veterinary hematology || case studies

C A S E 1: E S T RO G EN - I N D U C ED A P L A S T I C A N EM I A

Patient: German shepherd dog, spayed female, 10 years of ageHistory: Urinary incontinence began about a month earlier.

The referring veterinarian treated the dog with diethylstil-bestrol (DES), increasing the dosage to 3 mg orally once each day when the incontinence persisted. A single treat-ment of estradiol cypionate (ECP) of unknown dose was also given 2 1

2 weeks before referral. The animal was referred with a primary complaint of blood-stained peri-neal area.

Physical examination: Slightly depressed with normal hydra-tion, mucous membrane color, pulse rate, respiratory rate, and temperature. Moderate dental tartar and gingivitis were present. An open wound was present on the lateral aspect of the left stifle. Isolated ecchymotic hemorrhages were observed on the ventral abdomen.

Notable Laboratory FindingsHematology: Hematocrit (HCT), 23% with normal erythro-

cyte indices; platelet count, 6000/µL; neutrophil count, 500/µL; lymphocyte count, 2000/µL; monocyte count, 100/µL; eosinophil count, 0/µL; erythrocyte morphology, 1+ echinocytosis and moderate rouleaux; lymphocyte mor-phology, frequently reactive

Clinical chemistry: Not doneBone marrow: Aspirate and core biopsies were markedly

hypocellular. The marrow particles present in aspirate smears consisted primarily of reticular cells, macrophages, plasma cells, and mast cells. Low numbers of erythroid precursor cells and even lower numbers of granulocytic precursor cells were present. No megakaryocytes were observed. Large amounts of stainable iron were present.

AssessmentThe anemia in this dog was considered nonregenerative because no polychromasia was seen in the stained blood film. The reactive lymphocytes indicated increased antigenic stimu-lation, probably related to the profound neutropenia and open

wound. The subcutaneous hemorrhages resulted from the thrombocytopenia. Bone marrow evaluation revealed that the pancytopenia present resulted from a lack of bone marrow precursor cells. When erythroid precursors, granulocyte pre-cursors, and megakaryocytes are markedly reduced or absent, the term aplastic anemia is used. The lymphocyte count was normal because most lymphocytes in blood enter from lymph nodes and spleen rather than from the bone marrow. The reticular cells, macrophages, and plasma cells in the bone marrow were considered to be normal residual cells. Mast cells are rare in bone marrow of normal animals but are sometimes seen in aplastic bone marrow, possibly because microenviron-ment changes potentiate their development.

CommentThe dog was given a blood transfusion and antibiotic therapy was begun. Epistaxis began 5 days later. The HCT was 27%. A bone marrow aspirate collected at that time was again aplastic. A second blood transfusion was given. Marked hema-turia occurred 3 days later and the owner decided to have the dog euthanized. The aplastic anemia in this dog resulted from the prior administration of high doses of estrogens. ECP is much more toxic to canine bone marrow than is DES. Experi-mental studies have indicated that aplastic anemia develops about 3 weeks after toxic doses of estrogen are given, in agree-ment with the time course of this case. Only dogs and ferrets have been reported to develop estrogen-induced aplastic anemia. In addition to iatrogenic estrogen toxicity, dogs with endogenous hyperestrogenism (Sertoli cell tumor, interstitial cell tumor, seminoma of the testicle, and granulosa cell tumor of the ovary) can develop aplastic anemia, as can ferrets with protracted estrus.

R EF ER EN C E S

Kociba GJ, Caputo CA. Aplastic anemia associated with estrus in pet ferrets. J Am Vet Med Assoc. 1981;178:1293-1294.

Miura N, Sasaki N, Ogawa H, et al. Bone marrow hypoplasia induced by administration of estradiol benzoate in male beagle dogs. Jpn J Vet Sci. 1985;47:731-739.

Morgan RV. Blood dyscrasias associated with testicular tumors in the dog. J Am Anim Hosp Assoc. 1982;18:970-975.

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344 VETERINARYHEMATOLOGY

AssessmentIn the absence of identifiable peripheral tumors, a presumptive diagnosis of acute lymphoblastic leukemia was made. The severe neutropenia and anemia were explained by the replace-ment of normal marrow precursor cells with neoplastic cells. The normal platelet count was unexplained, as was the long history of intermittent epistaxis. The increased fibrinogen concentration suggested the presence of concomitant inflammation.

CommentThe horse was euthanized. Multiple submucosal hematomas were present in the maxillary sinuses, and mesenteric and sublumbar lymph nodes were enlarged. As in the antemortem biopsy, the bone marrow was diffusely filled with sheets of neoplastic lymphocytes. Lymphoid infiltrates were present in the spleen, liver, kidney, and lymph nodes. Moderate extra-medullary hematopoiesis was present in the spleen; conse-quently some of the blood platelets may have originated in the spleen. It is also possible that some bone marrow sites, not evaluated during the antemortem biopsy or necropsy, con-tained megakaryocytes. The necropsy findings were more supportive of a diagnosis of acute lymphoblastic leukemia than of lymphoma with secondary leukemia.

R EF ER EN C E

Lester GD, Alleman AR, Raskin RE, et al. Pancytopenia secondary to lymphoid leukemia in three horses. J Vet Intern Med. 1993;7:360-363.

C A S E 2: AC U T E LY M P H O B L A S T I C LE U K EM I A

Patient: Quarter horse, gelding, 15 years of ageHistory: Intermittent unilateral epistaxis for 4 months and

weight loss for 2 monthsPhysical examination: Pale mucous membranes, tachy-

cardia, temperature 103.8°F

Notable Laboratory FindingsHematology: HCT, 12% with normal erythrocyte indices;

fibrinogen, 1000 mg/dL; platelets, 142,000/µL; neutrophil count, 400/µL; lymphocyte count, 2200/µL; monocyte count, 100/µL; erythrocyte morphology, 2+ anisocytosis; lymphocyte morphology, 5% of lymphocytes were moder-ately large with fine nuclear chromatin and scant basophilic cytoplasm

Urinalysis: NormalClinical chemistry: UnremarkableCoggins’ test: NegativeCoagulation tests: Prothrombin time (PT) and activated

partial thromboplastin (APTT) normalPlatelet function tests: Normal platelet aggregation and

normal von Willebrand factor concentrationBone marrow biopsy: Replacement of normal marrow cells

with a monotonous population of moderately large lym-phocytes with fine nuclear chromatin and scant basophilic cytoplasm similar to those present in blood. Indistinct nucleoli were visible in some cells. As expected, these neo-plastic cells were peroxidase-negative.

Endoscopy: Normal nasopharynx, guttural pouch, and upper trachea

A p p EN d I x III n CaseStudies 345

massive flea infestation was believed to be the major source of blood loss in this dog. Some blood loss may have also occurred in the feces, but whipworms alone do not cause enough hemorrhage to result in iron-deficiency anemia. The increased RDW indicates that there is increased variation in erythrocyte volumes. In iron-deficiency anemia, this results from a mixture of normocytic erythrocytes and microcytic erythrocytes formed after iron becomes limiting for erythro-cyte development. The absolute reticulocyte count was not appropriately increased, indicating that decreased iron avail-ability is limiting the bone marrow response to the anemia. The normal total plasma and serum protein concentrations in a dehydrated animal suggest that the concentration will be low-normal or decreased after rehydration. Serum proteins are synthesized more rapidly than erythrocytes; consequently the total plasma protein concentration may be normal in animals with chronic blood loss. A majority of dogs with iron defi-ciency anemia have a thrombocytosis, as in this case. The neutrophilia, lymphopenia, monocytosis, and eosinopenia are likely the result of stress (endogenous glucocorticoid release), but the significant left shift and the magnitude of the neutro-philia indicate that a concomitant inflammatory response is also present. The slightly increased urea nitrogen concentra-tion is probably prerenal and secondary to dehydration.

CommentThe dog was given a whole blood transfusion (two units) and treated with intravenous lactated Ringer’s solution to correct the dehydration. The following day the HCT was 34%, total plasma protein was 6.2 g/dL, rectal temperature was 101.5°F, and marked clinical improvement was apparent. The animal was also treated for fleas and given an anthelmintic, and the client was instructed on appropriate flea-control measures for the dog’s environment. Oral iron therapy was not considered essential because of the amount of iron present in the trans-fused blood.

R EF ER EN C E

Harvey JW, French TW, Meyer DJ. Chronic iron deficiency anemia in dogs. J Am Anim Hosp Assoc. 1982;18:946-960.

C A S E 3: I RO N - D EF I C I EN C Y A N EM I A

Patient: Irish setter dog, female, 13 years of ageHistory: Weakness, anorexia, and weight loss for a week;

unable to walk at presentationPhysical examination: The dog was depressed, emaciated,

approximately 8% dehydrated, and nonambulatory because of extreme weakness. Pale mucous membranes, ocular and nasal discharges, excessive dental tartar, otitis externa, and large numbers of fleas were present. The rectal temperature was 99.6°F.

Notable Laboratory FindingsHematology: HCT, 11%; mean cell volume (MCV), 52 fL;

mean cell hemoglobin concentration (MCHC), 30 g/dL; red cell distribution width (RDW), 20%; reticulocyte count, 80,000/µL; total plasma protein, 6.8 g/dL; platelet count, 532,000/µL; band count, 3300/µL; neutrophil count, 24,800/µL; lymphocyte count, 500/µL; monocyte count, 3600/µL; eosinophil count, 0; erythrocyte morphology, 1+ polychromasia, 2+ anisocytosis, 2+ hypochromasia

Clinical chemistry: urea nitrogen, 29 mg/dL; creatinine, 1.0 mg/dL

Serum iron assays: Serum iron, 16 µg/dL (reference interval 84 to 233 µg/dL); total iron-binding capacity (TIBC), 462 µg/dL (reference interval 284-572 µg/dL; and ferri-tin, 140 µg/L (reference interval 80 to 800 µg/L)

Fecal flotation: Trichuris eggs

AssessmentThe presence of a severe microcytic hypochromic anemia indi-cates chronic iron deficiency. The low serum iron, normal serum TIBC, and low-normal serum ferritin concentrations support the diagnosis of iron deficiency. Serum ferritin con-centration generally correlates well with total body iron content, but ferritin is an acute-phase reactant protein that increases during inflammation. Consequently serum ferritin might have been lower in the absence of the inflammation documented in the physical examination. Iron deficiency is almost always the result of blood loss in adult animals. The


the animal’s regenerative bone marrow response. The increased total plasma protein concentration is the result of increased globulin concentrations and could represent an inflammatory reaction to the blood parasite. The slightly increased bilirubin concentration is attributable to the increased erythrocyte destruction accompanying these erythrocyte parasites. The slightly increased ALT may reflect hypoxic injury to the liver.

CommentDoxycycline and glucocorticoid therapy was initiated and the cat was discharged. The client was told that the M. haemofelis infection should respond to therapy but that the cat would probably remain FIV-positive, which would likely result in increased susceptibility to bacterial infections at a later date. Concurrent infections of M. haemofelis and FeLV generally result in more severe clinical signs and more severe anemia than occurs when a cat is infected with either agent alone. In contrast, concurrent infection with M. haemofelis and FIV does not appear to cause more severe anemia than does infec-tion with M. haemofelis alone. Consequently the regenerative anemia in this cat is attributable primarily to the M. haemofelis infection.

R EF ER EN C E

Harvey JW. Hemotrophic mycoplasmosis (hemobartonellosis). In: Greene CE, ed. Infectious Diseases of the Dog and Cat, 3rd ed. Philadelphia: Saunders Elsevier; 2006:252-260.

C A S E 4: M Y C O P L A S M A H A E M O F E L I S I N F E C T I O N

Patient: Domestic shorthaired cat, castrated male, 2 years of ageHistory: Presented for evaluation of deformed carpus, which

was present when the client acquired the cat as a strayPhysical examination: Deformity of carpus secondary to trau-

matic luxation, alopecia over pinna secondary to dermato-mycosis, slightly depressed and afebrile with marked splenomegaly

Notable Laboratory FindingsHematology: HCT, 13%; MCV, 86 fL; MCHC, 33% total

plasma protein, 8.3 g/dL; platelet count, normal; leukocyte counts, normal; nucleated erythrocytes, 1400/µL; erythro-cyte morphology, 1+ anisocytosis, 2+ polychromasia, 4+; Mycoplasma haemofelis organisms

Clinical chemistry: Bilirubin, 0.4 mg/dL; alanine aminotrans-ferase (ALT), 143 units/L; globulin, 5.8 g/dL

Serology: Feline leukemia virus (FeLV), negative; feline immunodeficiency virus (FIV), positive

AssessmentThe anemia was regenerative based on the degree of polychro-masia present. Reticulocyte counts may not be accurate when high numbers of M. haemofelis organisms are present. The macrocytosis and nucleated erythrocytes are consistent with


of endotoxin, which results in increased margination of neu-trophils, may also have contributed to this leukogram. The lymphopenia and eosinopenia probably resulted from the endogenous release of glucocorticoids. The slightly decreased plasma protein concentration probably resulted from the peri-tonitis with protein movement into the abdominal cavity. The increased serum AST activity was attributed to tissue injury.

CommentThe abdomen was lavaged with large volumes of saline solu-tion containing penicillin and streptomycin and the horse was treated with intravenous penicillin and intravenous fluids. Laboratory analyses were done again on day 3.

Notable Laboratory Findings (Day 3)Hematology: HCT, 42%; total plasma protein, 7.1 g/dL;

fibrinogen, 700 mg/dL; platelet count, normal; band count, 200/µL; neutrophil count, 900/µL; lymphocyte count, 300/µL; monocyte count, 200/µL; eosinophil count, 0/µL; neutrophilic morphology, 2+ toxicity.

Clinical chemistry: AST, 795 units/L.Abdominal fluid: HCT, 3%; protein; 2.9 g/dL; nucleated cell

count, 33,800/µL; most nucleated cells present were toxic neutrophils.

AssessmentThe abdominal fluid analysis revealed continued evidence of inflammation. The toxic neutropenia on day 3 resulted from peritonitis with movement of neutrophils into the abdominal cavity. The lymphopenia and eosinopenia resulted from the endogenous release of glucocorticoids. The fibrinogen increased in response to inflammation. The increased serum AST activity was attributed to tissue injury. The horse eventu-ally made a full recovery.

C A S E 5: VAG I N A L T E A R

Patient: Standard-bred horse, female, 10 years of ageHistory: Dystocia resulting in a vaginal tear and displacement

of intestines into the vagina. Attempts to repair the lacera-tion on the farm were initially unsuccessful because of hemorrhage and straining. Xylazine was administered as an analgesic and sedative, the intestines were replaced into the abdomen, and the laceration was sutured.

Physical examination: The horse was uncomfortable, exhibit-ing evidence of pain, but otherwise appeared normal.

Notable Laboratory Findings (Day 1)Hematology: HCT, 38%; total plasma protein, 6.0 g/dL,

fibrinogen, 300 mg/dL; platelet count, normal; metamy-elocyte count, 100/µL; band count, 600/µL; neutrophil count, 2400/µL; lymphocyte count, 600/µL; monocyte count, 200/µL; eosinophil count, 0/µL; neutrophilic mor-phology, 2+ toxicity.

Clinical chemistry: Aspartate aminotransferase (AST), 506 units/L.

Abdominal fluid: HCT, 8%; protein, 4.0 g/dL; nucleated cell count, 13,100/µL; most nucleated cells present were toxic neutrophils.

Microbiology: No bacterial growth was obtained from the abdominal fluid, but antibiotic therapy may have been initiated prior to culture.

AssessmentThe abdominal fluid analysis revealed evidence of hemorrhage and inflammation. The toxic left shift with low-normal neu-trophil numbers in blood resulted from peritonitis with move-ment of neutrophils into the abdominal cavity. The absorption


a diagnosis of hypereosinophilic syndrome was made. The etiology of this syndrome is unknown. Evidence that the overproduction of IL-5 may be involved in producing this disorder has been presented in humans with hypereosinophilic syndrome. A marked left shift in the eosinophilic series is expected in cats with eosinophilic leukemia. Eosinophilic leu-kemia was considered unlikely in this cat because most of the eosinophils in blood and tissues were mature. When present in animals, basophilia generally accompanies eosinophilia, possibly because certain growth factors (most notably IL-5) stimulate the production of both cell types. The slight neutro-philia and monocytosis present may be associated with the inflammation recognized in several tissues. The mild nonre-generative anemia is probably the result of the anemia of inflammatory disease. The increased serum protein concentra-tion was the result of increased globulins, further supporting the likelihood of an inflammatory reaction.

CommentThe cat was placed in an oxygen cage and treated with ami-nophylline (a bronchodilator) and an antibiotic pending the outcome of diagnostic tests. Once a diagnosis of hypereosino-philic syndrome was reached, glucocorticoid therapy was initiated. Clinical signs improved rapidly and the cat was discharged with a plan to taper the glucocorticoid dosage as clinical signs resolved.

R EF ER EN C E S

Huibregise BA, Turner JL. Hypereosinophilic syndrome and eosinophilic leukemia: a com-parison of 22 hypereosinophilic cats. J Am Anim Hosp Assoc. 1994;30:591-599.

Swenson CL, Carothers MA, Wellman ML, et al. Eosinophilic leukemia in a cat with naturally acquired feline leukemia virus infection. J Am Anim Hosp Assoc. 1993;29:467-501.

Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood. 1994;83:2759-2779.

C A S E 6: H Y P ER E O S I N O P H I LI C S Y N D RO M E

Patient: Himalayan cat, castrated male, 5 years of ageHistory: Respiratory distress developed 3 days earlier. The

referring veterinarian began treatment with an antibiotic, but the condition worsened.

Physical examination: The cat presented with abdominal res-piration and tachypnea. Harsh lung sounds were auscul-tated, the cat was underweight and may have been slightly dehydrated. Enlarged prescapular, axillary, and inguinal lymph nodes and splenomegaly were palpated. Papules and scabs on the head and base of the tail were believed to represent a flea-bite allergy. The rectal temperature was 102.6°F.

Notable Laboratory FindingsHematology: HCT, 29% with normal erythrocyte indices;

total plasma protein, 8.6 g/dL; platelet count, normal; neu-trophil count, 15,600/µL; lymphocyte count, 5100/µL; monocyte count, 1200/µL; band eosinophil count, 400/µL; eosinophil count, 22,300/µL; basophil count, 2100/µL; erythrocyte morphology, normal.

Clinical chemistry: Total serum protein, 8.1 g/dL; total glob-ulins, 5.9 g/dL.

Exfoliative cytology: Transthoracic lung aspiration revealed histiocytic eosinophilic inflammation. Increased numbers of eosinophils were also present in splenic and lymph node aspirates that appeared to exceed those present in contami-nating blood.

Histopathology: Chronic ulcerative eosinophilic dermatitis.Parasitology: ELISA heartworm test was negative.Thoracic radiograph: Patchy interstitial infiltrate.Abdominal ultrasound: Splenomegaly and slightly thickened

loops of bowel.

AssessmentBased on the magnitude of the eosinophilia and evidence of eosinophilic infiltration and injury in multiple organs,


C A S E 7: P YO M E T R A

Patient: Rottweiler dog, female, 2 years of ageHistory: Depression, lethargy, fever, and purulent bloody

vaginal discharge for several days; vomited the day of admission

Physical examination: Moderately depressed, panting respira-tion, slightly distended abdomen, dark pink mucous mem-branes, rectal temperature 102°F

Notable Laboratory Findings (Day 1)Hematology: HCT, 48%; total plasma protein, 7.5 g/dL;

fibrinogen, 200 mg/dL; manual platelet count, 180,000/µL; band neutrophil count, 3700/µL; neutrophil count, 57,400/µL; lymphocyte count, 7700/µL; monocyte count, 3700/µL; eosinophil count, 700/µL; basophil count, 0/µL; erythrocyte morphology, 1+ echinocytes; leukocyte mor-phology, 1+ toxicity of neutrophilic cells and occasional reactive lymphocytes

Clinical chemistry: UnremarkableCoagulation tests: PT, 9 seconds (control, 8 seconds); APTT,

20 seconds (control, 10 seconds); activated clotting time (ACT), 105 seconds (reference less than 95 seconds); fibrin degradation products (FDP), positive at 1:20 dilution

Abdominal radiographs: No abnormalities appreciatedAbdominal ultrasound: Large, fluid-filled uterus identified

AssessmentThe marked neutrophilia with toxic left shift and monocytosis indicated a severe inflammatory reaction. The presence of a dilated uterus and purulent vaginal discharge indicated that the dog had pyometra. The lymphocytosis may have reflected antigenic stimulation. The slightly decreased manual platelet count, prolonged APTT, slightly prolonged ACT, and positive FDP test indicated the presence of disseminated intravascular coagulation (DIC). Although the PT was normal, this test appears to be less sensitive than the APTT in the diagnosis of DIC. Fibrinogen is an acute-phase protein that tends to increase during inflammation; consequently, the normal fibrinogen value did not rule out DIC.

CommentAntibiotic and intravenous fluid therapy was begun after the first blood sample was taken. Epistaxis began on the following day and the animal became more depressed.

Notable Laboratory Findings (Day 2)Hematology: HCT, 32% with normal erythrocyte indices;

total plasma protein, 6.4 g/dL; fibrinogen, 400 mg/dL; manual platelet count, 61,000/µL; metamyelocyte count, 800/µL; band neutrophil count, 8400/µL; neutrophil count, 65,900/µL; lymphocyte count, 2100/µL; monocyte count, 7200/µL; eosinophil count, 0/µL; basophil count, 0/µL; erythrocyte morphology, 1+ echinocytes; leukocyte morphology, 1+ toxicity of neutrophilic cells and occasional reactive lymhocytes

Coagulation test: ACT, 150 seconds (reference less than 95 seconds)

AssessmentThe neutrophilia with toxic left shift and monocytosis were more pronounced on the second day. The decrease in lympho-cyte count and eosinopenia that developed suggested that increased endogenous glucocorticold release occurred as the dog’s clinical condition worsened. The decreased HCT on the second day was primarily the result of fluid therapy. The further decrease in the platelet count and the prolonged ACT suggested the continuation of DIC.

CommentOvariohysterectomy was performed after the blood sample was collected on the second day and the dog made an unevent-ful recovery.

R EF ER EN C E

Sevelius E, Tidholm A, Thoren-Tolling K. Pyometra in the dog. J Am Anim Hosp Assoc. 1990;26:33-38.


C A S E 8: S Y S T EM I C LU P U S ERY T H EM AT O S U S

Patient: Cocker spaniel dog, male, 4 years of ageHistory: Rear-leg lameness associated with bilateral hip dys-

plasia was diagnosed 2 years earlier, and erosive nonseptic arthritis involving the carpal and tarsal joints was recogn-lzed 4 months previously. The HCT and platelet counts were normal at that time, but the ANA test was positive at 1 : 100 dilution (reference less than 1 : 20). The dog has been treated with aspirin for the preceding 4 months.

Physical examination: The dog was depressed with pale mucous membranes. A polyarthropathy was present and all joints were painful. There were multiple raised pigmented skin lesions and small petechial hemorrhages on the penis and abdomen. The rectal temperature was normal.

Notable Laboratory FindingsHematology: HCT, 23%; MCV, 74 fL; MCHC, 33 g/dL;

reticulocyte count, 184,000/µL; total plasma protein, 7.9 g/dL; fibrinogen, 400 mg/dL; manual platelet count, 8000/µL; band neutrophil count, 600/µL; neutrophil count, 12,900/µL; lymphocyte count, 700/µL; monocyte count, 200/µL; eosinophil count, 1000/µL; nucleated erythrocyte count, 500/µL; erythrocyte morphology, 3+ anisocytosis, 2+ polychromasia, 3+ spherocytosis, occa-sional Howell-Jolly bodies, and autoagglutination of saline washed erythrocytes.

Clinical chemistry: Total serum protein, 8.2 g/dL; the total globulin, 5.6 g/dL.

Urinalysis: Specific gravity, 1.042; moderate bilirubinuria.Joint fluid: A direct smear from a swollen joint revealed

increased numbers of nondegenerate neutrophils and macrophages.

Antinuclear antibody (ANA) test: Positive at 1 : 320 dilution (reference less than 1 : 20)

Skin biopsy: Histologic lesions were consistent with pemphi-gus foliaceous, an immune-mediated skin disorder, but direct immunofluorescence examination for IgG deposits in skin was negative.

AssessmentThe presence of autoagglutination of saline-washed RBC-erythrocytes and spherocytosis points to an immune-mediated

anemia. The high-normal MCV and low-normal MCHC are consistent with the increased percentage of reticulocytes, and the absolute reticulocytosis indicates an appropriate bone marrow response to the anemia. The low number of nucleated erythrocytes is appropriate for the degree of reticulocytosis. The petechial hemorrhages can be attributed to the severe thrombocytopenia. Based on the presence of an immune-mediated hemolytic anemia and a positive ANA test, the thrombocytopenia was presumed to be immune-mediated. The combined presence of immune-mediated anemia and immune-mediated thrombocytopenia has been termed the Evans syndrome. The presence of high-normal numbers of eosinophils suggests that endogenous glucocorticoid release is not responsible for the neutrophilia, monocytosis, and lym-phopenia. The increased total globulins in serum and high-normal plasma fibrinogen concentration are consistent with inflammation, as is the mild neutrophilia with left shift and monocytosis. Bilirubinuria is common in dogs with hemolytic anemia even when bilirubinemia is not present because of the low renal threshold for bilirubin in dogs. A presumptive diag-nosis of systemic lupus erythematosus (SLE) was made based on the concomitant occurrence of immune-mediated hemo-lytic anemia, thrombocytopenia, nonseptic polyarthritis, and positive ANA test. The skin lesion may also have been a com-ponent of this syndrome, but an immune-mediated etiology could not be confirmed.

CommentTherapy consisted of glucocorticoid steroids and cyclophos-phamide. When examined 1 week later, the animal appeared to be feeling less pain, skin lesions were resolving, the HCT was 27%, MCV was 77 fL, and platelet count was 1.2 ×106/mL. The resolution of the thrombocytopenia following initia-tion of immunosuppressive therapy provides retrospective evidence that the thrombocytopenia was immune-mediated. It is assumed that the animal had high plasma thrombopoietin values when thrombocytopenic and that the subsequent thrombocytosis occurred as a rebound phenomenon when premature platelet destruction was reduced or eliminated by immunosuppressive therapy.

R EF ER EN C E

Grindem CB, Johnson KH. Systemic lupus erythematosus: literature review and report of 42 new canine cases. J Am Anim Hosp Assoc. 1983;19:489-503.

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