Each day, rheumatology nurses, nurse practitioners, and physician assistants field dozens of questions from their patients with rheumatic diseases, and they need to be able to properly and effectively communicate appropriate responses. This pocket guide includes a brief summary of evidence surrounding some of the most common—and challenging—questions that patients with rheumatoid arthritis, psoriatic arthritis, gout, and systemic lupus erythematosus are asking about. We hope you find this guide useful for your professional development and that it assists you with your day-to-day patient management.
How did I get gout?
Gout is a common condition, thought to affect roughly 4% of the U.S. population. It is the most common type of inflammatory arthritis in men. Overall, men are affected significantly more than women, by an estimated ratio of 5-10:1. Gout tends to occur primarily during or after middle age.1,2 Gout is associated with hyperuricemia, or abnormally elevated levels of serum uric acid. This can be due to either the overproduction of uric acid, or much more commonly, the inability of the kidneys to excrete enough uric acid into the urine.3
Unlike many other mammals, humans are missing an enzyme called uricase, which breaks uric acid down into a form that can be easily excreted in the urine.4 When serum uric acid concentrations reach a certain level, the solubility threshold for monosodium urate (the most common form of uric acid) is reached, and it leaks out of the serum to form crystals.3 These urate crystals can be deposited throughout various tissues in the body, causing a variety of conditions.5
When excess crystals are formed and deposited in the skeletal system (e.g., joints, bursa, tendons, cartilage), the immune system is activated, leading to an inflammatory response and acutely painful, warm, swollen, and red joints. Over time, the frequency and duration of acute attacks can increase and become chronic.6 This can lead to joint damage and the formation of subcutaneous tophi, which are nodules in and around the involved joint.7 While gouty arthritis is most common in the big toe, it also commonly affects the mid-foot, ankle, knee, upper limb, and fingers.2
Once thought to be a consequence of an indulgent lifestyle, it is now recognized that genetics are the primary contributor to the development of gout.4 Beyond age, sex, and genetics, other risk factors such as certain medications (e.g., diuretics or aspirin), renal disease, excess weight, hypertension, and dietary and alcohol intake are also believed to increase the risk of developing gout.7 However, a recent study showed that diet was responsible for less than 1% of variation in serum urate levels; in contrast, 24% of the variation was explained by common genetic factors.8
1. Singh JA. Racial and gender disparities among patients with gout. Curr Rheumatol Rep. 2013;15(2):307.
2. Dirken-Heukensfeldt KJ, Teunissen TA, van de Lisdonk H, Lagro-Janssen AL. Clinical features of women with gout arthritis. A systematic review. Clin Rheumatol. 2010;29(6):575-582.
3. Pittman JR, Bross MH. Diagnosis and management of gout. Am Fam Physician. 1999;59(7):1799-1806, 1810.
4. Benn CL, Dua P, Gurrell R, et al. Physiology of hyperuricemia and urate-lowering treatments. Front Med (Lausanne). 2018;5:160.
5. Nuki G, Doherty M, Richette P. Current management of gout: practical messages from 2016 EULAR guidelines. Pol Arch Intern Med. 2017;127(4):267-277.
6. Qaseem A, Harris RP, Forciea MA, Clinical Guidelines Committee of the American College of Physicians. Management of acute and recurrent gout: A clinical practice guideline from the American College of Physicians. Ann Intern Med. 2017;166(1):58-68.
7. Hainer BL, Matheson E, Wilkes RT. Diagnosis, treatment, and prevention of gout. Am Fam Physician. 2014;90(12):831-836.
8. Major TJ, Topless RK, Dalbeth N, Merriman TR. Evaluation of the diet wide contribution to serum urate levels: meta-analysis of population based cohorts. BMJ. 2018;363:k3951.