Two adult dogs were evaluated for hypercalcemia. Diagnostic evaluation identified elevated parathyroid hormone-related protein (PTHrP) and presumptive humoral hypercalcemia of malignancy. At necropsy, schistosomiasis was diagnosed. North American schistosomiasis is caused by Heterobilharzia americana. Clinical findings may include dermatitis, coughing, diarrhea, and anorexia. Clinicopathological findings may include hypercalcemia, hyperglobulinemia, hypoalbuminemia, anemia, and eosinophilia. Diagnosis by fecal examination is difficult. Praziquantel or fenbendazole treatment may be curative or palliative. These are the first reported cases of hypercalcemia with elevated PTHrP in animals without diagnosed malignancy. Elevation of PTHrP has not been previously reported in hypercalcemic humans or in animals with granulomatous inflammation.

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.Key words: Gastroduodenoscopy; Hypoalbuminemia; Intestinal biopsy; Lymphangiectasia P rotein-losing enteropathy (PLE) is a syndrome in which there is excessive loss of protein from the gastrointestinal tract. In general, PLE is only recognized after animals become hypoalbuminemic, 1,2 although enteropathies in people can produce excessive alimentary protein loss without causing abnormal serum protein concentrations. PLE has been well described in the dog, and certain breeds, such as the Lundehund, 3 Basenji, 4 and Soft-coated Wheaten Terrier 5 appear to be at increased risk of PLE. Various intestinal lesions may be associated with PLE, including lymphangiectasia, immunoproliferative enteropathy, lymphocyticplasmacytic enteritis, eosinophilic enteritis, gastrointestinal ulceration/erosion, giardiasis, chronic intussusception, small intestinal bacterial overgrowth, neoplasia, hypoalbuminemia causing mucosal edema, increased activation of tissue plasminogen activator, systemic lupus erythematosus, vascular lesions in the intestinal mucosa, and chemotherapy/ radiation therapy. [6][7][8][9][10][11][12][13][14][15][16][17][18][19] Most of these diseases can be diagnosed by gross examination or by light microscopic examination of small intestinal tissue samples. However, some of these diseases such as systemic lupus erythematosus or small intestinal bacterial overgrowth cannot reliably be identified with biopsy and routine histopathology. 15,20 Although lesions of small intestinal crypts have been associated with PLE in 1 dog, this dog also had absence of villi and large areas of mucosal ulceration. 21 In this paper, we describe 6 dogs with PLE in which a large number of intestinal crypts were dilated and filled with mucus, with or without inflammatory cellular debris. None of our dogs had discernable ulceration or lack of villi. The purpose of this report is to document this histologic lesion and its apparent association with PLE in the dog. Materials and MethodsThe cases reported were examined at Texas A&M University between 1989 and 1999, and at Michigan State University in 1997. All dogs had panhypoproteinemia...

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.

A 4-month-old female Siberian Husky was referred for a 2-month history of intermittent diarrhea, poor body condition, polyuria, and polydipsia. Based on the history, the diarrhea was thought to be of small intestinal or mixed origin because the dog had a ravenous appetite, poor body condition and failure to thrive, frequent defecations, and feces that occasionally were covered by mucus. The dog had been diagnosed with and repeatedly treated for hookworms and coccidia by the referring veterinarian with a combination of praziquantel, pyrantel pamoate, and febantel, a and metronidazole.b The dog also had been treated with amoxicillin, c sulfadimethoxine, d and prednisone e for short periods of time. Two weeks before presentation, the referring veterinarian changed the dog's regular diet f to a prescription diet g formulated for dogs with gastrointestinal disease. The antiparasitic medications, antibiotics, glucocorticoids, and diet change led only to transient responses, and the diarrhea always recurred with discontinuation of therapy despite the fact that both direct fecal examination and fecal flotation were negative. The dog's appetite was increased for the entire period of 2 months.At the time of presentation, the dog weighed 12 kg and was in poor body condition (body condition score 3/ 9; optimal, 5/9).1 Slightly thickened, gas-filled intestinal loops were identified by abdominal palpation. CBC and serum electrolyte concentrations were within normal limits. A serum biochemical profile revealed mild increases in alkaline phosphatase activity (ALP, 187 U/L; reference range, 10-150 U/L), creatine kinase activity (CK, 421 U/L; reference range, 10-200 U/L), and serum phosphorus concentration (8.8 mg/dL; reference range, 2.1-6.3 mg/dL), and a mild decrease in blood urea nitrogen concentration (BUN, 4 mg/dL; reference range, 7-27 mg/dL). Liver disease was suspected, and fasting and 2-hour postprandial total serum bile acid concentrations were evaluated and found to be normal (fasting serum bile acid concentration, ,1.0 mM/L; reference range, 0-5 mM/L; postprandial serum bile acid concentration, 1.5 mM/L; reference range, 3.9-12.7 mM/L). A relatively low specific gravity (1.017) was noted on urinalysis, and bacterial culture of urine yielded no growth.Radiographs of the abdomen were normal, but the layers of the small intestinal wall could not be differentiated on abdominal ultrasonography, and a prominent pancreas of normal echogenicity was identified. Serum concentrations of cobalamin, folate, canine pancreatic lipase immunoreactivity (measured as Spec cPL h ), and canine trypsin-like immunoreactivity (cTLI) were determined and results of these tests were Spec cPL ,29 mg/L (below the detection limit; reference range, 29-200 mg/L), cTLI 7.1 mg/L (reference range, 5.0-35.0 mg/L), cobalamin 1,001 ng/L (reference range, 249-733 ng/L), folate 39.3 mg/L (reference range, 6.5-11.5 mg/L). These findings were interpreted as consistent with small intestinal bacterial overgrowth (SIBO), also referred to as antibiotic-responsi...

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