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Biomedical subjects

Michael D Willard

Publications and source records attributed to Michael D Willard.

7 recordsLinked to original sources

Protein-losing enteropathies.

GI protein loss can result from a heterogeneous group of diseases, including lymphangiectasia, IBD, neoplasia, ulceration, intussusception, and histoplasmosis. PLE should be suspected in any hypoalbuminemic patient with no evidence of exudative protein loss, proteinuria, or HI. A minimum laboratory database for the suspected PLE patient should include a complete blood cell count, a biochemical and electrolyte profile, urinalysis (+/- urine protein:cretinine ratio), and pre- and postprandial bile acid determinations. Fecal alpha 1-PI concentrations may be used to confirm the presence of GI protein loss in cases with concurrent renal or hepatic disease. Because PLE is a syndrome and not a specific disease, the most effective therapy must be directed at the underlying cause. Multiple high-quality endoscopic biopsies are sufficient to diagnose most patients with PLE, although full-thickness biopsies are required in some cases. Patients with PLE are often clinically "fragile," and careful symptomatic therapy must be integrated with dietary and medical management strategies in most cases.

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Biopsy of the gastrointestinal tract.

Gastrointestinal biopsy is a potentially powerful tool, but it is easy to do it incorrectly. If clinicians are careless in performing or submitting biopsies, or if they blindly believe whatever the histopathology report says, they are abdicating their responsibility to the client and patient. Two comments seem most appropriate. First, the goal of endoscopy is not to be able to place the tip of an endoscope in a particular location; rather, the goal of endoscopy is to be able to access a particular location and then take a diagnostic specimen well enough that surgery can be avoided. Second, attention to detail is worth at least as much if not more than technology.

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Esophagitis and esophageal strictures.

Esophagitis and esophageal strictures are important causes of esophageal disease in dogs and cats. Clinical suspicion is created when the clinician recognizes the clinical signs suggestive of esophageal disease and accounts for historical information and physical examination findings. Once suspected, the diagnosis of esophagitis and esophageal strictures is a fairly simple one in most cases. Although the benefit of diminishing secretion of gastric acid in patients with esophagitis is unquestioned, other questions regarding adjunctive medical treatments, such as sucralfate and glucocorticoids for dogs and cats with esophagitis, have not been answered through appropriate clinical studies. Esophageal strictures are readily treated with balloon dilation or esophageal bougienage, and clients can expect most patients to become functional, although dietary change may be necessary.

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Interobserver variation among histopathologic evaluations of intestinal tissues from dogs and cats.

OBJECTIVE: To determine whether substantial interobserver variation exists among diagnostic pathologists for descriptions of intestinal mucosal cell populations and whether histopathologic descriptions accurately predict when a patient does not have clinically evident intestinal disease. DESIGN: Comparative survey. Sample Population-14 histologic slides of duodenal, ileal, or colonic tissue from 10 dogs and 3 cats. PROCEDURE: Each histologic slide was evaluated independently by 5 pathologists at 4 institutions. Pathologists, who had no knowledge of the tissues' origin, indicated whether slides were adequate for histologic evaluation and whether the tissue was normal or abnormal. They also identified the main infiltrating cell type in specimens that were considered abnormal, and whether infiltrates were mild, moderate, severe, or neoplastic. RESULTS: Quality of all slides was considered adequate or superior by at least 4 of the 5 pathologists. For intensity of mucosal cellular infiltrates, there was uniformity of opinion for 1 slide, near-uniformity for 6 slides, and nonuniformity for 7 slides. Five dogs did not have clinical evidence of intestinal disease, yet the pathologists' descriptions indicated that their intestinal tissue specimens were abnormal. CONCLUSIONS AND CLINICAL RELEVANCE: Substantial interobserver variation was detected. Standardization of pathologic descriptions of intestinal tissue is necessary for meaningful comparisons with published articles. Clinicians must be cautious about correlating clinical signs and histopathologic descriptions of intestinal biopsy specimens.

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Sustained strenuous exercise increases intestinal permeability in racing Alaskan sled dogs.

We assessed gastric and intestinal permeability and performed gastroscopy to evaluate the effects of sustained strenuous exercise on the gastrointestinal tract in racing sled dogs. Three teams of racing Alaskan sled dogs were examined approximately 1 week before and 24 hours after the 2003 Iditarod sled dog race (1,100 miles in 10 days). Each examination consisted of the administration of a solution of sucrose, lactulose, and rhamnose to evaluate gastric and intestinal permeability, as well as gastroscopy to visually inspect the gastric mucosa. Of the 54 dogs examined before the race, 16 completed the course and contributed data to the analysis. Sustained strenuous exercise was associated with an increased frequency of gastric erosions or ulcerations seen endoscopically (0% prerace versus 61% postrace). A significant postrace increase occurred in the median lactulose to rhamnose ratio in both serum and urine (0.11 versus 0.165, P = .0363; 0.11 versus 0.165, P = .0090, respectively). No significant differences were found in median serum or urinary sucrose concentrations when pre- and postrace values were compared. No correlation was found between visible gastric lesions and the concentration of sucrose in serum or urine samples obtained 4-5 hours after administration of the sugar solutions. We conclude that sustained strenuous exercise is associated with increased intestinal permeability, but the sucrose permeability test as we performed it did not correlate with visible gastric lesions.

Alaska↗

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.

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Clinicopathological abnormalities and treatment response in 24 dogs seroreactive to Bartonella vinsonii (berkhoffii) antigens.

Bartonella vinsonii (B. vinsonii) subspecies berkhoffii is a recently recognized cause of endocarditis, myocarditis, and granulomatous disease in dogs. In an effort to elucidate other potential disease manifestations, the case records of 24 dogs that were seroreactive to B. vinsonii (berkhoffii) antigens were studied retrospectively. Diagnoses included immune-mediated hemolytic anemia, neutrophilic or granulomatous meningoencephalitis, neutrophilic polyarthritis, cutaneous vasculitis, and uveitis. Repeated B. vinsonii (berkhoffii) antibody titers became negative after treatment. This study indicates that a diverse spectrum of disease manifestations and clinicopathological abnormalities can be detected in dogs that are seroreactive to B. vinsonii (berkhoffii) antigens.

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