Chronic gastritis is a histopathologic entity characterized by chronic inflammation of the stomach mucosa. Gastritides can be classified based on the underlying etiologic agent (eg, Helicobacter pylori, bile reflux, nonsteroidal anti-inflammatory drugs [NSAIDs], autoimmunity, allergic response) and the histopathologic pattern, which may suggest the etiologic agent and clinical course (eg, H pylori –associated multifocal atrophic gastritis). The image below depicts chronic active gastritis caused by H pylori.
Helicobacter pylori-caused chronic active gastritis. Genta stain (20X). Multiple organisms (brown) are visibly adherent to gastric surface epithelial cells.
Other classifications are based on the endoscopic appearance of the gastric mucosa (eg, varioliform gastritis). Although minimal inflammation is observed in some gastropathies, such as those associated with NSAID intake, these entities are discussed in this article because they are frequently included in the differential diagnosis of chronic gastritis.
Chemical or reactive gastritis is caused by injury of the gastric mucosa by reflux of bile and pancreatic secretions into the stomach, but it can also be caused by exogenous substances, including NSAIDs, acetylsalicylic acid, chemotherapeutic agents, and alcohol.1 These chemicals cause epithelial damage, erosions, and ulcers that are followed by regenerative hyperplasia detectable as foveolar hyperplasia, and damage to capillaries, with mucosal edema, hemorrhage, and increased smooth muscle in the lamina propria.
Inflammation in these lesions caused by chemicals is minimal or lacking; therefore, the term gastropathy or chemical gastropathy is more appropriate to describe these lesions than is the term chemical or reactive gastritis as proposed by the updated Sydney classification of gastritis.2 Importantly, mixed forms of gastropathy and other types of gastritis, especially H pylori gastritis, may coexist.
No single classification of gastritis provides an entirely satisfactory description of all types of gastritis.3 However, an etiologic classification provides a direct target toward which therapy can be directed, and, for this reason, the etiologic classification is used in this article. In many instances, chronic gastritis is a relatively minor manifestation of diseases that predominantly manifest in other organs or manifest systemically, such as gastritis in individuals who are immunosuppressed.
Helicobacter gastritis is a primary infection of the stomach and is the most frequent cause of chronic gastritis. Cases of histologically documented chronic gastritis are diagnosed as chronic gastritis of undetermined etiology or gastritis of undetermined type when none of the findings reflect any of the described patterns of gastritis and a specific cause cannot be identified.
The pathophysiology of chronic gastritis complicating a systemic disease, such as hepatic cirrhosis, uremia, or another infection, is described in the relevant disease articles. The pathogenesis of the most common forms of gastritis is described as follows.
H pylori- associated chronic gastritis
H pylori are gram-negative rods that have the ability to colonize and infect the stomach. The bacteria survive within the mucous layer that covers the gastric surface epithelium and the upper portions of the gastric foveolae. The infection is usually acquired during childhood. Once the organism has been acquired, has passed through the mucous layer, and has become established at the luminal surface of the stomach, an intense inflammatory response of the underlying tissue develops.4
The presence of H pylori is associated with tissue damage and the histologic finding of both an active and chronic gastritis. The host response to H pylori and bacterial products is composed of T- and B-cell lymphocytes, denoting chronic gastritis, followed by infiltration of the lamina propria and gastric epithelium by polymorphonuclear leukocytes that eventually phagocytize the bacteria. The presence of polymorphonuclear leukocytes in the gastric mucosa is diagnostic of active gastritis.
The interaction of H pylori with the surface mucosa results in the release of proinflammatory cytokine interleukin (IL)-8, which leads to recruitment of polymorphonuclear cells and may begin the entire inflammatory process. Gastric epithelial cells express class II molecules, which may increase the inflammatory response by presenting H pylori antigens, leading to further cytokine release and more inflammation. High levels of cytokines, particularly tumor necrosis factor-a (TNF-α)5 and multiple interleukins (eg, IL-6, IL-8, IL-10), are detected in the gastric mucosa of patients with H pylori gastritis.
Leukotriene levels are also quite elevated, especially leukotriene B4, which is synthesized by host neutrophils and is cytotoxic to gastric epithelium. This inflammatory response leads to functional changes in the stomach, depending on the areas of the stomach involved. When inflammation affects the gastric corpus, parietal cells are inhibited, leading to reduced acid secretion. Continued inflammation results in loss of parietal cells, and the reduction in acid secretion becomes permanent.
Antral inflammation alters the interplay between gastrin and somatostatin secretion, affecting G cells (gastrin-secreting cells) and D cells (somatostatin-secreting cells), respectively. Specifically, gastrin secretion is abnormal in individuals who are infected with H pylori, with an exaggerated meal-stimulated release of gastrin being the most prominent abnormality. When the infection is cured, neutrophil infiltration of the tissue quickly resolves, with slower resolution of the chronic inflammatory cells. Paralleling the slow resolution of the monocytic infiltrates, meal-stimulated gastrin secretion returns to normal.
Differences in virulence factors that characterize different strains of H pylori influence the clinical outcome of H pylori infection. People infected with H pylori strains that secrete the vacuolating toxin A (vacA) are more likely to develop peptic ulcers than people infected with strains that do not secrete this toxin. Another set of virulence factors is encoded by the H pylori pathogenicity island (PAI). The PAI contains the sequence for several genes and encodes the CAGA gene. Strains that produce CagA protein (CagA+) are associated with a greater risk of development of gastric carcinoma and peptic ulcers. However, infection with CagA- strains also predisposes the person to these diseases.6,7,8
H pylori- associated chronic gastritis progresses with the following 2 main topographic patterns that have different clinical consequences:
Antral predominant gastritis is characterized by inflammation and is mostly limited to the antrum. Individuals with peptic ulcers usually demonstrate this pattern of gastritis.
Multifocal atrophic gastritis is characterized by involvement of the corpus and gastric antrum with progressive development of gastric atrophy (loss of the gastric glands) and partial replacement of gastric glands by an intestinal-type epithelium (intestinal metaplasia). Individuals who develop gastric carcinoma and gastric ulcers usually demonstrate this pattern of gastritis.
Most of the people who are infected with H pylori do not develop significant clinical complications, and they remain carriers with asymptomatic chronic gastritis. Some individuals who carry additional risk factors may develop peptic ulcers, gastric mucosa–associated lymphoid tissue (MALT) lymphomas, or gastric adenocarcinomas.
An increased duodenal acid load may precipitate and wash out bile salts, which normally inhibit the growth of H pylori. Progressive damage to the duodenum promotes gastric foveolar metaplasia, resulting in sites for H pylori growth and more inflammation. This cycle results in the increasing inability of the duodenal bulb to neutralize acid entering from the stomach until changes in duodenal bulb structure and function are sufficient for an ulcer to develop. H pylori can survive in areas of gastric metaplasia in the duodenum, contributing to the development of peptic ulcers.
MALT lymphomas may develop in association with chronic gastritis secondary to H pylori infection. The healthy stomach lacks organized lymphoid tissue, but, following infection with H pylori, lymphoid tissue is universally present. Acquisition of gastric lymphoid tissue is thought to be due to persistent antigen stimulation from byproducts of chronic infection with H pylori. The continuous presence of H pylori results in the persistence of MALT in the gastric mucosa, which eventually may progress to form low- and high-grade MALT lymphomas. MALT lymphomas are monoclonal proliferations of neoplastic B cells that have the ability to infiltrate gastric glands. Gastric MALT lymphomas typically are low-grade T-cell–dependent B-cell lymphomas, and the antigenic stimulus of gastric MALT lymphomas is thought to be H pylori.
Another complication of H pylori gastritis is the development of gastric carcinomas, especially in individuals who develop extensive atrophy and intestinal metaplasia of the gastric mucosa. Although the relationship between H pylori and gastritis is constant, only a small proportion of individuals infected with H pylori develop gastric cancer. The incidence of gastric cancer usually parallels the incidence of H pylori infection in countries with a high incidence of gastric cancer and is consistent with H pylori being the cause of the precursor lesion, chronic atrophic gastritis.
Persistence of the organisms and associated inflammation during long-standing infection is likely to permit the accumulation of mutations in the gastric epithelial cells' genome, leading to an increased risk of malignant transformation and progression to adenocarcinoma. Studies have provided evidence of the accumulation of mutations in the gastric epithelium secondary to oxidative DNA damage associated with chronic inflammatory byproducts and secondary to deficiency of DNA repair induced by chronic bacterial infection.
Although the role of H pylori in peptic ulcer disease is well established, the clinical role of the infection in nonulcer dyspepsia remains very controversial. H pylori eradication may be beneficial for symptom relief in a small proportion of patients, but routine H pylori testing and treatment in nonulcer dyspepsia is not currently widely accepted. Therefore, consider H pylori eradication strategies in patients with nonulcer dyspepsia on an individual patient-by-patient basis.
Infectious granulomatous gastritis
Granulomatous gastritis (see image below) is a rare entity. Tuberculosis may affect the stomach and cause caseating granulomas. Fungi can also cause caseating granulomas and necrosis, a finding that is usually observed in patients who are immunosuppressed.
Granulomatous chronic gastritis. Noncaseating granulomas in the lamina propria. Courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.
Gastritis in patients who are immunosuppressed
Cytomegalovirus (CMV) infection of the stomach is observed in patients with underlying immunosuppression. Histologically, typical intranuclear eosinophilic inclusions and, occasionally, smaller intracytoplasmic inclusions are found (see image below).
Chronic gastritis. Typical cytomegalovirus inclusions in lamina propria capillary endothelial cells. Courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.
A patchy, mild inflammatory infiltrate is observed in the lamina propria. Viral inclusions are present in gastric epithelial cells and in endothelial or mesenchymal cells in the lamina propria. Severe necrosis may result in ulceration. Herpes simplex causes basophilic intranuclear inclusions in epithelial cells. Mycobacterial infections by Mycobacterium avium-intracellulare are characterized by diffuse infiltration of the lamina propria by histiocytes, which rarely form granulomas (see image below).
Chronic gastritis. Mycobacterium avium-intracellulare in gastric lamina propria macrophages. Courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.
This type of gastritis is associated with serum antiparietal and anti-intrinsic factor (IF) antibodies. The gastric corpus undergoes progressive atrophy, IF deficiency occurs, and patients may develop pernicious anemia.
The development of chronic atrophic gastritis limited to corpus-fundus mucosa and marked diffuse atrophy of parietal and chief cells characterize autoimmune atrophic gastritis. Autoimmune gastritis is associated with serum antiparietal and anti-IF antibodies that cause IF deficiency, which, in turn, causes decreased availability of cobalamin and, eventually, pernicious anemia in some patients.
Autoantibodies are directed against at least 3 antigens, including IF, cytoplasmic (microsomal-canalicular), and plasma membrane antigens. Two types of IF antibodies are detected (ie, types I and II). Type I IF antibodies block the IF-cobalamin binding site, thus preventing the uptake of vitamin B-12. Cell-mediated immunity also contributes to the disease. T-cell lymphocytes infiltrate the gastric mucosa and contribute to epithelial cell destruction and resulting gastric atrophy. A recent study reported that gender, age, vitamin B12, folate, renal function, atrophic gastritis and the methylenetetrahydrofolate (MTHF) 677TT genotype were significant determinants of homocysteine levels, which were positively related to incident cardiovascular diseases.9
Chronic reactive chemical gastropathy
This type of gastritis is associated with long-term intake of aspirin or NSAIDs. It also develops when bile-containing intestinal contents reflux into the stomach. Although bile reflux may occur in the intact stomach, most of the features associated with bile reflux are typically found in patients with partial gastrectomy, in whom the lesions develop near the surgical stoma. The mechanisms through which bile alters the gastric epithelium involve the effect of several bile constituents. Both lysolecithin and bile acids can disrupt the gastric mucous barrier, allowing the back diffusion of positive hydrogen ions and resulting in cellular injury. Pancreatic juice enhances epithelial injury in addition to bile acids. In contrast to other chronic gastropathies, minimal inflammation of the gastric mucosa typically occurs in chemical gastropathy.
Chronic noninfectious granulomatous gastritis
Noninfectious diseases are the usual cause of gastric granulomas and include Crohn disease, sarcoidosis, and isolated granulomatous gastritis. Crohn disease demonstrates gastric involvement in approximately 33% of the cases. Granulomas have also been described in association with gastric malignancies, including carcinoma and malignant lymphoma. Sarcoidlike granulomas may be observed in people who use cocaine, and foreign material is occasionally observed in the granuloma.
This is a type of chronic gastritis with dense infiltration of the surface and foveolar epithelium by T lymphocytes and associated chronic infiltrates in the lamina propria. Because of similar histopathology relative to celiac disease, lymphocytic gastritis has been proposed to result from intraluminal antigens. High anti-H pylori antibody titers have been found in patients with lymphocytic gastritis, and, in limited studies, the inflammation disappeared after H pylori eradication. However, many patients with lymphocytic gastritis are serologically negative for H pylori. A number of cases may develop secondary to intolerance to gluten and drugs such as ticlopidine.
Large numbers of eosinophils may be observed with parasitic infections such as those caused by Eustoma rotundatum and anisakiasis. Eosinophilic gastritis can be part of the spectrum of eosinophilic gastroenteritis. Although the gastric antrum is commonly affected and can cause gastric outlet obstruction, this condition can affect any segment of the GI tract and can be segmental.10 Patients frequently have peripheral blood eosinophilia. In some cases, especially in children, eosinophilic gastroenteritis can result from food allergy, usually to milk or soy protein. Eosinophilic gastroenteritis can also be found in some patients with connective tissue disorders, including scleroderma, polymyositis, and dermatomyositis.
Small doses of radiation (up to 1500 R) cause reversible mucosal damage, whereas higher radiation doses cause irreversible damage with atrophy and ischemic-related ulceration. Reversible changes consist of degenerative changes in epithelial cells and nonspecific chronic inflammatory infiltrate in the lamina propria. Higher amounts of radiation cause permanent mucosal damage, with atrophy of fundic glands, mucosal erosions, and capillary hemorrhage. Associated submucosal endarteritis results in mucosal ischemia and secondary ulcer development.
Ischemic gastritis is believed to result from atherosclerotic thrombi arising from the celiac and superior mesenteric arteries.
Approximately 35% of adults are infected with H pylori, but the prevalence of infection in minority groups and immigrants from developing countries is much higher. Children aged 2-8 years in developing nations acquire the infection at a rate of about 10% per year; whereas, in the United States, children become infected at a rate of less than 1% per year. This major difference in the rate of acquisition in childhood is responsible for the differences in epidemiology between developed countries and developing countries. Socioeconomic differences are the most important predictor of the prevalence of the infection in any group. Higher standards of living are associated with higher levels of education and better sanitation, thus the prevalence of infection is lower.
In the United States and in other countries with modern sanitation and clean water supplies, the rate of acquisition has been decreasing since 1950. The rate of infection in people with several generations of their families living at a high socioeconomic status is in the range of 10% to 15%. This is probably the lowest the prevalence can decline spontaneously until eradication or vaccination programs are instituted.
Lymphocytic gastritis has been estimated to represent approximately 1.4% of all gastritides. The disease has been reported in various parts of the world but more commonly in Europe, and it appears to be less common in the United States.
Chronic reactive chemical gastropathy is one of the most common and poorly recognized lesions of the stomach.
An estimated 50% of the world population is infected with H pylori; therefore, chronic gastritis is extremely frequent. H pylori infection is highly prevalent in Asia and in developing countries, and multifocal atrophic gastritis and gastric adenocarcinomas are more prevalent in these areas.11
Autoimmune gastritis is a relatively rare disease, most frequently observed in individuals of northern European descent1,12 and blacks. The prevalence of pernicious anemia, resulting from autoimmune gastritis, has been estimated at 127 cases per 100,000 members of the population in the United Kingdom, Denmark, and Sweden. The frequency of pernicious anemia is increased in patients with other immunologic diseases, including Graves disease, myxedema, thyroiditis, and hypoparathyroidism.
Morbidity of chronic gastritis is strongly related to the underlying cause. Chronic gastritis as a primary disease, such as H pylori- associated chronic gastritis, may progress as an asymptomatic disease in some patients, whereas other patients may report dyspeptic symptoms.
The clinical course may be worsened when patients develop any of the possible complications of H pylori infection such as peptic ulcer or gastric malignancy.
H pylori gastritis is the most frequent cause of MALT lymphoma. Patients with chronic atrophic gastritis may have a 12- to 16-fold increased risk of developing gastric carcinoma, compared with the general population. Approximately 1 in 6 infected persons develop peptic ulcer, and, in the United States, approximately 25% develop hypochlorhydria or achlorhydria. The lifetime risk of gastric cancer is in the range of 1% to 3%.
Environmental factors, such as diet and standard of living, are important in determining which pathway is prevalent in a country or area.
In patients with autoimmune gastritis, the major effects are consequent to the loss of parietal and chief cells and include achlorhydria, hypergastrinemia, loss of pepsin and pepsinogen, anemia, and an increased risk of gastric neoplasms. Autoimmune gastritis represents the most frequent cause of pernicious anemia in temperate climates. The risk of gastric adenocarcinoma appears to be at least 2.9 times higher in patients with pernicious anemia than in the general population.
H pylori -associated chronic gastritis appears to be more common among Asian and Hispanic people than in people of other races.
In the United States, H pylori infection is more common among black, Native American, and Hispanic people than among white people, a difference that has been attributed to socioeconomic factors.
Autoimmune gastritis is more frequent in individuals of northern European descent and in black people, and it is less frequent in southern European and Asian people.
Sarcoidosis is more frequent in young black people, whereas isolated granulomatous gastritis is more common in older white people.
Chronic H pylori- associated gastritis affects both sexes with similar frequency.
The female-to-male ratio for autoimmune gastritis has been reported to be 3:1.
Lymphocytic gastritis affects men and women at similar rates.
Age is the most important variable relating to the prevalence of H pylori infection, with persons born before 1950 having a notably higher rate of infection than people born after 1950. For example, roughly one half of people older than 60 years are infected, compared with 20% of people younger than 40 years. This increase in infection prevalence with age is largely apparent rather than real, reflecting a continuing overall decline in the prevalence of H pylori infection.
Because the infection is typically acquired in childhood and is lifelong, the high proportion of older individuals (eg, 60 y or older) who are infected is the long-term result of infection that occurred in childhood when standards of living were lower. The prevalence will decrease as people who are currently aged 40 years and have a lower rate of infection grow older (a birth cohort phenomenon).
H pylori gastritis is usually acquired during childhood, and complications typically develop later.
Patients with autoimmune gastritis usually present with pernicious anemia, which is typically diagnosed in individuals aged approximately 60 years. However, pernicious anemia can be detected in children (juvenile pernicious anemia).
Lymphocytic gastritis can be observed in children but is usually detected in late adulthood. On average, patients are aged 50 years.
Eosinophilic gastroenteritis mostly affects people younger than 50 years.
Patients who are symptomatic with idiopathic granulomatous gastritis usually present when they are older than 40 years.
H pylori infection: Acute H pylori infection is usually not clinically detected, but experimental infection results in a clinical syndrome characterized by epigastric pain, fullness, nausea, vomiting, flatulence, malaise, and (sometimes) fever. The symptoms resolve in about 1 week whether or not the organism is eliminated. Persistence of the organism causes H pylori chronic gastritis, which is usually asymptomatic but may manifest as gastric pain or, rarely, with nausea, vomiting, anorexia, or significant weight loss. Symptoms may occur with the development of complications of chronic H pylori gastritis, which include peptic ulcers, gastric adenocarcinoma, and MALT lymphoma.
Autoimmune gastritis: The clinical manifestations are primarily related to the deficiency in cobalamin, which is not adequately absorbed because of IF deficiency as a result of severe gastric parietal cell atrophy. The disease has an insidious onset and progresses slowly. Cobalamin deficiency affects the hematologic, gastrointestinal, and neurologic systems.
Hematologic manifestations: The most significant manifestation is megaloblastic anemia, but, rarely, purpura due to thrombocytopenia may develop. Symptoms of anemia include weakness, light-headedness, vertigo and tinnitus, palpitations, angina, and symptoms of congestive failure.
Gastrointestinal manifestations: The lack of cobalamin is associated with megaloblastosis of the gastrointestinal tract epithelium. Patients sometimes report having a sore tongue. Anorexia with moderate weight loss that is occasionally associated with diarrhea may result from malabsorption associated with megaloblastic changes of the small intestinal epithelial cells.
Neurologic manifestations: These result from demyelination, followed by axonal degeneration and neuronal death. The affected sites include peripheral nerves, posterior and lateral columns of the spinal cord, and cerebrum. Signs and symptoms include numbness and paresthesias in the extremities, weakness, and ataxia. Sphincter disturbances may occur. Mental function disturbances vary from mild irritability to severe dementia or psychosis. The neurologic disease may occur in a patient with hematocrit and red cell parameters within the reference range.
Patients with pernicious anemia have an increased frequency of gastric polyps and gastric carcinoid and a 2.9-fold increase in the frequency of gastric cancer.
Granulomatous gastritis: In multisystemic diseases, specific symptoms related to gastric involvement may be minor. Caseating granulomas secondary to tuberculosis may be found in the absence of lung disease in patients who are malnourished, immunosuppressed, or alcoholic. Patients with Crohn disease and gastric involvement may report gastric pain, nausea, and vomiting. Gastric involvement in Crohn disease is almost invariably associated with intestinal disease, and intestinal manifestations predominate. Sarcoidosis of the stomach is usually associated with granulomatous inflammation in other locations, especially the lungs, hilar nodes, or salivary glands. About 10% of patients with sarcoid involvement in the stomach are asymptomatic. Patients who are symptomatic present with gastric ulcers, hemorrhage, pyloric stricture, and gastric outlet obstruction.
Idiopathic isolated granulomatous gastritis: This diagnosis is established only when known entities associated with granulomas are excluded. Patients who are symptomatic usually are older than 40 years at presentation and have epigastric pain, weight loss, and vomiting secondary to pyloric obstruction.
Lymphocytic gastritis: This type mostly affects middle-aged or elderly patients. Lymphocytic gastritis may be associated with chronic H pylori infection, gluten-sensitive enteropathy, and Menetrier disease. It may represent a hypersensitivity reaction involving the gastric body. Lymphocytic gastritis has been described complicating MALT lymphoma and gastric carcinoma.
Eosinophilic gastroenteritis: Some patients have underlying connective tissue disorders. Patients with predominant mucosal involvement may report nausea, vomiting, and abdominal pain related to the ingestion of specific foods. Patients with involvement of the muscularis propria and resulting thickening and rigidity may present with outlet obstruction symptoms. Many patients have a history of allergy, peripheral eosinophilia, asthma, eczema, or food sensitivity. Some patients have a response to removal of these items from the diet, and their condition often responds to steroid treatment.
Gastritis in graft versus host disease: Graft versus host disease (GVHD) follows allogeneic bone marrow transplantation or transfusions, especially in patients who are immunocompromised. Patients with isolated gastric GVHD have symptoms of nausea, vomiting, and upper abdominal pain without diarrhea.13
The physical examination is of little contributory value in chronic gastritis. However, some findings are specifically associated with the particular complications of H pylori- associated gastritis and autoimmune gastritis.
In uncomplicated H pylori- associated atrophic gastritis, clinical findings are few and nonspecific.
Epigastric tenderness may exist.
If gastric ulcers coexist, guaiac-positive stool may result from occult blood loss.
Bad breath (ie, halitosis) and abdominal pain or discomfort may occur, with bloating associated with bacterial overgrowth syndrome.
Physical findings may result from the development of pernicious anemia and neurologic complications in patients with autoimmune atrophic gastritis.
With severe cobalamin deficiency, the patient is pale and has slightly icteric skin and eyes. The pulse is rapid, and the heart may be enlarged. Auscultation usually reveals a systolic flow murmur.
See Gastroesophageal Reflux Disease. Types of chronic gastritis include the following:
Chronic gastritis caused by H pylori infection - This is the most common cause of chronic gastritis.
Infection by Helicobacter heilmannii
Granulomatous gastritis associated with gastric infections in mycobacteriosis, syphilis, histoplasmosis, mucormycosis, South American blastomycosis, anisakiasis, or anisakidosis
Chronic gastritis associated with parasitic infections -Strongyloides species, schistosomiasis, Diphyllobothrium latum
Viral infections such as CMV and herpes virus infection14
Chemical gastropathy, usually related to chronic bile reflux or NSAID and aspirin intake
Chronic noninfectious granulomatous gastritis,15,16 associated with the following:
Isolated granulomatous gastritis
Chronic granulomatous disease of childhood
Allergic granulomatosis and vasculitis
Plasma cell granulomas
Tumoral amyloidosis and granulomas associated with gastric carcinoma
Langerhans cell histiocytosis
Lymphocytic gastritis, including gastritis associated with celiac disease (also called collagenous gastritis)17
Radiation injury to the stomach
Gastritis secondary to drug therapy
Chronic gastritis of undetermined etiology or gastritis of undetermined type (eg autistic gastritis
Abu Zubair meriwayatkan dari Jabir bin Abdullah bahwa Nabi Muhammad SAW bersabda:
"Setiap penyakit ada obatnya. Jika obat yang tepat diberikan dengan izin Allah, penyakit itu akan sembuh".
(HR. Muslim, Ahmad dan Hakim).
Kamis, 31 Desember 2009
Diposkan oleh FX di 23.41
The Holy Al-Qur'an (English version)
- Surah 1 - Al Fatiha THE OPENING
- Surah 2 - Al Baqarah THE HEIFER
- Surah 3 - Ali 'Imran - THE FAMILY OF 'IMRAN
- Surah 4 - Al-Nisa' THE WOMEN
- Surah 5 - Al Ma'idah THE REPAST
- Surah 6 - Al An'am THE CATTLE
- Surah 7 - Al A'raf THE HEIGHTS
- Surah 8 - Al Anfal THE SPOILS OF WAR
- Surah 9 - Al Tawbah THE REPENTANCE
- Surah 10 - Yunus JONAH
- Surah 11 - Hud THE PROPHET HUD
- Surah 12 - Yusuf JOSEPH
- Surah 13 - Al Ra'd THE THUNDER
- Surah 14 - Ibrahim ABRAHAM
- Surah 15 - Al Hijr THE ROCKY TRACT
- Surah 16 - Al Nahl BEES
- Surah 17 - Al Isra' THE NIGHT JOURNEY
- Surah 18 - Al Kahf THE CAVE
- Surah 19 - Maryam MARY
- Surah 20 - TA HA
- Surah 21 - Al Anbiya THE PROPHETS
- Surah 22 - Al Hajj THE PILGRIMAGE
- Surah 23 - Al Mu'minun THE BELIEVERS
- Surah 24 - Al Nur THE LIGHT
- Surah 25 - Al Furqan THE CRITERION
- Surah 26 - Al Shu'ara' THE POETS
- Surah 27 - Al Naml THE ANTS
- Surah 28 - Al Qasas THE NARRATIONS
- Surah 29 - Al 'Ankabut THE SPIDER
- Surah 30 - Al Rum THE ROMANS
- Surah 31 - Luqman LUQMAN
- Surah 32 - Al Sajdah THE PROSTRATION
- Surah 33 - Al Ahzab THE CONFEDERATES
- Surah 34 - Saba' SHEBA
- Surah 35 - Fatir THE ORIGINATOR OF CREATION
- Surah 36 - Ya Sin YA SIN
- Surah 37 - Al Saffat THOSE RANGED IN RANKS
- Surah 38 - Sad SAD
- Surah 39 - Al Zumar CROWDS
- Surah 40 - Ghafir FORGIVER
- Surah 41 - Fussilat EXPOUNDED
- Surah 42 - Al Shura CONSULTATION
- Surah 43 - Al Zukhruf THE GOLD ADORNMENTS
- Surah 44 - Al Dukhan THE SMOKE
- Surah 45 - Al Jathiyah THE KNEELING DOWN
- Surah 46 - Al Ahqaf WINDING SAND-TRACTS
- Surah 47 - Muhammad MUHAMMAD
- Surah 48 - Al Fath THE VICTORY
- Surah 49 - Al Hujurat THE CHAMBERS
- Surah 50 - Qaf QAF
- Surah 51 - Al Dhariyat THE WINDS THAT SCATTER
- Surah 52 - Al Tur THE MOUNT
- Surah 53 - Al Najm THE STAR
- Surah 54 - Al Qamar THE MOON
- Surah 55 - Al Rahman THE MOST GRACIOUS
- Surah 56 - Al Waq'iah THE INEVITABLE
- Surah 57 - Al Hadid IRON
- Surah 58 - Al Mujadilah THE WOMAN WHO PLEADS
- Surah 59 - Al Hashr THE MUSTERING
- Surah 60 - Al Mumtahinah THAT WHICH EXAMINES
- Surah 61 - Al Saff THE BATTLE ARRAY
- Surah 62 - Al Jumu'ah FRIDAY
- Surah 63 - Al Munafiqun THE HYPOCRITES
- Surah 64 - Al Taghabun THE MUTUAL LOSS AND GAIN
- Surah 65 - Al Talaq DIVORCE
- Surah 66 - Al Tahrim PROHIBITION
- Surah 67 - Al Mulk THE DOMINION
- Surah 68 - Al Qalam THE PEN
- Surah 69 - Al Haqqah THE SURE REALITY
- Surah 70 - Al Ma'arij THE WAYS OF ASCENT
- Surah 71 - Nuh NOAH
- Surah 72 - Al Jinn THE SPIRITS
- Surah 73 - Al Muzzammil THE ENFOLDED ONE
- Surah 74 - Al Muddaththir THE ONE WRAPPED UP
- Surah 75 - Al Qiyamah THE RESURRECTION
- Surah 76 - Al Insan MAN
- Surah 77 - Al Mursalat THOSE SENT FORTH
- Surah 78 - Al Naba' THE GREAT NEWS
- Surah 79 - Al Nazi'at THOSE WHO TEAR OUT
- Surah 80 - 'Abasa HE FROWNED
- Surah 81 - Al Takwir THE FOLDING UP
- Surah 82 - Al Infitar THE CLEAVING ASUNDER
- Surah 83 - Al Mutaffifin THE DEALERS IN FRAUD
- Surah 84 - Al Inshiqaq THE RENDING ASUNDER
- Surah 85 - Al Buruj THE CONSTELLATIONS
- Surah 86 - Al Tariq THE NIGHT STAR
- Surah 87 - Al A'la THE MOST HIGH
- Surah 88 - Al Ghashiyah THE OVERWHELMING EVENT
- Surah 89 - Al Fajr THE DAWN
- Surah 90 - Al Balad THE CITY
- Surah 91 - Al Shams THE SUN
- Surah 92 - Al Layl THE NIGHT
- Surah 93 - Al Duha THE GLORIOUS MORNING LIGHT
- Surah 94 - Al Sharh THE EXPANSION OF THE BREAST
- Surah 95 - Al Tin THE FIG
- Surah 96 - Al Alaq THE CLINGING CLOT
- Surah 97 - Al Qadr THE NIGHT OF POWER
- Surah 98 - Al Bayyinah THE CLEAR EVIDENCE
- Surah 99 - Al Zalzalah THE EARTHQUAKE
- Surah 100 - Al 'Adiyat THOSE THAT RUN
- Surah 101 - Al Qari'ah THE GREAT CALAMITY
- Surah 102 - Al Takathur THE PILING UP
- Surah 103 - Al 'Asr TIME THROUGH THE AGES
- Surah 104 - Al Humazah THE SCANDALMONGER
- Surah 105 - Al Fil THE ELEPHANT
- Surah 106 - Quraysh THE TRIBE OF QURAYSH
- Surah 107 - Al Ma'un THE NEIGHBOURLY ASSISTANCE
- Surah 108 - Al Kawthar THE ABUNDANCE
- Surah 109 - Al Kafirun THOSE WHO REJECT FAITH
- Surah 110 - Al Nasr THE HELP
- Surah 111 - Al Masad THE PLAITED ROPE
- Surah 112 - Al Ikhlas THE PURITY OF FAITH
- Surah 113 - Al Falaq THE DAYBREAK
- Surah 114 - Al Nas MANKIND
- Acute Coronary Syndromes
- Angina Pectoris
- Anomalous Left Coronary Artery From the Pulmonary Artery
- Aortic Coarctation
- Aortic Dissection
- Aortic Regurgitation
- Aortic Stenosis
- Aortic Stenosis, Subaortic
- Aortic Stenosis, Supravalvar
- Ashman Phenomenon
- Atrial Fibrillation
- Atrial Flutter
- Atrial Myxoma
- Atrial Septal Defect
- Atrial Tachycardia
- Atrioventricular Block
- Atrioventricular Dissociation
- Atrioventricular Nodal Reentry Tachycardia (AVNRT)
- Benign Cardiac Tumors
- Brugada Syndrome
- Complications of Myocardial Infarction
- Coronary Artery Atherosclerosis
- Coronary Artery Vasospasm
- Digitalis Toxicity
- Dissection, Aortic
- Ebstein Anomaly
- Eisenmenger Syndrome
- First-Degree Atrioventricular Block
- HACEK Group Infections (Infective Endocarditis)
- Heart Failure - Decompensatio Cordis
- Holiday Heart Syndrome
- Hypertensive Heart Disease
- Junctional Rhythm
- Loeffler Endocarditis
- Long QT Syndrome
- Lutembacher Syndrome
- Mitral Regurgitation
- Mitral Stenosis
- Mitral Valve Prolapse
- Myocardial Infarction
- Myocardial Rupture
- Paroxysmal Supraventricular Tachycardia
- Patent Ductus Arteriosus
- Patent Foramen Ovale
- Pericardial Effusion
- Pericarditis Acute
- Pericarditis, Constrictive
- Pericarditis, Constrictive-Effusive
- Pulmonic Regurgitation
- Pulmonic Stenosis
- Right Ventricular Infarction
- Saphenous Vein Graft Aneurysms
- Second-Degree Atrioventricular Block
- Sinus of Valsalva Aneurysm
- Sudden Cardiac Death
- Tetralogy of Fallot
- Third-Degree Atrioventricular Block
- Torsade de Pointes
- Tricuspid Regurgitation
- Tricuspid Stenosis
- Unstable Angina
- Ventricular Fibrillation
- Ventricular Septal Defect
- Ventricular Tachycardia
- Wolff-Parkinson-White Syndrome