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Record your medication and uric acid levels in brite, get reminded to take your daily tablet and arrive at your appointment with a clear overview. Free of charge.
Never stop an ongoing uric-acid-lowering therapy (e.g. Allopurinol) because of a gout attack — this can make the levels fluctuate and trigger further attacks. Conversely, it should also not be started fresh in the middle of an acute attack.
Gout is a metabolic disease in which too much uric acid builds up in the body. If the uric acid in the blood permanently exceeds its solubility limit, it forms fine, needle-shaped crystals that deposit mainly in joints and tendons. If the immune system suddenly reacts to these crystals, the joint becomes severely inflamed — this is the classic gout attack.
Uric acid is produced during the breakdown of purines. Purines are building blocks that arise partly in the body itself (during the constant turnover of cells) and are partly taken in through food — especially through meat, offal, certain fish and alcohol. Normally the kidneys excrete the excess uric acid with the urine. If this balance is disturbed — because too much uric acid is produced or too little is excreted — the level in the blood rises. This hyperuricaemia is the basic prerequisite for gout.
Important to understand: a raised uric acid level alone is not yet gout. Many people have raised levels for years without ever having an attack. Only when crystals form and trigger inflammation is it called gout. Conversely, the measured uric acid level can even appear normal during an acute attack, because the uric acid is just then "bound" in the crystals. Gout is therefore more than just a lab value — it is a genuine inflammatory joint disease.
Untreated, it rarely stops at a single attack. Over the years the attacks can become more frequent, affect several joints and eventually progress to chronic gout, in which visible uric acid nodules (tophi) form and joints are permanently damaged. The good news: this can almost always be prevented by consistently lowering uric acid.
Uric acid is measured in the blood in milligrams per decilitre (mg/dl) or in micromoles per litre (µmol/l). The decisive threshold is the point at which uric acid no longer stays fully in solution: it lies at about 6.8 mg/dl (around 400 µmol/l). Above this value crystals can form — which is why it is the reference point for the entire treatment.
| Range | Uric acid (mg/dl) | Meaning |
|---|---|---|
| Normal range (men) | about 3.5–7.0 | Usually unremarkable |
| Normal range (women) | about 2.5–6.0 | Lower before the menopause |
| Crystallisation threshold | from 6.8 | Crystals can form from here on |
| Treatment target in gout | below 6.0 | Crystals slowly dissolve |
| Target in severe gout / tophi | below 5.0 | Faster dissolution of the deposits |
The most important value you should remember is the target value below 6.0 mg/dl. It is the actual goal of any long-term therapy — not freedom from symptoms alone. Because even when no attack is currently occurring, more crystals can continue to deposit at higher values. In pronounced gout with visible nodules, an even lower target of below 5.0 mg/dl is aimed for, so that the deposits dissolve faster.
This is why gout is one of the few diseases in which a single lab value defines the treatment goal so clearly. Regular checks of uric acid show whether the medication dose is right — similar to blood pressure or long-term blood sugar.
The most striking feature of gout is the acute attack. It typically begins suddenly, often at night or in the early morning hours, and reaches its peak within a few hours. The affected joint is:
In more than half of cases the first attack strikes the base joint of the big toe — this classic picture is called podagra. Why there of all places? The toe is the coolest point of the body and the furthest from the trunk, and uric acid crystallises out more easily in a cooler environment. The mechanical load when walking also favours deposition. However, the ankle, knee, fingers, wrist or elbow joint can be affected just as well.
A single attack subsides on its own after a few days up to about two weeks, even without treatment. This misleads many into overlooking the fact that the actual cause — the high uric acid — persists. Between attacks the joint is often completely symptom-free (the so-called intercritical interval). Without long-term therapy, however, the next attack usually follows sooner or later, and the attack-free phases become shorter over time.
In long-standing, untreated gout, tophi can form: visible, usually painless nodules of uric acid crystals, for example on the ears, fingers, elbows or the Achilles tendon. They are a sign that a great deal of uric acid has been deposited in the body, and a clear reason for consistent lowering. General joint pain has many causes — but the sudden, deeply red single attack is typical of gout.
The basis of any gout is a permanently raised uric acid level. Whether it develops depends on two mechanisms: the body produces too much uric acid, or the kidneys excrete too little. In most people, reduced excretion predominates. Both routes are influenced by predisposition and lifestyle.¹
An attack is often set off by a concrete trigger: a lavish meal with lots of meat, an evening with plenty of alcohol, a fasting cure or heavy sweating with fluid deficiency, but also infections, operations or — importantly — the abrupt starting or changing of a uric-acid-lowering therapy. This is why such a therapy is never started fresh in the middle of an attack and is always dosed up slowly at the start.
The diagnosis rests on the typical symptom picture combined with uric acid and, where possible, direct detection of crystals.¹,²
The most important distinction is from a bacterial joint infection (septic arthritis): it too shows a red, swollen, painful joint, but it is an emergency. With high fever and a severe feeling of illness, this cause must always be ruled out — more on this in the warning below. So-called pseudogout can also resemble it, in which other crystals (calcium pyrophosphate) trigger the inflammation; it can only be reliably distinguished via the joint fluid.
In an acute gout attack it is about one thing: stopping the inflammation and the pain as quickly as possible. The earlier treatment is given, the better — ideally within the first few hours. Lowering uric acid plays no role at this point; it comes only afterwards.¹
Alongside medication, simple measures help: resting and elevating the joint, cooling it carefully and drinking plenty. For the drug treatment there are three well-established options, chosen according to any accompanying conditions.
The acute attack treats the symptom — the long-term therapy treats the cause. Its aim is to lower uric acid enough that no new crystals form and existing deposits dissolve over time. The goal is clear: below 6.0 mg/dl, and in pronounced gout with tophi below 5.0 mg/dl.¹,³
When permanent drug lowering makes sense is decided by the medical practice — as a rule with repeated attacks, with visible tophi, with gout damage on the X-ray, or with very high levels and accompanying kidney disease. Important: the therapy is designed for the long term. It only works as long as it is taken — if it is stopped, uric acid rises again and the attacks return.
A common misunderstanding: many people stop Allopurinol as soon as they have gone a few months without an attack — in the belief that they are "cured". But this is exactly what often leads to a relapse. The good state is the result of the treatment, not its end. Changes to the therapy always belong in medical hands. More on dealing with several preparations: drug interactions.
brite reminds you of every daily tablet and documents your uric acid levels seamlessly — ready for your next appointment with the doctor.
Diet can noticeably influence uric acid — sometimes enough on its own with slightly raised levels, and as a sensible complement to medication in pronounced gout. Important for perspective: diet alone usually lowers uric acid by only about 1 mg/dl. Anyone with a markedly excessive value will rarely reach the target with it alone — diet does not replace long-term therapy, it supports it.²,³
Purines are the raw material from which uric acid is formed. It is worth knowing purine-rich foods and placing them in realistic portion sizes — not every figure in tables refers to the same amount.
| Food (realistic portion) | Purine content | Recommendation |
|---|---|---|
| Offal (liver, kidney), 100 g | Very high | Avoid |
| Sardines, anchovies, herring, 100 g | Very high | Avoid |
| Beer, including alcohol-free, 0.5 l | High (plus alcohol effect) | Restrict strongly |
| Red meat/sausage, 150 g | High | Rarely, small portions |
| Seafood, 100 g | High | Rarely |
| Pulses, 100 g cooked | Medium | Okay in moderation |
| Vegetables (including spinach, mushrooms), portion | Low to medium | Harmless |
| Dairy products (low-fat), portion | Very low | Beneficial, tend to lower |
| Eggs, coffee, water | Practically purine-free | Harmless |
Two points surprise many people: firstly, plant-based purine-rich foods such as spinach, mushrooms or pulses are considerably less problematic than animal ones — they do not have to be strictly avoided. Secondly, fructose plays a big role: sugar-sweetened soft drinks and fruit juices drive uric acid up and should be strongly restricted. What tends to lower the levels, on the other hand, are low-fat dairy products, coffee and above all an adequate amount to drink.
Gout typically runs in phases: the first attack is often followed by symptom-free intervals, then — without treatment — more frequent attacks, and finally the chronic form with tophi and joint damage. The decisive lever against this course is the permanent lowering of uric acid. If the target value is reached and held, the process can practically be stopped and in part reversed.
Gout is not treated in days but over years — the acute attack is only the tip. The long-term therapy only works if it runs reliably and uric acid stays in view. That is exactly what brite supports.
Record in brite where your target value lies and how your measurements develop — ideal for seeing whether the therapy is taking effect.
