AMYLOIDOSIS
Figure 2.255 Amyloidosis involving antral mucosa. At low power, slight eosinophilic material focally expands the lamina propria.
Figure 2.256 Amyloidosis involving antral mucosa. Higher power shows the acellular eosinophilic material.
Figure 2.257 Amyloidosis involving antral mucosa (Congo Red). Amyloid is orange on direct light and apple green with polarized light (Congo Red) (not shown).
Amyloidosis is notoriously easy to miss, unless carefully searched for on every biopsy (Figs. 2.255 and 2.256). On low power, this antral biopsy looks almost normal, but on high power a subtle amorphous pink deposit is focally seen. The corresponding Congo red is positive for amyloid, confirming the H&E impressions (Fig. 2.257). This patient was ultimately found to have a plasma cell dyscrasia.
APOPTOTIC BODY PROMINENCE
Figure 2.258 Apoptotic gastropathy. Apoptotic bodies are tiny bits of nuclear debris or dust that are often variably sized (arrowheads), in contrast to lymphocytes (arrows).
As with every biopsy, apoptotic body evaluation is part of the routine biopsy assessment and requires at least a few fields with the 40× objective (Fig. 2.258). In the stomach, one apoptotic body per 100 glands is normal, so it takes very few apoptotic bodies to cross the required threshold for apoptotic gastropathy. Occasionally, lymphocytes can raise concerns for apoptotic bodies, but with experience the distinction is more easily made: apoptotic bodies are tiny bits of nuclear debris or dust that are often variably sized; lymphocytes are larger and more uniform in size (Figs. 2.258 and 2.259). Apoptotic gastropathy is most commonly seen in the following settings:
Figure 2.259 Apoptotic gastropathy. CMV viral cytopathic effect is seen (arrow) with nuclear megaly and prominent nucleoli, in addition to a mild prominence of apoptotic bodies (arrowheads). A CMV immunostain was positive. In this case, the patient had a history of Hodgkin lymphoma, bone marrow transplant, and febrile diarrhea. Excess apoptotic bodies can be a valuable red flag to the underlying (treatable) diagnosis.
• Infection (Helicobacter, CMV, among others)
• Medication (i.e., NSAIDS and CellCept (Mycophenolate) injury, among others)195–197
• Graft versus Host Disease (See also Graft versus Host Disease, Lymphocytic Esophagitis Pattern, Esophagus Chapter)
• Immune-Mediated Disease
POORLY DIFFERENTIATED ADENOCARCINOMA WITH SIGNET RING CELL FEATURES
Figure 2.260 Metastatic lobular breast carcinoma.
Figure 2.261 Metastatic lobular breast carcinoma. Atypical stromal cells are seen (bracket).
Figure 2.262 Metastatic lobular breast carcinoma. Pleomorphic cells are seen with abundant pink cytoplasm (arrowheads).
This specimen is from a gastric resection for gastric bypass surgery (Figs. 2.260–2.262). The surgeon detected a firm focus at the proximal margin which she submitted for frozen section analysis. At low power, unremarkable oxyntic-type mucosa is seen in the upper left corner, in addition to fragments of squamous mucosa (Fig. 2.260). At higher power, the lamina propria appears a bit more cellular than usual, prompting closer inspection (bracket) (Fig. 2.261). On highest power, the nuclei have approximately the same appearance as those of the neighboring endothelial cells (not particularly hyperchromatic and not particularly large); however, histiocytes do not have such an infiltrative architecture (arrowheads) (Fig. 2.262). A CAM5.2 IHC highlights all of the indicated cells, supporting a diagnosis of poorly differentiated adenocarcinoma with signet ring cell features (Fig. 2.263). But the story does not conclude here. Every poorly differentiated adenocarcinoma with signet ring cell features in a woman must be accompanied by breast markers to exclude a metastatic lobular carcinoma. In this case, the atypical cells also show strong nuclear positivity for progesterone receptor, supporting the diagnosis of metastatic lobular carcinoma (Fig. 2.264). The patient ultimately was found to have a breast mass requiring subsequent mastectomy.
Figure 2.263 Metastatic lobular breast carcinoma (CAM5.2). The atypical cells are diffusely cytokeratin reactive, supporting the diagnosis of poorly differentiated carcinoma with signet ring cell features.
Figure 2.264 Metastatic lobular breast carcinoma (Progesterone receptor). Every poorly differentiated carcinoma with signet ring cell features in a woman should be evaluated with breast markers. This case was PR reactive, and a subsequent breast mass was found.
RUSSELL BODY GASTRITIS
Figure 2.265 Russell body gastritis.
Figure 2.266 Russell body gastritis.
Figure 2.267 Russell body gastritis (PAS).
This case represents a not uncommon consultation case, typically submitted with a concern for poorly-differentiated adenocarcinoma (Figs. 2.265–2.267). At lowest power, the gastric mucosa shows peculiar cells just below the surface epithelium and dispersed between gastric pits. These cells have brightly eosinophilic cytoplasm (Fig. 2.265). On higher power, the pink cytoplasmic inclusions are smooth and homogenous, and the nuclear cytology is bland: no hyperchromasia, pleomorphism, nor mitotic figures are seen (Fig. 2.266). Under oil magnification, the bland nature of the nuclear cytology is best appreciated (PAS). Note, the nuclei of the indicated cells are much smaller than those in the adjoining foveolar epithelium and the cytoplasmic inclusions are PAS reactive (Fig. 2.267). This case is an example of Russell body gastritis. Russell bodies are bright pink cytoplasmic inclusions derived from entrapped immunoglobulins that are lodged in the rough endoplasmic reticulum of plasma cells. Supporting their benign nature, Russell bodies display a mixed kappa and lambda light chain distribution. When plasma cells acquire prominent Russell bodies, as in this case, they are termed “Mott cells.” In the stomach, Russell bodies are commonly associated with Helicobacter gastritis, but they can theoretically be seen with any type of long-standing chronic inflammation. Importantly, Mott cells can be mimics of poorly differentiated adenocarcinoma since both can be sparsely distributed in a quasi-infiltrative pattern and have PAS+ cytoplasmic inclusions (Figs. 2.266 and 2.267 vs. Figs. 2.268–2.269); however, Mott cells display a uniformly bland cytology. In Figure 2.267, for example, note that the Mott cell nuclei are smaller than those of the neighboring foveolar epithelium nuclei. In comparison, the nuclei of poorly differentiated adenocarcinoma are typically larger than normal cells and display irregular nuclear contours, prominent nucleoli, and hyperchromasia (Figs. 2.268 and 2.269). In challenging cases, a cytokeratin stain can be helpful (the Mott cells are cytokeratin nonreactive, whereas the adenocarcinoma is cytokeratin reactive).
Figure 2.268 Poorly differentiated adenocarcinoma.
Figure 2.269 Poorly differentiated adenocarcinoma (PAS).
MUCUS-NECK CELLS
Figure 2.270 Mucus neck cells (arrowheads).
Figure 2.271 Mucus neck cells.
Figure 2.272 Mucus neck cells (PAS, arrowheads).
This near miss case highlights another common mimic of poorly differentiated adenocarcinoma with signet ring cell features (Figs. 2.270–2.272). Mucus neck cells are normal cellular constituents and, as their name implies, they are mucus secreting cells found at the neck of the gastric pits. Occasionally, these cells become dislodged, dispersed, or crushed, in which case their eccentrically placed nuclei can raise concerns for a signet ring cell adenocarcinoma. In this case, the abused tissue fragment features quite a few dislodged mucus neck cells in the luminal space (Fig. 2.270). Oil immersion is necessary to detect the miniscule nucleoli of mucus neck cells (unlike adenocarcinoma); at this power the nuclear contours are smooth and uniform, the chromatin is fine, and no mitotic figures are seen, all features supporting a benign diagnosis (Fig. 2.271). These cells display cytoplasmic PAS reactivity, but again the nuclear cytologic features are bland (Fig. 2.272). In addition to the histology, the clinical setting is also reassuring&emdash;the biopsy originated from an 8-year-old boy with eosinophilic esophagitis who had an unremarkable endoscopic examination.
SARCINA
Figure 2.273 Sarcina. Luminal debris is often ignored, but this example shows a mixture of Sarcina (arrow) and Micrococcus (arrowheads) organisms. Both Sarcina and Micrococcus can be found in tetrad formations, but Micrococcus grows in dense bacterial micro-colonies clusters and each organism is smaller.
Figure 2.274 Sarcina in a gastric ulcer. These Sarcina tetrads are embedded within a gastric ulcer of a patient with delayed gastric emptying. Treatment of the gastric ulcer, such as with sucralfate, is reasonable given the rare reported cases of emphysematous gastritis and gastric perforation associated with Sarcina.
Sarcina is a Gram-positive anaerobic bacteria with carbohydrate fermentative metabolism as the sole energy source (Figs. 2.273 and 2.274).198 Although the organism is ubiquitous in the environment and is not invasive, Sarcina can cause deadly gaseous bloat in livestock and rare cases of emphysematous gastritis and gastric perforation have been described in humans. The organism is found most commonly in patients with delayed gastric emptying (gastroparesis, nearby mass, obstruction). The presence of an underlying mucosal defect, such as an erosion or ulceration, may predispose patients to more serious sequelae from this otherwise ubiquitous and noninvasive organism. The characteristic tetrad or octet packets of Sarcina organisms are approximately 10 microns across, or the size of a lymphocyte nucleus, and are typically found intermixed with luminal debris. The unusual morphology is the result of cell division in at least two planes of growth, and this morphologic finding is diagnostic for the organism on routine H&E stain. Micrococcus species also forms a tetrad and, consequently, is an important Sarcina mimic. Micrococcus, however, clusters in dense bacterial microcolonies and is considerably smaller (0.5 micron individual compared to Sarcina’s larger three micron size).
FAQ: What are Sarcina treatment recommendations?
Answer: At this time, there are no recommended guidelines for Sarcina treatment. In patients without underlying mucosal defects, there is no evidence to show that eradication of the bacteria with antibiotics is effective or necessary. Because the organism can be found in vegetable matter, air, soil, and the feces of healthy humans, it is unlikely that Sarcina causes injury in the absence of an underlying mucosal defect; however, treatment of any underlying mucosal erosion or ulceration, if present, would be reasonable. The role of antibiotics in humans has not been fully investigated.
BEZOAR AND OTHER FOREIGN MATERIAL
Figure 2.275 Trichobezoar. This is a gross photograph of a hair bezoar removed from the stomach of a patient who was ingesting hair.
A “bezoar” is a ball of swallowed foreign material that collects in the stomach and fails to pass through the intestines (Fig. 2.275). Common examples include hair, fiber, food, or medication. Often, these are recognized at the time of endoscopy and are simply documented as a gross finding. Occasionally, however, undigested material can pose unusual challenges by mimicking other disease entities (Figs. 2.276and 2.277). An important histologic clue to look for is whether there is tissue reaction or inflammation, the absence of which should raise suspicion that the findings may represent inert luminal debris.
Figure 2.276 Ingested mushroom. These fungal hyphae were seen in the duodenal biopsy of a patient who had undergone bone marrow transplantation for chronic lymphocytic leukemia. In the clinical setting of immunosuppression, it is reasonable to consider an fungal infection; however, the endoscopic impression was that of foreign material, such as ingested food.
Figure 2.277 Ingested mushroom. Lower power of previous figure. The lack of tissue invasion and tissue inflammation is a strong indicator that the fungal elements in the field are not pathogenic. Indeed, further investigation revealed this patient had an omelet with mushrooms prior to endoscopy.
MAST CELL DISEASE
Figure 2.278 Gastric involvement by systemic mastocytosis. At scanning magnification, this gastric oxyntic mucosa might appear to have a mere superficial erosion (arrow); however, this patient has a significant past medical history for systemic mastocytosis.
Figure 2.279 Gastric involvement by systemic mastocytosis. Higher magnification corresponding to the area of “erosion” seen in previous figure. Even with the knowledge of the patient’s clinical history, and high-power examination, this case is challenging on routine H&E stain.
Figure 2.280 Gastric involvement by systemic mastocytosis. Oil immersion 100× photomicrograph of mast cells within the “erosion” seen in previous figures. The mast cells have clear to eosinophilic granular cytoplasm with centrally located nuclei. These mast cells show some nuclear atypia with mild hyperchromasia and spindle cell morphology.
Figure 2.281 Gastric involvement by systemic mastocytosis (CD117 immunostain). A CD117 immunostain of the case shown in the previous figure highlights clusters of mast cells in the area of erosion.
Figure 2.282 Gastric involvement by systemic mastocytosis (CD25 immunostain). A CD25 immunostain of the case shown in the previous figures shows aberrant expression within the mast cells. This presence of mast cell clusters in an extracutaneous site that express CD25 fulfills the criteria for diagnosis of systemic mastocytosis (World Health Organization: one major and one minor criterion).
Mastocytosis refers to a group of disorders characterized by excessive mast cell accumulation in one or multiple tissues (Figs. 2.278–2.280).199–201 Involvement of neoplastic mast cells in the gastrointestinal tract fulfills one major criterion of the World Health Organization (WHO) diagnostic criteria for systemic mastocytosis. In addition, abnormal expression of CD2 or CD25 by immunohistochemistry in these cells satisfies one minor criterion and fulfills the diagnosis of systemic mastocytosis (Figs. 2.281 and 2.282).
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