Randomized controlled trial of hydrolyzed fish diets in dogs with chronic enteropathy.

BACKGROUND: The role of diet in the pathogenesis and treatment of chronic enteropathies (CE) in dogs is unresolved. OBJECTIVES: To compare the ability of diets composed of hydrolyzed fish, rice starch, and fish oil without (HF) or with prebiotics, turmeric, and high cobalamin (HF+) against a limited ingredient diet containing mixed nonhydrolyzed antigens and oils (control) to resolve clinical signs and maintain serum cobalamin and folate concentrations in dogs with nonprotein losing CE (non-PLE). To determine the ability of hydrolyzed fish diets to support recovery and remission in dogs with PLE. ANIMALS: Thirty-one client-owned dogs with CE: 23 non-PLE, 8 PLE. METHODS: Randomized, blinded, controlled trial. Diets were fed for 2 weeks; responders continued for 12 weeks. Nonresponders were crossed over to another diet for 12 weeks. Response was determined by standardized clinical evaluation with long-term follow-up at 26 weeks. Concurrent medications were allowed in PLE. RESULTS: Nineteen of 23 (83%; 95% confidence interval [CI], 60%-94%) non-PLE CE responded clinically to their initial diet, with no difference between diets (P > .05). Four nonresponders responded to another diet, with sustained remission of 18/18 (100%; 95%CI, 78%-100%) at 26 weeks. Serum cobalamin concentration was increased (P < .05) and maintained by diet. Serum folate concentration decreased posttreatment (P < .05) but was restored by dietary supplementation. Hydrolyzed fish diets supported weight gain, serum albumin concentration, and recovery (P < .05) in dogs with PLE. CONCLUSIONS AND CLINICAL IMPORTANCE: Changing diet, independent of antigen restriction or supplemental ingredients, induced long-term remission in dogs with non-PLE CE. Serum cobalamin and folate concentrations were maintained by diet. Hydrolyzed fish diets supported clinical recovery and remission in PLE.

Protein losing enteropathy caused by eosinophilic gastroenteritis: A case report.

Protein losing enteropathy (PLE), a very rare disease with hypoproteinemia and edema as its characteristics, is caused by various diseases resulting in protein depletion from the gut. The diagnosis is relatively difficult due to its complex pathogeneses. The present paper reported a case whose symptom started with acute diarrhea and hypoproteinemia. Gastrointestinal endoscopies showed digestive ulcers and colon polyp. The treatments contained albumin infusion, Chinese herbal decoction and other symptomatic therapies. The hypoproteinemia become even worse and edema occurred after 4 days' treatment. A larger dose of albumin infusion (40-60 g/d) and modified herbal decoctions were prescribed. A final diagnosis of eosinophilic gastroenteritis (EG) complicated with PLE was confirmed by histopathological examination of a repeated gastroscopy. After three weeks' treatment, the serum albumin level was raised and the edema subsided gradually. In conclusion, herbs may have an effect on PLE patients, but PLE resulting from EG is very complex and easy to misdiagnose, especially in atypical conditions. Further studies are required to find the exact mechanisms.

Selenium status and fungi in the protein-losing enteropathy of persistent diarrhea.

BACKGROUND AND OBJECTIVES: A vicious cycle of infection, malabsorption, and malnutrition has been implicated in the perpetuation of diarrheal disease. This study examined whether persistent diarrhea is associated with changes in selenium status and stool alpha-1 antitrypsin (AAT) concentration. METHODS AND STUDY DESIGN: This cross-sectional study included 30 children aged 1-12 years with persistent diarrhea who were hospitalized in Cipto Mangunkusumo Hospital and Fatmawati Hospital, Jakarta, and 30 apparently healthy children who were matched by age and sex and lived in a rural area of Jakarta. Clinical examinations, blood routine tests, erythrocyte glutathione peroxidase (GPX) activity and plasma selenium levels as well as AAT in fresh stool samples were performed in all the subjects. RESULTS: Of 30 children with persistent diarrhea, 17 had moderate malnutrition and 13 had severe malnutrition. The mean plasma selenium was significantly lower in children with persistent diarrhea than in children without diarrhea (86.0 µg/L [95% CI: 76.1-95.9] vs 110 µg/L [95% CI: 104-116, p<0.0001). The mean stool AAT concentration was significantly higher in children with persistent diarrhea than in those without diarrhea (115 mg/dL [95% CI: 38.5-191] vs 16 mg/dL [95% CI: 4.0-13.5, p<0.0001]). Selenium correlated with AAT (p=0.05). Fecal fungi were persistently present. CONCLUSIONS: Although selenium status in both groups was optimal for the obtained plasma GPX activity, children with persistent diarrhea exhibited lower plasma selenium levels. This study suggests that the decrease in the plasma selenium level may be the consequence of protein loss and that fungi may be involved.

Seizures Associated With Hypocalcemia in a Yorkshire Terrier With Protein-Losing Enteropathy.

A 7 yr old, male, castrated, Yorkshire terrier was presented on emergency for an acute onset of seizure activity. The owner also reported that the dog had previously exhibited other symptoms, including intermittent vomiting, diarrhea, and anorexia for several yr. The initial workup revealed a marked decrease in ionized calcium and total protein. Further diagnostics revealed decreases in magnesium, 25 hydroxyvitamin D, albumin, and globulins, and an increased parathyroid hormone level. Intestinal biopsies revealed inflammatory bowel disease and lymphangiectasia. The dog received intravenous calcium gluconate for treatment of hypocalcemia followed by oral calcium and vitamin D supplementation. Seizure activity ceased once calcium levels approached the normal range. Medical and dietary therapy for lymphangiectasia and inflammatory bowel disease consisted of prednisone, rutin, and a low-fat diet. Decreased serum total ionized calcium levels have been reported previously in dogs with protein-losing enteropathies. Typically, the hypocalcemia is not associated with clinical signs. Severe clinical signs of hypocalcemia are rarely reported in dogs with protein-losing enteropathy, but seizures, facial twitching, and tremors can occur. When presented with a dog with a history of seizure activity, panhypoproteinemia, and hypocalcemia, protein-losing enteropathy should be included on the list of differential diagnoses.

Acquired intestinal lymphangiectasia successfully treated with a low-fat and medium-chain triacylglycerol-enriched diet in a patient with liver transplantation.

Intestinal lymphangiectasia is defined as a dilatation of small bowel lymphatic capillaries and a loss of lymph into the bowel lumen. Clinically it is characterized by hypoproteinaemia and oedema. We present here a case of protein-losing enteropathy due to intestinal lymphangiectasia after liver transplantation in a 57-year-old man who was transplanted for hepatitis C virus. Four years after liver transplantation, the patient developed hypoalbuminaemia and ascites associated with recurrence of cirrhosis. The sudden fall in serum albumin led us to look for a cause of reduction other than or in addition to cirrhosis. Duodenal biopsies showed tall villi with dilated lymphatic vessels and widening of the villi caused by oedema, demonstrating intestinal lymphangiectasia. In this case a low-fat diet supplemented with medium-chain triacylglycerols achieved an early clinical improvement with increased serum albumin levels and ascites disappearance. Intestinal lymphangiectasia should be suspected in liver-transplanted patients developing hypoproteinaemia and hypoalbuminaemia after the recurrence of cirrhosis.

Intestinal lymphangiectasia in children: a study of upper gastrointestinal endoscopic biopsies.

From 1980-1986 intestinal mucosal lymphangiectasia was diagnosed histologically in eight patients (6 weeks to 16 years; four males/four females; seven white). The presenting features were diarrhea (six/eight), vomiting (four/eight), and growth deficit (seven/eight). Additional conditions in these patients included asthma, urinary tract infection, esophageal atresia, hydrops fetalis, inflammatory bowel disease, malabsorption syndrome, and thymic hypoplasia. Hypoalbuminemia and edema (four/eight) were more prominent in those patients under 5 years of age. Two had systemic lymphangiectasia and lymphopenia. The patients responded variably to hyperalimentation and dietary supplements, depending on the extent of their lymphangiectasia and the age at onset of symptoms. Dilated lymphatics were seen in the small intestinal mucosa under the surface epithelium. Lesions were often focal, requiring several biopsies or serial sections for detection. Other common findings were mild to moderate lymphoplasmacytic inflammation and mild to moderate villous injury with blunting and edema. Mild inflammation without lymphangiectasia was also present in esophageal, gastric, or colonic biopsies. Diagnosis should be made on the basis of endoscopic findings or in small-intestinal inflammatory conditions even in the absence of a classic clinical picture. Histologic confirmation may require more than one serially sectioned biopsy. This study confirms the diversity of disorders that may be associated with intestinal lymphangiectasia and shows that the disease in infants is more severe and generalized.