Introduction
A 49-year-old patient working as a grain inspector has a diagnosis of rheumatoid arthritis, episodic hemoptysis, and invasive aspergillosis. He shows up reporting several symptoms, which could have varied explanations. This analysis aims to explain the possible cause of the symptoms shown, the genes associated with the disease, and the process of immunosuppression. The analysis will thoroughly investigate and describe various aspects of the case study.
Explanation of Symptoms
The exposure to the dusty environment might have caused the coughing and chest pain. During his grain inspection, the patient might have inhaled dirt, thus developing respiratory infections such as hemoptysis. Hemoptysis is coughing up blood, which might be worsened by inhaling dirt (Scherer et al., 2020). The patient’s fever may be caused by rheumatoid arthritis because fever is one of its major symptoms. According to Scherer et al. (2020), people with rheumatoid arthritis could have a fever caused by inflammation or because the treatment of the disease makes people susceptible to infections. The prednisone medication could also cause it, and one of its side effects is high fever (Scherer et al., 2020). The unusual fatigue could be caused by rheumatoid arthritis and the side effects of various medicines the patient takes.
Possible Genes
At least four identified genetic markers are associated with the development of rheumatoid arthritis. HLA-DR4 is a common gene for people with rheumatoid arthritis. According to Okada et al. (2019), people with this gene are more likely to develop rheumatoid arthritis than those without it, and its symptoms could be worse. The other gene is STAT4 which regulates and activates a person’s immune system (Okada et al., 2019). The presence of this gene in the body can easily compromise a person’s immunity. It is responsible for most autoimmune diseases where the immune system fights its body instead of protecting it. TRAF1 and C5 genes play a major role in causing chronic inflammation associated with rheumatoid arthritis (Okada et al., 2019). According to Okada et al. (2019), people with TRAF1 and C5 genes could have worse conditions of rheumatoid arthritis due to increased inflammation. The last gene associated with the development of rheumatoid arthritis is PTPN22 (Okada et al., 2019). The gene influences the expression and progression of rheumatoid arthritis. People with PTPN22 genes could have prolonged rheumatoid arthritis.
Immunosuppression
The process of immunosuppression entails a reduction in the capacity of the immune system to respond to foreign antigens effectively. The existing paradigm of mechanisms of action of immunosuppressants is that they operate to prevent allograft rejection by inhibiting cell activation, proliferation, differentiation, and cytokine production (Mackay & Rose, 2020). Immunosuppression can result from destroying immune effector cells or blockage of intracellular paths vital for antigen recognition or other immune components. According to Mackay and Rose (2020), immunosuppression can naturally occur because some parts of the immune system have immunosuppressive effects on other parts of the system. Immunosuppression can also be induced with drugs in preparation for a bone marrow transplant to prevent rejection of the process.
Conclusion
The patient’s symptoms could be caused by the environment, which makes him susceptible to various infections. With a suppressed immune system, the patient has acquired additional conditions that weaken him. Four genes associated with rheumatoid arthritis could be the cause of the disease. The process of immunosuppression, in this case, is caused by autoimmune, where the immune system fights its body instead of protecting it.
References
Mackay, I. R., & Rose, N. R. (2020). The autoimmune diseases (6th ed.). Academic Press.
Okada, Y., Eyre, S., Suzuki, A., Kochi, Y., & Yamamoto, K. (2019). Genetics of rheumatoid arthritis: 2018 status. Annals of the rheumatic diseases, 78(4), 446-453. Web.
Scherer, H. U., Häupl, T., & Burmester, G. R. (2020). The etiology of rheumatoid arthritis. Journal of autoimmunity, 110, 102-400. Web.