Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No.

3 (July) 2009; 77 - 95

Studies On Feline Hepatic Lipidosis

By
Kelany, W. M.a ; Sherein, S. A. Elgayed b ; Mahran, K. M. A.c and
Dardery, M. A.d
a

Dept. of Int. Med. and Infectious diseases, Faculty of Vet. Med., Cairo Univ.,
b
Dept. of Pathology, Faculty of Vet. Med., Cairo Univ.,
c
Dept. of clinical pathology, Faculty of Vet., Med., Cairo Univ. and
d
Dept. of Pathology, Animal Health Research Institute.

SUMMARY

his study was performed on 40 cats, divided on the basis of history

and clinical presentation into two equal groups; a group of apparently healthy cats and a group of clinically diseased cats. All cats were
subjected to clinical evaluation, ultrasonographic and clinicopathological
examinations. The livers of three dead cats from the second group were
examined histopathologically. The clinical signs of clinically diseased
cats included anorexia, vomiting, diarrhea, lethargy, hepatoencephalopathic signs (muscle fasciculation, tremors and convulsions)
with hemorrhagic diathesis and ascites in 2 cats. Palpation revealed
enlarged liver extended beyond the last right rib while fluid thrill was
detected by the tactile percussion in ascetic cats. The hematological profile of clinically diseased cats showed a normocytic normochromic anemia associated with stress leukogram. Moreover, the biochemical profiles of these cats showed significant increases in hepatic enzymes (AST,
ALT, ALP and GGT), bilirubin, triglycerides, total cholesterol, HDL,
LDL and VLDL in comparison to control cats. Serum glucose, BUN,
total proteins, albumin and A/G ratio were significantly decreased. Serum creatinine and globulins were not significantly changed. The ultrasonographic findings included diffuse hyperechogenicity of hepatic parenchyma, decreased visualization of the intrahepatic blood vessels and
enlargement of liver. The liver parenchyma was isoechoic or hyperechoic, compared with falciform or omental fats. The liver was also hyperechoic with respect to the spleen and renal cortices. Also, there was
increased attenuation of ultrasound waves by liver parenchyma. Microscopic examination of the livers of dead cats revealed different degrees
of lipidosis. From the research, it was concluded that ultrasonogaphy and
serum chemistry panel were complementary to each other. It can also be
confirmed by autopsy and histopathology of dead cats. The serum chemistry panel could detect the hepatic dysfunction while ultrasonography
defined the nature of lesions.
77

Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95
Referred by
Prof. Dr. Sohir Sokkar

Professor of Pathology, Fac. Vet. Med.,

Cairo University
Professor of Clinical Pathology, Fac. Vet.
Med., Cairo University

Prof. Dr. Safaa Ramadan

The purpose of this study is to

compare the reliability of ultrasonography versus laboratory diagnosis and histopathological studies
in the diagnosis of feline hepatic
lipidosis.

INTRODUCTION
epatic lipidosis in cats is a
commonly diagnosed hepatobiliary disease of unknown cause
(De-Maria et al., 1998 and Brown
et al., 2000). The condition seems
to have no age, breed, or gender
predilection (Thornburg et al.,
1982; Center, 1986 and Jacobs et
al., 1989). Hepatic lipidosis is diagnosed in obese or formerly
obese cats with anorexia, hepatomegally, jaundice and muscle
wasting (Burrows et al., 1981;
Thornburg, 1982; Center, 1986;
Jacobs et al., 1989; Bennette et
al., 2007 and Posner et al., 2008).
Abnormal laboratory parameters
(serum liver enzymes, bilirubin
and bile acid concentrations,
etc) are rapid and accurate methods for diagnosis of feline hepatic
disorders (Burrows et al., 1981;
Thornburg et al., 1982; Center,
1986; Jacobs et al., 1989 and Nakamura et al., 2005). Liver biopsy
was found to be the most reliable
diagnostic procedure to detect hepatic lipidosis (De-Maria et al.,
1998 and Willard et al., 1999).

MATERIAL AND METHODS

Animals:
A total number of 40 cats
(1.6-10.0 years-old, Persian, Siamese and Egyptian Mau) admitted
to the clinic of Faculty of Veterinary Medicine, Cairo University
and to a private veterinary clinic in
Giza governorate in the period
from September, 2007 to August,
2008 were included in the study.
On the basis of history and clinical
presentation, the cats were divided
into 2 groups (each composed of
20 cats); group (1); a group of apparently healthy cats and group
(2); a group of clinically diseased
cats.
Clinical evaluation:
Age, gender, breed, respiratory rate, pulse rate, rectal temperature of the cats of the study
were recorded. All cats were thoroughly investigated and clinically
examined by abdominal palpation
and tactile percussion according to
the method described by Kelly
(1984).

Nowadays, use of ultrasonography enhanced the detection of

fatty infiltration in liver with high
sensitivity and specificity (Scatarige et al., 1984; Nakamura et al.,
2005 and Posner et al., 2008).
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Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

ces; mean corpuscular hemoglobin

concentration (MCHC), mean corpuscular volume (MCV) as well as
total (TLC) and differential leukocyte count (DLC).

Ultrasonography:
Ultrasonography was performed after 24 hours fasting. The
examined cats were positioned in
dorsal recumbency. Cranial ventral
ab domen were clipp ed and
sheaved then covered with coupling gel. Transverse and longitudinal scans were taken using PieMedical Scanner (Maastricht,
Netherlands) and sector transducer
with alternating frequency of 5.07.5 MHz according to the method
described by Nyland et al., (1989).

Serum liver function tests

were estimated using the commercial diagnostic kits supplied by
Sentinel (Milan, Italy). The aspartate aminotransferase (AST) and
alanine aminotransferase (ALT)
were estimated according to the
method described by Reitman and
Frankel (1957), -glutamyltransferase (GGT) as described by Szasz
(1976), alkaline phosphatase
(ALP) as described by Roy (1970),
total and direct bilirubin as described by Doumas et al., (1973),
glucose as described by Trinder
(1959), blood urea nitrogen (BUN)
as described by Tabacco et al.,
(1979), creatinine as described by
Fabiny and Ertingshausen
(1971), triglycerides as described
by Wahlefeld (1974), total cholesterols as described by Allain et al.,
(1974), high density lipoproteins
(HDL) as described by Warnick et
al., (1983), low density lipoproteins (LDL) and very low density
lipoproteins (VLDL) were calculated according to the equations of
Friedewald et al., (1972), albumin
as described by Doumas et al.,
(1971) and total proteins as described by Gornall et al., (1949)
while serum globulins and A/G ratio were calculated.

Collection of blood samples:

Blood samples were collected
from all animals of both groups
after 12 hours fasting from anterior
median vein. Blood samples were
divided into two portions. A portion was mixed with potassium salt
of EDTA as anticoagulant for hematological tests and the other portion was left to clot in clean and
dry test tube and then centrifuged
at 3000 rpm for 10 minutes. The
clear supernatant serum was then
frozen at -20OC for the biochemical studies.
Clinicopathological studies:
Complete blood count (CBC)
was performed for all blood samples with the standard techniques
described by Feldman et al.,
(2000). The CBC included red
blood cells (RBCs) count, hemoglobin (Hb) concentration, packed
cell volume (PCV), red cells indi79

Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

Although, the clinically diseased cats showed no significant

changes in the parameters of general clinical examinations (table 1)
except icteric color of mucous
membranes, there was a panorama
of clinical signs. The clinical signs
were including anorexia, vomiting,
d i a r r h e a , l e t h a r g y, h e p a t o encephalopathic signs (muscle fasciculation, tremors and convulsions) with hemorrhagic diathesis
and ascites in 2 cats (Photo 1-4).
Palpation revealed enlarged liver
extended beyond the last right rib
while fluid thrill was detected by
the tactile percussion in ascetic
cats. Three cats died and were subjected to histopathological examination (photo 1:5).

Histopathological studies:
Postmortem examination was
performed, on three dead cats from
the clinically diseased group, for
gross and histopathological examination. Samples were collected
from liver of investigated cases
and were fixed in 10% neutral
buffered formalin for preparing
paraffin tissue sections at 4-6
thickness, then stained with Hematoxylin and Eosin according to the
method described by Bancroft
and Stevens (1996). Special stains
as Masson's trichrome and Prussiun blue stains were used according to the methods described by
Masson (1929) and Perls (1867),
respectively.
Statistical analysis:
Analysis of the data was performed by ANOVA (Analysis Of
Variance) test using the computer
software Statistical Package for
Social Sciences (SPSS) for Windows (version 10.0) according to
the method described by Irwan
(1996).
RESULTS
Results of clinical evaluation
The clinically healthy cats
were characterized by absence of
any clinical signs of hepatobiliary
disorders and were taken as a
model of normal ultrasonography
of the liver and as a control negative group for clinicopathological
evaluation.
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Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

Table (1): General clinical examination of clinically healthy and clinically

diseased cats.
Parameters
Respiratory rate
Pulse rate
Rectal temperature (C)
Mucous membranes

Control cats

Diseased cats

27 3.66

32.38 3.22

82.18 3.79

91.38 5.11

38.6 0.30

38.8 0.50

Very faint rosy red

Icteric

Free

Free

Superficial lymph nodes

centration and PCV revealing a

normocytic normochromic anemia
associated with leukocytosis, neutrophilia, lymphopenia, monocytopenia and eosinopenia. Moreover,
the biochemical profiles of these
cats showed significant increases
in hepatic enzymes (AST, ALT,
ALP and GGT), bilirubin, triglycerides, total cholesterol, HDL,
LDL and VLDL in comparison to
control cats. Serum glucose, BUN,
total proteins, albumin and A/G
ratio were significantly decreased.
Serum creatinine and globulins
were not significantly changed.

Ultrasonographic results:
The findings included a diffuse hyperechogenicity of hepatic
parenchyma, decreased visualization of the intrahepatic blood vessels and enlargement of liver. The
liver parenchyma was isoechoic or
hyperechoic, compared with falciform or omental fats. The liver was
also hyperechoic with respect to
the spleen and renal cortices. Also,
there was increased attenuation of
ultrasound waves by liver parenchyma (Scan A:H).
Clinicopathological results:
Clinicopathological results
are illustrated in tables (2-3). The
hematological profile of clinically
diseased cats showed significant
decreases in RBCs count, Hb con81

Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

Table (2): Hematological parameters associated with cat lipidosis (mean values SD)

Parameters

Unit

Control cats

Diseased cats

RBCs count
PCV
Hb concentration
MCV
MCHC
TLC
Neutrophil count
Lymphocyte count
Monocyte count
Eosinophil count

6.34 0.81
40.86 1.64
12.76 1.35
64.02 5.78
31.53 2.48
8.95 0.73
5.53 0.37
2.44 0.17
0.420 0.024
0.527 .031

4.95 0.77*
32.35 1.27*
9.47 0.94*
65.20 6.20
29.87 1.58
10.04 0.85*
7.78 0.26*
1.37 0.11*
0.300 0.018*
0.401 0.029*

10 / L
%
g/dl
Fl
g%
103/L
103/L
103/L
103/L
103/L

Table (3): Biochemical parameters associated with cat lipidosis (mean values SD)

Parameters

Unit

Control cats

Diseased cats

AST

IU/L

63.5 2.1

138 12.3*

ALT

IU/L

62.7 3.4

121.6 7.12*

ALP

IU/L

31.8 0.2

69.2 8.1*

GGT

IU/L

18.1 0.13

38 2.2*

Total bilirubin

mg/dl

0.78 0.11

1.150.12*

Direct bilirubin

mg/dl

0.32 0.13

0.450.09*

Indirect bilirubin

mg/dl

0.46 0.12

0.700.02*

Glucose

mg/dl

89.1 0.9

69.3 1.6*

Total proteins

g/dl

8.18 0.61

7.11 0.2*

Albumin

g/dl

4.15 0.15

3.17 0.81*

Globulins

g/dl

4.03 0.31

3.93 0.28

A/G
BUN

-----

1.01 0.11

0.755 0.12*

mg/dl

22.3 0.22

16.31.7*

Creatinine

mg/dl

0.89

0.74 0.03

Triglycerides

mg/dl

54 3.43

115 10.84*

Total cholesterol

mg/dl

163 9.96

266 13.74*

HDL

mg/dl

66 3.47

78 4.18*

LDL

mg/dl

86.2 5.86

165 8.52*

VLDL

mg/dl

10.8 0.95

23 1.29*

*Significant difference at P value 0.05

82

0.07

Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

Prussiun blue stain, (Photomicrograph, 6). Furthermore, the

perilobular fibrosis infiltrating the
entire of the lobules as intralobular fibrosis, (Photomicrograph, 9
& 11) that appeared greenish in
color with Masson's trichome stain
(Photomicrograph 10). For the portal areas, there were bile duct hyperplasia, congestion and fibrosis
as Sclerosing cholangitis, (Photomicrograph, 12).

Pathological Results:
Gross appearance:
Examined livers showed diffuse icteric surface (Photo 6), distended gall bladder and presence
of echymotic hemorrhages around
the borders (Photo 7).
Microscopical examination:
Microscopic examination of
livers from dead cats which have
hepatic lipidosis as diagnosed
clinically and ultrasonography revealed different degrees of lipidosis as following; it may affect just
one hepatic lobule particularly
around the central vein as monolobular periacinar fatty degeneration. The rest of the hepatic
cells showed different degrees of
degenerative changes (Photomicrograph, 1 & 2).
Hepatic lipidosis may also
progressively extend to invade the
whole hepatic lobule and also infiltrating many other lobules as multilobular hepatic lipidosis, (Photomicrograph, 3 & 4). Moreover,
Fibrosis appeared surrounding the
hepatic lobules as perilobular fibrosis, (Photomicrograph, 5 & 7).
That appeared greenish in color
with Masson's trichome stain
(Photomicrograph, 8). Also, there
was congestion with infiltration of
hemosidren pigment (hemosiderosis) in-between the perilobular
fibrosis. Hemosidren pigments appeared as bluish pigment with
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Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

Photo (1): Egyptian Mau cat showed icteric conjunctival mucous membranes and skin of ears.
Photo (2): Egyptian Mau cat showed icteric gum and skin of ears.
Photo (3): Siamese cat showed marked icterus of the skin of the ventral
abdominal wall and ascites.
Photo (4): Persian cat showed severe ascites.
Photo (5): Egyptian Mau cat showed icteric gum.
Photo (6): Icteric liver with distended gall bladder and presence of
echymotic hemorrhage around the borders.
Photo (7): Liver showing diffuse icteric surface.
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Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

Scan (A): Normal sagittal scan of 1.6 years-old Siamese tom cat displaying echolucent gall bladder, hyperechoic diaphragm and
hepatic parenchyma which appeared moderately hypoechoic
interrupted with echogenic wall of portal veins.
Scan (B): Normal sagittal scan of the liver, spleen and left kidney in 1.6
years-old Persian queen showing the parenchyma of the liver
is little bit more echoic than the cortex of the left kidney and
less echoic than spleen.
Scan (C): Hepatic scan of 2.5 years-old Persian queen displaying
marked increase in echodensity of liver parenchyma (fatty
liver) than right renal cortex (which caudally displaced and
covered by liver due to hepatomegally).
Scan (D): Hepatic scan of 2.5 years-old Persian queen revealing marked
increase in echogenicity with absence of echogenic walls of
portal veins.

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Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

Scan (E): Hepatic scan of 2.5 years-old Persian queen showing drastic
increase in echogenicity with anechoic fluid (gall bladder)
with distant acoustic enhancement.
Scan (F): Hepatic scan of 5 years-old Persian queen displaying diffuse
hepatic hyperechogenicity which interrupted by portal veins
(with less clearance of echogenic walls).
Scan (G): Hepatic scan of 10 years-old castrated Siamese tom cat showing marked increase in echogenicity than spleen.
Scan (H): Hepatic scan of 10 years-old casterated Siamese tom cat revealing marked diffuse increase in echodensity than omental
fat.

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Photomicrograph 1: Liver of cat with lipidosis showing centrolobular fatty

degenerated hepatocytes (arrows) with central hepatic cell necrosis (n),
(H&E100).
Photomicrograph 2: Liver of cat with lipidosis showing periacinar fatty degenerated hepatocytes (arrows), (H&E200).
Photomicrograph 3: Liver of cat with lipidosis showing multilobular progressive diffuse lipid vacuolization (arrows), (H&E100).
Photomicrograph 4: Liver of cat with lipidosis showing multiple intracellular
fat vacuoles (arrows) which may coalesce with each other forming large fat
vacuoles pushing the nucleus to one side in the form of signet ring appearance
(S), (H&E100)
Photomicrograph 5: Liver of cat with lipidosis showing perilobular fibrosis
(arrows) with congestion (C) and hemosiderosis, (H&E100).
Photomicrograph 6: Liver of cat with lipidosis showing bluish hemosidren
pigments (arrows), (Prussiun blue X 400).
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Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

Photomicrograph 7: Liver of cat with lipidosis showing higher magnification of the

perilobular fibrosis (arrows), (H&E200).
Photomicrograph 8: Liver of cat with lipidosis showing greenish perilobular fibrosis
(arrow), (Masson's trichome 200).
Photomicrograph 9: Liver of cat with lipidosis showing perilobular and intralobular
fibrosis (arrows), (H&E100).
Photomicrograph 10: Liver of cat with lipidosis showing greenish perilobular (P)
and intralobular (arrows) fibrosis. (Masson's trichome 100).
Photomicrograph 11: Liver of cat with lipidosis showing intralobular fibrosis
(arrow), (H&E200).
Photomicrograph 12: Liver of cat with lipidosis showing portal fibrosis (F), congestion (C) and bile duct hyperplasia (H), (H&E100).
88

Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

clinical examination (hepatomegally on palpation and fluid thrill

with tactile percussion in ascetic
cats).

DISCUSSION

n the basis of our investigations; no predisposition of

age, gender and breed of cats were
found in feline hepatic lipidosis as
other hepatobiliary disorders.
These findings agreed with the results reported by Bennette et al.,
(2007) and Posner et al. (2008).

The hematological profile of

clinically diseased cats showed
significant decreases in RBCs
count, Hb concentration and PCV
revealing a normocytic normochromic anemia which seemed to
be nutritional anemia and could be
attributed to the anorexia which
was a consistent clinical finding in
all examined cases. Moreover,
stress leukogram was obvious and
characterized by leukocytosis, neutrophilia, lymphopenia, monocytopenia and eosinopenia (Feldman
et al., 2000).

The most common clinical

symptoms, which may indicate hepatic parenchyma degeneration are
anorexia, apathy, vomiting, diarrhea, polyuria, polydipsia, jaundice, coagulopathy, weight loss,
dehydration, discoloring of feces
and anemia (Blaxter, 1991;
Barsanti et al., 1997 and Weiss et
al., 1997). Clinical diagnosis of
feline hepatic diseases is relatively
difficult, because of the substantial
functional reserve of the liver.
Often pathological signs appear
when the function of 70 80% of
hepatic parenchyma is compromised. Rothuizen and Meyer (2000)
ascertain that the above mentioned
clinical signs, appear in multiple
diseases of different pathogenesis
and thus additional diagnostic
methods are essential to confirm
primary hepatic dysfunction. Basic
diagnostic methods (hematology,
biochemical blood parameters and
ultrasonography) used in the
identification of hepatic and bile
tract diseases are auxiliary in
nature and should be interpreted in
connection with anamnesis and

The significant increases in

AST, ALT, bilirubin, triglycerides,
total cholesterol, HDL, LDL and
VLDL with the significant decrease of BUN, total proteins, albumin and A/G indicate hepatocellular damage while the significant
increases of ALP and GGT indicate billary obstruction (Blanchard et al., 2002 and Blanchard et
al., 2004).
Both types of liver damage
were indicative of severe intrahepatic cholestasis. So in the present study, serum hepatic chemistry panel detected the alterations in
hepatic functions but failed to define the nature of hepatobiliary dis89

Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

we studied were based on these 2

properties and they were similar to
the criteria used to accurately detect fatty infiltration in human liver
(Gosink et al., 1979; Scatarige et
al., 1984 and Brown et al., 2000).

order.
The findings of ultrasonography included a diffuse hyperechogenicity of hepatic parenchyma,
decreased visualization of the portal blood vessels and enlargement
of liver which was observed by
caudal displacement of right kidney. The liver parenchyma was
isoechoic or hyperechoic, compared with falciform or omental
fats (normally, the liver is less
echoic than falciform or omental
fats). The liver was also hyperechoic with respect to the spleen
and renal cortices (normally, the
liver is less echoic than spleen and
more echoic than renal cortices).
Also, there was increased attenuation of ultrasound waves by liver
parenchyma. Ultrasonography is
useful in evaluating liver parenchymal structure as increased liver
echogenicity and attenuation of
sound are associated primarily
with cirrhosis and fatty infiltration
(Gosink et al., 1979; Joseph et
al., 1979; Foster et al., 1980 and
Nakamura et al., 2005). The excellent ability of ultrasonography
to identify severe hepatic lipidosis
in cats correctly was expected because fatty tissues, in general, are
hyperechoic and attenuate sound
more rapidly than other soft tissues
(Freese and Lyons, 1977; Behan
and Kazam, 1978; Willard et al.,
1999 and Nakamura et al., 2005).
The ultrasonographic criteria that

Ultrasonography which is a
quick, non-invasive method of imaging the abdominal viscera was
an accurate method of diagnosing
severe hepatic lipidosis in the
group of cats studied. In clinical
practice, ultrasonographic examination of the liver, prior to/or in
the absence of liver biopsy, should
be a useful, reliable diagnostic test
for detection of severe hepatic lipidosis in cat with hepatobiliary disease and these results confirmed
with those of histopathology which
revealed different degrees of lipidosis starting with monolobular
periacinar fatty degenerations, then
multilobular hepatic lipidosis.
These results come in accordance
with those of Jones (1989). Moreover, perilobular and intralobular
fibrosis together with congestion
and hemosiderosis were formed
and confirmed with Masson's
trichome stain and Prussiun blue
stain, (Hitt, 1989).
Our histopathological results
of portal tract changes agreed with
those reported by Thornburg et
al., (1982) and Edwards et al.,
(1983) and revealed Sclerosing
cholangitis.
90

Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

Barsanti, J.A.; Jones, B.D. and

Spano, J.S. (1997): Prolonged anorexia associated
with hepatic lipidosis in three
cats." Feline Pract.; 7: 52- 57.

CONCLUSION

rom the research, it was concluded that ultrasonogaphy

and serum chemistry panel were
complementary to each other. It
can also be confirmed by autopsy
and histopathology of dead cats.
The serum chemistry panel could
detect the hepatic dysfunction
while ultrasonography defined the
nature of lesions. Further diagnostic evaluation is recommended
which includes guided needle biopsy and computed tomography to
determine whether the liver is culprit and rule out diseases of other
organ system as well as to extend
the diagnostic value of ultrasonography.

Behan, M. and Kazam, E.

(1978): "The echogenic characteristics of fatty tissues and
tumors." Radiol.; 129: 143151.
Bennette, S.L.; Milne, M., Slocombe, R.F. and Landon,
B.P. (2007): "Gall-bladder
mucocele and concurrent hepatic lipidosis in a cat." Aust.
Vet. J.; 85(10): 397-400.
Blanchard, G.; Paragon, B.M.;
Milliat, F. and Lutton, C.
(2002): "Dietary L-carnitine
supplementation in obese cats
alters carnitine metabolism
and decreases ketosis during
fasting and induced hepatic
lipidosis." J. Nutr.; 132(2):
204- 210.

REFERENCES
Allain, C.C., Poon, L.S., Chan,
C.S., Richmond, W. and Fu,
P.C. (1974): "Enzymatic determination of total serum
cholesterol." Clin. Chem., 20:
470-475.

Blanchard, G.; Paragon, B.M.;

Serougne, C.; Ferezou, J.;
Milliat, F. and Lutton, C.
(2004): "Plasma lipids, lipoprotein composition and profile during induction and
treatment of hepatic lipidosis
in cats and the metabolic effect of one of daily meal in
healthy cats." J. Anim.
Physiol. Anim. Nutr.; 88(3-4):
73-87.

Alpers, D.H. and Sabesin, S.M.

(1987): "Fatty liver : Biochemical and clinical aspects." In: Schiff L, Schiff
ER, Disease of the liver,
6thed. Philadelphia: Lippincott
Co.; 949-978.
Bancroft, J.D. and Stevens, A.
(1996): Theory and practice
of histological technique. 4th
ed., Churchill, Livingston,
New York.

Blaxter, A. (1991): "Diagnosis

91

Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

and Mangement of Hepatic

Disorders." Feline Practice.
London , 17-138.

984-993.
Doumas, B.T., Watson W.A. and
Biggs H.G. (1971): "Albumin
standards and the measurement of serum albumin with
bromcresol green." Clin.
Chim. Acta; 31:87-96.

Brown, B.; Mauldin, G.E.; Armstrong, J.; Moroff, S.D. and

Mauldin, G. N. (2000):
"Metabolic and hormonal alterations in cats with hepatic
lipidosis." J. Vet. Intern.
Med.; 14 (1): 20-26.

Edwards, D.F., McCracken,

M.D. and Richardson, D.C.
(1983): "Sclerosing cholangitis in a cat." J. Am. Vet. Med.
Assoc.; 182:710.

Burrows, C.F.; Chiapella, A.M.

a n d J e z y k, P . (1981):
"Idiopathic feline hepatic lipidosis:The syndrome and
speculation on its pathogenesis." Florida Vet. J.Winter;1820.

Fabiny, D.L. and Ertingshausen,

G. (1971): "Automated Reaction-Rate Method for Determination of Serum Creatinine
with the Centrifi." Chem.
Clin. Chem., 17: 696-700.

Center, S.A. (1986): "Hepatic

lipidosis in the cat." In the
Proceedings of the 4th American College of Veterinary Internal Medicine Forum; 13:
71-79.

Feldman, B.F., Zinkl, J.G. and

Jain, N.C. (2000): "Schalms
Veterinary Hematology." 5th
(ed.), Lippincott Williams &
Wilkins, Philadelphia, USA.

De-Maria, R.; Divari, S.; Bo, S.;

Sonnio, S.; Lotti, D.; Capucchio, M.T. and Castagnaro,
M. (1998): "Beta-galactosidase deficiency in a Korat
cat: a new form of feline
GM1-gangliosidosis." Acta
Neuropathol.; 96(3): 307-314.

Foster, K.J.; Dewbury, K.C. and

Griffith, A.H. (1980): "The
accuracy of ultrasound in the
detection of fatty infiltration
of the liver." Br. J. Radiol.;
53: 440-442.
Freese, M. and Lyons, E.A.
(1977): "Ultrasonic back scatter from liver tissue: its dependence on frequency and
protein/lipid composition." J.
Clin. Ultrasound; 5: 307-312.

Doumas, B.T., Perry, B.W.,

Sasse, E.A. and Straumfjord, J.V. (1973): "Standardization in bilirubin assays:
Evaluation of selected methods and stability of bilirubin
solutions." Clin. Chem., 19:

Friedewald, W.T., Levy, R.I. and

Fredrickson, D.S. (1972):
"Estimation of the concentra92

Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

tion of LDL cholesterol in

plasma, without use of the
preparative ultracentrifuge."
Clin. Chem., 18: 499-504.

Kelly, W.R. (1984): "Examination

of abdomen in small animals."
Textbook of Veterinary Clinical Diagnosis, 3rd (ed.); 26-46.

Gornall, A.G.; Bardwill, C.J.

and David, M.M. (1949):
"Determination of serum proteins by means of the Biuret
reaction." J. Biol. Chem.; 177:
75.

Masson, P. (1929): "Trichrome

stainings and their preliminary technique." J. Techn.
Meth.; 12, 75-90.
Nakamura, M.; Chen, H.M.;
Momoi, Y. and Iwasaki, T.
(2005): "Clinical application
of computed tomography for
the diagnosis of feline hepatic
lipidosis." J. Vet. Med. Sci.;
67(11): 1163- 1165.

Gosink, B.B.; Lemon, S.K. and

Scheible, W. (1979): "Accuracy of ultrasonography in diagnosis of hepatocellular disease." A.J.R.; 133: 19-23
Hitt, M.E. (1989): "Feline hepatic
lipidosis." In the proceedings
of 56th Annual AAHA Meeting, St Louis, Mo; April; 714; 374-377.

Nyland, T.G.; Hager, D.A. and

Herring, D.S. (1989):
"Sonography of the liver, gall
bladder and spleen." Seminars
in Veterinary Medicine and
Surgery (Small Animal); 4:
13 31.

Irwan, T.M. (1996): In "Applied

Linear Statistical models",
Neter, Kutner, Neachtsheim
Wasserman. 4th (ed.).

Perls, N. (1867): Virchows Arch.

Path. Anat., 39: 42.

Jacobs, G.; Cornelius, L. and Allen, S. (1989): "Treatment of

idiopathic hepatic lipidosis in
cats." J. Am. Vet. Med.
Assoc.; 195: 635-638.

Posner, L.P.; Asakawa, M. and

Erb, H.N. (2008): "Use of
propofol for anesthesia in cats
with primary hepatic lipidosis." J. Am. Vet. Med. Assoc.;
232(12): 1841-1843.

Jones, B.R. (1989): "Feline liver

disease." Aust. Vet. Pract.;
19:28.

Reitman, S. and Frankel, S.

(1957): "Colorimeteric method for aspartate and alanine
aminotransferases." Am. J.
Clin. Path.; 28: 56.

Joseph, A.E.A.; Dewbury, K.C.

and McGuire, P.G. (1979):
"Ultrasound in the detection
of chronic liver disease (the
bright liver)." Br. J. Radiol.;
52: 184-188.

Rogers, Q.R. (1994): "Experimental induction of hepatic lipidosis in cats." Am. J. Vet.
93

Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

of Enzymatic Analysis", Vol.

5, Bergmeyer, H.U., Academic Press, New York, pp.
1831-1835.

Res.; 55 (9): 1291- 1302.

Rothuizen, J. and Meyer, H.P
(2000): "History, physical examination and signs of liver
disease. Textbook of Veterinary Internal Medicine." W.B.
Saunders comp., Philadelphia.

Warnick, G.R., Benderson, V.

and Albers, N. (1983): "Selected methods." Clin. Chem.,
10: 91-99.

Roy, A.V. (1970): "Rapid method

for determining alkaline phosphatase activity in serum with
thymolphthalein monophosphate." Clin. Chem., 16: 431.

Weiss, D.j., Armstrong, P.J. and

Gagne, J. (1997): "Inflammatory liver disease." Am
Small Anim., 12: 22-27.
Willard, M.D.; Weeks, B.R. and
Johnson, M. (1999): "Fineneedle aspirate cytology suggesting hepatic lipidosis in
four cats with infiltrative hepatic disease." J. Feline Med.
Surg.; 1 (4): 215-220.

Scatarige, J.C.; Scott, W.W. and

Donovan, P.H. (1984): "Fatty
infiltration of the liver: ultrasonographic and computed
tomographic correlation." J.
Ultrasound Med.; 3(1): 9-14.
Szasz, G. (1976): "Determination
of serum GGT." Clin. Chem.;
22: 2051.

Yeager, A.E. and Mohammed,

H. (1992): "Accuracy of ultrasonography in the detection
of severe hepatic lipidosis in
cats", Am. J. Vet. Res.; 53
(4): 597-599.

Tabacco, A., Meiattini, F., Moda,

E. and Tarli, E. (1979):
"Simplified enzymic/colorimetric serum urea nitrogen
determination". Clin. Chem.,
25: 336-337.
Thornburg, L.P.; Simpson, S.
and Digilio, K. (1982): "Fatty
liver syndrome in cats." J.
Am. Anim. Hosp. Assoc.; 18:
397-400.
Trinder, P. (1959): "Determination of blood glucose using
4-Amino-phenazone". J. Clin.
Pathol., 22: 246.
Wahlefeld (1974): In: "Methods
94

Egypt. J. Comp. Path. & Clinic. Path. Vol. 22 No. 3 (July) 2009; 77 - 95

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