Dr. Mahatma is a board certified gastroenterologist in clinical practice for 30 years. He is a graduate of the University of Wales College of Medicine in Cardiff, U.K. He completed his residency in Internal Medicine at Cook County Hospital in Chicago. IL. He then completed his fellowship in Gastroenterology at Tulane University School of Medicine in New Orleans, LA. He received his board certification in Internal Medicine in 1986. Pulmonology in 1988, and Gastroenterology in 1991. He is a member of the American College of Gastroenterology, American Gastroenterology Association, American Society of Gastrointestinal Endoscopy, Texas Medical Association, and Dallas County Medical Society.
His primary focus includes colon cancer screening and gastrointestinal diseases such as esophagitis (GERD), ulcers, inflammatory bowel disease, gallbladder disease, and liver disease. He routinely performs colonoscopy with removal of polyps, EGD, esophageal dilatation, PEG(Endoscopic retrograde cholangio-pancreatography) placement, and ERCP(Endoscopic retrograde cholangio-pancreatography)
1. Dig Dis Sci. 1991 Nov;36(11):1562-8.
Misoprostol but not antacid prevents endotoxin-induced gastric mucosal injury: role of tumor necrosis factor-alpha.
Mahatma M, Agrawal N, Dajani EZ, Nelson S, Nakamura C, Sitton J.
Department of Medicine, Tulane University School of Medicine, New Orleans,
Many of the complications of septic shock are believed to be a consequence of elevated circulating levels of tumor necrosis factor (TNF), which is an important mediator of tissue injury. Prostaglandins (PGs) of the E series have recently been reported to inhibit TNF production in vitro. We investigated the in vivo effect of misoprostol, a PGE1 analog, on endotoxin-induced gastric mucosal injury and TNF production. For the gastric mucosal injury studies, groups of animals were pretreated with intragastric misoprostol (100 and 200 micrograms/kg) or with antacid (2 ml/animal of Maalox Plus) 30 min prior to a challenge with intravenous E. coli lipopolysaccharide (LPS) at 5.0 mg/kg. Stomachs were examined 3 hr after LPS. Systemic endotoxin alone induced microscopic edema, vascular congestion, and polymorphonuclear (PMN) infiltration of the gastric mucosa. Pretreatment with misoprostol, but not with antacid, significantly and dose-dependently reduced the gastric mucosal injury. For the TNF studies, groups of rats were given either misoprostol (100 or 200 micrograms/kg, intragastric), or saline 1 hr prior to LPS challenge. Serum samples were obtained 1.5 hr after LPS challenge.
Misoprostol dose-dependently and significantly (P less than 0.01) inhibited TNF activity. We conclude that misoprostol is a potent inhibitor of TNF systemic production and inhibits the gastric mucosal injury induced by endotoxemia. These studies suggest a potentially important therapeutic role for misoprostol in inflammatory diseases in which TNF exerts a contributory role.