Page 1361 - Clinical Small Animal Internal Medicine

144 Pancreatic Endocrine Tumors 1299

N1), and distant metastasis (M0 or M1). Therefore, full resulting in elevation of blood sugar. The catabolic effects
VetBooks.ir staging (thoracic radiographs, abdominal ultrasound, of glucagon result in hypoaminoacidemia. Requirements
for histidine and lysine‐rich keratohyalin granules in the
serum chemistry, complete blood count, and urinalysis)
is recommended.
Overall, the prognosis is guarded because of the high stratum granulosum make the epidermis susceptible to
hypoaminoacidemia.
rate of metastasis and recurrence of clinical signs.
Approximately 36–51% of dogs have detectable meta­
static disease at the time of surgery. With surgery alone, Epidemiology
stage I (T1N0M0), II (T1N1M0), and III (T1N0M1 or Glucagonomas are rare in people (<250 reported) with
T1N1M1) dogs have an expected median survival of 19 only a few case reports in dogs. They have not been
months, nine months, and six months respectively. reported in cats.
Survival time for dogs treated medically is less than
when surgery combined with medical management is
used. In one study, medical management with pred­ Signalment
nisone and dietary change alone resulted in a median The typical signalment is an older dog. There are no
survival time (MST) of 74 days. In a separate study, the reported breed dispositions.
median survival time for dogs that had a partial pancrea­
tectomy was reported at 496 days. In a subset of nine
dogs that received postsurgical medical treatment History and Clinical Signs
(diazoxide and prednisone) at the time of relapse, the Dermatologic manifestations include lesions of the foot­
median survival time was extended to 1316 days. pad, pressure points, periocular area, and mucocutane­
Streptozotocin therapy, especially as an adjunctive to ous junctions such as the perineum, genitalia, and
surgery, should be considered. Although data are lim­ muzzle. Hyperkeratosis of the footpads also occurs.
ited, normoglycemia has been shown to be prolonged Weight loss is associated with the catabolic effects of the
with use of streptozotocin when compared to dogs that glucagon. Hyperglucagonemia can cause diabetes melli­
were medically managed with diet and prednisone (163 tus resulting in polyuria and polydipsia.
versus 90 days respectively). In addition, reduction in
metastatic lesions and resolution of hypoglycemic poly­
neuropathy in dogs have been reported. Diagnosis
Persistent postoperative hypoglycemia has also been An elevated plasma glucagon level in the absence of
reported to be prognostic. In one study, dogs that became hypoglycemia is supportive of the presence of a gluca­
normoglycemic postoperatively had a median survival of gonoma. Histopathology of skin biopsies will be consist­
680 days compared to those that remained hypoglyce­ ent with superficial hydropic dermatitis and marked
mic, which had a MST of 90 days. parakeratosis. A definitive diagnosis is obtained through
histopathology of the pancreatic tumor. In animals with
Glucagonoma skin lesions, elevations in liver enzymes and hypoalbu­
minemia may also be present.
Etiology/Pathophysiology
Therapy
Alpha‐cells secrete glucagon and constitute about
20–25% of the endocrine pancreas. Glucagon has a pro­ Surgical debulking or resection is the treatment of
found hyperglycemic effect. In people, glucagonomas are choice. Octreotide may be helpful in animals that have
commonly associated with diabetes mellitus and severe alpha‐cells that are expressing somatostatin receptors.
paraneoplastic dermatologic disease. Dogs with gluca­ Streptozotocin has been used with limited success in
gonomas can have a similar dermatologic syndrome people for palliative treatment. When dermatologic
called superficial necrolytic dermatitis, necrolytic migra­ lesions are present, a high‐quality protein diet such, as
tory erythema, or metabolic epidermal necrosis. This Hill’s Science Diet a/d should used in nonencephalo­
dermatologic disease has been identified in multiple pathic animals. Supplementation with 3–6 egg yolks per
dogs with glucagonomas but it is more commonly asso­ day may also be beneficial. Intravenous amino acid ther­
ciated with liver disease and is not pathognomonic for a apy has been useful. A 10% crystalline amino acid solu­
glucagonoma. tion (Aminosyn®, Abbott Labs) at 25 mL/kg over 6–8
Glucagon has catabolic effects and opposes the effects hours repeated every 7–10 days has been used to treat
of insulin. It causes gluconeogenesis, glycogenolysis, and hypoaminoacidemia. Ideally, the hypertonic amino acid
lipolysis that cause the conversion of glycogen to glucose, solution is administered via a central vein to decrease