Chronic Illness – Gout
- Gout is the most common form of inflammatory arthritis in men that is increasing in prevalence (Roddy & Choi, 2014). It is more common in men (3-6% incidence) than women (1-2% incidence), occurs more often with increasing age, and is more common in certain ethnic groups (Pacific Islanders) (Dehlin, Jacobsson, & Roddy, 2020).
- The incidence of gout varies depending on the population being studied (Dehlin et al., 202). Current reports show that the prevalence range from < 1 % to 6.8%, with an incidence of 0.58-2.89 per 1,000 person-years (Dehlin et al., 2020).
- Risk factors for gout include obesity, dietary factors, and comorbid conditions (Dehlin et al., 2020). The rise of obesity and comorbidities is likely contributing to the rising prevalence of gout (Dehlin et al., 2020).
Pathology and Course of Illness
- Uricase is an enzyme that degrades uric acid to a more soluble form known as allantoin (Kratzer et al., 2014). Through evolution, humans have lost this gene, which has resulted in the uric acid build-up (hyperuricemia) that plays a significant factor in the development of gout that we see today (Kratzer et al., 2014).
- Gout can be an acute or chronic disease that occurs due to a build-up of monosodium urate (MSU) crystals in joints, bones, and soft tissues (Merriman, Dalbeth, & Romain, 2020). It can result in gout flare-ups (acute arthritis), chronic gouty arthritis (chronic arthritis), or tophaceous gout (tophi) (Merriman et al., 2020).
- Non-modifiable risk factors include male gender, advanced age, and ethnicity (e.g., Pacific Islanders) (Merriman et al., 2020). Modifiable risk factors include obesity, alcohol-containing beverages (especially beer and distilled spirits), beverages containing high fructose/sucrose, hypertension, thiazide or loop diuretic use, chronic kidney disease, postmenopausal, organ transplant recipient status, and use of certain medications (e.g., cyclosporin A or low-dose aspirin) (Merriman et al., 2020).
- Hyperuricemia is a pathogenic factor necessary for the build-up of gout (Merriman et al., 2020). Factors that promote the build-up of hyperuricemia include renal underexcretion of urate, extrarenal underexcretion of urate, and overproduction of urate (Merriman et al., 2020).
- Build up of urate crystals in the joints interact with undifferentiated phagocytes, which results in an inflammatory response that leads to synovitis (synovial inflammation), cartilage loss, and bone damage by inhibiting osteoblasts, and bone erosions (Merriman et al., 2020).
- The inflammatory response consists of tumor necrosis factor (TNF)-alpha, interleukin (IL)-8, and chemokine signaling that leads to neutrophil adhesion to endothelium, influx, and amplification resulting in the inflammation (Merriman et al., 2020).
- Clearance of urate crystals by differentiated phagocytes, coating the crystals with proteins, neutrophil apoptosis, and inactivation of inflammatory mediators will resolve gout attacks (Merriman et al., 2020).
Diagnosis and Management
Diagnosis made by clinical findings
- Diagnosis of gout can be made based on clinical findings coupled with a reliable history of recurrent monoarthritis of the first metatarsophalangeal joint (big toe) (Gaffo, 2021).
- Additionally, a diagnosis of gout can also be made if the patient has at least 6 of the criteria written below by the American College of Rheumatology (ACR) (Gaffo, 2021).
- > 1 Attack of acute arthritis
- Maximum inflammation developed within one day
- Monoarthritis attack, redness observed over joints
- First metatarsophalangeal joint painful or swollen
- Unilateral first metatarsophalangeal joint attack
- Unilateral tarsal joint attack
- Tophus (confirmed or suspected)
- Asymmetric swelling within a joint on x-ray film
- Subcortical cyst without erosion on x-ray film
- Joint culture negative for organism during attack
- The patient should be assessed for previous gout attacks, medications, dietary habits, and family history (Gaffo, 2021). Gout commonly presents as acute monoarticular arthritis with sudden-onset severe pain and swelling (Gaffo, 2021). Gout can affect any joint but most commonly affects the first metatarsophalangeal, tarsometatarsal, ankle, and knee joints (Gaffo, 2021).
- A physical examination of the affected joint will reveal warmness, redness, swollenness, tenderness, and limited range of movement (Gaffo, 2021). Tophi (hard subcutaneous nodules) may also be present in the extensor surface of the affected joint (e.g., over the elbows, knees, and Achilles tendons) (Gaffo, 2021).
Diagnosis made by lab/imaging
- An arthrocentesis that is positive for monosodium urate crystals can provide a definitive diagnosis (Gaffo, 2021). A serum urate level ≥6.8 mg/dL can also assist in diagnosing gout; however, this is usually hard to interpret during the initial gout episode and is more reliable two weeks after the actual gout attack (Gaffo, 2021).
- Other imaging that could be ordered includes an ultrasound, dual-energy computer tomography (DECT), and radiography (Gaffo, 2021).
- First-line treatment options for an acute gout attack include NSAIDs, corticosteroids, and colchicine unless they are contraindicated (Gaffo, 2021).
- NSAIDs (e.g., naproxen, ibuprofen, diclofenac potassium) may be used for up to 10-14 days to relieve an acute attack unless contraindicated (Gaffo, 2021). Reasons for contraindications may include a eGFR < 60, hyperkalemia, duodenal or gastric ulcer, uncontrolled hypertension, moderate to severe uncompensated heart failure, cirrhosis, and unmodifiable drug interactions (e.g., anticoagulation), NSAID allergy intolerance (Gaffo, 2021).
- Corticosteroids (e.g., prednisone, methylprednisolone acetate, triamcinolone acetonide) can also be used unless contraindicated (Gaffo, 2021). Reasons for contraindications may include brittle diabetes mellitus, history of glucocorticoid intolerance, recent surgery with a wound that has not healed, and suspected concurrent infection (Gaffo, 2021).
- Lastly, colchicine may also be used, but patients must be educated about the common side effects of diarrhea, nausea, and vomiting that often precede pain relief (Gaffo, 2021). Colchicine is less effective in gout that has been ongoing for greater than 24-36 hours (Gaffo, 2021). Contraindications for colchicine include history of allergy to the medication, renal or hepatic impairment (or both), recently taking a P450 3A4 inhibitor, or P-glycoprotein multidrug-resistant transported inhibitor (Gaffo, 2021).
- The first-line treatment for chronic management of gout is allopurinol (Gaffo, 2021). This urate-lowering drug aims to lower serum urate levels to < 6 mg/dL (Gaffo, 2021). Treatment with allopurinol is recommended for patients with frequent gout flares (≥2 annually), gout with ≥1 subcutaneous tophi, and evidence of radiographic damage due to gout (Gaffo, 2021). The typical starting dosage for allopurinol is 100 mg orally once daily for 2-3 weeks post a gout episode (Gaffo, 2021). Allopurinol can be increased by 100 mg/day increments every week depending on the serum urate levels (Gaffo, 2021). The max dose is 800 mg/day (Gaffo, 2021). Allopurinol is contraindicated to people with hypersensitivity to allopurinol or formulation components (Gaffo, 2021).
- Treatment with allopurinol can also be combined with suppressive therapy using NSAIDs unless otherwise contraindicated (Gaffo, 2021).
- The second-line treatment for ongoing gout management is febuxostat 40-80 ng once daily, reducing uric acid production (Gaffo, 2021). However, typical side effects of this medication include elevated liver function tests, headache, hypertension, diarrhea, and arthralgias/stiffness (Gaffo, 2021). Febuxostat is not recommended as first-line therapy by the FDA unless patients are not able to tolerate allopurinol (Gaffo, 2021).
- Aside from management using medications, patients can also decrease gout incidence by avoiding food triggers (food containing purines, alcohol, fructose), exercising (to reduce obesity), and proper management of other comorbidities (Gaffo, 2021).
- Patients who develop worsening gout flare-ups will eventually experience gout in other parts of their body, such as the knee and ankle. If left untreated, the urate levels will crystalize into tophis (bumps under the skin). Gout will result in chronic pain and limited mobility for the patient. Experiencing chronic pain and limited mobility puts the patients at risk for falls. This will interrupt their daily activities and social life.
- A retrospective study conducted in 2015 displayed that depression had a higher occurrence in gout patients who did not use antigout medications when compared to those who did (Changchien et al., 2015). This study also found that patients with gout had a 1.18-fold increase in developing depressive disorders (Changchien et al., 2015).
- Additionally, the study found that men ≤49 years, without comorbidities, who do not use NSAID or prednisone also had a higher risk for depression (Changchien et al., 2015). This shows that proper control of gout is needed to prevent depressive disorders, especially for younger men with gout (Changchien et al., 2015).
Nurse Practitioner Implications
- Gout is a common chronic disease seen in the primary care setting. With a proper history assessment and diagnostic tools, this is a disease that can be diagnosed during an office visit. Nurse practitioners must educate patients that gout is a form of arthritis that results in pain and swelling in the joints due to the buildup of uric acid and can worsen if not treated and appropriately managed (Roddy & Choi, 2014).
- The first-line treatment options for an acute gout flare-up are NSAIDs, corticosteroids, and colchicine (Gaffo, 2021). Allopurinol combined with NSAIDs is the primary treatment for ongoing/chronic gout flare-ups (Gaffo, 2021). Nurse practitioners should educate patients on avoiding foods high in purine (e.g., alcohol, seafood, fructose/sucrose, and offal) (Gaffo, 2021). Additionally, we must encourage lifestyle modifications such as weight loss and exercise (Gaffo, 2021).
- As nurse practitioners, we must show awareness and understanding of the chronic pain that our patients are experiencing and empathize with them during their visits. Ultimately this condition limits their mobility and affects their daily lives. As providers, we must equip our patients with the proper tools to manage recurrent gout flare-ups and have the appropriate education to prevent future recurrence.
Changchien, T. C., Yen, Y. C., Lin, C. L., Lin, M. C., Liang, J. A., & Kao, C. H. (2015). High Risk of Depressive Disorders in Patients With Gout. Medicine, 94(52), e2401. https://doi.org/10.1097/md.0000000000002401
Dehlin, M., Jacobsson, L., & Roddy, E. (2020). Global epidemiology of gout: prevalence, incidence, treatment patterns and risk factors. Nature Reviews Rheumatology, 16(7), 380–390. https://doi.org/10.1038/s41584-020-0441-1
Gaffo, A. (2021, December 1). Clinical manifestations and diagnosis of gout. Up-To-Date. Retrieved April 15, 2022, from https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-gout?search=gout%20diagnosis&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H87543138
Gaffo, A. (2022, April 7). Treatment of gout flares. Up-To-Date. Retrieved April 15, 2022, from https://www.uptodate.com/contents/treatment-of-gout-flares?search=gout%20man&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H85444272
Kratzer, J. T., Lanaspa, M. A., Murphy, M. N., Cicerchi, C., Graves, C. L., Tipton, P. A., Ortlund, E. A., Johnson, R. J., & Gaucher, E. A. (2014). Evolutionary history and metabolic insights of ancient mammalian uricases. Proceedings of the National Academy of Sciences, 111(10), 3763–3768. https://doi.org/10.1073/pnas.1320393111
Merriman, T., Dalbeth, N., & Romain, P. (2020, July 14). Pathophysiology of gout. Up-To-Date. Retrieved April 13, 2022, from https://www-uptodate-com.eu1.proxy.openathens.net/contents/pathophysiology-of-gout?search=GOUT%20PATHOPHYSIOLOGY&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
Prior, J., Ogollah, R., Muller, S., Chandratre, P., Roddy, E., & Mallen, C. (2015). Gout, anxiety, and depression in primary care: a matched retrospective cohort study. Scandinavian Journal of Rheumatology, 44(3), 257–258. https://doi.org/10.3109/03009742.2015.1022215
Roddy, E., & Choi, H. K. (2014). Epidemiology of Gout. Rheumatic Disease Clinics of North America, 40(2), 155–175. https://doi.org/10.1016/j.rdc.2014.01.001
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