Arthritis is a medical condition that affects the joints, causing inflammation and, to some extent, tenderness. In the U.S., close to 54.4 million individuals have been diagnosed with at least one form of arthritis, of which approximately 23.7 million persons have low work productivity as a result of the condition (Center for Disease Control and Prevention [CDC], 2018). The major symptoms of the disease include such conditions as joint pain, stiffness, itching, and inflammation. Notably, the indications progress gradually or abruptly and worsen with age. Arthritis is more regular among aging adults, though it can be diagnosed in any other person irrespective of age, including children.

The main common type of arthritis is osteoarthritis, though other common forms include such diseases as gout, fibromyalgia, lupus, and rheumatoid arthritis. Osteoarthritis causes cartilage to break down, whereas RA is an autoimmune disorder where the immune system of an individual attacks its organs, in this case, the joints. It is marked by symmetric, erosive synovitis and, in most cases, extraarticular connection. Patients with RA experience a chronic variation of the disease, and regardless of therapy, it may lead to advanced joint obliteration, distortion, disability, and even premature cell apoptosis (Zhang et al., 2018). In gout, arthritis results from uric acid crystals accumulation in the blood (Macfarlane, Seibel and Zhou, 2020). In other forms of arthritis, underlying diseases condition such as psoriasis or lupus can cause the development of arthritis. Based on this analysis, individuals suffering from a rare form of arthritis might manifest significant and various symptoms, thus requiring the application of different treatment modalities.

Treatment of arthritis varies and depends on the various kinds of arthritis and their underlying disease conditions. However, the main objectives of arthritis treatments are to lower the symptoms of the disease condition and to promote quality of life and well-being (Gale et al., 2018). The prescribed drug for the patient in the case study is prednisone. Therefore, to comprehend the need for alternative drugs for the case of a patient with arthritis, the mechanism of action of prednisone is necessary.

Prednisone is a glucocorticoid drug whose main action is to lower inflammation, yet it suppresses the immune systems. The mechanism of action involves the prednisone stimulating the glucocorticoid receptors in the body cells, which results in the suppression of the harmful cytokines (Berardicurti et al., 2020). Prednisone reduces the swelling through the inhibition of the relocation of polymorphonuclear white blood corpuscle and retreating amplified blood vessel absorbency (Zheng, Guo and Wu, 2018). It also stifles the immune system by decreasing the action and capacity of the defense system.

In this case, the antineoplastic properties may relate to the hindrance of glucose conveyance. Furthermore, such obstruction includes phosphorylation and stimulation of cell apoptosis in undeveloped white blood cells (Rice et al., 2017). Furthermore, it may have antiemetic capacities by obstructing the brain excitation of the emetic center through suppression of prostaglandin (Chilkoti et al., 2019). Prednisone is a pro-drug to prednisolone, and with its immunomodulating properties, it can enter a cell upon surface receptor binding (Berardicurti et al., 2020). Once inside a cell and into the nucleus, prednisone attaches and stimulates certain nuclear receptors, which lead to transformed gene expression and suppression of pro-inflammatory cytokine excretion (Rice et al., 2017). Therefore, the drug lowers the number of lymphocytes circulating in the blood, thus promoting cell differentiation and inducing cell death in subtle tumor cells.

Through the inhibited cytokines, there is a reduction in inflammation, pain, and associated stiffness. Furthermore, prednisone acts as Cyclooxygenase-2 (COX-2) inhibitors, which are nonsteroidal anti-inflammatory drugs (NSAIDs) that mark and binds to the active sites of COX-2, an enzyme accountable for the pain and swelling in somatic cells (Verhoeven et al., 2019). Based on the illustrations above, with regards to underlying health conditions of an individual with arthritis and the mechanism of action of prednisone, other alternative treatments are necessary to reduce or lower the adverse effects of prednisone, a glucocorticoids molecule.

Some of the alternative therapeutic drugs for arthritis are fast-acting NSAIDs, which play a role in relieving pain and lowering swelling in arthritis. For example, Aspirin acts as an inhibitor of prostaglandins when used at high doses, thus reducing the sensation of pain and inflammation in arthritis, especially RA (Zhang et al., 2018). The disadvantages of using Aspirin include such side effects as tinnitus, loss of hearing, and gastrointestinal intolerance. Another newer drug in the market that acts the same way as Aspirin is celecoxib (Celebrex), a COX-2 inhibitor that has GI bowel effects (Krasselt and Baerwald, 2019). Celebrex’s mechanism of action involves the suppression of the enzyme COX-2, which further hampers the metabolism of prostaglandins, prostacyclin, and thromboxane (Krasselt and Baerwald, 2019). Other regular side effects include vomiting, nausea, abdominal pain, ulceration, and bleeding of the stomach walls. The adverse effects can be managed by taking antacids, proton pump inhibitors (PPI), or misoprostol (Cytotec) to reduce gastrointestinal bleeding or ulcers.