However, inadequate or excessive zinc intake can be harmful; excess zinc particularly impairs copper absorption because metallothionein absorbs both metals.The human dopamine transporter contains a high affinity extracellular zinc binding site which, upon zinc binding, inhibits dopamine reuptake and amplifies amphetamine-induced dopamine efflux in vitro. The human serotonin transporter and norepinephrine transporter do not contain zinc binding sites. Some EF-hand calcium binding proteins such as S100 or NCS-1 are also able to bind zinc ions. Nutrition
Dietary recommendations
The U.S. Institute of Medicine (IOM) updated Estimated Average Requirements (EARs) and Recommended Dietary Allowances (RDAs) for zinc in 2001. The current EARs for zinc for women and men ages 14 and up is 6.8 and 9.4 mg/day, respectively. The RDAs are 8 and 11 mg/day. RDAs are higher than EARs so as to identify amounts that will cover people with higher than average requirements. RDA for pregnancy is 11 mg/day. RDA for lactation is 12 mg/day. For infants up to 12 months the RDA is 3 mg/day. For children ages 1–13 years the RDA increases with age from 3 to 8 mg/day. As for safety, the IOM sets Tolerable upper intake levels (ULs) for vitamins and minerals when evidence is sufficient. In the case of zinc the adult UL is 40 mg/day (lower for children).
Removal or enucleation of the eye is a last resort option if the eye already has become blind and painful.Repeated blood transfusions may be needed to control anemia, and thrombocytopenia can be managed with splenectomy. Prognosis
The neurological symptoms are progressive and can lead to severe spasticity, bulbar symptoms and dysarthria within one to two decades. The life span is shorter than normal. Death occurs between 2 and 30 years of age, depending on the severity of the syndrome. The immediate cause of death is pneumonia, fulminant intestinal bleeding or multiple organ dysfunction.If not treated, the retinal detachment can lead to ischemia and growth of new blood vessels over the iris and anterior chamber angle. This in turn can cause secondary glaucoma, cataract and, ultimately, blindness of the eye. Epidemiology
This syndrome is usually sporadic although families with two or more affected siblings of both sexes are known. History
A child who was eventually diagnosed with cerebroretinal microangiopathy with calcifications and cysts was first described in the literature in 1987. The disorder was suspected of being allelic with either the Revesz syndrome or leukoencephalopathy with calcifications and cysts.