Yukiko писал(а): То есть они получается с фена вообще уходили не один год?
Hepatocutaneous Syndrome
Secondary to phenobarbital
Jason Berg, DVM, DACVIM (SAIM, Neurology),
Animal Specialty Center
Rex is a 10-year-old German Shepherd cross who initilly
presented to the neurology service at Animal Specialty
Center in 2003 for recurrent grand mal seizures. Rex
was normal interictal and did not have any relevant
medical history. Physical and neurological exams were
normal as was blood work including bile acids and a
thyroid profie. A presumptie diagnosis of idiopathic
epilepsy was given. MRI and CSF analysis are needed for
a defiitie diagnosis but these have a very low yield for
any actie disease process in a dog that starts seizing
between the ages of 1 and 5, is normal interictal, has
normal blood tests and has a normal neurological exam.
Rex did not have an MRI performed. Phenobarbital was
initited and Rex had a routie CBC and chemistry panel
performed twice yearly.
The only abnormality on any blood work done from
2003 through 2007 was an increase in ALP. In 2008
the ALT and AST showed slight elevatins. Potassium
bromide (KBr) was added to lessen the amount of
phenobarbital required. Rex was started on milk thistle
as a hepatoprotectant. Rex became ataxic and somnolent
even with a low dose of KBr so he was switched from KBr
to pregabalin (Lyrica®) for its twice-daily dosing, renal
excretin and reduced sedatie effct. His liver enzymes
improved slightly but the ALT and AST never normalized.
His phenobarbital dose was decreased initilly but could
never be completely eliminated.
Slowly the frequency and severity of seizures increased
over the next few months and multile antionvulsants
were trialed. In multile combinatins, these included
clorazepate, valproic acid, and acetazolamide. Zonisamide
and felbatol were not used due to liver metabolism and
associatin with possible hepati damage. Gabapenti
was not trialed because he was currently on pregabalin
which is a derivatie of gabapenti. Levitiacetam
(Keppra®) would be a wise choice due to renal excretin
but the dosing (every 8 hours) was problemati for the
family. Rex contiued to have an unacceptable number of
seizures (> 3/month).
In March 2011 rufiamide (Banzel®) was added.
Rufiamide is new and novel antionvulsant (FDA approved
in 2008). It is hepatially metabolized but does not induce
P450 enzymes as phenobarbital does. There is limited
informatin in the veterinary literature at the current tie,
but pharmacology data suggest it can be given BID.
Lyrica® and clorazepate were weaned and discontiued
aftr the rufiamide was started. Beginning in May
2011, Rex’s liver enzymes were increasingly elevated
and phenobarbital was weaned down to a 25%
reductin. In June 2011 Rex presented for ascites,
anorexia, and lethargy. Blood work supported liver
failure (elevated liver enzymes and low normal BUN,
albumin, and cholesterol). Restig bile acids were
elevated at 31 µmol/L (normal <10 µmol/L). An
abdominal ultrasound revealed an irregular nodular
small liver, a large amount of ascites, and no masses or
other pathology. A liver biopsy was not performed but
cirrhosis was the presumptie diagnosis. Analysis of
the ascites revealed a pure transudate with no signs of
infectin or malignancy.
Phenobarbital was stopped in 2 weeks and the only
antionvulsant Rex was taking from June 2011 on was
rufiamide. Treatment for hepati failure and ascites
was initited with a diet change to Hill’s L/D and oral
zinc gluconate, ursodiol, furosemide, spironolactone,
and Denamarin®. The milk thistle that Rex had been
on for years was contiued. Within 2 weeks the ascites
resolved and then the furosemide and spironolactone
were weaned. Appetie was poor and inconsistent.
Hepatocutaneous Syndrome
Secondary to phenobarbital
Jason Berg, DVM, DACVIM (SAIM, Neurology),
Animal Specialty Center
7
internal Medicine, neurologVOLUME 2 • IssUE 1 • WIntER 201
