82nd Western Veterinary Conference S12D Pearls of Feline Liver Disease David C. Twedt, DVM, DACVIM Colorado State University, Fort Collins, CO, USA OVERVIEW OF THE ISSUE Liver disease is common in the cat and the finding of icterus is a frequently a clinical clue that the cause is primary liver disease. The types of liver disease as well as differences in laboratory tests for the cat are very different from disorders observed in the dog. OBJECTIVES OF THE PRESENTATION Liver disease is common in the cat and our understanding of many conditions has advanced considerably over the recent years. The types of liver disease as well as interpretation of laboratory tests for liver disease for the cat are unique and very much different than the common disorders observed in the dog. This is due in part to specific anatomical and metabolic differences of the cat. The following sections will include an overview of these differences with specific pearls of newer information on feline hepatic disease, diagnostic testing and treatment strategies. KEY ETIOLOGIC AND PATHOPHYSIOLOGIC POINTS A study evaluating the utility of liver biochemistries in the diagnosis of feline liver disease found the best predictive tests for primary liver disease includes ALP, GGT, total bilirubin and bile acids.1 Both ALT and AST values are quite variable and elevations don’t always predict primary inflammatory liver disease (cholangitis) or hepatic lipidosis, both of which cause more cholestatic changes with increases in ALP, GGT rather than hepatocellular damage reflected by increases in ALT and AST. ALP is also unique in cats because the half-life of the enzyme is short (6 hours) and the feline liver is reported to contain only one- third the concentrations found in dogs.2 Consequently, increases in serum ALP due to cholestasis are not expected to increase with the same magnitude as would occur in dogs with a similar diseases. Corticosteroids do not induce a steroid isoenzyme of ALP nor do they cause a steroid hepatopathy. Cats having idiopathic hepatic lipidosis usually have marked increases in ALP with GGT concentrations having only mild increases.4 Gamma-glutamyl transpeptidase (GGT) is a similar to ALP in that GGT increases with cholestasis however this enzyme appears to have greater sensitivity for the diagnosis of cholangitis than does ALP. Presumably this is because GGT is found in higher concentrations in the bile ducts than in the hepatocyte where ALP appears to predominant and is affected more by intrahepatic cholestasis. Cats having cholangitis usually have higher elevations in GGT than ALP. Clinical Pearl: Elevations in GGT often suggests biliary tract disease while marked increases in ALP occur with lipidosis. Bile acids in the cat are most useful in screening for portal systemic shunts. Icterus is a common clinical and laboratory finding and the old saying that icteric cats have a poor prognosis is no longer true. Icterus can occur in cats from many etiologies of which not are all liver related and many etiologies are very treatable. Icterus occurs from alteration in the normal bilirubin pathway and there are many complexities in bilirubin metabolism and the ability to conjugate compounds is uniquely affected in the cat. Pre-hepatic icterus from hemolysis must first be ruled out. For icterus to occur secondary to hemolysis of RBCs the hematocrit (PCV) must fall significantly and usually >20%. Very treatable causes of hemolytic anemia such as Mycoplasma spp. or hypophosphatemia should be first excluded. Next causes of altered hepatic bilirubin metabolism should be considered. There are several steps involved in the pathways of bilirubin metabolism before it reaches the bile.3 This hepatic metabolism can be affected by not only structural damage but also metabolic alterations from inflammatory cytokines or endotoxins or from nutritional alterations due to mobilization of free fatty acids delivered to the liver. Also protein deficiencies resulting from starvation or catabolic conditions can lead to depletion of bilirubin binding proteins contributing to alterations in metabolism. Cats also have inherent low concentrations of glucuronyl transferase, an enzyme required to convert bilirubin to water- soluble form prior to hepatic excretion.4 It is these multiple steps in bilirubin pathway that can result in icterus often without evidence of significant structural liver disease. When I reviewed a series of cats with elevations in bilirubin and grouped them into either clinically icteric cats (bilirubin >3.0 mg/dl) or those with biochemical icterus (having only icteric serum with bilirubin ranging from 0.5 to 2.9 mg/dl). Cats with clinically icteric (bilirubin > 3.0 mg/dl) most often had primary hepatobiliary disease when hemolytic disease was ruled out. Clinical Pearl: Icteric cats without hemolysis often have primary liver disease. Cats having biochemical icterus (bilirubin < 3.0 mg/dl) do not always have a primary hepatobiliary disease but could also have other non-hepatic disorders with the liver being only secondarily affected. For example, it is not unusual to find elevations in bilirubin concentrations in cats with inflammatory disease such as pyothorax, abscesses or fat necrosis.5 Clinical Pearl: Cats with biochemical icterus (bilirubin < 3.0 mg/dl) do not always have primary liver disease. Liver Diseases in Cats The incidence of liver disease in the cat is unknown but is considered to be common. In an unpublished review by the author of 175 consecutive liver biopsies performed on cats at Colorado State University several large categories were apparent (Table1). Making up 87% of the liver biopsies were 4 groups: Lipidosis (both idiopathic and secondary, 26%), Cholangitis (25%), Neoplasia (20%) and Reactive hepatopathies (16%). Hepatic cysts are also an occasional finding in some cats but rarely cause problems. Lipidosis and cholangitis were the most common conditions and will be discussed below. Reactive hepatopathies refer to changes in the liver that occur secondary to a primary non-hepatic disorder such as inflammatory bowel disease, hyperthyroidism and cardiac disease to name a few examples. In many cases of secondary reactive hepatopathies there may also be some degree of secondary lipidosis. Often the leakage enzymes (ALT and AST) are the predominate enzyme abnormality. Hepatic neoplasia is also common with lymphoma the most common type of cancer observed. Cats are also different than dogs in the fact that benign tumors are more common than malignant hepatic neoplasia. Bile duct adenomas (cyst adenomas) were the most common benign tumor and bile duct carcinoma the most common malignant neoplasia when hematopoietic tumors (i.e., lymphoma) are excluded from the hepatic neoplasia group. Clinical Pearl: Cholangitis and hepatic lipidosis are the most common primary acquired liver disease in cats. Table 1. The approximate incidence of feline liver disease based on histology reports of 175 consecutive liver biopsies performed at Colorado State University. Histologic diagnosis Percent Lipidosis 26% Cholangitis 25% Neoplasia 20% Reactive hepatopathies 16% Vascular anomalies 4% Toxic hepatopathies 5% Cystic lesions 2% Miscellaneous 2% Hepatic Lipidosis Lipidosis by definition is the abnormal accumulation of lipid (most often triglycerides) in the cytoplasm of the hepatocyte. Hepatic lipidosis can occur in cats as either a primary idiopathic disorder or secondary to a number of other primary disease conditions. Hepatic lipidosis is simply the result of nutritional, metabolic or toxic insults to the liver that results in abnormal lipid accumulation. This process can be quite variable and the process is completely reversible.6 Cats appear to be unique when it comes to hepatic lipid accumulation because primary lipidosis in the dog is very uncommon. Causes for lipidosis in cats are many. For example, a common secondary cause resulting in significant hepatic triglyceride accumulation is diabetes mellitus. This diagnosis is generally obvious (hyperglycemia and glycosuria) and the lipidosis resolves with appropriate therapy. Hepatic lipid accumulation can also result secondary to a number of other disease syndromes associated with anorexia and weight loss including conditions such as pancreatitis, inflammatory bowel disease or other major organ dysfunction. These secondary conditions generally have less severe lipidosis than occurs with idiopathic hepatic lipidosis.2 The prognosis for secondary hepatic lipidosis is entirely dependant on the primary etiology causing lipidosis. Clinical Pearl: Sick and anorectic cats from almost most any cause can develop secondary hepatic lipidosis. The etiology of idiopathic hepatic lipidosis is unknown and many theories have been put forward without substantial documentation. Some suggest that there is a defect in hepatic lipid mobilization resulting in the decreased ability for hepatic fat oxidation, decreased synthesis of apoproteins and decreased lipoprotein removal from the liver.6 The cause for the rapid mobilization of peripheral fat however is as yet unknown. A novel unpublished theory speculated by some is that the disease is one causing a primary central anorexia disorder that then resultants in fat mobilization and hepatic lipidosis. In any event it is important to investigate all possible secondary conditions leading to anorexia and the hepatic lipidosis. One study reported on a number of cats with acute pancreatitis resembling the classic idiopathic form of hepatic lipidosis.7 Cats with idiopathic hepatic lipidosis are generally older and obese cats that have undergone a stressful episode in the recent history that is then followed by a period of complete anorexia. There does not appear to be a breed or sex predisposition. Cats will present with an acute history of rapid weight loss (up to 40–60% body weight over 1–2 weeks), depression and icterus.6 The weight loss is significant and is characterized by significant loss of muscle mass while abdominal and inguinal fat stores are often spared. Typical neurological signs commonly associated with hepatic encephalopathy in the dog are uncommon. Complete anorexia, lethargy and depression may however be in part the result of hepatic encephalopathy. These cats generally always have a total aversion to any type of food. The diagnosis of idiopathic hepatic lipidosis is made by ruling out all secondary causes and is supported by the clinical history and laboratory findings. Icterus is common and is associated with a very high ALP and often normal or a disproportionate increase in GGT. ALT concentrations may be abnormal but quite variable in magnitude of elevation. Clinical Pearl: Elevated ALP with low GGT is often suggestive of hepatic lipidosis. Hypercholesterolemia, hyperammoniemia and abnormal bile acid levels are characteristic. About 1/3 of the cats have a nonregenerative anemia, hypokalemia and clotting abnormalities and about 1/2 the cats demonstrate poikilocytes in the RBC’s.2 Finding severe hypokalemia, anemia or other concurrent disease (i.e., pancreatitis) the lipidosis has a poorer survival rate.2 The liver size may be normal or enlarged on palpation or radiographically. A lipidosis liver is usually diffusely hyperechoic on ultrasound examination. A definitive diagnosis requires a liver biopsy or hepatic cytology. A fine needle aspirates of the liver with cytological evidence of many vacuolated lipid containing hepatocytes helps support a diagnosis. Be aware however that cytological diagnosis does not always correlate with histology. A needle aspirate is best obtained using ultrasound guidance. A hepatic tissue biopsy confirms the diagnosis of lipidosis but does not differentiate primary idiopathic lipidosis vs. lipidosis secondary to other conditions. Care should be taken when obtaining a liver biopsy as some cats may have coagulation abnormalities. The therapy for idiopathic hepatic lipidosis requires aggressive management.8 At our hospital approximately an 80% survival rate should be expected in cats given appropriate therapy and when no underlying disease is present. Initial therapy requires rehydration with balanced electrolyte solutions. Replacement of potassium deficits is imperative as normokalemia improves survival.2 Some cats may also require magnesium supplementation as well.8 Administration of glucose containing solutions may actually cause marked hyperglycemia in these patients and could result in a refeeding syndrome (see below). Cats also have a tendency to develop lactic acidosis and therefore lactate-containing fluids (i.e., Lactated Ringers) should be avoided. The practice of adding B-vitamins to the fluids should also be avoided because their prolonged exposure to light in the fluid bag could inactivate them and parenteral administration is a better option. Adequate nutrition then becomes the most important part of the therapy for hepatic lipidosis. Force-feeding or appetite stimulation is generally not adequate to meet caloric needs and tube feeding is the best way to administer adequate calories.9 Nasogastric tubes can be used but due to the small size feeding is limited to liquid diets and they are less tolerated than larger tubes. I suggests placement of either an esophageal or gastrostomy feeding tube. In our hospital we find that esophageal tubes to be well tolerated and having less complications than gastric tubes. One should refer to specific articles on tube placement techniques. I find the 20 French red rubber feeding tubes ideal for esophageal feeding tubes. The nutritional recommendations for idiopathic hepatic lipidosis are completely empirical and poorly documented. There are numerous reports in the literature suggesting various diets (with a variety of protein and fat content recommendations). In general, dietary fat and protein should not be restricted in these cats because calories and protein are so important in providing nutritional balance. I generally feed a canned nutritional recovery formulation. The caloric requirements should be calculated based on an ideal body weight. At the onset of feeding I give approximately 25% of the cats caloric needs divided over 4 to 6 feedings and then gradually increasing the amount fed over a week or so to get to their caloric requirements. Feeding too much volume or rapid feeding can result in vomiting and possibly a re-feeding syndrome. Clinical Pearl: Hepatic lipidosis is managed by feeding a balanced diet to meet the cat’s caloric requirements. Some authors suggest arginine (1000 mg/day), thiamine (100 mg/day) and taurine (500 mg/day) for 3–4 weeks.8,9 There is some evidence that L-carnitine supplementation in cats may protect against hepatic lipid accumulation (at least in weight reduction studies in cats) and consequently may be an appropriate dietary adjunct for cats with lipidosis.10 Carnitine is required for transport of long chain fatty acids into the mitochondria for subsequent oxidation and energy production. A deficiency of carnitine may lead to impaired mitochondrial function. It appears that carnitine deficiency could result in liver disease and that supplementation may help protect against encephalopathy, hypoglycemia, and subcellular damage. Studies have however have failed to show carnitine deficiency in cats with hepatic lipidosis.11 Suggested dose is 250–300 mg/day. Clinical Pearl: There is yet no good data to support the benefit of various dietary supplements. There is also evidence to suggest many cats with hepatic lipidosis have or will develop cobalamin (B12) deficiency.12 Experimental cobalamin deficiency in cats results in lethargy, anorexia and weight loss—the signs observed with lipidosis. Anecdotal reports suggest cats improve faster with high doses of cobalamin given 250 µg SQ weekly. Serum cobalamin levels should first be determined to document the presence of a deficiency. There is not enough cobalamin in the B-complex vitamins to replace a cobalamin deficiency. Some clinicians suggested administration of S-adenosylmethionine (SAMe) a molecule found in all living organisms that is involved in the metabolism of glutathione (GSH). GSH participates in many metabolic processes and plays a critical role in detoxification mechanisms of the cell. Depletion of hepatic GSH can indirectly cause toxic effects in these cells by increasing oxidative stress. Exogenous administered SAM has been shown to increase intracellular GSH levels in hepatocytes and prevents GSH depletion when exposed to toxic substances thus acting indirectly as an antioxidant.7 SAMe is also important in hepatocyte membrane integrity and function. The suggested dose is 100 mg/day. The benefit of SAMe or other antioxidants in hepatic lipidosis is unknown. Another antioxidant hepatoprotectant is milk thistle or its extract silibinin (available as a silibinin-phosphatidylcholine combination that improves GI absorption). The prognosis must be guarded in the recovery of lipidosis however with aggressive nutritional therapy many if not most cats recover. Several complications that can occur with therapy include a re- feeding syndrome and vomiting. The re-feeding syndrome is associated with the development of an often life-threatening electrolyte disturbances that occurs within 24 to 48 hours of enteral feeding.13 This is well described in humans occurring with introduction of nutrition and resultant increased insulin levels driving potassium, phosphorous and magnesium into the cells causing a critical depletion of these electrolytes in the blood. Vomiting is also a frequent complication associated with feeding. To avoid these problems electrolyte abnormalities should be first corrected and then followed by feeding small frequent meals usually starting out with 25% of the daily calculated caloric needs and gradually increasing the diet volume over 3 to 7 days. If vomiting persists I will sometimes use maropitant (Cerenea™) or other antiemetics. Maropitant is metabolized by the liver but the dose I use in cats with hepatic lipidosis is lower (0.25–0.5 mg/kg SO q 24 h with the normal cat dose being 1.0 mg/kg SQ q 24 h). When the cat is consuming adequate calories without the need for tube supplementation the feeding tube can be removed. Tube feeding may extend for up to 4–6 weeks. A failure to respond to traditional hepatic lipidosis therapy should signal the need to investigate the likelihood of an underlying condition in the patient. Feline Inflammatory Liver Disease (Cholangitis) Cholangitis is an inflammatory disorder of the hepatobiliary system. It is a disease complex and may be associated with duodenitis, pancreatitis, cholecystitis and/or cholelithiasis. The terminology is somewhat confusing and pathologists often name the conditions differently. Based on the histological classification of the WSAVA Liver Standardization Group they have been separated cholangitis into three basic histological groups; neutrophilic cholangitis, lymphocytic cholangitis and cholangitis associated with liver flukes (Figure 3).14 Neutrophilic Cholangitis. This classification has previously also been referred to as suppurative or exudative cholangitis /cholangiohepatitis and is the most common type of biliary tract disease observed in cats in North America. Neutrophilic cholangitis is thought to be the result of biliary tract infection ascending from the gastrointestinal tract. In the acute neutrophilic form (ANF), the lesions are exclusively neutrophilic or suppurative but over time it is thought that cases may progress to a chronic neutrophilic form (CNF) having a mixed inflammatory pattern containing variable numbers of neutrophils, lymphocytes and plasma cells. The ANF is thought to be the result of an ascending bacterial infection.15 Usually coliforms (E. coli) or Enterococcus spp are cultured from the liver or bile. Inflammation can also extend into the hepatic parenchyma causing a cholangiohepatitis. Cats with this syndrome tend to be middle aged or younger and present with acute illness of a week or less in duration. They may have evidence of a fever, anorexia, vomiting or lethargy. Cats are also frequently icteric. A leukocytosis is generally identified on the CBC. Typically because of the primary bile duct involvement the GGT concentrations are much higher proportionally than the ALP. The ALT and AST increase is variable depending on the amount of inflammation extending into the hepatic parenchyma. Ultrasound should always be performed to rule out pancreatitis and biliary obstruction. Fine needle aspirate cytology may show suppurative inflammation. In some cases we will also perform an ultrasound-guided cholecystocentesis for cytology and culture. An elevated feline PLI would support concurrent pancreatitis. A liver biopsy is required for histology and will confirm the diagnosis. The liver should always be cultured because of the relationship of bacteria and cholangitis. If obstruction is identified surgery becomes indicated to decompress and flush the biliary system. However, I always try to avoid performing surgical diversion surgery of the biliary system unless it is the last resort and suggest to the surgeon to try first to flush the extrahepatic biliary system. We sometimes will place a temporary biliary stent to maintain patency. Therapy for affected cats includes fluid and electrolyte support as needed but antibiotics are a critical part of the therapy. Ampicillin, ampicillin-clavulanic acid, cephalosporins and metronidazole have been suggested as effective antibiotics. Unless a culture and sensitivity directs otherwise ampicillin or ampicillin-clavulanic acid are my choice of antibiotic therapy because of the likelihood of E. coli and the fact that both are concentrated in the bile. It is recommended that cats be treated for at least 1 month or even longer with antibiotics. Short duration of therapy may result in reoccurrence of clinical signs. Ursodeoxycholic acid (Actigall 10–15 mg/kg/day) should be used as well for the benefit of choleresis and hepatoprotection. Abdominal discomfort and vomiting may be signs of hepatobiliary pain and buprenorphine or other pain management should be administered. Clinical Pearl: Neutrophilic cholangitis is secondary to ascending enteric bacteria and should be treated with appropriate antibiotic therapy. The CNF (neutrophilic, mixed or lymphocytic-plasmacytic) cholangitis may be the result of progression of the acute neutrophilic cholangitis. In the chronic stage the liver lesions are associated with the presence of a mixed inflammatory infiltrates in the portal areas consisting of neutrophils, lymphocytes and plasma cells.14,16 Possibly fibrosis, ductular proliferation or extension of inflammation into the hepatic parenchyma will occur as well. There is also a direct relationship between chronic cholangitis and inflammatory bowel disease and chronic pancreatitis. One study found 83% of affected cats had inflammatory bowel disease and 50% had concurrent chronic pancreatitis.17 The association of the three together has been referred to as “feline triaditis”. Possibly the common channel theory where the pancreatic ducts and bile ducts join before entering the duodenum explain this triad of clinical signs. Ascending bacteria initiate the acute disease and possibly then over time it can become chronic. In a yet to be published study we identified over 68% of affected cats with CNF to have of bacteria in and around bile ducts suggesting that resident bacteria may be responsible for the chronic inflammation.18 Affected cats are usually middle aged or older and have a long duration of signs lasting weeks to months. Presenting complaints are often vomiting, lethargy and anorexia. Signs may wax and wane and weight loss may be present. Physical findings identify jaundice in most, possibly hepatomegaly and rarely abdominal effusion. The laboratory findings are variable. Most cats are icteric and there are variable increases in ALP/GGT or ALT/AST. Hyperglobulinemia is observed in over 50% if the cases. Ultrasound may reveal pancreatic, bile duct or gallbladder changes. The liver generally has a mixed echogenicity pattern with prominent portal areas. Cats with concurrent pancreatitis may have an increase in feline pancreatic lipase immunoreactivity (fPLI). A liver biopsy confirms the diagnosis. Cultures should always be performed. The traditional treatment usually suggests immunosuppressive therapy using prednisolone at 2–4 mg/kg daily and then slowly tapering over 6 to 8 weeks to 0.5–1 mg/kg given once or every other day. However this therapy does not always resolve the chronic disease but may slows its progression or minimize the clinical signs. In the recent identification of bacteria in many cats having cholangitis indicates a rigorous course of antibiotic therapy for the possibility of a bacterial component would be indicated. Ursodeoxycholic acid is a nontoxic hydrophilic bile acid that when administered changes the bile acid milieu. Ursodeoxycholic acid (10–15 mg/kg/day) is nontoxic and suggested for these cats having cholangitis and in fact may even be more beneficial than corticosteroids. This drug is reported to increase bile flow (choleresis), change bile acid concentrations to less toxic concentrations, reduce inflammation and fibrosis and improve liver enzymes. Other liver support therapy such as SAMe, Silybum or other antioxidants may be of benefit in the long-term management. The disease is slow and progressive often characterized with periodic flair ups. Approximately 50% of the cases will have a prolonged survival. The final stage of this disease complex can be biliary cirrhosis associated with extensive fibrosis and bile duct proliferation that may end with liver failure associated with ascites and hepatic encephalopathy. Clinical Pearl: Always culture a liver biopsy. Lymphocytic Cholangitis. This is a condition (severe lymphocytic portal hepatitis, progressive lymphocytic cholangitis or nonsuppurative cholangitis) described to be a very chronic lymphocytic inflammatory biliary tract disorder that is progressive over months and years.14 The pathology of the liver is characterized by a consistent moderate to marked infiltration of small lymphocytes predominately restricted to the portal areas, often associated with variable portal fibrosis and biliary proliferation. The later stages result in considerable distortion of liver architecture. The bile ducts can also become irregular with dilation and fibrosis. In some cases lymphocytic infiltrates in the portal areas may be confused with well-differentiated lymphocytic lymphoma. Bacteria is not primarily involved in the pathogenesis of this syndrome.14 It is postulated that lymphocytic cholangitis is the result of immune mediated mechanisms based on preliminary immunologic studies.19 This syndrome as a slow chronic disease that continues to progress over months to years. It is often first identified in younger.20 The most common clinical features observed late in the disease include ascites, jaundice, and hypergammaglobulinemia (in almost all cases). In advanced cases, ultrasonographic examination often demonstrates dramatic changes intra and extra-hepatic bile ducts with marked segmental dilations and areas of stenosis that may lead the operator to believe there is an obstruction. Ascites and hepatic encephalopathy occur late in the disease as a result of acquired portal hypertension and hepatic dysfunction. The treatment for the chronic lymphocytic cholangitis involves using anti-inflammatory or immunosuppressive therapy in addition to supportive therapy as described with neutrophilic cholangitis. One yet unpublished study suggests lymphocytic cholangitis cases had a better response when treated with ursodeoxycholic acid than with corticosteroids.20 This finding may not be completely unexpected because ursodeoxycholic acid has been shown to have a positive treatment effect in humans having chronic primary biliary cirrhosis having a very similar histologic pattern to these chronic cases. Clinical Pearl: Lymphocytic cholangitis is best treated with immunosuppression and ursodeoxycholic acid. Complications of Cholangitis Syndromes. The following are conditions often observed with the cholangitis cases. Bile sludge and or cholelithiasis often occur with inflammatory biliary tract disease. Thick inspissated bile or choleliths are thought to be the result of deconjugation of the normally soluble conjugated bilirubin from the action of bacterial enzymes or inflammatory products present in the biliary tree. Bile sludging is best managed by treating the primary cholangitis, treating any biliary tract infection, and by the use of choleretic agents to increase the flow of bile. Ursodeoxycholic acid should be prescribed at 10–15 mg/kg/day. The concerns of using ursodeoxycholic acid for fear of a bile duct obstruction is unfounded in the author’s opinion and in fact experimental studies evaluating it in bile duct obstruction models showed less histological damage than the placebo group.21 Corticosteroids have a similar effect on bile flow and may also be useful. Complete obstructions may require surgery and in rare conditions a cholecystoduodenostomy or cholecystojejunostomy is required but should be avoided if at all possible because of the complication of ascending cholangitis. KEY DRUGS, DOSAGES AND INDICATIONS Key Drug Drug Class Dose Range Frequency Route Indications L carnitine Supplement 250–300 mg/cat Daily PO Lipidosis Cobalamin B vitamin 250 µg/cat Weekly SQ With deficiency Ursodeoxycholic acid Bile acid 10–15 mg/kg Daily PO Cholangitis S-adenosyl-methionine Antioxidant 90 mg/kg Daily PO Liver disease Sibilin Antioxidant 5 mg/kg Daily PO Liver disease SUMMARY There are two unique liver diseases in the cat and with accurate diagnostics one should be able to adequately manage most cases. No doubt in the future we will have a better understanding of these diseases and appropriate therapies. REFERENCES 1. Center SA, Baldwin BH, Dillingham S, et al. Diagnostic value of serum gamma-glutamyl transferase and alkaline phosphatase activities in hepatobiliary disease in the cat, J Am Vet Med Assoc 188:507, 1986. 2. Center SA, Crawford MA, Guida L, et al. A retrospective study of 77 cats with severe hepatic lipidosis: J Vet Intern Med 7:349, 1993. 3. Rothuizen J, van den Brom WE, Fevery J. The origins and kinetics of bilirubin in dogs with hepatobiliary and haemolytic diseases. J Hepatol. 1992 May;15(1–2):17–24 4. Sherding RG. Feline jaundice. J Feline Med Surg 2(3):165, 2000. 5. Ottenjann M, Weingart C, Arndt G, Kohn B. Characterization of the anemia of inflammatory disease in cats with abscesses, pyothorax, or fat necrosis. J Vet Intern Med 20(5):1143, 2006. 6. Center SA. Feline hepatic lipidosis. In Richards JR, editor: Veterinary clinics of North America small animal practice, Philadelphia, 2005, Saunders, pp 246, 253, 256, 260. 7. Akol KG, Washabau RJ, Saunders HM, Hendrick MJ. Acute pancreatitis in cats with hepatic lipidosis. J Vet Intern Med. 1993 Jul–Aug;7(4):205–9. 8. Holan KM. Feline hepatic lipidosis. In Bonagura JD, Twedt DC eds: Kirk’s Current Veterinary Therapy XIV, St Louis, 2008, Saunders/Elsevier p 570. 9. Griffin B. Feline hepatic lipidosis: Treatment recommendations. Compend Cont Educ Pract Vet 22(10):910, 2000. 10. Center SA, Harte J, Watrous D, et al. The clinical and metabolic effects of rapid weight loss in obese pet cats and the influence of supplemental oral L-carnitine. J Vet Intern Med 14(6):598, 2000. 11. Jacobs G, Cornelius L, Keene B, et al. Comparison of plasma, liver, and skeletal muscle carnitine concentrations in cats with idiopathic hepatic lipidosis and in healthy cats. Am J Vet Res 51(9):1349, 1990. 12. Simpson KW, Fyfe J, Cornetta A, et al. Subnormal concentrations of serum cobalamin (vitamin B12) in cats with gastrointestinal disease. J Vet Intern Med. 2001 Jan–Feb;15(1):26–32. 13. Justin RB, Hohenhaus AE. Hypophosphatemia associated with enteral alimentation in cats. J Vet Intern Med 9:228, 1995. 14. van den Ingh TSGAM, Cullen JM, Twedt DC, et al. Morphological classification of biliary disorders of the canine and feline liver. In: Rothuizen J, Bunch SE, Cullen JM, et al, eds. WSAVA standards for clinical and histological diagnosis of canine and feline liver diseases. Saunders/Elsevier: Edinburgh, 2006, p61. 15. Twedt DC, Armstrong PJ. Feline inflammatory liver disease. In Bonagura JD, Twedt DC eds: Kirk’s Current Veterinary Therapy XIV, St Louis, 2008, Saunders/Elsevier, p 576. 16. Gagne JM, Weiss DJ, Armstrong PJ. Histopathologic evaluation of feline inflammatory liver disease. Vet Pathol 33:521, 1996. 17. Weiss DJ, Armstrong PJ, Gagne J. Inflammatory liver disease. Semin Vet Med Surg (Small Anim) 12:22, 1997. 18. Twedt DC, Janeczko SD, McCord KW, et al. Culture-independent detection of bacteria in feline inflammatory disease. J Vet Intern Med 23:729, 2009. 19. Lucke VM, Davies JD. Progressive lymphocytic cholangitis in the cat. J Small Anim Pract 25:249, 1984. 20. Rothuizen J. Cholangitis in cats—a review, Proceedings of the 31st World Small Animal Congress, Prague, Czech Republic, 2006, p 47. 21. Frezza EE, Gerunda GE, Plebani M, et al. Effect of ursodeoxycholic acid administration on bile duct proliferation and cholestasis in bile duct ligated rat, Dig Dis Sci 38:1291, 1993.
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