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Aceruloplasminemia
Reviewed by Medicinsk Expert•Last updated: 2026-10-22•Condition

Aceruloplasminemia

Aceruloplasminemia is a genetic disorder characterized by the gradual accumulation of iron in the brain and other organs, leading to progressive neurological issues and systemic health complications.

Overview

Aceruloplasminemia is a disorder in which iron gradually accumulates in the brain and other organs. Iron accumulation in the brain results in neurological problems that generally appear in adulthood and worsen over time.

Symptoms

People with aceruloplasminemia develop a variety of movement problems, including:

  • Involuntary muscle contractions (dystonia) of the head and neck, resulting in repetitive movements and contortions.
  • Rhythmic shaking (tremors).
  • Jerking movements (chorea).
  • Eyelid twitching (blepharospasm).
  • Grimacing.
  • Difficulty with coordination (ataxia).

Some individuals also develop psychiatric problems and a decline of intellectual function (dementia) in their forties or fifties. Additionally, affected individuals may have diabetes mellitus caused by iron damage to insulin-producing cells in the pancreas. The condition also leads to a shortage of red blood cells (anemia) and changes in the light-sensitive tissue at the back of the eye (retina), which can be observed during an eye examination.

Causes

Mutations in the CP gene cause aceruloplasminemia. This gene provides instructions for making a protein called ceruloplasmin, which is involved in iron transport and processing. When ceruloplasmin is unstable, nonfunctional, or unavailable, the body cannot effectively transport iron out of tissues. The resulting iron accumulation damages cells, leading to neurological dysfunction and other health problems.

Inheritance

This condition is inherited in an autosomal recessive pattern, meaning both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene but typically do not show signs or symptoms of the condition.

Frequently Asked Questions

Diagnosis relies on a combination of low serum ceruloplasmin, low copper, and elevated ferritin levels, together with MRI evidence of iron deposition in the basal ganglia, liver, and pancreas. Genetic testing for biallelic CP‑gene mutations confirms the diagnosis.
Rapid escalation of movement disorders (new or worsening dystonia, tremor, or ataxia), sudden onset of severe anemia, new‑onset diabetes, visual changes from retinal iron deposition, or acute neurological decline (confusion, seizures) should prompt immediate evaluation, as they may signal accelerated iron accumulation needing intensified chelation or hospitalization.
The mainstay is iron‑chelation therapy (e.g., deferoxamine, deferasirox) to reduce tissue iron, often combined with periodic phlebotomy if anemia is not severe. Antioxidant supplements (vitamin E, zinc) may help protect neurons, and symptomatic therapies such as antispasmodics for dystonia or insulin for diabetes are used as needed.
Because the disorder is autosomal recessive, each sibling has a 25 % chance of being affected if both parents are carriers. Targeted DNA testing for the known CP mutations is recommended for at‑risk relatives. Genetic counseling should discuss carrier testing, reproductive options (e.g., IVF with pre‑implantation genetic diagnosis), and the low likelihood of disease in heterozygous carriers.
Source: MedlinePlus, National Library of Medicine

MedlinePlus brings together authoritative health information from the National Library of Medicine (NLM), the National Institutes of Health (NIH), and other government agencies and health-related organizations.

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