Evaluation of serum values of pancreatic enzymes after endoscopic retrograde pancreatography in dogs

OBJECTIVE: To assess the safety of endoscopic retrograde pancreatography (ERP) in dogs by performing repeated clinical examinations and laboratory analyses of serum amylase, lipase, canine trypsin-like immunoreactivity (cTLI), and canine pancreatic elastase 1 (cE1) after the procedure. ANIMALS: 7 healthy Beagles. PROCEDURES: Clinical examinations were performed and blood samples obtained for serum enzyme determinations before and at intervals (10 minutes; 2, 4, and 6 hours; and 1, 2, and 3 days) after ERP. RESULTS: Repeated clinical examinations revealed no signs of ERP-induced complications in the 7 dogs. Results of repeated laboratory tests indicated a transient increase in serum values of amylase, lipase, and cTLI but not cE1. Mean +/- SD lipase activity increased from 120.7 +/- 116.4 U/L to 423.4 +/- 243.1 U/L at 4 hours after ERP. Median serum cTLI concentration increased from 16.2 microg/L (range, 77 to 26.5 microg/L) to 34.9 microg/L (range, 16.6 to 68.3 microg/L) 10 minutes after ERP. Enzyme values returned to baseline levels at the latest on day 2 in 6 of 7 dogs. Highest values for serum amylase, lipase, and cTLI and their delayed return to baseline values were detected in 1 dog with contrast filling of the pancreatic parenchyma. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that ERP appears to be a safe imaging technique of pancreatic ducts in healthy dogs, although it induced a transient increase in serum values of pancreatic enzymes. In dogs, repeated clinical examinations and serum enzyme determinations can be used to monitor ERP-induced complications such as acute pancreatitis.     

Asparaginase-associated pancreatitis in a dog

A dog with lymphosarcoma was evaluated for vomiting, lethargy, and abdominal pain 48 h after treatment with L-asparaginase. Based on drug administration, clinical signs, bloodwork, and elevated canine pancreatic lipase immunoreactivity, L-asparaginase-associated pancreatitis was diagnosed. This is an acknowledged toxicity; however, its pathophysiology and incidence rate in veterinary patients are unknown and sparsely documented.     

Pancreatic abscess in dogs: six cases (1978-1986)

Pancreatic abscess was diagnosed by exploratory celiotomy in 6 dogs. The most common clinical signs included acute onset of lethargy (n = 5), anorexia (n = 6), vomiting (n = 5), and diarrhea (n = 2). Physical examination revealed pain response to abdominal palpation (n = 5), depression (n = 5), icterus (n = 3), fever (n = 3), and cranial abdominal mass (n = 2). Consistent preoperative clinicopathologic abnormalities included leukocytosis with left shift, observance of toxic neutrophils on the blood smear, hyperlipasemia, hyperamylasemia, hyperbilirubinemia, and increased serum alkaline phosphatase activity. In 5 of 6 dogs, abdominal radiography revealed increased soft tissue density in the cranial portion of the abdomen. Ultrasonography performed on 4 dogs confirmed pancreatic mass. In all dogs, exploratory celiotomy revealed a cavitary pancreatic mass that contained sterile, mucopurulent material. Histopathologic diagnoses included acute necrotizing or chronic-active pancreatitis and steatitis. Two dogs were euthanatized at the time of diagnosis, and the remaining 4 were treated by use of pancreatic debridement(s), open abdominal drainage, and intensive administration of fluids and antibiotics. One dog was euthanatized 4 days after surgery, because of progressive pancreatic abscessation. Three dogs recovered and were discharged.     

Serum Pancreatic Lipase Immunoreactivity Concentrations in Dogs Treated with Potassium Bromide and/or Phenobarbital

Potassium bromide, phenobarbital, or a combination of both is commonly used in the treatment of canine epilepsy. Several cases of clinical pancreatitis have been reported in dogs after treatment with potassium bromide, but the risk of elevated serum canine pancreatic lipase immunoreactivity concentrations in dogs treated with potassium bromide and/or phenobarbital has not previously been evaluated in a large group of dogs. This study suggests an increased risk for elevated serum canine pancreatic lipase immunoreactivity concentrations and possibly pancreatitis in dogs treated with potassium bromide or phenobarbital alone or in combination.     

Observational study of 14 cases of chronic pancreatitis in dogs

This study reports the clinical, clinicopathological and ultrasonographic findings from dogs with chronic pancreatitis (CP). Fourteen dogs with clinical signs consistent with CP and histological confirmation of the disease were evaluated. Abdominal ultrasound and clinical pathology results were recorded. Sensitivities of pancreatic enzymes for diagnosis of CP were calculated with two different cut-off values. The mean age of affected dogs was 9.1 years. Spaniels were the most common breed with CP, representing seven of the 14 dogs in this study. CP was histologically severe in nine cases. Most dogs showed chronic low-grade gastrointestinal signs and abdominal pain. Five dogs had exocrine pancreatic insufficiency and five dogs had diabetes mellitus. The sensitivity of elevated trypsin-like immunoreactivity for CP was 17 per cent. The sensitivities of canine pancreatic lipase immunoreactivity, lipase and amylase for CP were 44 to 67 per cent or 14 to 28 per cent depending on the cut-off value used. Cholesterol was elevated in 58 per cent of samples. Liver enzymes were often elevated. The pancreas appeared abnormal on 56 per cent of ultrasound examinations. Ten dogs had died by the end of the study period; only one case was due to CP.     

CT angiographic changes in dogs with acute pancreatitis: A prospective longitudinal study

Computed tomographic angiography (CTA) has recently been shown to be a useful tool in the diagnosis of acute canine pancreatitis, the identification of pancreatic necrosis, and the detection of sequelae. Evidence of pancreatic necrosis on CTA has been shown to be correlated with a poorer outcome in both humans and dogs and early diagnosis and intervention may improve outcomes. In humans, pancreatic necrosis is typically evident on CTA within 48 h of clinical signs, thus, repeat CTA examinations are often performed to identify pancreatic necrosis that may not have been evident on CTA examinations performed early in the course of disease. Published information investigating the timing of CTA examinations and the use of serial CTA in dogs with acute pancreatitis is lacking. In this prospective, longitudinal study, CTA examinations were performed at the time of hospitalization and repeated 3‐5 days later in 11 dogs suffering from acute canine pancreatitis to determine if pancreatic necrosis or sequelae are under diagnosed on examinations performed at the time of hospitalization. Computed tomographic angiography studies were evaluated for changes in pancreatic size, pancreatic contrast enhancement, and peri‐pancreatic tissues and vessels. The only statistically significant difference between the initial and repeat CTA examinations was the improvement of fat stranding on the repeat CTA examinations (P < .045). Based on these results, CTA performed at the time of admission is likely adequate in the diagnosis and evaluation of dogs with acute pancreatitis. Repeat CTA examinations are unlikely to add additional information in the absence of worsening clinical signs.     

Increased canine pancreatic lipase immunoreactivity (cPLI) and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) lipase in dogs with evidence of portal hypertension and normal pancreatic histology: a pilot study

The clinical presentations of both liver disease and pancreatitis are nonspecific and overlapping, which may cause difficulty in diagnosis. In our retrospective pilot study, we assessed whether dogs with evidence of portal hypertension and absence of pancreatitis on pancreatic histology have increases in canine pancreatic lipase immunoreactivity (cPLI) and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) lipase. We included dogs that had been presented between 2008 and 2019 if they had normal pancreatic histology, histologically confirmed hepatopathy, and if canine pancreas-specific lipase (Spec cPL; Idexx) or DGGR lipase had been measured. Only dogs with portal hypertension were included. Six dogs fulfilled the inclusion criteria. Four of 6 and 2 of 6 dogs had Spec cPL and DGGR lipase exceeding the upper reference limit, respectively. From the 4 dogs with increased Spec cPL, 2 had concentrations of 200–400 µg/L and 2 had concentrations ≥ 400 µg/L. Our results suggest that canine portal hypertension might lead to increased Spec cPL and DGGR lipase values in the absence of pancreatitis on histology. Until more evidence in a larger number of dogs with portal hypertension is available, both tests should be interpreted cautiously in the presence of portal hypertension.     

Evaluation of 1,2-O-dilauryl-rac-glycero glutaric acid-(6′-methylresorufin) ester (DGGR) and 1,2-diglyceride lipase assays in dogs with naturally occurring hypercortisolism

1,2-O-dilauryl-rac-glycero glutaric acid-(6′-methylresorufin) ester (DGGR) lipase activity has been proposed as a faster and less expensive test used in the diagnosis of acute pancreatitis (AP) compared to canine pancreatic lipase immunoreactivity (cPLI), which is considered the most sensitive and specific serum test available for dogs. Elevations in lipase activity have been observed in dogs with naturally occurring hypercortisolism (HC) and in those treated with exogenous steroids, which complicates the diagnosis of AP in dogs with HC. We compared lipase activity measured by DGGR and 1,2-diglyceride (1,2-DiG) assays in 22 dogs with HC, 22 with AP, and 22 healthy dogs. The dogs with HC had no clinical signs or ultrasonographic findings consistent with AP. DGGR lipase activity was elevated in 64% and 73% of the dogs with HC and AP, respectively, and in 18% of healthy dogs. 1,2-DiG lipase activity was high in 23% and 36% of the dogs with HC and AP, respectively, and in 5% of the healthy dogs. Both DGGR and 1,2-DiG lipase activities were significantly different between the healthy dogs and the other 2 groups, whereas no differences were detected between the dogs with HC and those with AP. Our results support a lack of specificity for both DGGR and 1,2-DiG lipase activity assays in aiding the diagnosis of AP in dogs with HC.     

A pilot study evaluating changes in pancreatic lipase immunoreactivity concentrations in canines treated with L-asparaginase (ASNase), vincristine, or both for lymphoma

L-asparaginase (ASNase) is a common chemotherapy agent for the treatment of lymphoid malignancies. L-asparaginase has been reported to cause clinical pancreatitis in both humans and canines. Canine pancreatic lipase immunoreactivity (cPLI) is now a common diagnostic tool for evaluating pancreatitis in dogs. A total of 52 dogs were enrolled into this study. Canine pancreatic lipase immunoreactivity (cPLI) concentrations were evaluated before and after administration of ASNase, vincristine, or both. All dogs enrolled in the study were evaluated for signs compatible with clinical pancreatitis. No dogs receiving ASNase alone showed evidence of clinical pancreatitis after administration. Also, there was no statistically significant change in cPLI concentrations before or after treatment. Fourteen percent of dogs that received both vincristine and ASNase concurrently had elevated concentrations of cPLI after treatment. Of the 11 dogs with clinical signs compatible with pancreatitis after any chemotherapy treatment, no dog had a cPLI concentration > 400 μg/dL. In conclusion, ASNase did not cause clinical pancreatitis in this cohort of dogs but larger sample sizes are required to further validate this data.     

Occurrence, clinical features and outcome of canine pancreatitis (80 cases)

Medical records of 80 dogs diagnosed with acute pancreatitis during a 4-year period were evaluated regarding history, breed predilection, clinical signs and additional examination findings. Cases were selected if compatible clinical symptoms, increased serum activity of amylase or lipase and morphologic evidence of pancreatitis by ultrasonography, laparotomy or necropsy were all present. Like in other studies, neutered dogs had an increased risk of developing acute pancreatitis. Although breed predilection was consistent with earlier reports, some notable differences were also observed. Apart from Dachshunds, Poodles, Cocker Spaniels and Fox Terriers, the sled dogs (Laikas, Alaskan Malamutes) also demonstrated a higher risk for pancreatitis according to our results. Concurrent diseases occurred in 56 dogs (70%), diabetes mellitus (n = 29, 36%) being the most common. Clinical signs of acute pancreatitis were similar to those observed in other studies. The study group represented a dog population with severe acute pancreatitis, having a relatively high mortality rate (40%) compared to data of the literature. Breed, age, gender, neutering and body condition had no significant association with the outcome. Hypothermia (p = 0.0413) and metabolic acidosis (p = 0.0063) correlated significantly with poor prognosis and may serve as valuable markers for severity assessment in canine acute pancreatitis.     

Toxicoses associated with administration of mitoxantrone to dogs with malignant tumors

One hundred twenty-nine dogs with histologically confirmed malignant tumors were used in a prospective study to determine the toxicity of the new dihydroxyquinone derivative of anthracene, mitoxantrone, which was administered IV at 21-day intervals at dosages ranging from 2.5 to 5 mg/m2 body surface area. Each dog was evaluated for signs of toxicosis for 3 weeks after each dose was administered or until the dog died, whichever came first. The number of dogs in each evaluation period were as follows: 1 dose (n = 129), 2 doses (n = 82), 3 doses (n = 43), 4 doses (n = 26), 5 doses (n = 19), 6 doses (n = 9), 7 doses (n = 6), 8 doses (n = 5), 9 doses (n = 3), and 10 doses (n = 1). The most common signs of toxicosis were vomiting, diarrhea, anorexia, and sepsis secondary to myelosuppression. None of the dogs died of complications resulting from mitoxantrone treatment. Dogs with signs of toxicosis during the 21-day interval from administration of the first dose of mitoxantrone were 95 times (P = 0.003) more likely to develop signs of toxicosis during the 21-day interval from the second dose of mitoxantrone. Similarly, dogs that developed signs of toxicosis during the 21-day interval from the administration of the second dose were 34 times (P less than 0.001) more likely to develop signs of toxicosis during the 21-day interval from the administration of the third dose. With each 1 mg/m2 increase in mitoxantrone, the odds of developing signs of toxicosis increased by 5.9 fold (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Elevated canine pancreatic lipase immunoreactivity concentration in dogs with inflammatory bowel disease is associated with a negative outcome

O bjectives : To investigate whether elevated canine pancreatic lipase immunoreactivity (CPLI) concentrations in dogs with inflammatory bowel disease (IBD) is associated with a worse clinical outcome.
M ethods : Serum CPLI assays were performed on serum stored from cases diagnosed with IBD. Thirty-two dogs with CPLI results within the reference range were designated as the control group and 15 dogs had CPLI above the reference range. Clinical signs, age, serum lipase and amylase activities, serum albumin and cobalamin concentrations, abdominal ultrasound examination, histopathology on small intestinal biopsies, management of IBD and outcome were compared between the two groups.
R esults : No significant differences were found in clinical activity score (P=0·54), number of antibiotic-responsive disease cases (P=0·480), number of steroid-responsive disease cases (P=0·491), serum amylase activity (P=0·058), serum cobalamin concentration (P=0·61), serum albumin concentration (P=0·052), abdominal ultrasound score (P=0·23) and histopathology scores for IBD (P=0·74) between the two groups. Dogs with increased CPLI concentration were significantly older and had a higher serum lipase activity than dogs with a CPLI concentration within the normal reference range (P=0·001, P=0·001, respectively). Moreover, dogs with increased CPLI concentration responded poorly to steroid treatment (P=0·01) and were significantly more likely to be euthanased at follow-up (P=0·02).
C linical S ignificance : CPLI should be measured in cases of canine IBD as elevated CPLI was associated with a worse outcome.     

Foramen magnum decompression with cranioplasty for treatment of caudal occipital malformation syndrome in dogs

Objectives— To describe a cranioplasty procedure used in conjunction with foramen magnum decompression (FMD) for the treatment of canine caudal occipital malformation syndrome (COMS), and to evaluate the clinical outcome. Study Design— Prospective clinical study. Animals— Dogs (n=21) with COMS diagnosed by magnetic resonance imaging (MRI). Methods— After FMD, titanium screws were placed around the perimeter of the foramen magnum defect and a skull plate fashioned from titanium mesh and polymethylmethacrylate was attached to the back of the skull, using the titanium screws as anchor posts. Follow‐up was obtained by direct examination by the authors, telephone interviews with owners and referring veterinarians, and a questionnaire sent to owners of surviving dogs designed to assign objective measures of response to surgical intervention. Surgical success was defined as improvement in ≥1 aspects of clinical dysfunction (e.g. scratching, pain) postoperatively. Owner‐assigned pre‐ and postoperative quality‐of‐life (QOL) scores (1–5) for surviving dogs were compared using a Wilcoxon's signed rank test for paired data (P≤.05). Results— No intraoperative complications occurred and postoperative complications were limited to transient worsening of a pre‐existing head tilt and ataxia in 1 dog, and the need for oral pain medication for 1–4 weeks in 3 dogs. Seventeen dogs (81%) had clinical improvement after surgery. Although clinical signs resolved in 1 dog, it died after being hit by a car, 5 months after surgery. One dog had no change in clinical signs; this patient's clinical signs were not severe and the owners had opted for surgery primarily to prevent progression of disease. Two dogs were euthanatized; 1 because of no improvement of severe clinical signs, and 1 because of sustained recurrence of apparent head and neck pain 7 months later. One dog required a dorsal laminectomy at a second site (C1/C2 vertebral level), 2 months later. Four dogs has transient “flare‐ups” of apparent head/neck pain 2–13 months later; all resolved with transient re‐institution of oral analgesic therapy. Further surgery at the FMD was not needed. Based on the returned questionnaires, there was an overall significant improvement in QOL scores. Conclusions— FMD with cranioplasty was well tolerated, with no intraoperative complications, and minor postoperative complications. Most dogs improved clinically, and none required further surgery at the original FMD site. Clinical Relevance— FMD with cranioplasty may be an effective surgical method of treating dogs with COMS and is well tolerated. Based on prior reports of FMD for this disorder, it appears that cranioplasty may reduce the rate of surgical failure caused by formation of compressive scar tissue at the FMD site in the short term. Results of this preliminary study support further evaluation of the cranioplasty procedure in a larger group of dogs over a more extended follow‐up period.     

Amanita muscaria toxicosis in two dogs

Objective: To report the manifestations, history, and pathophysiologic basis of disease in 2 dogs with Amanita muscaria toxicosis. Case summaries: Two dogs were evaluated for an acute onset of gastroenteritis and seizures. A. muscaria toxicosis was suspected in each dog after confirmation of environmental exposure and visualization of ingested mushrooms in vomitus. The diagnosis was confirmed following identification of toxic Amanita metabolites in the urine and serum of each dog. Administration of supportive and symptomatic therapies resulted in the complete recovery of each animal. Unique information provided: Ingestion of the mushroom, A. muscaria, by dogs can result in acute gastrointestinal distress that precedes a potentially life‐threatening central neurologic syndrome characterized by seizures, tremors, and somnolence. Central nervous system dysfunction results primarily from the actions of ibotenic acid and its decarboxylation product, muscimol, which are analogues of the neurotransmitters glutamate and γ‐aminobutyric acid (GABA), respectively. Identification of these toxins in the urine and serum of affected dogs using high‐performance liquid chromatography (HPLC) provides a definitive diagnosis.     

Acute blindness associated with intracranial tumors in dogs and cats: eight cases (1984-1989)

Rostral and middle cranial fossa tumors affecting the optic chiasm and resulting in acute visual deficits were diagnosed in 7 dogs and 1 cat. Blindness and dilated nonresponsive pupils were the primary signs in all animals. Other concurrent neurologic deficits were either absent or were equivocal. Behavioral changes, including signs of depression and lethargy, were noticed in 1 dog and the cat subsequent to the onset of blindness. Retinal function was assessed as normal by electroretinography in all animals. The histologic necropsy diagnosis was pituitary carcinoma in 1 dog and the cat and paranasal sinus carcinoma with intracranial extension in 1 dog. A cytologic diagnosis of polycentric lymphosarcoma affecting the optic chiasm was diagnosed in 1 dog. In the remaining 4 dogs, results of computed tomographic imaging or endocrine function testing suggested pituitary gland neoplasia. Four dogs were treated with cobalt-60 radiation or chemotherapy. There was partial return of visual function in only 1 of the dogs treated with radiation.     

Exfoliative cutaneous lupus erythematosus in German shorthaired pointer dogs: disease development,progression and evaluation of three immunomodulatory drugs (ciclosporin,hydroxychloroquine, and adalimumab) in a controlled environment

Six German shorthaired pointer dogs (two females, four males) with exfoliative cutaneous lupus erythematosus (ECLE) were studied in a controlled setting until disease progression necessitated euthanasia. During investigations into the heredity of disease, five dogs received immunomodulatory drugs to alleviate clinical signs (lameness, erythema, scaling, erosions/ulcers). One dog served as a control and received only baths and oral fatty acids. Four dogs received ciclosporin (5–10 mg/kg once daily) for 4.5 months to 2 years. Ciclosporin decreased erythema and arthralgia, but did not halt worsening of lesions. Three dogs received hydroxychloroquine (5–10 mg/kg once daily) for 8 weeks, 7 months, and 9 months, respectively, with no side effects. Hydroxychloroquine appeared to slow clinical progression in two dogs on extended treatment and normalized globulin levels in all three dogs while receiving the drug. Four dogs, including the control dog, were euthanized between 1 and 4.5 years of age. Two remaining male dogs received a tumour necrosis factor (TNF)‐α antagonist, adalimumab, at 0.5 mg/kg every 2 weeks for 8 weeks then weekly for 8 weeks. Serum TNF‐α levels were not significantly altered nor were quantifiable changes seen in skin lesions or lameness. Subsequently, the dogs were maintained on hydroxychloroquine for another year. This is the first study to evaluate the use of a TNF‐α inhibitor for canine lupus and the first to address the safety of long‐term administration of hydroxychloroquine, albeit in a small number of dogs. The study documents the progression of ECLE and generally poor response to therapy.     

5-Hydroxytryptophan toxicosis in dogs: 21 cases (1989-1999)

OBJECTIVE: To determine epidemiologic characteristics, clinical findings, and treatment outcome of 5-hydroxytryptophan (5-HTP) toxicosis in dogs. DESIGN: Retrospective study. ANIMALS: 21 dogs with evidence of accidental 5-HTP ingestion. PROCEDURE: Information was retrieved from the National Animal Poison Control Center database. Records of dogs ingesting 5-HTP between January 1989 and February 1999 were reviewed for information on signalment, dose ingested, clinical signs (onset, severity, duration), treatments administered, and outcome. RESULTS: Clinical signs of toxicosis developed in 19 of 21 (90%) dogs. Neurologic signs included seizures (9 dogs), depression (6), tremors (5), hyperesthesia (5), and ataxia (4). Gastrointestinal tract signs included vomiting or diarrhea (12 dogs), signs of abdominal pain (3), and hypersalivation (2). Other clinical signs were hyperthermia (7 dogs) and transient blindness (3). Three dogs died. No important clinical laboratory or necropsy findings were reported. The doses of 5-HTP ingested ranged from 2.5 to 573 mg/kg (1.1 to 260 mg/lb) of body weight; the minimum toxic dose reported in our study was 23.6 mg/kg (10.7 mg/lb), and the minimum lethal dose was 128 mg/kg (58.1 mg/lb). Onset of signs ranged from 10 minutes to 4 hours after ingestion, and signs lasted up to 36 hours. Of 17 dogs with clinical signs of toxicosis that received treatment, 16 recovered; treatment consisted of decontamination, seizure control, thermoregulation, fluid therapy, and supportive care. CONCLUSIONS AND CLINICAL RELEVANCE: Ingestion of 5-HTP in dogs can result in a potentially life-threatening syndrome resembling serotonin syndrome in humans, which requires prompt and aggressive care.     

Acute aldicarb toxicity in dogs: 15 cases (2001–2009)

Objective – To describe the common clinical signs, laboratory abnormalities, treatment, and prognosis associated with acute aldicarb toxicosis in dogs. Design – Retrospective observational study from 2001 to 2009. Setting – Urban referral hospital. Animals – Fifteen client‐owned dogs. Interventions – None. Measurements and Main Results – The most common clinical signs associated with acute aldicarb toxicosis were vomiting, ptyalism, diarrhea, and tremors. Of the 15 dogs, 11 were admitted to the hospital for treatment, 2 were euthanized at presentation and 2 were discharged against medical advice following minimal treatment and lost to follow‐up. Laboratory abnormalities included lactic acidosis and hyperglycemia in 12 and 9 patients, respectively. Treatment of hospitalized dogs included induction of emesis with apomorphine (4 dogs), activated charcoal (5), IV fluids (11), atropine (7), methocarbamol (3), diazepam (1), pralidoxime (1) and diphenhydramine (1). Ten of 11 hospitalized dogs survived to discharge; 1 was euthanized following a respiratory arrest after 36 hours of hospitalization. One patient received mechanical ventilation and treatment for pneumonia before discharge from the hospital. The median duration of hospitalization was 22 hours (range 12–168 h). Conclusions – Acute aldicarb toxicosis carries a good prognosis for survival and hospital discharge with treatment. Supportive care should be considered for at least 18–24 hours to monitor for response to therapy and development of respiratory failure.     

Increased toxicity of P-glycoprotein-substrate chemotherapeutic agents in a dog with the MDR1 deletion mutation associated with ivermectin sensitivity

Lymphoma was diagnosed in a 4-year-old spayed female Collie, and treatment with a combination chemotherapy protocol incorporating prednisone, L-asparaginase, vincristine, vinblastine, doxorubicin, and cyclophosphamide was initiated. The dog had signs of gastrointestinal tract toxicosis and myelosuppression after treatment with P-glycoprotein-substrate drugs (vincristine, vinblastine, and doxorubicin) even when dosages were reduced, but did not have signs of toxicosis after treatment with cyclophosphamide, a non-P-glycoprotein-substrate drug, even when administered at the full dosage. It was postulated that a deletion mutation in the canine MDR1 gene (deltaMDR1 295-298) could be responsible for the drug toxicoses in this dog. This mutation has been identified as the cause of a functional P-glycoprotein defect in Collies susceptible to the toxic effects of ivermectin, another P-glycoprotein-substrate drug. The MDR1 genotype of this dog consisted of 1 normal and 1 mutant MDR1 allele. Because P-glycoprotein contributes to renal, biliary, and intestinal excretion of P-glycoprotein-substrate drugs, it is possible that drug excretion was delayed in this patient, resulting in clinical signs of toxicosis.     

Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide

Necrolytic migratory erythema (NME; also known as superficial necrolytic dermatitis) is a syndrome most often associated with certain chronic liver diseases or pancreatic glucagonomas. In humans with glucaconoma‐associated NME, skin lesions usually respond to octreotide, a somatostatin analogue that inhibits glucagon release. In this report an 11‐year‐old golden retriever dog with pancreatic glucononoma and metastasis to the regional lymph nodes, spleen and liver was diagnosed with NME. The dog exhibited erosions, ulcers and crusts on the paws, pressure points, muzzle, periocular area and prepuce. The dog was also anorexic and had difficulty walking. Because metastasis precluded surgery, treatment was initiated with subcutaneous octreotide (2 μg/kg twice daily). Skin lesions and systemic clinical signs improved markedly within 5 days. The dosage was increased to nearly 3 μg/kg twice daily and signs almost completely resolved within 10 days. Anorexia was the major adverse effect observed. During the following month, both dosage (1–3.7 μg/kg) and frequency (two to four times daily) of the octreotide injections were adjusted to permit control of clinical signs while maintaining adequate appetite. Temporary cessation of octreotide administration resulted in the rapid recurrence of skin lesions. Resuming injections led to improvement of clinical signs within 48 h. The dog was later euthanized because of progressive metastatic disease. In conclusion, subcutaneous octreotide injections were beneficial in this dog with glucagonoma‐associated NME. This somatostatin analogue could be a valuable option to treat canine patients with non‐resectable or relapsing pancreatic glucagonoma‐associated NME.