Secondary hypoparathyroidism attributed to hypomagnesemia in a dog with protein-losing enteropathy.

Severe hypomagnesemia (0.8 mg/dl; reference range, 1.6 to 2.3 mg/dl), hypocalcemia, and protein-losing enteropathy were identified in a 5-year-old castrated male 3-kg (6.6 lb) Shih Tzu examined because of anorexia, lethargy, paresis, and abdominal distention. Histologic examination of intestinal biopsy specimens revealed lymphangiectasia and lymphocytic, plasmacytic, neutrophilic infiltrates. Initial treatment included administration of magnesium (0.80 mEq/kg [0.36 mEq/lb]) of body weight in a balanced electrolyte solution. This treatment resulted in normalization of the serum magnesium concentration (1.7 mg/dl); resolution of the lethargy, paresis, and tachycardia; and an increase in the serum parathyroid hormone and ionized calcium concentrations. Findings were consistent with secondary hypoparathyroidism attributable to hypomagnesemia. Magnesium concentration should be monitored in all dogs with gastrointestinal tract disease, especially those with protein-losing enteropathy, anorexia, and weakness.     

Hypomagnesemia and hypocalcemia associated with protein-losing enteropathy in Yorkshire terriers: five cases (1992-1998)

OBJECTIVE: To determine clinical and laboratory findings associated with protein-losing enteropathy, hypomagnesemia, and hypocalcemia in Yorkshire Terriers. DESIGN: Retrospective study. ANIMALS: 5 purebred or crossbred Yorkshire Terriers with protein-losing enteropathy, hypomagnesemia, and hypocalcemia. PROCEDURE: Medical records were reviewed for dogs with protein-losing enteropathy, hypomagnesemia, and hypocalcemia. RESULTS: Of 8 dogs with these signs, 5 had Yorkshire Terrier breeding. Common findings were diarrhea, abdominal effusion, leukocytosis, neutrophilia, hypocalcemia (ionized calcium), hypomagnesemia, hypoproteinemia, hypoalbuminemia, hypocholesterolemia, and increased serum activity of aspartate aminotransferase. CONCLUSIONS AND CLINICAL RELEVANCE: Yorkshire Terriers are at increased risk for development of protein-losing enteropathy with hypomagnesemia and decreased ionized calcium concentration. Hypomagnesemia and hypocalcemia may have a related pathogenesis involving intestinal loss, malabsorption, and abnormalities of vitamin D and parathyroid hormone metabolism. Serum electrolyte replacement may be required to avoid neurologic and metabolic problems.     

Dexamethasone for treatment of multisystemic eosinophilic epitheliotropic disease in a horse

A 4-year-old Paint mare was examined because of respiratory tract infection, dermatitis, and weight loss of 2 months' duration. Initial examination revealed generalized pruritic dermatitis, ocular and nasal discharges, and stranguria. Laboratory abnormalities included leukopenia and hypoalbuminemia. Further examination of the respiratory tract revealed grade III of IV pharyngitis and pyogranulomatous pneumonia. Endoscopic examination of the bladder revealed a prolific mass at the junction of the bladder and urethra. Hypoproteinemia was suspected to be caused by protein-losing enteropathy. On histologic examination, skin, rectal, pharyngeal, and urethral biopsy specimens were characterized by infiltration of eosinophils and lymphocytes, and a diagnosis of multisystemic eosinophilic epitheliotropic disease was made. The horse improved following treatment with dexamethasone, trimethoprim-sulfamethoxazole, and an antihistamine and was discharged after 19 days of hospitalization. Treatment with dexamethasone was continued for 4 weeks after hospitalization but was then discontinued. Eight months after discharge, the horse was performing as a pleasure horse and did not require any medical treatment. Multisystemic eosinophilic epitheliotropic disease is typically associated with a poor prognosis in horses. The dermatitis, protein-losing enteropathy, and lower respiratory tract disease in this horse were consistent with previous reports; however, pharyngitis and urethritis have not, to our knowledge, been previously reported in horses with this disease.     

An outbreak of Lawsonia intracellularis infection in a standardbred herd in Ontario

An outbreak of protein-losing enteropathy associated with Lawsonia intracelluaris infection was diagnosed in 6 standardbred foals from a farm in Ontario. Wildlife exposure may have been involved in the perpetuation of disease in this outbreak. The clinical presentation, treatment, outcomes, and pathological findings are described.     

Lawsonia intracellularis proliferative enteropathy in a weanling foal,with a tentative histological diagnosis of lymphocytic plasmacytic enteritis

This Case Report describes a weanling filly with protein-losing enteropathy associated with Lawsonia intracellularis infection. This was diagnosed on the basis of a significant antibody response and a positive faecal PCR result. The histopathological lesion observed in proliferative enteropathy is mucosal hyperplasia, commonly affecting the ileum and colon in foals. Duodenal biopsies obtained from this filly revealed a lymphocytic plasmacytic infiltrate. The filly recovered completely following treatment with erythromycin and no additional medication was administered to treat the lymphocytic plasmacytic infiltrate. This Case Report suggests that lymphocytic plasmacytic infiltrates observed on duodenal biopsies may represent a nonspecific intestinal immune response.     

Large granular intestinal lymphosarcoma and leukemia in a dog

A rare, large granular lymphocyte (LGL) tumor causing a protein-losing enteropathy and thrombocytopenia was diagnosed in an Irish wolfhound. The case had an aggressive clinical course, like most LGL tumors in humans. Immunophenotyping suggested that the LGL tumor in this dog was derived from a natural-killer cell.     

Primary epitheliotropic intestinal T-cell lymphoma in a horse.

A 17-year-old Quarterhorse gelding with a clinical diagnosis of protein-losing enteropathy was submitted for necropsy following a 4-5-month duration of weight loss, decreased appetite, and hypoproteinemia. Gross findings included multiple 1-2-cm diameter ulcers on the luminal surfaces of the duodenum and ileum. Histologic examination revealed individual large, round cells infiltrating much of the mucosal epithelium of the duodenum, jejunum, ileum, and colon in addition to multifocal areas of ulceration. Similar round cells infiltrated Brunner's glands and expanded the submucosa beneath the foci of ulceration. Immunohistochemical staining indicated the round cell population was of T-lymphocyte origin. Several features of this equine neoplasm bear similarities to enteropathy-associated T-cell lymphoma in humans.     

Entéropathie, avec perte de protéines, secondaire à une lymphangiectasie intestinale, chez trois chiens

Protein-losing enteropathy secondary to intestinal lymphangiectasia in three dogs

Three cases of protein-losing enteropathy secondary to intestinal lymphangiectasia in the dog are presented.

In the three cases, common clinical findings were nonresponsive diarrhea and weight loss. Subcutaneous edema was observed in case 1. Polyphagia and polydipsia were evident in cases 2 and 3.

Serum examinations revealed low values of protein with a normal albumin/globulin ratio. There was histopathological evidence of dilatation of lacteals, as well as plasma cell and lymphocyte infiltration in the small intestine.

In the three cases, a corticotherapy was instituted and gave good results.

     

Protothecal enteritis as a cause of protein-losing enteropathy in a bull

Prototheca spp are achlorophyllic saprophytic algae found in wastewater, sewage, agricultural waste, and possibly elsewhere in the environment. Infections with these organisms have been reported in cattle, humans, and dogs; affected cattle commonly develop mastitis. A 5-year-old Brahman-cross bull was evaluated because of a history of diarrhea and weight loss. The history and physical examination and clinicopathologic findings were similar to those associated with granulomatous enteritis caused by Mycobacterium avium subsp paratuberculosis (Johne's disease), which is the most common protein-losing enteropathy of cattle. However, diagnostic tests for paratuberculosis yielded negative results. Biopsy specimens from the ileum, jejunum, and ileocecal lymph node were collected for histologic examination and preparation of tissue impression smears; Prototheca-like organisms were identified. Because of the poor prognosis associated with this infection and the lack of safe and economical therapeutic agents for cattle, the owner decided to euthanatize the bull. Infection with Prototheca organisms was confirmed postmortem. As this case illustrates, protothecosis may be a cause of granulomatous enteritis in cattle.     

Prognostic value of small intestinal dilatation in dogs with protein-losing enteropathy

To date, little is known about the prognostic significance of ultrasonographic findings in dogs with protein-losing enteropathy (PLE). The aim of this retrospective study was to examine the prognostic value of ultrasonographic findings in dogs with PLE. A total of 26 dogs with PLE were included: 20 dogs with chronic enteropathy and 6 dogs with gastrointestinal lymphoma. The presence of small intestinal dilatation was associated with shorter survival time in dogs with PLE (P=0.003). The presence of hyperechoic intestinal mucosal striations was associated with longer survival time in dogs with PLE (P=0.0085). The results of the current study indicate that the presence of small intestinal dilatation might be associated with poor prognosis in dogs with PLE.     

Lymphocytic-plasmacytic enteritis in two horses

The primary hematologic abnormalities in 2 adult horses with chronic weight loss were hypoalbuminemia and hyperglobulinemia. One horse was anemic, had subclinical disseminated intravascular coagulation, and prolonged plasma sulfobromophthalein half-life. Small-intestinal dysfunction with malabsorption was indicated by abnormal D-xylose absorption test results. Clinicopathologic and pathologic findings were consistent with a diagnosis of malabsorption and protein-losing enteropathy, attributable to lymphocytic and plasmacytic infiltration of the intestine.     

Protein-losing enteropathy associated with cystic mucoid changes in the intestinal crypts of two dogs

Two dogs were emaciated and hypoalbuminemic due to protein-losing enteropathy associated with a severe, focal, mucoid, cryptal ectasia of the duodenum and marked villus atrophy. In one case, diseased portions of the duodenum were obvious endoscopically and were limited to discrete, focal areas in the small intestine, with apparently more undiseased tissue than diseased tissue being present. The signs and lesions in one dog resolved after initiating combination dietary and pharmacological therapy.     

Strongyloidiasis in a Cope's grey tree frog (Hyla chrysoscelis).

A male Cope's grey tree frog (Hyla chrysoscelis) died spontaneously with ventral subcutaneous edema and was necropsied. Thickening of the intestinal mucosa was observed histopathologically, with villous atrophy and intraepithelial nematodes present. Adult female Strongyloides sp. nematodes were isolated from the fixed intestinal tract, the first time this nematode genus has been recovered from this frog genus. Intestinal strongyloidiasis should be considered as a cause for protein-losing enteropathy and death in frogs.     

A case of protein-losing enteropathy treated with methotrexate in a dog

A 9-year-old female Pug was presented to us with chronic diarrhea. Hematologic findings indicated severe hypoproteinemia and hypoalbuminemia, and endoscopy revealed severe edema of the duodenal mucosa. Based on these results and on additional histopathological findings, we made a diagnosis of protein-losing enteropathy caused by lymphocytic-plasmacytic enteritis with lymphangiectasia. The dog was initially treated with prednisolone and cyclosporine. This treatment regimen was not effective. However, when methotrexate was substituted for cyclosporine, progress was obtained and the diagnosis was confirmed.     

Myenteric ganglionitis and intestinal leiomyositis in a Jack Russell terrier

A 9-year, 6-month old spayed female Jack Russell terrier presented with a 3-week history of intermittent vomiting, diarrhoea and weight loss. Serum biochemistry demonstrated severe panhypoproteinaemia, mild hypocalcaemia and mild hypocholesterolaemia, consistent with protein-losing enteropathy. Full-thickness biopsies obtained from the stomach and different sections of small intestine demonstrated histological features of both myenteric ganglionitis and early intestinal leiomyositis. Complete resolution of clinical signs occurred within 1 week of implementing immunosuppressive therapy. At the time of writing, 9 months following diagnosis, the dog remains in remission.     

Comparison of ultrasonographic findings with clinical activity index (CIBDAI) and diagnosis in dogs with chronic enteropathies.

Intestinal wall thickness is neither a specific nor sensitive ultrasound parameter for detecting intestinal inflammation. We hypothesize that mucosal echogenicity, lymphadenomegaly, and secondary findings of the gastrointestinal tract would be more sensitive and specific markers for detecting and differentiating causes of chronic inflammatory bowel disease in dogs. Fifty-six client-owned dogs with chronic diarrhea and 10 control dogs were examined with two-dimensional, gray-scale ultrasound (time 0, 4, and 10 weeks post therapy) and small intestinal mucosal biopsies were performed at the 0- and 4-week time points. The clinical activity was assessed at each time point using the canine inflammatory bowel disease activity index (CIBDAI). Fifty-one dogs had inflammatory infiltration of the duodenal mucosa and were divided into three groups, food-responsive disease, idiopathic inflammatory bowel disease, and protein-losing enteropathy, based on their response to the different treatments and histology. Two different patterns of increased echogenicity of the mucosa were detected: hyperechoic speckles and hyperechoic striations. A normal, hypoechoic bowel mucosa in dogs with chronic diarrhea had a sensitivity of 80% and a specificity of 81% for the diagnosis of food-responsive disease. Hyperechoic striations had a sensitivity of 75% and a specificity of 96% for dogs with protein-losing enteropathy. Hyperechoic speckles were non-specific for diagnosing inflammatory bowel disease. There was a significant relationship between ultrasound score and CIBDAI at t0, but not following therapy. Mucosal echogenicity may be a better parameter for detecting inflammatory bowel disease than bowel wall thickness in dogs with chronic diarrhea.     

Pattern recognition and feature extraction of canine celiac and cranial mesenteric arterial waveforms: normal versus chronic enteropathy--a pilot study

In this pilot study, we hypothesize that waveform patterns of the celiac and cranial mesenteric arteries differ pre- and post-prandially in normal dogs compared to those with chronic enteropathy. We further suggest that it is possible to classify these findings according to the type of disease present. Eleven dogs with chronic enteropathy and eight normal dogs were examined. Doppler examinations were performed at times 0 (fasted), and at 20, 40, 60 and 90 min post-prandially. The waveform shapes were described and the following features were extracted: resistive and pulsatility index, mean maximum velocity, mean diastolic velocity, peak systolic velocity, early diastolic notch ratio and the deceleration time interval. Dogs with inflammatory bowel disease had either lower or absent flow at fasting in early diastole compared to the other groups. Resistive and pulsatility indices decreased during digestion in all groups except those with protein losing enteropathy. The increase in mean diastolic flow during digestion in affected dogs was either lacking (protein-losing enteropathy) or significantly lower (inflammatory bowel disease, P<0.05) compared to normal dogs. Dogs with chronic enteropathies had abnormal arterial waveform shapes and suboptimal increases in diastolic blood flow during digestion and these findings worsened with the severity of the histological lesions present. Doppler ultrasound of the celiac and mesenteric arteries has great potential to enhance our understanding of intestinal disease in conscious dogs.     

Small intestinal adenomatous polyposis resulting in protein-losing enteropathy in a horse

A 4-year-old Quarter Horse gelding was presented with a history of weight loss of 6 months duration, along with extensive ventral subcutaneous edema. Clinicopathologic findings included a markedly low serum total protein (2.9 g/dl) and a low packed cell volume (24%). The mucosal surface of the distal jejunum and entire ileum were carpeted with numerous polypoid, papillary, and glandular masses comprised of pseudostratified tall columnar cells and large numbers of interspersed goblet cells. Neoplastic change was diffuse throughout the mucosa of each mass, but abrupt demarcation occurred between neoplastic masses and adjacent mucosa. Immunohistochemical staining for protein of the p53 tumor suppressor gene revealed only occasional cytoplasmic reactivity within polyps and normal mucosa. Nuclear staining for papillomavirus antigens was not observed. Electron microscopic examination revealed features of well-differentiated intestinal epithelial cells, including apical tight junctions and microvilli, desmosomes, and the presence of numerous goblet cells. Microorganisms were not detected. Small intestinal polyposis should be considered as a rare differential diagnosis for protein-losing enteropathy in the horse.     

Familial protein-losing enteropathy and protein-losing nephropathy in Soft Coated Wheaten Terriers: 222 cases (1983-1997)

Records and pedigrees of Soft Coated Wheaten Terriers (SCWT) with protein-losing enteropathy (PLE) or protein-losing nephropathy (PLN) were studied retrospectively. Criteria for inclusion were defined based on analysis of blood (panhypoproteinemia for PLE, hypoalbuminemia for PLN) and urine (proteinuria for PLN) and histopathologic examination of tissue. Two hundred twenty-two affected dogs (female:male ratio = 1.6, P < .001) were clinically identified. Dogs were diagnosed with PLE earlier (P < .005; mean +/- SD age: 4.7+/-2.6 years, n = 76) than with PLN (6.3+/-2.0 years, n = 84) or with both diseases (5.9+/-2.2 years, n = 62). Clinical signs included vomiting, diarrhea, weight loss, pleural and peritoneal effusions, and less commonly thromboembolic disease. Dogs with PLE generally had panhypoproteinemia and hypocholesterolemia; intestinal lesions included inflammatory bowel disease, dilated lymphatics, and lipogranulomatous lymphangitis. Dogs with PLN generally had hypoalbuminemia, proteinuria, hypercholesterolemia, and azotemia; renal lesions typically showed chronic glomerulonephritis/glomerulosclerosis, and less commonly endstage renal disease. Dogs with combined PLE/PLN had intermediate mean values (P < .001) for serum total protein, albumin, globulin, and cholesterol but had a higher mean urine protein:creatinine ratio than did PLN dogs (P < .05); intestinal and renal lesions in these dogs were similar to those in the other groups. Two dogs had incidental mild renal dysplasia. Pedigree analysis from 188 dogs demonstrated a common male ancestor, although the mode of inheritance is unknown. Both PLE and PLN are common diseases in this small breed population. The prognosis is poor. Compared with previously reported intestinal and renal diseases in dogs, a new, distinctive familial predisposition for both PLE and PLN has been recognized in the SCWT breed.     

Ultrasonographic findings in a basenji with immunoproliferative enteropathy

The ultrasonographic findings in a one-and-a-half-year-old female basenji with immunoproliferative enteropathy are described. On ultrasonographic examination, generalised thickening of the small bowel wall was found, ranging between 4 and 6 mm. The normal layered appearance of the intestinal wall was replaced by three distinct layers; an innermost enlarged hyperechogenic layer; an enlarged poor echogenic layer, and an outer hyperechogenic layer. These findings are consistent with the histopathological appearance of this particular chronic inflammatory bowel disease, since the inner layer probably represents the infiltrated mucosa, the middle layer the infiltrated lamina propria and the outer layer the serosa. Thus, the ultrasonographic finding of generalised thickening of the intestinal wall in a basenji presenting with chronic diarrhoea, weight loss, anorexia or vomiting is strongly indicative of immunoproliferative enteropathy.