Case Study Analysis – Rheumatoid Arthritis
In the case presented in this assignment, a 42-year-old woman complains of fatigue, joint pains, and episodes of chills. She reports that the symptoms have exacerbated over the past few weeks. Her significant past medical history includes similar episodes characterized by elevated Electrolyte sedimentation rate (ESR) and a negative antinuclear antibody test (ANA). She has been using ibuprofen to relieve symptoms, but the joint pain persists in the mornings. These presentations, together with the history, are indications of an autoimmune or inflammatory response. This paper aims to explore the likely causes of these symptoms, elucidate the potential genetic factors involved in the disease process, and underscore the impact of immunosuppression on the body systems.
Explanation of the Symptoms
In this case, the patient’s symptoms align with an autoimmune disorder. For instance, fatigue and joint pain are the hallmark symptoms of autoimmune conditions such as rheumatoid arthritis, systemic lupus erythematous, and polymyalgia rheumatic. Elevated levels of ESR signify an ongoing inflammatory disease. The ANA test being negative does not rule out the possibility of autoimmune disease since others, such as seronegative rheumatoid arthritis, present with negative ANA. The joint pain over the whole day but worse in the mornings is a characteristic of rheumatoid arthritis. The fever, as evidenced by 1000F, is accompanied by episodes of chills, which indicates an inflammatory response by the immune system (Kurup & Pozun, 2022). Persistent pain, even after the use of the nonsteroidal anti-inflammatory drug (ibuprofen), justifies the need for a more focused therapeutic approach.
Genetic Factors Associated with the Disease
Some genetic composition predisposes one to autoimmune and inflammatory diseases. These factors include HLA-DRB1, a gene that presents the antigens to the immune cells. Individuals with variant alleles of this gene are at increased risk of developing rheumatoid arthritis due to abnormal immune response triggering joint inflammation. Secondly, the PTPN22 gene encodes the protein that regulates the T-cell functioning. Mutations in this gene can cause autoimmune attacks on joint tissues. The third genetic factor is based on STAT4, a gene that regulates the cytokines in the mediation of immune and inflammatory responses. Variations in this gene promote excessive inflammation, hence increasing the risk of autoimmune diseases. Lastly, TNFAIP3 mutations compromise the NF-Kb signaling pathway for the immune response. This impairment results in exaggeration of the immune responses that yield to autoimmune conditions and other inflammatory diseases (Vetchinkina et al., 2021).
Immunosuppression and its Impact on Body Systems
Immunosuppression is the reduction of the efficiency of the immune system, usually caused by medications such as corticosteroids, diseases, and treatment approaches such as post-organ transplant (Rice, 2019). During an autoimmune disease, the immune system attacks the healthy tissues, causing inflammatory symptoms in the affected areas. To evade the damage caused by this malfunction, immunosuppressive medications are administered to lower the overactivity of the immune system. Immunosuppression has impacts on the body. Firstly, immunosuppressive drugs reduce the inflammation of the joints, hence alleviating the pain and swelling. However, prolonged use of these agents may increase the risk of osteoporosis and also inhibit further joint degradation. Secondly, immunosuppression affects the immune system by reducing its efficacy in surveillance, making the patient more susceptible to infections. Thirdly, immunosuppression affects the cardiovascular and respiratory systems through increased risk of respiratory infections. Autoimmune conditions increase the risk of cardiovascular disease due to chronic inflammation. Immunosuppression lowers the inflammatory burden, hence mitigating cardiovascular disease. Additionally, autoimmune diseases such as diabetes can affect kidney function. As Handley and Hand (2021) suggested, immunosuppression therapy may prevent damage to the renal system by controlling inflammation but may also increase the risk of renal infections.
References
Handley, G., & Hand, J. (2021). Adverse Effects of Immunosuppression: Infections. Pharmacology of Immunosuppression, 287–314. https://doi.org/10.1007/164_2021_550
Kurup, S., & Pozun, A. (2022). Biochemistry, Autoimmunity. PubMed; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK576418/
Rice, J. M. (2019). Immunosuppression. Nih.gov; International Agency for Research on Cancer. https://www.ncbi.nlm.nih.gov/books/NBK570319/#:~:text=In%20the%20absence%20of%20adequate
Vetchinkina, E. A., Mikhaylenko, D. S., Kuznetsova, E. B., Deryagina, T. A., Alekseeva, E. A., Bure, I. V., Zamyatnin, A. A., & Nemtsova, M. V. (2021). Genetic Factors of Predisposition and Clinical Characteristics of Rheumatoid Arthritis in Russian Patients. Journal of Personalized Medicine, 11(6), 469. https://doi.org/10.3390/jpm11060469
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Question
Develop a 1- to 2-page case study analysis in which you:
Explain why you think the patient presented the symptoms described.
Identify the genes that may be associated with the development of the disease.
Explain the process of immunosuppression and the effect it has on body systems.

Case Study Analysis – Rheumatoid Arthritis
A 42-year-old female presents to the clinic with chief complaint of increased fatigue and joint pain worsening over the last few weeks. Her past medical history includes similar episodes with a prior ESR of 56 mm/hr and a negative ANA. She reports that she has had some episodes of chills but hasn’t taken her temperature. The patient reports that she takes ibuprofen for the pain which partially relieves her symptoms. The pain is sometimes worse in the morning but also occurs throughout the day. Her blood pressure is 124/78, heart rate 74, temperature 100 F.