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**λ±μ¬λ©νμ(Dexamethasone)**μ κ°λ ₯νκ³ μ§μ μκ°μ΄ κΈ΄ ν©μ± κΈλ£¨μ½μ½λ₯΄ν°μ½μ΄λλ‘, κ°λ ₯ν νμΌ λ° λ©΄μ μ΅μ νΉμ± λλ¬Έμ μμνμμ λ리 μ¬μ©λ©λλ€. * **μκ°:** νλλ‘μ½λ₯΄ν°μ(μ½λ₯΄ν°μ)λ³΄λ€ μ½ 25~30λ°° λ κ°λ ₯νλ©°, 무기μ§μ½λ₯΄ν°μ½μ΄λ(μλΆ μ λ₯) νμ±μ΄ κ±°μ μμ΅λλ€. * **μ ν:** μμ½μ¬ λ² μ΄μ€ λλ μΈμ°μΌ μ λ체(ννμ‘, μ©μ‘ λλ μ°κ³ )λ‘ μ 곡λ©λλ€. μμ½μ¬ ννμ νμΌμ¦ ν¨λ₯μ μΌλ°μ μΌλ‘ μΈμ°μΌ μ λμ²΄λ³΄λ€ μ°μν©λλ€. > **μμ μμ :** μλ¬Όνμ λ°κ°κΈ°κ° κΈΈκ³ (>36-72μκ°) 무기μ§μ½λ₯΄ν°μ½μ΄λ νμ±μ΄ μκΈ° λλ¬Έμ κ³ μ©λ λ©΄μ μ΅μ μλ²μ΄λ κΈμ± μλ λ₯΄κΈ° λ°μμ λ§€μ° μ ν©νμ§λ§, μμνλΆ-λνμ체-λΆμ (HPA) μΆμ μ¬κ°νκ² μ΅μ ν μνμ΄ μμΌλ―λ‘ κ²©μΌ μ μ§ μλ²μΌλ‘λ **μ ν©νμ§ μμ΅λλ€**.
μμ© κΈ°μ : Dexamethasone exerts its effects by diffusing across cell membranes and binding to specific cytosolic **glucocorticoid receptors (GR)**. * **Transactivation:** The receptor-ligand complex translocates to the nucleus β binds to glucocorticoid response elements (GREs) on DNA β upregulates the expression of anti-inflammatory proteins like **lipocortin-1** (annexin A1). Lipocortin-1 inhibits **phospholipase A2**, thereby blocking the release of arachidonic acid and the subsequent synthesis of inflammatory prostaglandins and leukotrienes. * **Transrepression:** It inhibits transcription factors such as **NF-ΞΊB** and **AP-1** β downregulates the production of pro-inflammatory cytokines (e.g., IL-1, IL-6, TNF-Ξ±).
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- Systemic fungal infections
- Active viral infections
- Corneal ulcers (especially for ophthalmic preparations)
- Concurrent use of NSAIDs
- Known hypersensitivity to the drug
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- Polyuria (PU) and Polydipsia (PD)
- Polyphagia (increased appetite)
- Panting (especially in dogs)
- Gastrointestinal ulceration or bleeding
- Iatrogenic hyperadrenocorticism (Cushing's syndrome) with chronic use
- Secondary infections due to immunosuppression
- Delayed wound healing
- Muscle wasting and weakness
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- NSAIDs (e.g., carprofen, meloxicam) Β· Significantly increased risk of severe gastrointestinal ulceration and bleeding.
- Insulin Β· Dexamethasone induces insulin resistance, antagonizing the hypoglycemic effect of insulin and increasing requirements in diabetic patients.
- Phenobarbital Β· May induce hepatic enzymes, increasing the metabolism and clearance of dexamethasone.
- Diuretics (potassium-depleting) Β· Increased risk of hypokalemia.
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- Clinical signs of disease resolution
- Water intake and urination (PU/PD)
- Appetite and body weight
- Blood glucose levels (especially in predisposed patients)
- Signs of gastrointestinal bleeding (melena, hematemesis)
- ACTH stimulation test (if assessing HPA axis suppression)
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Acute overdose is rarely life-threatening but may cause significant gastrointestinal upset, profound PU/PD, and panting. Chronic overdosage leads to **iatrogenic hyperadrenocorticism (Cushing's syndrome)**, characterized by alopecia, pot-bellied appearance, muscle wasting, and immunosuppression. Treatment is supportive and requires gradual tapering of the drug.
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