Chronic oesophagitis in the cat.

BACKGROUND: Our understanding of the pathophysiology of gastro-oesophageal reflux disease (GERD) in man is limited. The aim of the present study was to establish a long-term (>1 year) animal model for reflux oesophagitis which would allow us to study various aspects of the development of chronic reflux oesophagitis. METHODS: Myotomy was carried out in the gastro-oesophageal junction in eight cats; seven other cats were sham-operated. Before the operation, and every 2 months thereafter, oesophagoscopy was carried out, biopsies were taken for histology, and manometry was performed to determine the lower oesophageal sphincter pressure (LESP). The cats were killed 1 year after the operation. RESULTS: The myotomy operation resulted in a significantly decreased LESP. In oesophageal biopsies from these cats, there was a varying degree of oesophagitis starting already 2 months after surgery. In six of the eight myotomized cats there was hyperplasia of the stratum basale, and cardiac type metaplasia was observed in two cats. The control cats showed no significant changes in LESP or in the histology of the oesophagus. CONCLUSIONS: In cats followed for more than a year, myotomy in the gastro-oesophageal junction results in reflux oesophagitis similar to that seen in patients with chronic gastro-oesophageal reflux.

Signal transduction pathways in esophageal and lower esophageal sphincter circular muscle.

Esophageal reflux is a common condition that affects children and 1 in 10 adults, and if untreated may result in chronic esophagitis, aspiration pneumonia, esophageal strictures, and Barrett's esophagus, a premalignant condition. Although esophagitis is a multifactorial disease that may depend on transient lower esophageal sphincter (LES) relaxation, speed of esophageal clearance, mucosal resistance, and other factors, impairment of LES pressure is a common finding in patients complaining of chronic heartburn. Our data suggest that esophageal and LES circular muscle utilize distinct Ca2+ sources, phospholipid pools, and signal transduction pathways to contract in response to acetylcholine (ACh): (1) In esophageal muscle ACh-induced contraction requires influx of extracellular Ca2+ and may be linked to phosphatidylcholine metabolism, production of diacylglycerol (DAG) and arachidonic acid, and activation of a protein kinase C (PKC)-dependent pathway. (2) In LES muscle ACh-induced contraction utilizes intracellular Ca2+ release arising from metabolism of phosphatidylinositol (PI), and a calmodulin-myosin light chain kinase-dependent pathway. Resting LES tone, on the other hand, may be due to relatively low basal PI hydrolysis resulting in submaximal levels of inositol triphosphate (IP3)-induced calcium release and interaction with DAG to activate PKC. (3) After induction of experimental esophagitis, basal levels of PI hydrolysis and intracellular calcium stores are substantially reduced, resulting in a reduction of resting tone. In addition the signal transduction pathway responsible for LES contraction in response to ACh changes from one that depends on IP3 production, calcium release, and calmodulin activation to one that relies on influx of extracellular calcium and activation of PKC.

Resolution of focal fatty infiltration of the liver.

Focal fatty infiltration of the liver has been recognized as a distinct entity only since 1980. It may simulate neoplastic or other low-density parenchymal lesions, including abscesses and hemangiomas. I report a case of histologically confirmed focal fatty infiltration of the liver in a man with obesity and alcoholism; the lesion disappeared after the patient began a program of exercise, weight loss, and abstinence from alcohol. The possible pathogenesis of focal fatty infiltration of the liver is reviewed, diagnostic techniques are described, and reversibility of the lesion is discussed.

Long-term survival in a patient with verrucous carcinoma of the esophagus.

A 66-yr-old white male with a long-standing history of gastroesophageal reflux and Barrett's esophagus developed squamous cell dysplasia proximal to the site of the metaplastic epithelium. Two months later, he presented with progressive dysphagia. Upper endoscopy revealed near obliteration of the lumen from a large friable mass in the distal esophagus. Repeat endoscopic biopsies revealed areas of focal dysplasia but were inconclusive for the presence of malignancy. At surgery, a large inflammatory fibrotic mass was resected that was confirmed histologically to be a verrucous squamous cell carcinoma. Twenty-two months after the resection, there is no evidence of tumor recurrence. The case and relevant literature is discussed.