Gastritis, and Gastric and Duodenal Ulcers

Gastritis refers to inflammation of the gastric mucosa, and can be classified in a number of different ways:

  • severity: gastritis can be either erosive or nonerosive based on the severity of damage to the mucus membranes
  • location: gastritis can be classified on the basis of what part of the stomach is involved, including the cardia (upper stomach), corpus (middle stomach), and antrum (lower stomach)
  • onset and duration: gastritis can also be classified on the basis of either an acute onset or chronic manifestation, based in part on the case history, but also from a histological examination of the inflammatory cells. (Berkow 1992, 796).

Acute gastritis is a very serious and life-threatening condition that usually occurs in very ill patients, typically experienced as a vague abdominal discomfort. Life-threatening clinical manifestations include hemorrhaging from the mouth or nose, and symptoms of gastric perforation. Histological examination reveals an infiltration of polymorphonuclear leukocytes in the gastric mucosa, usually in the antrum or corpus. The most common cause of acute erosive gastritis are drugs such are anti-inflammatory drugs and other NSAIDs (e.g. acetaminophen, acetyl salicylic acid), as well as alcohol consumption and acute emotional stress. If the patient has a history of chronic NSAID they may present with anemia, incating chronic gastric bleeding. Less common but important causes include radiation burns, viral infections (e.g. cytomegalovirus), vascular injury, and direct trauma (e.g. nasogastric tubes). In very ill patients the overall mortality can be between 40-50%. (Berkow 1992, 762; Rubin and Farber 1990, 359-61)

Patients with chronic erosive gastritis typically present with a vague dyspepsia, with epigastric pain and nausea, and can even be asymptomatic. Endoscopy reveals the presence of multiple punctate or apthous ulcers, while further histological examination will show some degree of atrophy or metaplasia. If it involves the the antrum there will be a loss of G cells and thus decreased gastrin secretion, or if the corpus, a loss of oxyntic glands facilitating reduced HCl, pepsin, and intrinsic factor secretion. The causes of chronic gastritis are essentially the same as for its acute forms. (Berkow 1992, 763; Rubin and Farber 1990, 359-61)

Nonerosive gastritis is typically associated with Helicobacter pylori, a spiral-shaped, gram-negative bacteria that thrives in the high acid environment of the stomach. It is thought that infection with H. pylori invariably leads to gastric mucosal inflammation, which in turn alters gastric secretion, leaving the mucosa more susceptible to damage by acid. The highest concentrations of H. pylori are typically found in the antrum. (Berkow 1992, 764-65; Rubin and Farber 1990, 359-61)

H. pylori is a very common chronic infection, and in developing countries is most frequently acquired in childhood, although infection of children is much less common in industrialized societies. Although the exact mode of transmission is unclear, the organism has been cultured from stool, saliva, and dental plaque, which suggesting an oral-oral or fecal-oral transmission. Infections tend to predominate in families and in hospital workers, frequently in nurses and gastroenterologists. (Carroll 2005; Sepulveda 2005b)

Although H. pylori is fingered as the cause of almost all cases of nonerosive gastritis, less than 20% of all H. pylori infected persons will develop significant clinical consequences in their lifetime, suggesting that H. pylori may not be as pathogenic as previously thought.There are many different strains of H. pylori, with apparently different degrees of virulence. Furthermore, H. pylori appears to have co-evolved in humans and is thought by many to be a commensal. The typical treatment of H. pylori is the use of several different kinds of antibiotics, administered over a long period of time. This treatment will result in the destruction of beneficial bacterial strains and may provoke esophageal disease or gastric cancer of the cardia. (Hunt et al 2001; Sepulveda 2005)

Autoimmune factors can also promote chronic nonerosive gastritis. Auto-antibodies are produced against the parietal cells and intrinsic factor, leading to a reduction or complete inhibition of gastric secretion. Further investigation usually reveals increased serum gastrin (due to G-cell hyperplasia in the antrum) and gastric enterochromaffin-like hyperplasia due to gastrin stimulation. (Sepulveda 2005b; Rubin and Farber 1990, 359-61)

The mildest form of nonerosive gastritis is superficial gastritis, which even more than the other, more serious forms of gastritis, can yield very mild symptoms. The inflammatory process can involve all parts of the stomach but is not accompanied by atrophic or metaplastic changes. Upon histological examination the infiltrating cells are usually found to be lymphocytes, plasma cells and neutrophils. (Rubin and Farber 1990, 359-61)

Atrophic gastritis is often an evolute of chronic, superficial gastritis, typically presenting as a definite but nonetheless mild dyspepsia. Histological examination yields lymphocytes and plasma cells often penetrating the mucosa all the way to the muscularis. The condition also involves degenerative changes in HCl and pepsin secreting cells leading to a loss of gastric secretions, including intrinsic factor which promotes a vitamin B12 deficiency (Berkow 1992, 765; Sepulveda 2005a).

Gastric metaplasia is common in chronic nonerosive gastritis, typically occurring with severe atrophy of the gastric glands, which are progressively replaced by mucous glands, typically in the antral mucosa. The gastric mucosa may resemble small intestinal mucosa, with goblet cells, endocrine (enterochromaffin or enterochromaffin-like) cells, and rudimentary villi, and may even assume functional (absorptive) characteristics. In complete metaplasia, gastric mucosa is completely transformed into small intestinal mucosa, with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits dysplasia. Both cell types are associated with an increased risk of stomach cancer. (Sepulveda 2005b; Rubin and Farber 1990, 359-61)

Peptic ulcer disease refers to an excoriated segment of the gastrointestinal mucosa, typically in the stomach (gastric ulcer) or first few centimeters of the duodenum (duodenal ulcer), which proceeds to penetrate through the muscularis. The ulcers may range in size from several millimeters to several centimeters. The etiology of peptic ulcer disease was at one time considered to be due to excess gastric acid secretion but this theory has given way to factors that disrupt normal mucosal defense mechanisms, including H. pylori infection and NSAIDs usage, which make the mucosa more susceptible to the effects of the stomach acid. Gastric ulcers typically arise from chronic nonerosive gastritis, and in most cases patients secrete less acid than healthy individuals. (Berkow 1992; Rubin and Farber 1990, 361-65)

The mechanism by which H. pylori promotes damage to the gastric mucosa is thought to be a result of the organism synthesizing the enzyme urease that breaks down urea into ammonia. This chemical reaction allows the organism to survive the acidic environment of the stomach, but at the same time erodes the mucous membrane. H. pylori also produces cytotoxins that promote epithelial damage, as wellas mucolytic enzymes such as protease and lipase. The host response to these events are thought to promote the release of cytokines that further promote damage and the process of ulcerogenesis. (Berkow 1992; Rubin and Farber 1990, 361-65)

NSAIDs promote damage to the gastric mucus membranes through a directly toxic effect and by modifying the host response on a systemic basis. When ingested NSAIDs diffuse into gastric epithelial cells and promote the release of H+ ions, promoting mucosal injury. NSAIDs also inhibit the cyclooxygenase pathway and the synthesis of prostaglandins that maintain gastric integrity. The interruption of this metabolic pathway results in significant changes to the gastric mucosa, inhibiting blood flow, reducing mucus and HCO3 secretion, and inhibiting cellular repair mechanisms (Berkow 1992; Rubin and Farber 1990, 361-65)

The signs and symptoms of peptic ulcer disease can vary. While in some cases, such as in the elderly, the pain can be minimal or even absent, others can experience a burning pain in the epigastrum that refers to the back. In some cases the pain is relieved by eating, whereas for others it makes little difference. Very often the symptoms come and go. Pyloric ulcers are often associated with symptoms of obstruction such as bloating, nausea, vomiting. In duodenal ulcers the pain tends to be consistent, frequently absent when the patient awakens but appearing later in midmorning. The pain of duodenal ulcers is often relieved by food but recurs within a few hours after eating. (Berkow 1992, 768-69)

The most common complication of peptic ulcer disease is hemorrhaging, and occurs in up to 20% of patients. Symptoms include vomiting of blood (“coffee grounds”), occult blood in the stools and iron-deficiency anemia. The penetration of the gastric or duodenal wall by an ulcer results in stomach acids leaking into the abdominal cavity, causing peritonitis, and can attack the pancreas or liver. The overall mortality rate for perforated ulcers is 10-40% with gastric ulcers, and 5-13% with duodenal ulcers. (Berkow 1992; Rubin and Farber 1990, 361-65)

Medical Treatment

The medical treatment of gastritis and peptic ulcer disease doesn’t differ all that much from GERD or hiatus hernia, with a reliance upon suppressing acid secretion through the use of antacids, bismuth subsalicylate, H2 antagonists and proton pump inhibitors. This is despite the fact that patients with gastritis and ulcers have been shown to have lower acid levels than normal. With the discovery of the possible role of H. pylori in the etiology of peptic ulcers however, it is now common for these drugs to be used along with one or more antibiotics such as metronidazole, tetracycline, clarithromycin, and amoxicillin, referred to as “triple therapy.” The claim is that this treatment has an 80-90% cure rate must be regarded with some skepticism, as even though the supposed etiological agent has been removed, the symptoms may continue: such is the danger of defining a disease based upon the etiology alone. In 1997 a follow-up study of patients that had received antibiotic therapy for H. pylori over a two year period indicated an overall treatment failure rate of 23%, with H. pylori showing high levels of resistance to clarithromycin (30%), metronidazole (66%), or to both of these antibiotics (23%) (McMahon, et al. 2002). Even in patients that have undergone successful treatment for H. pylori may find that the initially positive results may be replaced by a gradual onset of recurring symptoms. As for the usage of antibiotics, treatment will almost certainly result in the destruction of beneficial bacterial strains and in some cases, may provoke esophageal disease or gastric cancer of the cardia (Hunt et al 2001). The larger issue of antibiotic resistance, which is increasingly shown to be an important and vital issue, must also be taken into account.

Holistic treatment

The treatment of gastritis and peptic ulcer disease is once again similar to that of GERD and hiatus hernia, with an acknowledge of the increased severity of symptoms and the inherent difficulty in treating a condition that can be life-threatening, as is the case of a perforating ulcer. Another important factor to take into account is the loss of intrinsic factor and chronic bleeding, which leads to anemia.

In Ayurvedic medicine peptic and duodenal ulcers are generally classified under the term Amla-pitta, and are caused by eating incompatible foods, foods that promoting a burning sensation, and the aggravation of Pitta.

Among the various treatments for gastritis, peptic and duodenal ulcer are:

1. Reduce insult to gastric and duodenal epithelium

  • eliminate NSAIDs and if required replace with anti-inflammatory compounds that are not toxic to the gastric mucosa, e.g. Turmeric (Curcuma longa), Devil’s Claw (Harpagophytum procumbens), EPA/DHA, MSM, glucosamine/chondroitin sulfate
  • reduce exposure to xenobiotics such as pesticides, insecticides and herbicides, emphasizing organically grown vegetables and free range, hormone/antibiotic-free animal produce
  • increase intake of high fiber foods and foods rich in antioxidant phytochemicals such as broccoli, cabbage, cauliflower, beets, carrots and onions
  • increase intake of omega 3 fatty acids, found in foods such as wild salmon, halibut and arctic char, or supplement with EPA/DHA, 1000 mg daily.
  • supplement with a chelated multimineral and trace mineral supplement to provide for the manufacture of detoxification enzymes and antioxidants

2. Reduce gastric inflammation

  • Laxative botanicals to purge excess heat, used for a short period during the initial stages of treatment, e.g. Turkey Rhubarb (Rheum palmatum), Cascara (Rhamnus purshiana), Huang Qin (Scutellaria baicalensis), Trivrit (Operculina turpethum) etc.
  • Flavonoids and flavonoid-containing botanicals to limit acid production via inhibiting histamine release, e.g. Nettles (Urtica dioica), Marigold (Calendula officinalis), Meadowsweet (Filipendula ulmaria), Chamomile (Matricaria chamomilla), Huang Qin (Scutellaria baicalensis), Chai Hu (Buplerum chinense), quercitin, catechin, etc.
  • Astringing vulneraries, to promote muscular tone of the LES, check hemorrhaging and heal ulcerations, e.g. Avens (Geum urbanum), White Oak (Quercus alba), Goldenseal (Hydrastis canadensis), Bayberry (Myrica cerifera), Canada Balsam (Abies balsamea), etc.
  • Neutralizing cordial, useful for those going through chemotherapy. Dosage is 5 mL, 4-6 times daily
  • Banana (Musa paradisiacal), as ripened fruit, banana chips, or leaf powder, ad. lib.
  • Cold infusions of Slippery Elm (Ulmus fulva), Marshmallow (Althaea officinalis) or Comfrey (Symphytum officinale), 50 g per 1 liter, taken as needed, up to 1-2 liters daily; OR powders of Licorice (Glycyrrhiza glabra), Marshmallow (Althaea officinalis) or Slippery Elm (Ulmus fulva), 5-10 g mixed with cool water, taken as needed; OR De-glycyrrhized Licorice (Glycyrrhiza glabra) (DGL), suitable in patients where obesity or hypertension is an issue, in doses of 2-3 tablets as needed; OR Aloe juice, up to one liter daily, may promote diarrhea
  • eat a low fat, low protein diet until inflammation is reduced; e.g. soup stock, steamed and baked vegetables, rice, dhal etc.

3. Promote healing of epithelium

  • Vitamin A, 25,000-50,000 IU daily
  • Vitamin C, 1-2 g bid-tid, to bowel tolerance
  • Vitamin E, 800-1200 IU daily
  • Methylsulfonylmethionine (MSM), 2-3 g, bid-tid; OR 500-1000 mL of freshly juiced cabbage daily; OR the Chinese patent formula Vitamin U (Fare You), 3 tabs tid are alternatives to MSM

4. Promote proper gastric digestion

  • Bitters, taken in small doses before meals, e.g. Barberry (Berberis vulgaris), Yellow Gentian (Gentiana lutea), Centuary (Centaurium umbellatum), Buckbean (Menyanthes trifoliata), Goldenseal (Hydrastis canadensis), Huang Lian (Coptis chinense),Bhunimba (Andrographis paniculata), Katuka (Picrorrhiza kuroa) etc. NOTE: the usage of bitters are often avoided at the outset of treatment because the initial stimulation of acid production may worsen any ulceration
  • Aromatics, used in chronic conditions to ease spasm, pain and cramping, e.g. Calamus (Acorus calamus), Caraway (Carum carvi), Fennel (Foeniculum vulgare), Mints (Mentha spp), Chamomile (Matricaria chamomilla), Dong Gui (Angelica sinensis),Anise (Pimpinella anisum), Cardamom (Elettaria cardamomum), Bitter Orange (Citrus aurantium); care must be taken if acid reflux is a part of the clinical presentation
  • Antispasmodics, e.g. Valerian (Valeriana officinalis), Cramp Bark (Viburnum opulus), Kava (Piper methysticum), Wild Yam (Dioscorea villosa), etc.
  • Digestive enzymes, full spectrum (HCl), pancreatic enzymes, ox bile), 2-3 caps with meals
  • Food combining: avoid mixing animal proteins with starchy food, fruit should only be consumed on an empty stomach
  • Avoid dairy and flour products, which due to their sticky and heavy properties impair gastric motility
  • Avoid overeating, do not eat within three hours of bedtime
  • Avoid alcohol
  • Avoid tobacco
  • Avoid deep-fried foods, e.g. French fries, potato chips, etc.
  • Weight loss, to reduce intra-abdominal pressure

5. Restore the bowel ecology

  • Once acute inflammation is resolved, introduce live-culture foods, e.g. pickled vegetables etc
  • Probiotics: e.g. lactobacilli, bifidobacterium
  • Prebiotics: e.g. fructo-oligosaccharides, inulin (e.g. found in Inula and Taraxacum root)

6. Specific formulations

  • Robert’s Formula, 20 gtt, tid in water, before meals
  • Shatavari ghrita, 6-12 g, tid before meals
  • Avipattikara churna, 3-6 g tid before meals, with honey
  • Sai Mei An, for pain and burning sensations, without bleeding, 3 pills tid
  • Yunnan Pai Yao, for ulceration with bleeding, 2 capsules tid-qid

7. Treat underlying anemia

  • avoid direct iron supplementation as this tends to promote intestinal infection; once acute phase is resolved, use herbs, e.g. Yellow Dock (Rumex crispus), Nettles (Urtica dioica), foods (red meat, eggs, yams, prunes, figs), Vitamin C (to bowel tolerance), Vitamin B (50-100 mg daily), and low-iron supplements (e.g. Floradix®)