Solzin

Wilson's disease (also called hepatolenticular degeneration) is an autosomal recessive metabolic defect. The liver can't excrete copper properly into the bile, so too much copper builds up in the liver and then in other organs, including the brain, kidneys, eyes, bone and muscles. The liver cells store the extra copper for a while. When their capacity is exceeded, copper is released into the blood and taken up in sites outside the liver, such as the brain. This causes motor disorders (ataxia, tremors, speech difficulties) and psychiatric manifestations (irritability, depression, deterioration of work performance).

Redistribution of the excess copper within the hepatocytes leads to hepatocellular injury, inflammation, necrosis and eventually cirrhosis. Patients may present clinically with mainly hepatic, neurologic or psychiatric symptoms.

The disease has been treated by restricting copper in the diet and by using chelating agents, which bind free copper to reduce its toxicity and help its excretion. In symptomatic patients, the purpose of the first treatment with a chelating agent is to detoxify copper. Once the patient's symptoms have stabilized clinically, maintenance treatment begins. Clinical measures are then used to decide whether the patient remains stable.

Pregnancy: Studies in pregnant women haven't shown that zinc acetate or zinc sulfate raises the risk of fetal abnormalities when given in any trimester of pregnancy. If Zinc Acetate Dihydrate is used during pregnancy, harm to the baby looks unlikely. But the studies can't rule out harm completely, so zinc acetate should be used in pregnancy only if clearly needed. There is also a risk on the other side, because copper toxicosis can develop during pregnancy if anti-copper therapy is stopped.

Lactation: Zinc does appear in breast milk, and zinc-induced copper deficiency may occur in the nursing baby. For this reason, women on zinc therapy are advised not to nurse their babies.

Paediatric use of Zinc Acetate Dihydrate has been looked at in only a small number of patients across two clinical trials. From those observations, children aged 10 years and above seem to be kept well controlled on 75 to 150 mg of elemental zinc daily, given in divided doses. No patients below 10 years of age have been studied.

Acute oral overdose with inorganic zinc salts is rarely reported in humans. If it happens, the zinc salt that hasn't been absorbed should be removed from the stomach by lavage as quickly as possible. The plasma level of zinc should be measured, and heavy metal chelation therapy should be considered if the level is markedly raised (>1000 μg/dL). Any signs or symptoms of toxicity should also be treated as medically indicated.

One death linked to zinc sulfate overdose has been reported. An adult woman accidentally swallowed about 28 g of zinc sulfate. She died on the fifth day after ingestion, and the death was put down to renal failure. The overdose had also caused hemorrhagic pancreatitis and hyperglycemic coma. The amount she took was 500 mg/Kg of zinc sulfate, which is in the same order of magnitude as the amount found to be lethal in animals.

Store Zinc Acetate Dihydrate below 30°C, and keep it away from light and moisture. Keep it out of the reach of children.