Gout

Gout ( Urikopathie ) is a purine metabolic disorder that runs in spurts and ( in case of insufficient treatment) by deposits of uric acid crystals ( urate ) in various peripheral joints and tissues to a periarticular bone and cartilage changes as well as by long-term damage to the excretory organ kidney ultimately to renal failure leads. The damage to the kidneys painlessly, but it is a bigger problem than the painful gout attacks to the joints.

• 5.1 Acute gout attack
• 5.2 Chronic Gout

• 9.1 The history of gout

Symptoms

Acute

Acute symptoms include sudden severe pain in a joint, and severe pain when touched: gouty arthritis. The joint is red, extremely painful, swollen and warm up ( dolor - tumor - Calor - rubor ), also general signs of infection such as fever, increased white blood cells and increased uric acid levels before the attack (often normal in acute attack of gout uric acid levels ), rarely headache.

A joint is without an injury or other reasonable cause highly painful, swollen and hot. Often, the big toe joint is affected, it is called gout ( gout from the Greek, in Latin, as used by Seneca, Cicero and others; Agra stands for, catch, Bondage ', for pod, foot '). Chiragra are gout- related pain in the wrist ( chir stands for ' hand '). In principle, the acute attack of gout - and the first - affect every joint. The attack of gout keeps untreated, usually two to three weeks, the duration of seizures may increase during disease progression. The seizures can also merge into one another in the chronic phase, so that there is no pain-free intervals longer.

Chronic

If multiple seizures are expired, a chronic gout develops. The joints are destroyed, are characteristic of the radiograph juxtaarticular punch defects in the cancellous bone of the condyle has significant defects. The consequences are limiting the performance, uric acid crystal deposits in joints, joint deformation, kidney stones, kidney failure. If the gout passes into the chronic phase, acute attacks are often less clear and less painful.

Hyperuricemia

There are two causes of hyperuricemia, ie the increased uric acid levels in the blood: the primary and the secondary form.

• The primary form is a disruption of purine metabolism. It is caused by a disorder of the kidney excretion. In very rare cases may be the cause also an overproduction of uric acid. The primary form occurs more frequently than the secondary.
• The secondary type of various comorbidities cause the increased uric acid levels.

Causes

In well over 99 % of all cases ( without any external influence ) of hyperuricemia is a renal disorder based, it can be inherited as an autosomal dominant. In these patients is a hereditary disorder of the kidney excretion of uric acid before with otherwise normal renal function. Hyperuricemia may also in renal impairment from other causes, such as Diabetes mellitus may be a sequence, since a high blood sugar levels damage blood vessels over a long period, so that the renal function is impaired. In addition, harm, excessive alcohol intake, as carboxylic acids compete with uric acid excretion mechanism of the kidney. In addition, beer supplies by the yeast residues still present in addition uric acid forming purines.

Next may be a disorder of purine metabolism. Most is a fault of HGPRT ( enzyme) in the recycling of purine bases. Total absence of this enzyme, this leads to the Lesch -Nyhan syndrome.

Diagnostics

An elevated uric acid levels can be detected in blood. One should however keep in mind that the blood levels, depending on what was eaten or drunk, can fluctuate quite quickly. If there is an attack of gout, uric acid levels in the blood can be in the normal range, this does not exclude gout. In most cases the clinical picture is sufficient.

( optional changes )

• Leucocytes
• Increase in erythrocyte sedimentation rate (ESR)
• Increase in uric acid > 6.5 mg / dl

With an increase in uric acid > 8 mg / dl suffer 25% of patients, with an increase to> 9 mg / dl almost every patient suffers an attack of gout. Recent studies report that actually develops in only about 5 % of patients with high levels of uric acid gout.

In addition, in chronic course of the disease typical changes in bone can be detected in the X-ray image (eg, joint destruction and periarticular erosions, tophi ). In urography, the indirect presentation of individual Uratsteine ​​diagnosis is ( can not be represented on the radiograph ). Finally, uncertainty may confirm the diagnosis, a direct joint puncture in the presence of urate crystals in the Synovialanalyse.

Treatment options

Acute gout attack

All of these drugs combat the symptoms.

Chronic gout

• Benzbromarone
• Probenecid

Uric acid formation by food (selection)

• High uric acid concentration ( 200 mg/100 g): trout, herring, sprat, grilled chicken, liver, kidneys, sweetbreads, heart meat, broth, bouillon cubes and baker's yeast.
• Average amount of uric acid ( 80-150 mg/100 g): plaice fillet, ham sausage, lean meat (beef, pork, chicken, game), legumes and peanuts
• No / little uric acid (0-50 mg/100 g): milk, yogurt, egg, pumpkin, pepper, potato, apple, whole grain bread, white bread and cheese. However, dairy products are often enriched with fructose. When converting to the consumption IMP apply, the concentration of uric acid in the body can rise above the Purinabbau.
• For beverages are primarily beer ( 10-23 mg/100 g) and Coke (10 mg/100 g) Purinquellen.

The purines contained in coffee, black tea and cocoa are not degraded to uric acid, so they can continue to be consumed.

Gout in animals

Even the dinosaurs had gout. After they had observed in the metacarpal bone of a Tyrannosaurus Rex bone lesions that were similar to those of gout patients have been studied further 83 skeletons. Just another specimen showed similar changes. On the affected bone and holes at the edges of bone neoplasms were observed. The bone density of the intact bone showed it to no abnormality. You could, however, prove by any method remains of gout crystals to clear evidence of the etiology of the bone changes to be provided. Indications for urate -driven genesis remain the gout typical bone changes that are substantially different from those of similar diseases such as reticulohistiocytosis or amyloidosis.

Niggles

An obsolete term for an acute attack of gout is " niggles " that was derived from late Middle High German Zipperlin, Middle High German from Zipfen for ' mince ' and mockingly referred to the transition of the patient. Advanced was the importance for other ailments. So Adelung described in his 1801 published dictionary already niggles as

" A legacy in High German greater part naming, both of gout, as the Chiragra. The ache you have, get. The niggles on the hands. There is no healing of the. Cyprian, the Holy resist this disease, as Zeiler will, but zips from a still existing in the low voice types Verbo, zippeln, and often twitch and tear into small paragraphs formed as podagrische patients are accustomed to do in the pain of gout. This lowness of the verb is because the cause that you can become obsolete the derived substantive, zumahl as well as its form, as a diminutive, no understandable reason has. "

The application as a remedy was stiftend name for the Zipperleinskraut ( Giersch ).