, or high doses need a gradual reduction, sometimes over months.
2. Increase the dose during illness — the sick day rules.
During fever or significant illness, the dose is typically doubled, because the body would normally produce far more cortisol under stress and cannot.
For vomiting, diarrhoea, major injury or surgery, injected hydrocortisone is needed — because a tablet that comes back up has done nothing.
3. Carry a steroid card or alert bracelet.
So that in an emergency, when you may not be able to explain, the people treating you know.
And this applies to inhaled and topical steroids at high doses too, not only tablets — high-dose inhaled steroids and potent topical steroids over large areas can suppress the adrenals.
Reducing the harm
Lowest effective dose, shortest duration.
Take it in the morning, matching the natural rhythm and reducing suppression and insomnia.
Steroid-sparing agents — methotrexate, azathioprine and biologics exist largely so that people do not have to stay on long-term steroids (Chapter 21.5).
Bone protection — calcium, vitamin D, and a bisphosphonate for anyone expected to be on significant doses for months.
Gastric protection where there is added risk.
Monitoring — blood pressure, glucose, weight, bone density, eyes.
Vaccination before starting where possible, and live vaccines avoided while immunosuppressed.
And use a targeted route where you can: inhaled for asthma, topical for skin, injected into a joint, enteric-coated budesonide for gut disease. The whole point of these formulations is high local concentration with minimal systemic exposure.
Topical steroids
And the practical problem here is the opposite of what people expect: under-use, not over-use.
Fear of steroids leads to applying too little, too briefly, so the eczema never clears, so the cream gets applied on and off for months — which delivers more total steroid than a proper short course would have (Chapter 21.7).
Potency is matched to the site: mild on the face and in skin folds, where the skin is thin and absorbs more; stronger on the body; strongest on palms and soles.
The fingertip unit — the amount from the fingertip to the first crease, covering about two adult palms — gives a way to apply enough.
Used for a defined period until the skin is clear, then stopped or stepped down.
Emollients continue regardless, because they are treating the barrier problem underneath.
NSAIDs — the other anti-inflammatories
Covered in detail in Chapter 22.5, and the comparison is worth making explicitly.
| Steroids | NSAIDs | |
|---|---|---|
| Acts on | Gene expression | COX enzymes |
| Speed | Hours | Under an hour |
| Strength | Very strong | Moderate |
| Main long-term risk | Bone, glucose, adrenal | Stomach, kidney, heart |
| Stopping | Must taper | Stop freely |
And they should not be combined casually, because the ulcer risk together is considerably higher than either alone.
Colchicine — for gout, working by disrupting the microtubules that inflammatory cells use to move. Effective, and the dose-limiting side effect is diarrhoea. It is also being used at low dose for cardiovascular inflammation, where trials have shown benefit — an old plant-derived drug finding a new role.
Biologic anti-inflammatories — targeting one cytokine rather than the whole response (Chapter 21.5). Far more selective, and correspondingly more specific in their infection risks.
Anabolic steroids
Included briefly because the confusion causes real harm.
Testosterone derivatives used to build muscle. Legitimate medical uses exist — testosterone replacement in genuine deficiency, some anaemias, and muscle wasting in certain conditions.
Non-medical use at high doses causes: reduced natural testosterone production with testicular shrinkage and infertility; breast tissue growth in men, because excess testosterone is converted to oestrogen; acne; hair loss; liver damage with oral forms; raised LDL and lowered HDL cholesterol; thickened heart muscle; and mood changes including aggression and depression, particularly on withdrawal.
Much of this is reversible; some is not.
And this is a different category of drug entirely from the corticosteroids in the rest of this chapter — different molecules, different receptors, different effects.
The summary worth carrying
Steroids are among the most useful drugs in medicine, and they save lives.
They take hours to work, because they act on gene expression.
The harm is mostly a function of dose and duration.
And the single rule that matters most: long-term steroids are never stopped suddenly, doses are increased during illness, and everyone taking them should carry a card.
What the next page fixes
Chapter 22.13 covers side effects and interactions — the combinations that cause the most harm, and how to spot when a new symptom is actually a drug.