What is gout?
Gout is a painful rheumatic inflammation as a result of crystallized uric acid in a joint. In the warm blood uric acid dissolves easily, but at too high a concentration thereof may precipitate the acid in the form of small needle-shaped crystals. In a relatively cold environment, such as hands and feet, this is done most easily. In 60% of the cases, the base joint of the big toe is affected.
Gout symptoms
The crystallization of uric acid in the joint leads to an often rapidly emerging severe inflammatory reaction with redness, swelling, pain, heat and disability. Patients are at night suddenly woke up in pain and often can barely walk. In addition in the toes gout may also occur at other places, for example, in the ankle, knee, finger or the auricle. In someone with gout are often seen tophi. These are uric acid crystals that are visible through the skin. This example, on the hands, feet, elbows and ears are found.
Epidemiology
Gout occurs worldwide but has a large variation in prevalence. This is due to different regional genetic, dietary and environmental factors. The condition is more common in men. Estrogens namely, have a protective effect on the development of gout. This gout is rare in women before menopause.
In the age group 30 to 60 years is the most common gout average. In men with a genetic predisposition or meet a number of risk factors, the condition can occur earlier. In women, however, the peak is reached between the 60th and 80th year of life.
The higher prevalence in the elderly is caused by the higher incidence of congestive heart failure and hypertension, and the consequent use of diuretics and cardio aspirin in this age group.
Gout also has a difference in preventing related to ethnic factors. In addition to possible genetic factors contribute to the difference in diet to these differences. In the US, for gout at 3:11 per 1,000 people in African Americans and 1.82 per 1,000 Caucasians. In Africa itself gout occurs very rarely.
In the Netherlands and Belgium a few per thousand inhabitants suffer from gout.
What causes gout?
In primary gout congenital enzyme deficiency leads to the accumulation of urate. This form is extremely rare. In secondary gout the disorder is the result of several possible factors which either lead to an increased production of uric acid or a reduced excretion of uric acid by the kidneys. A combination of both is also possible.
Factors that lead to an increased production of uric acid:
- Increased purine degradation by chronic alcohol or cytostatics.
- An increased cell breakdown in the body by, for example, tumors, obesity and psoriasis.
- A purine-rich diet consisting of organ meats, certain fish such as anchovies, sardines, mussels, lobster, poultry and game.
Factors that lead to an increased uric acid levels in the blood due to the decreased excretion by the kidneys:
- Certain kidney diseases, including as a result of hypertension or lead intoxication.
- Alcohol.
- Certain medications such as diuretics, aspirin and laxatives.
- Some disease conditions such as dehydration, excessive fasting and an underactive thyroid.
Gout treatment
Gout treatment may consist of three phases:
- Treating the acute phase and the associated pain
- Preventing new acute exacerbations
- The lowering of the amount of uric acid in order to prevent the precipitation of urate crystals
The treatment of the acute phase is mainly aimed at reducing the pain and the inflammation. The drugs that do qualify are mainly the strong non-steroidal anti-inflammatory drugs such as indomethacin, diclofenac, naproxen and ketoprofen. Also, corticosteroids, have systemically or administered intra-articularly here their place in the short-term suppression of the inflammatory response in an acute attack of gout. Also, the parent drug colchicine, with a small therapeutic interval, reduces the inflammation in the joints in gout and has a limited place in the treatment of the acute phase. Also, combinations of these above drugs can be used.
The treatment of the underlying hyperuricemia is usually not appropriate as long as the acute attack of gout is not under control.
The long-term treatment is based on reducing the amount of uric acid and may consist of drugs such as allopurinol, febuxostat, and probenecid. These means change the amount of uric acid in both the serum and the tissues, but may in certain cases still elicit acute attacks of gout. This undesirable effect can be suppressed by prophylactic drugs such as colchicine, to apply low doses of NSAIDs, low doses of prednisone.
Other therapeutic agents that may be considered are uricase and pegloticase, vitamin C, anakinra and fenofibrate.
Non-pharmacological measures to prevent new flare-ups of gout are the following:
- Limiting or avoiding the consumption of food with high purine concentration.
- The avoidance of large amounts of alcoholic beverages and especially beer.
- The avoidance of soft drinks with a high amount of fructose.
- The limited use of natural juices, sugary food and salt.
- Avoid dehydration and drinking 3 to 4 liters of water per day.
- A balanced diet and reduce cholesterol.
- Weight loss in obese people is a valuable measure.
Causes, diagnosis and risk factors
For the formation of crystals, it is not strictly necessary to have an abnormally high levels of uric acid in the blood, and vice versa gives a lot of uric acid in the blood is not always lead to gout. A diagnosis can be confirmed by decrease of moisture to show from an inflamed joint and the characteristic needle-shaped crystals. This is particularly necessary when it is desired to determine whether there is any gout or pseudo-gout. Many - if not most - doctors, however, this will not find in a typical presentation required.
The reason may lie in a greater production of uric acid (a waste product of the purine bases adenine and guanine in DNA degradation), or in an inability to adequately remove uric acid, or in a combination of both.
An elevated uric acid in serum may remove a result of food or the inability uric acid are adequate:
- Meat, especially red meat and organ meats. People who eat red meat are 40% more likely to have gout compared with those who eat little red meat.
- Alcoholic beverages, especially beer and spirits. Two to four glasses of wine a week has no effect on the risk of gout. Alcohol causes dehydration (extra fluid loss) and therefore can also trigger an attack.
- A high intake of sea food increases the risk of gout by 50% compared with a low intake.
- Fructose-containing foods. Consumption of fructose-rich beverages such as fruit juices but particularly soft drinks, is strongly along with gout, especially in men. In people who drink two or more glasses of soda a day doubles the risk of gout. The large amount of fructose may lead to an elevated uric acid level in the blood. Fructose increases the production of uric acid due to an increased degradation of nucleotides. Hereditary fructose intolerance is probably a fairly common cause of gout.
- Also, degradation of own tissue (e.g., tumor after treatment with chemotherapy) may also be a ooraak of elevated uric acid production.
- An inability to adequately remove uric acid is hereditary and / or may have to do with renal impairment; Gout is also more common in people with heart failure.
- Also, a heavy metal poisoning, such as lead or cadmium, may cause gout, in that with the metal affected kidneys can no longer remove it from the blood uric acid.
There are a number of foods that were previously associated with gout, but which turn out to have no effect on the gain of gout.
- Vegetable protein (eg tofu)
- Purine-rich vegetables such as legumes
- Wine (two to four drinks per week)
Foods that might reduce the chance of getting gout:
- Consumption of low-fat dairy products is associated with reductions in uric acid levels and may protect against gout. The milk protein casein and lactalbumin promote renal excretion of uric acid. When a group of nuns who as an experiment for four weeks did not use dairy, uric acid levels increased significantly.
- Coffee Consumption. In people who drink a lot of coffee is less for gout. Antioxidants in coffee, such as chlorogenic acid, presumably improve insulin sensitivity and reduce insulin levels, making the renal excretion of uric acid increases.
- A traditional remedy is eating a few ounces sweet cherries per day. In women, these cherries seem to actually reduce uric acid concentrations.
- By drinking plenty of water, the concentration of uric acid in the blood.
There is a very old remedy that works well: colchicine, an alkaloid from autumn crocus, Colchicum autumnale. However, the therapeutic index of this is small.
Usually, therefore started with anti-inflammatory analgesics of the NSAID group, such as ibuprofen, diclofenac, or naproxen. Is the ignition once mastered it can be started with a preventive acting drug, if the attacks recur with some regularity. There are various effective means such benzbromarone or allopurinol, which, however, have unpleasant side effects in some people. The duration of treatment can be started only after the acute attack has been contained. Otherwise, this could easily flare up again.
Also, vitamin C can decrease the uric acid level in the serum. It is in competition with the uric acid absorption by the renal tubules in the kidneys, and also lowers the level of uric acid through the increase of the overall glomerular filtration rate in the kidney. In a twenty-year study in nearly 50,000 men showed the risk of gout by almost half reduced by daily intake of 1,500 mg of vitamin C or more.
Supplementation with polyphenols can also likely to reduce the risk of gout by an effect of reducing the uric acid levels in the body, and an inhibitory effect on the enzyme xanthine oxidase.