Portal Vein Thrombosis in Cats: 6 Cases (2001–2006)

Background: Portal vein thrombosis (PVT) in cats is sparsely reported.
Purpose of Study: To evaluate the clinical signs and diseases associated with PVT in cats.
Animals: 6 client-owned cats.
Methods: Medical records for cats with a portal vein thrombus diagnosed on abdominal ultrasound or at necropsy were reviewed. Signalment, historical data, underlying disorders, clinical findings, clinicopathologic and histopathologic data, diagnostic imaging findings, treatment, and outcome were recorded.
Results: All 6 cats identified with PVT also had hepatic disease. Evidence of a congenital portosystemic shunt was present in 3/6 cats. Two cats had primary or metastatic hepatic neoplasia. One cat had acute cholangitis, acute pancreatitis, and locally extensive acute centrilobular hepatic necrosis. Two cats were suspected to have acute thrombi and 4 cats had chronic thrombi.
Conclusion and Clinical Significance: PVT might be an important concurrent finding in cats with hepatic disease.     

Acute Hepatic Necrosis And Liver Failure Associated With Benzodiazepine Therapy In Six Cats, 1986–1995.

A retrospective analysis was conducted of all feline necropsies performed during a nine year period to identify cases of sever, acute, centrilobular (periacinar), hepatic necrosis (ACHN). After exclusion of cats with anemia, a series of seven cases of ACHN was identified. In addition, two similar cases were identified from tissue submitted for histopathology following, and eight had bile duct hyperplasia. Seven of the nine cats received diazepam prior to dath, and one received zolazepam. Of the seven cats that received diazepam, five were healthy prior to treatment and received oral diazepam for the treatment of inappropriate urination, intercat aggression, or skin disease. Two cats which received diazepam exhibited other clinical signs: one had chronic vomiting, and the other received diazepam after biochemical evidence of hepatocellular necrosis was present. Onset of clinical sings in cats receiving oral diazepam occurred 7–13 days following the initiation of treatment. Clinical signs and clinical biochemical analysis were compatible with severe hepatocellular necrosis and acute liver failure. All cats had lesions in other organs: five had pancreatic disease, five had cardiac disease, and five had renal disease. All cats died, or were euthanized, within 4 dyas of the onset of clinical signs and 2 days after presentation to a veterinarian. Fatal, acute, centrilobular hepatic necrosis appears to be a serious adverse reaction to diazepam therapy in certain cats.     

Clinical features of inflammatory liver disease in cats: 41 cases (1983-1993)

OBJECTIVE: To compare the clinical and clinicopathologic findings in and prognosis for cats with lymphocytic portal hepatitis (LPH) versus cats with acute or chronic cholangiohepatitis (CH). DESIGN: Retrospective study. ANIMALS: 25 cats with LPH; 16 cats with CH (7 acute, 9 chronic). PROCEDURE: Cats with LPH and CH were selected by evaluating records from liver biopsy specimens submitted to the University of Minnesota Veterinary Teaching Hospital during a 10-year period. Clinical and clinicopathologic data were retrieved. RESULTS: Cats with CH had higher segmented and band neutrophil counts, alanine aminotransferase activities, and total bilirubin concentrations than did cats with LPH. Cats with acute CH had higher segmented and band neutrophil counts and lower serum alkaline phosphatase activities and total bilirubin concentrations than did cats with chronic CH. Twelve of 14 cats with LPH or CH had coarse or nodular texture to the liver on ultrasonography, with loss of portal vein wall clarity noticed in 4 of 8 cats with LPH. Sixteen of 23 cats with LPH and 8 of 15 cats with CH survived > 1 year. Of those cats living < 1 year, all cats with LPH and 5 of 7 cats with CH had a serious concurrent illness that may have been responsible for their deaths. CLINICAL IMPLICATIONS: LPH and CH can be detected and tentatively differentiated through evaluation of clinical laboratory test results, but histologic evaluation of liver specimens is necessary for definitive differentiation. Survival time was good regardless of the type of inflammatory liver disease.     

Acute Pancreatitis in Cats With Hepatic Lipidosis

The purpose of this study was to characterize the incidence, clinical features, and prognosis of acute pancreatitis in cats with hepatic lipidosis. Of 13 cats histologically diagnosed with hepatic lipidosis between July 1988, and November 1989,5 (38%) were also histologically diagnosed with acute pancreatitis. In cats with hepatic lipidosis alone, the signalment, history, physical examination, and clinicopatho-logic findings were generally indistinguishable from those of cats with concurrent acute pancreatitis except that cats with acute pancreatitis were more likely to be cachectic and to have coagulation abnormalities. Hepatomegaly was seen on abdominal radiographs in both groups. Of the 5 cats with concurrent acute pancreatitis, abdominal ultrasonography detected 1 cat with a hypoechoic pancreas and 5 with peritoneal effusion; those abnormalities were not seen in cats without concurrent acute pancreatitis. Cats with concurrent acute pancreatitis had only a 20% recovery rate, compared with a 50% recovery rate in cats with hepatic lipidosis alone. We conclude that cats with hepatic lipidosis should be rigorously evaluated for concurrent acute pancreatitis because of 1) the rate of disease coincidence, 2) the inability of signalment, history, physical examination, and clinicopathologic findings to adequately distinguish between hepatic lipidosis and acute pancreatitis, 3) the worse prognosis associated with concurrent acute pancreatitis, and 4) the opposing nutritional strategies for hepatic lipidosis and acute pancreatitis. (Journal of Veterinary Internal Medicine 1993; 7:205–209. Copyright © 1993 by the American College of Veterinary Internal Medicine.)     

Possible Hemolytic Uremic Syndrome in Three Cats After Renal Transplantation and Cyclosporine Therapy

OBJECTIVE: To describe the clinical history of 3 cats with possible hemolytic uremic syndrome (HUS) after renal transplantation. STUDY DESIGN: This case series documents historical findings, physical examination findings, clinical pathologic features, necropsy and histopathologic findings of 3 cats with possible HUS. RESULTS: Two cats had chronic renal failure; 1 cat had acute renal failure secondary to ethylene glycol toxicity. A renal transplant was performed in each of the 3 cats without obvious problems. Complications that would support a diagnosis of HUS, including anemia, thrombocytopenia, and azotemia occurred within 24 hours in 1 cat, within 8 days in a second cat, and 2 months after transplantation in the third cat. In 2 cats, HUS was likely secondary to cyclosporine immunosuppression. In the third cat, HUS may have been secondary to allograft rejection. Renal biopsies from all 3 cats were suggestive of HUS. CONCLUSION AND CLINICAL RELEVANCE: In human beings, HUS in transplant recipients may occur secondary to immunosuppressive drugs, vascular rejection, or recurrence of original disease. Graft loss occurred in all 3 cats in this study and the mortality rate was 100%. Clinicians caring for these patients need to be aware of this disorder because early recognition and treatment is critical in the management of post-transplant HUS.     

Ultrasonographic findings in cats with clinical,gross pathologic,and histologic evidence of acute pancreatic necrosis: 20 cases (1994-2001)

OBJECTIVE: To determine ultrasonographic findings in cats with clinical, gross pathologic, and histologic evidence of acute pancreatic necrosis. DESIGN: Retrospective study. ANIMALS: 20 cats. PROCEDURE: Ultrasound reports and permanent ultrasonographic images were reviewed, and ultrasonographic findings were recorded. Thoracic and abdominal radiographs were also reviewed, when available. Anatomic localization of pancreatic necrosis was determined from the gross pathology report; duration and severity of pancreatic necrosis were determined by reviewing histologic specimens. The presence of concurrent disease was recorded from the final pathology report. RESULTS: The pancreas was considered ultrasonographically normal in 10 cats and was not observed in 3. Ultrasonographic findings were considered compatible with pancreatitis in the remaining 7 cats. Gross pathologic findings indicated that pancreatitis was multifocal in all 7 of these cats; histologically, pancreatitis was acute or subacute in 5 and associated with severe or moderate necrosis in 6. In the remaining 13 cats, gross pathologic findings indicated that pancreatitis was multifocal (n = 8) or focal (2), or gross pathologic findings were normal (3). Histologically, pancreatitis was peracute or acute in 11 of these 13 cats and associated with severe or moderate necrosis in 8. Thoracic and abdominal radiographic findings were nonspecific. CONCLUSIONS AND CLINICAL RELEVANCE: Results of ultrasonography were consistent with a diagnosis of pancreatitis in only 7 of 20 cats with acute pancreatic necrosis in the present study. This suggests that new diagnostic criteria must be established if abdominal ultrasonography is to be an effective tool in the diagnosis of pancreatitis in cats.     

Clinical signs, underlying cause, and outcome in cats with seizures: 17 cases (1997-2002)

OBJECTIVE: To determine clinical signs, results of diagnostic testing, underlying cause, and outcome in cats with seizures. DESIGN: Retrospective study. ANIMALS: 17 cats with seizures. PROCEDURE: Only those cats in which an underlying metabolic abnormality causing the seizures had been identified, diagnostic imaging of the brain and CSF analysis had been done, or a necropsy had been performed were included. Seizures were classified as being a result of metabolic disease, symptomatic epilepsy (ie, epilepsy resulting from a structural lesion of the brain), or probably symptomatic epilepsy (ie, epilepsy without any extracranial or identifiable intracranial disease that is not suspected to be genetic in origin). RESULTS: 3 cats had seizures associated with an underlying metabolic disease (hepatic encephalopathy), 7 had symptomatic epilepsy (3 with neoplasia and 4 with meningoencephalitis), and 7 had probably symptomatic epilepsy. Six of the 7 cats with symptomatic epilepsy died or were euthanatized within 3 months after the diagnosis was made, whereas 6 of the 7 cats with probably symptomatic epilepsy survived for at least 12 months after the diagnosis was made. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that cats with probably symptomatic epilepsy may have a good long-term prognosis.     

Cholecystoenterostomy for treatment of extrahepatic biliary tract obstruction in cats: 22 cases (1994-2003)

OBJECTIVE: To identify factors associated with outcome in cats with extrahepatic biliary tract obstruction (EHBTO) that undergo biliary diversion surgery. DESIGN: Retrospective case series. ANIMALS: 22 cats. PROCEDURES: Medical records of cats with surgically confirmed EHBTO that underwent cholecystoenterostomy were reviewed. RESULTS: Clinical signs and physical examination findings included vomiting, anorexia, icterus, lethargy, weakness, and weight loss. Common clinicopathologic abnormalities included high serum hepatic enzyme activities and serum bilirubin concentration. Abdominal ultrasonography was performed in 21 cats, and all 21 had findings consistent with EHBTO. Eleven of 15 cats in which blood pressure was monitored had intraoperative hypotension. Eighteen cats had anemia following surgery, and 14 cats had persistent hypotension. Extrahepatic biliary tract obstruction was a result of neoplasia in 9 cats and chronic inflammatory disease in 13. Fourteen cats survived long enough to be discharged from the hospital, but only 6 survived > 6 months after surgery, all of which had chronic inflammatory disease. Median survival time for cats with neoplasia (14 days) was significantly shorter than that for cats with inflammatory disease (255 days). No other variable was associated with outcome. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that cats with EHBTO secondary to neoplasia have a poorer prognosis than cats with EHBTO secondary to chronic inflammatory disease. However, the overall prognosis for cats with EHBTO undergoing cholecystoenterostomy must be considered guarded to poor, and the incidence of perioperative complications is high.     

Comparisons between cats with normal and increased fPLI concentrations in cats diagnosed with inflammatory bowel disease

Objectives : The aim of this study was to compare age, serum albumin and cobalamin concentrations, serum alanine amino transferase and alkaline phosphatase activities, feline inflammatory bowel disease clinical disease activity index, pancreatic ultrasound findings, intestinal histopathology scores, outcome, treatment and clinical response between cats diagnosed with inflammatory bowel disease with normal or increased serum feline pancreatic lipase immunoreactivity concentrations. Methods : Medical records for 23 cats diagnosed with inflammatory bowel disease and with serum feline pancreatic lipase immunoreactivity concentrations available were reviewed. Three groups were compared; cats with serum feline pancreatic lipase immunoreactivity concentrations 2·0 to 6·8 µg/l (group A), 6·9 to 11·9 µg/l (group B) and ≥12·0 µg/l (group C). Results : Sixteen of the 23 cats had increased serum feline pancreatic lipase immunoreactivity concentrations; 9 cats in group B and 7 cats in group C. The remaining seven cats were in group A. Cats with serum feline pancreatic lipase immunoreactivity concentrations ≥12·0 µg/l had significantly lower median serum albumin and cobalamin concentrations. No significant differences were identified between the three groups for age, serum alanine amino transferase and alkaline phosphatase activities, feline inflammatory bowel disease clinical disease activity index, pancreatic ultrasound findings, intestinal histopathology scores, clinical outcome, treatment or clinical response. Clinical Significance : Hypoalbuminaemia and hypocobalaminaemia were more frequently observed in cats with serum feline pancreatic lipase immunoreactivity concentrations ≥12·0 µg/l.     

Evaluation of serum feline trypsin-like immunoreactivity for the diagnosis of pancreatitis in cats

OBJECTIVE: To evaluate serum feline trypsin-like immunoreactivity (fTLI) concentration and results of abdominal ultrasonography, CBC, and serum biochemical analyses for diagnosis of pancreatitis in cats. DESIGN: Prospective study. ANIMALS: 28 cats with clinical signs compatible with pancreatitis. PROCEDURE: Serum fTLI concentrations were determined, and abdominal ultrasonography, CBC, and serum biochemical analyses were performed prior to histologic evaluation of pancreatic, hepatic, and intestinal specimens. On the basis of histologic results, cats were categorized as having a normal pancreas (n = 10), pancreatic fibrosis with ongoing inflammation (9), pancreatic fibrosis without inflammation (4), and acute necrotizing pancreatitis (5). Serum fTLI concentrations and results of CBC, serum biochemical analyses, and histologic evaluation of hepatic and intestinal specimens were compared among groups. RESULTS: Significant differences in serum fTLI concentrations or any hematologic or biochemical variable were not detected among the 4 groups of cats. Median serum fTLI concentrations were 51 micrograms/L (range, 18 to 200 micrograms/L) in cats with a normal pancreas, 32 micrograms/L (range, 12 to > 200 micrograms/L) in cats with pancreatic fibrosis and ongoing inflammation, 124 micrograms/L (range, 36 to > 200 micrograms/L) in cats with pancreatic fibrosis without ongoing inflammation, and 30 micrograms/L (range, 24 to 84 micrograms/L) in cats with acute necrotizing pancreatitis. We detected a high prevalence of concurrent hepatic and intestinal tract disease in cats with pancreatitis. CONCLUSIONS AND CLINICAL RELEVANCE: In cats with clinical signs of pancreatitis, serum fTLI concentration is poorly associated with histopathologic diagnosis.     

Phase I clinical trial evaluating STI571 in tumor bearing cats

Introduction: STI571 (Gleevec, imatinib mesylate) is a receptor tyrosine kinase inhibitor with selectivity for Bcr‐Abl, platelet‐derived growth factor (PDGF), stem cell factor (SCF), and c‐Kit. Side effects with use in humans include vomiting, diarrhea, nausea, myalgia, edema, and cutaneous reactions. Renal and hepatic toxicity have also been reported. In dogs, there is significant hepatic toxicity at sub‐clinical doses. The purpose of this prospective study was to determine the toxicity level and potential treatment protocol in tumor bearing cats. Methods: A phase I clinical trial was performed in client owned cats using an escalating dose of STI571 in tumor bearing cats. Cats included in the study had a histologic diagnosis of fibrosarcoma or other tumors and were staged with CBC, biochemical profile, thoracic radiographs, and abdominal ultrasound. None of the cats received concurrent chemotherapy, but those previously treated with surgery, radiation therapy, or chemotherapy, were not excluded. The initial starting dose was 5 mg/cat PO SID and was gradually increased to 10 and 20 mg/cat PO SID at a 2–6 week interval depending on laboratory work and disease progression. A repeat physical examination, CBC, and biochemical profile, were performed every 2 weeks for 2 rechecks, then every 4 weeks. Results: Six cats were enrolled in the study. Four cats had oral squamous cell carcinoma, and two cats had cutaneous fibrosarcoma. One cat demonstrated leukocytosis, increased liver enzymes, and signs of acute renal failure two weeks after initiating therapy (5 mg PO SID). No dose escalation was made in this cat. Five cats endured dose escalations of 10 mg PO SID in two cats and 20 mg PO SID in three cats and were treated for 2–4 months. None of these cats experienced any signs of toxicity as measured by CBC and biochemical profile. Conclusions: Only one cat experienced toxicity that may have been associated with low dose administration of STI571. As most cats tolerated the drug without an adverse effect, further evaluation of STI571 in a phase II clinical trial is warranted.     

Indications for and outcome of positive-pressure ventilation in cats: 53 cases (1993-2002)

OBJECTIVE: To determine indications for and outcomes of positive-pressure ventilation (PPV) in cats, document ventilator management, and identify factors associated with outcome. DESIGN: Retrospective study. ANIMALS: 53 cats that underwent PPV. PROCEDURE: Information on signalment, history, concurrent diseases, clinical findings, results of venous blood gas analyses and clinicopathologic testing, treatment, ventilator settings, and outcome was retrieved from the medical records. Data for cats that survived were compared with data for cats that died or were euthanatized while undergoing PPV RESULTS: PPV was initiated for management of respiratory failure (36 cats [68%]), cardiac arrest (9 [17%]), neurologic impairment (6 [11%]), and nonresponsive hypotension (2 [4%]). Eight cats (15%) survived, 19 (36%) died, and 26 (49%) were euthanatized while undergoing PPV. Cats that survived had a longer duration of ventilation than did those that died or were euthanatized and had a significantly higher incidence of ventilator-associated pneumonia. Signalment and ventilator settings were not associated with outcome. Cats that had no clinical evidence of pulmonary disease but required PPV because of primary neurologic disease had a higher survival rate (2/6) than did cats that required PPV because of respiratory failure (5/36), cardiac arrest (1/9), or nonresponsive hypotension (0/2). CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that the survival rate for cats requiring PPV may be lower than reported survival rates for dogs. Death was attributable to progressive respiratory failure, non-responsive hypotension, kidney failure, or neurologic impairment.     

Bile acid concentrations in the diagnosis of hepatobiliary disease in the cat

The clinical usefulness of measuring serum bile acid concentrations as a diagnostic test for hepatobiliary disease was examined in 80 cats that were suspected of having hepatic disease. Serum values of total bilirubin, alkaline phosphatase (ALP), alanine transaminase (ALT), and aspartate transaminase (AST) also were measured. Fasting serum bile acid values were determined by use of solid-phase radioimmunoassay for total conjugated bile acids or by a direct enzymatic spectrophotometric method. A definitive diagnosis was established by histologic examination of the liver, and on the basis of these findings, cats were assigned to groups (1 to 8, respectively) including: extrahepatic bile duct obstruction, hepatic lipidosis, cirrhosis, intrahepatic cholestasis (cholangiohepatitis, cholangitis), neoplasia, hepatic necrosis, portosystemic vascular anomalies, and miscellaneous. Cats in group 8 had no morphologic evidence of hepatobiliary disease or had hepatic lesions that were mild. Test efficacy of fasting serum bile acids, total bilirubin, ALP, ALT, and AST were expressed by use of 4 indices: sensitivity, specificity, positive predictive value, and negative predictive value. The diagnostic efficacy of fasting serum bile acids was examined alone and in combinations with the other tests. There was wide overlapping of values of fasting serum bile acids, total bilirubin, ALP, ALT, and AST among cats in groups 1 to 7. The specificity of fasting serum bile acids for the diagnosis of hepatic disease exceeded 90% at values greater than or equal to 5 mumol/L and reached 100% at greater than or equal to 15 mumol/L.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical and Clinicopathologic Features in 11 Cats with Cuterebra Larvae Myiasis of the Central Nervous System

The medical records of 11 cats with histopathologic findings consistent with central nervous system (CNS) Cuterebra larvae myiasis were retrospectively examined to determine if clinical features could identify this disorder antemortem. Young to middleaged indoor-outdoor domestic shorthaired cats presenting with acute neurologic signs from July through September predominated. Many cats recently had clinical signs consistent with upper respiratory disease. Most cats presented for depression, lethargy, or seizures. Almost all cats had abnormal rectal temperatures, either hyperthermia or hypothermia. Peripheral leukocytosis and eosinophilia were not characteristic of cats with CNS cuterebriasis. Cerebrospinal fluid analysis did not consistently disclose evidence of inflammation. Common neurologic deficits included blindness, abnormal mentation, and signs of unilateral prosencephalic disease. No specific clinical or clinicopathologic test was diagnostic for CNS cuterebriasis.     

Clinical, cerebrospinal fluid, and histological data from twenty-seven cats with primary inflammatory disease of the central nervous system.

The purpose of this report is to present the clinical, cerebrospinal fluid (CSF) and histological data from 27 cats with inflammatory disease of the central nervous system (CNS). The cats were part of a study of 61 cats admitted to two university clinics over an eight-year period because of signs of CNS disease. The most frequent diseases were feline infectious peritonitis (FIP) (12/27) and suspected viral disease other than FIP (10/27). Typical CSF findings in cats with FIP were a protein concentration of greater than 2 g/L (200 mg/dL) and a white cell count of over 100 cells/microL, which consisted predominantly of neutrophils. In contrast, the CSF of cats with suspected viral disease had a protein concentration of less than 1 g/L (100 mg/dL) and a total white cell count of less than 50 cells/microL. In general, cats with FIP or suspected viral disease were less than four years of age. Neurological signs were usually multifocal in cats with FIP, but focal in cats with suspected viral disease. The CSF findings were variable in five other inflammatory diseases represented. Two cats with protozoan infection had normal CSF total cell counts but abnormal differential counts. The CSF findings were invaluable in differentiating FIP from other causes of inflammatory CNS disease.     

Fibrocartilaginous embolic myelopathy in five cats

Five cats had clinical signs, radiographic findings, and cerebrospinal fluid analyses consistent with fibrocartilaginous embolic myelopathy. All cats had an acute onset of nonpainful, asymmetrical spinal cord signs (paresis or paralysis of one or more limbs). Magnetic resonance imaging was performed in three cats. On T2-weighted images, an intramedullary lesion was revealed that was hyperintense to normal spinal cord gray matter. On T1-weighted images, the lesion was isointense. Three of the cats were euthanized, and postmortem examination confirmed myelomalacia with intralesional fibrocartilaginous emboli. Two cats survived and were clinically improved within 3 weeks.     

Acquired portosystemic shunting in two cats.

Acquired portosystemic shunts (PSS) are a clinical entity distinct from congenital PSS. Their apparent incidence in cats is low, which may reflect the rarity of predisposing hepatic parenchymal disease, such as cirrhosis, in this species. Two cats with acquired PSS associated with primary hepatobiliary disease are described. Relevant findings in acquired PSS are discussed, as are potential reasons for the apparently low incidence in the cat.     

Lymphocytic/plasmacytic gastroenteritis in cats: 14 cases (1985-1990).

Over a 5-year period, lymphocytic/plasmacytic gastroenteritis was diagnosed in 14 cats. Purebred cats were affected significantly (P less than 0.025) more often than nonpurebred cats. Mean age at onset of clinical signs was 6.8 years (range, 1 to 13 years); 11 cats were male. Vomiting and weight loss, each reported in 10 of 14 cats, were the most common clinical signs. Diarrhea was reported in 7 of 14 cats. Alopecia was found in 4 of 14 cats. High hepatic enzyme activities and low plasma protein concentrations were frequent biochemical findings. Hyperemia, hemorrhage, and a roughened or "cobblestone" mucosa were visualized by endoscopy in only 2 of 8 cats with duodenal disease and in 2 of 5 cats with gastric disease. Lymphocytic/plasmacytic inflammation was detected in biopsy specimens from the stomach or duodenum or both in all cats; the duodenum was affected most commonly. Degree of inflammation frequently varied among gastric, duodenal, and colonic specimens from the same cat. Glucocorticoid treatment and dietary management adequately controlled clinical signs in 7 cats, but treatment was ineffective in 6 cats, 5 of which were euthanatized because of severity of clinical signs.     

Anemia, splenomegaly, and increased osmotic fragility of erythrocytes in Abyssinian and Somali cats

OBJECTIVE: To determine clinical and clinicopathologic features of a chronic intermittent severe hemolytic anemia characterized by erythrocyte osmotic fragility in Abyssinian and Somali cats. DESIGN: Case series. ANIMALS: 13 Abyssinian and 5 Somali cats. PROCEDURES: History, pedigree information, and results of routine laboratory tests, special erythrocyte studies, and histologic evaluation of splenic and hepatic specimens were analyzed. RESULTS: Age at which clinical signs of anemia were first apparent ranged from 6 months to 5 years. Ten cats had splenomegaly. Most often, the PCV was between 15 and 25%, but it was as low as 5% at some times. The anemia was characterized by macrocytosis and mild to moderate reticulocytosis, but no poikilocytosis. Hyperglobulinemia, lymphocytosis, mild hyperbilirubinemia, and high hepatic enzyme activities were common findings. Results of Coombs tests and tests for infectious diseases were negative. The erythrocytic osmotic fragility was high in affected cats (mean osmotic fragility, 0.66 to 0.78%), compared with healthy cats (0.48 to 0.58). No specific membrane protein abnormality, erythrocyte enzyme deficiency, or hemoglobinopathy was identified. Histologic evaluation of splenic and hepatic specimens revealed extramedullary hematopoiesis and hemosiderosis. Four of the 5 Somali cats were closely related. CONCLUSIONS AND CLINICAL RELEVANCE: On the basis of results of pedigree analyses, the apparent breed predilection, and the exclusion of other known causes of anemia in cats, we believe that the hemolytic anemia in these cats was likely a result of a novel hereditary erythrocyte defect. A genetic predisposition to immune-mediated destruction of erythrocytes could not be ruled out.