Gastritides

• gastropathies:
  1. reactive gastropathy: irritated or reactive or regenerative foveolar cellularity and little or no lamina propria cell infiltrate (unless eroded area or fairly acute [S-01-7429])
     • endoscopic:
       1. milder: erythema
       2. more severe: petechial hemorrhage or even diffuse superficial hemorrhage; erosions and ulcers may supervene
     • foveolar nuclei may look reactive (even large nucleoli)
     • reduction of foveolar cell mucous
     • increase of foveolar cell cytoplasmic amphophilia
     • microscopic foveolar hyperplasia with pit elongation and serrate profile & pseudovillous appearance of the antral biopsies, microscopically, as becomes more chronic.
     • hemorrhages: subepithelial; biopsy artifact is also subepithelial; if involves more than 25% of the biopsy, it is less likely to be artifact¹
     • due to endogenous (bile reflux) or exogenous (alcohol; NSAIDs) chemical, stress
       1. NSAIDs by far most common cause¹
       2. alcohol
       3. iron and potassium
       4. hepatic arterial infusion chemotherapy¹; HAIC may induce bizarre gastric nuclei²
       5. prolapse gastropathy (see below)
       6. physical injury: corrosive agents, radiation, instrumentation
       7. postgastrectomy reflux (but can be seen in intact stomach): endoscopy shows petechiae, erosions, and bile staining¹ and may even produce polypoid change [S-01-7383].
       8. ischemia
       9. physiological and/or emotional stress
       10. no cause identified in significant percentage
  2. atrophic gastropathy: body biopsies show some chronic gastritis plus a spectrum of focal appearance of pseudopyloric metaplasia filling in where parietal cells beginning to drop out to paietal atrophy so severe that the histology resembles antral mucosa...the stage of pernicious anemia [L06-9901].
  3. gastroparesis:
     • structural: as a consequence of mechanical pyloric outlet obstruction (partial or complete), gastric emptying can be delayed.
       1. obstructive pyloric muscular hypertrophy
          • muscular only
          • fibromuscular (post-erosional/ulcerative)
          • amyloid deposits
       2. benign polyp or tumor obstruction.
       3. malignant polyp or tumor obstruction.
       4. food or foreign body impaction/obstruction (bezoar).
     • functional:
       1. intermittent or episodic gastroparesis:
          • food & chemical overload (too much food & alcohol).
          • as a less-than-N&V manifestation of viral gastroenteritis.
       2. chronic or progressive gastroparesis:
          • fibrosis (scarring) from erosions.
          • peripheral neuropathy (diabetic?).
          • vasculopathy injury with subsequent dysfunction (diabetic?).
          • as an autoimmune GI dysmotility (AGID): as a limited form of autoimmune autonomic neuropathy (autoantibodies attacking the GI ganglioneuronal elements). Often as a paraneoplastic phenomenon (thymoma & small cell lung cancer).
  4. pigment: brownish pigment is likely to be demonstrable by the iron stain as hemosiderin in the following significant patterns^{7, 8}...
  • gastric lumenal surface pattern: probaly reflects therapeutic iron intake.
  • within lamina propria or granulation tissue: probaly reflects direct iron therapy pill damage.
  • within lamina propria histiocytes only: probably reflects prior mucosal hemorrhage from any number of possible etiologies.
  • within glandular or surface epitilial cells: rule out systemic hemosiderosis or hemochromatosis^{7, 8}; &, if not, think of a a late phase⁷ of iron absorption after recent coating of the mucosal surface [S07-12785, L08-9114].
  5. amyloid gastropathy:
  6. portal hypertensive gastric hyperemia: may be relatively localized & suggest "gastritis" & biopsy show lamina propria "hypervascularization" [LMC-02-291].
  7. Menetriere's syndrome:
  8. limited enlarged fold(s):
  9. gastric xanthelasma: pale when thin (endoscopist may call it leukoplakia) & yellow when thicker patches at endoscopy and histology shows foamy macrophages ²...synonym = "lipid island" & found in about 1% of EGDs & associated with or reflection of some factor in arterial atherosclerosis, cholesterolosis of the GB, and diabetes mellitus; not known to be related to any particular hyperlipidemia. When scant macrophage collections & less well defined, may reflect prior erosive & hemorrhagic lesion which is mostly organized [S-07-3222].
• gastritis:
  1. acute infectious:
     • "usual":
       1. viral: almost never biopsied except as problem situations in immunocompromised patients¹
       2. syphilitic: usually a picture of densely plasmacytic, glandular destructive infiltrate¹
       3. fungal: mostly in immunocompromised patients¹
     • phlegmonous: nearly always fatal, rare, suppurative filing and thickening mostly of submucosa by polys; mostly in alcoholics with history of pharyngitis; usually culture out streptococcus.¹ 
  2. nonspecific chronic: more than a rare lamina propria plasma cell and not otherwise fitting a specific pattern; some allow fewer than 5 mononuclear cells per hpf...fewer than 3 mononuclears between crypts...clusters of 3-5 or more plasma cells³
  3. active chronic Helicobacter pylori gastritis:
     • tends to be assoc. with antral and duodenal ulcer disease; endoscopically antrocentric when unmodified by medications.
     • increased lamina propria chronic inflammatory cells (may include polys and eos).
     • may see lamina propria lymphoid aggregates or nodules.
     • polys infiltrate antral pit neck epithelial zone....always suspect diagnosis when see this.
     • special stain positivity for morphologically typical curved or coccoid bacteria or the longer spiral bacteria of H. heilmannii or H. felis (there are many other helicobacteria in stomachs of various animals).
     • majority who get to GI biopsier docs have already been extensively self-medicated or primary-care medicated & biopsy features not classical & may especially lack polys & organisms may be quite sparse and as short rods & coccoid and even geographically relocated to more fundic & may be associated with focal parietal cell hypertrophy (proton pump inhibitors also may cause focal hypertrophy)⁵.
     • these incompletely treated cases often present with a markedly refractory non-ulcer dyspepsia⁵.
     • IHC is much more sensitive than the CLO test performed on biopsies⁵; the breath test is problematic; the stool antigen test may be the best way to feel that H. p. is ruled out because it reflects status of entire stomach.
  4. active chronic Helicobacter-pylori-like gastritis:
     • like H. p. gastritis but can't demonstrate organisms in biopsy
  5. lymphocytic gastritis: resembles "protein sensitivity enteropathy" and "lymphocytic colitis".
  6. collagenous gastritis: very rare & may be associated with celiac disease.
  7. Crohn's associated gastritis: a highly focal non-Helicobacter gastritis.
  8. eosinophilic gastritis (EG)and/or gastroenteritis (EGE):
     • eosinophilic esophagitis (EE) is the best described of the eosinophilic gastrointestinal diseases (EGIDs)⁶.
     • eosinophilic gastric infiltrate in a patient with GI symptoms (usually postprandial) and negative for parasites and extra-intestinal disease¹.
     • almost always have absolute peripheral blood eosinophilia; may have bone marrow eosinophilia¹.
     • symptoms depend on the variant¹:
       1. iron deficiency and/or malabsorption if primarily alters the small bowel mucosa
       2. obstructive if primarily involves muscular layers
       3. eosinophilic ascites when serosa prominently involved
     • eosinophilia related to collagen vascular disease may be accompanied by a prominent mast cell infiltrate¹
     • has no relation to inflammatory fibroid polyp (eosinophilic granuloma)¹
  9. granulomatous gastritis: infectious, sarcoidal, Crohn's-related [S-02-3531]
• ulcers:
  1. NOTE: inflammatory cell negativity in biopsy of immediately adjacent mucosa around an ulcer connotes a NSAIDs ulcer until proven otherwise¹
  2. Erosion is superficial; when reaches the submucosa, anyone would define it as an ulcer¹
  3. reactive gastropathy mostly erodes and rarely ulcerates¹
  4. HAIC (hepatic artery intravascular chemo) may induce ulcers with bizarre nuclei mimicking ulcerated gastric ca.²
  5. Cameron or Cameron's ulcers or erosions: ulcers having special endoscopic features of longitudinal linearity and being at the diaphragmatic hiatus in large hiatal hernias (some 10% of chronic iron deficiency anemia workups turn out to have large hiatal hernias...anemia on basis of coming and going of these erosions?⁴).
  6. Dieulafoy's "ulcer": usually in proximal stomach and is a persisting mucosal defect (not really an ulcer) ulcer having a central conspicuous artery...thought likely to reflect an AVM. May also find in duodenum & bronchus.
• lymphovascular abnormalities:
• motility lesions:
  1. gastroparesis, non-obstructive
• anatomic problems:
  1. gastric outlet obstruction and gastroparesis:
     • acquired pyloric muscle hypertrophy (see above).
  2. chronic relapsing antral prolapse (prolapse gastropathy):
     • produces endoscopic finding of patulous antral mucosa with erythematous longitudinal stripes ("watermelon stomach")

1. Rodger Haggitt, seminar notes, 5/97
2. R. E. Petras, seminar notes, 1991
3. Dayharsh & Burgart, of Mayo Clinic Dept. of Surg. Path, CAP Today, page 104, 7/2001
4. Yamada, et. al., Textbook of Gastroenterology, 2nd Ed.
5. Neil Goldstein, CME in Chicago (JBC) June 2006.
6. Furuta GT, Children's Hosp. Boston, editorial: "Eructations From Eosinophils", Gastroenterology 131(5):1629-30, November 2006.
7. Kaye P, et. al., "Iron-induced mucosal pathology of the upper gastrointestinal tract: a common finding in patients on oral iron therapy ", Histopathology 53(3):311-317, September 2008.
8. Marginean EC, et. al., "Gastric Siderosis: Patterns and Significance. ", American Journal of Surgical Pathology 30(4):514-520, April 2006.