Genetic Welfare Problems of Companion Animals

An information resource for prospective pet owners

Miniature Schnauzer

Pancreatitis and Hyperlipidaemia

Related terms: hyperlipaemia, hyperlipoproteinaemia, hypertriglyceridaemia, acute pancreatitis, chronic pancreatitis, diabetes mellitus, exocrine pancreatic insufficiency.

Outline: Miniature Schnauzers are predisposed to pancreatitis (lifetime risk of developing the disease may be about 5%) but the genetic basis of this predisposition is not clear at present. In this disease, digestive enzymes made in the pancreas for use in digestion of food in the intestine, become active in the tissue of the pancreas itself. The resulting damage can be acute and serious and can cause severe pain, but it is thought that more commonly, the diseases process is more gradual and this is likely to cause episodes of chronic lower-grade pain.

Summary of Information

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1. Brief description

The pancreas is situated in the abdomen, close to the small intestine and liver. It has two distinct functions. The first is an endocrine (hormonal) function: the regulation of the blood glucose level by secretion of the hormones insulin and glucagon. The second, its exocrine function, is the secretion of digestive enzymes (chemicals vital for the digestion of food) into the intestines. Various mechanisms exist to prevent these digestive enzymes from damaging the pancreas itself and the surrounding body tissues. However, when the pancreas is damaged, these chemicals and enzymes often become active inside the pancreas and cause significant damage. This can either be due to a sudden-onset severe disease (acute pancreatitis) causing destruction of the pancreas with significant systemic effects or a lower-grade process with local inflammation and scarring (chronic pancreatitis). Chronic pancreatitis is much more common than acute pancreatitis but is often symptom-less, with important signs only being seen late in the course of disease (Xenoulis 2008).

Pancreatitis can be caused by a variety of factors and the cause in a particular individual dog is often not known. A high fat diet, being overweight, exposure to certain drugs, trauma and disruption to the blood supply of the pancreas can all cause acute pancreatitis (Hess et al 1999). The predisposition of Miniature Schnauzers to the disease is probably related to their tendency to have high levels of triglycerides (fats) in the blood (see below) (Xenoulis et al 2010) but there is also evidence that they have a genetic defect affecting the function of pancreatic secretory trypsin inhibitor (Bishop et al 2007).

Pancreatitis probably develops because trypsin (a digestive enzyme which breaks down protein) becomes active within the pancreatic tissue and leads to the release of additional damaging enzymes. Damage to the pancreas leads to local inflammation, swelling, disruption of its blood supply, which can lead to death of parts or the entire pancreas. The damaged pancreatic tissue is susceptible to infection as bacteria move up the pancreatic duct from the intestine. Inflammatory products and toxins from the diseased pancreas enter the general circulation and cause effects elsewhere in the body (Kalli et al 2009). Dogs with acute pancreatitis often suffer from systemic effects (Kalli et al 2009).

Other consequences of pancreatitis can include: liver damage, diabetes mellitus, intestinal obstruction, abscesses in the pancreas, peritonitis and septicaemia (Kalli et al 2009).

The commonest clinical signs of pancreatitis itself are anorexia (loss of appetite), vomiting and diarrhoea, but many other signs may be seen including: weakness, depression, fever, haemorrhagic diarrhoea or sudden death (Lewis 2007).

One complication on recovery from acute pancreatitis is chronic pancreatitis. This can also occur without an initial acute episode. Chronic pancreatitis is a lower grade inflammatory condition that persists and leads to permanent damage of the pancreas and loss of pancreatic function (production of pancreatic juice and hormones) (Watson 2003). Ongoing chronic pancreatitis is often clinically silent (inapparent) until complications arise secondary to the loss of pancreatic function such as increased thirst due to diabetes mellitus or diarrhoea due to exocrine pancreatic insufficiency (see below). Chronic pancreatitis is therefore difficult to detect until a late stage when virtually all functional pancreatic tissue has been lost.

2. Intensity of welfare impact

Acute pancreatitis is thought to be always a painful condition even if the dog shows no obvious clinical signs of this (Xenoulis et al 2008). Bouts of acute pancreatitis also cause suffering from nausea, vomiting and diarrhoea, and from the malaise associated with depression and collapse (Hall et al 2003, Kalli et al 2009). Death from shock and multiple organ failure is frequent (Kalli et al 2009, Papa et al 2011).

Chronic pancreatitis is more common than the acute form, but mostly causes welfare problems when acute episodes occur. However, there must be concern that episodes of self-resolving abdominal pain occur in dogs with chronic pancreatitis without owners noticing.

There are also significant welfare impacts from the consequences of chronic pancreatitis. Diabetes mellitus often causes severe illness with vomiting, anorexia, collapse and death. Treatment of diabetes mellitus is often successful but may have adverse welfare effects through frequent veterinary visits, injections, forced changes to lifestyle through controlled feeding and exercise, and from possible side effects of treatment eg over-dosage of insulin often causes hypoglycaemia and the signs of weakness, collapse and, sometimes, death. Exocrine pancreatic insufficiency causes chronic hunger and unpleasant diarrhoea. Although veterinary treatment is often helpful, it has to be life-long and sometimes is difficult (Hall et al 2003).

3. Duration of welfare impact

Those dogs that recover from acute pancreatitis usually do so within a few days or a week but recurrence is quite common (Hall et al 2003; Kalli et al 2009). The outcomes from chronic pancreatitis have not been studied but it is assumed that most affected dogs will continue to have at least low-level disease and to be at risk of bouts of acute pancreatitis, the development of diabetes mellitus or the persistence of exocrine pancreatic insufficiency (Xenoulis et al 2008).

4. Number of animals affected

Around one third of Miniature Schnauzers have been shown to have an abnormally high blood triglyceride levels and are presumed to have idiopathic hyperlipidaemia (Xenoulis et al 2007).

Miniature Schnauzers are predisposed to pancreatitis and have the highest prevalence of this disease (Lewis 2007, Mori et al 2010). Lewis (2007) reported that, in a survey of in-patients at a chain of veterinary hospitals in the USA during 2006, 92 of 15,765 Miniature Schnauzers were found to have pancreatitis. This suggests a prevalence of 0.58% per annum. If we estimate lifespan in these dogs to average 10 years, then the risk of an individual developing the disease during its lifetime may be in the order of about 5%. As most cases of pancreatitis are chronic in nature, not acute, it is possible that this may be an underestimate (Xenoulis et al 2008).

From data on estimates of total dog population in the UK and on the percentage of all micro-chip registered dogs that are Miniature Schnauzers (Lucy Asher, 2011, personal communication), we estimate that the UK population size of this breed may be around 60,000.

5. Diagnosis

6. Genetics

The predisposition to pancreatitis seen in Miniature Schanuzers is assumed to be connected to their known predisposition to hyperlipidaemia (Whitney et al 1993, Xenoulis et al 2010). Investigations into the genetics of idiopathic hyperlipaemia in Miniature Schnauzers have been initiated but so far the cause has not been determined (Schickel et al 2005).

Mutant forms of the pancreatic secretory trypsin inhibitory gene (known as the SPINK1 gene) are widespread in the breed but it has been shown that this mutation is not the only factor contributing to the occurrence of pancreatitis (Bishop et al 2007, Bishop et al 2010).

7. How do you know if an animal is a carrier or likely to become affected?

Carriers (animals which pass the disease to their offspring without showing signs of it themselves) may exist but their importance in propagation of the disease is uncertain and detection is currently not possible.

Hyperlipidaemia can be evaluated by a simple and widely available blood test that measures levels of triglycerides and cholesterol. It seems reasonable to suggest that Miniature Schnauzers with hyperlipidaemia should not be bred as this is both an undesirable trait in itself and a marker for increased likelihood of acute and chronic pancreatitis and the associated diseases of diabetes mellitus and exocrine pancreatic insufficiency. However, the hyperlipidaemia may not appear until after the animal has been bred from and, as such, this test is not useful for testing puppies prior to purchase.

8. Methods and prospects for elimination of the problem

As far as we are aware, there are currently no programmes to reduce the incidence of hyperlipidaemia in Miniature Schnauzers.

Hyperlipidaemia is so common in Miniature Schnauzers (Xenoulis et al 2007) that attempting to breed only from unaffected individuals could cause a significant reduction in the gene pool that might lead to other serious unintended consequences on the health of the population. This could be avoided or alleviated by out-crossing with dogs of unaffected breeds.

For further details about this condition, please click on the following:
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1. Clinical and pathological effects

The pancreas is situated in the abdomen, close to the small intestine and liver. It has two distinct functions. The first is an endocrine (hormonal) function: the regulation of the blood glucose level by secretion of the hormones insulin and glucagon. The second, its exocrine function, is the secretion of digestive enzymes (chemicals vital for the digestion of food) into the intestines. Of these, only around 2% of pancreatic cells (the islets of Langerhans) are involved in the endocrine function. Most are involved in the exocrine, with the production of enzymes, chemicals and fluids that flow, via the main pancreatic ducts, into the small intestine as “pancreatic juice”. The main chemical in this juice is bicarbonate which acts to neutralise the acid produced in the stomach. Enzymes are proteins that act as catalysts in the chemical reactions that break down foodstuffs into molecules small enough to pass through the intestinal wall. These enzymes include: proteases that break down protein into amino acids; pancreatic lipase and phospholipase that break down fats; nucleases that breakdown nucleic acids (DNA and RNA) and pancreatic amylase that breaks down starch and glycogen. Some of the enzymes are secreted as inactive forms that only become active and able to contribute to digestion once activated in the small intestine.

Various mechanisms exist to prevent these potentially corrosive chemicals and enzymes from damaging the pancreas and the surrounding body tissues. The particularly dangerous enzymes, such as trypsin which breaks down proteins, are stored in the pancreas as inert proenzymes eg trypsinogen. These become activated by substances produced in the duodenum (the first part of the small intestine). Other enzymes, in turn, are only activated once exposed to trypsin itself. A second protective mechanism is the presence of enzyme inhibitory substances within the pancreas, which are produced both by the organ and are found in the circulating blood (Kalli et al 2009). There is evidence from investigations into the genetics of pancreatitis in Miniature Schnauzers that one of these inhibiting substances is defective (Bishop et al 2007).

When the pancreas is damaged, these chemicals and enzymes often become active inside the organ and cause significant damage. This can occur as a sudden-onset, severe disease (acute pancreatitis) causing destruction of the pancreas with significant systemic effects (effects throughout the body) or as a lower-grade process with local inflammation and scarring (chronic pancreatitis). Chronic pancreatitis is much more common than acute pancreatitis. It is often clinically silent, that is, inapparent, with signs only being seen late in the course of disease (Xenoulis 2008). Repeat bouts of mild but acute pancreatitis occur in some individuals (Hall et al 2003).

Pancreatitis can be caused by a variety of factors and the cause in a particular individual is often not known. A high fat diet, being overweight, exposure to certain drugs, trauma and disruption to the blood supply of the pancreas, may all cause acute pancreatitis (Hess et al 1999). The predisposition of Miniature Schnauzers to the disease is probably related to their tendency to have high levels of triglycerides (fats) in the blood (see below) (Xenoulis et al 2010) but there is also evidence that they have a genetic defect affecting the function of pancreatic secretory trypsin inhibitor (Bishop et al 2007).

Miniature Schnauzers are predisposed to idiopathic hyperlipidaemia (high levels of fat in the blood for an unknown reason) (Ford 1993, Whitney et al 1993, Stockham & Scott 2002, Xenoulis et al 2007). This is recognised most often in middle-aged and older Miniature Schnauzers and tends to worsen with age (Barrie and Watson 1995, Xenoulis et al 2007). The lipids (fats) include triglyceride and cholesterol. Triglycerides are used as cellular energy reserves and cholesterol is largely used as a component of hormones and cellular structures. Miniature Schnauzers are prone to high blood levels of triglyceride, and cholesterol levels are also sometimes elevated, especially in more advanced disease.

In general, high levels of fats in the blood are usually due to the recent eating of a fatty meal or to metabolic diseases but they can also be caused by a defect in lipid (fat) metabolism. Lipids are carried in the blood, to and from the intestines, liver and other tissues, in complexes that they form with proteins, and these are known as lipoproteins. There are four types of lipoproteins: chylomicrons, very low density lipoproteins (VLDLs), low density lipoproteins (LDLs), and high density lipoproteins (HDLs) (Duncan 2005). In affected Miniature Schnauzers the concentration of VLDLs, and sometimes also the number of chylomicrons, is increased (Whitney et al 1993). The particular defect in Miniature Schnauzers that causes this, has not been determined but the possibilities include: increased production of VLDLs; reduced activity of the enzyme (lipoprotein lipase) that breaks down VLDLs; low levels of one of the proteins important in forming lipoproteins; or a defect in a liver cell receptor that compromises the normal processing of fats by the liver (Bauer 2000, Stockham and Scott 2002, Jaeger et al 2003).

One study showed that, while all members of the breed were predisposed, female Miniature Schnauzers are more likely to develop hyperlipidaemia than males (Mori et al 2010). However, in another, no differences were found in lipid levels between the sexes (Xenoulis et al 2007).

The high levels of triglycerides may cause abdominal pain, lack of appetite, vomiting, diarrhoea and seizures (Duncan 2005, Jaeger et al 2003). High triglyceride levels are an important factor in the development of pancreatitis in humans and it is likely that this is also the case in dogs (Whitney et al 1993, Yadav & Pitchumoni 2003, Kalli et al 2009; Xenoulis et al 2008). It has been shown that high blood triglyceride levels are associated with high levels of a blood marker of pancreatic damage (Xenoulis et al 2010).

Pancreatitis is probably due to the enzyme trypsin becoming active within the pancreas and triggering activity of other enzymes too. Damage to the pancreas leads to local inflammation and swelling. Disruption to its blood supply can lead to the death of parts, or the entire, pancreas. The damaged tissue is also susceptible to infection by bacteria moving up the pancreatic duct from the intestine. Inflammatory products and toxins from the diseased pancreas enter the general circulation and cause effects elsewhere in the body (Kalli et al 2009). Dogs with acute pancreatitis often suffer from systemic effects – systemic inflammatory response syndrome (SIRS), in which circulation collapses and breathing is compromised - and which leads to multiple organ failure and death in many cases (unless this can be averted through intensive care). Problems with blood clotting are also seen, with thrombus (clot) formation, emboli (clots free floating in the blood) and, paradoxically, an increased tendency to bleed (disseminated intravascular coagulopathy). Both peritonitis (infection and inflammation in the abdominal cavity) and septicaemia (blood poisoning) may occur (Kalli et al 2009).

Pancreatic damage often also results in obstruction of the bile duct, which conveys bile from the liver to the duodenum and which travels through the pancreas, leading to jaundice and liver damage. Local inflammatory products and toxins, as well as bacteria from the intestine can also contribute to liver damage and failure secondary to pancreatitis (Kalli et al 2009).

Acute pancreatitis may additionally cause diabetes mellitus if pancreatic tissue damage is extensive enough to effect the production of insulin in the cells of the Islets of Langerhans, and thus to compromise the control of blood glucose levels. This was found to occur in 36% of dogs with severe acute pancreatitis in one study (Papa et al 2011). Some dogs recover from acute pancreatitis but develop an abscess in the pancreas that causes more chronic (longer-term) illness (Kalli et al 2009). Scar tissue around the pancreas can sometimes cause intestinal obstruction.

The commonest clinical signs of pancreatitis are inappetance (anorexia), vomiting, and diarrhoea. There can be many other signs including weakness, depression, fever, haemorrhagic (bloody) diarrhoea or sudden death (Lewis 2007). Abdominal pain is obvious in about 15% of affected dogs (Lewis 2007) and, in attempting to alleviate the pain, some dogs will adopt a “praying” body position with the head lowered, the fore-legs stretched out in front and the rear end raised (Kalli et al 2009).

The prognosis for recovery from acute pancreatitis is very variable. One recent study suggested that the death rate is around 40% (Papa et al 2011). A scheme to predict prognosis, based on the number of additional disease consequences has been proposed but assumes that there is comprehensive veterinary attention. The existence of the following criteria were considered as significant: marked white blood cell response in the blood, significant liver damage, kidney failure, disruption of blood acidity or high glucose levels. When only one of these was present the death rate was 11%; when three were of these factors were found the death rate was 66%, and all dogs died when four or five of these factors were involved (Ruaux and Atwell 1998, Ruaux 2000).

One complication on recovery from acute pancreatitis is chronic pancreatitis. Chronic pancreatitis can also occur without an initial acute episode. Chronic pancreatitis is a lower grade inflammatory condition that persists and leads to permanent damage of the pancreas and loss of pancreatic function (Watson 2003). Ongoing chronic pancreatitis is often clinically silent, that is, symptom-less until complications arise secondary to the loss of pancreatic function such as increased thirst and urine production due to diabetes mellitus. It is, therefore, difficult to detect until the late stages when virtually all functioning pancreatic tissue has been lost. Exocrine pancreatic insufficiency (EPI) occurs when the damage has been of such severity that not enough pancreatic juice is produced for digestion. The main signs of EPI re intractable diarrhoea and weight loss despite a normal or excessive appetite (Hall et al 2003, Watson 2003). (Chronic pancreatitis, however, is not the commonest cause of EPI in dogs [Hall et al 2003]).

Dogs with chronic pancreatitis are probably also more likely to have bouts of acute pancreatitis.

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2. Intensity of welfare impact

Acute pancreatitis is thought to be always a painful condition, even if the dog shows no obvious clinical signs of this (Xenoulis et al 2008). Certainly, it is known to be a painful condition in humans. In attempting to alleviate the pain, some dogs will adopt a “praying” body position - with their head lowered, the fore-legs stretched out in front and the rear end raised (Kalli et al 2009). Bouts of acute pancreatitis also cause suffering from nausea, vomiting and diarrhoea, and from the malaise associated with depression and collapse (Hall et al 2003, Kalli et al 2009). Death from shock and multiple organ failure is frequent (Kalli et al 2009, Papa et al 2011).

There are also significant welfare impacts from the consequences of chronic pancreatitis. Diabetes mellitus often causes severe illness with vomiting, anorexia, collapse and death. Treatment of diabetes mellitus is often successful but may have adverse welfare effects through the frequent veterinary visits, injections, forced changes to lifestyle through controlled feeding and exercise, and from possible side effects of treatment eg over-dosage of insulin often causes hypoglycaemia and signs of weakness, collapse and, sometimes, death. Exocrine pancreatic insufficiency causes chronic hunger and unpleasant diarrhoea. Although veterinary treatment is often helpful, it has to be life-long and sometimes is difficult (Hall et al 2003).

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3. Duration of welfare impact

Those dogs that recover from acute pancreatitis will usually do so within a few days or a week but recurrence is quite common (Hall et al 2003; Kalli et al 2009). The outcomes from chronic pancreatitis have not been studied but it is assumed that most affected dogs will continue to have at least low-level disease and to be at risk of bouts of acute pancreatitis, the development of diabetes mellitus or the persistence of exocrine pancreatic insufficiency (Xenoulis et al 2008) throughout their life.

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4. Number of animals affected

Around one third of Miniature Schnauzers have been shown to have an abnormally high blood triglyceride levels and are presumed to have idiopathic hyperlipidaemia (Xenoulis et al 2007).

Miniature Schnauzers are predisposed to pancreatitis and have the highest prevalence of this disease (Lewis 2007, Mori et al 2010). Lewis (2007) reported that the overall prevalence of acute pancreatitis in dogs admitted during 2006 to a multi-centre practice in the USA was 23 cases per 10,000 patients per year. The prevalence in Miniature Schnauzers was about twice this. Lewis (2007) reported that, in this survey, 92 of the total of 15,765 Miniature Schnauzers admitted were found to have pancreatitis. This suggests a prevalence of 0.58% per annum. If we estimate lifespan of dogs of this breed to average 10 years, then the risk of an individual developing the disease during its lifetime may be in the order of about 5%. As most cases of pancreatitis are chronic in nature, not acute, it is possible that this may be an underestimate (Xenoulis et al 2008).

From data on estimates of total dog population in the UK and on the percentage of all micro-chip registered dogs that are Miniature Schnauzers (Lucy Asher 2011, personal communication), we estimate that the UK population size of this breed may be around 60,000.

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5. Diagnosis

The diagnosis of acute pancreatitis is not straightforward (Hess et al 1998). The presentation is similar to that of many diseases of other abdominal organs (Hall et al 2003, Kalli et al 2009). The diagnosis of chronic pancreatitis is even more difficult and may depend on repeated diagnostic tests in order to detect bouts of mild acute pancreatitis which are indicative of ongoing chronic pancreatitis (Xenoulis et al 2008). Blood tests can be helpful in making the diagnosis of acute pancreatitis, especially the test for canine pancreatic lipase immunoreactivity (cPLI) or canine specific pancreatic lipase (Spec cPL). Imaging of the cranial abdomen, especially using ultrasound or CT scans may be helpful in diagnosis of both conditions (Kalli et al 2009, Xenoulis et al 2008). Determining the underlying cause is usually impossible although there may be a clue from the history (Kalli et al 2009). Hyperlipidaemia can be a consequence of pancreatitis as well as a cause of it, so the presence of high blood triglyceride levels in a dog with pancreatitis does not mean that this was the cause, even in a Miniature Schnauzer (Xenoulis et al 2008).

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6. Genetics

The Miniature Schnauzer’s breed predisposition to pancreatitis is assumed to be associated with its predisposition to hyperlipidaemia (Whitney et al 1993, Xenoulis et al 2010). Investigations into the genetics of idiopathic hyperlipaemia in the breed, based on the 105 genetic mutations known in analogous disease in humans, have been initiated, but so far the cause has not been determined (Schickel et al 2005).

In humans, several mutant genes have been identified that are associated with pancreatitis (cationic trypsinogen gene, cystic fibrosis transmembrane regulator gene, pancreatic secretory trypsin inhibitor [PSTI] gene) (Ellis 2004). It has been found that affected Miniature Schnauzers are more likely to be homozygous for mutant forms of the pancreatic secretory trypsin inhibitory gene (known as the SPINK1 gene) than those that are unaffected. This mutation is widespread in the breed but it has been shown that it is not the only factor contributing to the occurrence of pancreatitis (Bishop et al 2007, Bishop et al 2010). Further investigations into the genetic basis of the disease have so far been unsuccessful (Bishop et al 2004, Schickel 2005, Schickel et al 2005, Sahin-Tóth et al 2006).

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7. How do you know if an animal is a carrier or likely to become affected?

The recent work indicating that dogs homozygous for the mutant SPINK1 gene have increased risk of pancreatitis suggests that there is a possibility that carriers (animals which can pass the disease to their offspring but which are unaffected themselves) may exist but it is too early to draw firm conclusions. Hyperlipidaemia can be evaluated by a simple and widely available blood test (measuring levels of triglycerides and cholesterol). Blood must be taken after a 12-16 hour period of starvation (Duncan 2005). It seems reasonable to suggest that Miniature Schnauzers with hyperlipidaemia should not be used for breeding as hyperlipidaemia is both an undesirable trait in itself and a marker for the increased likelihood of acute and chronic pancreatitis and its associated diseases of diabetes mellitus and exocrine pancreatic insufficiency. However, hyperlipidaemia may not develop until after the animal has been used for breeding and, as such, the test is not useful for testing puppies prior to purchase. There may be a case for testing of parents and grandparents to ensure that these do not have hyperlipidaemia.

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8. Methods and prospects for elimination of the problem

As far as we are aware, there are currently no programmes aimed at reducing the incidence of hyperlipidaemia in Miniature Schnauzers.

It may be advisable to avoid purchasing puppies with close relatives (siblings, parents, siblings of parents) that are known to have suffered from any form of hyperlipidaemia, pancreatitis or diabetes mellitus (Bell 2010).

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9. Acknowledgements

UFAW is grateful to Rosie Godfrey BVetMed MRCVS and David Godfrey BVetMed FRCVS for their work in compiling this section.

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10. References

Barrie J and Watson TDG (1996) Hyperlipidemia. In: Bonagura JD (editor) Kirk’s Current Veterinary Therapy XII Small Animal Practice pp 430-434. WB Saunders: Philadelphia, USA

Bauer JE (2000) Hyperlipidemia. In: Ettinger SJ and Fledman EC (eds) Textbook of Veterinary Internal Medicine 5th edition pp 283-292. WB Saunders: Philadelphia, USA

Bell JS (2010) Genetic Testing and Genetic Counselling in Pet and Breeding Dogs. World Small Animal Veterinary Association World Congress Proceedings

Bishop MA, Steiner JM, Moore LE and Williams DA (2004) Evaluation of the cationic trypsinogen gene for potential mutations in Miniature Schnauzers with pancreatitis. Canadian Journal of Veterinary Research68: 315–318

Bishop MA, Xenoulis PG, Suchodolski JS and Steiner JM (2007) Identification of three mutations in pancreatic secretory trypsin inhibitor gene of Miniature Schnauzers. Proceedings of the American College of Veterinary Internal Medicine (abstract): 151

Bishop MA, Xenoulis PG, Levinski MD, Suchodolski JS and Steiner JM (2010) Identification of variants of the SPINK1 gene and their association with pancreatitis in Miniature Schnauzers. American Journal of Veterinary Research 71: 527-533

Duncan J (2005) Laboratory evaluation of lipids. In: Villiers E and Blackwood L (eds) BSAVA Manual of Canine and Feline Clinical Pathology 2nd edition pp 241-246. British Small Animal Veterinary Association: Cheltenham, UK

Ellis I (2004) Genetic counseling for hereditary pancreatitis—the role of molecular genetics testing for the cationic trypsinogen gene, cystic fibrosis and serine protease inhibitor Kazal type 1. Gastroenterology Clinics of North America 33: 839-854

Ford RB (1993) Idiopathic hyperchylomicronaemia in Miniature Schnauzers. Journal of Small Animal Practice 34: 488-492

Kalli I, Adamama-Moraitou K and Rallis TS (2009) Acute pancreatitis in dogs: a review article. European Journal of Companion Animal Practice 19: 147-155

Hall EJ, Murphy KF and Darke PGG (2003) Pancreas. In: Notes on Canine Internal Medicine pp 194-197. Blackwell Publishing: Oxford, UK

Hess RS, Saunders HM, Van Winkle TJ, Shofer FS and Washabau RJ (1998) Clinical, Clinicopathologic, Radiographic, and Ultrasonographic Abnormalities in Dogs with Fatal Acute Pancreatitis: 70 Cases (1986-1995) 1998. Journal of the American Veterinary Medicine Association 213: 665-670

Hess RS, Kass PH, Shofer FS, Van Winkle TJ and Washabau RJ (1999) Evaluation of Risk Factors for Fatal Acute Pancreatitis in Dogs. Journal of the American Veterinary Medical Association 214: 46-51

Jaeger JQ, Johnson S, Hinchcliff KW, Sherding R, Jensen W, Brunzell J and Murdock S (2003) Characterization of Biochemical Abnormalities in Idiopathic Hyperlipidemia of Miniature Schnauzer Dogs. Proceedings of the American College of Veterinary Internal Medicine

Lewis HB (2007) Risk factors for canine pancreatitis. Available at: http://www.banfield.com/Banfield/files/ae/ae47fac6-da51-4de4-8bc8-f735f8324313.pdf. Accessed 31.5.2011

Mori N, Lee P, Muranaka S, Sagara F, Takemitsu H, Nishiyama Y, Yamamoto I, Yagishita M and Arai T (2010) Predisposition for primary hyperlipidemia in Miniature Schnauzers and Shetland sheepdogs as compared to other canine breeds. Research in Veterinary Science 88: 394-399

Papa K, Máthé A, Abonyi-Tóth Z, Sterczer A, Psáder R, Hetyey C, Vajdovich P and Vörös K (2011) Occurrence, clinical features and outcome of canine pancreatitis (80 cases). Acta Veterinaria Hungarica 59: 37-52

Ruaux CG and Atwell RB (1998) A severity score for spontaneous canine acute pancreatitis. Australian Veterinary Journal 76: 804-808

Ruaux CG (2000) Pathophysiology of organ failure in severe acute pancreatitis in dogs. Compendium of Continuing Education for the Practising Veterinarian 22: 531-543

Sahin-Tóth M, Sahin-Tóth V, Schickel R and Steiner JM (2006) Mutations of the Trypsinogen Gene Associated with Pancreatitis in Humans Are Absent from the Gene for Anionic Trypsinogen of Miniature Schnauzers with Pancreatitis. 16th European College of Veterinary Internal Medicine-Companion Animals Congress

Schickel R (2005) Identification of the nucleotide sequence of the lipoprotein lipase gene as well as its role in the development of hyperlipidemia and pancreatitis in the Miniature Schnauzer [Dr med vet thesis]. Munich: Ludwig-Maximilians University

Schickel R, Steiner JM, Cox ML and Williams DA (2005) Evaluation of Seven Exons of the Lipoprotein Lipase Gene in Miniature Schnauzers with Hypertriglyceridemia and Pancreatitis Proceedings of the American College of Veterinary Internal Medicine

Stockham SL and Scott MA (2002) Lipids. In: Stockham SL and Scott MA 2002 Lipids. In: Fundaments of Veterinary Clinical Pathology pp 529- 537. Iowa State Press: Ames, Iowa USA pp 529- 537. Iowa State Press: Ames, Iowa USA

Watson PJ (2003) Exocrine pancreatic insufficiency as an end stage of pancreatitis in four dogs. Journal of Small Animal Practice 44: 306-12

Whitney MS, Boon GD, Rebar AH, Story JA and Bottoms GD (1993) Ultracentrifugal and electrophoretic characteristics of the plasma lipoproteins of Miniature Schnauzer dogs with idiopathic hyperlipoproteinemia. Journal of Veterinary Internal Medicine 7: 253–260

Yadav D and Pitchumoni CS (2003) Issues in hyperlipidemic pancreatitis. Journal of Clinical Gastroenterology 36: 54-62

Xenoulis PG, Suchodolski JS, Levinski MD and Steiner JM (2007) Investigation of Hypertriglyceridemia in Healthy Miniature Schnauzers. Journal of Veterinary Internal Medicine 21: 1224–1230

Xenoulis PG, Suchodolski JS and Steiner JM (2008) Chronic pancreatitis in dogs and cats. Compendium of Continuing Education for the Practising Veterinarian 30: 166–181

Xenoulis PG, Suchodolski JS, Ruaux CG, Jörg M and Steiner JM (2010) Association Between Serum Triglyceride and Canine Pancreatic Lipase Immunoreactivity Concentrations in Miniature Schnauzers. Journal of the American Animal Hospital Association 46: 229-234

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Animal Welfare Information

Genetic Welfare Problems of Companion Animals

Miniature Schnauzer

Pancreatitis and Hyperlipidaemia

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Summary of Information

1. Clinical and pathological effects

2. Intensity of welfare impact

3. Duration of welfare impact

4. Number of animals affected

5. Diagnosis

6. Genetics

7. How do you know if an animal is a carrier or likely to become affected?

8. Methods and prospects for elimination of the problem

9. Acknowledgements

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Please help

10. References

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Animal Welfare Information

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Genetic Welfare Problems of Companion Animals

Miniature Schnauzer

Pancreatitis and Hyperlipidaemia

Please help

Summary of Information

1. Clinical and pathological effects

2. Intensity of welfare impact

3. Duration of welfare impact

4. Number of animals affected

5. Diagnosis

6. Genetics

7. How do you know if an animal is a carrier or likely to become affected?

8. Methods and prospects for elimination of the problem

9. Acknowledgements

Please help If you found this information useful please donate to help us keep it up to dateDonate now

Please help

10. References

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