Full text of DOI:10.1111/j.1751-0813.2001.tb10671.x

Clinical
Successful treatment of hypereosinophilic syndrome
in a dog
MC PERKINS and ADJ WATSON
Faculty of Veterinary Science, The University of Sydney, New South Wales 2006
vomiting, diarrhoea and coughing extending over 2 years. The
An 11-year-old crossbred dog was presented with a history of
cough had been diagnosed without investigation as allergic
episodic vomiting, diarrhoea, abdominal discomfort and
bronchitis and was partially controlled with a preparation
coughing. These signs had been present for several years.
containing prednisolone and chlorpheniramine. Diarrhoea had
Marked peripheral eosinophilia (10.3 x 109/L) was found. No
underlying cause of reactive eosinophilia was apparent. Bone
been attributed to pancreatic maldigestion based on low serum
concentration of trypsin-like immunoreactivity; it was partially
controlled by dietary manipulation and pancreatic enzyme
supplementation, though diarrhoea and vomiting recurred on
occasions. Hypothyroidism had been diagnosed as well, based
on low basal plasma thyroxine concentration without thyroid
stimulation testing.
Medications being given at the time of referral were
chlorpheniramine-prednisolone, thyroxine, pancreatic enzymes,
and stilboestrol (for urinary incontinence).
marrow aspiration biopsy showed hyperplasia of the
eosinophilic cell line, with some increase in immaturity,
although all cells were morphologically normal. There were
numerous eosinophils in bronchial wash fluid and eosinophilic
infiltrates were evident in biopsies of pancreas, liver, small
intestine and colon but not stomach. Hypereosinophilic
syndrome was diagnosed. The dog responded well to twice
daily treatment with hydroxyurea and prednisolone. Clinical
signs are well-controlled 16 months later.
Aust Vet J 2001;79:686-689
On physical examination the dog was mildly pyrexic
(39.70C) and had slight abdominal discomfort on palpation.
The liver and spleen were not palpably enlarged. There were
several subcutaneous well-circumscribed masses on the ventral
abdomen and neck which had not been previously investigated.
Otherwise the skin appeared normal and superficial lymph
nodes were not enlarged.
Abdominal ultrasonographic examination revealed an
irregularly thickened pancreas with loss of detail around the
right craniodorsal quadrant, suggesting chronic pancreatitis
with localised peritonitis. There was questionable thickening of
part of the stomach wall, indicating possible gastropathy, but
visibility was poor due to regional gas. All other structures
appeared normal.
Routine blood biochemical tests (including amylase and
lipase) were performed. The only abnormality was low plasma
urea concentration (0.93 mmol/L, reference range 3.0 to 10.0);
this might be attributable to the low protein diet prescribed
previously for gastrointestinal disease, as no other biochemical
changes indicated liver dysfunction. Haematological
examination revealed moderate mature neutrophilia (20.9 x
109/L, reference range 4.1 to 9.4) and marked mature
eosinophilia (10.3 x 109/L, reference 0.14 to 1.2). Numbers of
erythrocytes, lymphocytes, monocytes and platelets were within
reference ranges.
Key words: dog, hypereosinophilic syndrome, hydroxyurea, prednisolone.
ES was first described in humans in 1968.1
Subsequently, similar syndromes have been reported
H
occasionally in cats2-7 and rarely in dogs.8-10 HES is
characterised by persistent and marked peripheral eosinophilia
of unknown aetiology, bone marrow hyperplasia of eosinophilic
precursors, and multiple organ infiltration by mature
eosinophils.6,11 The diagnosis of HES is reached by excluding
the many known causes of eosinophilia. There is much
discussion as to whether EL is distinct from HES or whether
HES is a pre-malignant form of EL.2,6,12 Some human cases of
HES have shown transformation to acute EL,12 but HES can be
initially distinguished from EL by the maturity of the
eosinophils in peripheral blood and bone marrow.6,12,13
Virtually any organ can be infiltrated by eosinophils in HES,
but those most often affected in cats and dogs are the
gastrointestinal tract, bone marrow, spleen, lymph nodes, lung
and liver.6-8,10 In humans the heart, skin, and central nervous
system are also commonly affected.4,13,14
This article describes a dog with HES that had a protracted
illness. Unlike many human and feline HES patients, the dog
responded well to treatment, in this case with a combination of
prednisolone and hydroxyurea.
Additional testing was undertaken to identify potential causes
of eosinophilia. A heartworm antigen test was negative. Faecal
flotation and faecal sedimentation tests for endoparasites were
negative. Cytological evaluation of fine needle aspirates of the
subcutaneous masses indicated they were lipomas. As signs of
illness had abated, the dog was sent home on enrofloxacin and
amoxycillin-clavulanate for suspected localised peritonitis. The
chlorpheniramine-prednisolone combination was withdrawn,
because of concern that prednisolone might exacerbate
pancreatitis, and dexchlorpheniramine was substituted.
Stilboestrol and thyroxine were also withdrawn, in case the
eosinophilia was induced by a drug reaction.
Case report
An 11-year-old desexed female crossbred dog weighing 21 kg
was referred with a 2-week history of recurrent vomiting,
diarrhoea, abdominal discomfort and mild persistent cough.
The owner reported previous episodes of intermittent, recurrent
CGL
EG
EL
HES
IL-2
IL-5
IFN-α
Chronic granulocytic leukaemia
Eosinophilic gastroenteritis
Eosinophilic leukaemia
Hypereosinophilic syndrome
Interleukin-2
Interleukin-5
Interferon-α
The dog had no clinical signs for 1 week but returned 10 days
after discharge with recurrence of vomiting and worsening
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Clinical
cough. Eosinophilia was increased (25.1 x 109/L) and a systolic
heart murmur was audible on the right hemithorax.
Echocardiography revealed mild tricuspid insufficiency and a
mass within the left atrium that was suspected to be a ball
thrombus.
The dog was anaesthetised and a bronchial wash and
exploratory laparotomy were performed. The liver and spleen
appeared smaller than normal while the pancreas appeared
thickened and nodular. There was a fleshy nodular mass in the
body of the pancreas. There was no evidence of peritonitis.
Biopsies were taken from stomach, small intestine, colon,
pancreas and liver. Cytology from the bronchial wash revealed
numerous inflammatory cells with eosinophils predominating
(48% eosinophils, 36% neutrophils, 12% macrophages, 4%
lymphocytes), groups of ciliated columnar epithelial cells and
some mucus strands.
increased and there was resolution with dietary change. On three
occasions the dog vomited once or twice, but eosinophil counts
were unchanged and medication was continued. When
examined after 3 months of treatment, the heart murmur had
resolved and cardiac ultrasound examination showed the
presumed ball thrombus was no longer present. After 4 months a
second low serum trypsin-like immunoreactivity concentration
confirmed ongoing exocrine pancreatic insufficiency. The
pancreatic enzyme supplementation was therefore continued.
Hydroxyurea dosage will be reduced further if possible to reduce
both dog's and owners' exposure to this drug.
Discussion
Eosinophils are tissue-dwelling cells, found in loose
connective tissue of organs that serve as entry points for foreign
substances, such as the skin and respiratory and gastrointestinal
tracts.15 They are secretory cells containing several cytotoxic and
neurotoxic proteins.15 These proteins although important for
defence against parasites can contribute to tissue destruction.15
Eosinophils have the potential to produce cytokines, act as
antigen-presenting cells, and contribute to chronic
inflammation and fibrosis.15 It is these effects which cause
multi-organ damage in HES.
Histologic examination of the pancreatic mass revealed
adipose tissue, scarring and granulation tissue with pockets of
heavy infiltration by neutrophils and small to moderate
numbers of eosinophils. In the right limb of the pancreas,
lobules of pancreatic tissue were separated by a large amount of
fibrous tissue that was heavily infiltrated with an almost pure
collection of eosinophils. There were many dilated ducts
adjacent to the exocrine parenchyma. The parenchyma,
although partially replaced by fibrous tissue, was essentially
normal. No islets were seen in the biopsy specimen examined.
In the liver there was a moderate portal infiltrate composed of
mononuclear cells and moderate numbers of eosinophils. There
were also scattered nodules in the liver parenchyma composed
mostly of mononuclear cells and occasional eosinophils. A
heavy infiltrate of eosinophils (many of which appeared to have
degranulated) was seen in deeper lamina propria of small
intestine and colon. No histologic changes were found in the
stomach. Chronic eosinophilic pancreatitis, eosinophilic
enteritis and mild to moderate portal hepatitis were diagnosed.
A bone marrow aspirate revealed hypercellularity of the
neutrophilic and eosinophilic lines. The eosinophilic line
showed a shift toward immature forms, but development
appeared orderly and no abnormal forms were seen. Other bone
marrow constituents appeared normal.
Based on these findings, HES was diagnosed. Due to poor
success reported with glucocorticoid therapy alone in feline and
human HES patients, treatment was begun with a combination
of hydroxyurea (25 mg/kg) and prednisolone (1.5 mg/kg),
given twice daily. Omeprazole 20 mg was given once daily as
prophylaxis against corticosteroid-induced gastrointestinal
ulceration. Pancreatic enzyme supplementation was continued.
The dog responded well to treatment and clinical signs ceased
almost immediately. After 7 days the peripheral eosinophil
count was zero. Prednisolone and hydroxurea doses were slowly
tapered over a 4-month period. Clinical signs and eosinophil
count were stabilised at final doses of hydroxyurea 15 mg/kg
and prednisolone 0.8 mg/kg, given on alternate days.
Omeprazole was given only while the dog was receiving high
prednisolone doses. Onychomadesis (sloughing of nails), a
known side-effect of hydroxyurea, occurred on two occasions
soon after treatment began. Mild anaemia developed and
persisted while hydoxyurea dosages were high, but resolved as it
was reduced.
A diagnosis of HES is made by excluding all known causes of
eosinophilia. The most common cause of eosinophilia in the
dog is parasitism. This may occur with both endoparasites and
ectoparasites, although the response is greater with
endoparasites because of the prolonged host-tissue contact.16
Sensitised T-lymphocytes initiate and maintain eosinophilia by
production of IL-5.16
Inflammation or local hypersensitivity reactions in mast cell
rich sites, such as skin and alimentary, respiratory and
genitourinary systems, also cause eosinophilia.16 The stimulus
for eosinophil accumulation at sites of inflammation may be
mediated by products of mast cell or basophil degranulation,
deposition of immune complexes within tissues, cytokines and
vasoactive amines, or complement-derived chemotactic
factors.16 Neoplastic conditions of various kinds have resulted
in eosinophilia;11,16,17 disseminated mast cell neoplasia is the
most common, but a number of other neoplasms have been
implicated. Although the mechanism of this paraneoplastic
eosinophilia is unknown, it is thought to involve T-lymphocyte-
derived cytokine mediators such as IL-5 and IL-2.16
Eosinophilia has occasionally been seen in association with drug
administration and various other disease processes, although the
reason for eosinophilia in many of these is unclear.16 Conditions
reportedly associated with eosinophilia in dogs are listed in
Table 1.
Some human references state that eosinophilia must be
evident for >6 months for the syndrome to be defined as
HES.13 This can create diagnostic difficulties as endogenous
cortisol release and glucocorticoid therapy, often begun early
in the illness, can reduce eosinophil counts.16,17 As the
intravascular half-life of eosinophils is <1 hour in dogs,15,17 the
number of eosinophils in tissues and bone marrow may not
necessarily be reflected by the circulating eosinophil count. This
discrepancy has been noticed also in human medicine.19
There is uncertainty as to whether HES is a distinct entity or
a premalignant form of EL.6,12,13 Some human HES cases have
transformed to acute leukaemia over a period as long as 24
years.12 Although transformations are probably rare, regular
follow-up is advisable.
There have been only mild clinical signs during an 8-month
follow-up period. On two occasions there was some
semi-formed faeces but blood eosinophil numbers were not
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Clinical
Table 1. Conditions reportedly associated with eosinophilia in dogs.6, 7, 9, 13, 16-18
Parasites
Nematode
Arthropod
Hypersensitivity
Neoplasia
Miscellaneous
Atopy/ flea allergy
Disseminated mastocytosis
Hypoadrenocorticism
Oral granuloma
Fibrosarcoma
Breed predisposition in Rottweiler
Snake bite
Ulcerative/eosinophilic enteritis
Gastrointestinal eosinophilic granuloma
Mammary carcinoma
Lymphosarcoma
Liver disease
Trematode
Protozoa
Pyometra
Myositis
Mast cell tumour
CGL
Chronic renal failure
Juvenile nephropathy
Panosteitis (enostosis)
Rectal polyp
Thymoma
EL
Urinary tract disease
Mastitis
Pulmonary infiltrates with eosinophilia
Canine eosinophilic granuloma
Sterile eosinophilic pustulosis
Hypocalcaemia
Arthrosis
Fungi/yeastlike fungal infection
Drug administration (eg tetracycline,
recombinant IL-2)
Immune-mediated diseases
HES
predominantly male.3,11
There is general agreement that HES can be distinguished
from EL by the maturity of eosinophils in peripheral blood,
bone marrow and tissues.6,13 There may be immature
eosinophils in the blood, bone marrow, and tissues in HES but
these are fewer than in EL.6 In true EL there is usually more
than 10% blasts in the bone marrow, and anaemia and
thrombocytopaenia are often present, as with other acute
leukaemias.13
Clinical signs of canine HES can vary depending on organ
involvement. Gastrointestinal signs (weight loss, vomiting,
diarrhoea, anorexia) seem to predominate although coughing
and dyspnoea are also reported.8-10 One dog with suspected EL
showed similar signs but more aggressive organ infiltration and
fatal outcome.18 Additional findings reported in feline HES are
fever, pruritis, congestive heart failure, seizures and weakness.5
In human HES, skin involvement is common,19 and
neurological dysfunction (encephalopathy, peripheral
neuropathy, thromboembolic cerebral infarctions) can
occur.13,19 Thromboembolic events are common in human
HES.13,19 Eosinophilic cardiomyopathy is the major cause of
morbidity and death in affected people;13 eosinophilic
infiltration leads to myocardial necrosis, mural thrombus
formation and eventually subendocardial and endocardial
fibrosis, terminating in congestive heart failure caused by
restrictive-type cardiomyopathy.6 Clinical features in the case
reported here comprised typical gastrointestinal signs and
coughing. There was also some tricuspid valve insufficiency and
a mass in the left atrium thought to be a thrombus.
The hypercoaguable state associated with high numbers of
eosinophils is thought to be multifactorial. Major basic protein
(an eosinophil product) causes endothelial damage resulting in
platelet aggregation and activation, while eosinophilic cationic
protein is thought to activate coagulation factor XII (Hageman
factor).4 Decreased fibrinolytic activity and increased levels of
monocyte-derived procoagulants may render HES patients
hypercoagulable.4 In one report, a cat with HES had a large
thrombus containing numerous eosinophils attached to the left
atrial wall.4 In the present case, ultrasonography suggested
presence of a similar mass that resolved with treatment.
Human EL is regarded as a variant of CGL.13 The
Philadelphia chromosome (a specific chromosomal
abnormality) is associated with CGL in people, but has not
been identified in domestic species.20 Determination of
leukocyte alkaline phosphatase activity has been used to identify
CGL in humans,18,20 but its value for differentiating CGL, EL
and HES in the dog is unknown.20,21 Measurement of
immunoglobulin-E has been used to predict response to
treatment in human HES.20 Such procedures would need to be
evaluated in dogs to see whether they can aid diagnosis and
predict treatment response.
Just as EL and HES can be difficult to diagnose and
distinguish from one another, so too can EG. EG is a rare
disease of unknown aetiology characterised by eosinophilic
infiltration of gastrointestinal tract and bone marrow.22 The
clinical, biological and evolutive findings suggest that EG may
evolve into idiopathic HES with involvement of other organs in
addition to the gastrointestinal tract.22
Eosinophilia without proliferation of other cell lines is usually
accompanied by an overproduction of IL-5.11,15 Up to one
quarter of human HES patients may have proliferation of a
clone of abnormal IL-5-secreting T-cells.12 Flow cytometry can
aid identification of these aberrant T-lymphocytes in HES
patients.12 Although patients with aberrant T-cell populations
may respond similarly to corticosteroids and other proposed
treatments for HES, therapy directed more specifically toward
T-cells is more appropriate in such cases.
Too few dogs have been diagnosed with HES to identify
common features. In cats, middle-aged individuals are more
commonly affected, although the age range is 8 months to 12
years.6,7 About 75% of affected cats are female.7 There are no
reports of purebred cats affected with HES.7 Humans diagnosed
with HES average 35 years of age (range 5 to 66) but are
Dogs with HES have shown involvement of bone marrow,
lymph nodes, gastrointestinal tract, spleen, lungs, skin, kidneys
and peritracheal tissue.8-10 In the present case there was
involvement of lungs, liver, pancreas, large and small intestine,
bone marrow and possibly the heart, but lesions may also have
existed in unexamined tissues. As with HES, EL can affect any
organ. One canine EL report described a dog with eosinophilic
infiltrates throughout the liver, lungs, kidney, lymph nodes and
bone marrow.18 The eosinophilic infiltrates were of varying
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Clinical
4. Saxon B, Hendrick M, Waddle JR. Restrictive cardiomyopathy in a cat with
hypereosinophilic syndrome. Can Vet J 1991;32:367-369.
5. Plotnick A. Hypereosinophilic syndrome in a cat. Fel Pract 1994;22:28-31.
6. Huibregtse BA, Turner JL. Hypereosinophilic syndrome and eosinophilic
leukaemia: a comparison of 22 hypereosinophilic cats. J Am Anim Hosp Assoc
1994;30:591-599.
7. Wilson SC, Thomson-Kerr K, Houston DM. Hypereosinophilic syndrome in a
cat. Can Vet J 1996;37:679-680.
8. Goto N, Kawamura M, Inoue M, Sato A. Pathology of two cases of canine
disseminated hypereosinophilic disease. Jpn J Vet Sci 1983;45:305-312.
9. Jensen AL, Nielsen OL. Eosinophilic leukaemoid reaction in a dog. J Small
Anim Pract 1992;33:337-340.
maturity and mitotic figures were abundant, making the
diagnosis of EL straightforward.18
Treatment for human HES has predominantly been with
corticosteroids,11,12,19 supplemented with hydroxyurea when
necessary.11-13,19 More recently, IFN-α has been used
successfully in human HES and Churg-Strauss syndrome
patients resistant to other treatments.11,12,23,24 IFN-α has now
been described as a potential first line treatment for human
HES,25 combined with hydroxyurea in cases resistant to other
treatments.24
Other therapies effective in some human HES patients
include cyclophosphamide, vincristine, dapsone, and
cyclosporine.11,24 The nucleotide analogue 2-chlorode-
oxyadenosine suppresses helper T-cells and may have a role in
treating HES but requires further assessment.26 Other potential
strategies involve identification of molecules that regulate
function or production of eosinophils. Antibodies against IL-5
are promising and have been effective in animals with allergic
airway disease.11 Allogenic bone marrow transplantation has
been effective in human drug-resistant HES patients.25
Glucocorticoids have been the mainstay of treatment in feline
HES, but most have responded poorly.3-5,7 A few affected cats
have been treated with prednisolone and hydroxyurea,
although too few to judge efficacy.3,5 Use of IFN-α has not
been reported in canine or feline HES. There are no reports
of use of hydroxyurea in canine HES, although it has been used
in dogs with chronic myelogenous leukaemia.27
10. Ballmer-Rusca E, Hauser B. Case report: persistent eosinophilia in a dog:
hypereosinophilic syndrome. Kleintierpraxis 1993;38:137-138,140.
11. Rothenberg ME. Eosinophilia. N Engl J Med 1998;338:1592-1600.
12. Bain BJ. Eosinophilia-idiopathic or not? N Engl J Med 1999;341:1141-1143.
13. Brigden ML.
1999;105:193-210.
A practical workup for eosinophilia. Postgrad Med
14. Jameson MD, Segraves SD. Idiopathic hypereosinophilic syndrome.
Postgrad Med 1988;84:93-101.
15. Young KM. Eosinophils. In: Feldman BF, Zinkl JG, Jain NC, editors.
Schalm's veterinary hematology. 5th edn. Lippincott Williams and Wilkins,
Philadelphia, 2000:297-307.
16. Schultze AE. Interpretation of canine leukocyte responses. In: Feldman BF,
Zinkl JG, Jain NC, editors. Schalm's veterinary hematology. 5th edn. Lippincott
Williams and Wilkins, Philadelphia, 2000:366-381.
17. Lilliehook I, Gunnarsson L, Zakrisson G, Tvedten H. Diseases associated
with pronounced eosinophilia: a study of 105 dogs in Sweden. J Small Anim
Pract 2000;41:248-253.
18. Ndikuwera J, Smith DA, Obwolo MJ, Masvingwe C. Chronic granulocytic
leukaemia/eosinophilic leukaemia in a dog? J Small Anim Pract 1992;33:553-
557.
19. De Vriese AS, Kips JC, Vogelaers DP et al. Pitfalls in the diagnosis of
hypereosinophilic syndrome: a report of two cases. J Intern Med 1997;241:165-
170.
The prognosis for cats with HES is generally poor although
some have shown short-term improvement: survival times were
1 week to 3.5 years, averaging 7.5 weeks.4-7 People with HES
also have had a poor prognosis, although aggressive
combination therapy has been associated with improved
survival in recent years.13 Too few cases of canine HES have
been reported to comment on overall prognosis.
20. Goldman EE, Graham JC. Clinical diagnosis and management of acute
nonlymphoid leukaemias and chronic myeloproliferative disorders. In: Feldman
BF, Zinkl JG, Jain NC, editors. Schalm's veterinary hematology. 5th edn.
Lippincott Williams and Wilkins, Philadelphia, 2000:706-716.
21. Raskin RE, Valenciano A. Cytochemistry of normal leukocytes. In: Feldman
BF, Zinkl JG, Jain NC, editors. Schalm's veterinary hematology. 5th edn.
Lippincott Williams and Wilkins, Philadelphia, 2000:337-346.
22. Malaguarnera M, Restuccia N, Pistone G et al. Eosinophilic gastroenteritis.
Eur J Gastroenterol Hepatol 1997;9:533-537.
The dog described in this report is now monitored every 2
months to check for leukaemic transformation and drug-
induced bone marrow suppression. Since hydroxyurea is highly
teratogenic,28 the dose will be slowly reduced and potentially
stopped if control is maintained.
It is not clear whether recurrent vomiting, diarrhoea,
coughing and pancreatic destruction earlier in this dog's life
were related to early HES. The prednisolone administered for
the chronic cough may have controlled clinical signs somewhat
and suppressed peripheral eosinophilia. However, it is pleasing
to see that a dog with such a long history of recurrent disease
has responded well to treatment for HES.
23. Tatsis E, Schnabel A, Gross WL. Interferon-alpha treatment of four patients
with the Churg-Strauss syndrome. Ann Intern Med 1998;129:370-374.
24. Malbrain MLNG, Zachee P. Combination of interferon-alpha and
hydroxyurea in the treatment of idiopathic hypereosinophilic syndrome
[correspondence]. Br J Haematol 1997;97:929-930.
25. Butterfield JH. Hypereosinophilic syndromes-established and new treatment
options. Biodrugs 1997;7:341-355.
26. Ueno NT, Zhao S, Robertson LE, Consoli U, Andreeff M. 2-
Chlorodeoxyadenosine therapy for idiopathic hypereosinophilic syndrome.
Leukaemia 1997;11:1386-1390.
27. Vail DM. Hematopoietic tumors. In: Ettinger SJ, Feldman EC, editors.
Textbook of veterinary internal medicine, 5th edn. Saunders, Philadelphia,
2000:507-523.
28. Watson ADJ, Peaston AE, Malik R, Swinney GR. Guidelines for handling
antineoplastic and immunosuppressive drugs. Aust Vet J 1997;75:868-876.
(Accepted for publication 21 May 2001)
Acknowledgments
We thank P Martin, P Canfield, and M France for cytological
and histopathological interpretations, K Hoffman and G Allen
for assistance with imaging, and GB Hunt for surgical support.
Addendum
The dog is currently being maintained on 25 mg/kg
hydroxyurea once weekly and 0.5 mg/kg prednisolone every
other day. Clinical signs are well controlled 16 months later.
Since writing this report a recent article describing idiopathic
HES in three Rottweilers has been published in J Vet Intern Med
2001;15:162-166.
References
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2. Hendrick M. A spectrum of hypereosinophilic syndromes exemplified by six
cats with eosinophilic enteritis. Vet Pathol 1981;18:188-200.
3. Scott DW, Randolph JF, Walsh KM. Hypereosinophilic syndrome in a cat. Fel
Pract 1985;15:22-30.
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