Results suggest that dogs with diabetes mellitus may have many concurrent disorders. The most commonly identified concurrent disorders included hyperadrenocorticism, urinary tract infection, dermatitis, otitis, acute pancreatitis, neoplasia, and hypothyroidism.

The aim of this study was to retrospectively describe the outcome of 127 dogs with naturally occurring diabetic ketoacidosis (DKA) and to examine the association between outcome of canine DKA and clinical and clinicopathologic findings. Eighty-two (65%) dogs were diagnosed with DKA at the time of initial diagnosis of diabetes mellitus (DM). Eighty-seven dogs (69%) had one or more concurrent disorders diagnosed at the time of hospitalization. Commonly identified concurrent conditions included acute pancreatitis (52, 41%), urinary tract infection (21, 20%), and hyperadrenocorticism (19, 15%). Dogs with coexisting hyperadrenocorticism were less likely to be discharged from the hospital (P = .029). Of 121 treated dogs, 89 dogs (70%) survived to be discharged from the hospital, with a median hospitalization of 6 days. Nonsurvivors had lower ionized calcium concentration (P < .001), lower hematocrit (P = .036), lower venous pH (P = .0058), and larger base deficit (P = .0066) than did survivors. Time from admission to initiation of subcutaneous insulin therapy was correlated with lower serum potassium concentration (P = .0056), lower serum phosphorus concentration (P = .0043), abnormally high white blood cell count (P = .0060), large base deficit (P = .0015), and low venous pH (P < .001). Multivariate analysis showed that base deficit was associated with outcome (P = .021). For each unit increase in the base deficit, there was a 9%) greater likelihood of discharge from the hospital. In conclusion, the majority of dogs with DKA were not previously diagnosed with DM. Concurrent conditions and electrolyte abnormalities are common in DKA and are associated with length of hospitalization. Survival was correlated to degree of anemia, hypocalcemia, and acidosis.

The objective of this study was to determine whether dogs with atherosclerosis are more likely to have concurrent diabetes mellitus, hypothyroidism, or hyperadrenocorticism than dogs that do not have atherosclerosis. A retrospective mortality prevalence casecontrol study was performed. The study group included 30 dogs with histopathological evidence of atherosclerosis. The control group included 142 dogs with results of a complete postmortem examination, a final postmortem examination diagnosis of neoplasia, and no histopathological evidence of atherosclerosis. Control dogs were frequency matched for age and year in which the postmortem examination was performed. Proportionate changes in the prevalence of diabetes mellitus, hypothyroidism, and hyperadrenocorticism were calculated by exact prevalence odds ratios (POR), 95% confidence intervals (95% CI), and P values. Multiple logistic regression analysis was used to examine the combined effects of prevalence determinants while controlling for age and year of postmortem examination. Dogs with atherosclerosis were over 53 times more likely to have concurrent diabetes mellitus than dogs without atherosclerosis (POR ϭ 53.6; 95% CI, 4.6-627.5; P ϭ .002) and over 51 times more likely to have concurrent hypothyroidism than dogs without atherosclerosis (POR ϭ 51.1; 95% CI, 14.5-180.1; P Ͻ .001). Dogs with atherosclerosis were not found to be more likely to have concurrent hyperadrenocorticism than dogs that did not have atherosclerosis (POR ϭ 1.8; 95% CI, 0.2-17.6; P ϭ .59). Diabetes mellitus and hypothyroidism, but not hyperadrenocorticism, are more prevalent in dogs with atherosclerosis compared to dogs without atherosclerosis on postmortem examination.

Intestinal lymphangiectasia in dogs appears to be a heterogeneous disorder characterized by various degrees of panhypoproteinemia, hypocholesterolemia, lymphocytopenia, and imaging abnormalities. In most dogs, the severity of hypoalbuminemia appears to offer the best correlation with severity of histologic lesions of lymphangiectasia. Imaging abnormalities are common in dogs with intestinal lymphangiectasia but are not specific enough to differentiate this disorder from other gastrointestinal disorders, nor are they predictive of histologic severity.

The pathophysiology of canine diabetes remains poorly understood, in part due to enigmatic clinical features and the lack of detailed histopathology studies. Canine diabetes, similar to human type 1 diabetes, is frequently associated with diabetic ketoacidosis at onset or after insulin omission. However, notable differences exist. Whereas human type 1 diabetes often occurs in children, canine diabetes is typically described in middle age to elderly dogs. Many competing theories have been proposed regarding the underlying cause of canine diabetes, from pancreatic atrophy to chronic pancreatitis to autoimmune mediated β-cell destruction. It remains unclear to what extent β-cell loss contributes to canine diabetes, as precise quantifications of islet morphometry have not been performed. We used high-throughput microscopy and automated image processing to characterize islet histology in a large collection of pancreata of diabetic dogs. Diabetic pancreata displayed a profound reduction in β-cells and islet endocrine cells. Unlike humans, canine non-diabetic islets are largely comprised of β-cells. Very few β-cells remained in islets of diabetic dogs, even in pancreata from new onset cases. Similarly, total islet endocrine cell number was sharply reduced in diabetic dogs. No compensatory proliferation or lymphocyte infiltration was detected. The majority of pancreata had no evidence of pancreatitis. Thus, canine diabetes is associated with extreme β-cell deficiency in both new and longstanding disease. The β-cell predominant composition of canine islets and the near-total absence of β-cells in new onset elderly diabetic dogs strongly implies that similar to human type 1 diabetes, β-cell loss underlies the pathophysiology of canine diabetes.