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Note: written for beardies,
but may be applied to PONS.
Chronic small intestinal disease
is a problem for many beardies. In young dogs especially, chronic
intermittent small bowel diarrhea often accompanied by weight loss
or failure to gain weight may be the result of bacterial overgrowth.
This isn’t the only presentation, some dogs may not have diarrhea,
others may vomit or have mild colitis, but in general they are young
and not doing well. Bad bacteria can become established for a
variety of reasons, but mostly these can be grouped as due to
defective production of stomach acid, defective gut motility,
defective local immunity, exocrine pancreatic insufficiency,
defective mucus production, unabsorbed nutrients and malnutrition.
Where possible the underlying cause of the problem should be
treated. If this cannot be determined oral oxytetracycline or
tylosin are usually effective treatments.
Dietary sensitivity (allergic
reaction) and food intolerance can also cause chronic diarrhea.
Usually the two conditions are difficult to distinguish, and are
treated similarly. Exclusion diets using a protein and carbohydrate
source the dog has not previously experienced. Owners should never
feed any treats during this phase, just the prescribed diet. It can
take 6 to 8 weeks for an improvement to be seen. At this point to
confirm diagnosis the dog should be challenged with the original
diet – which should cause problems to reappear (surprisingly many
owners are reluctant to complete this step). Foods should be
reintroduced one item at a time. Unfortunately, truly allergic dogs
develop allergies to the new ingredients over time. Steroids may
help reduce the allergic response. Raw and home cooked diets may
also prove successful for these dogs, and evidence of allergy to the
grain mites in kibble has recently been reported.
Infiltration of the lamina
propria of the small intestine wall is characteristic of
inflammatory bowel disease (IBD). In the most common form the
invading cells are lymphocytes and plasma cells; less commonly the
invading cells are eosinophils. This condition may also co-occur
with dietary sensitivity, bacterial overgrowth, giardia,
campylobacter and histoplasmosis and other fungal infections as well
as lymphosarcoma. Co-existing problems should be addressed. Grossly
the intestinal wall may appear normal or thickened, and definitive
diagnosis is made from biopsy samples taken during endoscopic
examination. Treatment is similar to that for dietary sensitivity.
Reducing carbohydrate and/or replacing other sources with rice can
be very helpful, as can replacing long chain fatty acids with medium
chain ones.
Intestinal lymphangiectasia is a
protein losing condition in which flow of lymph from the intestines
is blocked, the lymph ducts can rupture and release plasma proteins
into the intestines. It may be congenital or acquired, most often
subsequent to congestive heart failure. A diet high in good quality
protein and low in fat, supplemented with fat soluble vitamins is
helpful. Steroids may help relieve clinical signs. Where possible
the underlying cause should be treated.
Adenocarcinoma is the most common
intestinal tumor, although lymphosarcoma, leiomyoma, leiomyosarcoma,
fibrosarcoma and intestinal polyps can occur. Signs of these are
vague and progress slowly. Anorexia and weight loss are usually the
first signs. Adenocarcinoma usually occurs in the duodenum or large
intestine, and may spread locally and sometimes to more distant
sites. Mean survival after surgery is about 7 months. Lymphosarcoma
usually spreads to the lymph nodes and response to chemotherapy in
dogs is poor. Leiomyoma and leiomyosarcoma are tumors of the muscle
wall, and if you can resect the tumor this is usually curative as
they rarely metastasize.
The Large Intestine
is between 28 and 90 cms in dogs, and runs from the end of the ileum
to the anus. There are three sections. The cecum is an 8 to 30 cms.
long pouch off the colon shortly after it leaves the ileum. The
colon has two distinct bends as it passes through the abdomen to the
rectum. The cell layers of the wall are similar to those of the
small intestine; however, there are no villi and fewer microvilli,
but more mucous secreting cells. Cell turnover here is slower (4 to
7 days). The large intestine’s primary function is to extract
water and electrolytes from the effluent from the ileum, and to
store feces prior to defecation. A small amount of fermentation of
organic material occurs in the first part of the colon, but this is
of little significance, unlike the same process in herbivores. Most
muscle contractions are actually away from the rectum, slowing down
the passage of the contents while they are mixed, stored and
dehydrated. Towards the anus, spontaneous giant contractions propel
the contents into the rectum. The large bowel has a limited capacity
for removing water. Normally it removes 90% of the remaining water,
but if excess water comes from the small intestine, it may be
overwhelmed, and the result is diarrhea. Sodium is also absorbed,
and potassium and bicarbonate secreted. The latter neutralizes acids
produced by fermentation. Bacterial content in the gut is highest in
the large intestine, with 10 11 organisms in each gram of feces –
nearly 50% of its dry weight. The bacteria resist bacterial
overgrowth with unfriendly bacteria, while metabolizing any
remaining carbohydrates, proteins and lipids.
Diarrhea is the most common sign
of large bowel disease. It is characterized by a lot of mucous, and
often accompanied by straining. Blood will be red rather than the
black tarry melena seen with small intestinal bleeding. Frequency of
defecation is increased, but the amount is diminished. Dogs usually
remain bright and normal; weight loss is uncommon. Strictures or
tumors may result in the production of abnormally shaped feces.
Vomiting and weight loss indicate small intestinal disease is
present too. Diarrhea can be the result of dietary indiscretion or
changing diet too quickly for the enzymes to adapt; whipworm
infection; IBD or neoplasia. Tumors can be benign – adenoma,
leiomyoma or malignant – adenocarcinoma, lymphosarcoma or
leiomyosarcoma – although the latter can usually be surgically
removed completely. Irritable bowel syndrome, also called nervous or
spastic colon, is a vague term for large bowel diarrhea that is
often fiber responsive (psyllium is curative) or caused by toxins
produced by clostridial bacteria. Other causes of large bowel
diarrhea are fungal, bacterial or parasitic.
Constipation may result from too
efficient removal of fluid from the bowel or insufficient mucous
production. Megacolon – enlargement of the colon leading to poor
motility – is rare in dogs, and is usually acquired secondary to
prolonged mechanical or functional obstruction of defecation.
Function of the rectum and anus
depends on the coordination of conscious and unconscious muscular
movements. The rectum begins as the colon enters the pelvis. The
region is rich in mucous secreting cells. If these cells become
inflamed then mucous secretion increases, as does straining and the
presence of blood in the feces. Three kinds of glands empty into the
anal region. Anal glands are modified sweat glands that secrete
lipid into the lumen of the anus. The glands of the paired anal sacs
that lie at positions 4 and 8 just below the skin around the anus
secrete a mixture of dead cells, protein, sebaceous fluid and
bacteria into the sacs. The circumanal glands surround the anus and
are non-secretory. The anus has two sphincters, the internal one is
not under conscious control. The external sphincter surrounds the
internal one, and is under conscious control. The two sphincters are
normally perfectly coordinated, but damage to the pudendal nerve can
result in fecal incontinence.
While the anus is not involved in
digestion, problems can frequently result in owners deciding to
euthanatize the dog. Problems in the area can include: perineal
hernia – rectum, urinary bladder or prostate gland can herniate
into the anal region; rectal polyps and other tumors; rectal
prolapse; proctitis – inflammation often secondary to colitis;
rectal stricture – usually the result of trauma or surgery; rectal
foreign bodies – these may lodge in the rectum having passed
through the rest of the intestinal tract. Foreign bodies can cause
secondary fistulas and abscesses. Perianal fistulas are extremely
painful and consist of one or multiple tracts running from the lumen
of the anus through the skin in the region around the anus. Dogs
with broad tail bases that clamp their tails are at increased risk.
Low thyroid and poor immune function may also be inciting factors.
Surgery and/or topical tacrolimus usually is curative.
Anal sac impaction, inflammation
and/or abscessation is common, and owners notice their dog licking
or biting at the area, scooting their butts, having trouble sitting
(or showing reluctance to do so), pain and straining on defecation.
One or both sacs may be involved, and they can readily be palpated
through the skin. Normal secretions are clear to pale yellowish
brown. Granular material, pus, blood and turbidity are all abnormal.
Normally impacted sacs can be expressed easily, but sometimes the
secretions form a cement-like block which has to be cleared before
you can express them. Abscesses are extremely painful, and can cause
fever. They can also lead to fistulas forming. In dogs with a
chronic problem, removal of the sacs is recommended. Feeding a high
fiber diet may help express the sacs. Adenocarcinomas may affect the
anal sacs, and usually metastasize to the nearby lymph nodes.
The Liver
carries out at least 1500 biochemical functions essential to a
dog’s survival. It is involved in the metabolism of carbohydrates,
lipids, protein, vitamins and endocrine hormones; immune function;
storage; making blood clotting factors, iron regulation and even
making blood in utero and in extreme situations; making, storing and
regulating the secretion of bile; and the detoxifying and excreting
of drugs, hormones and several other substances. Its storage
capacity, functional reserve and regenerative capabilities are the
stuff of legend, but this doesn’t make it easy to recognize when
something is amiss; and often disease is severe and advanced before
a problem is detected.
The liver is composed of six
lobes. About 80% of the volume consists of hepatocytes. Another
important cell type is the Kupffer cell, these line the blood
vessels passing through the liver. These are fixed macrophages –
cells that ingest and detoxify substances. They are also needed for
the metabolism of iron, lipid, cholesterol and certain hormones. In
addition, they have several important functions in the immune
system. Ito cells are rich in retinoids and store lipids; they also
produce most of the collagen that results in fibrosis of the liver.
The capillaries passing through the liver have fenestrae or gaps
allowing the passage of much larger molecules than most blood
vessels. When blood pressure increases in the liver though, these
close and become less permeable. Blood sinusoids serve to dissipate
the pressure of blood entering the liver and store blood; the system
is usually maintained at low pressure. Certain bile salts can
increase blood flow and pressure within the liver.
Hepatocytes are arranged in cords
with one side abutting a blood vessel and the other a bile
canaliculus. On both sides surface area is magnified by the presence
of microvilli, greatly increasing the surface for nutrient,
metabolite, drug, toxin and bile exchange. These cords are supported
on a framework of collagen and reticulin fibers.
Bile is formed in the hepatocytes
and passes into the canaliculi, then to ductules, ducts and
ultimately the gallbladder. Electrolyte and fluid content is
modified during this passage. In the gall-bladder it is concentrated
and stored until it is expelled into the duodenum to aid in
digestion.
Nutrient rich blood from the
stomach, intestines, spleen, pancreas, colon and gall-bladder flows
into the portal circulation and passes through the liver before
entering the rest of the circulation. Nutrients are removed and
further processed while undesirable substances absorbed from the gut
are removed and/or detoxified. At any one time 10-25% of the blood
is in the liver. Much of it is being stored. The liver can actually
double its blood storage which alone can lead to liver congestion.
During hemorrhage, it can compensate for loss of 25% of the total
blood volume. At rest about 25% of cardiac output is passing through
the liver, this changes with exercise, posture and at meal times.
While two-thirds of the blood in the liver comes from the portal
vein, one third comes through the hepatic artery, which supplies the
oxygen needed for liver function. Even brief interruption of blood
flow through the hepatic artery can lead to lethal, septic necrosis.
In newborn puppies most of the
abdominal cavity is occupied by the liver, in the young dog the
ratio of liver to body weight is about 4 to 5: 100, but in older
dogs this drops to 2:100. Small livers may be the result of reduced
blood perfusion, chronic fibrosis, atrophy of the hepatocytes, or
loss of their cellular content. Enlarged liver can result from
passive congestion, infiltrative or inflammatory conditions,
blockage of the bile ducts and cystic liver disease. Drug exposure
– barbiturates etc.; infection or inflammation of the hepatocytes
can result in increased liver mass secondary to enlargement of the
organelles within the cells. If 70% of the liver is removed, in 6
weeks the remaining liver can have regrown to pretty much normal
size and functional capacity. During that time, the body must have
adequate glucose and coagulation factors provided, however.
Bile acids are formed from
cholesterol and bound to an amino acid, usually taurine but
sometimes glycine. Bile is secreted in volume into the intestines
when food is consumed, and helps digestion and absorption of fat.
Bile is released in smaller quantities, sometimes by-passing the
gallbladder, at other times. Some dogs will vomit up bile if they
have not been fed – particularly before the morning feed. Giving a
bed-time cookie is usually enough to prevent this happening.
Early signs of hepatobiliary
disease are usually vague – anorexia, vomiting,
diarrhea/constipation, weight loss, intermittent fever. A more
specific sign would be jaundice – yellowing of the mucous
membranes and non-pigmented skin and eye whites – this can appear
rapidly with major occlusion of the bile duct or very slowly.
Gastrointestinal ulceration and hemorrhage may occur as disease
progresses. Bleeding tendencies, due to Vitamin K deficiency,
usually take a couple of weeks to appear. Feces may become dark
green or dark-green/orange due to increased blood break down or pale
gray or tan and fatty if bile flow is obstructed. Significant
bleeding into the bowel produces black tarry feces. Increased
drinking and urination and the appearance of urobilinogen in urine
indicate liver disease, although some animals have problems
urinating. Change in liver size can often be palpated.
Neurobehavioral changes – ataxia, lethargy, stupor, head-pressing,
obsessive circling, sudden unexplained blindness, seizures or coma
can indicate severe acquired liver insufficiency or congenital
portosystemic shunt – where some or all blood from the digestive
tract by-passes the liver and goes directly into the main
circulation. Ascites, the accumulation of fluid in the abdomen, is
often the result of increased blood pressure in the portal vein
usually indicating obstruction.
Diagnosis of liver disease begins
with basic blood testing a complete blood count and biochemistry
profile, in fact in many cases liver disease can be discovered
before any physical signs become apparent. However, liver enzymes
can be elevated by a number of unrelated conditions – bone
disorders or growth; endocrine disease; gastrointestinal and splenic
disease; hypoxia; drugs; low blood pressure; neoplasia; systemic
infection; trauma; fever; wasp stings or after general anesthesia!
If none of these are apparent follow up with ultrasound and biopsy
are probably the most helpful procedures for characterizing the
cause of the liver disease. X-rays and nuclear scintigraphy may also
be helpful.
Acute hepatic failure
occurs when a sudden severe insult to the liver results in
compromise of at least 70 to 80% of functional liver mass, exceeding
the liver’s functional reserve and resulting in signs of liver
failure. Diffuse necrosis of liver tissue is the most obvious and
consistent sign. Causes can include hepatotoxic drugs and anesthetic
agents; chemical and biologic substances (aflatoxin; amanita
mushrooms; blue green algae; pennyroyal oil; heavy metals;
herbicides; fungicides; rodenticides; household cleaners; industrial
chemicals, etc.); infectious or parasitic agents (viral hepatitis,
acute bacterial cholangiohepatitis; leptospirosis; liver abscess;
extrahepatic infections and sepsis; systemic fungal infection –
esp histoplasmosis; toxoplasmosis; postcaval heartworm infection);
systemic or metabolic disease (acute pancreatitis; acute hemolytic
anemia); trauma; diaphragmatic hernia with liver entrapment; heat
stroke; surgery where blood pressure and oxygen perfusion is
compromised; liver lobe torsion. Treatment depends on the underlying
cause of the liver failure. Given the liver’s role it is
especially vulnerable to a vast array of substances, and this is
something we should consider before introducing any substance into
our dog’s or our family’s environment. Apart from acetaminophen
antidotes exist for most acute hepatotoxins.
Cholestatic hepatobiliary
disease is the result of impaired flow or excretion of
normal volumes of bile. Substances normally secreted in the bile
build up in circulating blood serum – bile acids, bilirubin,
cholesterol – and there is increased activity of enzymes
associated with the cells of the biliary tract – alkaline
phosphatase (ALP) and gamma-glutamyltransferase (GGT). Jaundice is
the hallmark of this condition. Cholestasis can result from blockage
or rupture of the bile ducts. This often requires surgical
correction. Common causes are pancreatic disease (edema, abscesses,
cysts or cancer), or gallstones. Retention of bile in the liver can
cause secondary injury to hepatocytes.
Chronic
liver disease – hepatic fibrosis and cirrhosis – can
also result from a great many causes. Repeated exposure to drugs or
toxins; infection; cholestasis; immune injury (chronic idiopathic
hepatitis) and hypoxia often secondary to cardiac failure are all
potential problems. A single episode of massive hepatic necrosis
could cause end stage liver disease. However, the cause is never
determined in most cases. One study showed that cirrhosis was
responsible for 15% of the cases of liver disease as determined by
biopsy.
In cirrhosis fibrous tissue
replaces much of the normal liver and the remaining cells become
disorganized further limiting function. It is irreversible, and
while removing the underlying cause may slow progression of the
disease it can not restore the liver. Blood flow to the liver is
compromised, and blood pressure increased, so remaining cells are
less able to function.
Nodular hyperplasia
is a common post-mortem finding in dogs over the age of 8. These
nodules are not precursors to cancerous lesions, and they are not
associated with clinical signs. Unfortunately, they cannot be
distinguished from primary or secondary neoplasia on ultrasound,
only by biopsy.
Liver cancer may
be primary or metastatic and virtually all types of cancer have been
reported. Metastatic cancer from pancreas, lymph nodes, spleen,
mammary glands, adrenal glands, bone, bone marrow, lungs, thyroid
glands and gastrointestinal tract is more common, and lymphosarcoma
and pancreatic carcinoma are the most common types. Primary tumors
are rare, and they are not associated with viral infection, exposure
to chemical carcinogens, toxins, drugs or prior liver disease as
they are in humans. These tumors can be benign or malignant.
I am not aware of any cases of
congenital portosystemic shunts being reported in Beardies. Multiple
acquired portosystemic shunts can result as a compensatory response
to prolonged elevated portal blood pressure. Likewise hepatic
arteriovenous fistulas can form as a result of elevated blood
pressure in the hepatic artery diverting blood into the portal
system. Neither condition is common. Both are more common in younger
dogs, and in certain breeds, but not in beardies.
Hepatic lipidosis
is an excessive accumulation of fat (triglycerides) in the liver. It
is caused by an imbalance between rate of deposition and dispersal
of fat, and can be nutritional, metabolic, hormonal, toxic or
hypoxic in origin. The clinical significance depends on the severity
and underlying cause. Excess fat does not impair liver function, but
results in a large, pale yellow liver – such as that of the foie
gras goose. Diabetes mellitus is one of the most common causes.
Treating the underlying cause is desirable.
Hypertriglyceridemia
– elevated triglyceride (TG) levels in serum - is the most
prevalent lipid disorder in dogs. It may result in vomiting,
diarrhea and non-localized abdominal pain. Signs frequently resolve
with fasting. Seizures may also be a presenting sign. Reducing
dietary fat is often curative, but feeding gastrointestinal diets
(such as Hill’s i/d) may make the condition worse. Blood
triglycerides must be measured after fasting the dog to distinguish
the condition from normal post feeding elevation of TG. Other
rule-outs include diabetes mellitus, which can result in marked
increase in TG and mild elevation of cholesterol (CH); protein
losing nephropathy due to kidney disease which increases both TG and
CH. The primary cause of elevated CH is hypothyroidism, although 30%
of dogs with Cushing’s Disease (hyperadrenocorticism) have
elevated CH, too.
The major function of the exocrine
pancreas is to secrete digestive enzymes and coenzymes. It
also secretes bicarbonate to help neutralize stomach acid, and
factors that assist in absorption of Vitamin B 12, zinc and probably
other nutrients. Pancreatic fluid inhibits bacterial overgrowth in
the duodenum and jejunum, helps with normal degradation of old brush
border cells, and promotes growth of the mucosa together with
biliary secretions. The pancreas protects itself from digestion by
several mechanisms, including producing an enzyme inhibitor
(pancreatic secretory trypsin inhibitor), which it secretes together
with the digestive enzymes.
The pancreas has left and right
lobes and a small central body where they join together.
Embryonically it grows out from the duodenum to which it stays
connected by two secretory ducts –pancreatic duct and accessory
pancreatic duct. The right lobe lies alongside the duodenum and the
left lobe along the pyloric region of the stomach.
The acinar cells of the pancreas
secrete enzymes to degrade proteins, lipids and polysaccharides.
Proteolytic and phospholipolytic enzymes are stored as inactive
zymogens, which are normally activated in the intestines by cleaving
a small peptide from the zymogen, so trypsinogens become trypsins
etc. This is achieved by an enzyme – enteropeptidase – formed in
the enterocytes. The trypsins, chymotrypsins and elastases cleave
polypeptides at specific sites, while carboxypeptidases lop off
terminal carboxyl residues.
At rest the pancreas secretes
about 2% of the bicarbonate and 10% of the enzymes it does when the
animal eats a meal. There are cyclic increases though in the amounts
secreted. After a meal secretion occurs in two phases, the first,
which peaks an hour or two after eating, is rich in enzymes. The
second phase occurs about 8 to 11 hours after the meal, is more
voluminous and rich in bicarbonate. Low levels of amylase, lipase
and zymogens leak into the blood stream.
Pancreatitis is
inflammation of the exocrine pancreas. Acute pancreatitis has a
sudden onset, may occur repeatedly, but causes little or no
permanent pathologic change. Chronic pancreatitis is a continuing
inflammatory condition resulting in permanent impairment of
function. Pancreatitis seems to result when the proteolytic enzymes
are activated while still in the pancreas causing autodigestion.
This is probably because of a failure of the normal secretory
process. In most cases the inciting cause is unknown. Some potential
causes are: nutrition/hyperlipoproteinemia – low protein, high fat
diets, and especially prevalent in obese animals; drugs, toxins,
hypercalcemia; duct obstruction – gall stones, tumors, parasites,
trauma, edema, sphincter spasm; duodenal reflux, pancreatic trauma,
loss of circulation/reperfusion injury; viral, fungal or parasitic
infection.
Signs usually include depression,
anorexia, vomiting, sometimes diarrhea and pain – splinting the
stomach (praying). In severe cases the dog may have collapsed and be
in shock. They are usually mildly to moderately dehydrated and have
a fever. In some dogs a mass at the front of the abdomen can be
felt. CT scans are the most useful for diagnosing pancreatitis, but
ultrasound may be helpful. Fluids and careful electrolyte balance
together with nothing given by mouth is the basis for treatment. In
uncomplicated cases, prognosis is good for complete recovery,
although it is recommended that high fat foods be avoided in future.
Exocrine pancreatic
insufficiency (EPI) is quite common in Beardies. Pancreatic
acinar cells are progressively lost and replaced by fibrous tissue
so that the body ultimately fails to produce sufficient digestive
enzymes and food is not absorbed but passes through to the feces
largely unchanged. Signs do not appear until most of the tissue is
lost, for example fat in the feces is usually not observed until
85-90% of the secretory capacity has been lost. Even without
pancreatic enzymes, alternate pathways do exist, and up to 63% of
ingested protein and 84% ingested fat will be absorbed without
pancreatic enzymes.
In the majority of dogs
pancreatic acinar atrophy is the primary cause of EPI. The cause is
unknown, although nutritional deficiencies – amino acid imbalance,
copper deficiency, protein-calorie malnutrition – have been
postulated. Malnourishment secondary to small intestinal mucosal
abnormality has also been suggested as dogs often show g/I
disturbance long before there is significant weight loss. In humans,
and apparently in quite a lot of Beardies, chronic pancreatitis is
the cause of EPI. In some cases diabetes mellitus may co-exist with
EPI. In some dogs congenital EPI has been reported, as well as EPI
secondary to surgical resection of the duodenum.
In many dogs with EPI, enzymes
malfunction, there are changes in the mucosa of the small intestine
resulting in abnormalities of transport mechanisms and changes in
bacterial presence. Dogs have often suffered from malabsorption a
long time before diagnosis is made or help sought however, and this
may result in some of the associated changes that have been
reported.
The best test for EPI is a blood
test – serum trypsin-like immunoreactivity (TLI). This test rules
out small intestinal disease (IBD) as the cause of the
malnourishment. Dogs are managed by supplementing each meal with
pancreatic enzymes and most do quite well. The enzymes –
especially lipase – are largely digested themselves though before
they reach the small intestine. Attempts to maximize enzyme efficacy
- such as predigesting food with enzymes prior to feeding - have not
proven to have any advantage. Highly digestible diets should be fed,
and in most cases dogs require slightly more food than their healthy
counterparts to maintain their ideal weight. Like all exocrine
pancreatic diseases, EPI can be very painful and dogs may become
more aggressive as a result of the pain as well as hunger. Vitamins
B 12 and E may need to be supplemented in dogs with EPI.
Adenocarcinoma
of the acinar or pancreatic duct cells is relatively uncommon in
dogs. When it does occur, the dogs are older. These tumors are
highly malignant and have usually metastasized to the duodenal wall,
liver and lymph nodes prior to diagnosis. Signs are usually
non-specific - anorexia, depression, vomiting. If the bile ducts are
involved the dog may develop jaundice, if the pancreatic duct is
blocked there will be signs of EPI, and if the beta cells are
affected signs will be of diabetes mellitus. An abdominal mass may
be palpated, or a tumor visualized via ultrasound, but diagnosis is
usually made via exploratory surgery. Prognosis is extremely poor
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