Tophaceous Gout: A Comprehensive Overview

Tophaceous gout represents the most advanced and severe manifestation of gout, a form of inflammatory arthritis. This condition arises from the sustained accumulation of uric acid crystals, which then coalesce into distinct growths known as tophi. These tophi typically develop around joints and within the soft tissues affected by chronic gout. It is a critical progression from earlier stages of the disease, demanding vigilant management to prevent irreversible damage and functional impairment. Understanding its origins and impact is paramount for effective intervention.

Gout itself is a prevalent type of inflammatory arthritis, impacting over 9 million adults across the United States. Its root cause lies in hyperuricemia, a condition characterized by abnormally high levels of uric acid in the bloodstream. When individuals experience chronic gout, where uric acid levels remain persistently elevated, they are at risk of developing tophaceous gout. The continuous excess of uric acid leads to the ongoing formation and deposition of urate crystals, primarily concentrating around affected joint structures.

The presence of tophaceous gout can severely impact various joints and soft tissues throughout the body. The resulting growths can be considerably painful, frequently leading to significant joint damage and, in advanced cases, severe disability. Fortunately, modern medical advancements offer a range of effective treatment strategies. These interventions are designed not only to alleviate the acute symptoms and reduce the frequency of painful flare-ups but also to prevent further joint damage and mitigate the potential for long-term disability, offering hope for improved quality of life.

This comprehensive article aims to elucidate the intricate journey of gout, detailing its four distinct stages of progression. We will explore the characteristic symptoms associated with tophaceous gout, delve into its underlying causes, and outline the established diagnostic procedures. Furthermore, we will discuss the various treatment modalities available, encompassing pharmacological interventions, essential lifestyle modifications, and surgical considerations, alongside crucial strategies for preventing the onset and progression of this challenging condition.

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Tophaceous Gout: The Most Severe Form of Gout

Medical professionals classify gout into four progressive stages, a framework that assists in predicting the disease's trajectory and guiding therapeutic approaches. This categorization helps clinicians understand the severity and development of the condition, allowing for more targeted and timely interventions. Each stage presents unique characteristics, ranging from initial biochemical changes to overt clinical manifestations and chronic complications. Recognizing these stages is vital for both diagnosis and the formulation of an effective long-term management plan.

The four recognized stages of gout include:

• Asymptomatic hyperuricemia
• Acute gout
• Intercritical gout
• Chronic tophaceous gout

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Asymptomatic Hyperuricemia

Asymptomatic hyperuricemia marks the initial phase of gout, characterized by an elevated concentration of uric acid within the bloodstream without any noticeable joint pain, redness, or swelling. This biochemical imbalance occurs as the body processes purines—naturally occurring substances produced by the body and also found in certain foods and beverages. Consuming foods high in purines, such as red meats, organ meats, and specific seafood, along with excessive alcohol intake, can significantly contribute to these elevated uric acid levels.

High uric acid levels can also arise if the body's kidneys are unable to efficiently excrete uric acid through urine. Various underlying health conditions, including chronic kidney disease, diabetes, and an underactive thyroid, can impair this excretory function. Furthermore, the use of certain medications, particularly diuretics often referred to as "water pills," can also contribute to an increase in serum uric acid. Although uric acid blood tests will show elevated levels in this stage, hyperuricemia alone is not sufficient for a gout diagnosis. Many individuals with high uric acid may never develop gout, with studies indicating that only a fraction, specifically up to 36% of those with hyperuricemia, will progress to clinical gout. Nonetheless, urate crystals begin to silently accumulate in the joints during this period, setting the stage for potential future complications.

Acute Gout

The acute stage of gout is marked by sudden, intensely painful attacks, frequently occurring during the nighttime. These episodes, commonly referred to as flares, attacks, or flare-ups, typically present with severe joint pain, pronounced redness, and noticeable swelling in the affected area. The joints most often targeted during an acute gout flare include the big toes, other parts of the feet, ankles, and knees, though any joint can be affected. The onset is often abrupt and can be debilitating, profoundly impacting daily activities.

A characteristic feature of these acute attacks is their relatively short duration in the early stages, often lasting only a few days before symptoms begin to subside. In some instances, a flare might also be accompanied by systemic symptoms such as chills or fever, indicating a significant inflammatory response. While a subsequent attack may not occur for several months or even up to a year, it is critical to note that if these episodes are not promptly and effectively managed, they tend to become progressively more severe, more frequent, and last for considerably longer durations over time, leading to more chronic issues.

Intercritical Gout

Following an acute gout flare, many individuals enter the intercritical stage, a period characterized by the absence of symptoms. Despite this apparent remission, it is a crucial phase for disease management, as up to 75% of people with gout will experience a second flare within a year of their initial attack. However, it is also possible for some individuals to go several years without another symptomatic episode, highlighting the variability of the disease. This asymptomatic interval between flares represents an optimal window for initiating long-term therapeutic strategies.

During the intercritical stage, the primary objective is to implement measures that prevent future gout flares and mitigate the risk of long-term complications. This involves a dual approach: pharmacologically lowering uric acid levels through prescribed medications and adopting significant dietary adjustments and other lifestyle modifications. By proactively managing uric acid concentrations during this symptom-free period, patients can effectively interrupt the progression of the disease, thereby reducing the likelihood of recurrent attacks and protecting joint health before damage becomes irreversible.

Chronic Tophaceous Gout

Chronic tophaceous gout represents the most advanced and potentially debilitating stage of the disease, occurring when uric acid levels remain inadequately controlled over prolonged periods. This stage is distinctly characterized by the development of tophi—visible accumulations of urate crystals that manifest as hard, palpable lumps beneath the skin. These tophi can form in various locations, notably impacting the small joints of the fingers, where they can cause noticeable physical deformities and significant limitations in joint movement and dexterity, profoundly affecting fine motor skills.

If these tophi are allowed to develop within the bone and cartilage, they can lead to severe and irreversible joint damage and progressive deformity. Furthermore, tophi located under the skin can be acutely painful and are susceptible to infection, adding another layer of complication to the disease. While the progression to chronic tophaceous gout often takes a decade or longer, resulting from persistent inflammation and recurrent attacks, it is now considered rare due to the availability of effective treatment options. Even if gout reaches this advanced stage, consistent use of uric acid-lowering medications can significantly reduce the risk of complications and the development of new or visible tophi, underscoring the importance of adherence to treatment.

Tophaceous Gout Symptoms

Gout is fundamentally an inflammatory condition, primarily affecting joints and the surrounding soft tissues. The inflammatory response triggered by uric acid crystal deposition leads to a distinct set of symptoms. During a flare-up, individuals typically experience severe pain, which is often described as excruciating and incapacitating. This pain is accompanied by noticeable swelling around the affected joint, along with a sensation of warmth and extreme tenderness upon touch. The skin overlying the inflamed joint often becomes visibly red, a classic sign of inflammation.

When gout progresses to its chronic form, it can lead to more persistent and damaging issues beyond these acute flare symptoms. Chronic gout is associated with synovitis, which is the inflammation of the joint lining, contributing to ongoing discomfort and stiffness. The persistent presence of urate crystals can also cause bony erosions, leading to irreversible loss of bone tissue, and significant damage to the joint cartilage, compromising joint integrity. Critically, the formation of tophi—deposits of uric acid crystals—becomes a hallmark of chronic tophaceous gout, representing a severe complication of uncontrolled disease.

Gout is characterized by its fluctuating nature, alternating between periods of symptomatic flare-ups and periods of remission where symptoms are absent. A typical gout flare usually strikes suddenly, often waking individuals from sleep due to its rapid onset and escalating intensity. The recovery period from a flare can vary, potentially taking several days or even weeks for complete resolution. However, chronic gout introduces additional and more persistent symptoms, primarily due to the presence of tophi, which are masses of uric acid that accumulate under the skin.

The manifestations associated with tophi can vary significantly in number, size, and location, impacting patients differently. These include direct joint or tissue damage, which may be apparent visually or detectable only through advanced imaging techniques. Tophi can cause pronounced stiffness and a significant reduction in the affected joint's range of motion, severely impairing function. In advanced cases, this can lead to disability or a diminished capacity to effectively use the affected joint. Furthermore, tophi can induce nerve pain due to direct compression or entrapment of nearby nerves, adding another layer of discomfort. It's crucial to understand that tophi can inflict severe and lasting damage to joint and bone tissue. The combination of joint swelling and nerve compression can also lead to the skin breaking down over a tophus, resulting in the drainage of uric acid crystals and a heightened risk of infection in the affected joint or surrounding tissue.

What Causes Tophaceous Gout?

Gout develops when the concentration of uric acid in the blood becomes excessively high, a condition known as hyperuricemia. Under normal physiological circumstances, the kidneys play a vital role in filtering uric acid from the bloodstream and excreting it efficiently through urine. However, in certain situations, the kidneys may become overwhelmed, either due to an overproduction of uric acid or an impaired ability to eliminate it, leading to an undesirable buildup of this compound in the circulation.

When uric acid levels reach a critical saturation point, the excess uric acid can precipitate and crystallize, forming sharp urate crystals that are then deposited within the joints. Upon recognizing these urate crystals as foreign invaders, the body's immune system mounts a robust inflammatory response. This activation of the inflammatory cascade is what ultimately leads to the characteristic swelling, intense pain, and other debilitating symptoms commonly associated with a gout attack, underscoring the intricate interplay between metabolism and immune function in the disease's pathogenesis.

Certain individuals face an increased predisposition to developing gout, influenced by a combination of both non-modifiable and modifiable risk factors. Non-modifiable risk factors are inherent characteristics that cannot be altered, such as age, sex, genetic predisposition, and ethnic background. In contrast, modifiable risk factors are lifestyle and environmental elements that can be actively managed or changed to potentially reduce the risk of developing a health condition. Examples of these changeable factors include dietary habits, smoking status, body weight, and the level of physical activity engaged in, all of which offer opportunities for intervention and risk reduction.

Non-Modifiable vs. Modifiable Risk Factors

Non-modifiable risk factors for gout encompass elements that are beyond an individual's control, yet significantly influence their susceptibility to the condition. These inherent predispositions include:

• Sex: Individuals assigned male at birth exhibit a notably higher propensity to develop gout compared to those assigned female at birth, although the risk for women increases after menopause.
• Age: A clear association exists between advancing age and an elevated risk for both hyperuricemia and the subsequent development of gout. The body's metabolic processes and kidney function can become less efficient with age.
• Family history: A genetic predisposition plays a significant role; having close family members with a history of gout substantially increases an individual's own risk compared to the general population, suggesting a hereditary component in uric acid metabolism.

Modifiable risk factors for gout are elements within an individual's control that, if managed, can significantly influence the likelihood of developing the condition. These factors include:

• Alcohol: Excessive consumption of alcohol, particularly beer and spirits, can acutely elevate uric acid levels in the blood, predisposing individuals to gout flares. Limiting intake is a key preventive measure.
• Diet: A diet rich in purines, found abundantly in organ meats, certain seafood, and high-fructose corn syrup-sweetened beverages, directly contributes to increased uric acid production. Adopting a low-purine diet is often recommended.
• Medical conditions: Certain pre-existing health issues, such as high blood pressure, various kidney diseases, diabetes, and anemia, can all contribute to elevated uric acid levels. Effective management of these underlying conditions can substantially reduce gout risk.
• Medications: Several commonly prescribed medications can inadvertently raise uric acid concentrations. These include diuretics (water pills), beta-blockers (used for blood pressure control), cyclosporine (an immunosuppressant), and even low-dose aspirin. For individuals at higher risk for gout, healthcare providers may consider substituting these with less risky alternatives.

The progression to chronic tophaceous gout is often a direct consequence of untreated or inadequately managed gout over an extended period. Individuals who experience frequent and severe gout flares are particularly at risk, as such episodes signify persistently elevated uric acid levels that are not being effectively controlled. This sustained hyperuricemia creates an environment conducive to the formation and growth of tophi. Adhering diligently to a healthcare provider’s treatment plan, maintaining careful dietary habits, and consistently taking prescribed medications are critical steps. These measures are pivotal in lowering uric acid levels, preventing recurrent flares, and significantly reducing the risk of tophi development and the debilitating complications associated with chronic tophaceous gout.

Diagnosis

The definitive diagnosis of gout, particularly tophaceous gout, is typically confirmed through a joint aspiration test. In this procedure, a healthcare professional carefully uses a needle to draw a sample of synovial fluid—the lubricating fluid found within joints—or, in cases of tophaceous gout, a sample from the tophus deposit itself. This collected fluid or tissue sample is then meticulously sent to a specialized laboratory for microscopic examination, where the presence of characteristic urate crystals can be directly identified, providing a conclusive diagnosis.

While serum uric acid concentrations can offer supportive evidence for a gout diagnosis, it's crucial to understand that hyperuricemia (elevated uric acid levels) alone does not conclusively signify the presence of gout. Many individuals may have high uric acid without developing the condition. The most opportune time to confirm a diagnosis of gout is often during an active attack, when the inflammatory response is most pronounced and crystals are more readily identifiable. For chronic tophaceous gout, a microscopic examination of the tophi deposits themselves provides the definitive confirmation, directly demonstrating the presence of urate crystals.

In addition to the joint aspiration test, several other diagnostic tools may be employed to either confirm a gout diagnosis or differentiate it from other forms of joint inflammation. These supplementary tests include:

• Blood work: A uric acid blood test is routinely performed to measure the concentration of uric acid in the bloodstream. Furthermore, other blood tests may be ordered to identify additional markers that could indicate other types of arthritis or related systemic conditions, providing a broader diagnostic picture.
• Imaging: X-rays can be a valuable tool, primarily to rule out other potential causes of joint inflammation and to assess for joint damage over time. Ultrasound scans are increasingly utilized for their ability to non-invasively detect urate crystals within joints and visualize tophi masses, even before they become clinically apparent. A dual-energy computerized tomography (DECT) scan offers advanced imaging capabilities, capturing images from multiple angles to precisely visualize urate crystal deposits within joints and comprehensively characterize tophi masses, providing detailed anatomical information.

How Is Tophaceous Gout Treated?

While there is currently no definitive cure for tophaceous gout, the condition is highly manageable and treatable through a combination of therapeutic approaches. Effective management typically involves a regimen of medications, crucial lifestyle modifications, and in select, advanced cases, surgical intervention may be considered as a last resort. The overarching goal of treatment is to lower uric acid levels, alleviate symptoms, prevent further joint damage, and enhance the patient's overall quality of life, transforming a debilitating condition into a controllable one.

Medications

Pharmacological interventions aimed at lowering uric acid levels are a cornerstone of gout management and are strongly recommended for specific patient profiles. These include individuals who experience two or more gout flare-ups annually, those who exhibit clear evidence of joint damage on imaging studies, or patients who have already developed tophaceous gout. The American College of Rheumatology guidelines even suggest initiating these critical uric acid-lowering medications during an acute flare, rather than delaying treatment until the symptomatic episode has fully subsided, to optimize long-term outcomes.

A range of uric acid-lowering medicines is employed in the comprehensive treatment of gout, each targeting different aspects of uric acid metabolism. These include:

• Allopurinol: This medication works by preventing the overproduction of uric acid, thereby reducing overall levels in the body.
• Uloric (febuxostat): Similar to allopurinol, febuxostat also reduces the formation of uric acid, offering an alternative for patients who may not tolerate allopurinol.
• Probenecid: This drug enhances the kidneys' ability to filter and excrete uric acid, thus increasing its elimination from the body.
• Krystexxa (pegloticase): Administered intravenously, pegloticase is a more potent agent reserved for severe, refractory cases, functioning by breaking down urate crystals directly.

During acute gout flares, various medications are used to rapidly reduce symptoms and alleviate pain. Over-the-counter (OTC) non-steroidal anti-inflammatory drugs (NSAIDs) are a common initial choice to manage discomfort and inflammation. For more severe or persistent flares, healthcare providers can prescribe stronger medications. These may include Colcrys (colchicine), which is effective in both treating and preventing gout flares by disrupting the inflammatory process. Prescription-strength NSAIDs, such as Indocin (indomethacin), are also utilized for their powerful pain-relieving and anti-inflammatory properties. Additionally, interleukin-1 blockers, a newer class of biologics, target specific inflammatory pathways to reduce the processes that lead to inflammation. Oral or injectable corticosteroids are another option, widely used for their potent anti-inflammatory effects during intense gout flare-ups, providing rapid relief.

Lifestyle and Self-Care

Beyond pharmacological interventions, incorporating specific lifestyle changes and adopting diligent self-care strategies can significantly contribute to reducing tophaceous gout symptoms and preventing recurrent flare-ups. These non-pharmacological approaches play a crucial role in complementing medical treatment, offering patients practical ways to manage their condition daily. Embracing these habits can lead to a substantial improvement in symptom control and a reduction in the overall burden of the disease, empowering individuals in their management journey.

Key lifestyle and self-care strategies include:

• Diet: Individuals with gout should strictly avoid foods and beverages notoriously high in purines, as these directly contribute to elevated uric acid levels. Conversely, certain foods have been shown to be beneficial in mitigating gout flares, including low-fat dairy products, citrus fruits, and other sources rich in vitamin C, which can aid in uric acid excretion.
• Use cold therapy: Applying ice packs or cold compresses to the gout-affected joint during a flare can provide significant relief from inflammation and pain. It is advisable to apply ice for up to 20 minutes at a time, several times throughout the day, to maximize its anti-inflammatory effects.
• Rest the affected joints: During a gout flare, it is crucial to rest the affected joint to minimize pain and swelling. If possible, elevating the affected joint with a pillow can further help reduce swelling and improve comfort, facilitating faster recovery.
• Drink water: Adequate hydration is paramount in gout management. Insufficient water intake can lead to an increase in uric acid levels in the body. Staying well-hydrated helps the kidneys efficiently flush out uric acid, thereby assisting in bringing levels down and potentially reducing recovery time from a flare.

Surgery

In rare and specific circumstances, surgical intervention may become a necessary treatment option for tophaceous gout. This is typically considered when tophi masses become significantly problematic and conservative medical management is no longer sufficient. Surgical removal might be indicated if tophi become infected, posing a risk of systemic complications. Furthermore, surgery may be necessary if tophi cause severe pain, or if they grow to a size that results in nerve compression, leading to debilitating neurological symptoms.

Extensive or deeply embedded tophi that cause considerable damage to joint structures or surrounding tissues may also warrant surgical removal. The objective of such procedures is to alleviate symptoms, restore function, and prevent further irreversible joint destruction. However, it is important to emphasize that the vast majority of individuals living with gout will never require surgery. The effectiveness of uric acid-lowering medications means that surgical intervention for gout remains an infrequent and last-resort option, primarily reserved for the most complicated and resistant cases where joint integrity and function are severely compromised.

How to Prevent Tophaceous Gout

Preventing the progression of gout, especially to its chronic tophaceous form, hinges critically on consistent adherence to treatment protocols and diligent self-management. It is paramount for individuals diagnosed with gout to faithfully follow their healthcare provider’s advice and rigorously comply with all prescribed treatment instructions. Proactive and sustained efforts in managing uric acid levels are the most effective defense against the disease advancing to its more severe stages, ensuring long-term joint health and overall well-being.

For individuals who are overweight or obese, achieving and maintaining a healthy weight is a powerful preventative strategy. Losing excess weight can significantly reduce uric acid levels, thereby decreasing the risk of future gout attacks. Additionally, weight reduction helps alleviate mechanical pressure on painful joints, enhancing comfort and mobility. Regular physical activity, particularly low-to-moderate intensity exercises, has also been shown to lower uric acid levels and can mitigate pain while reducing the potential for disability associated with gout. Aiming for at least 150 minutes per week of moderate-intensity activity is a good target, with preference given to joint-friendly activities like walking and swimming.

Beyond weight management and exercise, dietary discipline and healthy lifestyle choices are indispensable for gout prevention. This includes consistently consuming a healthy, balanced diet and maintaining adequate hydration, which supports the kidneys in their uric acid excretion function. Critically, strict avoidance of foods known to be high in purines is essential, as these directly contribute to uric acid spikes. Furthermore, limiting alcohol consumption and refraining from smoking are vital. While smoking may not directly cause gout, research indicates that cigarette use can elevate uric acid levels, thereby increasing the risk of both gout flares and the development of severe complications, including tophi.

Summary

Tophaceous gout represents the most severe and advanced stage of gout, characterized by the formation of urate crystal deposits known as tophi. These distinct lumps typically develop under the skin, often over joints and within nearby tissues, signaling a progression of the disease due to uncontrolled uric acid levels. The presence of tophi can lead to significant discomfort, inflammation of the joint lining (synovitis), loss of bone tissue, and irreversible damage to cartilage, substantially impacting joint function and overall mobility.

Although there is currently no definitive cure for gout, the condition is highly manageable, and its complications, including the formation of tophi, can be effectively prevented. This is achieved through a multi-faceted approach that integrates uric acid-lowering medications with essential lifestyle modifications. Key lifestyle adjustments include adopting a healthy diet low in purines, maintaining a healthy weight, and engaging in regular physical activity. By diligently implementing these strategies, individuals can significantly reduce their risk of gout progression, preventing it from becoming a chronic, debilitating condition and averting the development of tophi.

It is crucial to understand that gout progression is not inevitable, and the disease does not have to become chronic or lead to the formation of tophi. Vigilance and prompt action are key. Individuals should promptly inform their healthcare provider if they experience more than two gout attacks within a year, if their gout attacks become increasingly severe, or if they notice any suspicious lumps or nodules under their skin. Early identification of tophaceous gout is critical, as it allows for the immediate initiation of appropriate treatments to effectively bring uric acid levels under control, thereby minimizing joint damage and preserving long-term quality of life.

Read more:

• Health A-Z
• Arthritis
• Gout

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