A Case Study of Acute Gout Attack on Obese and Diabetic Patients
Gout is associated with obesity, diabetes type 2, and high blood pressure. Over 85% of people with diabetes also have hypertension, which increases the level of acid in the body, which causes insulin resistance. Almost 88% of people diagnosed with diabetes are obese (Schumacher, 2008). The risk of getting gout for people with obesity is four times higher than people with average weight.
Gouty arthritis is an intense inflammatory response resulting from articular layers of monosodium urate (MSU) crystals. MSU crystals cause inflammation through Toll-like receptors (TLR) that stimulate cells by giving surface to C5, thus causing membrane attack complex (C5b-9), leading to chemokine’s secretion cytokines with other inflammatory receptors that cause an influx of neutrophils into the joint. The TLR2 and TLR4‘s recognition of the MSU crystals causes defense response reaction to the infectious pathogens. This process causes inflammation and degeneration of tissue linked to gouty arthritis.
Inflammation is a physical process in which receptors are released from cutaneous nerves to cause inflammatory reaction. When the unmyelinated afferent somatic c-fibers are stimulated they release inflammatory mediators which in turn produce neuropeptides that trigger a release of inflammatory responses. Tissue damage in the body such as in gout arthritis will trigger the sensory neurons which will send impulse through the dorsal root to the nervous system for processing. The neurological process of inflammatory induced pain, and fever happens when prostaglandin E2 binds to EP3 in the preoptic hypothalamus which causes thermogenesis. The proinflammatory cytokines via their receptors on the brain endothelial cells trigger pain and fever, through prostaglandin E2 which is the final mediator of fever. Fever and pain are the main symptoms of inflammatory diseases such as gout arthritis.
African Americans are affected by gout arthritis disease more than whites, and are unlikely to get proper treatment. In 2008, 4% of whites in the US were affected by the disease compared to 25.7% of Africans diagnosed with it. In the case study done, the patient is a white male thus, he is not affected by the race prevalence for the gout disease. In his case it is likely to be caused by underlying conditions such as obesity, diabetes, and hypertension.
This is a case of a 58-year-old obese white male presented for the treatment of fever, chills, pain, and swelling in the right great toe. The patient states that the symptoms mentioned above presented sudden and that the pain is felt in the right great toe. He is unable to exert any weight on the right limb because of the intense pain. He has a past medical history of diabetes mellitus type 2 and hypertension. On physical examination, he reveals pain on assessing of metatarsophalangeal the right first toe. He is on medication: hydrochlorothiazide 50 mg PO to treat hypertension and diabetes combined, metformin 500mg PO bid to treat diabetes type 2 in obese patients. The tests real that he has an elevated sedimentation rate (ESR) of 33mm/hr, which indicates inflammation and infection. The C-reactive protein (CRP) is 24mg/L, which also indicated infection. The metabolic panels were standard, and uric acid levels were 6.7mg/dl, slightly higher than the standard rates.
Management and Outcome
The first goal is rapid alleviation of acute pain and inhibits inflammation. After that, a long term goal is recommended to stop further acute gout attacks in the future and stop joint destruction. It is done by continuously reducing uric acid levels; the uric acid levels should be maintained below 6.0 mg/dl (Cronstein & Terkeltaub, 2006). In the acute treatment of gout attack, resting, elevating, and cooling of the affected limb is recommended, together with administration of NSAIDs such as diclofenac 250mg/dl or ibuprofen up to 2400mg/d (if the patient does not have stomach ulcers or bleeding). Alternatively, colchicine o.5mg 2hourly can be administered (Cronstein & Terkeltaub, 2006). The treatment is likely to settle the gout attack in less than a day.
Long-term treatment aims to lower uric acids. The patient should be sensitized to life adjustments to make to improve his metabolic profile. The adjustments can include; reduction of consumption of fructose drinks, purine containing foods such as seafood. His diet should be rich in milk, vegetable proteins, and water. He should avoid alcohol drinks and meat. Light exercises and body weight loss of 1kg per month is also recommended for the patient. The medications for long-term treatment include; allopurinol and uricosuric agents such as benzbromarone (Sun, et al., 2015). Further, the patient is advised to adhere to the drug regimen of hypertension and diabetes treatment.
Recommendation and Conclusion
Treatment of acute gouty arthritis should be followed by managing its cause and lowering the uric acid level. The goal is to destroy stores of uric acid crystals in the body. Early treatment of gout is known to be effective.