Journal of Small Animal Practice • Vol 59 • April 2018 • © 2017 British Small Animal Veterinary Association
Journal of Small Animal Practice (2018) 59, 222–227
Accepted: 19 September 2017; Published online: 24 November 2017
25-Hydroxy vitamin D3 serum
concentration in dogs with acute
polyradiculoneuritis compared to
E. J. L
* , A. K * , T. R. H-B * , N. G
† , ‡
J. H. R
*School of Veterinary Sciences , University of Bristol, Langford Small Animal Hospital , Langford , Bristol , BS405DU , UK
The Royal Veterinary College , Hatfield , AL9 7TA , UK
Cave Veterinary Specialists, George’s Farm Nr Wellington , Wellington, TA21 9LE, UK
Fizpatrick Referral Hospital, Godalming, GU07 2QQ , UK
Corresponding author email: email@example.com
: To determine if dogs with acute polyradiculoneuritis have lower serum 25-hydroxy vitamin D3
concentration compared to a control group of dogs with idiopathic epilepsy.
: Retrospective case–control study of 21 dogs with acute canine polyradiculoneuritis
and 21 control dogs with idiopathic epilepsy matched for year and season of presentation from a referral
hospital population in the UK. Serum concentration of 25-hydroxy vitamin D3 was compared between
groups using Student’s t-test.
: Dogs with acute canine polyradiculoneuritis had significantly lower (P=0·033) serum 25-hydroxy
vitamin D3 concentration (87·1 nmol/L ±55·4 nmol/L) compared to a control group with idiopathic
epilepsy (113 nmol/L ±66·3 nmol/L).
: The cause and clinical significance of the altered vitamin D status in dogs with acute
polyradiculoneuritis are not clear and require further investigation. Our findings pave the way for improved
understanding of acute canine polyradiculoneuritis and, potentially, improved clinical management, if a
causal role for 25-hydroxy vitamin D3 is defined.
Acute canine polyradiculoneuritis (ACPRN) is the most com-
mon form of acute polyneuropathy in dogs (Cuddon 2002 ).
Definitive diagnosis of ACPRN requires histopathology of
nerve root biopsies, which show an inflammatory infiltrate of
mononuclear cells predominantly in the ventral motor nerve
roots (Cummings et al . 1982 ). Nerve root biopsies are rarely per-
formed ante-mortem in dogs and therefore a presumptive diag-
nosis is made by excluding other diseases and using supportive
clinical criteria, electrodiagnostics and cerebrospinal fluid (CSF)
analysis (Cummings et al . 1982 ).
The aetiopathogenesis of ACPRN is currently unknown but
an immune-mediated process is suspected with a postulated
molecular mimicry mechanism although the trigger has yet to
be identified (Holt et al . 2011 ). ACPRN has been likened to
the acute demyelinating and occasionally axonal forms of Guil-
lain–Barré syndrome (GBS) in humans (Holmes et al . 1979 ).
A recent study demonstrated anti-GM2 ganglioside antibod-
ies in ACPRN suggesting that it may share a similar autoim-
mune pathophysiology with GBS (Rupp et al . 2013 ). These
anti-GM2 ganglioside antibodies appear to have a low diag-
nostic specificity (60%) but a high sensitivity (97%) and can
therefore be used as a supportive ancillary diagnostic test for