Background: The detailed pathological phenotype of diet-responsive chronic enteropathy (CE) and its modulation with dietary therapy remain poorly characterized.Hypothesis/Objectives: Key mucosal lesions of diet-responsive CE resolve with dietary therapy.Methods: This was a prospective observational study of 20 dogs with diet-responsive CE. Endoscopic duodenal biopsies collected before and 6 weeks after the start of a dietary trial were assessed by means of qualitative and quantitative histopathological, immunohistochemical, and ultrastructural criteria. Control duodenal biopsies were obtained from 10 healthy Beagle dogs on 1 occasion.Results: Compared with control dogs, the CE dogs had higher villus stunting scores and higher overall WSAVA scores, a lower villus height-to-width ratio, and higher lamina propria density of eosinophils. The CE dogs also had ultrastructural lesions of the mitochondria and brush border. In common with other studies in which the disease and control populations are not matched for breed, age, sex, and environment, these comparisons should be interpreted with caution. Comparing biopsies collected at presentation and 6 weeks after starting the dietary trial, mean lamina propria mononuclear cell score and lamina propria densities of eosinophils and mononuclear cells decreased. Dietary therapy also improved ultrastructural lesions of the mitochondria and brush border, eliciting a decrease in intermicrovillar space and an increase in microvillus height.Conclusions and Clinical Importance: In dogs with diet-responsive CE, the remission of clinical signs with dietary therapy is associated with subtle decreases in lamina propria density of eosinophils and mononuclear cells, and resolution of ultrastructural lesions of the enterocyte.

A dentigerous cyst is an odontogenic cyst associated with the crown of the impacted or unerupted teeth. Such cyst remain initially completely asymptomatic unless when infected and can be discovered only on routine radiographic examination. Here, such a case of dentigerous cyst, which was discovered on routine radiographic examination, is discussed here.

Drug-induced liver injury (DILI) presents as a broad spectrum of adverse drug reactions which can range from a mild elevation in liver enzymes to fulminant liver failure. The primary goal is to identify DILI early when the patient’s liver enzymes are elevated and to discontinue the offending agent as soon as possible to prevent further injury. Herbal, dietary supplements and anabolic steroids represent a significant component of the drugs thought to cause DILI in the United States. Unlike all other drugs known to cause DILI, these drugs fall into a category of injury that is neither intrinsic nor idiosyncratic due to overlapping characteristics between the two. Here, we present a case of the off-label use of androgenic anabolic steroids inducing liver injury. A combination of clinical, laboratory, and histologic workup eventually led to the diagnosis of DILI. This can be a diagnostic challenge for practitioners. The American College of Gastroenterology (ACG) published guidelines to aid the clinician in diagnosing DILI. Proving that an episode of liver injury is caused by a drug is difficult in many cases as it requires the exclusion of alternative etiologies. Some of the variables include temporal association, clinical-biochemical features, type of injury (hepatocellular and/or cholestatic), extrahepatic features, and the likelihood that a given agent is the culprit based on its known manifestations with prior cases. This case illustrates the utility of the diagnostic tools used for DILI as recommended by the ACG, along with a supplemental histopathologic diagnosis.