TOP CAUSES OF STOMACH DISEASES YOU SHOULD KNOW

The stomach is a vital organ in the digestive system, responsible for storing food, mixing it with digestive juices, and propelling the mixture into the small intestine. Its unique environment, particularly its high acidity, makes it susceptible to a range of specific conditions and diseases. Understanding these classifications is fundamental for diagnosis, treatment, and research in gastroenterology.

Classification of Diseases of the Stomach

Stomach diseases can be broadly classified based on their underlying cause, the tissue layers affected, or their clinical presentation. A common approach involves categorizing them as follows:

1. Inflammatory Conditions (Gastritis):
   • Definition: Inflammation of the gastric mucosa (lining of the stomach).
   • Characteristics: Can be acute (sudden onset, short duration) or chronic (long-standing, persistent inflammation). Further classified by cause (e.g., H. pylori, NSAIDs, alcohol, stress, autoimmune, chemical) and location/pattern (e.g., antral, pangastritis).
   • Significance: A very common group, ranging from asymptomatic to causing significant pain, bleeding, and leading to pre-malignant changes or ulceration. This category is discussed in detail below.
2. Peptic Ulcer Disease (PUD):
   • Definition: Defined breaks in the gastric or duodenal mucosa extending through the muscularis mucosae. While technically involving the duodenum, ulcers are often associated with gastric pathology, particularly H. pylori or NSAID use, which primarily affect the stomach lining.
   • Characteristics: Can be acute or chronic. Causes include H. pylori infection (most common), NSAID use, Zollinger-Ellison syndrome, stress (stress ulcers), and rare conditions.
   • Significance: A major cause of upper gastrointestinal bleeding, perforation, and obstruction if left untreated.
3. Infectious Gastropathies (Other than H. pylori):
   • Definition: Inflammation or damage to the stomach lining caused by infections other than H. pylori.
   • Characteristics: Less common than H. pylori-induced disease. Can include viral infections (e.g., Cytomegalovirus, Herpes Simplex Virus, especially in immunocompromised individuals), fungal infections (e.g., Candidiasis), parasitic infections, and bacterial infections (e.g., Syphilis – leading to luetic gastritis, or potentially granulomatous infections like Tuberculosis in rare cases).
   • Significance: Often occur in specific patient populations (immunocompromised) or geographic areas and require targeted antimicrobial therapy.
4. Chemical/Reactive Gastropathies:
   • Definition: Damage to the gastric mucosa caused by chemical irritants or bile reflux. This is distinct from true inflammation (gastritis) although often grouped together.
   • Characteristics: Common causes include chronic bile reflux (e.g., after gastric surgery), alcohol abuse, chronic NSAID or aspirin use (low dose), and chemotherapy. Characterized by foveolar hyperplasia, smooth muscle proliferation, and often minimal acute inflammatory cells.
   • Significance: Can cause chronic upper abdominal pain, nausea, and bleeding.
5. Autoimmune Gastritis:
   • Definition: A form of chronic gastritis caused by an autoimmune attack against the parietal cells and/or intrinsic factor.
   • Characteristics: Typically affects the body and fundus of the stomach. Leads to parietal cell atrophy, loss of acid production (achlorhydria), and deficiency of intrinsic factor, causing Vitamin B12 malabsorption (pernicious anemia). Often associated with antibodies to parietal cells or intrinsic factor.
   • Significance: Increases the risk of gastric carcinoid tumors (due to hypergastrinemia secondary to achlorhydria) and gastric adenocarcinoma (specifically the diffuse type, though the link is complex).
6. Motility Disorders:
   • Definition: Conditions affecting the ability of the stomach muscles to contract and move food properly.
   • Characteristics: Can include gastroparesis (delayed gastric emptying, often associated with diabetes, post-surgical changes, or idiopathic), functional dyspepsia (symptoms suggestive of stomach disease without identifiable structural or biochemical abnormality, thought to involve motility or sensation issues), and sometimes rapid gastric emptying.
   • Significance: Cause symptoms like early satiety, nausea, vomiting, bloating, and upper abdominal discomfort. Diagnosis often requires specialized motility testing.
7. Polyps and Tumors:
   • Definition: Abnormal growths arising from the gastric mucosa or submucosa.
   • Characteristics:
     • Polyps: Benign growths like fundic gland polyps (often associated with PPI use), hyperplastic polyps (often related to chronic gastritis), or adenomatous polyps (premalignant).
     • Benign Tumors: Leiomyomas, GISTs (Gastrointestinal Stromal Tumors – can be benign or malignant potential), Schwannomas, etc.
     • Malignant Tumors:
       • Gastric Carcinoma (Adenocarcinoma): The most common gastric malignancy, classified into intestinal type (often linked to gastritis, H. pylori, metaplasia) and diffuse type (often genetic, poorer prognosis).
       • Lymphoma: Primarily MALT Lymphoma (strongly associated with H. pylori) and aggressive lymphomas.
       • Neuroendocrine Tumors (Carcinoids): Can arise sporadically or secondary to conditions causing hypergastrinemia (like autoimmune gastritis or Zollinger-Ellison syndrome).
       • Sarcomas: Rare.
   • Significance: Ranging from incidental findings (many polyps) to highly aggressive cancers requiring complex multi-modal treatment.
8. Vascular Lesions:
   • Definition: Conditions involving abnormal blood vessels in the stomach wall.
   • Characteristics: Examples include Gastric Antral Vascular Ectasia (GAVE syndrome, or “watermelon stomach”), angiodysplasias, or Dieulafoy’s lesion (a large caliber artery that erodes through the mucosa).
   • Significance: Common causes of acute or chronic upper gastrointestinal bleeding.

This classification provides a framework for understanding the diverse array of conditions that can affect the stomach. Among these, gastritis is exceptionally common, with Helicobacter pylori being a primary driver of chronic forms.

Gastritis and Helicobacter pylori-Induced Gastritis

Gastritis is defined as inflammation of the gastric mucosa. It is a histological diagnosis, meaning inflammation is seen on a biopsy. However, the term “gastropathy” is often used clinically when there is mucosal injury without evidence of significant inflammation (e.g., reactive gastropathy from NSAIDs or bile reflux).

Gastritis can be acute or chronic. Acute gastritis is typically transient inflammation, often caused by NSAIDs, alcohol, or severe stress. Chronic gastritis is more persistent and is most commonly caused by Helicobacter pylori infection, or less often by autoimmune mechanisms.

Detailed Examination of Helicobacter pylori-Induced Gastritis

Helicobacter pylori (H. pylori) is a Gram-negative, microaerophilic bacterium that colonizes the gastric mucosa of humans. It is estimated to infect over half of the world’s population, though the prevalence varies significantly by geography and socioeconomic status. H. pylori is now recognized as the primary cause of chronic gastritis, peptic ulcer disease, and a significant risk factor for gastric cancer and MALT lymphoma.

Pathogenesis of Helicobacter pylori-Induced Gastritis

The ability of H. pylori to colonize the harsh, acidic environment of the stomach and cause chronic disease relies on several key factors:

1. Survival in Acid: H. pylori produces large amounts of the enzyme urease. Urease hydrolyzes urea (present in gastric juice and tissue) into ammonia and carbon dioxide. The ammonia neutralizes the gastric acid in the immediate vicinity of the bacterium, creating a more hospitable microenvironment.
2. Motility and Access to Mucosa: H. pylori is helical-shaped and possesses multiple flagella, allowing it to move through the viscous gastric mucous layer. This enables it to reach the relatively pH-neutral environment near the surface epithelial cells, underneath the protective mucous layer.
3. Adhesion: The bacterium expresses outer membrane proteins (OMPs), such as adhesins (e.g., BabA, SabA), which bind to specific receptors on the gastric epithelial cells (e.g., blood group antigens, sialyl-dimeric Lewis x). This adherence allows the bacteria to resist being sloughed off with gastric mucus and provides a stable location to deliver virulence factors.
4. Virulence Factors & Tissue Damage: H. pylori produces various factors that directly damage epithelial cells, modulate the host immune response, and alter gastric physiology:
   • Cytotoxin-associated gene A (CagA): Injected into host cells via a Type IV secretion system. Inside the cell, CagA interferes with host cell signaling pathways, altering cell morphology, polarity, and proliferation. CagA-positive strains are strongly associated with more severe inflammation, atrophy, and increased risk of peptic ulcer disease and gastric cancer.
   • Vacuolating cytotoxin A (VacA): Secreted toxin that forms pores in the host cell membrane, leading to vacuolation (formation of vesicles) and potentially apoptosis (programmed cell death) of epithelial cells. VacA also affects immune cells.
   • Other factors: Phospholipases, proteases, and other enzymes that degrade the mucous layer and damage cell membranes.
   • Induction of Inflammation: H. pylori components (like LPS) and virulence factors trigger an innate and adaptive immune response. Epithelial cells and immune cells release pro-inflammatory cytokines (e.g., IL-1β, TNF-α, IL-8), recruiting neutrophils, lymphocytes, and plasma cells to the gastric mucosa. This chronic inflammation is central to the pathogenesis of gastritis.
5. Alteration of Gastric Physiology: H. pylori infection can affect acid secretion. Initial infection, particularly in the antrum, often leads to increased gastrin release and increased acid production. Chronic infection, especially when spreading to the body and fundus, can lead to parietal cell loss and reduced acid production (hypo- or achlorhydria).

The interplay between the host’s genetic susceptibility, environmental factors, and the specific H. pylori strain’s virulence factors determines the pattern and severity of gastritis and the likelihood of developing complications. Antral-predominant gastritis is often associated with increased acid and is linked to duodenal ulcers. Pangastritis or body-predominant gastritis is often associated with decreased acid, atrophy, and a higher risk of gastric ulcers and cancer.

Pathologic Features of Helicobacter pylori-Induced Gastritis

The appearance of H. pylori-induced gastritis varies depending on the stage (acute vs. chronic) and distribution (antrum, body, pangastritis).

• Gross/Endoscopic Features:
  • Acute: Mucosal edema, redness (erythema), maybe scattered erosions.
  • Chronic: Mucosal redness, fine nodularity, thickened folds (early), or flattened, thin, and pale mucosa in areas of atrophy (late). In some cases, visible lymphoid follicles may be seen as raised white spots.
• Microscopic/Histologic Features (Diagnosis confirmed by biopsy):
  • Chronic Inflammation: Presence of increased numbers of lymphocytes and plasma cells in the lamina propria (the connective tissue layer beneath the epithelium).
  • Activity (Acute Inflammation): Presence of neutrophils migrating through the epithelium and into the gastric pits and lumen. This is the “activity” component of chronic active gastritis, indicating ongoing epithelial injury.
  • Intestinal Metaplasia: The transformation of the gastric epithelial lining cells into cells resembling those found in the small or large intestine (goblet cells, absorptive cells). This is a pre-malignant change. It is typically patchy and starts in the antrum before potentially spreading.
  • Glandular Atrophy: Loss of the specialized gastric glands (parietal cells and chief cells), particularly in the body and fundus in cases of pangastritis or body-predominant disease. This leads to reduced acid and intrinsic factor production. Atrophy is also considered a pre-malignant condition.
  • Lymphoid Aggregates/Follicles: Formation of organized collections of lymphocytes with germinal centers in the lamina propria. This represents the host’s immune response and is particularly prominent in H. pylori infection. Persistent stimulation can potentially progress to MALT lymphoma.
  • Identification of H. pylori Organisms: The bacteria are typically seen on the surface of the epithelium, within the mucous layer, or sometimes in the gastric pits. They are curved or spiral rods. They are often difficult to see on routine hematoxylin and eosin (H&E) stains, so special stains like Giemsa, Warthin-Starry silver stain, or immunohistochemistry are used to visualize them clearly.

Complications of Helicobacter pylori-Induced Gastritis

Chronic H. pylori infection and the resulting gastritis can lead to several significant complications:

1. Peptic Ulcer Disease (PUD): H. pylori is the cause of approximately 70-80% of gastric ulcers and over 90% of duodenal ulcers. In the duodenum, the bacteria themselves don’t typically colonize the duodenal lining, but the increased acid load caused by antral H. pylori gastritis leads to gastric metaplasia in the duodenum (patches of duodenal lining become like gastric lining), which H. pylori can then colonize, causing duodenitis and ulceration. Eradication of H. pylori significantly reduces the recurrence rate of peptic ulcers.
2. Chronic Atrophic Gastritis (CAG): As described under pathologic features, chronic inflammation leads to the loss of gastric glands and specialized cells (parietal and chief cells), leading to atrophy. CAG is a consequence of long-standing H. pylori infection (or autoimmune disease).
3. Intestinal Metaplasia (IM): Also described under pathologic features, IM is a direct consequence of chronic epithelial injury and inflammation, strongly associated with H. pylori. Complete IM (resembling small intestine) and incomplete IM (resembling large intestine) exist, with incomplete IM carrying a higher risk of dysplasia and cancer.
4. Dysplasia: This refers to pre-cancerous cellular changes in the gastric epithelium, often arising within areas of intestinal metaplasia or atrophy. Dysplasia can be low-grade or high-grade; high-grade dysplasia is considered an immediate precursor to invasive adenocarcinoma.
5. Gastric Adenocarcinoma (Intestinal Type): H. pylori is classified as a Class I carcinogen by the WHO. Chronic H. pylori gastritis, particularly when it progresses through the Correa cascade (chronic gastritis -> atrophy -> intestinal metaplasia -> dysplasia -> carcinoma), is the leading cause of intestinal-type gastric cancer. Eradication of H. pylori, especially before the development of widespread atrophy or metaplasia, can reduce the risk of gastric cancer.
6. Gastric MALT Lymphoma: Mucosa-Associated Lymphoid Tissue (MALT) lymphoma of the stomach is a low-grade lymphoma strongly linked to chronic H. pylori infection. The persistent immune stimulation by the bacteria leads to the proliferation of lymphoid tissue in the gastric wall. In many cases, successful eradication of H. pylori leads to complete remission of early-stage gastric MALT lymphoma.
7. Iron Deficiency Anemia: Chronic, low-grade bleeding from severely inflamed or eroded mucosa due to gastritis or associated ulcers can lead to iron deficiency anemia over time. Additionally, some studies suggest that H. pylori might impair iron absorption or increase iron loss.

In conclusion, diseases of the stomach are varied, ranging from common inflammatory conditions like gastritis to complex neoplastic processes. Helicobacter pylori remains a central figure in gastric pathology, driving chronic inflammation that can progress through a well-defined sequence of histological changes, ultimately leading to potentially severe complications including peptic ulcer disease and gastric malignancy. Accurate classification and thorough investigation, often involving endoscopy and biopsy, are crucial for managing these conditions effectively.

Defining Peptic Ulcer Disease and its Significance

Peptic Ulcer Disease (PUD) is a condition characterized by breaks or erosions in the protective lining (mucosa) of the gastrointestinal tract, specifically in locations exposed to acid-pepsin secretion. The most common sites are the stomach (gastric ulcers) and the first part of the small intestine, the duodenum (duodenal ulcers). These ulcerations penetrate through the muscularis mucosae layer, differentiating them from more superficial erosions.

PUD is a prevalent condition globally, historically associated with significant morbidity due to complications like bleeding and perforation. While advancements in understanding its primary causes and developing effective treatments have reduced its severity in many cases, it remains a clinically important condition requiring accurate diagnosis and management.

Etiology – The Causes of Peptic Ulcer Disease

Peptic ulcers develop when there is an imbalance between factors that damage the mucosal lining (aggressive factors) and factors that protect it (defensive factors). While historically attributed solely to lifestyle or stress, the vast majority of PUD cases are now known to be caused by specific factors:

1. Helicobacter pylori (H. pylori) Infection: This gram-negative bacterium is the most common cause of PUD worldwide. It colonizes the stomach and can persist for decades, causing chronic inflammation (gastritis). H. pylori contributes to ulcer formation through multiple mechanisms, including direct mucosal injury, induction of inflammation, disruption of the mucosal barrier, and alteration of gastric acid secretion (often increasing acid production, especially in duodenal ulcer formation).
2. Nonsteroidal Anti-inflammatory Drugs (NSAIDs): Regular use of NSAIDs (such as aspirin, ibuprofen, naproxen, celecoxib) is the second most common cause. NSAIDs damage the mucosa through two main mechanisms:
   • Topical Injury: Direct irritation to the epithelial cells.
   • Systemic Injury: Inhibition of cyclooxygenase (COX) enzymes. COX-1 is crucial for producing prostaglandins, which play a vital role in maintaining gastric mucosal defense (promoting mucus and bicarbonate secretion, maintaining mucosal blood flow, and stimulating cell regeneration). NSAID-induced reduction in prostaglandins weakens these defenses, making the mucosa vulnerable to acid and pepsin.
3. Less Common Causes:
   • Zollinger-Ellison Syndrome (ZES): A rare condition characterized by gastrin-producing tumors (gastrinomas), usually in the pancreas or duodenum. Excessive gastrin leads to hypersecretion of gastric acid, causing severe, often multiple, and sometimes refractory ulcers.
   • Other Medications: Corticosteroids (especially when combined with NSAIDs), potassium chloride tablets, and some chemotherapy drugs can contribute to ulcer formation.
   • Smoking: Impairs mucosal blood flow, reduces prostaglandin synthesis, decreases bicarbonate secretion, and delays ulcer healing.
   • Severe Physiological Stress: While classic PUD is typically chronic, acute, superficial ulcers can occur in critically ill patients due to severe stress (see Step 6).
   • Genetics: A family history of PUD is a modest risk factor.

It’s important to note that diet and stress, while potentially exacerbating symptoms, are not considered primary causes of PUD in the absence of H. pylori or NSAID use.

Pathogenesis – How Ulcers Develop

The pathogenesis of peptic ulcers revolves around the disruption of the delicate balance between aggressive factors (acid, pepsin, H. pylori, NSAIDs, bile) and defensive factors.

• Aggressive Factors: Gastric acid and pepsin are essential for digestion but can autodigest the stomach and duodenal lining if the protective barrier is compromised. H. pylori and NSAIDs directly compromise this barrier.
• Defensive Factors: These include the pre-epithelial mucous-bicarbonate layer (creating a pH gradient), the epithelial cell layer (rapid turnover, tight junctions), subepithelial factors (mucosal blood flow delivering oxygen and nutrients, nerves, and inflammatory cells), and production of protective mediators like prostaglandins.

Specific Pathogenic Mechanisms:

• H. pylori: The bacterium possesses virulence factors that facilitate colonization (urease to create a neutral microenvironment), adherence to epithelial cells, and damage (toxins like VacA, CagA). The ensuing chronic inflammatory response also contributes to tissue injury. In addition, H. pylori can indirectly affect gastrin and somatostatin levels, leading to increased acid secretion, particularly in duodenal ulcer patients.
• NSAIDs: As discussed, their primary mechanism is reducing protective prostaglandins by inhibiting COX enzymes, particularly COX-1. This diminished prostaglandin production impairs mucus and bicarbonate secretion, reduces mucosal blood flow, and hinders epithelial cell repair, leaving the mucosa vulnerable to acid and pepsin attack.
• Zollinger-Ellison Syndrome: The excessive gastrin release overwhelms the defensive capacity of the mucosa through sheer volume of acid.

The breakdown of these defenses allows acid and pepsin to injure the underlying layers, leading to inflammation, necrosis, and the formation of an ulcer crater that can extend deeply into the stomach or duodenal wall.

Types of Peptic Ulcers

Peptic ulcers are primarily classified by their location:

1. Duodenal Ulcers (DU):
   • Occur in the duodenum, most commonly the first portion (duodenal bulb), within a few centimeters of the pylorus.
   • Historically more common than gastric ulcers, though the incidence has shifted with changes in H. pylori prevalence and NSAID use patterns.
   • Strongly associated with H. pylori infection (over 90% of cases).
   • Often associated with increased gastric acid secretion.
2. Gastric Ulcers (GU):
   • Occur in the stomach, most commonly along the lesser curvature.
   • More evenly split between H. pylori infection and NSAID use as causes. Other causes like bile reflux are also considered.
   • Gastric acid secretion may be normal or even reduced, but the mucosal defense is significantly impaired.
   • Crucially, a subset of gastric ulcers (especially those not clearly linked to H. pylori or NSAIDs) can be malignant (cancerous), requiring biopsy for definitive diagnosis. Duodenal ulcers are almost always benign.

While symptoms can overlap, classic patterns sometimes exist: DU pain may improve with food and worsen several hours after a meal (or at night), while GU pain may be exacerbated by eating.

Pathology – The Appearance and Structure of Peptic Ulcers

Understanding the pathology involves examining the ulcer both macroscopically (how it looks to the naked eye or during endoscopy) and microscopically (how the tissue appears under a microscope).

• Macroscopic Appearance:
  • Shape: Typically round or oval, with clearly defined edges.
  • Size: Variable, usually ranging from a few millimeters up to several centimeters in diameter.
  • Depth: Extends through the muscularis mucosae and often into the submucosa and muscularis propria. A defining feature that distinguishes it from a superficial erosion.
  • Edges: In benign ulcers, the edges are clean, sharply demarcated, and often appear “punched-out.” In malignant ulcers, the edges tend to be irregular, raised, nodular, and thickened.
  • Base: Covered with a fibrinous exudate and necrotic debris. Below this lies granulation tissue (indicating attempted healing), and eventually a layer of dense fibrous tissue (scarring). A visible blood vessel (sentinel vessel) in the base indicates a risk of bleeding.
• Microscopic Appearance: A cross-section of a chronic peptic ulcer reveals characteristic layers from the lumen inward:
  1. Surface Layer: Necrotic debris and acute inflammatory cells (neutrophils).
  2. Inflammatory Layer: Active inflammation with neutrophils and mononuclear cells. H. pylori (if present) can be seen in the mucus layer or adhering to epithelial cells at the ulcer margin.
  3. Granulation Tissue Layer: Vascularized connective tissue with fibroblasts, endothelial cells, and chronic inflammatory cells (lymphocytes, plasma cells, macrophages). Represents the body’s attempt at healing.
  4. Fibrous Tissue Layer: Dense collagenous scar tissue that extends into the submucosa and muscularis propria, replacing the destroyed muscle tissue. This layer accounts for the potential for stricture formation during healing.

Malignant ulcers microscopically show cancerous cells within the ulcer base and edges, invading the surrounding tissues, which is distinct from the benign inflammatory and repair processes seen in non-malignant PUD.

Complications of Peptic Ulcer Disease

While many ulcers heal with treatment, some can lead to serious complications that require immediate medical intervention:

1. Bleeding: This is the most common and potentially life-threatening complication. It occurs when the ulcer erodes into a blood vessel. Symptoms range from occult blood loss (leading to iron deficiency anemia) to acute, severe hemorrhage. Manifestations include hematemesis (vomiting blood, which can be red or look like coffee grounds) and melena (black, tarry stools due to digested blood).
2. Perforation: The ulcer erodes through the entire wall of the stomach or duodenum, allowing gastric or duodenal contents to leak into the abdominal cavity. This causes severe peritonitis, a medical emergency presenting with sudden, intense abdominal pain, rigidity of the abdominal wall, and signs of shock.
3. Penetration: The ulcer erodes into an adjacent organ (such as the pancreas, liver, or colon) rather than into the free abdominal cavity. This causes severe, localized pain that may radiate, often presenting differently than classic ulcer pain.
4. Obstruction: Scarring and inflammation associated with chronic ulcers, particularly in the pyloric channel or proximal duodenum, can narrow the lumen, obstructing the passage of food. Symptoms include recurrent postprandial vomiting (often containing undigested food from hours earlier), early satiety, bloating, and weight loss.

These complications underscore the importance of prompt diagnosis and treatment of peptic ulcers.

Other Types of Gastric Ulcerations

Beyond the classic PUD caused by H. pylori or NSAIDs, other conditions can cause ulcerations in the stomach lining. While sharing the appearance of an ulcer, their etiology and clinical context differ:

1. Acute Gastric Mucosal Lesions (Stress Ulcers): These are superficial erosions or ulcers that occur rapidly in the stomach (and sometimes duodenum) in patients experiencing severe physiological stress. Triggers include major trauma, burns (Curling ulcers), severe sepsis, head injury (Cushing ulcers, often deep and perforated), shock, or multi-organ failure. Pathogenesis involves reduced mucosal blood flow (ischemia) and impaired defense mechanisms rather than chronic inflammation or altered acid/defense balance driven by H. pylori or NSAIDs. They tend to be multiple and located predominantly in the fundus and body of the stomach. Prophylaxis is often given in critical care settings.
2. Malignant Ulcers: Gastric adenocarcinoma (stomach cancer) can present as an ulcerated lesion. Unlike benign ulcers, malignant ulcers have irregular, raised margins and a different microscopic appearance (cancer cells). Any gastric ulcer not clearly caused by NSAIDs or H. pylori (or which doesn’t heal with treatment) requires biopsy to rule out malignancy.
3. Ischemic Ulcers: Can result from reduced blood flow to a specific area of the stomach, potentially due to vasculitis or other vascular compromise.
4. Radiation-Induced Ulcers: Can occur after radiation therapy to the upper abdomen.
5. Crohn’s Disease: While more commonly affecting the small and large intestines, Crohn’s can cause inflammation and ulceration anywhere in the GI tract, including the stomach and duodenum.
6. Drug-Induced (Non-NSAID): Certain other drugs can cause gastric ulcers, although less frequently than NSAIDs (e.g., bisphosphonates like alendronate, specifically if not taken with enough water or if the patient lies down afterwards).
7. Caustic Ingestion: Swallowing corrosive substances can cause severe, widespread ulceration and necrosis of the stomach lining.

These conditions highlight that an ulceration in the stomach can have diverse underlying causes, necessitating a thorough medical investigation to determine the specific etiology and guide appropriate treatment.