Prevalence of acromegaly, Cushing’s disease and pancreatitis
in cats with diabetes
Theo Vlamings
Research internship article
Supervised by H.S. Kooistra
Feb 2011 - Okt 2013
Acknowledgements
I would like to thank my fellow students for joining in on this research and help gather
samples to increase statistical significance in our results. And M. Kuyten in particular for the
interesting debates on the subject of diabetes. The clinics in Eindhoven and Best were also
most helpful in their aid to gather clients with diabetic cats to participate in this research,
and further supported me in my quest to gather the (last) milliliters of blood required. I
would like to thank dr. H.S. Kooistra for providing me with this interesting subject to
research, and for his help whenever I needed it. Finally, I would like to give thanks to Laura
Stokhof for her support in finalizing this report.
Contents
Achknowledgements
Contents
Abstract
Introduction
Diabetes Mellitus
Etiology
Signs and complications
Aim of this research
Materials and methods
Results
Discussion
Conclusion and recommendations
References
Appendix
Abstract
The regulation of cats with diabetes is a difficult path with countless factors that can
complicate matters. Recognizing acromegaly, Cushing’s disease or pancreatitis in an early
stage can aid in both the therapeutic path ahead as well as the prognosis. 138 cats with
diabetes in the Netherlands have been examined for aforementioned diseases, they have
undergone physical examination and lab tests have been done on their blood and urine.
Particularly in the case of acromegaly, the high prevalence found in this study (31,1%) is in
line with recent research. What immediately draws notice is the increased prevalence in
male cats (39,1%) compared to female specimens (11,4%). Which could prove to be
additional leverage in veterinary practice in the decision whether or not to test a cat when
the diagnosis of diabetes has been made. Diagnosing pancreatitis and Cushing’s disease is
challenging, and the absence of an affordable yet reliable test made it difficult to provide
significant data regarding these conditions.
Introduction
Diabetes mellitus (DM) is a disease that affects many species of animals as well as humans.
What is interesting is that there are some differences have been found between the types of
diabetes that commonly affect these animals. For example, dogs seem to suffer more from a
congenital form of diabetes or as a result of concurrent disease or corticoid therapy. Cats as
well as humans, however, seem to be often affected by diabetes as a result of their lifestyle. 1
The trend in human lifestyle is that we slowly transition to a sugar-rich diet with processed,
short chain carbohydrates.2 While cats usually don’t eat a great deal of sugar, they are often
provided with very energy-dense diets. Cats also tend to have a more dormant lifestyle in
the current age; rather than hunting to meet their dietary requirements, they are kept
indoors with their meals provided for them at regular intervals by their owners. While there
is currently no proof that indoor cats are predisposed to acquire diabetes as opposed to
outdoor cats, the resulting obesity from eating too much and exercising too little has proven
to be a predisposing factor. 3
When at least part of the cause of diabetes stems from the management and daily care of
the cat, one implies that the owner is at fault. While this could be true, there is a primary
role for the veterinarian to provide the owner with information about the risk factors that
play a role in this disease. Then, if the veterinarian could be convinced that the owner
provides the correct care for their cat, one could start sooner on the diagnostic steps to
prove or disprove any concurrent diseases in a diabetic cat. However, in order to have a
sound diagnostic plan to do this, it is necessary to know the prevalence of the various
diseases that can cause DM in cats. This was the veterinarian can make a good judgment call
of the value of these tests in each individual diabetic cat.
A recent study in the United Kingdom showed that 59 out of the 184 diabetic cats examined
had elevated plasma IGF-1 levels. Of these 59 cats, 18 were further examined and 17 were
found to have acromegaly. (2) Another study showed that of 24 diabetic cats, 4 were found
to have (pituitary-dependent) hyperadrenocorticism and 4 were diagnosed with
acromegaly.4
Diabetes mellitus
Etiology
For a long time, there has been a division of diabetes into four types; the congenital type 1
where a patient’s autoimmune system is targeting pancreatic cells. Type 2 is acquired as a
result of increased insulin resistance and decreased production of insulin by the pancreatic
Beta cells. Type 3 is caused by another disease such as Cushing’s Disease or acromegaly.
Type 4 diabetes can arise during pregnancy. In cats, only type 2 and type 3 as described here
are commonly found. What all types have in common is that there is an insulin deficiency,
which leads to an increase in glycogenolysis and gluconeogenesis, and a decrease in glucose
consumption by the tissues. These three effects together create an increase of plasma
glucose.5
Diabetes type 2 in man shows some degree of genetic predisposition in certain populations.
This also seems to be the case with DM in cats, where the Burmese cat is overrepresented
when compared to other pure breed cats. 6 Recent research shows that this may be related
to their tendency towards a deregulated lipid metabolism, due to which even lean Burmese
cats are shown to have higher percentages of very low density cholesterol compared to
obese domestic cats. 7
In addition to obesity there are several other risk factors that contribute to insulin resistance
and which may result in diabetes. Glucocorticoid excess is an example of such a factor,
whether provided as therapy or through an increased endogenous production.
Pheochromocytoma, pregnancy and acromegaly can also cause increased insulin resistance.
The sex of a cat is a risk factor as well, since male cats have a higher insulin resistance than
female cats. Finally, inflammatory diseases may also cause insulin resistance. 8, 9 So obesity
may not be directly linked to diabetes in current literature despite the increased amount of
apodikines in both different kinds as in absolute amounts. Because of the pro inflammatory
effect of apodikines such as interleukine and tumor necrosis factor there is an indirect link to
increased insulin resistance. 10 It has even been calculated in a previous research that each
kilogram of bodyweight in cats leads to about a 30% loss in insulin sensitivity and glucose
effectiveness. 11
Increased resistance to insulin by itself does not lead to diabetes. In most cases, this is
compensated for through an increased production of insulin. However, if the insulin
resistance is profound or of long enough duration, hyperglycemia and eventually glucosuria
and diabetes can develop. It has been hypothesized that this was due to glucose toxicity or
amyloid deposition but the details in these remain unclear. The exact pathophysiologic
mechanism that causes the beta cells of the pancreas to fail in keeping up with the increased
insulin demand remains unclear.
Signs and complications
When the blood glucose level rises beyond 14-16 mmol/l the renal capacity to reabsorb
glucose from the urine is exceeded and causes glucosuria. 12 As these glucose modules are
osmotic they will cause an osmotic diuresis and thus polyuria. This is often accompanied
with polydipsia, but dehydration is not uncommon and therefore fluid intake should always
be monitored. If the glucosuria persists it may lead to weight loss due to the energetic value
of the glucose lost, which causes additional breakdown of muscle protein into glucose. In
some cases however, this weight loss is not as profound as in other due to an increase in
appetite. The increased plasma glucose levels can also give cause for diabetic neuropathy to
develop. This presents itself with muscle weakness of the hind legs.
As a result of decreased intracellular glucose in the absence of sufficient insulin, more
triglycerides will breakdown into acetone, β-hydroxybutyrate and acetoacetate, also known
as ketone bodies. The chemoreceptor trigger zone in the medulla oblongata is susceptible to
these ketone bodies, which can cause a patient to vomit or become anorexic due to nausea.
These ketone bodies further contribute to the osmotic diuresis already in place, which can
lead to a profound dehydration, hypovolemia, hypokalemia and acidosis that is seen during
diabetic ketoacidosis. A recent study in dogs show that during diabetic ketoacidosis, some
dogs show normal levels of insulin, showing that a period of insulin resistance due to a
secondary disease could also be a factor in cats in causing diabetic ketoacidosis. 13
Hyperosmolar hyperglycemic state is characterized by a marked increase in plasma glucose
and plasma osmolarity with often dehydration, hypokalemia and acid-base abnormalities. It
has also been known in the past as hyperosmolar nonketotic coma, but it was found that
ketone bodies were sometimes present as well, while coma often was not. The exact cut off
values of plasma osmolarity (>320->350 mOsm/kg) and blood glucose (>30 mmol/L) on
which the diagnosis of hyperosmolar hyperglycemic state is made, varies between different
studies. 5, 14
Aim of this research
The current paradigm among Dutch veterinarians regarding feline diabetes is that other
disease processes play a minor role in its pathogenesis. Recent research indicates that
acromegaly may be a more important factor than was previously assumed to be the case.
There is even less information available on the prevalence of pancreatitis and Cushing’s
disease in cats with diabetes. Regulating a cat with diabetes is not an easy task, and even
though the odds of remission are encouraging if diabetes mellitus is diagnosed early, this
requires a fast and adequate therapy. Diagnosis of complicating factors is important because
a more accurate prognosis to the owner can be provided this way before therapy has
started. An early diagnosis can also offer additional therapeutic option. While it is not
reasonably possible to check for every predisposing disease when the diagnosis of diabetes
mellitus is made, it is paramount to look at each case with an open mindset to avoid missing
any concurrent illness.
Materials and methods
For the purpose of this research, a few dozen , non-referral based clinics were approached
based on their location to cooperate with this research. They were asked to provide
information of any owners of diabetic cats so that these owners could be requested to have
their cat participate in this research. The sole entry condition was that the cat was currently
receiving treatment for diabetes with insulin. The owners were then asked several questions
(see appendix) and each cat was subsequently examined and approximately 10 ml of blood
was drawn from the jugular vein. The owners received a bag of Katkor® which they were
asked to replace the litter content with in the evening before the cats were examined, and
the owners were to take a urine sample during the morning before the examination.
The urine was then examined in the veterinary diagnostic lab (UVDL) at the faculty of
veterinary medicine in Utrecht. The urine was then checked for specific gravity, pH, protein,
glucose, ketone bodies, cortisol, creatinine, blood cells and the cortisol/creat ratio was
determined. The blood, glucose and ketone bodies were evaluated with a semi-quantitative
analysis. Each urine sample was also subject to a microscopic urine evaluation. Hematology
was also performed at the UVDL, where the following parameters were determined:
hematocrit, mean cell hemoglobin, mean cell hemoglobin concentration, mean cell volume,
leukocytes, segmented neutrophils, banded neutrophils, eosinophils, basophils, monocytes,
lymphocytes and lymphoblasts.
Plasma samples were sent to the veterinary lab in Zürich (UZH), where the following
parameters were determined; bilirubin, glucose, fructosamine, urea, creatinine, protein,
albumin, cholesterol, triglyceride, alkaline, phosphatase, amylase, lipase, ASAT, ALAT,
sodium, potassium, chloride, calcium, phosphate, T4 and IGF-1. Plasma samples were sent to
the veterinary lab in Texas as well, where fPLI, fTLI, Folate (vitamin B9) and Cobalamine
(vitamin B12) were tested.
Results:
Out of the 138 diabetic cats examined. 95 were male while 43 were female. The following
breeds were present: 107 European short hair cats, 8 Persian cats, 6 Norwegian Forest cats,
4 Maine Coons, 2 British short hair cats, 2 Siamese cats. Of these breeds only one cat each
was examined: American short hair, Blue Russian cat, Burmese cat, Havana Brown,Ragdoll,
Somali cat and Siberian cat. The youngest cat was 4 years old while the oldest was 18 years
old. The average age was 12,28. The average body weight was 5,57 kilograms with the
lightest cat weighing 2,7 kilograms and the heaviest weighing 11,6 kilograms. Nutrient status
was noted by the researcher on a scale of 1-9 with 1 being cachectic, 3 being lean, 5 ideal, 7
clearly overweight and 9 severely adipose. One cat was found to be cachectic. 16 cats were
found to be lean. Five cats were found to be somewhere between lean and ideal. 46 cats
were found to be ideal. 15 cats were found to be somewhere between lean and clearly
overweight. 40 cats were found to be overweight. Four cats were found to be somewhere
between clearly overweight and severely adipose. Eight cats were found to be severely
adipose out of a total of 135 cats.
When asked, 42 out of 133 owners found that water intake did not decline since the start of
diabetes therapy for their cat. 28 out of 133 owners observed that general condition did not
improve in the same period of time. 96 out of 133 owners found that there no in appetite in
the same period of time. 34 out of 133 owners saw there was no decrease in urination
frequency or amount since the start of diabetes therapy. 43 out of 136 owners believed
there was a change in body contour, size of head and/or size of paws since diabetes therapy
was initiated. 58 cats were said to vomit at regular intervals out of 137 cats, though this is
including frequencies from once a week to about three times a year. Similarly 23 out of 137
cats were said to have diarrhea with a frequencies between continuous to twice a year.
The average plasma glucose was 13,41 (reference value was set at 4,0-9,0) out of 123
samples, with the lowest at 1,00; highest at 48,20 and a standard deviation of 8,84. The
average Fructosamine was 512,54 (reference value at 202-299); the lowest value was 221,00
and highest 849,00 with a standard deviation of 145,27. The average plasma amylase was
1241,41 (reference 700-1538) with the lowest value being 463 and the highest 11310, the
standard deviation was 1018 and 11 cats had a value of >1538. The average plasma lipase
was 26,39 (reference value was 8-26) with the highest value at 119 and lowest at 10, the
standard deviation was 17,19 and 40 samples had a value of >26.
Out of the 112 urine samples, 96 were tested positive for glucose. Out of those 96 positive
samples, 90 were tested +++ for glucose. The average cortisol/creatinine ratio was 23,06
(reference value was <42) with the lowest value being 0,4 and the highest 139,3; the
standard deviation was 21,93 and 17 cats had a value of >42.
The average fPLI was 6,88 (reference value was <3,5 to <5,3) out of 119 samples with the
lowest value being 0,7 and the highest 33,2; the standard deviation was 6,78 with 56 cats
having a value of >5,3. The average fTLI was 50,33 (reference value was 12,0-82,0) with the
lowest value being 12,8 and the highest 187,3; the standard deviation was 33,0 with 15 cats
having a value of >82,0. The average Folate was 21,17 (reference value was 8,9-19,9) with
the lowest value being 4,0 and the highest 56,6; the standard deviation was 11,03 with 49
cats having a value of >19,9. The average Cobalamine was 564,08 (reference value was 2761405) with the lowest value being 170 and the highest 971; the standard deviation was
234,47 with 18 cats having a value of <276.
The average IGF-1 was 714,8 (reference value was 200-800) with the lowest value being
15,15 and the highest 2470,97; the standard deviation was 473 with 38 cats having a value
of >800.
Using IBM® SPSS® Statistics Version 22, an attempt was made to link age with our findings.
No significant link could be made, short of kidney disease (minimum expected result of 0.06
and a Chi-Square significance value of 0,045 was found). Kidney disease however was not
further investigated in this research.
It was remarkable that only four female specimens had elevated IGF-1 while 31 females had
a IGF-1 value within reference range. On the other hand of the males, 34 had elevated IGF-1
while 53 males had a normal IGF-1. Using Fisher’s test with a two-tailed P value this resulted
in a P value of 0.0025. Which means that the difference in IGF-1 between females and males
was significant. There seems to be a trend for cats with elevated IGF-1 to develop azotemia,
but without statistical significance.
A pancreatitis score was also made, in an attempt to find a combined high fPLI, high fTLI,
high serum amylas and high serum lipase. If any of these parameters was above the
reference value, the cat got a score of “1”. If any two parameters were above the reference
value, the cat got a score of “2”, and so on. Using this system, 28 cats got a score of “1”, 24
cats got a score of “2”, 20 cats got a score of “3” and 1 cat got a score of “4”.
Using this data, it is possible to create suspicion whether or not the Somogyi effect might be
in effect in certain cats. This was done by selecting the cases that had a serum glucose below
reference value, a fructosamin above reference value as well as glucosuria. As this means
the cat had a high glucose over a longer period of time because of the high fructosamin and
glucosuria. But the low glucose indicates that the insulin dosage could be too high. This was
the case in 21 cats out of 107 complete samples.
Discussion:
The high incidence of diabetic cats, 38 out of 122 or 31,1%, with increased IGF-1 is in line
with what was found in previous studies. A similar study was performed in the United
Kingdom where 334 diabetic cats had an IGF-1 suggestive of acromegaly out of 1222 cats
examined (26,4%). In particular however, it appears that male cats are at an increased risk to
develop acromegaly. An increased IGF-1 can be predictive for acromegaly, since previous
research showed that 94% of the cats with elevated IGF-1 had acromegaly. 15 Yet there is
also evidence that insulin increases the hepatic production of IGF-1 which can require some
degree of interpretation in cases that are on the edge of the reference range. Routine
measurements are thus advised in diabetic cats that are either difficult to regulate or require
high doses of insulin, with added emphasis on the testing of male cats due to the increased
predisposition for acromegaly. Fortunately, while IGF-1 was previously often measured using
a radioimmunoassay, the more affordable option of using an ELISA for this parameter is
being researched which should facilitate its use in veterinary practice when validated. 16
Non iatrogenic hyperadrenocorticism with or without diabetes is a relatively rare disease in
cats, with only about 100 cases being reported in literature thus far. 17, 18 Measuring the
urine cortisol/creat ratio gives us a good idea of what the prevalence could be at the very
most. However in order to actually diagnose hyperadrenocorticism it would be needed to do
additional testing, a dexamethasone suppression test for example. This way a differentiation
could be made whether cortisol is excreted in the urine due to stress, for example because
the litter content is abnormal, or if there is adrenal hyperfunction. There has also been some
discussion regarding the typing of diabetes, there has been evidence that in humans,
corticosteroids are a precipitating factor for people that already have a decreased insulin
secretion to develop DM. Thus people that already meet various risk factors in the
pathogenesis of diabetes type 2 are more apt to develop diabetes when treated with
corticosteroids. 19 Subsequently, though cats have increased odds of remission when treated
with corticosteroids before the onset of diabetes, they often relapse as well. 20 This result
shows that corticosteroids are likely not the sole contributor in the pathogenesis of diabetes.
21
Pancreatitis is frequently seen as a possible cause for diabetes through the destruction of
Beta cells and for inducing peripheral insulin resistance. Though 56 cats out of 120 had
elevated fPLI, other studies show non diabetic cats having elevated fPLI in ratios such as
66%. 22 Though it should be said that severely increased values of over 20 ug/l were not
found in that study in diabetic cats, while on the other hand 8 cats in this study had a value
of >20ug/l out of 119 cats. Concurrent disease of the bowels and liver or bile ducts, so called
triaditis, is a frequent finding in cats with pancreatitis. Despite the high rate of cats with
vomiting (58) and diarrhea (23) in the anamnesis, these phenomena are at such low
frequencies that it is difficult to draw any conclusions with regard to possible pathologies.
The nonspecific symptoms of pancreatitis do not aid in its diagnosis. A veterinarian can gain
more information through echographic examination of the abdomen, but it is often best to
focus on the therapy of diabetes along with supportive care in case of dehydration and
anorexia. Fortunately, cats with acute pancreatitis during the start of diabetes frequently go
into remission once the pancreatitis subsides with little to no increased insulin resistance. 22
The average fructosamin was 512,54; which is far beyond its upper reference range of 299.
This elevated level was found despite most of the cats being diagnosed with diabetes
months or years prior to this study. A considerable portion of the cats also lack a diet that is
low in carbohydrates and high in protein as is recommend in cats with DM, though some
have a concurrent illness that prevents this like with kidney disease or urolithiasis, many
don’t have such a contraindication. 54 cats out of 135 are also overweight without a
reduction in this weight after onset of the diagnosis of diabetes. In 21 out of 107 cats there is
a suspicion of the Somogyi effect playing a role. All these findings point to a poor regulation
of diabetes, likely not as a result of concurrent disease but due to poor management.
Though it is difficult, and possibly erroneous to put the blame on the veterinarian or the
owner, fact remains that these findings worsen the prognosis.
Even though care has been taken to get a group of cats that represents the diabetic
population in the Netherlands, it has been difficult to be completely unbiased. The clinics
were approached based on their topographic location, which could result in a difference of
breeds proportions, different rates of indoor and outdoor cats and the diet they are
provided. It is certainly possible that people would choose to participate in this research
because they suspect a concurrent illness playing a role and this would be an easy way to
find out. It’s also plausible that the owners of cats which are well regulated don’t see a point
in participating or don’t come in the clinic very often. The data gathered from owners by
anamnesis can be hard to interpret, and harder yet to compare to other data. The
parameters from the physical examination were gathered by 4 different students in different
stages of their veterinary education, thus making it harder to compare. Some of the samples
have been stored in less ideal environments prior to being examined and some cases’
samples have also been in transit for various periods of time which may influence certain
measurements.
Conclusion and recommendations
The high prevalence of acromegaly in male cats is something to keep in mind not only when
a cat is diagnosed with diabetes but also when insulin resistance is taking hold and the
veterinarian is inclined to increase insulin dosage. Further testing of high urinary
cortisol/creatinine cats to prove or disprove Cushing’s disease is recommended. Diagnostic
imaging of elevated IGF-1 cats on the pituitary gland would also strengthen our findings.
Regardless of any concurrent illness however, the results of the data gathered show that
there is still much to improve when managing a cat with diabetes. There are some
remarkable high levels of remission reported in recent literature, and this author refuses to
accept that we cannot reach similar results.
References
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Appendix
Date:
Practice:
Name cat owner:
Signalement
Age:
Sex:
Breed:
body weight:
name cat:
Diabetes was diagnosed (date, year):
Current treatment
Type of insulin:
Dose of insulin:
BID or SID:
Food/diet:
Food additives:
Other treatment:
Did appetite change since start of diabetes therapy?
Current impression of owner on appetite:
Did general condition improve since start of diabetes therapy?
Current impression of owner on general condition of the cat:
Did water intake decline since start of diabetes therapy?
Current impression of owner on amount of water intake:
Did amount of urine/frequency of urination decline since start of therapy?
Current impression of owner on amount of urine/frequency of urination:
Since therapy of diabetes was started did the cat gain weight? Lose weight?
Did body contour/size of head/size of pawns change since start of diabetes therapy?
Hair coat and skin:
Vomiting:
Diarrhea:
Locomotion:
Nervous system:
Vision:
Any other problem: