Polymyositis: The Autoimmune Disorder Research Paper

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A common disease of the muscular system in human beings is polymyositis. The illness is an unusual inflammatory condition that causes general muscle weakness, specifically the body’s back, leg, and side muscles. The disease was first described in 1863 and 1887 in publications by Ernst Leberecht. In 1916, it was linked to dermatomytosis and malignancy. According to Leclair et al. (2021) polymyositis could make an individual find it challenging to lift objects, rise from seated positions, and climb stairs. It is common in persons over thirty years until the aging period and more commonly affects women than men. The exact cause of the condition is unknown, but the illness shares several characteristics with existing autoimmune disorders. The primary symptoms include weakness in specific muscles including the ones close to the neck, upper arms, shoulders, and hips. As a result, the weakness is predominant in the right and left parts of the body. The prevalence of the illness is approximately twenty-two in every one hundred thousand persons.

While polymyositis affects many muscles, the most affected are the back muscles. This muscle’s normal autonomy begins at the top of the neck and progresses toward the tailbone. Sasaki and Kohsaka (2018) postulate that the issues caused by polymyositis are directly associated with the complex structure of the back. In this case, the concern is advanced by the back muscles being made up of several nerve muscles, tendons, fasciae, ligaments, and tendons. The ligaments, as the primary tissue, hold the vertebrae that are mainly affected by polymyositis. The muscle is connected to other body parts using the nerves that extend directly toward the small holes located in the vertebrae that allow a solid connection to other body parts. This connection of this muscle to other parts of the body makes polymyositis a crucial muscle illness.

The illness, commonly systematic inflammation, mainly affects the muscle’s endomysium. While it is closely related to other muscular conditions, specific differences differentiate it. For example, by affecting the endomysium, it differentiates from dermatomyositis, whereby perimysal inflammation presents the leading emphasis of inflammation. There exists a T-cell-mediated response in the polymyositis against the muscle fiber surface that results in necrosis. Recent studies demonstrate that polymyositis is associated with hypoxia that often minimizes adenosine triphosphate and creatine phosphate (Yang et al. 2019). Due to hypoxia, a significant decrease in muscles causes muscle weakness and fatigue. Certain muscular dystrophies, including biochemical muscle disease, metabolic myopathies, and Becker’s muscular dystrophy, could mimic this condition and must be excluded.

Although the causes of polymyositis are unknown, a practical treatment approach includes the use of corticosteroids. This medication involves drugs like prednisone, which effectively controls all symptoms associated with polymyositis (Sasaki & Kohsaka, 2018). Nonetheless, Yang et al. (2019) warn that prolonged use of this drug could present severe and broad side effects to the patient. A healthcare provider can address this by gradually regulating the dose down to low levels. According to Leclair et al. (2021) steroids are also an effective treatment strategy for the illness. The treatment strategy helps to manage instances of muscle inflammation, which is a predominant effect of the disease. Additionally, steroids help to reduce pain and enhance muscle strength. Although steroids are a practical approach, they have diverse side effects that require a close view of the patient. Physical therapy also guarantees an effective prevention method (Yang et al. 2019). Besides these treatment approaches, polymyositis can be prevented by advising individuals to work out regularly or consider physical exercises to prevent the illness and its severity in later years.

References

Leclair, V., Notarnicola, A., Vencovsky, J., & Lundberg, I. E. (2021). Polymyositis: Does it really exist as a distinct clinical subset? Current Opinion in Rheumatology, 33(6), 537-543.

Sasaki, H., & Kohsaka, H. (2018). . Modern rheumatology, 28(6), 913-921. Web.

Yang, S. H., Chang, C., & Lian, Z. X. (2019). . Journal of translational autoimmunity, 2, 100018. Web.

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