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Gout is a common form of inflammatory arthritis that causes sudden, severe pain, swelling and tendernes.


Patients present with one or more erythematous, swollen and painful joints with restricted movement. The big toe is frequently involved (podagra). Other commonly involved joints include the instep, ankle, knee and wrist joints. The attacks are sudden and typically last up to 8 to12 hours. Systemic involvement is rare and may be indicated by the presence of fever.

  • The elderly patients were more likely to have fever (51.1%) during the attack than the young (20.8%) and middle-aged (30.8%) patients (P 0.001 by χ² test).[ncbi.nlm.nih.gov]
  • [ 713.6 ] Staphylococcus 711.0 Streptococcus 711.0 syphilis (see also Syphilis) 094.0 [ 711.4 ] syringomyelia 336.0 [ 713.5 ] thalassemia (see also Thalassemia) 282.40 [ 713.2 ] tuberculosis (see also Tuberculosis, arthritis) 015.9 [ 711.4 ] typhoid fever[icd9data.com]
  • Lupus Multiple sclerosis Osteoarthritis Osteoporosis Polymyositis Psoriatic arthritis Rheumatic fever Rheumatoid arthritis Scleroderma Type 1 diabetes[uvahealth.com]
  • Systemic involvement is rare and may be indicated by the presence of fever. A detailed history and physical examination is often sufficient to form a diagnosis.[symptoma.com]
  • He had intermittent fever and acute arthritis in several joints leading to hospitalization and enforced bed rest for 6 weeks. The details of his illness and its possible etiology are reviewed.[oadoi.org]
Family History of Gout
  • The family history of gout was found in one-third of the cases (p   0.05). Uricemia was higher in cases than controls (p 0.05).[ncbi.nlm.nih.gov]
  • Patients with non-synonymous allelic variants had an earlier onset of gout (42 vs 48 years, P 0.0143) and a greater likelihood of a familial history of gout (41% vs 27%, odds ratio 1.96, P 0.053).[ncbi.nlm.nih.gov]
  • history of gout can be obtained in less than half patients' male / female ratio ranging from 7:1 to 9:1 females with gout tend to be postmenopausal; pathophysiology predisposing conditions: common chronic diseases assoc w/ gout include alcoholism, obesity[wheelessonline.com]
  • Diagnosis Your doctor will ask you about your medications, diet, alcohol use, and about any family history of gout. Your doctor will examine you, and he or she will look at your painful joints and search your skin for tophi.[drugs.com]
  • You are more likely to get gout if you: Have a family history of gout. Have had an organ transplant. Are a man. Are an adult. Are overweight. Drink alcohol. Eat a lot of foods rich in purines. Have been exposed to lead.[niams.nih.gov]
Toe Pain
  • The big joint toe pain may be so severe that even the weight of bedsheets causes discomfort. Gouty arthritis is easily treated with nonsteroidal anti-inflammatory drugs (NSAIDs).[everydayhealth.com]
Gouty Tophus
  • The surgery combined with decreasing trioxypurine treatment can improve the treatment outcome of gouty tophus.[ncbi.nlm.nih.gov]
  • Gouty tophus presenting at a soft tissue mass diagnosed by fine-needle aspiration: a case report. Diagn Cytopathol. 1996 ; 15: 246 – 9. Google Scholar Crossref Medline ISI 4. Mackford, BJ, Kincaid, RJ, Mackay, I.[doi.org]
  • Histopathology confirmed the excised tissue as gouty tophus. Following this, the patient was placed on allopurinol, a xanthine oxidase inhibitor to prevent recurrent attacks.[ncbi.nlm.nih.gov]
  • Malignant fibrous histiocytoma arising in a gouty tophus at the second metacarpophalangeal joint. J Plast Reconstr Aesthet Surg. 2006;59:775–8. [ PubMed ] 2. Gentili A. The advanced imaging of gouty tophi.[ncbi.nlm.nih.gov]
Joint Swelling
  • These are the presence of a clear history of at least two attacks of painful joint swelling with complete resolution within two weeks, a clear history or observation of podagra, the presence of a tophus, and a rapid response to colchicine within 48 hours[bmj.bmjjournals.com]
  • Clinical outcomes evaluated included pain, joint swelling and tenderness, activities of daily living, patient global assessment, recurrence, intermediate outcomes of serum urate levels, and harms.[ncbi.nlm.nih.gov]
  • Outcomes included pain, bleeding, joint swelling, erythema, tenderness, activity limitation, response to therapy, quality of life, time to resolution, supplementary analgesics, and adverse events.[doi.org]
Joint Deformity
  • If left untreated, gout can cause painful joint deformities and lead to kidney disease. Gout was once associated with overindulgence of rich foods and wine, but in truth, anyone can get gout.[nm.org]
  • Chronic symptoms such as joint deformity and limitation of motion in affected joints may occur if several attacks of gout occur each year. Uric acid deposits called tophi develop in cartilage tissue, tendons, and soft tissues.[mountsinai.org]
  • Surgery may be required to excise or drain infected or ulcerated tophi, to correct joint deformities, or to improve joint function.[medical-dictionary.thefreedictionary.com]
  • Gout Complications In addition to joint damage, joint deformity, bone loss, and loss of mobility, gout may lead to, or develop into, the following conditions: Recurrent gout (chronic gouty arthritis) People with recurrent gout experience flare-ups, or[everydayhealth.com]
Knee Pain
  • Case 2 involved a 69-year-old man who presented to the emergency department with acute onset of atraumatic left knee pain.[ncbi.nlm.nih.gov]
  • Critical Essential Core Tested Community Questions (9) Sorry, this question is for PEAK Premium Subscribers only (OBQ13.256) A 65-year-old patient who recently underwent abdominal surgery for a diverticular abscess is referred for right knee pain and[orthobullets.com]
  • Our physicians are also available to consult on other musculoskeletal disorders including shoulder, hip and knee pain and will work closely with your integrated care team to provide a comprehensive plan for treatment. Article Navigation[nm.org]
Joint Effusion
  • Joints joint effusion (earliest sign) preservation of joint space until late stages of the disease an absence of periarticular osteopenia eccentric erosions the typical appearance is the presence of well-defined “punched-out” erosions with sclerotic margins[radiopaedia.org]
  • The medical term for excessive fluid in a joint is a "joint effusion." Gout frequently involves joints in the lower extremities. The classic location for gout to occur is the big toe.[medicinenet.com]
Foot Pain
  • People with gout demonstrated a reduced peak ankle joint angular velocity which may reflect gait-limiting factors and adaptations from the high levels of foot pain, impairment and disability experienced by this population.[ncbi.nlm.nih.gov]
  • Uremia Invest. 1985; 9 (2):127–130. [ PubMed ] [ Google Scholar ] Markowitz ME, Rosen JF. Assessment of lead stores in children: validation of an 8-hour CaNa2EDTA provocative test.[ncbi.nlm.nih.gov]


A detailed history and physical examination is often sufficient to form a diagnosis.

Laboratory Tests

  • Complete blood count
  • Serum uric acid levels
  • Serum electrolytes
  • Serum creatinine 


The imaging techniques that currently have a role in the imaging of gout include conventional radiography, ultrasound, computed tomography, dual energy computed tomography, magnetic resonance imaging and nuclear medicine [8]. 

Test results

Axial gouty arthropathy should be included in the differential diagnosis of chronic low back pain, mainly when several risk factors for gout are present [9]. The presence of tophi is diagnostic. In other cases, a diagnosis can be based on physical examination and confirmed by lab tests.

  • Uricosuric agents are alternative therapies in patients with preserved renal function and no history of nephrolithiasis.[ncbi.nlm.nih.gov]
  • Uricosuric agents can cause hyperuricosuria, a risk factor for nephrolithiasis and acute uric acid nephropathy.[ncbi.nlm.nih.gov]
  • […] gout in women should prompt a more detailed work up of enzyme deficiency; patients may complain of very mild attacks developing w/o provocation that abate w/o specific treatment; podagara : classic presentation of acute attack of first MTP joint; hand: nephrolithiasis[wheelessonline.com]
  • The association between gout and nephrolithiasis: the National Health and Nutrition Examination Survey III, 1988–1994. Complete Listing of References[arthritis-health.com]
  • ZURAMPIC Prescribing Information At doses greater than 200 mg a day of ZURAMPIC with an XOI, the risk of renal-related adverse events and nephrolithiasis was higher and should not be used.[fda.gov]
  • CASE REPORT: 56-year old male patient, with history of arterial hypertension, hypertriglyceridemia, obesity, glucose intolerance and alcohol abuse, diagnosed with gout in his fifth decade of life.[ncbi.nlm.nih.gov]
  • Hypertension, renal insufficiency, hypertriglyceridemia, hypercholesterolemia, hyperuricemia, diabetes, obesity, and early menopause were each associated with a higher risk of incident gout and/or gout flares.[ncbi.nlm.nih.gov]
  • […] obtained in less than half patients' male / female ratio ranging from 7:1 to 9:1 females with gout tend to be postmenopausal; pathophysiology predisposing conditions: common chronic diseases assoc w/ gout include alcoholism, obesity, hypertension, CAD, and hypertriglyceridemia[wheelessonline.com]
  • Hypertriglyceridemia and hyperuricemia: effects of two fibric acid derivatives (bezafibrate and fenofibrate) in a double‐blind, placebo‐controlled trial. Metab Clin Exp 1988 37 217–220. [ PubMed ] [ Google Scholar ] 27.[ncbi.nlm.nih.gov]
Uric Acid Increased
  • Avoidance of uric acid-increasing drugs (e.g., diuretics, aspirin in low doses, cyclosporine, ethambutol). Alcohol consumption (especially beer!). Strive for normal weight.[lecturio.com]


Gout, whilst in principle considered to be well understood and simple to treat, often presents diagnostic and management challenges, with evidence to suggest that it is often inadequately treated and poor compliance is a major issue [9].


Treatment of gout is mainly the use of nonsteroidal anti-inflammatory drugs, corticosteroids and colchicine. Colchicine is a potent anti-inflammatory drug that has a narrow therapeutic index. Indicated for treating gout and familial mediterranean fever, it inhibits mitosis by interfering with microtubule formation and arresting cell division [10]. Analgesics may be prescribed to relieve pain. For prophylaxis, xanthine oxidase inhibitors like Allopurinol and Febuxostat may be given.

Lifestyle Modifications

Obese patients must be encouraged to reduce weight and to start light, regular exercise. Diet should be low in foods which have a high purine content.


The natural course of gout has 4 stages. First is asymptomatic hyperuricemia which mostly occurs near puberty in males and after menopause in females. After a few years, the second stage, acute gouty arthritis, occurs. This stage is characterized by sudden, excruciating pain, usually in just one joint; 50% occur in the first metatarsophalengeal joint [6]. Eventually other joints become involved. This stage, if left untreated, may last for a few weeks after which gradual resolution occurs, called the asymptomatic intercritical stage.

Now the prognosis varies. The patient may have a second gout attack and progress to the fourth stage called chronic tophaceous gout. Or in some patients, the disease may completely resolve. Overall, with appropriate treatment, gout has a good prognosis.

Patients with gout have as much as 1000 times more uric acid in the body as unaffected individuals do and are almost twice (1.97 times) as likely to develop renal stones as healthy individuals are [7]. They also are prone to develop metabolic syndrome which increases chances of diabetes. Other complications include urate nephropathy due to tophi production in the kidneys resulting in pyelonephritis, recurrent fractures, secondary infections and nerve damage.



The heritability of serum urate levels is estimated at 63% [2]. Gout tends to run in families and several genes have been implicated like URAT1, GLUT9, ABCG2.


Although genetic factors have been strongly associated with hyperuricemia, environmental and other state-of-health factors are responsible for the majority of the gout burden in developed countries [3]. Consumption of fructose-rich foods and beverages is associated with an increased risk of gout in both men and women [4]. Other factors include anemia, obesity, renal insufficiency, cancer and hypertension.



Gout has a high prevalence and is estimated to affect 1-2% population of the United States, and is becoming more common [5].


It is more common in males.


Gout is more common in some races and rare in others. It is more common in African-Americans than in Whites.

Sex distribution
Age distribution


Gout is marked by transient attacks of acute arthritis initiated by crystallization of urates within and about joints. It occurs either due to one of two pathways.

  • Overproduction of uric acid

Uric acid is the end product of purine metabolism. One of the pathways involved in purine metabolism is called the salvage pathway in which the enzyme hypoxanthine guanine phosphoribosyl transferase (HGPRT) plays an important role. If this enzyme is deficient, it may lead to increased production of uric acid by the de novo pathway, resulting in gout.

  • Reduced excretion

Plasma levels of uric acid are kept within normal range by the four-part excretion system (filtration, reabsorption, secretion and post-secretory reabsorption) of the kidneys. 90% of the filtered urate is reabsorbed by the action of URAT1 gene. Decreased filtration and underexcretion is the primary cause behind gout.

Morphological Changes

Central to the pathogenesis of the arthritis is precipitation of monosodium nitrate (MSU) crystals into the joints [6]. The synovium is edematous, congested and filled with an inflammatory infiltrate.

  • Chronic tophaceous arthritis

Tophi are the pathognomonic hallmark of gout. They are large aggregates of urate crystals surrounded by inflammatory cells and they may occur in joint cavities, articular cartilage, tendons, ligaments, even inside kidneys and skin. This subtype occurs due to repetitive precipitation of urate crystals in acute attacks.


Gout can be prevented by taking a balanced diet which is particularly low in high protein sources such as liver, kidney or sardines, and by avoiding drinks with high sugar content. Lifestyle modifications such as a regular 30 minute walk and weight control can also help.


Gout is defined as an arthritic condition resulting from the deposition of monosodium urate (MSU) crystals in and/or around joints, following long-standing hyperuricemia [1]. It is a very common condition in both developing and developed countries, but fortunately, it can be easily managed.

Patient Information


Gout is a painful inflammatory condition that can affect a variety of joints, causes significant distress and is associated with a number of comorbidities. 


Several genetic and environmental factors play a role in causing this disease. Whatever the underlying etiology, gout is primarily due to increased levels of uric acid in blood.


Symptoms include swelling, redness and pain in joints. The most commonly involved joint is of the big toe. Gradually, more joints become involved such as the rest of the toes, instep, ankle, knee, hip, wrist and elbow. In some cases, joints of the vertebrae also become involved. 


Treatment includes dietery modifications, lifestyle changes, weight reduction and analgesic and anti-inflammatory medications. Gout can easily be managed.



  1. Bardin T, Richette P. Definition of hyperuricemia and gouty conditions. Curr Opin Rheumatol. 2014 Mar;26(2):186-91. 
  2. Yang Q, Guo CY, Cupples LA, Levy D, Wilson PW, Fox CS. Genome-wide search for genes affecting serum uric acid levels: the Framingham Heart Study. Metabolism. Nov 2005;54(11):1435-41. 
  3. Vitart V, Rudan I, Hayward C, Gray NK, Floyd J, Palmer CN, et al. SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout. Nat Genet. Apr 2008;40(4):437-42.
  4. Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ. Feb 9 2008;336(7639):309-12. 
  5. Chen LX, Schumacher HR. Gout: an evidence-based review. J Clin Rheumatol 2008 14 (5 Suppl): S55–62. 
  6. Robbins and Cotran. Pathologic Basis of Disease. 8th ed. V Kumar, AK Abbas, N Fausto, JC Aster, et al, eds. Pa: Saunders Elsevier. Ch 26 p 1242-46.
  7. Bernad B, Narvaez J, Diaz-Torné C, Diez-Garcia M, Valverde J. Clinical image: corneal tophus deposition in gout. Arthritis Rheum. Mar 2006;54(3):1025
  8. Chowalloor PV, Siew TK, Keen HI. Imaging in gout: A review of the recent developments. Ther Adv Musculoskelet Dis. 2014 Aug;6(4):131-43. 
  9. Cardoso FN, Omoumi P, Wieers G, Maldague B, Malghem J, Lecouvet FE, Vande Berg BC. Spinal and sacroiliac gouty arthritis: report of a case and review of the literature. Acta Radiol Short Rep. 2014 Sep 17;3(8):2047981614549269.
  10. Stromberg P, Wills BK, Rose SR. Gout exacerbation, weakness, hypotension--Dx? J Fam Pract. 2014 Aug;63(8):455-6. 

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Last updated: 2017-08-09 18:25