Gout

Gout is a complicated form of arthritis, which can affect anyone. Patients with gout suffer from sudden pain attacks, edema, redness, and painfulness in one or several joints (most often, it is the one in the big toe). A gout attack can wake a patient in the middle of the night. The affected joint will be hot, swollen, and will extremely painful. 
Gout develops in people with increased uric acid (hyperuricemia). It is manifested by salt deposition in joints and other body tissues. 

• Hyperuricemia is a concentration of uric acid in the serum over 360 μmol/l. 
• Uric acid is a final product of purine decomposition in the body. 
• Purines are chemical compounds that are the basis of nucleic acids needed for DNA and RNA synthesis.

We obtain approximately 1/3 of the uric acid with food, and 2/3 is produced by the decomposition of internal purines. Uric acid does not decompose in the human body due to the lack of an enzyme called uricase. 

Gout is the most widespread form of inflammatory arthritis, affecting approximately 9.2 million adults (3.9%) across the USA.

Facts About Gout

• Gout is not often seen in men under 30 and in women of the pre-menopause age.
• Gout is the most frequent cause of acute inflammation of the joint in males over the age of 40.
• When gout develops in males under the age of 25, it is caused by an inherited defect in the purine metabolism, alcoholism, or renal failure.
• Gout has become more widespread in recent years due to the use of diuretics.

Gout has a long-term asymptomatic progression (months or years) when tissues accumulate sodium monourate. Crystal deposition within the tissues occurs when the uric acid levels are increased for a long time. However, not everyone with hyperuricemia develops gout!

Mechanism of Gout Development

Gout is always accompanied by an increased level of serum uric acid, over 420 μmol/l. In women, this number is a little lower – 360 μmol/l.
Main reasons for the uric acid increase in the blood.

• Genetic factors. Ethnic and genetic predisposition affects the prevalence of gout. There is also a familial form of gout. 
• Excess weight and obesity. 
• Alcohol intake. Alcohol contributes to the increase in the level of serum urates and the development of uric acid precursors. Despite this, it can obstruct the secretion of urates by kidneys.
• Eating large amounts of meat. Diet rich in animal purines (for example, red meat and crustaceans) is associated with hyperuricemia. Products and drinks with high fructose content are considered risk factors for gout development. Fructose is the only carbohydrate, which increases the urate level in the serum.
• Taking diuretics.
• Organ transplants. Patients that have had a kidney transplant are more susceptible to the development of gout due to existing renal failure and the use of cyclosporine to prevent transplant rejection.

Monourate crystals are built up in the joint and the surrounding tissues and induce the body’s immune response. Severe inflammation develops together with an acute arthritic attack. The chronic inflammatory process takes place in the patient’s body even when there is no acute arthritic attack.

Gout Classification

Primary Gout

Primary gout is usually related to.

• Inherited isolated dysfunction in the function of kidney channels.
• Increased secretion of uric acid for an unknown reason.

Secondary Gout

Reasons for secondary gout are.

• Diseases and conditions related to increased secretion of uric acid (approximately 10-15%) — lymphoproliferative diseases, malignancies, hypothyroidism, polycythemia, Paget disease, Gaucher disease, psoriasis, obesity. 
• Dysfunction of its removal (85-90%) – chronic renal failure, hypothyroidism, hyperparathyroidism, sarcoidosis, starvation, toxicosis of pregnant women, Down syndrome, lead intoxication, toxin poisoning, lactic acidosis with alcohol intake, diuretics, acetylsalicylic acid

The Severity of Gout

• Mild — arthritis attacks once or twice a year. No more than 2 joints are inflamed, no kidney damage or joint destruction, there are no tofuses (nodules of urate salt deposits under the skin), or they are single with a diameter of no more than 1 cm.
• Moderate— 3-5 attacks a year. The disease affects 2-4 joints. The person develops multiple tofuses, and kidney damage is limited to urolithiasis.
• Severe — attacks occur over 5 times a year. The patient has large pronounced tofuses, nephropathy (severe kidney damage).

Clinical Manifestation of Gout

Asymptomatic Hyperuricemia

The patient is not concerned about anything; the disease is not manifested. Blood tests show high uric acid containment. Disease development can take up to 30 years.

Acute Gout Arthritis

The joint lesion begins from the lower extremities — from the first metatarsophalangeal joint (the base of the big toe), joints of the midfoot, ankle, knee joints. The elbow joint may also be involved. In women, the disease may begin with joints of the hands and elbow.

Typical signs of acute gout arthritis.

• The rapid development of symptoms, increasing to a maximum within a few hours. Intensive pain, even when the joint is touching a bedsheet during the early morning. 
• The patient cannot move the affected joint.
• Oedema, redness, shiny glossy skin over the joint.

There is a possibility for a milder course of attacks and their independent disappearance at the onset of the disease.

Interictal Gout

There are no acute symptoms or unpleasant and painful feelings. Joints remain physiologically active. Uric acid accumulates in tissues during all this time. The gout attack can occur for a long time – after months or even years.

Chronic Gout Arthritis

The following sodium monourate crystal deposition causes the development of a chronic pain syndrome, significant deformations of joints, and dysfunction, especially or feet and hand joints. The disease develops relatively quickly. It affects other joints, urinary bladder, kidneys, and other organs.

Chronic Tofus Gout

Significant accumulations of the sodium monourate cause development of tofuses. These are developed on the bending surface of hand fingers and feet, forearms, elbow joints, around the Achilles tendons, auricle. And the higher the concentration of urates – the quicker is the formation of tofuses. Often tofuses are signs of the length of the disease. Painful, bursting, and suppurating tophi in the hands are typical of gout in older patients!