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It blocks the activation of T cells by inhibiting the enzyme calcineurin, which is required for the transcription of interleukin-2: This mechanism of action is associated with a different class of immunosuppressive medications called calcineurin inhibitors, such as cyclosporine. Prednisone does not directly block T-cell activation by inhibiting calcineurin.

It interferes with the synthesis of nucleic acids, which are essential for the replication and function of immune cells: While prednisone may have some impact on nucleic acid synthesis, it is not the primary mechanism of action for its therapeutic effects in rheumatoid arthritis. The anti-inflammatory and immunosuppressive effects of prednisone primarily result from the inhibition of inflammatory mediators and immune cell activity.

It binds to specific antigens or receptors on the surface of immune cells and either neutralizes them or induces their destruction: This mechanism of action is associated with targeted therapies such as monoclonal antibodies. Prednisone, as a glucocorticoid, exerts its effects through genomic mechanisms by binding to cytoplasmic receptors and modulating gene expression, rather than direct binding to specific antigens or receptors on immune cells.

It reduces inflammation, pain, fever, and allergic reactions by inhibiting the synthesis of prostaglandins and leukotrienes: This description corresponds to the pharmacologic effects of glucocorticoids rather than mineralocorticoids like fludrocortisone. While glucocorticoids can have anti-inflammatory effects, fludrocortisone primarily focuses on the mineralocorticoid actions related to electrolyte balance.

It regulates the secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland, maintaining the feedback loop of cortisol production: Fludrocortisone does not directly regulate the secretion of ACTH. It primarily acts at the level of the kidneys to promote sodium reabsorption and potassium excretion.

It influences the carbohydrate, protein, and fat metabolism in various tissues, increasing blood glucose and suppressing immune response: These effects are associated with glucocorticoids rather than mineralocorticoids. Fludrocortisone primarily focuses on the mineralocorticoid effects related to electrolyte balance rather than the metabolic and immunosuppressive actions of glucocorticoids.

The drug may cause nephrotoxicity and increase the risk of renal impairment and electrolyte imbalances: While azathioprine can have adverse effects on the kidneys in some cases, nephrotoxicity is not a commonly reported side effect. It is not a primary concern when using azathioprine in the treatment of Crohn's disease.

The drug may cause neurotoxicity and increase the risk of tremor, headache, and seizures: Neurotoxicity is not a commonly reported side effect of azathioprine. The potential for neurotoxicity is relatively low compared to other adverse effects associated with the medication.

The drug may cause hepatotoxicity and increase the risk of liver impairment and jaundice: Azathioprine has the potential to cause hepatotoxicity in some individuals, but it is not a commonly observed side effect. Liver impairment and jaundice are rare adverse effects associated with azathioprine use.

Decreased frequency and severity of diarrhea, abdominal pain, and rectal bleeding . These are the main symptoms of ulcerative colitis, a chronic inflammatory condition of the colon and rectum that causes ulcers, bleeding, and mucus production in the lining of the bowel. Infliximab is a monoclonal antibody that works by blocking the action of tumor necrosis factor-alpha (TNF-alpha), a cytokine that mediates inflammation and tissue damage in ulcerative colitis. Infliximab can reduce the inflammation and ulceration of the bowel and improve the clinical symptoms of ulcerative colitis .

Improved endoscopic findings and mucosal healing . Endoscopy is a procedure that uses a flexible tube with a camera and light to examine the inside of the digestive tract. Mucosal healing is the restoration of the normal structure and function of the bowel lining. Infliximab can improve the endoscopic appearance and mucosal healing of the colon and rectum in patients with ulcerative colitis . This may reduce the risk of complications such as strictures, fistulas, abscesses, or cancer .

Decreased levels of inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) . CRP and ESR are blood tests that measure the level of inflammation in the body. CRP is a protein produced by the liver in response to inflammation, and ESR is a measure of how fast red blood cells settle in a tube of blood. Both tests are elevated in patients with ulcerative colitis due to the chronic inflammation of the bowel. Infliximab can lower the levels of CRP and ESR by reducing the inflammation and tissue damage in ulcerative colitis . This may reflect the improvement in disease activity and prognosis .

Resolution of extraintestinal manifestations associated with ulcerative colitis (e.g., joint pain, skin lesions) . Extraintestinal manifestations are symptoms or conditions that affect other organs or systems outside the digestive tract. They occur in about 25% of patients with ulcerative colitis and may include arthritis (joint inflammation), uveitis (eye inflammation), erythema nodosum (skin nodules), pyoderma gangrenosum (skin ulcers), primary sclerosing cholangitis (liver inflammation), or ankylosing spondylitis (spine inflammation) . Infliximab can resolve or improve some of these extraintestinal manifestations by blocking TNF-alpha, which is involved in their pathogenesis .