Use of octreotide for the treatment of protein-losing enteropathy in dogs: Retrospective study of 18 cases.

BACKGROUND: More than 50% of dogs with protein-losing enteropathy (PLE) fail to respond to standard therapies. Octreotide, a somatostatin analogue, is used in cases of intestinal lymphangiectasia (IL) in humans with some success. OBJECTIVES: Describe the use of octreotide in dogs with PLE including reason for and details of prescription, adverse effects, and apparent response. ANIMALS: Eighteen dogs with PLE, 13 with histopathology available. Ninety-two percent (12/13) had IL diagnosed on biopsy. All 13 dogs had intestinal inflammatory infiltrates noted. METHODS: Multicenter, retrospective, descriptive study. Cases were volunteered for inclusion by individual attending veterinarians who reported the use of octreotide in cases of PLE. RESULTS: In 16/18 (89%) cases octreotide was prescribed to PLE dogs with a clinical suspicion or confirmed diagnosis of IL that were refractory to standard therapies. Median serum albumin at the time of octreotide prescription was 1.7 g/dL (range, 1.0-3.1 g/dL). The median dose of octreotide prescribed was 20 µg/kg, SQ, daily with a range of 4-39 µg/kg, SQ, daily. Adverse effects were noted in 3/18 (17%, 95% CI [4%, 41%]) of dogs; discontinuation of the drug was necessary in 1 dog. Improvement in clinical signs was noted in 6/12 (50%, 95% CI [21%, 79%]). CONCLUSIONS AND CLINICAL IMPORTANCE: Octreotide was most commonly prescribed to dogs with PLE and suspected or confirmed IL that had failed to respond to standard therapies. Though a benefit to PLE dogs cannot be confirmed, octreotide was well tolerated by the majority of dogs at the doses prescribed in this study.

An undernutrition screening score for dogs with protein-losing enteropathy: A prospective multicenter study.

BACKGROUND: The impact of undernutrition in dogs with protein-losing enteropathy (PLE) caused by inflammatory enteritis, intestinal lymphangiectasia, or both and which variables are most predictive of outcome are unknown. OBJECTIVES: Develop an undernutrition screening score (USS) for use at the time of diagnosis of PLE in dogs, which is predictive of outcome. ANIMALS: Fifty-seven dogs with PLE prospectively recruited from 3 referral hospitals in the United Kingdom. METHODS: An USS based on the presence and severity of 5 variables: appetite, weight loss, and body, muscle, and coat condition and scored out of 15, with higher scores reflecting worse undernutrition, was calculated at the time of diagnosis. Follow-up information was obtained for at least 6 months. RESULTS: Dogs that failed to achieve clinical remission within 6 months had higher USS at diagnosis compared with dogs that achieved remission (median, 7.5; range, 2-14 and median, 5; range, 0-14, respectively). The USS at diagnosis gave an area under the receiver operating characteristic curve (AUC) of 0.656 for predicting nonclinical remission within 6 months, whereas a score consisting of just epaxial muscle loss and coat condition resulted in a larger AUC of 0.728. CONCLUSIONS AND CLINICAL IMPORTANCE: Of the 5 variables assessed in the USS, a combination of epaxial muscle loss and coat condition was most predictive of not achieving clinical remission within 6 months in dogs with PLE. Additional studies will help determine the effect of changes in USS and the 5 associated variables after diagnosis on outcome variables in these dogs.

Evaluation of the degree and distribution of lymphangiectasia in full-thickness canine small intestinal specimens diagnosed with lymphoplasmacytic enteritis and granulomatous lymphangitis.

Intestinal lymphangiectasia (IL) is often observed in dogs with chronic small intestinal diseases. Hypoplasia of the lymphatic vessel due to decreased lymphangiogenesis, which has been suggested in human idiopathic IL, may contribute to the pathogenesis of canine IL. This study aimed to evaluate the diameter and number of lymphatic vessels in full-thickness small intestinal specimens of dogs with IL. Immunohistochemical labeling of lymphatic endothelial cell markers was performed on retrospectively retrieved full-thickness small intestinal specimens. Sixteen dogs with histologically confirmed IL were included, of which 10 had lymphoplasmacytic enteritis (LPE), and six had granulomatous lymphangitis (GL). Nine dogs that died from non-gastrointestinal disorders and with little or no abnormalities in the small intestine were used as controls. Lymphatic vessel diameters in dogs with IL were significantly increased in all layers of the small intestine, including the villus lacteal, lamina propria, submucosa, muscularis, and mesentery, compared with controls (all P<0.01). There was no significant difference in the lymphatic vessel diameters between dogs with LPE and GL (all P>0.05). There was no significant difference in the number of lymphatic vessels between dogs with IL and the controls in all layers of the small intestine (all P>0.05). This study demonstrated that IL was observed in all layers of the small intestine, including the submucosa, muscularis, and mesentery, independent of the underlying disease. Factors other than reduced lymphatic vessels would contribute to the pathogenesis of IL in dogs.

Ultrasound and endoscopic findings in dogs with lymphangiectasia / [Conclusões ultrassonográfica e endoscópica em cães com linfangiectasia ]

Lymphangiectasia is a heterogenous inflammatory bowel disease characterized by lymphatic vessel dilation, chronic diarrhea and protein loss such as serum albumin and globulin. The most common cause of lymphangiectasia is considered to be the congenital malformation of the lymphatics. The study was conducted between 2012-2015 on 76 dogs suffering from intestinal disorders and manifesting digestive symptoms such as diarrhea or weight loss. In order to assess the origin of disorder, physical examination, biochemistry profile, ultrasound and endoscopic examinations were performed. Ultrasound examination tried to assess the changes of intestines' echogenicity, changes in wall thickness, wall layering and presence of striations or / and speckles (hyperechoic structures along intestinal mucosal layer). Endoscopic examination findings included dilated lacteals (59.2%) and erythema (21.1%). Although increased friability was observed in 33 dogs, it was not considered in the study due to limitations represented by the evaluation of the endoscopic images only. The study proved that an extremely significant statistical correlation exists between the presence of speckles and dilated lacteals in dogs with lymphangiectasia (P<0.05). Up to now, there is no other study to make an association between the white spots observed in ultrasound examination and dilated lacteals revealed after endoscopy in dogs with intestinal lymphangiectasia.(AU)

A linfangiectasia é uma doença inflamatória intestinal heterogênea, caracterizada por dilatação dos vasos linfáticos, diarreia crônica e perda de proteínas, como albumina sérica e globulina. A causa mais comum de linfangiectasia é considerada a malformação congênita dos linfáticos. O presente estudo foi realizado entre 2012 e 2015, em 76 cães que sofrem de distúrbios intestinais e manifestam sintomas digestivos, como diarreia ou perda de peso. Para avaliar a origem do distúrbio, foram realizados exame físico, perfil bioquímico, ultrassonográfico e endoscópico. O exame ultrassonográfico tentou avaliar as alterações da ecogenicidade do intestino, as alterações na espessura da parede, a estratificação e a presença de estrias e / ou de manchas (estruturas hiperecoicas ao longo da camada mucosa intestinal). Os resultados do exame endoscópico incluíram lacteais dilatadas (59,2%) e eritema (21,1%). Embora tenha sido observada maior friabilidade em 33 cães, ela não foi considerada no estudo devido às limitações representadas pela avaliação apenas das imagens endoscópicas. O estudo demonstrou que existe uma correlação estatística extremamente significativa entre a presença de manchas e lacteais dilatadas em cães com linfangiectasia (P <0,05). Até o momento, não há outro estudo para associar as manchas brancas observadas no exame ultrassonográfico e lacteais dilatadas reveladas após endoscopia em cães com linfangiectasia intestinal.(AU)

Lymphatic endothelial cell immunohistochemical markers for evaluation of the intestinal lymphatic vasculature in dogs with chronic inflammatory enteropathy.

BACKGROUND: Lymphatic endothelial cell (LEC) immunohistochemical markers have identified intestinal lymphatic vasculature abnormalities in humans with inflammatory bowel disease, but have not been used to evaluate intestinal lymphatic vasculature in a group of dogs with chronic inflammatory enteropathy (CIE). OBJECTIVES: To utilize LEC markers to identify and measure intestinal lymphatic vasculature in endoscopic biopsy samples of CIE dogs. To evaluate whether measured lymphatic vasculature variables correlate with serum albumin concentrations. ANIMALS: Twenty-four dogs with CIE; n = 13, serum albumin concentration <2.5 g/dL (CIE-protein-losing enteropathy [PLE]), n = 11, serum albumin concentration ≥2.5 g/dL (CIE-N). METHODS: Prospective study. Lymphatic endothelial cell immunolabeling with Prox-1 and LYVE-1 performed on endoscopic biopsy samples from 24 dogs with CIE. Duodenal and ileal villous lacteal width (VLW) and proprial mucosal lacteal width (MLW) were determined for each case and analyzed for correlation with serum albumin concentration. Lacteal dilatation scores using routine H&E histopathology were assessed for correlation with immunohistochemistry (IHC)-calculated VLW and MLW. RESULTS: Lower serum albumin concentrations were correlated with increased VLW (rho = -.4644; P = .02) and MLW (rho = -.6514; P < .001) in the ileum. Lymphatic endothelial cell IHC identified presumptive proprial mucosal lymphangiectasia in some dogs that was not recognized with routine H&E staining. Lacteal dilatation scores were correlated with VLW in duodenum (rho = .4634; P = .02) and ileum (rho = .5292; P = .008), but did not correlate with MLW. CONCLUSIONS AND CLINICAL IMPORTANCE: Lymphatic endothelial cell immunolabeling identified presumptive proprial mucosal lymphangiectasia in CIE dogs, particularly in the ileum of hypoalbuminemic dogs. Routine evaluation of villous lacteals likely underestimates abnormalities of the lymphatic vasculature in dogs with CIE.

Comparative pathophysiology and management of protein-losing enteropathy.

Protein-losing enteropathy, or PLE, is not a disease but a syndrome that develops in numerous disease states of differing etiologies and often involving the lymphatic system, such as lymphangiectasia and lymphangitis in dogs. The pathophysiology of lymphatic disease is incompletely understood, and the disease is challenging to manage. Understanding of PLE mechanisms requires knowledge of lymphatic system structure and function, which are reviewed here. The mechanisms of enteric protein loss in PLE are identical in dogs and people, irrespective of the underlying cause. In people, PLE is usually associated with primary intestinal lymphangiectasia, suspected to arise from genetic susceptibility, or "idiopathic" lymphatic vascular obstruction. In dogs, PLE is most often a feature of inflammatory bowel disease (IBD), and less frequently intestinal lymphangiectasia, although it is not proven which process is the true driving defect. In cats, PLE is relatively rare. Review of the veterinary literature (1977-2018) reveals that PLE was life-ending in 54.2% of dogs compared to published disease-associated deaths in IBD of <20%, implying that PLE is not merely a continuum of IBD spectrum pathophysiology. In people, diet is the cornerstone of management, whereas dogs are often treated with immunosuppression for causes of PLE including lymphangiectasia, lymphangitis, and crypt disease. Currently, however, there is no scientific, extrapolated, or evidence-based support for an autoimmune or immune-mediated mechanism. Moreover, people with PLE have disease-associated loss of immune function, including lymphopenia, severe CD4+ T-cell depletion, and negative vaccinal titers. Comparison of PLE in people and dogs is undertaken here, and theories in treatment of PLE are presented.

The clinical efficacy of dietary fat restriction in treatment of dogs with intestinal lymphangiectasia.

BACKGROUND: Intestinal lymphangiectasia (IL), a type of protein-losing enteropathy (PLE), is a dilatation of lymphatic vessels within the gastrointestinal tract. Dietary fat restriction previously has been proposed as an effective treatment for dogs with PLE, but limited objective clinical data are available on the efficacy of this treatment. HYPOTHESIS/OBJECTIVES: To investigate the clinical efficacy of dietary fat restriction in dogs with IL that were unresponsive to prednisolone treatment or showed relapse of clinical signs and hypoalbuminemia when the prednisolone dosage was decreased. ANIMALS: Twenty-four dogs with IL. METHODS: Retrospective study. Body weight, clinical activity score, and hematologic and biochemical variables were compared before and 1 and 2 months after treatment. Furthermore, the data were compared between the group fed only an ultra low-fat (ULF) diet and the group fed ULF and a low-fat (LF) diet. RESULTS: Nineteen of 24 (79%) dogs responded satisfactorily to dietary fat restriction, and the prednisolone dosage could be decreased. Clinical activity score was significantly decreased after dietary treatment compared with before treatment. In addition, albumin (ALB), total protein (TP), and blood urea nitrogen (BUN) concentration were significantly increased after dietary fat restriction. At 2 months posttreatment, the ALB concentrations in the ULF group were significantly higher than that of the ULF + LF group. CONCLUSIONS AND CLINICAL IMPORTANCE: Dietary fat restriction appears to be an effective treatment in dogs with IL that are unresponsive to prednisolone treatment or that have recurrent clinical signs and hypoalbuminemia when the dosage of prednisolone is decreased.

Effects of corn oil administered orally on conspicuity of ultrasonographic small intestinal lesions in dogs with lymphangiectasia.

Lymphangiectasia is one of the causes of protein-losing enteropathy in dogs and characteristic ultrasonographic small intestinal lesions have been previously described. The purpose of this study was to determine whether corn oil administered orally (COAO) would result in increased conspicuity of these characteristic small intestinal ultrasonographic lesions in dogs with lymphangiectasia. Affected dogs were included if they underwent corn oil administered orally and had a surgical full-thickness intestinal biopsy diagnosis of lymphangiectasia. Control dogs had normal clinical examination and standard laboratory test findings. Ultrasound images of duodenum, jejunum, and ileum were obtained prior to and 30, 60, 90, and 120 min after corn oil administered orally for all dogs. Parameters recorded for each ultrasound study were intestinal wall thickness, mucosal echogenicity, and presence or absence of hyperechoic mucosal striations (HMS) and a parallel hyperechoic mucosal line (PHML). Nine affected and five controls dogs were included in the study. Seven of the nine dogs with lymphangiectasia had hyperechoic mucosal striations prior to corn oil administered orally. Jejunal hyperechoic mucosal striations were significantly associated with lymphangiectasia at multiple time points (P < 0.05) and were best identified in dogs with lymphangiectasia 60 or 90 min after corn oil administered orally. Increased mucosal echogenicity was observed in all dogs at multiple time points after corn oil administered orally. A parallel hyperechoic mucosal line was present in the jejunum in 4/5 healthy and 6/9 dogs with lymphangiectasia at one or more time points after corn oil administered orally. Findings indicated that corn oil administered orally improves conspicuity of characteristic ultrasonographic lesions in dogs with lymphangiectasia, however some of these lesions may also be present in healthy dogs that recently received a fatty meal.

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.

Duodenal endoscopic findings and histopathologic confirmation of intestinal lymphangiectasia in dogs.

BACKGROUND: The diagnosis of intestinal lymphangiectasia (IL) has been associated with characteristic duodenal mucosal changes. However, the sensitivity and specificity of the endoscopic duodenal mucosal appearance for the diagnosis of IL are not reported. HYPOTHESIS/OBJECTIVES: To evaluate the utility of endoscopic images of the duodenum for diagnosis of IL. Endoscopic appearance of the duodenal mucosal might predict histopathologic diagnosis of IL with a high degree of sensitivity and specificity. ANIMALS: 51 dogs that underwent upper gastrointestinal (GI) endoscopy and endoscopic biopsies. METHODS: Retrospective review of images acquired during endoscopy. Dogs were included if adequate biopsies were obtained during upper GI endoscopy and digital images were saved during the procedure. Images were assessed for the presence and severity of IL. Using histopathology as the gold standard, the sensitivity and specificity of endoscopy for diagnosing IL were calculated. RESULTS: Intestinal lymphangiectasia (IL) was diagnosed in 25/51 dogs. Gross endoscopic appearance of the duodenal mucosa had a sensitivity and specificity (95% confidence interval) of 68% (46%, 84%) and 42% (24%, 63%), respectively for diagnosis of IL. Endoscopic images in cases with lymphopenia, hypocholesterolemia, and hypoalbuminemia had a sensitivity of 80%. CONCLUSIONS AND CLINICAL IMPORTANCE: Endoscopic duodenal mucosa appearance alone lacks specificity and has only a moderate sensitivity for diagnosis of IL. Evaluation of biomarkers associated with PLE improved the sensitivity; however, poor specificity for diagnosis of IL supports the need for histopathologic confirmation.

White spots on the mucosal surface of the duodenum in dogs with lymphocytic plasmacytic enteritis.

Distended lacteals, described as expanded white villi in duodenum, are strongly indicative of primary intestinal lymphangiectasia. In the present study, we evaluated the significance of white spots present in the duodenal mucosa of dogs with lymphocytic plasmacytic enteritis (LPE). Fifty dogs with LPE were included in this study, and white spots were detected in the duodenal mucosa in 22 dogs during endoscopy. Hypoproteinemia was more frequent in dogs with white spots than in dogs without spots (p = 0.02). Serum protein and albumin concentration were significantly lower in LPE dogs with white spots (p = 0.038) compared to LPE dogs without white spots (p = 0.039). There was a significant correlation between white spots density and lymphatic dilatation histological scores (p = 0.023; ρ = 0.481). These results suggest that the presence of white spots in the duodenal mucosa of dogs is not a finding exclusive for intestinal lymphangiectasia. Low serum protein and albumin concentrations together with lymphatic dilatation seem to be related to the presence of white spots in the duodenal mucosa of LPE dogs.

Ultrasonographic intestinal hyperechoic mucosal striations in dogs are associated with lacteal dilation.

In this retrospective study, the medical records of 23 dogs with the sonographic feature of small intestinal hyperechoic mucosal striations and an endoscopic or surgical intestinal biopsy were reviewed. Histopathologic lacteal dilation was present in 96% of dogs with mucosal striations. Sonographic findings associated with mucosal striations included: mild jejunal wall thickening (96%), mild duodenal wall thickening (78%), mucosal speckles (70%), and abdominal effusion (87%). The mucosal striations were diffuse (70%) or multifocal (30%) and did not cause loss of wall layering, except in one dog with a severe mural lipogranuloma. Mesenteric lymphadenopathy was identified in 9% of dogs. Thirteen dogs with endoscopic biopsies had mild to moderate villus lacteal dilation and the nine dogs with surgical biopsies had moderate to severe dilation. Inflammatory infiltrates were mild (61%) or moderate (30%) with variable numbers and combinations of cells, including eosinophils (65%), plasma cells (61%), lymphocytes (57%), and neutrophils (30%); one dog had disseminated villus histiocytic sarcoma. The biochemistry changes and clinical signs were consistent with protein-losing enteropathy in 78% of dogs. Hyperechoic mucosal striations in dogs are associated with lacteal dilation and are frequently associated with mucosal inflammation and protein losing enteropathy.

Case study in canine intestinal lymphangiectasia.

A 9.52 kg, 9-year-old, spayed female beagle was presented with the chief complaint of abdominal distention of 1 week's duration. A presumptive diagnosis of canine intestinal lymphangectasia was arrived at by exclusion of other causes for the patient's ascites. The patient was successfully treated with dietary modification and immunosuppressive therapy.

Ultrasonographic diagnosis--small bowel lymphangiectasia in a dog.

A 7-year-old, West Highland White Terrier had a 5-month history of diarrhea, dysorexia, and weight loss. Sonographically, there was a focal area of intestinal thickening with loss of layering. A neoplastic or severe inflammatory condition was suspected and intestinal lymphangiectasia was diagnosed histopathologically. This patient seems to be the first description of intestinal lymphangiectasia appearing as an intestinal mass.

Primary lymphangiectasia in a dingo (Canis familiaris dingo).

A 3-yr-old intact male dingo (Canis familiaris dingo) presented with a 3-mo history of diarrhea. The diarrhea did not resolve with antibiotics or intestinal protectants. Fecal examination for parasites, fecal cultures, physical examination, and radiographs were unremarkable. Enteroscopic duodenal biopsies showed dilated lacteals without inflammation. Results of serum folate, cobalamin, and trypsin-like immunoreactivity were normal. Low serum total protein and albumin combined with increased fecal levels of alpha-1 protease inhibitor suggested the diagnosis of lymphangiectasia. Full-thickness intestinal biopsies of the duodenum, jejunum, and ileum revealed dilated mucosal and submucosal lacteals without associated inflammation, confirming the diagnosis of primary lymphangiectasia. Currently, the dingo is being maintained with nutritional management.

Clinical, clinicopathologic, radiographic, and ultrasonographic characteristics of intestinal lymphangiectasia in dogs: 17 cases (1996-1998).

OBJECTIVE: To characterize the clinical, clinicopathologic, and imaging findings in dogs with intestinal lymphangiectasia and to compare the histologic grade of lymphangiectasia with clinicopathologic and imaging abnormalities. DESIGN: Retrospective study. ANIMALS: 17 dogs with a histologic diagnosis of intestinal lymphangiectasia. PROCEDURE: Medical records of dogs with a histologic diagnosis of intestinal lymphangiectasia were reviewed for signalment, history, clinical signs, results of exploratory laparotomy, and clinicopathologic, radiographic, ultrasonographic, and histologic findings. RESULTS: Mean age of dogs was 8.3 years; the most common clinical signs were diarrhea, anorexia, lethargy, vomiting, and weight loss. Abnormal physical examination findings included dehydration, ascites, and signs of pain on palpation of the abdomen. The most notable clinicopathologic findings were low serum ionized calcium concentration and hypoalbuminemia. Abdominal ultrasonography was performed in 12 dogs and revealed intestinal abnormalities in 8 dogs and peritoneal effusion in 7 dogs. Exploratory laparotomy revealed abnormalities in 9 of 16 dogs including thickened small intestine, dilated lacteals, lymphadenopathy, and adhesions. On histologic examination of the small intestine, concurrent inflammation was observed in 15 of 17 dogs, crypt ectasia in 5 of 17, and lipogranulomas in 2 of 17. CONCLUSIONS AND CLINICAL RELEVANCE: 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.

Intestinal crypt lesions associated with protein-losing enteropathy in the dog.

Six dogs were diagnosed with protein losing enteropathy (PLE). There was no evidence of inappropriate inflammatory infiltrates or lymphangiectasia in multiple mucosal biopsies of the small intestine of 4 of the dogs. The 5th and 6th dogs had obvious lymphangiectasia and a moderate infiltrate of inflammatory cells in the intestinal mucosa. All 6 dogs had a large number of dilated intestinal crypts that were filled with mucus, sloughed epithelial cells, and/or inflammatory cells. Whether PLE occurs in these dogs because of protein lost from the dilated crypts into the intestinal lumen or whether the dilated crypts are a mucosal reaction due to another undetermined lesion that is responsible for alimentary tract protein loss is unknown. However, when large numbers of dilated intestinal crypts are present, they appear to be associated with PLE even if there are no other remarkable lesions in the intestinal mucosa.

Chyloabdomen in a neonatal foal.

A 12-hour-old female standardbred foal developed signs of abdominal pain, tachycardia, tachypnoea and fever associated with chylous ascites. Small intestinal obstruction was due to segmental, mid-jejunal lymphangiectasia. Post mortem examination revealed a lack of communication between afferent and efferent lymphatic vessels in the mesenteric lymphocentre, a defect which was suspected to be congenital.

Gastropathies in the Lundehund. I. Gastritis and gastric neoplasia associated with intestinal lymphangiectasia.

The results from gross and microscopic examination of the stomachs of Lundehunds and examination of stomachs of control dogs from other breeds were compared. Over a 13-year period, 12 of 14 autopsied Lundehunds have been diagnosed as having intestinal lymphangiectasia. In the present study, histological examination revealed gastritis as manifested by an increase in the number of mononuclear cells infiltrating the lamina propria in all the Lundehunds. The inflammation was chronic and restricted to the fundic and body regions, except in one Lundehund where antral gastritis was also present. Computer-assisted morphometric analysis was used to quantify the increased number of mononuclear cells. Atrophy of mucosal fundic glands was prominent in most Lundehunds and mucous metaplasia was often present. Conventional morphometry revealed a significant decrease in the height of the gastric mucosa. A relative expansion in area of the basal part of the lamina propria in Lundehunds with chronic atrophic gastritis corresponded to the observed increase in mononuclear cells and stromal elements. Primary gastric carcinoma with neoplastic cells infiltrating layers of the stomach wall was found in four Lundehunds. The high incidence of gastric carcinoma and the consistent presence of gastritis in Lundehunds suffering from intestinal lymphangiectasia suggest that these changes represent features of a single pathogenetic process.