Pathology Associates Of Lexington, P.A.
Pathology Associates Of Lexington, P.A.
Pathology Associates Of Lexington, P.A.
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        Gastritides, a linking classification outline


Acute gastroenteritis (AGE) affecting the stomach is unlikely to be biopsied. Transferred through the air or by human contact, it comes on suddenly. When afebrile, without fever, without seriously ill feelings and very primarily nausea and vomiting and stomach cramps, it is likely viral; if it includes a touch of feverish feeling or low grade fever plus general aches and pains, folks refer to it as "stomach flu". If diarrhea, it is almost always non-bloody. Notorious in our area in the winter of 2012-13 is the norovirus GII.4 genotype of the various small round-structured viruses (SRSVs). There can also be bacterial causes and causes by other organisms and toxins. A really-ill, sudden onset with higher fever & bloody diarrhea, a bacterial cause comes into the differential diagnosis. AGE can also come from "food poisoning", norovirus being only one cause. Much of the below has to do with work up of less dramatic situations, except for C. diff. colitis workups.

It is the much more chronic complaint situations which produce biopsies sent to pathologists. Criteria have been set for gastric biopsies (Sydenham criteria of the AGA) so that more than a rare plasma cell defines "chronic gastritis". Atrophic GI changes are greatly more difficult to discern histologically than they are endoscopically. So, proper interpretation of biopsies relies on the pathologist having knowledge of age, sex, the key clinical question to be addressed by the pathologist (for example, "watery diarrhea" workup or "celiac disease" workup), pertinent endoscopic positive or negative findings, and the key question to be answered ("UC, r/o dysplasia"). Clinicians are often concerned that provision of this info will cause "expectation bias" in the pathologist's interpretation; the pathologist "controls" for expectation bias by looking at the biopsies PRIOR to getting any further case information. When a pathologist uses the term "nonspecific" (for example, "nonspecific chronic gastritis"), it simply means that he/she is not in possession of enough histological or other information to achieve a more specific diagnosis.

[on-line endoscopic atlas]

  • gastropathies:
    1. reactive gastropathy (RG): irritated or reactive or regenerative foveolar cellularity and little or no lamina propria cell infiltrate (unless eroded area or fairly acute [S-01-7429]); it can sometimes be hyperplastic [L09-5392].
      • 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. Blood in lamina propria anywhere in GI tract can be ASA/NSAID or other antithrombotic associated & may or may not be related to bowel prep.
      • RG 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. oxyntic-cell gastropathy: if truly present, apparently related to long-term useage of proton pump inhibitors, being a spectrum of increasingly prominent and more widely distributed lamina propria parietal cells (e. g., becoming prominent on antral areas), with formation of dilated acinar-like vertical spaces into which hypertrophied parietal (oxyntic) cells may protrude in a sawtooth, hobnail fashion [L09-6228; L10-8922]9; then increase into micronudular cell clusters, and then begin to maybe form "fundic gland polyps". Because the normal extent of the histological antrum can be so highly variable, some experts limit the diagnosis to cases of a very late degree of adaptational expression where the endoscopist thought they were biopsying a polypoid lesion10.
    4. polyps: (HERE)
    5. hemorrhagic gastropathy: this may be freshly present as blood in lamina propria as mechanical artifact of the endoscopic process and/or a result of intentional (prescribed) or unintentional anticoagulation or antiplatelet therapy.
    6. gastroparesis:
      • structural: as a consequence of mechanical pyloric gastric outlet obstruction...GOO (partial or complete), gastric emptying can be delayed.
        1. obstructive pyloric muscular hypertrophy
          • muscular only
          • fibromuscular (post-erosional/ulcerative)
          • amyloid deposits
          • pyloric muscle torus malformation and greater curve, pyloric pseudodiverticulum formation which, in overcapacity, kicks the outlet superomedial to obstruct and cause acute gastroparesis in someone who has been shown (or is subsequently shown) to have an anatomically nonstenotic gastric outlet (FA12-111) which the filled pseudodiverticulum could push into functional gastric outlet obstruction (GOO), see below.
        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).
    7. pigment: if one iron-stains each gastric biopsy, around 4%8 of cases will be positive; but, simply noting brownish pigment by H&E is a lower percentage & pigment is likely to be demonstrable by the iron stain as hemosiderin in the following significant patterns7, 8...
      • gastric lumenal surface pattern: probaly reflects therapeutic iron intake.
      • within lamina propria or granulation tissue: probaly reflects direct oral iron therapy pill damage.
      • within lamina propria histiocytes only: probably reflects prior mucosal hemorrhage from any number of possible etiologies or oral intake [L09-4478].
      • within glandular or surface epithelial cells: rule out systemic hemosiderosis or hemochromatosis7, 8,(only about a third of known hemochromatosis cases are positive8); &, if not, think of a a late phase7 of iron absorption after recent oral intake coating of the mucosal surface [S07-12785, L08-9114].
    8. amyloid gastropathy: less likely to see in mucosa than in muscle wall.
    9. portal hypertensive gastric hyperemia: may be relatively localized & suggest "gastritis" & biopsy show lamina propria "hypervascularization" [LMC-02-291].
    10. Menetriere's syndrome: an endoscopic DX.
    11. limited enlarged fold(s): an endoscopic DX.
    12. 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 
      • granulomatous: fungal & mycobacterial [S09-11393].
    2. Watch out!: any type of the following ongoing, longstanding chronic gastritis types can lead to intenstinal metaplasia & thereafter to adenomatous change [L12-4171]. So, intestinal metaplasia should be an "eye stopper" inducing a search for adenomatous change. Uncertainty of an adenomatous quailty can be fortified toward that diagnosis if (1) Ki-67 is claerly quite increased in the suspect cells (2) along with the same cells having nuclear p53 positivity (both markers in claerly increased contrast to adjecent epithelials.
    3. nonspecific chronic: very common in endoscopic biopsied population & is 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. Helicobacter can be present and generate little or no cellular reaction in the biopsy sample processed; therefore, we test all gastric biopsies for helicobacter [S11-6897].
    4. 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 short curved or coccoid [L11-12158] bacteria or the longer spiral bacteria [S10-8353] of H. heilmannii or H. felis (there are many other helicobacteria in stomachs of various animals). Coccoid forms indicate damaged organisms11 "hunkered down" into non-culturable survival mode.
      • majority who get to GI-biopsy 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 areas & 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 way more sensitive than the old CLO test performed on biopsies usually in the endoscopy suites5; the breath test is a global mucosal test but problematic relative to patient preparation and medication abstention; but we began offering it @ LML in 2010; the stool antigen test may be the best way to feel that H. p. is ruled out when the negative biopsy is supicious, because it reflects status of entire stomach & done in our hospital microbiology lab.
      • In our experience prior to bariatric screening for helicobacter gastritis, maybe 2-4% of cases of obesity surgery "sleeve" gastrectomies have a helicobacter gastritis which is positive for the organisms [L08-5767, L08-11800].
      • may be associated with (sometimes causitive?) borderline-to-increased duodenal IELs as in the villus-tip-score (VTS) [S13-1201].
    5. active chronic Helicobacter-pylori-like gastritis:
      • like H. p. gastritis but can't demonstrate organisms in biopsy [L10-7955]...suggest follow up stool antigen or breath test (see above).
    6. gastric body or antral intestinal metaplasia: this can be highly focal and is a "marker" of chronicity. If diffuse enough, it causes a pale endoscopic change referred to as "gastric leukoplakia" [L09-2302].
    7. lymphocytic gastritis: resembles "protein sensitivity enteropathy" and "lymphocytic colitis".
    8. collagenous gastritis: very rare & may be associated with celiac disease.
    9. Crohn's associated gastritis13: a histologically granulomatous or non-Helicobacter gastritis that tends to have pit abscesses, most commonly as helicobacter-like (but negative) [S13-3495] in patchy fashion.
    10. eosinophilic gastritis (EG) and/or gastroenteritis (EGE): the mean normal eosinophile count may be about 16/square mm of lamina propria with a wide SD (range of 0-110) & in USA normal usually less than 38/square mm & abnormal if greater than 30 eos. per 40x hpf (4-5 hpfs = a square mm)12.
      • eosinophilic esophagitis (EE) is the best described of the eosinophilic gastrointestinal diseases (EGIDs)6, HERE.
      • "histological eosinophilc gastroenteritis": recommended term when biopsy eosinophilic concentration is clearly above an average of greater than 127 eos/ (30 or greater per 40x hpf)12.
      • classical EG/EGE:
        • 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.
    11. granulomatous gastritis: AFB pos. gastritis case (S09-5638); infectious, sarcoidal [CG13-2026], 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. we have found a small regenerative mucosal post-ulcer repair proliferation on an enlarged fold in a "sleeve gastrectomy" [L09-5502].
    5. HAIC (hepatic artery intravascular chemo) may induce ulcers with bizarre nuclei mimicking ulcerated gastric ca.2
    6. 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 ); histology nonspecific & variable [S10-8896].
    7. Dieulafoy lesion or Dieulafoy's "ulcer": usually in proximal stomach and is a persisting mucosal defect (not really an ulcer) having a central conspicuous artery...thought likely to reflect an AVM. May also find in duodenum & bronchus.
    lymphovascular abnormalities:
    1. dilated vessels
      • think of portal hypertension & check out that possibility, especially when no evidence of prolapsed, redundant mucosa associated watermelon stomach.
      • GAVE: gastric antral vascular ectasia = a type of watermelon stomach & associated with GI bleeds and chronic anemia & may reflect "portal hypertensive gastropathy or scleroderma [HERE].
  • motility lesions:
    1. gastroparesis, non-obstructive: pyloric muscle torus malformation and greater curve, pyloric pseudodiverticulum formation which, in overcapacity, kicks the outlet superomedial to obstruct and cause acute gastroparesis in someone who has been shown (or is subsequently shown) to have a nonstenotic gastric outlet (FA12-111). See above.
    2. gastroparesis, related to over-capacity obstruction: there can be an acute or subacute, temporary immobilty that lasts hours to days when over-eating plus irritant contents lead to obstruction at a relatively tight outlet & motility stops. And, the key is that a subsequent post-crisis gastric emptying study turns out pretty normal. More commonly, the setting is of partial peptic or other chronic, incomplete or subtotal obstruction. Also, see immediately-previous #1.
  • 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.
  9. Odze, Goldblum, Crawford, Surg. Path. of the GI Tract, Liver, Biliary Tract, and Pancreas, 1067 pages, 2004 [EBS's office].
  10. Shari Taylor, MD, GI Pathologist, personal communications.
  11. Kusters JG, et. al., "Coccoid forms of Helicobacter pylori are the morphologic manifestation of cell death", Infect. Immun., 65(9): 3672-3679, September 1997 [HERE].
  12. Lwin T, et. al., Eosinophilic gastritis: histopathological characterization and quantification of the normal gastric eosinophil content, Modern Pathology 24(4):556-563, April 2011 HERE.
  13. Kefalas CH, 2003, HERE.
(posted 2001; latest addition 9 November 2013)


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