Metabolic and hormonal alterations in cats with hepatic lipidosis

Hepatic lipidosis in cats is a commonly diagnosed hepatobiliary disease of unknown cause. The purpose of this prospective study was to characterize the blood hormone and lipid status of cats with hepatic lipidosis, and to compare this status to that of cats with other types of liver disease and to control cats. Twenty-three cats with hepatic disease were assigned to 1 of 2 groups on the basis of cytopathologic or histopathologic examination of the liver: group 1, hepatic lipidosis (n = 18); or group 2, cholangiohepatitis (n = 5). Ten healthy young adult cats were used as controls. Food was withheld from control animals for 24 hours before blood collection. Concentrations of plasma glucagon and serum insulin, cortisol, thyroxine, triglycerides, cholesterol, phospholipids, and nonesterified fatty acids (NEFAs) were determined in all cats, in addition to routine hematologic and serum biochemical testing. Cats with hepatic lipidosis had higher serum NEFA concentrations than cats with cholangiohepatitis or control cats (P < .05). Cats with cholangiohepatitis had higher serum cholesterol and phospholipid concentrations than those of cats with lipidosis or control cats (P < .05); their plasma glucagon concentrations were higher than those of control cats (P < .05), but were not different from those of cats with hepatic lipidosis. Serum insulin concentrations were significantly higher in control cats than in diseased cats (P < .05), but neither serum insulin nor the insulin to glucagon ratio was significantly different among the cats with hepatic disease. The high concentration of NEFAs in cats with hepatic lipidosis suggests that at least 1 factor in the pathogenesis of this syndrome may involve the regulation of hormone-sensitive lipase.     

Liver glutathione concentrations in dogs and cats with naturally occurring liver disease

OBJECTIVE: To determine total glutathione (GSH) and glutathione disulfide (GSSG) concentrations in liver tissues from dogs and cats with spontaneous liver disease. SAMPLE POPULATION: Liver biopsy specimens from 63 dogs and 20 cats with liver disease and 12 healthy dogs and 15 healthy cats. PROCEDURE: GSH was measured by use of an enzymatic method; GSSG was measured after 2-vinylpyridine extraction of reduced GSH. Concentrations were expressed by use of wet liver weight and concentration of tissue protein and DNA. RESULTS: Disorders included necroinflammatory liver diseases (24 dogs, 10 cats), extrahepatic bile duct obstruction (8 dogs, 3 cats), vacuolar hepatopathy (16 dogs), hepatic lipidosis (4 cats), portosystemic vascular anomalies (15 dogs), and hepatic lymphosarcoma (3 cats). Significantly higher liver GSH and protein concentrations and a lower tissue DNA concentration and ratio of reduced GSH-to-GSSG were found in healthy cats, compared with healthy dogs. Of 63 dogs and 20 cats with liver disease, 22 and 14 had low liver concentrations of GSH (micromol) per gram of tissue; 10 and 10 had low liver concentrations of GSH (nmol) per milligram of tissue protein; and 26 and 18 had low liver concentrations of GSH (nmol) per microgram of tissue DNA, respectively. Low liver tissue concentrations of GSH were found in cats with necroinflammatory liver disease and hepatic lipidosis. Low liver concentrations of GSH per microgram of tissue DNA were found in dogs with necroinflammatory liver disease and cats with necroinflammatory liver disease, extrahepatic bile duct occlusion, and hepatic lipidosis. CONCLUSIONS AND CLINICAL RELEVANCE: Low GSH values are common in necroinflammatory liver disorders, extrahepatic bile duct occlusion, and feline hepatic lipidosis. Cats may have higher risk than dogs for low liver GSH concentrations.     

Diagnostic value of serum gamma-glutamyl transferase and alkaline phosphatase activities in hepatobiliary disease in the cat

The diagnostic value of serum gamma-glutamyl transferase (GGT) activity and serum alkaline phosphatase (ALP) activity in the detection of liver disease in the cat (n = 69) was compared. On the basis of histologic examination of the liver, cats were assigned to 8 groups: group 1--complete extrahepatic bile duct obstruction (n = 5), group 2--cholangiohepatitis-cholangitis syndrome (n = 11), group 3--hepatic lipidosis (n = 15), group 4--neoplasia, including lymphosarcoma and myeloproliferative disease (n = 9), group 5--hepatic necrosis (n = 7), group 6--cirrhosis (n = 3), group 7--portosystemic vascular anomaly (n = 4), and group 8--miscellaneous (n = 15). Cats assigned to group 8 lacked substantial histologic abnormalities of the liver. The mean value +/- SD of GGT in 20 clinically normal cats was 0.44 +/- 0.26 IU/L. The highest GGT activity in clinical patients developed in groups 1, 2, and 6. The highest ALP activity developed in groups 1 to 4. Significant correlations between GGT and ALP activities were detected only in groups 2 (P less than 0.001) and 5 (P less than 0.10). Among 54 cats with hepatic disease, only 11% had both the GGT and ALP activities within the normal ranges. Comparatively, 52% had ALP activities within the normal range, and 17% had GGT activities within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)     

A Retrospective Study of 77 Cats With Severe Hepatic Lipidosis: 1975–1990

The physical, clinicopathologic, and survival rates of 77 cats with severe spontaneous hepatic lipidosis are detailed in this report. Cats were subdivided into groups designated as idiopathic lipidosis if no other disease process was recognized, or secondary lipidosis if another disease process was diagnosed. Cats were also subdivided into groups designated as survivors or nonsurvivors on the basis of successful recuperation at 4 months after initial diagnosis. Differences between disease and survival groups were evaluated for significance. Overall, more female cats and middle-aged cats were affected. Presenting complaints of vomiting, anorexia, weakness, and weight loss were common. Physical assessment of most cats showed obvious hepatomegaly, jaundice, dehydration, and a weight loss ≥ 25% of usual body weight. Neurobehavioral signs indicative of hepatic encephalopathy, other than ptyalism and depression, were rare. Clinicopathologic features are characterized by hyperbilirubinemia and increased activities of serum ALT, AST, and ALP, with only small if any increase in γGT activity. Clinical features distinguishing cats with hepatic lipidosis from those with other serious cholestatic disorders include absence of hyperglobulinemia and low γGT activity relative to ALP activity. Although coagulation tests were abnormal in 45% of cats tested (n = 44), few cats showed clinical bleeding tendencies. Most cats received prophylactic vitamin K₁ therapy. Forty two cats received aggressive nutritional and supportive care and of these 55% survived. Cats with idiopathic disease were significantly younger, had significantly higher ALP activity and bilirubin concentration, and had a slightly better survival rate than cats with secondary lipidosis. Low PCV, hypokalemia, and an older age were significantly related to nonsurvival. Because of the variety of diets and food supplements used in case management, the influence of nutritional factors on survival could not be evaluated. (Journal of Veterinary Internal Medicine 1993; 7:349–359. Copyright © 1993 by the American College of Veterinary Internal Medicine.)     

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.)     

Proteins invoked by vitamin K absence and clotting times in clinically ill cats

The clinical utility of the Thrombotest, a method for determining the prothrombin time that is uniquely sensitive to the presence of proteins invoked by vitamin K absence (PIVKA), was prospectively evaluated and compared to routine coagulation tests in cats with clinically suspected bleeding tendencies. Abnormal PIVKA clotting values were determined by comparison to results of a concurrently evaluated pooled feline plasma sample and by use of an absolute cutoff value of 25.2 seconds. To be recognized as abnormal, PIVKA clotting values had to be >20% of the pooled feline plasma PIVKA clotting time (the "20% rule") or > or =25.2 seconds (mean + 2 standard deviations of 150 different pooled feline plasma samples). Among the disorders in the population examined were 74 cats with liver disease and 19 cats with severe inflammatory bowel disease. Overall, a prolonged PIVKA clotting time based on the 25.2-second cutoff was found in 39.3% of cats, and based on the 20% rule in 40.7% of cats. An abnormal prothrombin time (PT) developed in 5.8% of cats, an abnormal APTT in 14% of cats, subnormal fibrinogen in 8.8% of cats, and thrombocytopenia in 3.3% of cats. Bleeding tendencies were confirmed in 22 cats, of which abnormal PIVKA clotting times were recognized in 95.5%, abnormal PT in 21%, abnormal activated partial thromboplastin time in 25%, hypofibrinogenemia in 16.7%, and thrombocytopenia in 4.5%. Response to treatment with vitamin K was demonstrated in 21 of 24 cats with an abnormal PIVKA clotting time. In these cats, an abnormal PIVKA clotting time normalized within 3 to 5 days of parenteral vitamin K administration. Cats responding to vitamin K administration had hepatic lipidosis (n = 7), severe inflammatory bowel disease (n = 4), severe inflammatory bowel disease associated with cholangiohepatitis (n = 5), and miscellaneous disorders (n = 5). Using either endpoint, the PIVKA clotting time is more sensitive for the detection of cats with coagulopathies than routinely used coagulation assessments in our hospital. Our findings confirm that cats with hepatic lipidosis, severe cholangiohepatitis, and severe inflammatory bowel disease develop coagulopathies responsive to vitamin K administration.     

Lack of associations between ultrasonographic appearance of parenchymal lesions of the canine liver and histological diagnosis

Objective: To assess if there are any ultrasonographic features that may enable tentative diagnosis of hepatic parenchymal disease. Methods: Records of 371 dogs that had abdominal ultrasonography and abnormal liver on biopsy or necropsy were reviewed. Results: Histological diagnoses were hepatitis (n=77), nodular hyperplasia (n=47), vacuolar change (n=45), fibrosis (n=32), primary hepatic carcinoma (n=30), lymphoma (n=28), metastatic neoplasia (n=27), necrosis (n=21), lipidosis (n=17), haemangiosarcoma (n=13), round cell tumour (n=9), hepatocellular adenoma (n=8), degenerative change (n=6), steroid hepatopathy (n=7) and extramedullary haematopoiesis (n=4). The most prevalent ultrasonographic features were multifocal lesions (63% livers with haemangiosarcoma and 43% livers with hepatocellular carcinoma), diffuse lesions (71% livers with steroid hepatopathy, 44% livers with fibrosis and 40% livers with vacuolar hepatopathy), hyperechoic lesions (71% livers with steroid hepatopathy, 41% livers with lipidosis and 38% livers with fibrosis), heterogeneous lesions (62% livers with haemangiosarcoma), hepatomegaly (43% livers with steroid hepatopathy) and peritoneal fluid (62% livers with haemangiosarcoma). Target lesions were associated with malignancy in 67% instances. Marked variability in ultrasonographic appearance of lesions was observed for all diagnoses, and no statistically significant associations between ultrasonographic appearance and diagnosis were found. Clinical Significance: Histological examination remains essential for diagnosis of canine hepatic disease.     

Pulmonary thromboembolism in cats

Pulmonary thromboembolism (PTE) is rarely diagnosed in cats, and the clinical features of the disease are not well known. PTE was diagnosed at postmortem examination in 17 cats, a prevalence of 0.06% over a 24-year period. The age of affected cats ranged from 10 months to 18 years, although young (<4 years) and old (>10 years) cats were more commonly affected than were middle-aged cats. Males and females were equally affected. The majority of cats with PTE (n = 16) had concurrent disease, which was often severe. The most common diseases identified in association with PTE were neoplasia, anemia of unidentified cause, and pancreatitis. Cats with glomerulonephritis, encephalitis, pneumonia, heart disease, and hepatic lipidosis were also represented in this study. Most cats with PTE demonstrated dyspnea and respiratory distress before death or euthanasia, but PTE was not recognized ante mortem in any cat studied. In conclusion, PTE can affect cats of any age and is associated with a variety of systemic and inflammatory disorders. It is recommended that the same clinical criteria used to increase the suspicion of PTE in dogs should also be applied to cats.     

Coagulation Abnormalities in 22 Cats with Naturally Occurring Liver Disease

Twenty-two cats with liver disease were evaluated for coagulation abnormalities including alterations in prothrombin time, activated partial thromboplastin time, thrombin time, factor VII activity, and platelet count. The purpose of the study was to determine the prevalence of coagulation abnormalities in this population of cats, classify abnormalities according to underlying pathogenesis, and determine if serum biochemical parameters typically used as indicatiors of liver disease showed any correlation with the coagulation abnormalities present. Study results indicated that at least 1 coagulation abnormality was present in 82% of the cats. Prolongation of prothrombin time was most common (16/22 cats) and factor VII activity was below reference range (<60%) in 15 cats. When classified according to underlying pathogenesis, vitamin K deficiency was the most common abnormality found (11/22). Other abnormalities were less common and included hepatic synthetic failure (3/22), indeterminate (3/22), and disseminated intravascular coagulation (1/22). Increase in alkaline phosphatase (ALP) activity was the only biochemical abnormality that showed statistically significant correlation with coagulation abnormalities ( P = .023). Cats with marked increases in ALP activity were more likely to have coagulation abnormalities than those with only mild increases in ALP activity.     

Hypokalemia in cats: 186 cases (1984-1987)

Retrospective review of serum biochemical data obtained from 501 cats over a 3-year period (1984-1987) indicated that 186 (37%) had hypokalemia (serum potassium concentration less than 4.1 mEq/L). After adjusting for disease diagnosis, cats fed either of 2 commercial diets were 4 times more likely to be hypokalemic than cats fed other diets. Odds ratios (OR; measure of association), adjusted for diet type, were calculated to determine the odds of hypokalemia for a given disease, compared with odds of normokalemia for the same disease. Chronic renal failure (OR = 14.4), hepatic disease (OR = 5.7), systemic infectious diseases (viral or bacterial; OR = 2.7), and neuromuscular or CNS disease (OR = 2.4) were all significantly associated (P less than 0.05) with the occurrence of hypokalemia. Significant differences in age or sex between hypokalemic and normokalemic cats were not found. Within the group of 186 hypokalemic cats, hypercholesterolemia (89 cats; 48%), hyperglycemia (88 cats; 47%), high serum urea nitrogen concentration (86 cats; 46%), hyperchloridemia (80 cats; 43%), and high serum creatinine concentration (73 cats; 39%) were the most common biochemical abnormalities. When disease diagnosis was compared among cats with severe hypokalemia (serum potassium concentration less than 3.0 mEq/L) and those with moderate hypokalemia, cats with severe hypokalemia were 3.5 times more likely to have chronic renal failure than cats with less severe hypokalemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Accuracy of ultrasonography in the detection of severe hepatic lipidosis in cats.

The accuracy of ultrasonography in detection of feline hepatic lipidosis was studied retrospectively. The following ultrasonographic criteria were associated positively with severe hepatic lipidosis: the liver hyperechoic, compared with falciform fat; the liver isoechoic or hyperechoic, compared with omental fat; poor visualization of intrahepatic vessel borders; and increased attenuation of sound by the liver. In a group of 36 cats with clinically apparent hepatobiliary disease and in which liver biopsy was done, liver hyperechoic, compared with falciform fat, was the best criterion for diagnosis of severe hepatic lipidosis with 91% sensitivity, 100% specificity, and 100% positive predictive value.     

Comparison of plasma, liver, and skeletal muscle carnitine concentrations in cats with idiopathic hepatic lipidosis and in healthy cats

Concentrations of total, free, and esterified carnitine were determined in plasma, liver, and skeletal muscle from cats with idiopathic hepatic lipidosis and compared with values from healthy cats. The mean concentrations of plasma, liver, and skeletal muscle total carnitine; plasma and skeletal muscle free carnitine; and plasma and liver esterified carnitine were greater (P less than 0.05) in cats with idiopathic hepatic lipidosis than in control cats. The mean for the ratio of free/total carnitine in plasma and liver was lower (P less than 0.05) in cats with idiopathic hepatic lipidosis than in control cats. These data suggest that carnitine deficiency does not contribute to the pathogenesis of feline idiopathic hepatic lipidosis.     

Hypercalcemia in cats: a retrospective study of 71 cases (1991-1997)

A retrospective study was conducted to characterize the diseases, clinical findings, and clinicopathologic and ultrasonographic findings associated with hypercalcemia (serum calcium concentration >11 mg/dL) in 71 cats presented to North Carolina State University Veterinary Teaching Hospital. The 3 most common diagnoses were neoplasia (n = 21), renal failure (n = 18), and urolithiasis (n = 11). Primary hyperparathyroidism was diagnosed in 4 cats. Lymphoma and squamous cell carcinoma were the most frequently diagnosed tumors. Calcium oxalate uroliths were diagnosed in 8 of 11 cats with urolithiasis. Cats with neoplasia had a higher serum calcium concentration (13.5 ± 2.5 mg/dL) than cats with renal failure or urolithiasis and renal failure (11.5 ± 0.4 mg/dL; P <.03). Serum phosphorus concentration was higher in cats with renal failure than in cats with neoplasia ( P < .004). Despite the fact that the majority of cats with uroliths were azotemic, their serum urea nitrogen and creatinine concentrations and urine specific gravity differed from that of cats with renal failure. Additional studies are warranted to determine the underlying disease mechanism in the cats we identified with hypercalcemia and urolithiasis. We also identified a small number of cats with diseases that are not commonly reported with hypercalcemia. Further studies are needed to determine whether an association exists between these diseases and hypercalcemia, as well as to characterize the underlying pathophysiologic mechanism for each disease process.     

X‐RAY ATTENUATION OF THE LIVER AND KIDNEY IN CATS CONSIDERED AT VARYING RISK OF HEPATIC LIPIDOSIS

X‐ray attenuation of the liver has been measured using computed tomography (CT) and reported to decrease in cats with experimentally induced hepatic lipidosis. To assess the clinical utility of this technique, medical records and noncontrast CT scans of a series of cats were retrospectively reviewed. A total of 112 cats met inclusion criteria and were stratified into three hepatic lipidosis risk groups. Group 1 cats were considered low‐risk based on no history of inappetence or weight loss, and normal serum chemistry values; Group 2 cats were considered intermediate risk based on weight loss, serum hepatic enzymes above normal limits, or reasonably controlled diabetes mellitus; and Group 3 cats were considered high risk based on poorly controlled diabetes mellitus due to hypersomatotropism. Mean CT attenuation values (Hounsfield units, HU) were measured using regions of interest placed within the liver and cranial pole of the right kidney. Hepatic and renal attenuation were weakly positively correlated with each other (r = 0.2, P = 0.03) and weakly negatively correlated with body weight (r = ?0.21, P = 0.05, and r = ?0.34, P = 0.001, respectively). Mean (SD) hepatic and renal cortical attenuation values were 70.7 (8.7) HU and 49.6 (9.2) HU for Group 1 cats, 71.4 (7.9) HU and 48.6 (9.1) HU for Group 2, and 68.9 (7.6) HU and 47.6 (7.2) HU for Group 3. There were no significant differences in hepatic or renal attenuation among groups. Findings indicated that CT measures of X‐ray attenuation in the liver and kidney may not be accurate predictors of naturally occurring hepatic lipidosis in cats.     

Liver function in cats with hyperthyroidism before and after 131I therapy

BACKGROUND: The clinical significance of high serum concentration or activity of markers of liver damage in cats with hyperthyroidism is unknown. OBJECTIVE: To evaluate serum markers of liver function and damage, and ultrasonographic changes in cats with hyperthyroidism and with high liver enzymes, and to determine if abnormalities resolve after treatment with 131I. ANIMALS: Nineteen cats with hyperthyroidism (15 with high serum activities of liver enzymes) and 4 age-matched healthy control cats. METHODS: Serum bile acids, albumin, ammonia, cholesterol, and blood urea nitrogen concentrations, and activities of liver-derived enzymes, and blood glucose concentrations were measured before and after 131I therapy. These values were compared with those of cats that were euthyroid. In addition, gross liver parenchymal changes detected by abdominal ultrasonographic examination, before and after 131I therapy were evaluated. RESULTS: High serum liver enzyme activities were not associated with abnormalities in hepatic parenchyma and liver functional variables, regardless of the degree of increase. Serum liver enzyme activities return to normal after control of hyperthyroidism with 131I therapy. Cats with hyperthyroidism have a significantly higher serum fasting ammonia concentration than cats who were euthyroid (P = .019). Cats with hyperthyroidism also have significantly lower serum cholesterol (P = .005) and glucose (P = .002) concentrations before compared with after 131I therapy. Nine of 19 cats with hyperthyroidism had trace ketonuria. CONCLUSIONS AND CLINICAL IMPORTANCE: These results demonstrate that extensive examination for hepatobiliary disease in most cats with hyperthyroidism is unnecessary.     

Adverse events in 50 cats with allergic dermatitis receiving ciclosporin

Ciclosporin is an immunosuppressive drug that has been used to treat allergies and other immune-mediated diseases in cats, dogs and humans. Information about the adverse effects of ciclosporin in cats has been limited to smaller studies and case reports. Adverse effects in dogs are mainly gastrointestinal in nature, but humans can also experience hypertension and altered renal function. The aim of this retrospective case series study was to document the occurrence and clinical appearance of adverse events in cats receiving ciclosporin to treat allergic skin disease. The medical records of 50 cats with allergic dermatitis treated with oral ciclosporin (1.9-7.3 mg/kg/day) were reviewed. Adverse events occurred in 66% (33 cats). Adverse events likely to be associated with ciclosporin included the following: vomiting or diarrhoea within 1-8 weeks of receiving ciclosporin (24%), weight loss (16%), anorexia and subsequent hepatic lipidosis (2%) and gingival hyperplasia (2%). Other adverse events less likely to be associated with ciclosporin therapy included the following: weight gain (14%), dental tartar and gingivitis (10%), otitis (4%), chronic diarrhoea (4%), inflammatory bowel disease with indolent gastrointestinal lymphoma (2%), urinary tract infection (2%), cataract (2%), elevated liver enzymes (2%), hyperthyroidism and renal failure (2%) and transient inappropriate urination (2%). Some cats experienced multiple adverse events. Case-control studies are needed to prove cause and effect of ciclosporin with regard to these adverse events.     

Treatment of idiopathic hepatic lipidosis in cats: 11 cases (1986-1987)

Idiopathic hepatic lipidosis was diagnosed in 11 cats. Cats were treated by delivery of balanced nutrients supplemented with L-carnitine via a surgically placed gastrostomy tube. Feeding through the gastrostomy tube was initiated in the hospital and was continued at home in all cats. The mean duration of gastrostomy tube feeding was 48 days (range, 22 to 98 days). Vomiting associated with feeding (3 cats) and localized cellulitis at the gastrostomy site (2 cats) were the most frequent complications. Vomiting was controlled by reducing the volume of food administered at each feeding or by administration of metoclopramide. Cellulitis was treated successfully by parenteral administration of antibiotics and local wound cleansing. Seven of 11 cats (65%) survived and have remained clinically healthy for 15 to 29 months (mean, 20 months) since diagnosis. The other 4 cats died of peritonitis (n = 1), pneumonia (n = 1), hepatic encephalopathy (n = 1), or cardiopulmonary arrest (n = 1) between 0 and 10 days after surgery.     

Obesity increases initial rate of fibrin formation during blood coagulation in domestic shorthaired cats

Obesity predisposes to a prothrombotic state in humans, but whether a similar state occurs in obese animals is unknown. The objective of the current study was to examine the effect of body fat percentage (BF) on haemostatic parameters including thromboelastography with tissue factor as activator (TF-TEG) in client owned indoor-confined physically inactive cats. Seventy-two cats were included following an initial thorough health examination, and a complete blood count, biochemistry panel, conventional coagulation panel and a TF-TEG analysis were performed with tissue factor (1:50,000) as activator. The cats were anaesthetized, and BF was measured using Dual-energy X-ray absorptiometry. Significant difference between lean (BF < 35%, n = 26), overweight (35% < BF < 45%, n = 28) and obese (BF > 45%, n = 18) cats was identified using ANOVA. The correlation between BF, serum leptin and total adiponectin, respectively, with individual TEG and conventional coagulation parameters was evaluated. Obese cats showed a faster rate of fibrin formation (TF-TEG(R), p < 0.05), and TF-TEG(R) was positively correlated with plasma leptin levels. Increasing BF did not affect other conventional coagulation or TF-TEG parameters. In conclusion, this study indicates a connection between body fat content and altered haemostasis, also in cats. Whether feline obesity causes a hypercoagulable state of clinical relevance should be further investigated.     

Evaluation of acute congestive heart failure in dogs and cats: 145 cases (2007–2008)

Objective – To characterize the clinical presentation, management, and in‐hospital outcomes of dogs and cats diagnosed with acute congestive heart failure (CHF). Design – Retrospective study of animals seen between January 2007 and May 2008. Setting – Emergency service at a university teaching hospital. Animals – Ninety dogs and 55 cats with CHF. Measurements and Main Results – Patient characteristics, including age, clinical signs, clinicopathologic abnormalities, diagnostic testing, and outcome were recorded. Forty‐eight of the animals already were receiving cardiac medications at the time of presentation. The most common diseases represented were chronic valvular disease and cardiomyopathies. Cats had significantly lower median body temperature at admission compared with dogs (P<0.001). The most common abnormalities were elevated lactate (64%), elevated BUN (52%), hypochloremia (31%), hyperglycemia (27%), and elevated liver enzymes (26%). Many of these became even more prevalent during hospitalization. One hundred and sixteen animals were discharged from the hospital, for a survival rate of 80%. There was no survival difference between dogs and cats (P=0.39). Dogs that developed hypokalemia during hospital stay (P=0.04) were more likely to survive compared with those without hypokalemia and initial body temperature was lower for those cats that did not survive (P=0.02). Of those that did not survive, the majority were euthanized (n=25), while 4 dogs died. Conclusions – Dogs and cats presented to the emergency service with CHF had a high survival rate. In cats, initial body temperature was lower for those cats that did not survive. Although clinicopathologic abnormalities were common in both species, only dogs with hypokalemia had improved survival to hospital discharge.     

Hemostatic biomarkers in dogs with chronic congestive heart failure

BACKGROUND: Chronic congestive heart failure (CHF) in humans is associated with abnormal hemostasis, and abnormalities in hemostatic biomarkers carry a poor prognosis. Alterations in hemostatic pathways can be involved in the pathogenesis of CHF in dogs, and microthrombosis in the myocardium could contribute to increased mortality. HYPOTHESIS: That plasma concentration or activity of hemostatic biomarkers is altered in dogs with CHF and that these factors predict mortality. ANIMALS: Thirty-four dogs with CHF caused by either dilated cardiomyopathy (DCM, n=14) or degenerative valvular disease (CDVD, n=20) compared with 23 healthy age-matched control dogs were included in this study. Dogs with CHF were recruited from 2 referral cardiology clinics, and control dogs were owned by friends or colleagues of the investigators. METHODS: Clinical examination and echocardiography were performed in all dogs. Plasma fibrinogen and D-dimer concentrations, antithrombin and protein C activity, and thrombin-antithrombin complex (TAT) were measured in all dogs. RESULTS: Dogs with CHF had significantly higher fibrinogen (P = .04), D-dimer (P = .002), and TAT concentration (P < .0001), lower antithrombin (P < .0001) and protein C activity (P < .001) compared with control dogs. None of the hemostatic biomarkers were associated with risk of death. CONCLUSIONS AND CLINICAL IMPORTANCE: There is evidence of a procoagulant state in dogs with CHF. The lack of predictive value for survival might be due to the small number of dogs examined. Further studies are necessary to investigate the presence and importance of microthrombosis in dogs with CHF.