Gout is one of the most painful forms of rheumatism. It affects the joints and soft tissues, usually the basic joint of the big toe first.
Gout has been known since ancient times as a disease of abundance affecting those who indulge daily wine and meat. The way of life plays a certain role in it. Being overweight, sedentary and eating meat weighing more than 50 kilos per person per year all contribute to the fact that gout is still a widespread rheumatic disease in United States today.
80% of people suffering from gout are male. Around 3% of men reaching retirement age are affected. Gout is the most common inflammatory joint disease in men over the age of 40. The first attack of gout occurs on average in the middle of a man's life (between 40 and 45 years of age).
Women, on the other hand, are protected by female sex hormones until the menopause. In women, the first attack of gout occurs on average between the ages of 55 and 60.
Typical triggers for a nighttime gout attack are heavy alcohol consumption the night before and a large meal of meat, fish and seafood. It's the drop that makes the vase overflow - but the vase was already full a long time ago: Gout can progress over a long period of time. It is caused by an excessive concentration of uric acid in the blood: hyperuricemia.
The role of heredity in the disease was identified as early as the middle ages. Most people with gout have a congenital predisposition to a reduced ability of the kidneys to eliminate uric acid, which inevitably leads to an increase in uric acid levels (hyperuricemia).
Lifestyle also contributes to increased uric acid levels. Many people suffering from gout have a diet rich in meat, which leads to a high intake of purines and hinders the elimination of uric acid by the kidneys through excessive alcohol consumption.
Increased uric acid levels (hyperuricemia)
Purines play a central role in increasing uric acid levels (hyperuricemia). Purines are components of deoxyribonucleic acid (DNA), the genetic material enclosed in cell nuclei. Purines are partly supplied by food and partly synthesized by the body.
They are converted into uric acid through metabolism. If their concentration in the blood exceeds a certain level, the uric acid begins to crystallize and is deposited in the joints, the bursae and the connective tissue near the joints. Sharp-edged uric acid crystals irritate tissues, cause inflammation and severe pain.
The metabolic syndrome
Primary gout is caused by increased uric acid levels due to hereditary factors and diet. It is called secondary gout when it follows other diseases.
75% of patients with gout have a metabolic syndrome, which is the "fatal quartet" of obesity, hypertension, abnormal blood lipid levels and disorders of sugar metabolism. The metabolic syndrome is explained by various genetic mutations, but is very closely related to lifestyle. A poor diet and a sedentary lifestyle increase the risks. Patients can combat these risks by losing weight, adopting a healthy diet and improving their physical fitness.
Kidney damage caused by certain drugs such as laxatives or toxic substances such as lead can also cause gout. The kidneys' ability to eliminate uric acid is reduced. The old warning that wine causes gout may be linked to lead, which was commonly used to sweeten wine until the second half of the 18th century.
Gout is caused by high levels of uric acid in the blood: hyperuricemia. A high uric acid level is defined as more than 6 mg/dl of uric acid in the blood. Above this value, uric acid can be deposited in a crystalline form in the joints and soft tissues. This occurs in about 30% of men. Above 9 mg/dl a gout attack is inevitable.
The gout attack
A gout attack is an inflammation of a terribly painful joint that often strikes during sleep. It is most often the base joint of the big toe that is affected. The joint and the skin around it are swollen, very red and extremely sensitive to pressure and touch. The inflammation can extend to the tendon sheaths and bursae.
The most common causes of a gout attack are related to diet: a large meat-based dinner, excessive alcohol consumption, a restrictive diet or fasting.
In hospitalized patients, a gout attack can occur following the administration of diuretics. Diuretics may be necessary to lower blood pressure or improve circulation. They increase urinary secretion without increasing uric acid elimination.
When the disease becomes chronic
In the case of high uric acid levels, the pain associated with the disease occurs in flare-ups at increasingly shorter intervals. Without treatment, the disease becomes chronic and affects several joints at the same time. Gouty tophus, which is unsightly nodules, can also develop. These are benign deposits of uric acid crystals in a rounded shape that form in the coldest parts of the body, such as the earlobes, elbows, feet and fingers.
In the case of chronic gout, uric acid deposits can be found in the kidneys. The resulting kidney stones can irritate the pelvis and cause colic.
In addition, chronic gout can develop into osteoarthritis (known as secondary osteoarthritis).
The preliminary stage of gout can be easily established. A blood test can measure an increase in uric acid levels (hyperuricemia).
The doctor diagnoses a gout attack after a medical examination and from the patient's history. The symptoms of gout are clear: swelling, redness, severe pain and severely limited functional capacity of the affected joint.
Gout can be confused with pseudogout (chondrocalcinosis). To differentiate between the two diseases (differential diagnosis), the affected joint can be punctured and the synovial fluid can be analyzed in the laboratory. Gout manifests itself as uric acid crystals, pseudogout as calcium pyrophosphate crystals. The two types of crystals can be clearly distinguished under the microscope.
With chronic gout, the damage to the affected joints is visible on X-rays.
Anti-inflammatory drugs for gout attacks
The most effective method of stopping the violent pain caused by a gout attack is to act on the inflammation of the affected joint. There are anti-inflammatory drugs that are applied locally, ingested or injected directly into the joint (intra-articular injection or infiltration).
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Non-steroidal anti-inflammatory drugs (NSAIDs) based on diclofenac. They have an anti-inflammatory and analgesic effect.
Cortisone medications are suitable for short-term treatment. Cortisone can be injected directly into the joint in the event of a gout attack.
Colchicine was the classic treatment for gout. It is a natural medicine with toxic effects made from the autumn colchicum (Colchicum autumnale). Colchicine limits the proliferation of inflammatory cells, thus shortening the gout attack. However, treatment with colchicine requires a great deal of experience. The drug has significant side effects, even when used correctly.
At the worst moment of a gout attack (when the patient cannot tolerate the slightest touch of the inflamed area) pain ointments are of little help.
Long-term drug therapy for gout
Two groups of drugs are available for long-term treatment. They reduce excessive uric acid levels to the lower limit of the norm.
Allopurinol or febuxostat drugs are involved in the metabolism of purines. They inhibit the breakdown of purine into uric acid and thus reduce the level of uric acid. Uricostats are generally well tolerated but may induce side effects.
Medicines containing the active ingredients benzbromarone, probenecid or hesinurad also help to lower uric acid levels. They increase the kidneys' ability to evacuate uric acid in the urine. Losartan, an anti-hypertensive, also has the same effects. Uricosurics have the disadvantage of straining the kidneys. This is why it is important to drink plenty of water to help with elimination. Some uricosuric drugs should not be prescribed for kidney damage and kidney stones.
Reducing uric acid levels with medication is a long-term treatment. If it is stopped, the symptoms of gout may reappear. In consultation with the doctor, it may be attempted to discontinue the drug carefully after five years.
Alternative medicine and grandmother's remedies
Traditional herbal medicine can also help in the treatment of gout. Currently, herbal infusions with diuretic, purifying and anti-inflammatory effects are recommended, such as horsetail, angelica, nettle, goldenrod, chamomile, yarrow and licorice.
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Cataplasms and wraps
Cataplasms and wraps can complement a treatment for gout - cold in the case of a gout attack, warm in the case of chronic gout.
However, the effect of cold poultices is double-edged: while cold reduces inflammation and pain, it also promotes the crystallization of uric acid.
Conversely, warm poultices for chronic gout help to remove crystallised uric acid deposits from the joint. But heat can also increase inflammation.
Patients therefore have no choice but to experience hot and cold wraps. They will quickly see which ones give the best results. The cooling effect can be reinforced with poultices made of cottage cheese, medicated clay or vinegar.
Feet are usually a little colder than the rest of the body, especially in cases of limited physical activity. This explains why many gout attacks affect the basic joint of the big toe. To prevent a gout attack, you can wear thick socks and warm shoes in winter, and regularly take a foot bath at a maximum temperature of 37°C to stimulate circulation.
Another grandmother's remedy: consume natron (sodium hydrogen carbonate or baking soda) regularly. Natron changes the acidity of the urine from the normal acidic zone (pH between 5 and 6) to the basic zone (pH > 7). Due to the reduction of its acidity, the urine assimilates and eliminates more uric acid. The acidity of the urine can be checked with test strips available in drugstores.
Predisposition to gout is congenital. Too much uric acid can be hereditary. Do you have parents who you know have high uric acid levels (hyperuricemia)? Do any of your parents, grandparents, aunts or uncles have gout? If so, you need to take preventative measures: talk to your doctor and ask to have your uric acid levels measured.
If the blood test shows a particularly high uric acid level, we advise you to reduce your personal risk of contracting the disease by changing your eating habits. The dietary rules are the same as those recommended after a (first) attack of gout.
Dietary rules to prevent new gout attacks
The following advice is intended to prevent the occurrence of new attacks after an attack of gout, to prevent chronicity of the disease and to support the medical treatment of gout. The dietary rules set out below are based on the findings of the latest observational studies involving several thousand patients. As a result of these studies, the diet usually recommended in cases of gout has been rethought. Today, gout is not considered to be the only food-related health problem for many patients. In addition, foods that are difficult to remove from the diet are no longer strictly prohibited.
Less meat, fish and offal
Large portions of meat provide the body with considerable amounts of purines, which increase the level of uric acid. Reduce your consumption of meat, cold cuts, meat broth, aspic, fish and seafood. People with gout should not eat offal or livers, whether pork, beef or veal. In general, they should eat small portions of meat (100 g) and give preference to meats that are low in purines.
More dairy products
Consumption of dairy products reduces uric acid levels. Cow, sheep and goat's milk, which is produced by glandular secretion, does not contain cell nuclei that could contain purines. Butter, cream, kefir, faisselle, plain yoghurt and cottage cheese are also free of purines. On the other hand, purines are present in varying amounts in cheeses. Dairy substitutes based on almonds, oats, rice or soya contain purines in varying amounts. Tofu is low in purines.
People with gout should supplement their meals with generous portions of vegetables and salad. Vegetable foods are rich in healthy nutrients such as protein, vitamins, minerals and dietary fibre. Recent studies have shown that people with gout benefit from foods of plant origin that are traditionally avoided in the diet, such as legumes (peas, beans, lentils), mushrooms, spinach and cabbage. The nutritional qualities of plant-based foods prevailed.
Beware of sugar!
Eating fruit sugar (fructose) increases the level of uric acid. People with gout should not drink soft drinks or lemonades that are sweetened with fructose or sucrose. The same applies to fruit juices such as apple juice, orange juice, fruit smoothies and multivitamin juices. Fruit also contains fructose, but also valuable nutrients. So it is important to find the right balance. Two servings of fruit (300 g) a day are more than enough. Red fruits are particularly recommended. Avoid dried fruit, especially "sugar bombs" such as raisins and figs.
Excessive alcohol consumption increases the production of uric acid and slows down its elimination. Patients with gout and those predisposed to gout are advised to eliminate beer and spirits from their diet and to limit their consumption of wine. Two glasses of beer a day increase the risk of gout by 200% because of the purine in the yeast used to activate the fermentation process (including in alcohol-free beers).
Wine consumption is less harmful. A daily consumption of two glasses of wine for men and one glass of wine for women does not significantly increase the risk of gout.
Drink two to three liters of water or herbal tea every day. All cells in the body need enough fluid to function properly, especially the cells in the kidneys, which need it to filter uric acid from the blood and eliminate it in the urine. Elimination is stimulated by diuretic herbal infusions. Coffee lovers will be happy to know that their favorite drink has a positive effect on gout. According to international studies, coffee (normal and decaffeinated), unlike tea, lowers uric acid levels.
Overweight patients with gout should begin a gradual reduction in weight. However, those who are predisposed should not impose too restrictive a diet. Fasting and drastic diets destroy many muscle cells within a few days, releasing huge quantities of cell nuclei and thus purines. The metabolism does not distinguish between the purines provided by food and the purines resulting from the destruction of cells. An excess of purines increases the level of uric acid and can trigger a gout attack.
The basic joint of the big toe is most often affected by a gout attack.
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