Register
Community
Overview
Experts
Editors
Fellows
Code of conduct
AI Guidelines for Physicians
Company
About Us
FAQs
Privacy Policy
Terms of Use
Careers
Programs
News
News Releases
Press Coverage
Publications
Blog
Contact Us
Sign in
Please select the option that best describes you:
Topics:
Hepatology
•
Genetic Liver Disease
If a patient has a low ceruloplasmin with normal 24 hours urine copper excretion, how would you go about an approach to evaluation of other disorders of copper metabolism as a cause of liver disease?
Related Questions
How do you differentiate primary from secondary iron overload?
What management considerations should we be aware of in the care of aging patients with biliary atresia?
How would you differentiate neurologic manifestations of a patient with Wilson's disease versus manifestations of hepatic encephalopathy due to end-stage liver disease?
How would you approach a referral for concern for hemochromatosis with ferritin elevation but otherwise normal iron studies?
In a PSC patient who has received liver transplant, what graft and/or patient factors predispose to a more rapid return of their disease and how do you manage these peri-operatively and post-transplant?
How do you diagnose cystic fibrosis related liver disease?
In Fontan-associated liver disease (FALD), what clinical scenario would lead you to pursue an evaluation for simultaneous liver-heart transplant as opposed to heart alone if there is evidence of fibrosis on a liver biopsy?
What variables do you weigh most heavily when choosing which copper chelation therapy you'll recommend for a patient?
In what clinical scenario would you consider liver transplant evaluation for a patient with sickle cell hepatopathy?
How would you approach the management of a patient with elevated iron saturation (60%) and ferritin (500s) with negative genetic testing for hemochromatosis? What kind of further monitoring do you perform?