Zinc (Acetate, Sulfate, Gluconate)
Zinc is an essential trace element and nutritional agent critical for the function of over 200 metalloenzymes in the body. It plays a vital role in maintaining the structural integrity of cell membranes and nucleic acids, and is necessary for cell growth, immune response, wound healing, and vision. In veterinary medicine, zinc is primarily utilized for: * **Zinc-Responsive Dermatoses**: * *Syndrome I*: A genetic defect in zinc absorption seen primarily in Northern breeds (e.g., Siberian Huskies, Alaskan Malamutes). * *Syndrome II*: Occurs in rapidly growing large-breed puppies fed diets high in phytates or calcium, which bind dietary zinc and prevent its absorption. * **Hepatic Copper Toxicosis**: Used in susceptible breeds (e.g., Bedlington Terriers, West Highland White Terriers, Labrador Retrievers) to block the intestinal absorption of copper. * **Hepatic Fibrosis & Lipidosis**: Used as an adjunctive hepatoprotectant and antifibrotic agent. > **Clinical Pearl**: It is critical to distinguish between **elemental zinc** and **zinc salts** when calculating doses. For example, zinc sulfate contains 23% elemental zinc, while zinc gluconate contains only 14.3%. Always verify which form the dosage protocol is referencing.
กลไกการออกฤทธิ์: Zinc acts as a critical cofactor for numerous metalloenzymes, including **alkaline phosphatase**, **alcohol dehydrogenase**, **carbonic anhydrase**, and **RNA polymerase**. **Mechanism in Copper Toxicosis**: When administered orally in large doses, zinc induces the synthesis of **metallothionein** in intestinal enterocytes. Metallothionein is a cysteine-rich protein that has a much higher binding affinity for copper than for zinc. Dietary zinc → Induces enterocyte metallothionein → Binds dietary and biliary copper → Traps copper within the enterocyte → Enterocyte is sloughed into the feces (normal turnover) → **Negative copper balance**.
ขนาดยาตามชนิดสัตว์
- Adjunctive therapy of severe hepatic lipidosis · 7-10 mg/kg PO once daily, in B-Complex mixture if possible · PO · q24h
- Appetite stimulant · 1 mg/kg of elemental zinc PO once a day · PO · q24h
- Zinc-responsive dermatoses, copper storage disease · 1-2 mg elemental zinc p.o. q24h (zinc sulphate: 5 mg/kg p.o. q24h or in divided doses; zinc gluconate: 2 mg/kg p.o. q24h; zinc acetate: 1 mg/kg p.o. q24h) · PO · q24h · Not specified · Give with food to minimize vomiting.
- Adjunctive treatment and prophylaxis of hepatic copper toxicosis · Initially, give a loading dose of 100 mg elemental zinc (zinc acetate used in this study) twice daily (separate doses by at least 8 hours) for about 3 months; then reduce dose to 50 mg (elemental zinc) twice daily. · PO · q12h · Lifetime/Maintenance · If animal vomits, give doses with a small piece of meat. Do not give within one hour of a meal. Target zinc levels are 200-500 micrograms/dL.
- Adjunctive treatment and prophylaxis of hepatic copper toxicosis · 5-10 mg/kg elemental zinc q12h; use high end of dosage range initially for 3 months, then 50 mg PO q12h for maintenance. · PO · q12h · Lifetime/Maintenance · Separate dosage from meals by 1-2 hours. In dogs with active copper-induced hepatitis, do not use zinc alone, but in combination with a chelator.
- Adjunctive treatment and prophylaxis of hepatic copper toxicosis · 10 mg/kg elemental zinc (given as zinc acetate or zinc gluconate) PO twice daily. · PO · q12h · Give one hour before each meal.
- Adjunctive treatment and prophylaxis of hepatic copper toxicosis · 1.5-2.5 mg/kg zinc gluconate PO three times daily; 0.67 mg/kg zinc sulfate PO three times daily; or 100 mg (total dose) elemental zinc (as zinc acetate) PO twice daily. · PO · q8h or q12h · 3-6 month loading, then half dose · Goal is to achieve zinc plasma concentrations of 200-600 micrograms/dL.
วิธีการให้ยา
ข้อห้ามใช้
- Patients with pre-existing copper deficiency
- Patients with copper deficiency
อาการไม่พึงประสงค์
- Gastrointestinal disturbances (vomiting, nausea, anorexia)
- Hematologic abnormalities (hemolytic anemia, particularly at serum levels >1000 mcg/dL)
- Hypotension (with overdose)
- Jaundice (with overdose)
- Pulmonary edema (with overdose)
- Nausea
- Vomiting
- Diarrhoea
- Haemolysis (at high doses)
อันตรกิริยาระหว่างยา
- Copper · Large doses of zinc inhibit copper absorption in the intestine; separate supplements by at least 2 hours. · moderate
- Fluoroquinolones (e.g., enrofloxacin, ciprofloxacin) · Zinc salts may reduce the oral absorption of fluoroquinolones.
- Penicillamine · May potentially inhibit zinc absorption; clinical significance is not clear. · minor
- Tetracyclines · Zinc salts may chelate oral tetracycline and reduce its absorption; separate doses by at least 2 hours. · major
- Ursodiol · May potentially inhibit zinc absorption; clinical significance is not clear.
- Iron · Long-term administration of zinc may lead to decreased iron stores and functional deficiency · moderate
- Ursodeoxycholic acid · May potentially inhibit zinc absorption · minor
- Fluoroquinolones · Zinc salts may reduce the absorption of fluoroquinolone antibiotics · major
การติดตาม
- Serum zinc levels (Target 200-500 mcg/dL for copper toxicosis; do not exceed 1000 mcg/dL)
- Gastrointestinal signs (vomiting, anorexia)
- Complete Blood Count (CBC) to monitor for hemolysis/anemia
- Clinical response (resolution of dermatosis or hepatic signs)
- Serum zinc levels
- Serum copper levels
- Complete Blood Count (CBC) / PCV to monitor for haemolysis
การได้รับยาเกินขนาด
Signs associated with overdoses of zinc in mammals include **hemolytic anemia**, hypotension, jaundice, vomiting, and pulmonary edema. > **Toxicity Alert**: Ingestion of U.S. pennies minted after 1982 is a common cause of severe zinc toxicosis in dogs, as these coins are 97.5% zinc. **Treatment in Mammals**: * Remove the source (e.g., endoscopic or surgical removal of coins). * Dilution with milk or water. * Chelation therapy using edetate calcium disodium (Calcium EDTA). **Avian Toxicity**: Zinc intoxication in birds is relatively common (often from cage wire or hardware). Clinical signs are varied and nonspecific: lethargy, anorexia, regurgitation, polyuria, polydipsia, hematuria, hematochezia, pallor, dark or bright green diarrhea, foul-smelling feces, paresis, seizures, and sudden death. Treatment involves removing the source, chelation therapy (Calcium EDTA or succimer), and supportive care.
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