Pancreatitis associated with potassium bromide/phenobarbital combination therapy in epileptic dogs

In a retrospective study, at least 10% of dogs receiving potassium bromide/phenobarbital combination therapy, compared with 0.3% of dogs receiving phenobarbital monotherapy, had probable pancreatitis. Pancreatitis may be a more frequent and more serious adverse effect of potassium bromide/phenobarbital combination therapy than has been reported previously.     

Pancreatitis in Cats

Pancreatitis was considered a rare disease in the cat until a couple of decades ago when several retrospective studies of severe acute pancreatitis were published. It was apparent that few of the diagnostic tests of value in the dog were helpful in cats. With increasing clinical suspicion, availability of abdominal ultrasonography, and introduction of pancreas-specific blood tests of increasing utility, it is now accepted that acute pancreatitis is probably almost as common in cats as it is in dogs, although the etiology(s) remain more obscure. Pancreatitis in cats often co-exists with inflammatory bowel disease, less commonly with cholangitis, and sometimes with both. Additionally, pancreatitis may trigger hepatic lipidosis, while other diseases, such as diabetes mellitus, may be complicated by pancreatitis. Therapy is similar to that used in dogs, with added emphasis on early nutritional support to prevent hepatic lipidosis. Less is known about chronic pancreatitis than the acute form, but chronic pancreatitis is more common in cats than it is in dogs and may respond positively to treatment with corticosteroids.     

Acute Necrotizing Pancreatitis and Acute Suppurative Pancreatitis in the Cat

Medical records and histologic sections of 40 cats with acute pancreatitis were reviewed. Two distinct groups of cats with pancreatitis were established by histologic analysis of tissue. Group I (32 cats) had acute pancreatic necrosis (APN). Group 2 (8 cats) had suppurative pancreatitis. Ages of affected cats ranged from 3 weeks to 16 years. l h e majority consisted of indoor cats of the Domestic Short-Haired breed but Siamese cats were over-represented relative to the general population ( P > 0.05). Twenty-two percent of cats were obese and 57%were underweight. Thirty-eight percent of cats had acute disease. In the other cats, two stages in the progression of the disease were evident: (1) anorexia. weight loss, and lethargy, followed by (2) acute deterioration, development of shock, and a moribund state, despite fluid therapy. The most common clinical signs were severe lethargy (100%), reduced appetite (97%), dehydration (92%), and hypothermia (68%). The initial hemogram occasionally showed a neutrophilia (30%) and anemia (2670)but packed cell volume (PCV) decreased markedly to the extent that 555% of cats were anemic terminally. Serum biochemical abnormalities included increased activities of A1, T (68%) and ALP (50%). and increased conrentrations of bilirubin (64%) and cholesterol (64%).Cats with APN were hyperglycemic (64%)), glycosuric (60%) and ketonuric (20%), whereas cats with suppurative pancreatitis tended to be hypoglycemic (7%). Renal failure and electrolyte abnormalities were mild or infrequent escept for hypokalemia (56%)).This study characterizes a severe necrotizing pancreatitis in the cat similar to that reported in other species, and a histologically distinct suppurative pancreatitis.     

Chronic Pancreatitis in Dogs

Chronic pancreatitis used to be considered uncommon in dogs, but recent pathological and clinical studies have confirmed that it is in fact a common and clinically significant disease. Clinical signs can vary from low-grade recurrent gastrointestinal signs to acute exacerbations that are indistinguishable from classical acute pancreatitis. Chronic pancreatitis is a significant cause of chronic pain in dogs, which must not be underestimated. It also results in progressive impairment of endocrine and exocrine function and the eventual development of diabetes mellitus or exocrine pancreatic insufficiency or both in some affected dogs at end stage. The etiology is unknown in most cases. Chronic pancreatitis shows an increased prevalence in certain breeds, and recent work in English Cocker Spaniels suggests it is part of a polysystemic immune-mediated disease in this breed. The histological and clinical appearance is different in different breeds, suggesting that etiologies may also be different. Diagnosis is challenging because the sensitivities of the available noninvasive tests are relatively low. However, with an increased index of suspicion, clinicians will recognize more cases that will allow them to institute supportive treatment to improve the quality of life of the patient.     

Acute Pancreatitis in Cats With Hepatic Lipidosis

The purpose of this study was to characterize the incidence, clinical features, and prognosis of acute pancreatitis in cats with hepatic lipidosis. Of 13 cats histologically diagnosed with hepatic lipidosis between July 1988, and November 1989,5 (38%) were also histologically diagnosed with acute pancreatitis. In cats with hepatic lipidosis alone, the signalment, history, physical examination, and clinicopatho-logic findings were generally indistinguishable from those of cats with concurrent acute pancreatitis except that cats with acute pancreatitis were more likely to be cachectic and to have coagulation abnormalities. Hepatomegaly was seen on abdominal radiographs in both groups. Of the 5 cats with concurrent acute pancreatitis, abdominal ultrasonography detected 1 cat with a hypoechoic pancreas and 5 with peritoneal effusion; those abnormalities were not seen in cats without concurrent acute pancreatitis. Cats with concurrent acute pancreatitis had only a 20% recovery rate, compared with a 50% recovery rate in cats with hepatic lipidosis alone. We conclude that cats with hepatic lipidosis should be rigorously evaluated for concurrent acute pancreatitis because of 1) the rate of disease coincidence, 2) the inability of signalment, history, physical examination, and clinicopathologic findings to adequately distinguish between hepatic lipidosis and acute pancreatitis, 3) the worse prognosis associated with concurrent acute pancreatitis, and 4) the opposing nutritional strategies for hepatic lipidosis and acute pancreatitis. (Journal of Veterinary Internal Medicine 1993; 7:205–209. Copyright © 1993 by the American College of Veterinary Internal Medicine.)     

Serum Phospholipase A2 in Canine Acute Pancreatitis

During 3 years 28 cases of acute pancreatitis were diagnosed in dogs. In 26 of these dogs, the disease was fatal. The most frequent symptoms were vomiting, anorexia and lethargy. Two thirds showed tenderness upon abdominal palpation. Ascites was found in 3 cases. Of the blood, parameters, serum amylase level was elevated in 86 % and lipase in 89 % of the cases. Sixteen dogs were uremic and half of the dogs were hyperglycemic. Two thirds of the dogs had leukocytosis. Using stepwise multiple regression the best blood parameters explaining acute pancreatitis were leukocytes together with lipase and glucose.In an attempt to find a more specific serum test for dogs to diagnose acute pancreatitis serum phospholipase A2 (PLA₂) activity was measured. In sixteen out of the 28 dogs with acute pancreatitis, serum PLA₂ activity was increased. The ascites fluids were rich in PLA2. Serum PLA₂ is more often increased in the severe necrotizing pancreatitis (80 %) than in the milder forms of acute pancreatitis (44 %). All dogs with increased serum PLA₂ had also increased serum amylase and lipase activities. The dogs with an increased serum PLA₂ and dogs with ascites had fat necrosis in the vicinity of the pancreas. Experimental pancreatitis was induced in 4 dogs by injecting Na-taurocholate and trypsin into the pancreas. In these cases, very high PLA₂ activities in the serum and ascites fluids were detected, but none seemed to be present in the urine samples.Key words: dog, acute pancreatitis, phospholipase A2     

Serum Adipokine Concentrations in Dogs with Acute Pancreatitis

Background

Limited information is available about the role of adipokines in the development and progression of acute pancreatitis (AP) in dogs.

Objectives

To determine whether the circulating concentrations of adipokines differed between healthy dogs and dogs with AP, and whether the circulating concentrations differed between AP survivors and AP nonsurvivors.

Animals

Twenty‐eight healthy dogs and 25 client‐owned dogs with AP.

Methods

Prospective observational cohort study of 25 client‐owned dogs with newly diagnosed AP and 28 otherwise healthy dogs with similar body condition scores. The serum concentrations of leptin, adiponectin, resistin, visfatin, interleukin (IL)‐1β, IL‐6, IL‐10, IL‐18, and tumor necrosis factor (TNF)‐α were measured.

Results

The serum concentrations of leptin (P = .0021), resistin (P = .0010), visfatin (P < .0001), IL‐1β (P < .0001), IL‐6 (P = .0002), IL‐10 (P < .0001), and IL‐18 (P < .0001) were significantly higher in dogs with AP than healthy dogs, whereas the adiponectin concentration (P = .0011) was significantly lower. There were significant differences in the serum concentrations of leptin (P = .028) and adiponectin (P = .046) in survivors and nonsurvivors. After the disappearance of clinical signs, the concentrations of resistin (P = .037) and IL‐1β (P = .027) decreased significantly, whereas the serum concentrations of leptin (P > .999), adiponectin (P = .11), visfatin (P = .83), IL‐6 (P = .82), IL‐10 (P = .82), IL‐18 (P = .56), and TNF‐α (P = .94) did not differ significantly.

Conclusion and Clinical Importance

This study showed that dysregulation of adipokines might be involved in the pathogenesis of AP. In addition, leptin and adiponectin are likely to be associated with mortality rate in AP.     

10例犬胰腺炎的诊断与治疗

胰腺炎是胰腺自身被消化所导致的炎症,是兽医临床的常见病,给犬带来极大危害。论文采用发病情况调查,临床症状观察,实验室检查方法相结合对2012年-2016年西北农林科技大学西安动物医院所确诊的10例犬胰腺炎病例进行统计分析。发病情况调查的主要内容包括既往病史调查,既往用药史调查,问诊等;临床症状主要有剧烈的呕吐,食欲废绝,腹部按压疼痛;实验室检查采用美国IDEXX胰腺炎检测试纸条检测宠物脂肪酶水平,若发现脂肪酶水平显著升高,试纸条呈阳性,即可确诊。胰腺炎患犬的治疗原则为禁食、止吐、补液、止痛、消炎,补充营养物质,调节内环境平衡。经过治疗,所有病犬均康复,转归良好。通过对这10例胰腺炎患犬的诊断和治疗,能够为临床上该病的诊断、治疗以及预后评估等提供一定的参考。     

Pancreatitis associated with clomipramine administration in a dog

A three-year-old, male, entire, Yorkshire terrier was presented with peracute onset of abdominal pain and vomitus. Clinicopathological abnormalities included severely increased serum lipase activity, immeasurably high serum trypsin-like immunoreactivity and mild hypocalcaemia. Canine pancreatic lipase immunoreactivity (cPLI) was intended to be measured, however, the sample got lost. Ultrasonography revealed a hypoechoic pancreas with small amounts of peripancreatic fluid and hyperechogenic mesentery. Acute pancreatitis (AP) was diagnosed and the dog recovered with appropriate therapy within 48 hours. Clomipramine, a selective serotonin reuptake inhibitor (SSRI) for alleviating signs of separation anxiety had been given for seven weeks. Two similar, albeit less severe, episodes associated with previous courses of clomipramine had occurred eight months earlier that responded to discontinuing clomipramine and supportive care. As SSRIs are associated with AP in human beings and no other trigger could be identified, we conclude that clomipramine should be considered as a potential cause when investigating causes for AP in susceptible breeds or other dogs presenting with compatible clinical signs.     

Pancreatitis in hyperlipemic mink (Mustela vison)

In both man and animals, inflammatory changes in the pancreas often occur with disturbances in lipid metabolism, including hypertriglyceridemia and an excess of free fatty acids. Hyperlipoproteinemia type I is a human condition caused by a deficiency of lipoprotein lipase. A similar metabolic disturbance that occurs in mink is of considerable comparative interest, as it is also followed by pancreatitis. Pancreatic lesions in hyperlipoproteinemic mink included overt variably sized nodules with hemorrhage and necrosis. These lesions began as intralobular necrosis of exocrine cells and progressed to total lobular destruction, with eventual involvement of interlobular tissue. Remnants of epithelial cells and lipid-filled macrophages were seen in necrotic areas, along with other types of inflammatory cells scattered in a lipid-rich exudate. Granulation tissue developed rapidly in necrotic areas. Additional observations included ductal proliferation, replacement of epithelial cells with fat, and mural arterial thickening, most conspicuously with vacuolated cells and endothelial proliferation. Extravasation of lipid-rich plasma is thought to be a major intensifier of the inflammatory response.