Gout is triggered by an excess of uric acid in the body, known as hyperuricemia, which is influenced by genetic, metabolic, and environmental factors¹⁾. This process of uric acid saturation occurs locally in certain areas of the body (usually the joint), where precipitation of monosodium urate (MSU) crystals occurs, leading to development of gout²⁾. Gout, which induces acute arthritic symptoms, is characterized by recurrent episodes. Distinct manifestations can be observed during acute attacks in patients with the prevalent form of gout, including the sudden onset of pain, swelling, and inflammation in the joints or surrounding tissues, accompanied by a heat sensation. The first metatarsophalangeal joint is the joint most commonly affected by gout, accounting for 56%-78% of cases. However, gout can also affect various other joints, including the midfoot, ankle, and upper limb joints³⁾. Redness may occasionally manifest in small joints as well. The peak of pain and swelling usually persists for approximately 6-12 hours, and development of periarthritis, tendinitis, or bursitis may occur subsequent to the acute attack, in accordance with the circumstances^4,5). Spontaneous resolution commonly occurs within a few days of the onset of an acute attack. Chronic gout, which occurs after recurring acute attacks over a period of several years, is characterized by pain and stiffness caused by destruction of joints and damage to surrounding tissue, as well as the presence of tophi, which are aggregates of MSU crystals and dead immune cells. Tophi, a distinctive feature of gout, are deposited in subcutaneous tissue, inducing local or systemic inflammation similar to granuloma-like foreign body reactions. Usual locations include the ear, olecranon bursa, and the finger pulps¹⁾.

Although detection of gout arthritis in the hip joint is not common, gout is the most common form of inflammatory arthritis, with increasing prevalence worldwide. As life expectancy is increasing, and lower kidney function can affect older patients, the risk of uric acid accumulation may be higher in old age. Compared with other subspecialties, elderly patients are more often seen by hip surgeons, suggesting a potential need for hip surgeons to attain a more thorough understanding of gout. However, gout is still not widely regarded as one of the differential diagnoses for acute pain affecting the hip joint. The aim of this review is to provide an overview of the pathophysiology of gout and subsequently examine current diagnostic methods and therapeutic agents for treatment of gout, based on an understanding of its underlying mechanisms. A review of literature on previous studies regarding gout-related hip joint issues was also conducted in order to provide a useful reference for hip surgeons.

The reported worldwide prevalence of gout is around 1%-4% (Table 1)^5-7). In western high-income countries, higher prevalence of 3%-6% has been reported for males, compared to 1%-3% for females, meaning that gout is approximately 2-6 times more common in males than in females. The prevalence of gout increases with age, with a prevalence of 10% for males over 80 years old and a prevalence of 6% for females. The annual incidence of gout is approximately 2.68 per 1,000 individuals. Factors such as lack of exercise, changes in dietary habits (increased consumption of fast foods), and the increased incidence of obesity and metabolic syndrome contribute to the increasing global incidence of gout.

Table 1 . Prevalence and Incidence Rate of Gout.

Prevalence and incidence	Rate
Worldwide prevalence (%)	1-4
Prevalence in males (%)	3-6
Prevalence in females (%)	1-3
Prevalence in males over 80 years old (%)	10
Prevalence in females over 80 years old (%)	6
Annual incidence	2.68/1,000 persons

Serum uric acid levels show a pattern of gradually increasing from a low level in childhood and reaching normal adult levels after adolescence⁸⁾. In adulthood, the levels of uric acid are typically higher in males compared to females. However, after menopause, the levels of uric acid are increased in females, reaching levels similar to those of adult males. This phenomenon is helpful in explaining the higher prevalence of gout in middle-aged and older males, as well as postmenopausal females.

Deposition of urate crystals in tissues may commence when levels of uric acid in serum exceed 6.8 mg/dL⁵⁾. Urate, the ionized form of uric acid, has a weakly acidic nature with a pH 5.8. Various factors, including the pH of the synovial fluid, water concentration, electrolyte levels, and other components present in synovial fluid such as proteoglycans and collagen influence the solubility of uric acid within the joint. These factors can affect the solubility and potential crystallization of uric acid within the joint⁹⁾. Hyperuricemia is regarded as the main pathogenesis of gout. However, development of gout does not occur in every person with hyperuricemia. According to previous studies, development of gout occurred in only 5% of individuals with serum uric acid levels above 9 mg/dL¹⁰⁾. This finding suggests that factors other than hyperuricemia also contribute to development of gout, including genetic predisposition.

A homeostatic balance of production and excretion is responsible for maintenance of serum uric acid levels⁶⁾. Disruption of this balance can lead to an increase in the levels of uric acid. Approximately two-thirds of uric acid is excreted through the kidneys, while one-third is eliminated via the gastrointestinal tract¹¹⁾. Approximately 90% of hyperuricemia cases can be attributed to impaired excretion, with insufficient renal excretion as the cause in the majority of cases. In the gastrointestinal tract, involvement of the transporter ABCG2 in uric acid excretion, and in the kidneys, involvement of urate and organic anion transporters in uric acid excretion have been reported^12,13). Mutations in the genes encoding these transporters can also be a cause of impaired uric acid excretion, and development of hyperuricemia^14,15).

Factors that can increase production of uric acid include genetic disorders that can cause abnormalities in enzymes related to purine metabolism, increased dietary intake of purine-rich foods, and an increase in production of endogenous urate⁶⁾. Among the genetic disorders, Lesch–Nyhan syndrome is an X-linked recessive genetic disorder that causes a deficiency of hypoxanthine-guanine phosphoribosyltransferase. In addition, superactivity of phosphoribosyl pyrophosphate synthetase is an X-linked dominant inherited disorder. Association of both syndromes with renal stones and various neurological abnormalities has been reported¹⁶⁾. Dietary sources of purines include meat and seafood^17,18). Therefore, regulating intake of these foods is important. However, consumption of plant-based purines, such as beans, lentils, mushrooms, peas, and legumes, and dairy products does not increase the risk of hyperuricemia and gout. In fact, vitamin C, low-fat dairy products, and olive oil have been reported to decrease the risk of hyperuricemia. Alcohol can be a risk factor for hyperuricemia; however, the risk can vary depending on the amount and type. Beer is associated with the highest risk and wine the lowest. Factors that can increase production of endogenous urate include conditions that can cause an increase in cellular turnover, such as malignancies, hematological disorders, and inflammatory diseases⁶⁾. In addition, increased production of purine due to chemotherapy or tissue damage can also contribute to elevated levels of urate. Weight gain and obesity have also been associated with increased production of endogenous urate.

Necroinflammation is a key aspect in the pathophysiology of acute gout (Fig. 1)^6,19). Supersaturation and crystallization of uric acid within the joint causes direct damage to synovial epithelial cells, leading to the release of damage-associated molecular patterns or alarmins from the dead cells. MSU crystals are taken up by mononuclear phagocytes within the joint, leading to activation of the NLR family pyrin domain-containing 3 (NLRP3)/interleukin (IL)-1β inflammasome, resulting in local secretion of mature IL-1β and IL-1α. IL-1R/NF-κB–mediated cytokines and chemokines are also released by parenchymal cells. These inflammatory cytokines facilitate recruitment of neutrophils into the joint. Once inside the joint, MSU crystals are phagocytized by neutrophils, which then undergo necroptosis via activation of receptor-interacting protein kinase (RIPK)-1 and RIPK-3 and mixed-lineage kinase domain-like protein (MLKL). This process leads to the release of proinflammatory mediators such as histones and proteases, further perpetuating the vicious cycle. Continuation of the cycle may eventually lead to development of a cytokine storm. However, resolution of an acute gout attack typically occurs within a few days due to counter-regulatory mechanisms involving macrophages. Apoptotic neutrophils are cleared by macrophages in a noninflammatory manner. Negative feedback regulators including pyrin and caspase-containing domains, as well as anti-inflammatory cytokines such as TGF-β1 (transforming growth factor-beta1) are also released by macrophages, which inhibit proinflammatory mediators such as TNF I and II, and IL-10.

Figure 1. The molecular mechanisms in acute and chronic gout arthritis. (A) The key pathophysiology of acute gout is necroinflammation. (1) Monosodium urate (MSU) crystals elicit direct cytotoxic effects on epithelial cells by activating necroptosis. (2) Epithelial cell death releases damage-associated molecular patterns (DAMPs) and alarmins. (3) Mononuclear phagocytes take up MSU crystals, a process activating the NLR family pyrin domain-containing 3 (NLRP3)/interleukin (IL)-1β inflammasome and inducing local secretion of mature IL-1β as well as IL-1α. (4) Both forms of IL-1 activate the IL-1R on parenchymal and immune cells to secrete numerous proinflammatory mediators. (5) Among these mediators, several promote the rapid recruitment of neutrophils. (6) Neutrophils encounter MSU crystals, undergo necroptosis and neutrophil extracellular trap (NET) formation. (7) Necrotic neutrophils and NETs release various proinflammatory mediators, such as lytic proteases and cytotoxic histones, that further contribute to the crescendo of the auto-amplification loop of necroinflammation (vicious cycle). (B) Granuloma formation with tophus masses at the center, surrounded by giant cells and epitheloid cell layers can lead to bony lesions, soft tissue damage, and tissue remodeling.

Tophi, which are observed in cases of chronic gout, are similar to granulomas and can be divided into three layers. The first layer consists of a core composed of MSU crystals. The second layer surrounding the central core contains dense populations of innate immune cells, including CD68+ macrophages, plasma cells, and an abundance of neutrophil extracellular traps. The third layer is the fibrovascular outer region, which contains smaller numbers of T and B lymphocytes. Tophi may manifest without apparent signs of acute gout-related inflammation, despite the continued presence of MSU crystal deposits at the center of the lesions. The viability and differentiation of osteoclasts can be inhibited by MSU crystals, subsequently diminishing the capacity for formation of new bone. Consequently, osteoclasts are not observed in the vicinity of tophi-associated bony erosions. In addition, the viability and functionality of chondrocytes can be diminished by MSU crystals, leading to loss of cartilage.

As recommended by all included reports, confirmation of MSU crystals in synovial fluid or tophi has been the gold standard for definitive diagnosis^20-25). Evaluation of the clinical signs, laboratory results, and imaging results is generally required for a diagnosis of gout when MSU crystals have not been detected^26-28). The level of uric acid in serum required for diagnosis of hyperuricemia differs among studies. In general, a cut-off level of 6.8 to 7.0 mg/dL of serum uric acid has been reported^21,29,30). When suggesting standards according to gender, 6.0 mg/dL (or ~360 µmol/L) for females and 7.0 mg/dL (or ~420 µmol/L) for males were recommended^25,31). Various imaging modalities include plain radiography, ultrasonography, and dual-energy computed tomography. Changes in plain radiographs occur over several years due to slow disease progression. Therefore, despite the limited usefulness of plain radiographs in early gout, they can be helpful in supporting the diagnosis in later stages. Typical radiologic features of an established diagnosis of gout include bony erosions with protruding edges and sclerotic margins, bone hyperplasia, joint space narrowing, and soft tissue masses (tophis) that may be calcified. Musculoskeletal ultrasonography can assist in the diagnosis of gout, particularly in the case of atypical symptoms and when obtaining microscopic proof of the presence of MSU crystals is not possible. In the results of a systematic review, ultrasound findings of double contour signs, tophi, punctate deposits in the synovial membrane, and hyperechoic spots in the synovial fluid showed good specificity ranging from 0.65 to 1.00 for diagnosis of gout, using MSU crystal identification as the reference standard³²⁾. A meta-analysis of diagnostic studies on ultrasonographic assessment of joints for diagnosis of gout reported a sensitivity of 0.71 (95% confidence interval [CI] 0.64-0.78), specificity of 0.62 (95% CI 0.56-0.67), and an area under curve (AUC) of 0.8549 when a double contour sign was observed³³⁾. According to findings from several meta-analysis studies, dual-energy computed tomography, a diagnostic tool, has a high sensitivity of 88% (95% CI 84-90), specificity of 90% (95% CI 85-93), and AUC of 0.9565 for diagnosis of gout³⁴⁾.

Medications for gout are administered for treatment and prevention of gout attacks.

1. Medical Treatment of Gout Attacks

An acute attack of gout can be accompanied by sudden severe joint pain, swelling, redness, and localized heat in the joint area. Treatment should include administration of one or more anti-inflammatory drugs as soon as possible to reduce pain. There are three available medication types: colchicine, non-steroidal anti-inflammatory drugs (NSAIDs), and oral glucocorticoids. In comparative studies between drugs, colchicine, NSAIDs, and oral glucocorticoids showed similar effects³⁵⁾. In a randomized, double-blind study comparing indomethacin and oral glucocorticoids, more side effects were observed in the group receiving indomethacin compared with the group receiving oral glucocorticoids³⁶⁾. In the case of a recurrent gout attack, the patient's experience and preference for anti-inflammatory drugs used in the treatment of previous gout attacks should be considered when selecting medication. Colchicine provides relief from joint pain and inflammation during gout attacks. Immediately after a gout attack, 1.2 mg colchicine should be taken, followed by 1.6 mg 1 hour later, then 1.6 mg 12 hours later, which is a gout prevention dose and can be repeated 1-2 times a day³⁷⁾. Colchicine is cleaved by cytochrome P450 3A4 and excreted via the P-glycoprotein transporter³⁸⁾. A reduction of the dose of colchicine may be required for patients taking cytochrome P450 3A4 inhibitors. Both general NSAIDs and drugs capable of selective inhibition of cyclooxygenase-2 are effective in the treatment of gout attacks, therefore, it is presumed that no significant difference in effectiveness will be observed between the drugs³⁹⁾. In a large-scale randomized controlled study, the effects observed in the group taking high-dose 800 mg and 400 mg celecoxib daily were similar to those observed in the indomethacin group, while inferior effects were observed in the low-dose 100 mg daily group⁴⁰⁾. Considering the side effects, the course of treatment should be as brief as possible, although there may be a recurrence of gout attacks if the drug is stopped too early. Glucocorticoids may be the most appropriate treatment option for patients with renal, cardiac, hepatic, or gastrointestinal diseases. In a multicenter, randomized, double-blind study, the effects of administration of 30 mg of prednisolone once a day for five days were similar to those of NSAIDs³⁶⁾. The 2016 European Society of Rheumatology guidelines recommend administering 30-35 mg of prednisolone and glucocorticoids at the same dose for 3-5 days as the primary treatment for gout attacks⁴¹⁾.

2. Medication for Prevention of Gout Attacks

According to the results of a clinical trial, the frequency of gout attack was 36% in the group not receiving prophylaxis for gout attack, and as low as 19% in the group taking low-dose colchicine⁴²⁾. The appropriate dose of colchicine for prophylaxis is 0.6 mg 1-2 times a day. Anti-inflammatory drugs should be taken for at least 3-6 months, until the level of uric acid in serum reaches the target value, and the gout attacks stop occurring³⁷⁾. In the first randomized, placebo-controlled trial of colchicine prophylaxis, among 43 subjects, fewer attacks were reported in subjects who were treated with colchicine compared with those who did not use colchicine⁴³⁾. Indications for treatment with uric acid-lowering drugs include patients with gout who have subcutaneous gout-related nodules, damage from radiation therapy, or more than two gout attacks per year³⁷⁾. The urate lowering efficacy of febuxostat 80 mg was superior to that of febuxostat 40 mg and allopurinol (300/200 mg), and both doses of febuxostat were more effective and equally effective than allopurinol in patients with mild/moderate renal impairment⁴⁴⁾. Uric acid-lowering drugs are not immediately used in patients experiencing a gout attack for the first time. However, it should be started in cases involving decreased renal function, a blood uric acid level of 8-9 mg/dL or higher, and uric acid urolithiasis. The 2020 American College of Rheumatology guidelines recommended simultaneous treatment of gout attack and prescription of uric acid-lowering drugs for patients visiting the hospital with gout attacks³⁷⁾. The guidelines reflect the opinion that the number of patient visits can be reduced and that compliance with uric acid-lowering drugs can be increased for patients suffering from gout attacks. In a randomized, double-blind study of 1,027 patients evaluating the efficacy of drugs (febuxostat and allopurinol) for lowering the levels of serum urate, serum urate levels <6.0 mg/dL were maintained in the febuxostat group compared to the allopurinol group⁴⁰⁾. A treat-to-serum urate target approach is important for achieving the sustained therapeutic effect of uric acid-lowering drugs³⁷⁾. In order to lower the level of uric acid in blood to a target below 6 mg/dL, uric acid-lowering drugs are started at a low dose and gradually increased, and follow-up testing is performed for management of the blood uric acid level. Allopurinol has been reported as the most prescribed and first-choice uric acid-lowering drug in clinical practice⁴⁵⁾. Allopurinol is converted in the liver to the active metabolite oxypurinol. Prescribing 300 mg once a day can be effective in increasing medication compliance⁴⁶⁾. According to the results of a recent study, the average dose of allopurinol to reach a serum uric acid level of less than 6 mg/dL was approximately 400 mg⁴⁷⁾. In the first two weeks of treatment for gout attack, serum uric acid level, renal function, and HLA-B*5081 genotype testing are performed at the same time. Two weeks later, uric acid-lowering drugs are started along with drugs for prevention of gout attack. If the result of the HLA-B*5081 gene test is positive and chronic kidney disease stage 3, febuxostat should be administered as the first-line drug, instead of allopurinol. Febuxostat is an inhibitor of uric acid formation, which inhibits xanthine oxidase like allopurinol⁴⁸⁾. According to the 2020 American College of Rheumatology guidelines, febuxostat, like allopurinol, should be started at a low dose (≤40 mg/day) and gradually increased³⁷⁾. In a study mandated by the European Medicines Agency in 2020, no difference in terms of the incidence of adverse cardiovascular events, total mortality, and cardiovascular mortality was observed between the two drugs⁴⁹⁾. According to a recommendation by the 2020 French Matisse Society, allopurinol was banned and febuxostat was preferred in cases involving very poor renal function of stage 4-5 (estimated glomerular filtration rate <30 mL/min/1.73 m²)⁵⁰⁾. Benzbromarone is a uricosuric agent. Benzbromarone is often administered concurrently in cases where the concentration of uric acid in blood does not reach the target value even when using uric acid-lowering drugs. As reported, benzbromarone has not been approved in the United States due to the risk of fatal liver toxicity. Therefore, the need for regular testing of liver function should be considered when prescribing.

3. Arthroscopy for Detection and Treatment of Gout

Gout that affects the hip joint can cause severe pain and significant joint effusion. Among treatment options, arthroscopic evaluation and treatment offer minimal morbidity while enabling analysis of joint fluid, synovial biopsy, and decompression and lavage of the joint⁵¹⁾.

Hadler et al.⁵²⁾ reported on the clinical presentation and characteristics of 102 patients with acute polyarticular gout. Involvement of the lower limb joint was detected in 83% of these patients and 39% had polyarthritis as the initial manifestation. However, among the patients included in their study, involvement of the hip joint was only suspected in two cases.

Gout can occur in any joint, including the spine, pubic symphysis, and sacroiliac joint^1,3). However, involvement of central joints in the body is less frequent, which is related to the solubility of MSU. The solubility of MSU is reduced by lower pH or temperature, which promotes the accumulation of MSU crystals⁵³⁾. Therefore, peripheral joints such as the first metatarsophalangeal, knee, and ankle joints, with an environment that is more likely conducive to such changes, are more commonly affected⁵⁴⁾. However, fewer variations in pH or temperature are likely to affect joints like the hip, which are closer to the heart and well-perfused, resulting in a lower incidence of gout. In addition, the atypical presentation of standard gout symptoms, acute joint swelling, severe pain, or an increase in skin temperature, can be attributed in part to the deep location of these joints.

1. Ultrasound Findings of Hip Joint Involvement in Gout

Analysis of joint fluid, specifically for detection of MSU crystals, is considered the gold standard for diagnosis of gout⁵⁵⁾. Due to the deep location of the hip joint, use of ultrasound guidance during aspiration of joint fluid can be helpful, as it can uncover specific findings related to inflammatory and structural changes in the joint that can be considered in the diagnosis prior to analysis of joint fluid. One such finding is the double contour sign observed on ultrasound. The double contour sign on ultrasound refers to an echogenic line on the outer surface of the joint cartilage, parallel to the subchondral bone, caused by the deposition of MSU crystals on the surface of hyaline articular cartilage (Fig. 2). Zhu et al.⁵⁶⁾ reported that observation of this sign can support the diagnosis of gout. Di Matteo et al.⁵⁷⁾ reported that the double contour sign commonly observed around the hip joint in patients with gout is observed more frequently with longer disease duration, a higher frequency of gout-like attacks, and the presence of subcutaneous tophi.

Figure 2. In the longitudinal ultrasound scan of the hip joint it is possible to observe the formation of a double contour (arrowheads) on the overlying hyaline cartilage of the femoral head. This double contour is caused by the intraarticular aggregation of monosodium urate crystal deposits.

2. Unusual Cases of Hip Involvement in Gout

Xu et al.⁵⁸⁾ reported on a case of gout in a 28-year-old female. The patient presented to the hospital with worsening pain affecting the right hip that had started several days prior. Laboratory tests showed an elevated white blood cell count, C-reactive protein level, and erythrocyte sedimentation rate. Aspiration of the joint revealed a yellow cloudy fluid, and arthroscopic irrigation and debridement were performed. Ultimately, no bacterial growth was detected in the joint fluid culture, confirming the diagnosis of gout. The authors noted that previous cases of gout in young individuals involved known risk factors; however, this patient was the youngest reported case and had no known risk factors for gout or family history of gout.

Tolin and Navarra⁵⁹⁾ reported on the case of a 57-year-old male patient with chronic gout who presented with persistent vague pain affecting the right knee that had been ongoing for two months while on irregular medication. The patient’s pain was not related to activity and showed improvement with administration of tramadol but gradually progressed to involvement of the right hip and inguinal area. This case features the occurrence of acute involvement of the hip joint in a patient with chronic gout, with an initial manifestation of knee joint symptoms caused by referred pain.

Shah et al.⁶⁰⁾ reported on the case of a 71-year-old male patient who underwent a metal-on-metal total hip arthroplasty procedure for treatment of osteoarthritis 13 years prior. The patient had MPO/p-ANCA-positive vasculitis and was on low-dose rituximab as a chronic medication. He presented with acute hip pain, and aspiration of the joint revealed cloudy brown fluid. The results of fluid analysis indicated the presence of cobalt, chromium, and MSU crystals. The authors performed a revision surgery for replacement of the polyethylene liner and femoral head. They also observed pseudocapsule formation, an adverse reaction to metal debris, and amyloid deposition in the joint capsule. Huang et al.⁵³⁾ reported on the case of a 74-year-old male patient who presented with pain affecting the left hip, left ankle, and bilateral knee. The patient was a heavy alcoholic, and osteonecrosis of both femoral heads was detected by hip magnetic resonance imaging (MRI). The femoral head was irregular in shape and had collapsed, and the acetabulum was deformed, resulting in leg length discrepancy. The patient underwent a hip arthroplasty procedure for treatment of the severe deformity. Both cases demonstrate the coexistence of multiple pathological conditions.

Parisien et al.⁶¹⁾ reported on the case of a pathological femoral neck fracture associated with rare osseous lesions in a patient with gout. A 76-year-old female patient presented to the hospital with pain affecting the left hip following a low-energy fall. Despite having multiple medical comorbidities there was no history or family history of gout. On admission, joint osteoarthritis was detected on plain radiographs; however, the fracture was not clearly visible in computed tomography. Therefore, an MRI was performed, which showed a joint effusion and a non-displaced femoral neck fracture accompanied by nonspecific bone lesions. The authors performed a bone biopsy and internal fixation using a cephalomedullary nail. The results of the biopsy showed no signs of malignancy or infection, and the presence of tophi, a characteristic of gout, was ultimately confirmed. Needle-shaped negatively birefringent crystals were also observed.

Although gout arthritis of the hip joint could have clinical importance, it is currently underrecognized. In addition, as we have described in specific cases, making a diagnosis can be challenging in certain situations. However, the possibility of gout should not be overlooked and a diagnosis should be attempted using various available methods.

3. Debates on the Risk of Non-Vertebral Osteoporotic Fracture

The elevation of proinflammatory cytokine levels caused by gout can induce an inflammatory response in the body, leading to increased bone resorption and decreased bone formation^62,63). In addition, it can inhibit activation of vitamin D through suppression of 1-alpha-hydroxylase, resulting in lower levels of 1,25-dihydroxyvitamin D and higher levels of parathyroid hormone^64,65). In theory, this can promote development of osteoporosis and increase the risk of fractures.

Paik et al.⁶⁶⁾ conducted a prospective observational study on the relationship between gout and the risk of developing wrist and hip fractures in female patients. Among 3,769 patients with wrist fractures and 2,147 patients with hip fractures, patients with gout had 107 wrist fractures and 117 hip fractures. The authors reported that a history of gout increased the risk of hip fracture by 1.38 times; however, the risk of wrist fracture did not increase. In contrast, Kim et al.⁶⁷⁾, who performed an analysis of the risk of non-vertebral fractures between 73,202 patients with gout and 219,606 non-gout patients through matching, found that the risk of nonvertebral fractures was not increased in patients with gout. Therefore, the relationship between gout and the risk of osteoporotic fractures has not been fully established and conduct of additional research is needed in order to better understand this association.

Appropriate treatment methods and lifestyle modifications should be applied for patients with gout based on an adequate understanding of the pathophysiology and factors that contribute to development of gout. Gout, which is commonly encountered in medical settings, is an easily treatable disease. Hyperuricemia has been established as the primary cause, and with few available drugs, treatment selection is straightforward, the drugs are effective, and the price is relatively cheap. Most patients only visit the hospital in the case of an acute attack of gout, receive emergency treatment, and then go home. However, gout is not a disease that can be resolved with emergency treatment, but rather a chronic disease requiring the ongoing use of uric acid-lowering drugs. Therefore, patients should be educated on treatment strategies according to target blood uric acid concentration in order to achieve better results from treatment. In cases of gout that affects the hip joint, the clinical features may not be as apparent, underscoring the need for clinicians to proceed with caution during the process of diagnosis.

This research was supported by “Regional Innovation Strategy (RIS)” through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (MOE) (2021RIS-001).

This review article was presented at the Clinical Practice Guidelines Symposium of the Korean Hip Society on May 13, 2023.

No other potential conflict of interest relevant to this article was reported.