Page 858 - Small Animal Internal Medicine, 6th Edition

830 PART VI Endocrine Disorders

Systemic Hypertension histologic findings in the pancreatic islets include islet-
Diabetes mellitus and hypertension commonly coexist in specific amyloidosis, β-cell vacuolar degeneration, and a
VetBooks.ir dogs. Struble et al. (1998) found the prevalence of hyperten- reduction in the number of pancreatic islets, insulin-
containing β cells in the islet, or both. Genetics undoubtedly
sion to be 46% in 50 insulin-treated diabetic dogs in which
hypertension was defined as systolic, diastolic, or mean
the United Kingdom, but the role of genetics in other breeds
blood pressure greater than 160, 100, or 120 mm Hg, respec- plays a role in Burmese cats in Australia, New Zealand, and
tively. The development of hypertension was associated with remains to be determined. Additional risk factors for type 2
the duration of diabetes and an increased albumin/creatinine diabetes mellitus include male neutered cat, inactivity
ratio in the urine. Diastolic and mean blood pressure values (indoor cat), increasing age, insulin-resistant medications
were higher in dogs with longer duration of disease. A cor- (e.g., glucorticoids) and disease (e.g., hypersomatotropism),
relation between control of glycemia and blood pressure was and perhaps most important – obesity.
not identified. Systemic hypertension may result from exist- Adipose tissue produces two important adipokines: adi-
ing subclinical kidney disease or develop secondary to the ponectin, an adipokine that enhances insulin sensitivity and
effects of diabetes on vascular compliance, glomerular func- has antiinflammatory properties, and leptin, an adipokine
tion, or some other mechanism. Treatment for hypertension involved in appetite suppression, energy expenditure, and
should be initiated if the systolic blood pressure is consis- modulation of insulin sensitivity (Hoenig, 2012). Obesity
tently greater than 160 mm Hg. results in a decrease in circulating adiponectin and causes
leptin resistance. Adipose tissue also secretes a number of
Prognosis proinflammatory cytokines (e.g., TNF-α, IL-6) that nega-
The prognosis for dogs diagnosed with diabetes mellitus tively influence insulin signaling and cause insulin resistance
depends, in part, on owner commitment to treating the dis- (Hoenig et al., 2006). All of these actions promote the devel-
order, ease of glycemic regulation, presence and reversibility opment of diabetes, and all of these actions are potentially
of concurrent disorders, avoidance of chronic complications reversible with weight loss.
associated with the diabetic state, and minimizing the impact Islet amyloidosis also plays an important role in the
of treatment on the quality of life of the owner (see Table development of type 2 diabetes in cats. Islet-amyloid poly-
49.2). In a large study involving insured dogs in Sweden, the peptide (IAPP), or amylin, is the principal constituent of
median survival time after the first diabetes mellitus claim amyloid in adult cats with diabetes, is stored in β-cell secre-
(686 dogs) was 57 days and for dogs surviving at least one tory granules, and is co-secreted with insulin by the β cell.
day (463 dogs) was 2.0 years (Fall et al., 2007). For dogs Stimulants of insulin secretion also stimulate the secretion of
surviving at least 30 days after the first diabetes mellitus amylin. Chronic increased secretion of insulin and amylin,
claim (347 dogs), the proportion of dogs surviving 1, 2, and as occurs with obesity and other insulin-resistant states,
3 years was 40%, 36%, and 33%, respectively. However, sur- results in aggregation and deposition of amylin in the islets
vival times will vary between countries and between socio- as amyloid (Fig. 49.12). IAPP-derived amyloid fibrils are
economic regions within a country, and survival time is cytotoxic and may lead to a decline in β-cell function and
somewhat skewed because dogs are often 8 to 12 years old β-cell apoptosis (Costes et al., 2013). Loss of β-cell function
at the time of diagnosis, and a relatively high mortality rate may be present before amyloid depositions are visible in
exists during the first 6 months because of concurrent life- the islets.
threatening or uncontrollable disease (e.g., ketoacidosis, If deposition of amyloid is progressive, as occurs with a
acute pancreatitis, kidney failure). In our experience, dia- sustained demand for insulin secretion in response to per-
betic dogs that survive the first 6 months can easily maintain sistent insulin resistance, islet cell destruction progresses and
a good quality of life for longer than 5 years with proper care eventually leads to diabetes mellitus. The severity of islet
by the owners, timely evaluations by the veterinarian, and amyloidosis and β-cell destruction determines, in part,
good client-veterinarian communication. whether the diabetic cat is insulin-dependent or not and
whether diabetic remission is possible. Total destruction of
the islets results in insulin-dependent diabetes mellitus
DIABETES MELLITUS IN CATS (IDDM) and the need for insulin treatment for the rest of
the cat’s life. Partial destruction of the islets may or may not
Etiology, Classification, and Diabetic result in clinically evident diabetes, insulin treatment may or
Remission may not be required to control glycemia, and diabetic remis-
Type 1 diabetes mellitus with an underlying immune- sion may or may not occur once treatment is initiated. If
mediated etiology appears to be rare in cats. Although lym- amyloid deposition is progressive, the cat will progress from
phocytic infiltration of islets has been described in diabetic subclinical diabetes to noninsulin dependent diabetes
cats, this histologic finding is not common, and β-cell and (NIDDM; i.e., glycemia can be controlled with correction of
insulin autoantibodies have not been identified in newly insulin resistance and diet) and ultimately to IDDM. The
diagnosed diabetic cats. difference between IDDM and NIDDM is primarily a differ-
Type 2 diabetes predominates in cats and is characterized ence in severity of loss of β cells and severity and reversibility
by insulin resistance and dysfunctional β cells. Common of concurrent insulin resistance.