Protein-losing enteropathy in dogs is associated with decreased fecal proteolytic activity

Background: Measurement of proteolytic activity in feces is a traditional method for the diagnosis of exocrine pancreatic insufficiency (EPI). A drawback of this method is the occurrence of falsely low results that may lead to a false‐positive diagnosis of EPI. We hypothesized that intestinal loss of serum proteinase inhibitors in protein‐losing enteropathy (PLE) may inhibit fecal proteolytic activity and be a potential source of false low results. Objective: The objective of this study was to determine the effect of PLE on fecal proteolytic activity in dogs. Methods: Fecal proteolytic activity was measured using a radial diffusion casein digestion assay in 12 samples from 4 clinically healthy control dogs and 30 samples from 16 dogs with PLE. Gastrointestinal protein loss was assessed using an ELISA to determine fecal canine α₁‐proteinase inhibitor concentration. The relationship between the concentration of canine α₁‐proteinase inhibitor in the feces and the diameter cleared in the casein digestion assay was determined. The mean clearing diameter was compared between control dogs and dogs with PLE. Results: A significant negative correlation was observed between fecal canine α₁‐proteinase inhibitor concentration and casein clearing diameter (P < .001, Pearson r=—.6317, r 2 =.3999). Mean clearing diameter was significantly lower in dogs with PLE than in control dogs (12.63 vs 16.83 mm, P < .001, two‐tailed Student's t‐test). Conclusion: Increased fecal loss of α₁‐proteinase inhibitor in dogs with PLE is associated with a significant decrease in fecal proteolytic activity and may result in a false positive diagnosis of EPI.     

Protein-losing enteropathy in the Lundehund

Protein-losing enteropathy in the Lundehund, a possible hereditary disease, characterized clinically by intermittent diarrhoea, vomiting, wasting, ascites and oedema, is described. Serum examinations revealed low values of protein and calcium.
Post-mortem changes consisted of thickened duodenal and jejunal mucosa with blunt, short, anastomosing villi and plasma cell infiltration. Distended lacteals and dilated cystic glands were found together with elongated ducts, lymphangiectasis and ascites.
Aetiological mechanisms are discussed.     

Prognostic value of small intestinal dilatation in dogs with protein-losing enteropathy

To date, little is known about the prognostic significance of ultrasonographic findings in dogs with protein-losing enteropathy (PLE). The aim of this retrospective study was to examine the prognostic value of ultrasonographic findings in dogs with PLE. A total of 26 dogs with PLE were included: 20 dogs with chronic enteropathy and 6 dogs with gastrointestinal lymphoma. The presence of small intestinal dilatation was associated with shorter survival time in dogs with PLE (P=0.003). The presence of hyperechoic intestinal mucosal striations was associated with longer survival time in dogs with PLE (P=0.0085). The results of the current study indicate that the presence of small intestinal dilatation might be associated with poor prognosis in dogs with PLE.     

Hypercoagulability in dogs with protein-losing enteropathy

Background: Dogs with protein‐losing enteropathy (PLE) have previously been reported to present with thromboembolism; however, the prevalence and pathogenesis of hypercoagulability in dogs with PLE have not been investigated so far. Hypothesis: Dogs with PLE are hypercoagulable compared with healthy control dogs. Animals: Fifteen dogs with PLE. Thirty healthy dogs served as controls (HC). Methods: A prospective study was performed including 15 dogs with PLE. All dogs were scored using the canine chronic enteropathy activity index (CCECAI). Thromboelastography (TEG) and other measures of coagulation were evaluated. Recalcified, unactivated TEG was performed and reaction time (R), kinetic time (K), alpha angle (α), and maximum amplitude (M_A) values were recorded. Nine dogs were reassessed after initiation of immunosuppressive treatment. Results: All dogs with PLE in the study were hypercoagulable with decreased R (PLE: median 7.8, range [2.4–11.2]; HC: 14.1 [9.1–20.3]), decreased K (PLE: 2.5 [0.8–5.2]; HC: 8.25 [4.3–13.1]), increased α (PLE: 56.7 [38.5–78.3]; HC: 25.6 [17–42.4]), and increased M_A (PLE: 68.2 [54.1–76.7]; HC: 44.1, [33.5–49]) (all P < .001). Median antithrombin (AT) concentration was borderline low in PLE dogs; however, mean serum albumin concentration was severely decreased (mean 1.67 g/dL ± 5.1, reference range 2.8–3.5 g/dL). Despite a significant improvement in serum albumin and CCECAI, all 9 dogs with PLE were hypercoagulable at re‐examination. Conclusions and Clinical Importance: The hypercoagulable state in dogs with PLE cannot be solely attributed to loss of AT. Despite good clinical response to treatment, dogs remained hypercoagulable and could therefore be predisposed to thromboembolic complications.     

Myotonia associated with hyper-adrenocorticism in two dogs

Two dogs developed a disabling gait abnormality characterised by stiffness. The abnormality was consistent with a diagnosis of myotonia secondary to hyper-adrenocorticism. The first dog had iatrogenic hyperadrenocorticism, and its signs improved substantially after corticosteroid administration was gradually withdrawn. The second had pituitary-dependent hyperadrenocorticism, but myotonic signs progressed despite effective mitotane therapy. Procainamide administration reduced the myotonic stiffness in the second case.     

Protein-losing enteropathy in a dog with lymphangiectasia,lymphoplasmacytic enteritis and pancreatic exocrine insufficiency

This is a report of seven-year-old male Akita mixed dog, with protein-losing enteropathy (PLE). He had a history of chronic vomiting and diarrhea with anorexia/hyporexia. Previously he suffered acute abdomen about eight months prior to this visit. Our dog showed uncommon combination of diseases that could cause PLE since it was affected by inflammatory bowel disease (IBD), intestinal lymphangiectasia (IL), and exocrine pancreatic insufficiency (EPI). The dog had most of the abnormalities found in IL, as well as hypoalbuminemia, hyperglobulinemia, lymphopenia, hypocalcemia, and hypercholesterolemia. During endoscopy exam, we found changes characteristic of IL such as irregular small white spots. We took biopsies from stomach, duodenum, and cecum. These biopsies showed infiltration by lymphocytes and plasmatic cells in the lamina propria also, the duodenal biopsies showed moderate dilation of the lymphatic vessels. The patient had 2.1?µg/mL of TLI, this result was compatible with EPI. We assume that the first pathology in this animal was IBD, which caused chronic pancreatitis (CP) that in turn progressed to EPI. It is also possible that IL was secondary to IBD. We have reported for the first time the correlation of IBD and EPI in dogs. This should change our approach to treating chronic diarrhea in dogs. Therefore, we propose that dogs diagnosed with EPI should also be subjected to endoscopy and intestinal biopsy. Similarly, to rule out secondary EPI, TLI should be measured routinely in dogs with IBD.     

Retinopathy associated with ivermectin toxicosis in two dogs

CASE DESCRIPTION: 2 dogs (dogs 1 and 2) were examined for sudden onset of blindness. Both dogs had mild obtundation and mydriasis in both eyes. It was thought that dog 1 may have ingested ivermectin; dog 2 had been treated with ivermectin for demodectic mange. CLINICAL FINDINGS: On initial examination, both dogs had mydriasis and decreased pupillary light reflexes in both eyes. Dog 1 had an absent menace response bilaterally. Fundic examination of both eyes in both dogs revealed regions of multifocal retinal edema and folds with low-lying retinal separation. The electroretinogram was extinguished in dog 1 and attenuated in dog 2. Ivermectin was detected in serum samples from both dogs. TREATMENT AND OUTCOME: Both dogs made a complete clinical recovery following cessation of exposure to ivermectin; electroretinographic findings improved, and retinal edema resolved with some residual chorioretinal scarring. CLINICAL RELEVANCE: To our knowledge, this is the first report of resolution of retinal edema and electroretinographic changes associated with ivermectin toxicosis in dogs. In dogs that develop blindness suddenly, fundic examination, electroretinography, and assessment of serum ivermectin concentration are diagnostically useful, even if exposure to ivermectin is unknown.     

Electrocardiographic abnormalities associated with tetanus in two dogs

Bradycardia, sinus arrest, and second-degree atrioventricular block developed in 2 dogs with tetanus. Clinical signs attributable to bradycardia were not apparent. Administration of atropine resulted in resolution of the arrhythmias. Both dogs responded well to supportive treatment; the bradycardia resolved within 4 days of onset without specific treatment. Tetanus should be included in the differential diagnosis when increased neuromuscular excitability and bradycardia are evident, as is found in toxicity with acetylcholinesterase inhibitors, increased intracranial pressure, and other neurologic disorders.     

Hematologic changes associated with half-body irradiation in dogs with lymphoma

BACKGROUND: Reports describe the technique and efficacy of half-body irradiation (HBI) of dogs with lymphoma, but few describe the distinctive toxicoses associated with the combination of HBI and chemotherapy. HYPOTHESIS: HBI would transiently affect myelocytic and erythroid variables as assessed by serial analysis of complete blood counts. ANIMALS: Twenty-nine dogs with lymphoma treated with HBI during 2002 and 2003. METHODS: A retrospective study of medical records of 29 dogs was performed. Two HBI protocols were used, resulting in delivery of either 6 Gy or 8 Gy to each half of the body, 1 month apart. Dogs received chemotherapy before, during, or after irradiation, or at multiple times. Serial hematology was available for all dogs. Data were analyzed between collection periods by analysis of variance (ANOVA) RESULTS: The mean granulocyte count significantly (P < .01) decreased from 10,017 cells/microL (data range 3,001-20,170 cells/ microL) before the first radiation treatment to 3,250 cells/microL (820-4,400 cells/microL) at week 5 (P < .01). Three weeks after this nadir, the mean increased to 10,150 cells/microL (900-26,700 cells/microL). The hematocrit did not change (36-38%). Thrombocytopenia (<100,000/microL) occurred in 10 dogs. Two dogs died because of complications associated with thrombocytopenia. No significant difference in toxicity was found between the 6 Gy and 8 Gy group. CONCLUSIONS AND CLINICAL IMPORTANCE: HBI was myelosuppressive but effects were short term and resolved in 22 of 24 dogs. Further studies are needed to elucidate the safety and role of HBI in the treatment of dogs with lymphoma.     

Ulcerative colitis and protein losing enteropathy associated with intestinal salmonellosis and histoplasmosis in a horse

Ulcerative colitis, protein losing enteropathy and intestinal histoplasmosis-salmonellosis were diagnosed in a six-year-old Quarterhorse stallion. For six months before examination, the horse experienced a slow continual loss of weight. During the 17 day period of hospitalisation the horse developed progressive generalised oedema. On the 12th day of hospitalisation a severe profuse watery diarrhoea began; the horse was killed five days later.