Page 860 - Small Animal Internal Medicine, 6th Edition

832 PART VI Endocrine Disorders

Cat has pancreatic pathology and subclinical diabetes BOX 49.10
VetBooks.ir Inflammation, infection, neoplasia, hormonal Factors Involved in Diabetic Remission in Cats

disorder, or drug causes insulin antagonism
Recently diagnosed diabetic cat
Correction of glucose toxicity
Maintaining good glycemic control
Carbohydrate intolerance and hyperglycemia develop
Using long-acting insulin preparations twice daily
Feeding low carbohydrate diets
Avoiding insulin resistant medications (e.g.,
Glucose toxicity causes apparent IDDM
glucocorticoids)
Nature and reversibility of concurrent disorders
Insulin treatment and correction (control) Frequent evaluations
of concurrent disorders initiated Intensity of home blood glucose monitoring
Ability to attain blood glucose targets

Control of hyperglycemia
secretion and insulin sensitivity are poorly understood,
although oxidative stress and inflammatory cytokines are
Resolution of glucose toxicity
believed to play a role (Zini et al., 2009a). Reversal of glucose
toxicity is an important mechanism to explain diabetic
β cells regain function remission. The key to diabetic remission lies in the ability to
and insulin resistance resolves correct insulin resistance and attain and maintain good gly-
cemic control of the diabetic state. Factors involved in dia-
betic remission are listed in Box 49.10. Published remission
Loss of insulin requirements
and resolution of IDDM rates vary, but most veterinary internists report rates between
25% and 50%. A recent study among primary care veterinar-
ians in the southern United States under “everyday condi-
Cat returns to subclinical diabetic state tions” reported an approximate remission rate of 26% (Smith
et al., 2012).
FIG 49.13
Sequence of events in the development and resolution of an
insulin-requiring diabetic episode in cats with transient Clinical Features
diabetes. (From Feldman EC et al: Canine and feline
endocrinology and reproduction, ed 3, St Louis, 2004, WB SIGNALMENT AND RISK FACTORS
Saunders.) Although diabetes mellitus may be diagnosed in cats of any
age, most diabetic cats are 7 to 15 years of age at the time of
diagnosis. Diabetes mellitus occurs predominantly in neu-
insulin secretagogues, thereby mimicking type 1 IDDM. The tered male cats. Studies with a large cohort of cats performed
effects of glucose toxicity are potentially reversible upon cor- in in Sweden and the United Kingdom identified Burmese,
rection of the hyperglycemic state. The clinician makes a Russian Blue, Norwegian Forest, and Abyssinian cats at
correct diagnosis of diabetes mellitus; insulin therapy, dis- increased risk for diabetes mellitus. Additional risk factors
continuation of insulin antagonistic drugs, and treatment of included age, increasing body weight, indoor confinement,
insulin-antagonistic disorders improve hyperglycemia and and possibly dry cat food in normal weight cats.
insulin resistance; glucose toxicity resolves; β-cell function
improves; insulin secretion returns; and an apparent IDDM HISTORY
state resolves (Nelson et al., 1999). Diabetic remission usually The history in virtually all diabetic cats includes polydipsia,
occurs during the first 2 to 3 months of treatment, but we polyuria, polyphagia, and weight loss. A common complaint
have seen cats undergo remission up to a year or longer after of cat owners is the constant need to change the litter and an
initiating insulin treatment. Cats that experience diabetic increase in the size of the litter clumps. Additional clinical
remission have impaired glucose tolerance. Approximately signs include lethargy; decreased interaction with family
30% of cats relapse, usually within 5 to 6 months of discon- members; lack of grooming behavior and development of a
tinuing insulin. The future requirement for insulin treatment dry, lusterless, unkempt, or matted haircoat; and decreased
depends on the underlying abnormality in the islets. If the jumping ability, rear limb weakness, or development of a
abnormality is progressive (e.g., amyloidosis), eventually plantigrade posture (Fig. 49.14; Video 49.1). If the client does
enough β cells will be destroyed and IDDM will develop. not notice clinical signs associated with uncomplicated dia-
Glucose toxicity is a secondary event that only becomes betes, a diabetic cat may be at risk for developing DKA. The
apparent after hyperglycemia has occurred. The cellular time sequence from the onset of initial clinical signs to the
mechanisms by which chronic hyperglycemia affects insulin development of DKA is unpredictable.