Gastroesophageal reflux disease (GERD) is a chronic, relapsing condition with associated morbidity and an adverse impact on quality of life. The disease is common. Approach Considerations, Reflux Esophagitis, Infectious Esophagitis. Dellon ES, Gibbs WB, Fritchie KJ, Rubinas TC, Wilson LA, Woosley JT, et al. Clinical, endoscopic, and histologic findings distinguish eosinophilic esophagitis from gastroesophageal reflux disease. The Power of Together. Welcome to Nutricia Learning Center (NLC), a community hub and trusted, collective resource for health care providers managing patients with.
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AJR Am J Roentgenol. Prasad GA, Alexander JA, Schleck CD, Zinsmeister AR, Smyrk TC, Elias RM, et al. Epidemiology of eosinophilic esophagitis over three decades in Olmsted County, Minnesota. Clin Gastroenterol Hepatol. Nurko S, Rosen R, Furuta GT. Esophageal dysmotility in children with eosinophilic esophagitis: a study using prolonged esophageal manometry. Am J Gastroenterol. Review article: Helicobacter pylori and gastro- oesophageal reflux disease- -the European perspective. Aliment Pharmacol Ther. Suppl 8: 3. 6- 9. Chen LI, Chang JM, Kuo MC, Hwang SJ, Chen HC. Combined herpes viral and candidal esophagitis in a CAPD patient: case report and review of literature. Am J Med Sci. 3. 33(3): 1. De. Gaeta L, Levine MS, Guglielmi GE, Raffensperger EC, Laufer I. Herpes esophagitis in an otherwise healthy patient. AJR Am J Roentgenol. Levine MS, Laufer I, Kressel HY, Friedman HM. Herpes esophagitis. AJR Am J Roentgenol. Levine MS, Loevner LA, Saul SH, Rubesin SE, Herlinger H, Laufer I. Herpes esophagitis: sensitivity of double- contrast esophagography. AJR Am J Roentgenol. Shortsleeve MJ, Levine MS. Herpes esophagitis in otherwise healthy patients: clinical and radiographic findings. Borowitz SM. Diagnosis: herpes simplex esophagitis. Clin Pediatr (Phila). Geagea A, Cellier C. Scope of drug- induced, infectious and allergic esophageal injury. Curr Opin Gastroenterol. Baroco AL, Oldfield EC. Gastrointestinal cytomegalovirus disease in the immunocompromised patient. Curr Gastroenterol Rep. Buckner FS, Pomeroy C. Cytomegalovirus disease of the gastrointestinal tract in patients without AIDS. Clin Infect Dis. 1. Bonacini M, Young T, Laine L. Histopathology of human immunodeficiency virus- associated esophageal disease. Am J Gastroenterol. Bonacini M, Young T, Laine L. The causes of esophageal symptoms in human immunodeficiency virus infection. A prospective study of 1. Arch Intern Med. 1. Calore EE, Cavaliere JM, Perez NM, Campos Sales PS, Warnke KO. Esophageal ulcers in AIDS. Pathologica. 8. 9(2): 1. Edwards P, Wodak A, Cooper DA, Thompson IL, Penny R. The gastrointestinal manifestations of AIDS. Aust N Z J Med. 2. Levine MS, Loercher G, Katzka DA, Herlinger H, Rubesin SE, Laufer I. Giant, human immunodeficiency virus- related ulcers in the esophagus. Levine MS, Woldenberg R, Herlinger H, Laufer I. Opportunistic esophagitis in AIDS: radiographic diagnosis. Infectious esophagitis in AIDS: what have we learned in the last decade? Am J Gastroenterol. Sor S, Levine MS, Kowalski TE, Laufer I, Rubesin SE, Herlinger H. Giant ulcers of the esophagus in patients with human immunodeficiency virus: clinical, radiographic, and pathologic findings. Villanueva JL, Torre- Cisneros J, Jurado R, Villar A, Montero M, L. Leishmania esophagitis in an AIDS patient: an unusual form of visceral leishmaniasis. Am J Gastroenterol. Yangco BG, Kenyon VS. Epidemiology and infectious complications of human immunodeficiency virus antibody positive patients. Adv Exp Med Biol. Mimidis K, Papadopoulos V, Margaritis V, Thomopoulos K, Gatopoulou A, Nikolopoulou V, et al. Predisposing factors and clinical symptoms in HIV- negative patients with Candida oesophagitis: are they always present? Int J Clin Pract. Hiremath GS, Hameed F, Pacheco A, Olive A, Davis CM, Shulman RJ. Esophageal food impaction and eosinophilic esophagitis: a retrospective study, systematic review, and meta- analysis. Dig Dis Sci. 6. 0 (1. Guidelines for the diagnosis and management of gastroesophageal reflux disease. Am J Gastroenterol. Herpes esophagitis. Gastrointest Endosc. Nonevski IT, Downs- Kelly E, Falk GW. Eosinophilic esophagitis: an increasingly recognized cause of dysphagia, food impaction, and refractory heartburn. Cleve Clin J Med. Dellon ES, Gonsalves N, Hirano I, et al. ACG clinical guideline: evidenced based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis (Eo. E). Am J Gastroenterol. Hakansson B, Montgomery M, Cadiere GB, et al. Randomised clinical trial: transoral incisionless fundoplication vs. Aliment Pharmacol Ther. Wilheim AB, Miranda- Filho Dde B, Nogueira RA, R. The resistance to fluconazole in patients with esophageal candidiasis. Arq Gastroenterol. Jan- Mar. Dellon ES, Liacouras CA. Advances in clinical management of eosinophilic esophagitis. Gastroenterology. Straumann A, Conus S, Degen L, Felder S, Kummer M, Engel H, et al. Budesonide is effective in adolescent and adult patients with active eosinophilic esophagitis. Gastroenterology. Rothenberg ME, Wen T, Greenberg A, et al. Intravenous anti- IL- 1. Ab QAX5. 76 for the treatment of eosinophilic esophagitis. J Allergy Clin Immunol. Reuters Health. Elimination diet helps adult eosinophilic esophagitis: study. Medscape Medical News. February 1. 5, 2. Available at http: //www. Accessed: March 4, 2. Lucendo AJ, Arias A, Gonz. Empiric 6- food elimination diet induced and maintained prolonged remission in patients with adult eosinophilic esophagitis: A prospective study on the food cause of the disease. J Allergy Clin Immunol. Cotton CC, Erim D, Eluri S, et al. Cost utility analysis of topical steroids compared with dietary elimination for treatment of eosinophilic esophagitis. Clin Gastroenterol Hepatol. Asher Wolf W, Huang KZ, Durban R, et al. The six- food elimination diet for eosinophilic esophagitis increases grocery shopping cost and complexity. Agency for Healthcare Research and Quality. Comparative Effectiveness of Management Strategies for Gastroesophageal Reflux Disease. AHRQ: Agency for Healthcare Research and Quality. Available at http: //effectivehealthcare. Info. cfm? infotype=rr& Process. ID=1& Doc. ID=4. Accessed: January 3. Donnellan C, Sharma N, Preston C, Moayyedi P. Medical treatments for the maintenance therapy of reflux oesophagitis and endoscopic negative reflux disease. Cochrane Database Syst Rev. Apr 1. 8. Metz DC, Pilmer BL, Han C, Perez MC. Withdrawing PPI therapy after healing esophagitis does not worsen symptoms or cause persistent hypergastrinemia: analysis of dexlansoprazole MR clinical trial data. Am J Gastroenterol. Aceves SS, Chen D, Newbury RO, Dohil R, Bastian JF, Broide DH. Mast cells infiltrate the esophageal smooth muscle in patients with eosinophilic esophagitis, express TGF- . J Allergy Clin Immunol. Cho YK, Choi MG, Bak YT, et al. Efficacy of S- pantoprazole 2. Dig Dis Sci. 5. 7 (1. Ali MA, Lam- Himlin D, Voltaggio L. Eosinophilic esophagitis: a clinical, endoscopic, and histopathologic review. Gastrointest Endosc. Straumann A, Schoepfer AM. Therapeutic concepts in adult and paediatric eosinophilic oesophagitis. Nat Rev Gastroenterol Hepatol. Lee SP, Sung IK, Kim JH, Lee SY, Park HS, Shim CS. The clinical features and predisposing factors of asymptomatic erosive esophagitis. Dig Dis Sci. 6. 1 (1. Chehade M, Sher E. Medical therapy versus dietary avoidance in eosinophilic esophagitis: Which approach is better? Allergy Asthma Proc. Otani IM, Nadeau KC. True gastritis comes in several forms and is diagnosed using a combination of tests. In the 1. 99. 0s, scientists discovered that the main cause of true gastritis is infection from a bacterium called Helicobacter pylori (H. It has been associated with resulting ulcers, particularly peptic ulcers. And in some cases, chronic gastritis can lead to more serious complications. Nonerosive h. This form of nonerosive gastritis is the result of infection with Helicobacter pylori bacterium, a microorganism whose outer layer is resistant to the normal effects of stomach acid in breaking down bacteria. The resistance of H. Study of the role of H. Studies were also underway to determine the role of H. These commonly used pain killers, including aspirin, fenoprofen, ibuprofen and naproxen, among others, can lead to gastritis and peptic ulcers. Other forms of erosive gastritis are those due to alcohol and corrosive agents or due to trauma such as ingestion of foreign bodies. Other forms of gastritis. Clinicians differ on the classification of the less common and specific forms of gastritis, particularly since there is so much overlap with H. Other types of gastritis that may be diagnosed include: Acute stress gastritis- the most serious form of gastritis which usually occurs in critically ill patients, such as those in intensive care. Stress erosions may develop suddenly as a result of severe trauma or stress to the stomach lining. Atrophic gastritis is the result of chronic gastritis which is leading to atrophy, or decrease in size and wasting away, of the gastric lining. Gastric atrophy is the final stage of chronic gastritis and may be a precursor to gastric cancer. Superficial gastritis is a term often used to describe the initial stages of chronic gastritis. Uncommon specific forms of gastritis include granulomatous, eosiniphilic and lymphocytic gastritis. Causes and symptoms. Nonerosive h. It is believed that most infection occurs in childhood. The route of its transmission was still under study in 1. Its prevalence and distribution differs in nations around the world. The presence of H. However, physicians are still learning about the link of H. However, the majority of patients with H. Ulcer symptoms include dull, gnawing pain, often two to three hours after meals and pain in the middle of the night when the stomach is empty. Erosive and hemorrhagic gastritis. The most common cause of this form of gastritis is use of NSAIDS. Other causes may be alcoholism or stress from surgery or critical illness. The role of NSAIDS in development of gastritis and peptic ulcers depends on the dose level. Although even low doses of aspirin or other nonsteroidal anti- inflammatory drugs may cause some gastric upset, low doses generally will not lead to gastritis. However, as many as 1. NSAIDS, such as those with chronic arthritis, may develop gastric ulcers. In 1. 99. 8, studies were underway to understand the role of H. Any number of mechanisms may cause various less common forms of gastritis and they may differ slightly in their symptoms and clinical signs. However, they all have in common inflammation of the gastric mucosa. Diagnosis. Nonerosive h. This test detects active presence of H. Other serological tests, which may be readily available in a physician's office, may be used to detect H. Newly developed versions offer rapid diagnosis. The choice of test will depend on cost, availability and the physician's experience, since nearly all of the available tests have an accuracy rate of 9. Endoscopy, or the examination of the stomach area using a hollow tube inserted through the mouth, may be ordered to confirm diagnosis. A biopsy of the gastric lining may also be ordered. Erosive or hemorrhagic gastritis. Clinical history of the patient may be particularly important in the diagnosis of this type of gastritis, since its cause is most often the result of chronic use of NSAIDS, alcoholism, or other substances. Other forms of gastritis. Gastritis that has developed to the stage of duodenal or gastric ulcers usually requires endoscopy for diagnosis. It allows the physician to perform a biopsy for possible malignancy and for H. Sometimes, an upper gastrointestinal x- ray study with barium is ordered. Some diseases such as Zollinger- Ellison syndrome, an ulcer disease of the upper gastrointestinal tract, may show large mucosal folds in the stomach and duodenum on radiographs or in endoscopy. Other tests check for changes in gastric function. Treatment. H. In particular, relapse rates for duodenal and gastric ulcers has been reduced with successful treatment of H. Since the infection can be treated with antibiotics, the bacterium can be completely eliminated up to 9. Although H. In 1. No single antibiotic had been found which would eliminate H. Dual therapy involves the use of an antibiotic and a proton pump inhibitor. Proton pump inhibitors help reduce stomach acid by halting the mechanism that pumps acid into the stomach. This also helps promote healing of ulcers or inflammation. Dual therapy has not been proven to be as effective as triple therapy, but may be ordered for some patients who can more comfortably handle the use of less drugs and will therefore more likely follow the two- week course of therapy. TRIPLE THERAPY. As of early 1. H. It is estimated that triple therapy successfully eliminates 8. H. This treatment regimen usually involves a two- week course of three drugs. An antibiotic such as amoxicillin or tetracycline, and another antibiotic such as clarithomycin or metronidazole are used in combination with bismuth subsalicylate, a substance found in the over- the- counter medication, Pepto- Bismol, which helps protect the lining of the stomach from acid. Physicians were experimenting with various combinations of drugs and time of treatment to balance side effects with effectiveness. Side effects of triple therapy are not serious, but may cause enough discomfort that patients are not inclined to follow the treatment. OTHER TREATMENT THERAPIES. Scientists have experimented with quadruple therapy, which adds an antisecretory drug, or one which suppresses gastric secretion, to the standard triple therapy. One study showed this therapy to be effective with only a week's course of treatment in more than 9. Short course therapy was attempted with triple therapy involving antibiotics and a proton pump inhibitor and seemed effective in eliminating H. The goal is to develop the most effective therapy combination that can work in one week of treatment or less. MEASURING H. PYLORI TREATMENT EFFECTIVENESS. In order to ensure that H. The breath test is the preferred method to check for remaining signs of H. When symptoms do occur, patients may be treated with therapy similar to that for H. Avoidance of NSAIDS will most likely be prescribed. Other forms of gastritis. Specific treatment will depend on the cause and type of gastritis. These may include prednisone or antibiotics. Critically ill patients at high risk for bleeding may be treated with preventive drugs to reduce risk of acute stress gastritis. If stress gastritis does occur, the patient is treated with constant infusion of a drug to stop bleeding. Sometimes surgery is recommended, but is weighed with the possibility of surgical complications or death. Once torrential bleeding occurs in acute stress gastritis, mortality is as high as greater than 6. Alternative treatment. Alternative forms of treatment for gastritis and ulcers should be used cautiously and in conjunction with conventional medical care, particularly now that scientists have confirmed the role of H. Alternative treatments can help address gastritis symptoms with diet and nutritional supplements, herbal medicine and ayurvedic medicine. It is believed that zinc, vitamin A and beta- carotene aid in the stomach lining's ability to repair and regenerate itself. Herbs thought to stimulate the immune system and reduce inflammation include echinacea (Echinacea spp.) and goldenseal (Hydrastis canadensis). Ayurvedic medicine involves meditation. There are also certain herbs and nutritional supplements aimed at helping to treat ulcers. Prognosis. The discovery of H. Since treatment exists to eradicate the infection, recurrence is much less common. As of 1. 99. 8, the only patients requiring treatment for H. Research will continue into the most effective treatment of H. Regular treatment of patients with gastric and duodenal ulcers has been recommended, since H. It is believed that H. Detection and treatment of H. The prognosis for patients with acute stress gastritis is much poorer, with a 6. Prevention. The widespread detection and treatment of H. Until more is known about the routes through which H. Erosive gastritis from NSAIDS can be prevented with cessation of use of these drugs. An education campaign was launched in 1. NSAIDS and alternative drugs. Key terms. Duodenal — Refers to the duodenum, or the first part of the small intestine. Mucosa — The mucous membrane, or the thin layer which lines body cavities and passages. Ulcer — A break in the skin or mucous membrane. It can fester and pus like a sore. Resources. Periodicals. Podolski, J. 4: 1. Organizations. National Digestive Diseases Information Clearinghouse. Information Way, Bethesda, MD 2.
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