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

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.

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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.