Page 138 - Clinical Small Animal Internal Medicine

106 Section 2 Endocrine Disease

tests include histologic evaluation of liver biopsies and following glucose administration. The prognosis is good
VetBooks.ir specific enzyme assays that are rarely performed in vet­ if hypoglycemia is corrected before brain damage occurs.
The risk of developing hypoglycemia decreases with
erinary medicine. And lastly, GSD type IV has been doc­
umented in a family of Norwegian forest cats. It leads to
death as a result of perinatal hypoglycemic collapse or increasing age and body weight.
late juvenile‐onset neuromuscular degeneration.
Nonislet Cell Tumor‐Induced Hypoglycemia
Hypoglycemia can be a manifestation of neoplastic dis­
Idiopathic Causes of Liver‐Associated ease. Tumors related to the occurrence of hypoglycemia
Hypoglycemia in Young Animals: Neonatal can, as a general rule, be divided into three groups. First,
and Juvenile Hypoglycemia
tumors can produce excess insulin such as pancre­
Neonatal Hypoglycemia atic insulinomas or ectopic insulin‐producing tumors.
The blood glucose concentration in the healthy neonate Second, hypoglycemia can be caused by tumor‐related
falls during the first few hours after birth because of the factors such as destruction of the liver by massive tumor
loss of continuous transplacental infusion of glucose. infiltration. And lastly, there is now convincing evidence
Thereafter, the neonate is dependent on glycogenolysis that secretion of insulin‐like growth factor (IGF)‐2 and
and gluconeogenesis to maintain euglycemia between incompletely processed IGFs (e.g., pro‐IGF‐2 or “big”‐
feedings. Limited glycogen stores, small muscle mass, IGF‐2) causes hypoglycemia in humans. This mecha­
and lack of adipose tissue as alternative energy sources nism has also been documented in a few cases of
place the neonate at risk for hypoglycemia. That said, the hypoglycemia in dogs. Nonislet cell tumor‐induced
ill neonate should always be evaluated for hypoglycemia, hypoglycemia (NICTH) can arise in virtually every
especially if sepsis, toxic milk syndrome, or starvation is benign and malignant tumor. However, it mainly occurs
suspected or hypothermia is noted. Orally administered in patients with solid tumors of mesenchymal (e.g., leio­
glucose or frequent bottle feeding can help correct or myosarcoma, fibrosarcoma) and epithelial origin (e.g.,
prevent hypoglycemia. hepatoma, hepatocellular carcinoma), but rarely in
patients with tumors of hematopoietic or neuroendo­
Juvenile Hypoglycemia crine origin. The most frequent nonpancreatic tumors
Hypoglycemia of toy and miniature breed dogs younger associated with hypoglycemia are leiomyoma, leiomyo­
than 6 months of age is common. Deficiency of gluco­ sarcoma, hepatoma, hepatocellular carcinoma, and
neogenic precursors such as the amino acid alanine or an tumors with extensive hepatic metastasis.
age‐related transient malfunction or deficiency of
enzymes responsible for gluconeogenesis is implicated Pathophysiology
in this syndrome. Insufficient food supply of any cause Understanding the cause of hypoglycemia with NICTH
such as starvation or gastrointestinal disturbances may involves a brief review of the IGF system. The IGF sys­
cause hypoglycemia within 24 hours of fasting. In addi­ tem is composed of two IGF ligands (IGF‐1 and IGF‐2)
tion, underlying conditions such as PSVA that cause ano­ and two IGF receptors: the IGF‐1 receptor (IGF1R)
rexia or impaired liver function may contribute to the and IGF‐2 receptor (IGF2R). Both IGF‐1 and IGF‐2 are
precipitation of this syndrome. Many of these puppies structurally and functionally related to insulin but the
have a history of being recently purchased along with a glucose‐lowering effect of IGFs is 10 times lower than
recent change in environment and diet. Presenting signs that of insulin, although in healthy human subjects the
may include weakness, depression, vomiting and diar­ serum concentration of IGFs is about 1000 times
rhea with or without intestinal parasites, ataxia, stupor, higher than insulin. The crucial event in the develop­
and seizures. Similar forms of juvenile hypoglycemia ment of NICTH seems to be overexpression of the
have not been well documented in kittens. IGF‐2 gene by the tumor. NICTH is characterized by
recurrent fasting hypoglycemia and is associated with
Treatment and Prognosis the secretion of precursors of IGF‐2 (“big”‐IGF‐2) by
Intravenous administration of a 20% or 50% dextrose the tumor.
solution (0.8 mL to 0.2 mL per 100 g body weight respec­
tively) is indicated if there are neurologic signs. If the pup Diagnosis
can take the glucose solution orally, this is administered Dogs with hypoglycemia caused by NICTH are usually
at regular intervals until appetite returns. The small brought to the veterinarian with clinical signs of hypo­
amounts of food are given at two‐hour intervals. If tube glycemia, or hypoglycemia may be noted on a biochemi­
feeding is needed, oral rehydration is guided by electro­ cal profile in an asymptomatic patient during a wellness
lyte measurements. Clinical improvement occurs rapidly exam. The diagnosis of a nonislet cell tumor requires a