Hindlimb lameness associated with a focal osseous metaplasia in an 18‐year‐old Welsh Section D mare

This report describes a case of chronic lameness secondary to an extraskeletal osseous mass located in the plantaromedial aspect of the right hind pastern in a mature Welsh Section D mare. The lesion was confirmed to represent metabolically active osseous tissue in close apposition with the adjacent plantar digital neurovascular bundle and digital flexor tendons. Surgical resection of the mass resulted in a complete resolution of lameness and return to previous level of activity. Histopathological examination classified the mass as a focal osseous metaplasia, which was most likely to be the result of previous trauma causing local haemorrhage, which resulted in subsequent dystrophic mineralisation and eventually osseous metaplasia. Similar lesions have been described in man, but have not been previously reported in the horse.     

Chronic Gingivostomatitis with Esophagitis in Cats

Background

Chronic gingivostomatitis in cats (FCG) is a debilitating disease with potentially deleterious effects on overall health.

Hypothesis/Objectives

Little is known about the pathophysiology and overall impact of FCG. The aims of our study were to investigate whether gingivostomatitis occurs concurrently with esophagitis, if FCG treatment contributes to esophagitis and if esophagitis exacerbates signs of FCG.

Animals

Fifty‐eight cats with clinical signs of FCG and 12 healthy control cats exhibiting no signs of oral disease, all client‐owned.

Methods

Prospective study. Physical, oral and endoscopic examinations were performed on all cats. Measurements of salivary and esophageal lumen pH were obtained from both groups. Biopsies were acquired from sites of esophageal inflammation in cats with FCG and from normal‐appearing esophageal mucosa in control cats.

Results

The majority of cats with clinical signs of FCG exhibited some degree of esophagitis especially in the proximal (44/58) and distal (53/58) parts (P < 0.001) with or without columnar metaplasia, compared to controls. All cats lacked signs related to gastrointestinal disease. Salivary and esophageal lumen pH were not statistically different compared to controls.

Conclusions and Clinical Importance

Feline chronic gingivostomatitis seems to occur concurrently with esophagitis. Esophagitis also should be managed in cats with chronic gingivostomatitis because it may aggravate the existing condition.     

Immunohistochemical analysis of lens epithelial-derived membranes following cataract extraction in the dog

The objective of the study was to characterize the morphologic and immunohistochemical features of lens epithelial-derived proliferative membranes from the anterior segment of canine globes. These features were correlated with those previously identified for diseases resulting from lens epithelial cell (LEC) proliferation including posterior capsular opacification, traumatic subcapsular cataract, and subcapsular plaques associated with hypermature cataracts. Sixteen canine globes were removed as a result of glaucoma or other complications following cataract extraction. Light microscopic and immunohistochemical analysis was performed on sections from formalin-fixed, paraffin-embedded globes. The tissues were stained with a variety of antibodies for cellular markers for LECs, growth factors or other cellular constituents relevant to cellular metaplasia and proliferation. The membranes were composed of monolayers or multilayers of spindle-shaped cells on the external surfaces of the anterior and posterior lens capsule, ciliary processes, iris leaflets, and iridocorneal angle, and they could be seen extending from an obvious monolayer of LEC within the capsular sac. Variably, scattered pigment cells, presumably of uveal origin, were concurrently present. Cellular components of the membranes stained positive for vimentin, transforming growth factor-beta, basic fibroblast growth factor, and smooth muscle actin. An amorphous eosinophilic extracellular matrix consisting predominately of collagen was associated with the membranes. Proliferative anterior segment membranes following cataract surgery were morphologically and immunohistochemically similar to cellular and matrix components of posterior capsular opacification and capsular plaques seen with hypermature cataracts, both of which result from metaplasia and proliferation of LEC. The presence of these LEC-derived membranes in association with secondary glaucoma suggests that exuberant proliferation of LEC outside the confines of the lens capsular sac may cause pathologic alterations in the eye following cataract surgery in the dog.     

根除幽门螺杆菌对胃黏膜肠化生的影响

目的：了解幽门螺杆菌(HP)感染伴胃黏膜肠化生者经根除HP后肠化生的变化情况。方法：HP感染伴肠化生者28例口服抗菌药物三联疗法14d，另2l例不予根除HP，6个月后复查胃镜和病理活检。结果：28例中24例HP获根除，肠化生消失或明显减轻者有11／24例，对照组仅有3／2l例，两组差异具有显著性(P＜0．25)。结论：根除HP后肠化生可有效地消除或明显减轻，认为当HP感染伴肠化生时应积极根除HP。     

Intestinal metaplasia -the effect of Acid on the gastric mucosa and gastric carcinogenesis-

This review concerns stem cells and their relation to intestinal metaplasia. When gastric regions of mice, Mongolian gerbils or several strains of rats were irradiated with a total dose of 20 Gy of X-rays given in two fractions, intestinal metaplasia was only induced in rats. In addition, it was greatly influenced by rat strain and sex. Alkaline phosphatase (ALP) positive metaplastic foci were increased by administration of ranitidine (H(2) receptor antagonist), crude stomach antigens or subtotal resection of the fundus and decreased by cysteamine (gastric acid secretion stimulator), histamine or removal of the submandibular glands. Recent studies have shown that Cdx2 transgenic mice with gastric achlorhydria develop intestinal metaplasia and that in men and animals, Helicobacterpylori (H. pyrlori) infection can cause intestinal metaplasias that are reversible on eradication. Our results combined with findings for H. pylori infection or eradication and transgenic mice suggest that an elevation in the pH of the gastric juice due to disappearance of parietal cells is one of the principal factors for development of reversible intestinal metaplasia. When different organs were transplanted into the stomach or duodenum, they were found to transdifferentiate into gastric or duodenal mucosae, respectively. Organ-specific stem cells in normal non-liver tissues (heart, kidney, brain and skin) also differentiate into hepatocytes when transplanted into an injured liver. Therefore, stem cells have a multipotential ability, transdifferentiating into different organs when transplanted into different environments. Finally, intestinal metaplasia has been found to possibly increase sensitivity to the induction of tumors by colon carcinogens of the 1,2-dimethylhydrazine (DMH), azoxymethane (AOM) or 2-amino-1-methyl-6-phenylimidazo[4.5-b]pyridine (PhIP) type. This carcinogenic process, however, may be relatively minor compared with the main gastric carcinogenesis process induced by N-methy1-N'-nitro-N-nitrosoguanidine (MMNG) or N-methylnitrosourea (MNU), which is not affected by the presence of intestinal metaplasia. The protocol used in these experiments may provide a new approach to help distinguish between developmental events associated with intestinal metaplasia and gastric tumors.     

Idiopathic myelofibrosis accompanied by peritoneal extramedullary hematopoiesis presenting as refractory ascites in a dog

A 2.5‐year‐old spayed female American Pit Bull Terrier dog presented with a primary complaint of chronic refractory ascites. The dog's CBC displayed a moderate to severe macrocytic, hypochromic, nonregenerative anemia, and a moderate leukopenia as result of a moderate neutropenia and monocytopenia. Microscopic examination of the blood smear showed marked anisocytosis, mild polychromasia, mild acanthocytosis and ovalocytosis, moderate schistocytosis and poikilocytosis, and 4 metarubricytes/100 WBC. Abdominal ultrasonography revealed a homogenous, mild to moderately hyperechoic appearing liver as well as marked amounts of speckled anechoic to slightly hypoechoic peritoneal fluid. Cytology of the ascitic fluid demonstrated a sterile transudate, with evidence of a chronic inflammatory reaction as well as erythroid and myeloid precursor cells, and a few megakaryocytes with occasional micromegakaryocytes. Histologic sections of bone marrow, spleen, and liver were examined, using routine H&E stains, as well as a variety of immunohistochemistry and other special stains. Histopathology of the bone marrow and spleen revealed varying degrees of fibrosis, erythroid, and myeloid hyperplasia, as well as multiple small hyperplastic clusters of megakaryocytes. The megakaryocytes displayed many features of atypia such as increased cytoplasmic basophilia and occasional abnormal chromatin clumping with mitoses. Histopathologic examination of the liver disclosed evidence of mild extramedullary hematopoiesis. This case represents the first report of canine idiopathic myelofibrosis associated with peritoneal extramedullary hematopoiesis, resulting in refractory ascites. Although idiopathic myelofibrosis is a relatively rare condition in dogs, this case demonstrates that ascites caused by peritoneal implants of hematopoietic tissue may be the initial manifestation of myelofibrosis.