Question for Dr.'s/Professionals

Larry · medicine forum Guru Wannabe Joined: 09 May 2005 Posts: 151

My Dad, 83 y/o, 12 years post-bypass and has had two MIs (most recent in
1993) and 2 angioplasties. Seems to be doing much better since advent of
Lipitor. Also had a RFA successfully treated Atrial Flutter and has a
pacemaker for subsequent sick sinus syndrome. Good cardiac output for
someone in his condition (I believe it's up around 40-50%) and on
treadmill walking 3X/week. Current meds are Coumadin, Lipitor, Tenormin,
and Foltx.

Dad has history of "shooting pains", most of the time occuring in his
upper legs (thighs) and lower abdomen. Docs don't know what to make of
it ... thinking is that it might be circulatory or neurological. No
one's ever been able to fully diagnose and treat. They cause him to jump
and groan a bit ... and he is usually very pain tolerant.

He consulted with Neuro and had CT and electromyographic testing ...
everything negative. Neuro wants to start him on Neurontin. Is there any
reason why he should not be able to take Neurontin... given his Hx or
potential interactions with other meds that he is on?

Larry E.

outrider · medicine forum Guru Joined: 28 Apr 2005 Posts: 1155

I don't have cardiovascular disease but I experienced the pains you
describe when I was taking Lipitor and Baycol.

The standard liver function and nerve tests may not always show statin
damage. One needs to have muscle biopsies.

You may wish to take the following information to your father's
doctors. If you would like the full text PDF please e-mail me at the
address above. Search PUBMED for Dr. Paul S. Phillips work on statins,
statins and cardiopulmonary function, statin myopathy... . Zee

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Muscle Nerve. 2005 May;31(5):572-80.

Molecular clues into the pathogenesis of statin-mediated muscle
toxicity.

Baker SK.

Division of Physical Medicine and Rehabilitation, Department of
Medicine, McMaster University, McMaster University Medical Center, Room
4U4, Hamilton, Ontario, L8N 3Z5, Canada. bakersjj@hotmail.com

The pathophysiology of statin-mediated muscle dysfunction is poorly
defined. Reductions in skeletal muscle membrane cholesterol were
initially thought to account for the range of myopathic reactions,
e.g., myalgia, elevated serum creatine kinase, or rhabdomyolysis. This
assumption however, does not consider a potential role of the
isoprenoids in the pathophysiology of statin myopathy. The observation
that derangements in mevalonate kinase (MK), but not more distal
enzymes of cholesterologenesis, are associated with a skeletal myopathy
suggests a critical role for the isoprenoids in the maintenance of
muscle. Statins also deplete the isoprenoid pool by inhibiting the
enzyme, beta-hydroxy-beta-methylglutaryl coenzyme A reductase, which is
upstream of MK. Identifying candidate proteins that are both dependent
on isoprenoid-mediated modification and associated with muscle disease,
when genetically mutated, offers further insight into potential
mechanisms of statin myopathy. For example, lamin A/C, selenoprotein N,
alpha- and beta-dystroglycan, and cytoskeletal G-proteins all require
isoprenylation for optimal function. Understanding the pleiotropic
effects of protein prenylation, and the potential consequences of a
generalized insufficiency of this form of protein modification, may
help clarify the molecular pathogenesis of statin myopathy.

PMID: 15712281 [PubMed - in process]

Larry wrote:

Andrew B. Chung, MD/PhD · medicine forum Guru Joined: 25 Mar 2005 Posts: 8540

Larry wrote:

Google