Gout overview: Difference between revisions
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{{CMG}} {{AE}} {{Shivam Singla}} | {{CMG}} {{AE}} {{Shivam Singla}} | ||
==Overview== | ==Overview== | ||
<u>Gout is a common arthritis caused by deposition of monosodium urate crystals within joints after chronic hyperuricaemia. It affects 1-2% of adults in developed countries, where it is the most common inflammatory arthritis in men. Epidemiological data are consistent with a rise in prevalence of gout. Diet and genetic polymorphisms of renal transporters of urate seem to be the main causal factors of primary gout. Gout and hyperuricaemia are associated with hypertension, diabetes mellitus, metabolic syndrome, and renal and cardiovascular diseases. Non-steroidal anti-inflammatory drugs and colchicine remain the most widely recommended drugs to treat acute attacks. Oral corticosteroids could be an alternative to these drugs. Interleukin 1beta is a pivotal mediator of acute gout and could become a therapeutic target. When serum uric acid concentrations are lowered below monosodium urate saturation point, the crystals dissolve and gout can be cured. Patient education, appropriate lifestyle advice, and treatment of comorbidities are an important part of management of patients with gout.</u> | |||
Gout, otherwise called as [[metabolic arthritis]] is a [[congenital]] disorder of [[Uric acid]] [[metabolism]]. In this condition, monosodium urate or uric acid crystals are deposited on the articular [[cartilage]] of joints, tendons and surrounding tissues due to elevated concentrations of uric acid in the blood stream. This provokes an inflammatory reaction of these tissues. These deposits often increase in size and burst through the skin to form sinuses discharging a chalky white material. | Gout, otherwise called as [[metabolic arthritis]] is a [[congenital]] disorder of [[Uric acid]] [[metabolism]]. In this condition, monosodium urate or uric acid crystals are deposited on the articular [[cartilage]] of joints, tendons and surrounding tissues due to elevated concentrations of uric acid in the blood stream. This provokes an inflammatory reaction of these tissues. These deposits often increase in size and burst through the skin to form sinuses discharging a chalky white material. | ||
===Gout historical perspective=== | ===Gout historical perspective=== | ||
* Gout was first described by Egyptians in 2640 BC. | |||
* Hippocrates described [[podagra]] in 5th century BC as the unwalkable disease. | *Gout was first described by Egyptians in 2640 BC. | ||
* Galen described the [[monosodium urate]] crystal deposition following long standing [[hyperuricemia]] as [[Tophi]]. He described gout as a discharge of the four [[Four Temperaments|humors]] of the body in unbalanced amounts into the joints. | *Hippocrates described [[podagra]] in 5th century BC as the unwalkable disease. | ||
*Galen described the [[monosodium urate]] crystal deposition following long standing [[hyperuricemia]] as [[Tophi]]. He described gout as a discharge of the four [[Four Temperaments|humors]] of the body in unbalanced amounts into the joints. | |||
*The word Gout was first used in 1200s AD by Dominican monk Randolphus of Bocking and was derived from the Latin word 'Gutta'. | *The word Gout was first used in 1200s AD by Dominican monk Randolphus of Bocking and was derived from the Latin word 'Gutta'. | ||
*[[Aulus Cornelius Celsus]] discovered many symptoms of gout. | *[[Aulus Cornelius Celsus]] discovered many symptoms of gout. | ||
* | * | ||
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==References== | ==References== | ||
{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
Latest revision as of 22:29, 5 October 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[2]
Overview
Gout is a common arthritis caused by deposition of monosodium urate crystals within joints after chronic hyperuricaemia. It affects 1-2% of adults in developed countries, where it is the most common inflammatory arthritis in men. Epidemiological data are consistent with a rise in prevalence of gout. Diet and genetic polymorphisms of renal transporters of urate seem to be the main causal factors of primary gout. Gout and hyperuricaemia are associated with hypertension, diabetes mellitus, metabolic syndrome, and renal and cardiovascular diseases. Non-steroidal anti-inflammatory drugs and colchicine remain the most widely recommended drugs to treat acute attacks. Oral corticosteroids could be an alternative to these drugs. Interleukin 1beta is a pivotal mediator of acute gout and could become a therapeutic target. When serum uric acid concentrations are lowered below monosodium urate saturation point, the crystals dissolve and gout can be cured. Patient education, appropriate lifestyle advice, and treatment of comorbidities are an important part of management of patients with gout.
Gout, otherwise called as metabolic arthritis is a congenital disorder of Uric acid metabolism. In this condition, monosodium urate or uric acid crystals are deposited on the articular cartilage of joints, tendons and surrounding tissues due to elevated concentrations of uric acid in the blood stream. This provokes an inflammatory reaction of these tissues. These deposits often increase in size and burst through the skin to form sinuses discharging a chalky white material.
Gout historical perspective
- Gout was first described by Egyptians in 2640 BC.
- Hippocrates described podagra in 5th century BC as the unwalkable disease.
- Galen described the monosodium urate crystal deposition following long standing hyperuricemia as Tophi. He described gout as a discharge of the four humors of the body in unbalanced amounts into the joints.
- The word Gout was first used in 1200s AD by Dominican monk Randolphus of Bocking and was derived from the Latin word 'Gutta'.
- Aulus Cornelius Celsus discovered many symptoms of gout.
Pathophysiology
Gout occurs when mono-sodium urate crystals form on the articular cartilage of joints, on tendons, and in the surrounding tissues. Purine metabolism gives rise to uric acid, which is normally excreted in the urine. Defects in the kidney may cause uric acid to build up in the blood, leading to hyperuricemia, and the subsequent formation of gout crystals.
Differentiating Gout from other Diseases
Gout needs to be differentiated from other diseases such as cellulitis, rheumatoid arthritis, septic arthritis and sarcoidosis as they present with similar symptoms.
Epidemiology and Demographics
Gout affects men in age group 40-50 years. It is more common in people from the Pacific Islands, and New Zealand. In the United States, gout is twice as prevalent in African American males as it is in Caucasians.
Risk Factors
Several factors may put a person at risk for developing gout. These include the presence of; hypertension, diabetes, hypercholesterolemia, obesity, and alcohol abuse. Certain medications may also put a person at a higher risk for developing gout.
Prognosis
The prognosis of gout is good if it is treated early, and if the person maintains a healthy lifestyle with modification of their individual risk factors.
Diagnosis
Symptoms
The classic picture of an acute gouty attack, is sudden, excruciating, unexpected and burning pain. There will also be swelling, redness, warmth, and stiffness in the joint. In approximately 75% of first episodes, gout usually attacks the big toe.
Laboratory Findings
A definitive diagnosis of gout is made from light microscopy of the fluid aspirated from the joint. The fluid demonstrates intracellular negatively bi-refringent monosodium urate crystals and polymorphonuclear leukocytes in the synovial fluid. Although hyperuricemia is a common feature of gout, a high uric acid level does not necessarily mean a person will develop gout.
X-ray
An x-ray is done when gout is suspected to rule out other abnormalities of the bone that may be causing the pain. Most commonly in gout, the x-ray will show no abnormalities, or a small amount of soft tissue swelling.
Treatment
Medical Therapy
The first goal of therapy when treating gout, is pain relief. This can be acheived with NSAIDs, and oral or intra-articular glucocorticoids. If colchicine is given, it should be taken within the first 12 hours of the attack. Other, less standard methods of treatment include the use of hemorrhoidal ointment, ice, increasing mobility, and acetazolamide.
Surgery
For extreme cases of gout, surgery may be necessary to remove large tophi and correct joint deformity.
Secondary Prevention
There are several methods used to prevent a re-occurrence of gout. Dietary changes include reducing the intake of foods that increase the levels of purine in blood, such as protein and alcohol. Several foods, and vitamin C have been thought to decrease the levels of purine in the blood. Modification of the risk factors for gout has been shown to also be beneficial in reducing the reoccurrence of gout. There are medications which can increase the excretion of uric acid, and reduce uric acid levels through other mechanisms.