Dr. MahatmaGastroenterologist

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(Percutaneous endoscopic gastrostomy tube) 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,
Louisiana 70112.

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.

2. Am J Med. 1989 Jul;87(1):93-4.
Phenytoin-induced acute respiratory failure with pulmonary eosinophilia.

Mahatma M, Haponik EF, Nelson S, Lopez A, Summer WR.

Department of Medicine, LSU Medical Center, New Orleans 70112.

PMID: 2741988 [PubMed – indexed for MEDLINE]

3. J Assoc Acad Minor Phys. 1991;2(2):64-6.
Nonsteroidal anti-inflammatory drugs and acute upper gastrointestinal bleeding: a prospective study.

Agrawal NM, Patel R, Mahatma M, Dajani EZ.

Section of Gastroenterology, Tulane University School of Medicine, New Orleans, LA 70112.

One of the most serious side effects of nonsteroidal anti-inflammatory drugs (NSAIDs) is upper gastrointestinal mucosal damage that may result in hemorrhage, perforation, or even death. To determine the association between NSAID ingestion and acute upper gastrointestinal bleeding, we prospectively evaluated all hospitalized patients who underwent upper endoscopy for hematemesis and/or melena over a 12-month period at the Veterans Administration Medical Center of New Orleans and Tulane Medical Center. Forty of the 139 patients (29%) at the Veterans Administration Medical Center and 21 of the 90 patients (23%) at Tulane Medical Center were using NSAIDs at the time of referral for endoscopy. Erosive gastritis was the most common cause of bleeding attributed to NSAIDs (P less than
.005). Seventy percent of the patients with acute upper gastrointestinal bleeding who used NSAIDs were over age 55, compared with 55% of patients not using NSAIDs (P less than .05). This study indicates that NSAID use is found in 27% of hospitalized patients presenting with acute upper gastrointestinal bleeding.

Future prospective studies are needed to establish whether prophylactic therapy with synthetic prostaglandins may affect the prevalence of upper gastrointestinal bleeding in patients using NSAIDs.

PMID: 1810582 [PubMed – indexed for MEDLINE]

4. J Clin Gastroenterol. 1991 Dec;13(6):644-8.
HIV-1 gp41 antigen demonstration in esophageal ulcers with acquired immunodeficiency syndrome.

Jalfon IM, Sitton JE, Hammer RA, Agrawal NM, Ertan A, Mahatma M.

Department of Medicine, Tulane University School of Medicine, New Orleans,
Louisiana 70112.

Esophageal ulcers associated with acquired immunodeficiency syndrome (AIDS) may be chronic, debilitating, and resistant to antifungal or antiviral therapy. The therapeutic management of these lesions remains controversial due to the difficulty in identifying pathogenic agent(s). We review previously published cases and describe three AIDS patients with esophageal ulcers that stained by immunoperoxidase techniques for human immunodeficiency virus (HIV)-1 surface glycoprotein (gp41). All three showed symptomatic resolution and healing of their ulcers with corticosteroid therapy. We believe this documentation of HIV-1 gp41 antigen within mononuclear cells of esophageal ulcers in AIDS supports a role of the HIV-1 virus in the pathophysiology of idiopathic esophageal ulcers in patients with AIDS. These cases further support a role for corticosteroid therapy in the treatment of esophageal ulcers resistant to antifungal and antiviral therapy in patients with AIDS.

PMID: 1761837 [PubMed – indexed for MEDLINE]

5. Mahatma M, Nelson S, Hoda SA, Alptekin N, Brown DA, Agrawal N, Ertan
A: Prevention of gastric stress ulceration by misoprostol: Absence of relationship to tumor necrosis factor. Gastroenterology 98(5)2:A150, 1990.