- Clinical Finding
- Etiology
- Pathogenesis
- Pathology
- Epidemiology
- Management & Treatment
- Prevention
- Complications
- Prognosis
- Research Frontier
- Clinical Case Studies
- Study Questions
Liver manifestations usually do not begin until liver stores become saturated (6–7 g).
Iron deposition within cardiac tissue can lead to either dilated cardiomyopathy or a mixed dilated-restrictive picture. Conduction disturbances such as atrial fibrillation or sick sinus syndrome have also been linked with hereditary hemochromatosis. Dysrhythmias and cardiomyopathy are the leading cause of sudden death in patients with iron overload.
cirrhosis
Pathologically, the presence of “iron-free” nodules on histologic examination has correlated with onset of hepatocellular carcinoma.
With treatment, elevations in liver function tests and hepatomegaly are reversible. No strong evidence currently exists with respect to the reversibility of portal hypertension with treatment.
Content 3
Content 13
Content 11
What is the unifying common denominator in the pathogenesis of hereditary hemochromatosis?
Impaired expression of hepcidin
Enhanced expression of transferrin receptor
Enhanced expression of ferritin
Impaired expression of transferrin
Enhanced expression of ferroportin
The correct answer is A.
Hepcidin is the master regulator of iron homeostasis, suppressing both absorption of iron from the gastrointestinal tract and iron release from macrophages. Therefore, inactivating mutations of the hepcidin gene or of genes that support or promote transcriptional expression of hepcidin will result in iron overload. (The answer is A.)