Pharmacophore an International Research Journal
REVIEW ON DIAGNOSIS & MANAGEMENT OF GOUT IN PRIMARY HEALTH CARE
Gehan Hamdalla1, Noor Ali AlGhanem2*, Hatem Abdulaziz Mohammed AlGhamdi3, Bashayer Fahad AlHazmi4, Majed Rashed AlHarthi5, Mohammed Nawar AlOtaibi5, Amnah Ali Elagi6, Abobakr Ali AlQarni7, Jumanah Ali AlZahrani8, Abeer Fahad AlMutairi9, Saleh Abdullah Mohammed10
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ABSTRACT
With a countrywide incidence of 2.5% in the adult population, gout is the most prevalent inflammatory joint disease affecting men over 40 in the UK. Prevalences are similar in other industrialized nations, including the US and New Zealand. Monosodium Urate (MSU) crystals occur and are deposited in joints, most frequently the first metatarsophalangeal joint (MTP), as a result of the hyperuricemia that causes gout. Most gout patients in the UK are treated exclusively in primary care. To ensure that care is provided in accordance with need, it is critical to assess the socioeconomic status (SES) of a community afflicted by a condition. Being from a lower SES group is linked to more GP visits and worse health, according to numerous studies on social disadvantage and health consequences. Some of these studies have been conducted at the neighborhood and individual levels to determine whether any associations are caused by characteristics specific to the community or the patients.
Keywords: Gout, Health-related quality of life, Primary care, Comorbidity
Introduction
With a countrywide incidence of 2.5% in the adult population, gout is the most prevalent inflammatory joint disease affecting men over 40 in the UK [1]. Prevalences are similar in other industrialized nations, including the US and New Zealand [2, 3]. Monosodium Urate (MSU) crystals occur and are deposited in joints, most frequently the first metatarsophalangeal joint (MTP), as a result of the hyperuric emia that causes gout [4]. Most gout patients in the UK are treated exclusively in primary care. To ensure that care is provided in accordance with need, it is critical to assess the socioeconomic status (SES) of a community afflicted by a condition. Being from a lower SES group is linked to more GP visits and worse health, according to numerous studies on social disadvantage and health consequences [5, 6]. Some of these studies have been conducted at the neighborhood and individual levels to determine whether any associations are caused by characteristics specific to the community or the patients.
Little research has examined the link between SES and gout, producing conflicting findings. In a recent study conducted in the UK, it was discovered that those with gout who were 50 years of age or older were more likely than those without gout to see their financial income as inadequate. However, there was no correlation between having gout and occupational class, amount of education, or level of poverty in your neighborhood [7]. In Australia, no correlation with area-level disadvantage was discovered [8, 9]. Gout and SES were linked in research from Western Germany but not in a study of men [10].
More socioeconomically impoverished communities have the highest prevalence of gout, according to studies from England and New Zealand [4, 11]. Most of these earlier research contrasted SES between gout sufferers and non-gout sufferers. There are hardly any investigations on the connection between SES and the severity of gout. One study from Mexico found no association between tophi presence and socioeconomic class or educational attainment [12]. People frequently miss work due to acute gout severity, resulting in temporary sick leave [13]. People with gout have been demonstrated to be highly concerned about how their condition may affect their productivity, employability, and capacity to work [14]. Employees with gout take roughly five times as many days off from work each year due to illness as those without gout [15]. Employees with at least three gout attacks annually miss more days from work than those who experience fewer attacks [16]. In a study of individuals with severe chronic gout that was resistant to conventional therapy (mean number of attacks 8.8 per year), 78% of those under 65 reported missing work for at least one day owing to gout during a year, with the mean yearly number of workdays lost being 25 days [17].
It has been demonstrated that persons with insufficiently controlled gout, even receiving urate-lowering medication, have lower work productivity than those with satisfactory management [18]. Contrarily, a tiny study revealed no connection between the frequency of assaults or tophi and productivity at work [19].
Epidemiology
Globally, gout is the most prevalent kind of inflammatory arthritis. Gout is more prevalent in aging populations since the danger of developing it rises with advancing years. Gout is caused by a persistent increase in serum urate levels (hyperuricemia), which deposits monosodium urate crystals in joints, tendons, and other tissues. Gout flares are periodic episodes of severe acute inflammation. Despite being one of the few rheumatic diseases that can be "cured" with pharmacological urate-lowering treatments (ULTs), gout management remains insufficient in many parts of the world due to low ULT adoption and patient adherence. Gout frequently coexists with several comorbid illnesses, such as obesity, chronic renal disease, and cardiovascular disease [20].
Understanding changes in gout prevalence is crucial for facilitating adequate healthcare resource planning. Gout is the most prevalent inflammatory arthritis worldwide, not to mention that gout may be "cured" using readily available and affordable therapies. Due to the absence of data for many nations and the widely varying prevalence estimates across various geographic regions and demographics obtained using different illness classifications, it is challenging to determine the global prevalence of gout [20].
Diagnosis
Gout diagnostic criteria include two of the following:
Definitive diagnosis: the presence of monosodium urate crystals in the serum, in the joint fluid, or in the tissues.
The primary pathophysiologic events defining the clinical state of gout are the deposition of urate crystals in tissue and the ensuing inflammatory and potentially harmful effects. A gout flare is caused by monosodium urate (MSU) crystals, which can be seen when polarized light microscopy is used to identify these crystals in synovial fluid taken from joints or bursas [21]. While the joint spaces are typically intact and periarticular osteopenia is absent, unlike the radiographic alterations typical of rheumatoid arthritis, plain radiography may not detect early disease that does not show any abnormality. Bone erosions indicative of advanced gout frequently have an overhanging edge and sclerotic rim. In the event of a difficult diagnostic situation and for early detection, ultrasonography can be very helpful. Hyperechoic linear density (double contour sign) on the surface of hyaline cartilage or tophaceous deposits in joints or tendons are described as hyperechoic and encircled by a small anechoic rim, are crucial diagnostic findings [22].
Without joint fluid analysis, the primary care environment uses clinical diagnostic criteria to predict the likelihood of gout. The first metatarsal phalangeal joint is involved in the model along with seven other factors, including male gender (2 points), previous patient-reported arthritis (2 points), onset within a day (0.5 points), joint redness (1 point), hypertension or at least one cardiovascular disease (1.5 points), and serum urate level >5.88 mg/dL or 350 micromol/L (3.5 points) [22]. Patients can be classified as having a low (4 points), intermediate (>4 or 8 points), or greater (8 points) chance of gout based on their overall score. Patients in the intermediate category gain the most from additional assessment by synovial fluid analysis [22]. This clinical diagnostic criterion was tested on 390 Dutch primary care patients with acute monoarthritis, outperforming a doctor's diagnosis and providing a positive result in the derivation study [23]. Primary care physicians should be aware that acute calcium pyrophosphate crystal arthritis or septic arthritis may occasionally occur with gout flares (pseudogout). When a joint is aspirated, an orthopedic surgeon or rheumatologist will help determine the diagnosis by analyzing the synovial fluid [23]. In our routine clinical practice, we currently observe the three traditional stages of gout: acute gout flare, inter-critical gout, chronic gouty arthritis, and tophaceous gout).
Risk Factors
Factors that raise hyperuricemia are risk factors for gout. A baseline gender-associated 1 mg/dL greater uric acid in men increases the risk for gout compared to premenopausal women. The difference between the premenopausal and postmenopausal states is gone, and estrogen effects on uric acid clearance are most likely the cause [24]. The greater risk of hyperuricemia observed in the elderly is expected to be caused by comorbid renal illness in advanced age [24]. African Americans have higher serum uric acid levels than Caucasians do at baseline, which is one of the ethnic factors that affect risk [25]. Hyperuricemia and gout are linked to rare X-linked inborn metabolic abnormalities, such as Lesch-Nyhan syndrome (hypoxanthine-guanine phosphoribosyl transferase enzyme deficiency). Hyperuricemia and gout are also linked to metabolic comorbidities such as obesity, hypertension, hyperlipidemia, and metabolic syndrome [26]. Although it is recognized that endocrine disorders, such as hyperparathyroidism and hypopara thyroidism, and hypothyroidism, can affect kidney function, it is less apparent how these conditions affect blood urate levels and the risk of developing clinical gout [27].
Treatment
Treatment for acute gout should begin within 24 hours after the beginning of symptoms to obtain rapid and complete symptom relief [28]. Colchicine, NSAIDs, intravenous corticosteroids, and oral corticosteroids all work well to treat acute gout flare-ups [28]. The initial line of treatment is NSAIDs. Although Indocin (indomethacin) has traditionally been the drug of choice, there is no proof that it is more efficacious than other NSAIDs. It appears that intramuscular ketorolac works similarly [29].
After symptoms have subsided, any oral NSAID may be used at the maximum dosage for one to two days. For people who cannot tolerate NSAIDs or colchicine, corticosteroids are a suitable substitute [30]. Corticosteroids can be administered to patients with diabetes mellitus for brief periods with the proper monitoring for hyperglycemia. Due to their lower risk of side effects, intra-articular corticosteroid injections may be preferable to systemic corticosteroids when gout is restricted to a single joint [31].
Following the cessation of corticosteroid therapy for acute gout, rebound flares are frequent. After symptoms have subsided, preventative treatment and the start of a tapering course of corticosteroids over 10 to 14 days are advised to lower the likelihood of a return flare. Another alternative for acute gout treatment is colchicine. The US Food and Drug Administration (FDA) did not formally assess generic colchicine, which has been used for decades, for this indication until 2009, when branded colchicine (Colcrys) was approved. However, Colcrys is pricey, and there is no longer a generic version of colchicine.
Furthermore, when administered more than 72 to 96 hours after the onset of symptoms, colchicine may be less helpful at treating acute flares because it lacks analgesic qualities. Typical side effects include vomiting, diarrhea, and nausea [29]. Patients with renal or hepatic impairment should use colchicine with caution.
Conclusion
The condition of gout is easily treatable and can even be cured. The goal of care during an acute flare aims to relieve pain while preventing impairment and initiating treatment early. Although ULTs are widely accessible and efficient, allopurinol is still the first-line therapy [32]. Primary care practitioners should know the rationale for starting ULT, setting serum uric acid targets with patients, treating potential adverse effects of ULTs, and educating patients about dietary and lifestyle changes. Testing for hypertension, diabetes, hypercholesterolemia, and keeping an eye on weight is essential because gout is commonly a part of the metabolic phenomenon. Treatment should be used when necessary.
Acknowledgments: None
Conflict of interest: None
Financial support: None
Ethics statement: None
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