Disease Index Gastrointestinal Diseases

A Discussion of Gastritis with Keynotes of Leading Homeopathic Remedies

Last modified on August 15th, 2017

Dr. Devika Mehta presents a discussion of gastritis including keynotes of leading homeopathic remedies.

Stomach-Cancer.jpgGastritis is the most common silent disease of the gastrointestinal tract, affecting more than half of the world population. It is well known that H.pylori is the chief etiological agent of chronic gastritis, peptic ulcer, gastric adenocarcinoma, malt lymphoma. Helicobacter pylorus was discovered by Warren and Marshal in 1983. H. pylori has some unique characteristics:

  • It defied its detection by scientists for centuries.
  • It survives in the stomach, an organ which is devised by the nature to kill all bacteria.
  • 85% of the population hosts this organism asymptomatically.
  • It persists in the gastric mucosa for decades.
  • It does not penetrate the gastric mucosa for decades.
  • It reduces the risk of oesophagitis, Barrett’s esophagus, esophageal adenocarcinoma, in the infected individual.

 

Gastritis is defined as an inflammatory response of the gastric mucosa to infections or irritants.
In the histology of normal gastric mucosa, inflammatory cells – neutrophils are spare and lymphoid tissue is absent.

 

ACUTE GASTRITIS is diagnosed endoscopically in the presence of hyperemia, intermucosal hemorrhages, and erosions in the gastric antrum and/or body mucosa.
Erosions are flat, or elevated white based lesions with an erythematous margin, and are frequently seen in the antrum.
Histology shows marked surface epithelial degeneration and heavy infiltration with neutrophils, but it is rarely performed.

 

CHRONIC GASTRITIS may be classified as chronic active, non-atrophic (superficial), atrophic and pernicious anaemia.
On histology of the gastric mucosa, there is a predominant increase in the chronic inflammatory cells – lymphocytes, plasma cells and an occasional lymphoid follicle may be present.
Presence of numerous neutrophils indicates activity (chronic active gastritis).

In CHRONIC NON – ATROPHIC GASTRITIS inflammatory cells are restricted to upper one third and glandular atrophy is absent
In CHRONIC ATROPHIC GASTRITIS, infiltration extends much deeper and glandular atrophy (mild, moderate, marked) is present.

Gastric Atrophy, is diagnosed in the absence of inflammatory cells and extensive glandular damage is present(pernicious anaemia)

Endoscopy in the patients with advanced atrophic gastritis shows thinning of mucosa (loss of folds) and prominence of sub mucosal vascular patterns.

Atrophy is defined as the loss of appropriate glands and may be with or without intestinal metaplasia.

 

With atrophic gastritis, metaplastic changes in the glands – pseudo pyloric in the body mucosa or fundus – may be observed, fundus is inappropriate for location.

Metaplastic changes in the epithelium, intestinal in the antrum, body, fundus inappropriate for location, may be observed.

Intestinal metaplasia may be patchy and most frequently found in the gastric mucosal biopsy from the lesser curvature, near the incisura angularis.

Intestinal metaplasia extends proximately with increasing age and severity of ch. Gastritis.

INTESTINAL METAPLASIA may be complete –

Type I (enteric): Small intestinal epithelium with microvilli, goblet cells with acidic mucin, paneth cells at the base or incomplete.

 Type II (entrocolic):  Goblet cell with sulphomucin it is closely linked to the intestinal type of gastric adenocarcinoma, as the genetic abnormalities noted in pt with dysplasia (intraepithelial neoplasia) is observed in them.

Type III( colonic): Goblet cell with sulfomucin it is closely linked to the intestinal Types of gastric adenocarcinoma, as the genetic abnormalities noted in the pt with dysplasia (intraepithelial neoplasia) are observed in them.

Pernicious anaemia is defined as severe vita B12 malabsorption due to a marked intrinsic factor deficiency (‹ 200 units/hr) following a maximal stimulus.

A new definition of pernicious anaemia – the presence of intrinsic factor antibody in the serum or gastric juice with vita B12 malabsorption due to intrinsic factor deficiency was suggested in 1968.

Pt. of ‘pernicious anaemia’ without IFA should be accurately classified as atrophic gastritis, as the essential genetic factor the IFA, is absent in them.

Gastropathy should be differentiated from chronic gastritis by the absence of significant inflammation and the presence of vascular abnormalities.

 

ACUTE GASTRITIS

 

Damage to the gastric mucosa due to –

Medication – Aspirin, or non steroidal anti inflammatory drug (NSAID), cytotoxic drug, iron.

Irritants – Red and green chili, tobacco ingestion, alcohol.

Infections – Bacterial, viral, or fungal.

Uremia

Stress

 

Etiological factors for acute gastritis vary in developed and developing countries

In developed countries, drugs like Aspirin to prevent arterial thrombosis or NSAID for relief of the pain of arthritis are widely consumed by elderly and the commonest cause of acute gastritis.

Drug induced mucosal damage is predominantly in the antrum.

In acute gastritis, the gastric mucosa is intensely congested both in the body and antrum. The mucosal biopsy shows degenerative changes in the surface epithelium with mucus depletion and heavy infiltration with neutrophils.

Acute gastritis is characterized by sudden onset and quick resolution, at times within 3-4 days. To diagnose erosions, as the cause of haematemesis, gastroduodenoscopy examination should be performed within 48 hrs. In humans, the surface epithelium cells of the gastric mucosa are continuously exfoliated and replaced every 2-4 days – approximately half a million cells are exfoliated every minute and the same number replaced. Erosion occurs when there is an imbalance between the damage and repair of the surface epithelial cells. The deoxyribonucleic acid (DNA) content of the nuclei of the cells of different tissues is nearly identical. The number of the cells and the number of nuclei exfoliated during a period of time can be estimated by measuring the DNA content in the gastric juice. When the gastric mucosa is exposed to irritants, far more cells are exfoliated than can be replaced, resulting in the breakage of the gastric mucosal lining, causing erosion in the majority and bleeding in a few patients.

 

RED CHILI POWDER

Red chili powder and its active ingredient capsaicin were shown to significantly increase the exfoliation of surface epithelial cells of human gastric mucosa by estimating the DNA content in the gastric aspirates. Red chili powder also breaks the gastric mucosal barrier. In any patient with haemetemesis of unknown origin, ingestion of a highly spicy food in the previous meal should be determined.

The approximate amount of red chili powder per meal by Indian subjects, significantly increased gastric acid secretion – the effect of red chili powder on gastric acid secretion was studied by preventing reflux of H+ ions from the lumen, as the gastric mucosal barrier is also broken by the chilies. The DNA content of gastric aspirates significantly increased with intragastric infusion of black paper, asafetida, ginger, garlic. Substances such as red chili powder, aspirin, alcohol, which can break the gastric mucosal barrier, as well as stimulate acid secretion are likely to give conflicting results on acid secretion, depending upon the amount of gastric irritant used and the method employed to measure acid secretion.

 

TOBACCO

Tobacco contains carcinogens such as nicotine, polycyclic aromatic hydrocarbons, polonium, and 19- nitrosamines. Tobacco is used throughout the world for smoking but in two states of India, Maharashtra and Gujarat, it is ingested with or without pan or used as snuff or for cleaning teeth. In patients regularly chewing tobacco, the prevalence of gastric erosion on gastroduoendoscopy was as high as 20% . Further more, half an hour after the ingestion of 200 mg tobacco or one hour after the ingestion of 400 mg tobacco, per 50 patients., gastric erosions were observed in 35% and 38% patients. respectively.

 

ALCOHOL    

7% alcohol stimulates acid secretion but 12% and 16% alcohol fails to stimulate acid secretion. This is because the higher concentration of alcohol damage the gastric mucosal barrier, resulting in the loss of H+ ions from the lumen.

 

STRESS

Stress induced acute gastritis with erosion, is observed in the intensive care unit in patients with severe trauma, head injury, burns, sepsis, shock, ventilatory support etc. Inflammation plays a late and secondary role in its pathogenesis and hence may be termed ‘Stress gastropathy’.

 

INFECTION

Acute viral hepatitis causes damage to the gastric mucosal barrier in 70% of patients.

 

CHRONIC GASTRITIS

GASTRITIS

Environmental factors causing chronic gastritis may be:

  1. Helicobacter pylori infection
  2. Non helicobacter pylori infection

 

Various classifications of chronic gastritis based on vitamin B12 absorption, pathology, topography, immunology and endoscopic observations. In 1957 patients were separated in atrophic gastritis and pernicious anaemia on the basis of degree of vita B12 malabsorption. Those with ≥ 5 % excretion on the Schilling test were diagnosed as atrophic gastritis and those with severe B12 malabsorption ≤ 5 % excretion as pernicious anaemia.

In 1972 classified according to:

  1. The site of mucosa involved: pyloric, body, cardiac, transitional, interminate.
  2. The grade of gastritis: superficial or atrophic.
  3. The activity: quiescent or active.
  4. The presence of metaplasia: pseudo pyloric in the body mucosa, fundus or intestinal in the antrum, body or fundus mucosa.

 

The earliest immunological classification of chronic gastritis was reported in 1973. This classification was based on the immunological parameters, parietal cell antibody (PCA), intrinsic factor antibody (IFA), divided chronic gastritis into three types:

 

TYPE I:      Absence of both PCA and IFA in serum, e.g. post operative or corrosive gastritis.

TYPE II:     Presence of PCA and absence of IFA in the serum- superficial or atrophic gastritis

TYPE III:    Presence of both PCA and IFA in the serum- pernicious anaemia

 

PATHOPHYSIOLOGY

 

H. pylori colonizes the gastric mucosa because of:

  • Its motility with flagella
  • Capacity to produce abundant urease to form ammonia “ cloud” for its survival in intra luminal acid
  • Special affinity to adhere to the gastric epithelium and its ability to cause transient achlor or hypochlor hydria on initial exposure to the gastric mucosa

 

In the human stomach, H. pylori lies close to the intercellular junction of the gastric epithelial cells, underneath the surface mucus and within the gastric pits.

This location protects it from the intra luminal acid, to which it is sensitive.

Though H.pylori is non invasive, cytopathic changes are observed where it attaches to the gastric epithelial cells.

After colonization, H.pylori induces both a humoral and cellular inflammatory response.

For tissue injury important cytotoxins blamed are:

  1. Vacuolating cytotoxin A (vacA)
  2. Cytotoxin – associated gene A (cagA)
  3. Induced by with epithelium (iceA)
  4. Outer membrane inflammatory protein A(oipA)
  5. Bacteria adhesion

Various genotypes and their polymorphisms are identified by the polymerase chain reaction (PCR)

  • Helicobacter heilmanni
  • Glaucomatous
  • Eosinophilic
  • Lymphocytic
  • Collagenous
  • Reflux (reactive)
  • Corrosive
  • Post- irritation
  • Tobacco induced
  • Menetrier’s disease

 

NON H.PYLORI

  1. Helicobacter Heilmanni:

It is another gram negative spiral bacteria causing mild chronic gastritis.

It is probably transmitted from domestic pets. Less than 1 % of chronic gastritis results from this bacterial infection.

 

  1. Glaucomatous Gastritis:

It is diagnosed by the presence of granuloma in the mucosal biopsies which may vary in location, number, size and structure. Granuloma may occur with crohn’s disease, sarcoidosis, tuberculosis, histoplasmosis, syphilis, cryptococcal infection and post operative (structure material). The clinical radiology, endoscopy, histology and serology observations help to establish the etiology. In crohn’s disease, the focal active gastritis is present; the glaucomatous lesion is usually in antrum and may cause gastric outlet obstruction. In India, tuberculous granuloma should be excluded by staining for acid fast bacilli, performing polymerase chain reaction and/or culture.

 

  1. Eosinophilic Gastritis:

It is believed to be an allergic manifestation and may be a part of eosinophilic enteritis. It is characterized by eosinophilic infiltration of the gastric mucosa (20 eosinophils per high power field) with or without peripheral eosinophilia. Antral infiltration is common and may even cause an ulcer or a granuloma causing pyloric obstruction. A parasitic infection should be excluded.

 

  1. Lymphocytic Gastritis:

It is more often present in women and is usually asymptomatic; anorexia and weight loss occasionally occur. It is diagnosed by the presence of 30 or more lymphocytes / 100 epithelial cells (normally 3-8 intraepithelial lymphocytes). It is usually a pangastritis but occasionally affects the body mucosa only. On endoscopy, giant folds with some nodules and a few central apthous ulcer may be seen. It is associated with H.pylori infection (20%) or celiac disease (50%) and eradication of H.pylori or gluten withdrawal respectively, results in gradual improvement. In the absence of these conditions, MALT lymphoma or adenocarcinoma should be excluded.

 

  1. Collagenous Gastritis:

It is rare and is characterized by the presence of subepithelial collagen. Endoscopy shows erosions in the antrum and body mucosa and biopsy detected collagen deposition in the subepithelial region.

 

  1. Reflux (reactive) Gastritis:

It is due to reflux of duodenal contents especially bile in the gastric lumen, following operations on stomach – gastrojejunostomy, pyloroplasty or partial gastronomy.

 

  1. Corrosive Gastritis:

Corrosive ingestion, accidentally or with a suicidal intent of strong alkali or acid may result in acute gastritis mucosal damage causing erythema, oedema, erosions and ulcerations. The damage is determined by the concentration, volume, and duration of exposure and the occurrence of vomiting. Chronic gastritis and its complications – stricture may follow.

 

  1. Radiation Gastritis:

Acute gastritis may occur within a week of radiation on exposure. It usually occurs with higher doses of 4500 to 5900 CGY but may occasionally occur even with a low dose of 1800 CGY. With the availability of linear accelerator, the risk of gastritis with radiation has significantly reduced. Chronic gastritis and its complication, stricture and malignancy are observed in few patients.

 

  1. Tobacco:

Chronic gastritis has been reported in tobacco chewers. On electron microscopy, ultra structural changes fragmented basement membrane with reduction in hemidesmosome and widened intercellular spaces, similar to those observed in experimental carcinogenesis, were observed in the gastric mucosal biopsy of tobacco chewing patients.

 

10. Menetrier’s Disease i.e. Giant Hypertrophic Gastritis:

It is an uncommon disease in which gastric folds in fundus-body mucosa are prominent with occasional nodularity. The patient may present with edema of feet (protein losing enteropathy), diarrhea or weight loss. The histology shows elongation and dilation of gastric pits with reduction of gastric glands. Endo-sonography is helpful to differentiate prominent gastric mucosal folds, due to lymphoma, zollinger-ellison syndrome or gastric varices. Hypochlorhydria is usually present in this while basal, maximal acid output and serum gastrin are markedly elevated in patients with zollinger-ellison syndrome. The risk of malignancy is marginally increased.

 

 

SYMPTOMS AND COMPLICATIONS

In humans the absence of H.Pylori in the gastric mucosa is associated with a higher prevalence of endoscopic oesophagitis, Barrett’s esophagus and esophageal adenocarcinoma.

The presence of H.pylori in the gastric mucosa causes diseases such as:

Chronis gastritis

Duodenal ulcer

Gastric Ulcer

Mucosa-associated lymphoid tissue (MALT) lymphoma

‘Epidemic’ achlorhydria

Non Ulcer Dyspepsia(some patients)

 

H. PYLORI AND GASTRITIS

Symptoms:

The vast majority of chronic gastritis patients are asymptomatic. Non colicky pain in upper abdomen within 15 minutes after ingestion of a spicy meal and absence of pain on delaying or omission of a spicy meal are considered suggestive of chronic gastritis. Heaviness in upper abdomen immediately after a meal is also not an uncommon symptom. With a fiberoptic gastroscope a definite diagnosis of chronic gastritis is easy with biopsy from the body mucosa and the antrum. H.pylori causes chronic gastritis in all subjects. H.Pylori colonizes normal antrum and may extend into the body mucosa causing corpus gastritis. Chronic gastritis due to H.pylori slowly progresses over a few decades from the superficial to atrophic gastritis, intestinal metaplasia, dysplasia and gastric adenocarcinoma.

H. pylori was earlier responsible for more than 80% of chronic gastritis but its prevalence is decreasing in countries with improved sanitation.

 

H.PYLORI AND PEPTIC ULCER

DUODENAL ULCER:

The patients. with duodenal ulcer may present with dull aching pain in the epigastrium, occurring daily on an empty stomach or at midnight relieved soon after the ingestion of antacid, milk or non-spicy food. Nearly half of the numbers of patients with typical history of duodenal ulcer do not show any ulcer on endoscopy. The popular multi-factorial theory of stress and spices causing duodenal ulcer, died its natural death, with the discovery of H.pylori in 1983.

A major breakthrough in understanding of the etiology of duodenal ulcer was the discovery of H.pylori in the antral mucosal biopsy of humans, on upper gastrodudenal endoscopy- as; H.pylori is present in the antral mucosal biopsy of >90 % of duodenal ulcer patients., following the eradication of H.pylori from the gastric mucosa, annual duodenal ulcer recurrence reduced to less than 10% compared to 80%. Failure to eradicate H. pylori results in a higher recurrence rate of duodenal ulcer. H. pylori infection of the antral mucosa increases the risk of duodenal ulcer by 3-6 folds.

 

GASTRIC ULCER:

Pt. with benign gastric ulcer does not have any classical pattern of symptoms for a clinical diagnosis. Pt. may complain of dull aching pain in upper abdomen soon after food intake, nusea, heaviness, heamatemesis or symptoms of anemia.

Benign gastric ulcer is rare in Indian population, it may occur with ch.gastritis due to H.pylori or following ingestion of aspirin or NSAID. H. pylori increases the risk of benign gastric ulcer by 3 folds.

 

H.PYLORI AND GASTRIC MALIGNANCIES:

The patient with gastric malignancy presents with loss of weight, abdominal pain after food, nausea, vomiting, anaemia, haemetemesis and/or malena. Intestinal metaplasia is an important intermediary step in the development of gastric adencarcinoma (intestinal type). In India, intestinal metaplasia is uncommon in patients of atrophic gastritis and Type III (colonic) is rare, hence the incidence of gastric adenocarcinoma is low in South Asian population, despite a high prevalence of H. pylori in them. The exact cause for the low prevalence of intestinal metaplasia is not known but dietary factors are considered important.

 

MALT LYMPHOMA:

H.pylori infection increases the risk for the development of MALT lymphoma by 6-50 fold. In response to H. pylori infection, B and T lymphomas are attracted to the gastric mucosa. Monoclonal expansion and malignant transformation of B cells results in MALT lymphoma. H. pylori eradication usually cures MALT lymphoma in 70% of patients.

 

H.PYLORI AND ACHLORHYDRIA:

H. pylori has been blamed for the transient ‘epidemic’ hypo or achlorhydria at onset of infection, as it helps in its colonization in the gastric mucosa. Initial acid inhibition occurs due to a protein inhibition and pro-inflammatory cytokine interleukin 1B. Subsequently, acid output gradually increases over the next few months.

 

H.PYLORI AND NON ULCER DYSPEPSIA:

Non ulcer dyspepsia (functional dyspepsia) was initially defined as upper abdominal discomfort in the absence of an ulcer on endoscopy or barium meal.

About the author

Devika Kishorebhai Mehta

Devika Kishorebhai Mehta

Dr. Devika Kishorebhai Mehta DHMS, MD lives and works in Gujarat. In 1996 she received her D.H.M.S. from the Council of Homoeopathic System of Medicine and then her MD from H.N.G.University, Patan in 2011. From 2009 to the present she has been associated with Jawaharlal Nehru Homoeopathic Medical College as a reader and Head of Department of Organon of Medicine. Dr. Mehta has also worked as lecturer at Swami Vivekananda Homoeopathic Medical College, Bhavnagar and Rajkot Homoeopathic Medical College as a tutor. She is experienced in handling both OPD and IPD in homoeopathic hospitals. Her articles have been published in various periodicals, including the Vital Informer and on B. Jain’s website.

3 Comments

  • DEAR DR,
    YOUR LABOUR IS VERY EXTENSIVE. THE ARTICLE HAS COVERED ALL THE REMEDIES. IT IS BETTER IF THE COMMON SYMPTOMS OF REMEDIES ARE EXCLUDED. IT WOULD HAVE BEEN EASIER TO GRASP THE REMEDIES FOR THEIR PIN POINTED DIFFERENCES
    THANKS

  • kindly accept my sincere thanks for writing a beautiful article on gastritis with lot of information on etiology, pathology,diagnosis and homoeo treatment with appropriate drugs.

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