๋ํด๋ก๋ฅดํ๋๋ฏธ๋
**๋ํด๋ก๋ฅดํ๋๋ฏธ๋(Dichlorphenamide)**๋ ์ ์ ์ฑ **ํ์ฐํ์ํจ์ ์ต์ ์ (CAI)**๋ก, ์์ ์๊ณผ์์ **๋ น๋ด์ฅ**์ ๋ด๊ณผ์ ์น๋ฃ์ ์ ํต์ ์ผ๋ก ์ฌ์ฉ๋์์ต๋๋ค. * **์์ ์์ **: ๋์ฌ์ฑ ์ฐ์ฆ ๋ฐ ์ ์นผ๋ฅจํ์ฆ๊ณผ ๊ฐ์ ์ฌ๊ฐํ ์ ์ ๋ถ์์ฉ๊ณผ ์์ ์ ๊ณต๊ธ ๋ถ์กฑ์ผ๋ก ์ธํด, ์ ์ ์ฑ CAI๋ ๋๋ถ๋ถ **๋๋ฅด์กธ๋ผ๋ฏธ๋(dorzolamide)** ๋ฐ **๋ธ๋ฆฐ์กธ๋ผ๋ฏธ๋(brinzolamide)**์ ๊ฐ์ ๊ตญ์ ๋์ฒด์ ๋ก ๋์ฒด๋์์ต๋๋ค. * ํ์ฌ ์ฒ๋ฐฉ๋ ๊ฒฝ์ฐ, ์ผ๋ฐ์ ์ผ๋ก ์กฐ์ ์ฝ๊ตญ(compounding pharmacy)์ ํตํด ๊ตฌํด์ผ ํฉ๋๋ค. * ๊ฐ๋ฒผ์ด ํญ๊ฒฝ๋ จ ๋ฐ ์ด๋จ ํน์ฑ์ด ์์ง๋ง, ํ๋ ์์ํ์์๋ ์ด๋ฌํ ์ ์์ฆ์ผ๋ก ๊ฑฐ์ ์ฌ์ฉ๋์ง ์์ต๋๋ค.
์์ฉ ๊ธฐ์ : Dichlorphenamide exerts its effects via noncompetitive, reversible inhibition of the enzyme **carbonic anhydrase (CA)**. * **In the ciliary body**: Inhibition of **CA-II** โ decreased formation of bicarbonate (HCO3-) and hydrogen (H+) ions from carbon dioxide and water โ reduced active transport of sodium into the posterior chamber โ decreased aqueous humor production โ **lowered intraocular pressure (IOP)**. * **In the kidneys**: Inhibits CA in the proximal convoluted tubule โ increased renal tubular secretion of Na+, K+, and HCO3- โ alkaline diuresis and potential metabolic acidosis. * **In the CNS**: Exhibits mild anticonvulsant activity, likely secondary to localized metabolic acidosis or direct CA inhibition in the brain.
๋๋ฌผ ์ข ๋ณ ์ฉ๋
- Adjunctive treatment of glaucoma ยท 0.5-1.5 mg/kg PO two to three times daily ยท PO ยท q8-12h
- Adjunctive treatment of glaucoma ยท 1-2 mg/kg PO q8-12h ยท PO ยท q8-12h
- Adjunctive treatment of glaucoma ยท 2.2-4.4 mg/kg PO two to three times daily (q8-12h) ยท PO ยท q8-12h
- Adjunctive treatment of glaucoma ยท 10-15 mg/kg per day divided 2-3 times daily ยท PO ยท divided 2-3 times daily
- Adjunctive treatment of glaucoma ยท 2-5 mg/kg PO q8-12h ยท PO ยท q8-12h
์ฉ๋์ ๋ฉดํ ์์ ์ ๋ฌธ๊ฐ๋ฅผ ์ํ ์์ ์ฐธ๊ณ ์๋ฃ์ ๋๋ค. ํญ์ ์ต์ ๋ผ๋ฒจ๊ณผ ๊ฐ๋ณ ํ์์ ๋ํด ํ์ธํ์ญ์์ค.
ํฌ์ฌ ๊ฒฝ๋ก
๊ธ๊ธฐ
- Significant hepatic disease (may precipitate hepatic coma)
- Renal or adrenocortical insufficiency
- Hyponatremia
- Hypokalemia
- Hyperchloremic acidosis
- Electrolyte imbalance
- Severe pulmonary obstruction (unable to increase alveolar ventilation)
- Hypersensitivity to carbonic anhydrase inhibitors
- Chronic, noncongestive, angle-closure glaucoma (long-term use)
์ด์๋ฐ์
- Panting
- GI disturbances (inappetence, vomiting, diarrhea)
- CNS effects (sedation, depression, excitement)
- Hematologic effects (bone marrow depression)
- Renal effects (crystalluria, dysuria, renal colic, polyuria)
- Metabolic acidosis
- Hypokalemia
- Hyperglycemia
- Hyponatremia
- Hyperuricemia
- Hepatic insufficiency
- Dermatologic effects (rash)
- Hypersensitivity reactions
์ฝ๋ฌผ ์ํธ์์ฉ
- Antidepressants, Tricyclic ยท Alkaline urine caused by dichlorphenamide may decrease excretion of tricyclic antidepressants.
- Aspirin (or other salicylates) ยท Increased risk of dichlorphenamide accumulation and toxicity; increased risk for metabolic acidosis; dichlorphenamide increases salicylate excretion.
- Digoxin ยท Dichlorphenamide may cause hypokalemia, leading to an increased risk for digoxin toxicity.
- Insulin ยท Rarely, carbonic anhydrase inhibitors interfere with the hypoglycemic effects of insulin.
- Methenamine compounds ยท Dichlorphenamide may negate the effects of methenamine in the urine due to alkalinization.
- Potassium-depleting drugs (corticosteroids, amphotericin B, corticotropin, diuretics) ยท Concomitant use may exacerbate potassium depletion.
- Phenobarbital ยท Increased urinary excretion, which may reduce phenobarbital levels.
- Primidone ยท Decreased primidone concentrations.
- Quinidine ยท Alkaline urine caused by dichlorphenamide may decrease quinidine excretion.
๋ชจ๋ํฐ๋ง
- Intraocular pressure (IOP) / tonometry
- Serum electrolytes (may need to supplement potassium)
- Baseline CBC with differential and periodic retests if using chronically
- Clinical signs of adverse effects (GI upset, panting, CNS changes)
๊ณผ์ฉ๋
Information regarding acute toxicity of dichlorphenamide is limited. * **Clinical Signs**: Likely extensions of adverse effects, including severe electrolyte derangements (hypokalemia, hyponatremia), profound metabolic acidosis, CNS depression, and dehydration. * **Treatment**: * Monitor serum electrolytes, blood gases, volume status, and CNS status. * Provide aggressive supportive care, including IV fluid therapy to correct dehydration and acid-base/electrolyte imbalances (e.g., potassium supplementation). Treat symptomatically.
VetSheet ์ฝ๋ฌผ ๋ ํผ๋ฐ์ค๋ ๋ฉดํ ์์ ์ ๋ฌธ๊ฐ๋ฅผ ์ํ ์์ ์์ฌ๊ฒฐ์ ๋ณด์กฐ ๋๊ตฌ์ด๋ฉฐ, ์ ๋ฌธ์ ํ๋จ์ด๋ ์ ์กฐ์ฌ์ ์ต์ ๋ผ๋ฒจ์ ๋์ ํ์ง ์์ต๋๋ค.