The raison d'etre of this website is to provide you with hard scientific information which may help you make informed decisions in your quest for health (so far I have blogged concise summaries of over 1,500 scientific studies and have had three books published).

My research is mainly focused on the effects of cholesterol, saturated fat and statin drugs on health. If you know anyone who is worried about their cholesterol levels and heart disease, or has been told to take statin drugs you could send them a link to this website, and to my statin or cholesterol or heart disease books.

David Evans

Independent Health Researcher

Monday, 17 June 2013

Cholestatic jaundice induced by atorvastatin

This paper was published in the Israel Medical Association Journal 2009 Jul;11(7):440-1

Study title and authors:
Cholestatic jaundice induced by atorvastatin: a possible association with antimitochondrial antibodies.
Minha S, Golzman G, Adar I, Rapoport M.
Department of Internal Medicine C, Assaf Harofeh Medical Center, Zerifin, Israel.

This paper can be accessed at:

This paper describes the case of a man who developed cholestatic jaundice while taking atorvastatin. (Cholestatic jaundice is when the normal flow of bile from the liver to the small intestine is interupted).

(i) A 68 year old man was admitted to hospital complaining of fever, dark urine and hives (itchy rash).
(ii) He was taking atorvastatin 20 mg per day.
(iii) Physical examination revealed he had jaundice and large areas of hives.
(iv) Abnormal laboratory results included elevated liver function tests with a cholestatic pattern:
total bilirubin 7.4 mg/dl (normal 0.2–1.0 mg/dl)
alkaline phosphatase 555 U/L (normal 39–117 U/L)
alanine aminotransferase 250 U/L (normal 4–41 U/L)
aspartate aminotransferase 50 U/L (normal 5–38 U/L)
lactate dehydrogenase 540 U/L (normal 240–480 U/L)
(v) A diagnosis of drug-induced liver damage was made.
(vi) The patient stopped taking atorvastatin and he had a rapid biochemical and clinical improvement.
(vii) During the following four weeks the patient was discharged and readmitted twice with a similar clinical and laboratory findings.
(viii) A liver biopsy revealed on his next admission revealed severe inflammation.
(ix) Further investigation revealed that between admissions and prior to each recurrent bout of cholestatic hepatitis the patient had renewed his treatment with atorvastatin.  
(x) Complete cessation of atorvastatin was followed by a return to normal values of liver function tests and a complete clinical recovery.