Statin Neuropathy Masquerading as Diabetic
Autoimmune Polyneuropathy
Tom Brooks Vaughan, MD and David S.H.
Bell, MD
Statin-induced neuropathy is increasingly described. Proposed
mechanisms include an alteration in cholesterol synthesis,
producing a disturbance in the cholesterol-rich neuronal
membrane, or in the activity of ubiquinone (coenzyme
Q10), a mitochondrial respiratory chain enzyme inhibited
by statins leading to neuronal damage (1).
The entire class is implicated, and both polyneuropathy
and mononeuropathy have been described with improvement or even
complete resolution occurring with cessation of therapy (1).
In all cases, clinical improvement occurred soon after statins
were discontinued, and in the absence of specific clinical,
biochemical, or electrophysiological characteristics, this has
become the key diagnostic feature of statin-induced
neuropathy. To date, autonomic features accompanying
symmetrical neuropathy have not been described.
We present an 18-year-old white female with type 1 diabetes
for 5 years who, over several months, developed restless legs
followed by parasthesias, nocturnal diarrhea, fecal
incontinence, early satiety, and weight loss. Examination
revealed loss of pinprick sensation to the upper arms and
thighs accompanied by areflexia and loss of vibration
sense, a fixed tachycardia, and orthostatic hypotension.
Autoimmune demyelinating polyneuropathy was initially
suspected due to the relatively rapid onset of symptoms
and the combination of peripheral and autonomic findings.
Neuroelectrophysiological studies showed evidence of axonal,
sensory, and motor polyneuropathy but did not meet criteria
for demyelination. Supportive therapy included gabapentin,
clonazepam, metoclopramide, metronidazole, cholestyramine,
and fludrocortisone.
Before further investigations began, it was noted that the
subject
had been taking
atorvastatin
despite very
low lipid levels,
and it was discontinued. Within 1 week,
her symptoms improved
dramatically. Within 6 months, the
postural hypotension, diarrhea,
and symptoms of
gastroparesis had resolved, and all medicines
other than
insulin were discontinued. There remained a minimal
decrease in vibration sense, areflexia, and loss of sensation
to the wrist and ankle.
Isolated cases of statin-associated neuropathy have been reported
since 1994 (1).
Epidemiological and case-control studies from the U.K.
and Denmark suggest elevated odds ratios (ORs) of 2.5
(95% CI 0.3–14.2) to 3.7 (1.8–7.6), respectively, for the
development of neuropathy while on statin therapy (2,3).
The OR jumped to 26.4 (7.8–45.4) in patients with confirmed
neuropathy taking statins for >2 years (3).
The key to diagnosing statin-induced neuropathy is to discontinue
the statin and observe for potential improvement. In
conclusion, statins can infrequently cause an
idiosyncratic somatic and autonomic neuropathy that, in
the diabetic patient, will almost invariably be
attributed to diabetes. Awareness of this association and
a trial removal of the statin could result in restoration
of neurological function and a much-improved quality of life
in the diabetic patient.
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REFERENCES
1- Backes JM,
Howard PA:
Association of
HMG-CoA
reductase
inhibitors with
neuropathy. Ann
Pharmacother 37:
274–278, 2003
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2-- Gaist D, Rodriguez LA, Huerta C, Hallas J,
Sindrup S: Are users of lipid-lowering drugs at
increased risk of peripheral neuropathy? Eur J Clin
Pharmacol 56: 931–933, 2001 CrossRefMedline
3-Gaist D, Jeppesen U, Andersen M, Garcia Rodriguez
LA, Hallas J, Sindrup SH: Statins and risk of
polyneuropathy: a case-control study. Neurology 58:
1333–1337, 2002
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