Your Online Health Information Site

Advertisement

Gastritis

Introduction

Gastritis is a condition where the lining of the stomach is inflamed. It occurs typically from the late teens to old age. Children rarely develop it. Medically the lining of the stomach is called “mucosa”. In the introduction of the next chapter on ulcers I am explaining that there is a fine balance of several factors regarding the integrity of the mucosa.

For instance, when a person is extremely stressed (severe burns, head trauma, kidney or liver failure, shock etc.), the extra amount of acid production from the stimulation of ACTH production (stress hormone) coupled with a weakening effect of cortisol from the adrenal glands on the repair mechanisms of the mucosa will tip the balance.

Acute gastritis

Within only two to five days of such a major crisis as listed above acute stress gastritis will occur in a significant percentage. With the use of non-steroidal anti inflammatory drugs (NSAIDs) for arthritis or sports injuries the rate of acute erosive gastritis has increased. Alcohol abuse can cause the same thing. On endoscopy this condition can be diagnosed by the presence of spots of erosive changes throughout the stomach, but confined to the superficial layers. There is submucosal (petechial) bleeding associated with it.

H.Pylori

Another form of gastritis is the non-erosive gastritis. This type of gastritis is associated with the bacterium H. pylori (=helicobacter pylori). If this is not treated, as we learn in the next chapter, it can go on to chronic ulcers of the stomach and duodenum.

After decades of infection it can even lead to stomach cancer (adenocarcinoma of the stomach). In development countries H.pylori is very common and is usually acquired in childhood. In the U.S.A. it is rare in children and is more common in blacks and Hispanics than whites. It increases in frequency with age. It can be cultured from dental plaque and dental cavities, saliva and stool. Further comments about tests can be found under “diagnosis” of the chapter on “gastrointestinal diseases/ulcers” below. Non erosive gastritis is a superficial inflammatory change of the mucosa, which shows characteristic inflammatory cell infiltration on biopsy specimens taken by endoscopy. These more chronic forms of gastritis need the skills of an experienced gastroenterologist. The specialist may over the years have to do several gastroscopies with various attempts to culture bacteria and to take brushing samples and cancer biopsies for histological analysis to rule out malignancies. It may take several months of such testing before the specialist can give you a clear picture of what is going on inside.

Chronic gastritis can lead to three histological conditions: deep gastritis, gastric atrophy or metaplasia. Each of them have characteristic pathological appearances under the microscope and they have certain clinical significance as I will briefly mention. Deep gastritis is often associated with H.pylori infection and should be treated, as untreated it likes to progress to chronic ulcers.

Gastric atrophy is often found in older patients and is associated with autoantibodies against the acid producing cells of the gastric mucosa. This in turn leads to vitamin B12 malabsorption, a condition known as pernicious anemia. Metaplasia is found in some cases of severe atrophy and patches of gastric mucosa have been replaced with mucosa, which looks more like intestinal mucosa (“metaplasia”). This condition is important to watch as it can degenerate into stomach cancer.

Symptoms of gastritis

With acute stress gastritis the patient is too ill to communicate any symptoms. The physician in the ICU setting might therefore do an endoscopy to see whether or not stress ulcers are present.

If acute stress gastritis is not treated promptly, there is a high mortality rate from acute gastric or duodenal ulcerations, which can fairly quickly develop and from which profuse bleeding can occur. About 2% of ICU patients will develop profuse bleeding from stress ulcers. The mortality rate in these cases is in the order of 60 to 70% depending on the underlying disease.

Generally speaking, most gastritis cases are mild and of a more chronic nature.

Depending on how the pathology is, the severity of symptoms will vary. Some patients with non-erosive gastritis may hardly feel any symptoms at all, maybe some nausea or discomfort in the mid upper abdomen. If the pathology involves deeper aspects of the mucosa of the stomach, vomiting and more severe abdominal cramps, some burning and a “hunger feeling” are also not unusual. Sometimes there might be pain irradiating into the mid chest area and be confused with a heart attack. Particularly with biliary gastritis, where bile acids are flowing back into the stomach the symptoms can be fairly acute and vomiting occurs more frequently.

 Gastritis (Examined by Gastroscopy, Note Peptic Ulcer Also) Gastritis (Examined by Gastroscopy, Note Peptic Ulcer Also)

Gastritis (Examined by Gastroscopy, Note Peptic Ulcer Also)

Diagnosis

Mild cases are made on clinical grounds and treated according to the principles of the acid reflux chapter above. If H2-blockers do not give relief, there should be a high suspicion that perhaps H.pylori could be the reason for the gastritis.

The urea breath test (see next chapter)should be done to test that possibility. If it is positive, then a triple therapy program for one week would be successful in over 90% of the cases (see Ref. 1). This is a combination of amoxicillin and clarithromycin with a proton inhibitor or else a combination of clarithromycin and metronidazole with a proton pump inhibitor. If this fails, or if the symptoms are worse, endoscopy (also called “gastroduodenoscopy”or “panendoscopy”) is suggested, which is usually done by a gastroenterologist, but in smaller towns may still be done by a surgeon or internist. This allows the specialist to visually diagnose the condition and do biopsies to establish the severity of the gastritis to rule out a malignancy, if there are suspicious areas. A sample of secretions can also be tested directly with the rapid urease test for H.pylori.

Treatment

With positive test results triple therapy as mentioned above is ordered. With atrophic gastritis B12 injections have to be given regularly every months and the patient can learn how to do this him/herself. This will prevent the development of pernicious anemia. Gastric mucosa normally secretes a protein called intrinsic factor, which binds to the vitamin B12 of the food and gets absorbed in the small bowel. Patients with atrophic gastritis lack the intrinsic factor and that’s why this inexpensive vitamin needs to be given by injection. For the ordinary gastritis the antacid medications cimetidine, ranitidine or the stronger antacid medicines (proton pump inhibitors) are used for a few weeks.

Alternative treatment of gastritis

Dr. Murray explains that the cause of gastritis, gastric ulcer and duodenal ulcer is the breakdown of the mucosal barrier (Ref. 34, p.73-75). So the symptomatic treatment of the H. pylori infection with triple therapy (2 antibiotics and a PPI) may be the medical treatment commonly accepted as the norm, but it does not cure H. pylori in many cases. Some patients develop diarrhea from a Clostridium difficile super infection as a result of the antibiotics from the triple therapy requiring even more expensive antibiotics for that condition. This only happened, because the patients’ symptoms were treated instead of the cause. The cause of gastritis and duodenal ulcers is a weakening of the lining in the stomach and the duodenum resulting in a breakdown of the mucous barrier. In some people dietary habits play a role, like too much cereal and wheat consumption with too little alkaline vegetables in the meals to neutralize the acid formation (see Ref.35 for more details). However, when a simple licorice compound (DGL, which stands for deglycyrrhizinated licorice) is given, the symptoms from gastritis, acid reflux, and ulcers in the stomach or duodenum disappear. DGL supports the lining of the stomach and duodenum and reestablishes the defense against the acidy milieu. Not only that, but after a few weeks of DGL treatment all of the findings on endoscopy such as inflammation and ulcerations disappeared. Dr. Murray states that he has not encountered a case of gastritis or ulcer that would not have responded. It appears that the cause of gastritis and ulcers in the stomach and duodenum is not from too much acid, not from H. pylori infection, which appears to just be a concomitant infection, but actually is due to a breakdown of the barrier in the lining of the stomach and duodenum, which responds to DGL. The other interesting thing is that you can buy DGL in the health food store; the dosage is two to three chewable tablets on an empty stomach three times per day. According to Ref. 34 it needs to be taken 8 to 16 weeks, after which there is a full therapeutic response. Pepto-Bismol is another coating substance that is available over the counter and works well for minor stomach upsets.

More information about H. pylori and indigestion: http://www.askdrray.com/h-pylori-can-be-the-culprit-for-indigestion/

References:

1. M Frevel Aliment Pharmacol Ther 2000 Sep (9): 1151-1157.

2. M Candelli et al. Panminerva Med 2000 Mar 42(1): 55-59.

3. LA Thomas et al. Gastroenterology 2000 Sep 119(3): 806-815.

4. R Tritapepe et al. Panminerva Med 1999 Sep 41(3): 243-246.

5. The Merck Manual, 7th edition, by M. H. Beers et al., Whitehouse       Station, N.J., 1999. Chapters 20,23, 26.

6. EJ Simchuk et al. Am J Surg 2000 May 179(5):352-355.

7. G Uomo et al. Ann Ital Chir 2000 Jan/Feb 71(1): 17-21.

8. PG Lankisch et al. Int J Pancreatol 1999 Dec 26(3): 131-136.

9. HB Cook et al. J Gastroenterol Hepatol 2000 Sep 15(9): 1032-1036.

10. W Dickey et al. Am J Gastroenterol 2000 March 95(3): 712-714.

11. M Hummel et al. Diabetologia 2000 Aug 43(8): 1005-1011.

12. DG Bowen et al. Dig Dis Sci 2000 Sep 45(9):1810-1813.

13. The Merck Manual, 7th edition, by M. H. Beers et al., Whitehouse  Station, N.J., 1999.Chapter 31, page 311.

14. O Punyabati et al. Indian J Gastroenterol 2000 Jul/Sep 19(3):122-125.

15. S Blomhoff et al. Dig Dis Sci 2000 Jun 45(6): 1160-1165.

16. M Camilleri et al. J Am Geriatr Soc 2000 Sep 48(9):1142-1150.

17. MJ Smith et al. J R Coll Physicians Lond 2000 Sep/Oct 34(5): 448-451.

18. YA Saito et al. Am J Gastroenterol 2000 Oct 95(10): 2816-2824.

19. M Camilleri Am J Med 1999 Nov 107(5A): 27S-32S.

20. CM Prather et al. Gastroenterology 2000 Mar 118(3): 463-468.

21. MJ Farthing : Baillieres Best Pract Res Clin Gastroenterol 1999 Oct 13(3): 461-471.

22. D Heresbach et al. Eur Cytokine Netw 1999 Mar 10(1): 7-15.

23. BE Sands et al. Gastroenterology 1999 Jul 117(1):58-64.

24. B Greenwood-Van Meerveld et al.Lab invest 2000 Aug 80(8):1269-1280.

25. GR Hill et al. Blood 2000 May 1;95(9): 2754-2759.

26. RB Stein et al. Drug Saf 2000 Nov 23(5):429-448.

27. JM Wagner et al. JAMA 1996 Nov 20;276 (19): 1589-1594.

28. James Chin, M.D. Control of Communicable Diseases Manual. 17th ed., American Public Health Association, 2000.

29. The Merck Manual, 7th edition, by M. H. Beers et al., Whitehouse Station, N.J., 1999. Chapter 157, page1181.

30. Textbook of Primary Care Medicine, 3rd ed., Copyright © 2001 Mosby, Inc., pages 976-983: “Chapter 107 – Acute Abdomen and Common Surgical Abdominal Problems”.

31. Marx: Rosen’s Emergency Medicine: Concepts and Clinical Practice, 5th ed., Copyright © 2002 Mosby, Inc. , p. 185:”Abdominal pain”.

32. Feldman: Sleisenger & Fordtran’s Gastrointestinal and Liver Disease, 7th ed., Copyright © 2002 Elsevier, p. 71: “Chapter 4 – Abdominal Pain, Including the Acute Abdomen”.

33. Ferri: Ferri’s Clinical Advisor: Instant Diagnosis and Treatment, 2004 ed., Copyright © 2004 Mosby, Inc.

34. Michael T. Murray, ND: “What the drug companies won’t tell you and your doctor doesn’t know”. Atria Books, New York, 2009.

35. William Davis, MD: “Wheat belly. Lose the wheat, lose the weight, and find your path back to health.” HarperCollins Publishers Ltd., 2011.

Last modified: December 2, 2016

Disclaimer
This outline is only a teaching aid to patients and should stimulate you to ask the right questions when seeing your doctor. However, the responsibility of treatment stays in the hands of your doctor and you.