Neurological and Musculoskeletal Pathophysiologic Processes Accounting for the Patient Symptoms

Gouty attacks are often present with swelling, pain, erythema, and warmth of the affected joint. It results from tissue deposition of mono-sodium urate salt crystals. Deposition of uric acid crystals on the joints triggers an inflammatory response. Initially, monocytes and mast cells are activated, followed by the activation of neutrophils (Towiwat et al., 2019). Before the initial attack and in the inter-critical period, macrophages will engulf the deposited crystals. Less differentiated monocytes will trigger the production of interleukin-1,6, and 8, tumor necrosis factor, and cause endothelial activation. Mast cells will induce gouty attacks by producing interleukin-1 and histamine (Towiwat et al., 2019). This results in enhanced vascular permeability and vasodilation that causes swelling and redness in the affected area.

Local vasodilation and monocyte and mast cell productions trigger neutrophilic chemotaxis. Other chemotactic factors produced by mast cells and monocytes, such as leukotrienes, platelet-activating factors, and interleukins, will further aggravate the inflammatory response and neutrophilic migrations. The interleukin-1 produced triggers the recruitment of other monocytes, thereby amplifying the inflammatory response. It can also result in cartilage breakdown. These changes further result in the production of other inflammatory mediators such as bradykinin, prostaglandins, and other products of the lipoxygenase pathway. These inflammatory mediators activate the TRPV1 nociceptors. These stimuli are conducted to the spinal cord and transmitted to the dorsal horn before being relayed to the supraspinal structures. This signal is detected as pain (Towiwat et al., 2019). The fever and chills seen in gout attacks result from the production of inflammatory mediators.

Racial/Ethnic Variables and How They Interact to Affect the Patient

Traditionally, gout has been considered a disease of white men who indulge in overconsumption of gamey meat. However, epidemiologic findings have revealed that the disease also affects other racial/ethnic groups. Potential racial differences in the epidemiology of gout may be due to nongenetic social determinants of health. These include lifestyle, diet, health-seeking behavior, and others (McCormick et al., 2022). Environmental risk factors for the disease, such as obesity/overweight, alcohol consumption, and health-seeking behavior, make blacks more predisposed to the disease than other ethnic groups. Factors within this group that make them more vulnerable to the disease compared to their white counterparts include their culturally informed efforts to lower current gout-related disparities, diet, and lifestyle.

Conclusion

The case presented reveals the manifestation of gouty attacks. It also demonstrates individual manifestations and findings that help in diagnosing the disease. Gout is a musculoskeletal disorder. It manifests with pain and swelling. Systemic manifestations of the disease include fever and chills. The disease has a multi-factorial cause. Aspects of race and ethnicity, such as lifestyle and diet, have been shown to interplay in the pathophysiologic development of the disease.

References

Evans, P. L., Prior, J. A., Belcher, J., Mallen, C. D., Hay, C. A., & Roddy, E. (2019). Obesity, hypertension, and diuretic use as risk factors for incident gout: A systematic review and meta-analysis of Cohort studies. Arthritis Research & Therapy, 20(1). https://doi.org/10.1186/s13075-018-1612-1

McCormick, N., Lu, N., Yokose, C., Joshi, A. D., Sheehy, S., Rosenberg, L., Warner, E. T., Dalbeth, N., Merriman, T. R., Saag, K. G., Zhang, Y., & Choi, H. K. (2022). Racial and sex disparities in gout prevalence among us adults. JAMA Network Open, 5(8). https://doi.org/10.1001/jamanetworkopen.2022.26804