What is severe gout
Hyperuricemia and gout
Hyperuricemia: Accumulation of breakdown products of the purine metabolism with increased uric acid level in the blood as a result; mainly affects men between 40 and 60 years of age. Overeating, a meat-based diet and a hereditary predisposition promote the development of hyperuricemia, but chemotherapy for cancer can also be a trigger. If left untreated, the transition to gout threatens.
gout (Uricopathy, arthritis urica, arthropathica urica): Initially acute, then chronic inflammation of the joints due to uric acid crystals (urate), which crystallize out due to a permanently elevated uric acid level, are absorbed by white blood cells and are deposited in the joint spaces. Gout initially begins on one joint (monoarthritis) with an acute attack of gout. This is extremely painful, but relatively easy to treat. About 3% of men and less than 1% of women suffer an acute attack of gout once in their life, mostly around 40 years for men, and between 60–70 years for women. If the underlying increased uric acid level is not eliminated through a change in lifestyle and / or medication, there is a risk of transition to chronic gout - even after years without symptoms. It is characterized by gout attacks at ever shorter intervals, irrevocable destruction of the affected joints, gout nodules on bones and internal organs, in particular the development of kidney stones or a chronic gouty kidney.
Acute Attack of gout:
- Unbearable pain, swelling, overheating and reddening of the metatarsophalangeal joint of the big toe, and more rarely of the knee and other joints, usually occurring at night
- Severe touch sensitivity (the duvet is too heavy)
- Fever and general feeling of illness (increased heart rate, headache, and vomiting)
- Constant joint pain and complaints in the metatarsal, metatarsal, elbow, finger and knee joints, but also in the shoulder and spine
- Visible or palpable small nodules on the skin (gout nodules, e.g. auricle), but also on tendon attachments, tendon sheaths and bursa.
Become Purines (Building blocks of the genetic material DNA), the end product is uric acid, which is normally mainly excreted via the kidneys with the urine.
Hyperuricemia. If the balance between uric acid supply is disturbed to the detriment of uric acid excretion, the uric acid level in the blood rises, which the doctor calls hyperuricemia. Primary hyperuricemia (more than 95% of gout sufferers) is based on a congenital disorder of uric acid excretion, more rarely an increase in the body's own uric acid production due to enzyme defects in the purine metabolism. Secondary hyperuricemia is also a result of increased uric acid production, decreased uric acid excretion, or a combination of both. She comes z. B. as a result of the increased cell structure and cell breakdown in blood diseases or kidney damage.
Risk factors. An oversupply of uric acid in the blood occurs through food that is very rich in purine, heavy muscle work, the reduction of muscle mass or through increased consumption of alcohol (especially beer). Physical exertion, stress, weather changes, operations and infections are also discussed as triggers. More rarely, an increased breakdown of cells is responsible for the increased uric acid level when tumor tissue breaks down over a large area during cancer treatment, e.g. B. by radiation or chemotherapy.
Acute attack of gout. If the uric acid level is above a critical value, the excess uric acid forms crystals (uric acid stones = urates, precipitated uric acid). They are deposited in the joints and gout develops slowly but steadily. In an acute attack of gout, white blood cells migrate into the joint and eat up the uric acid crystals. A violent inflammatory reaction is set in motion by a large number of inflammatory substances attracted by this. Even a light touch with the duvet or through stockings is perceived as excruciatingly painful. An acute attack of gout is often triggered by excessive eating and drinking, but also by fasting. Especially when fasting is interrupted by the consumption of ice-cold drinks.
When the disease occurs for the first time, one of the two metatarsophalangeal joints of the big toe is usually affected, less often a knee joint.
Chronic gout. It is characterized by alternating acute gout attacks and symptom-free periods. The joints are destroyed, accompanied by deformation of the joints and misalignments of toes and fingers. Often are additional Gout nodules (Gouttophi) visible, which can be attributed to an increased deposition of uric acid stones - also in bones and soft tissues.
Kidney involvement. Hyperuricemia can also damage the kidneys when uric acid crystallizes in the kidneys. The uric acid crystals form uric acid stones, a type of kidney stone, and finally the chronic gout kidney with chronic kidney failure.
This is to be distinguished from acute damage to the kidneys by uric acid, which acute urate nephropathy: Uric acid is massively precipitated in the kidney tissue and acute kidney failure occurs suddenly. The same thing happens when highly concentrated acidic urine is formed - traceable to insufficient drinking.
That's what the doctor does
Diagnostic assurance. An acute attack of gout is so characteristic that the doctor recognizes it just by looking at the affected joint (visual diagnosis). The doctor takes blood because an increased uric acid level in the blood confirms the diagnosis. He uses other blood values to assess the course of the disease and check kidney function.
A bacterial joint inflammation with accumulation of pus (abscess) is rarely difficult to differentiate from an attack of gout, then a puncture of the joint to remove synovial fluid (puncture) is necessary for further clarification. Only in the case of an acute attack of gout are uric acid crystals found in the joint puncture, which are located within white blood cells.
Therapy. The aim of treatment is a permanent reduction in uric acid levels to around 5.5 mg / dl.
Therapy of hyperuricemia. If only the uric acid levels are increased (between 8.5 and 9 mg / dl), i.e. there is no acute gout attack, medication is usually avoided. The patient is required to change his or her lifestyle (low-purine diet). The exception is hyperuricemia as a result of chemotherapy, because there is a risk of tumor lysis syndrome: The amount of cell components released in the blood due to the disintegration of the tumor exceeds the excretory capacity of the kidneys. Mineral imbalances and metabolic disorders are the result; as it is an emergency situation, rapid action is required. Medicines are usually prescribed here.
Therapy of gout attack. If uric acid levels are above 9 mg / dl and gout attacks or kidney stones occur at the same time, drug treatment is required in addition to a change in diet. Above all else, the treatment of very severe pain with pain relievers (NSAIDs) is the first step.
Drug removal of uric acid stones from the kidneys is possible in two thirds of patients in the form of drug stone removal over a period of several months.
Prednisolone and / or non-steroidal anti-inflammatory drugs are used to treat the acute gout attack. Colchicine (cell poison obtained from the autumn crocus, e.g. Colchicum-Dispert®) is only used as a second choice because of its side effects. If oral medication does not work sufficiently, cortisone can alternatively be injected into the joint (intra-articular joint injection). However, there is an increased risk of infection, which is why this measure is only used in exceptional cases.
Drug prevention. Once the acute gout attack has been treated, further attacks must be prevented. Two drug groups are available for this:
- Uricostatics such as allopurinol (Zyloric®): They ensure that fewer purines are produced in the metabolism and thus inhibit the formation of too much uric acid; they are the first choice.
- Uricosurics such as benzbromaron and probenecid (probenecid Weimer®): They promote uric acid excretion via the kidneys. Because gout sufferers often have damaged kidneys, uricosuric drugs are risky.
For gout, the prognosis depends on the therapy, the course of the disease and the time of discovery, because the earlier it is diagnosed, the better the prospects - e.g. B. in the stage of an incipient hyperuricemia. If the disease has already taken a chronic course with changes in the joints, there is a risk of massive mobility restrictions (invalidity), and in the case of kidney damage, dialysis is even required.
Your pharmacy recommends
- In the event of an acute attack, keep the affected joint still and relieve the pain with cooling compresses (e.g. with alcohol).
- Avoid extreme nutritional situations such as fasting or gluttony, as this increases the uric acid level even further.
- Avoid alcohol (especially beer) and foods rich in purine (mainly internal organs, liver, kidneys), especially if an elevated uric acid level has been measured during a routine examination.
- At the beginning of the low-purine diet, it makes sense to weigh meat or fish portions, as the portion size is usually underestimated.
- Drink enough, at least two liters per day. This will prevent the kidneys from weakening, as uric acid is better excreted.
In an acute attack of gout, complementary medical measures are of little use.
In addition to drug therapy, cold treatments help relieve pain. Recommended are e.g. B. cold baths or ice packs that are wrapped in a sheet and placed on the affected area.
For some gout patients, the use of homeopathic remedies has proven effective, e.g. B. Bryonia or Belladonna.
in chronic gout is based on the measures that are also used in rheumatoid arthritis (self-help).
In the case of chronic gout, heat applications such as sweating cures, mud packs or mud baths support the standard therapeutic measures.
- www.ernaehrung.de - website of the Institute for Nutritional Information (DEBInet, Freudenstadt): For the search term gout, information about the disease, medication and numerous nutrition tips are provided. At www.ernaehrung.de/tipps/gicht/harnsaeure.pdf there is a table with the uric acid content of numerous foods to download free of charge. Very helpful and clear.
- E. Hund-Wissner; G. Wolfram: Delicious food for gout. Finally low uric acid levels. From snacks to festive menus: 130 varied recipes. Trias, 2006. Anyone who has problems with an elevated uric acid level does not need to forego a special diet or delicacies, as this guide impressively proves.
AuthorsKristine Raether-Buscham, Dr. med. Arne Schäffler in: Gesundheit heute, edited by Dr. med. Arne Schäffler. Trias, Stuttgart, 3rd edition (2014). Revision and update: Dr. med. Sonja Kempinski | last changed on at 17:02
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