Hi Andrew,
I would suspect atorvastatin induced intraheptic cholestasis as the explanation for this transient liver and lipid derangement. I suspect that withdrawal of atorvastatin was the key to resolution rather than fenofibrate per se.
Best regards
Mohammad
Dr. M A Al-Jubouri, MB ChB, MSc, EurClinChem, FRCP Edin, FRCPath
Consultant Chemical Pathologist
--------------------------------------------
On Wed, 29/7/15, Taylor Andrew (ROYAL UNITED HOSPITALS BATH NHS FOUNDATION TRUST) <[log in to unmask]> wrote:
Subject: puzzling lipids
To: [log in to unmask]
Date: Wednesday, 29 July, 2015, 10:31
Dear Mailbase
Any thoughts on this?
57y female hypertensive.
On atorvastatin, previous
results unremarkable, e.g. 2014: chol 6.4, HDL 2.7, tg
2.0
Going back to 2002, all
previous Tg less than 4
“Routine
bloods” in June 2015 grossly lipaemic: Tg 73.0
Advised GP switch atorva
to fenofibrate
1 week later: Tg now
reasonably well controlled, thank you, 6.4 mmol/L, BUT chol
now 20.6 mmol/L
All new investigations for
secondary hyperlipidaemia negative – e.g. I suspected
PBC but LFTs only mildly deranged (ALP 195 IU/L) except GGT=
700 IU/L, ultrasound = mild fatty liver only, immunology
normal
Recheck 1 week later: chol
13.4 mmol/L Tg normal, ApoB sent to check if it is LDL and
not LpX etc: 2.4g/L, i.e. consistent with a genuine marked
elevation of LDL
Recheck 2 weeks later:
LFTs normal, except GGT 90, lipids back to 2014 levels.
So, if gammaGT is the
clue: what liver disorder will produce gross
hypertriglyceridaemia responsive to fibrates but also
associated with transient marked LDL increase?
Suggestions on a postcard
please
Thanks
Worried of Bath
Andrew
Taylor
Consultant
Medical Biochemist RUH Bath
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