Demonstrative Experiment on the Favorable Effects of Static Electric Field Treatment on Vitamin D3-Induced Hypercalcemia

The purpose of this study was to elucidate the effects of static electric field (SEF) treatment on vitamin D3 (Vit D3)-induced hypercalcemia and renal calcification in mice. The mice were assigned to three groups: Vit D3-treated mice, mice treated with Vit D3 and SEF (Vit D3 + SEF), and untreated mice. After the administration of Vit D3, the Vit D3 + SEF-treated mice were exposed to SEF treatment by a high-voltage alternating current over five days. Serum biochemical examinations revealed that both the creatinine and blood urea nitrogen concentrations were significantly higher in the Vit D3-treated group. Significantly, decreased Cl concentrations, and increased Ca and inorganic phosphorus concentrations, were found in the Vit D3-treated group. In the Vit D3 + SEF-treated group, these parameters returned to the levels of the untreated group. In the Vit D3-treated group, histopathological examinations showed marked multifocal calcification in the lumens of the renal tubules and the renal parenchyma. The myocardium was replaced by abundant granular mineralization (calcification), with degeneration and necrosis of the calcified fibers. The stomach showed calcification of the cardiac mucosa. SEF treatment remarkably attenuated the Vit D3-induced hypervitaminotic injuries. In conclusion, this study provides important evidence that SEF treatment can reduce hypercalcemia and remove calcium deposits from the renal, cardiac, and gastric tissues. SEF treatment is useful in the regulation of disorders caused by an imbalance of serum electrolytes.

New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage

Summary Background Present diagnosis and management of gastroesophageal reflux disease (GERD) has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. This is due to failure to identify pathologic changes of early GERD; at present, pathology is limited to management of Barrett esophagus (BE). Methods Convincing evidence have confirmed that cardiac mucosa distal to the squamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium. Results When cardiac mucosa is recognized as a metaplastic esophageal epithelium, it becomes self-evident that the present endoscopic definition of the gastro-esophageal junction is incorrect, and there exists a dilated distal esophagus (DDE) in what is incorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It also becomes clear that the length of the DDE correlates with the presence and severity of GERD and represents the pathology of the entire spectrum of GERD. Further, it allows recognition that the DDE, measured as the gap between esophageal squamous epithelium and gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologic anatomy of damage to the abdominal segment of the lower esophageal sphincter (LES). Conclusion The new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause of GERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset. Ultimately, such early diagnosis has the potential to reverse the increasing trend of esophageal adenocarcinoma.

Peptic esophageal stricture in an adolescent with Barrett’s esophagus

Barrett’s esophagus (BE) is characterized by the replacement of distal esophageal stratified squamous epithelium by columnar epithelium. It is rare in children and the risk factors may include mental retardation, cerebral palsy, esophageal atresia, etc. Apart from corrosive ingestion, peptic stricture is the other leading cause of esophageal strictures in children. However, BE has not been well characterized in the pediatric population and in children presenting with esophageal strictures. A 16-year-old Indian boy presented with a history of gradually progressive dysphagia to solids (but not liquids) for 12 years along with heartburn and poor weight gain. Physical examination and routine blood investigations were unremarkable. Previously performed barium meal studies were suggestive of stricture in the mid and lower esophagus. Upper gastrointestinal (GI) endoscopy revealed a non-negotiable stricture with circumferential ulceration at 26 cm. The stricture was traversed using an ultrathin scope and the distal mucosa was found to be columnar. Biopsies revealed cardiac mucosa. The patient was treated with proton pump inhibitors (PPI) and four series of segmental dilatations with Savary Gilliard esophageal dilators. Peptic strictures occurring in the mid-upper esophagus should raise concerns about BE or malignancy. Here, we report a case of peptic esophageal stricture in a child without neurodevelopmental or trachea-esophageal abnormalities.