SNEAKY ADENOCARCINOMA
Figure 3.313 Acute duodenitis with gastric foveolar metaplasia and reactive epithelial change. The clinical impression of a mass lesion inspired deeper sections on this busy-appearing biopsy, although no histologic features of malignancy are readily apparent on this first level.
This case was received as “prominent ampulla, concerning for malignancy” (Fig. 3.313). The initial sections show duodenal mucosa with acute and chronic inflammation, gastric foveolar metaplasia, and marked reactive epithelial change (Fig. 3.313). Although these histologic features can account for a nodular clinical impression, deeper sections were pursued based on the clinical suspicion for malignancy. The first set of deeper sections were similarly concerning, but definitive malignancy was not seen. Deeper sections were repeated. And repeated. And repeated. In this case, the tissue block was exhausted and on the 38th level (!!!), clear lymphovascular invasion and infiltrating adenocarcinoma were seen (Figs. 3.314 and 3.315). When the histology does not fit the clinical scenario, consider deeper sections. When the deeper sections are not conclusive, consider repeat deeper sections or recommend rebiopsy (in this case, the patient was too unstable for a subsequent biopsy).
Figure 3.314 Infiltrating poorly-differentiated adenocarcinoma and lymphovascular space invasion. Deeper sections were performed until the block was exhausted. This photomicrograph represents the 38th (and final) section, which shows desmoplasia, infiltrating adenocarcinoma (arrowheads), and lymphovascular space invasion (asterisk). These deeper sections show an entirely different biopsy compared to the initial sections and were sufficient for chemotherapy initiation.
Figure 3.315 Sneaky adenocarcinoma involving the duodenal mucosa. Under oil immersion, note the nuclear irregularities, abundant pink cytoplasm, and cytoplasmic mucin droplet (arrowhead) characteristic of pancreatobiliary adenocarcinoma. Unfortunately, sometimes 38 levels are required for the ultimate diagnosis and sometimes only a few malignant cells are present! When the clinical scenario and the histology are not aligned, deeper sections (and deeper sections and deeper sections and deeper sections) are often required.
ISOSPORA
Figure 3.316 Isosporiasis. This intermediate power view shows how easy it is to miss Isospora. At low power, only gastric foveolar metaplasia and perhaps a slight increase in lamina propria eosinophils is seen. Other fields of this same case were essentially normal, emphasizing that every biopsy needs a few high power fields of attention for such extremely subtle diagnoses.
Figure 3.317 Isosporiasis. On higher power, a slight prominence of lamina propria eosinophils serves as a red flag to the diagnosis. Arrowheads highlight the Isospora organisms, which are obligate intracellular parasites and are found in the paranuclear or subnuclear cytoplasm.
Figure 3.318 Isosporiasis. On higher power, the Isospora organisms (arrowheads) are seen embedded within the epithelium. Unless the epithelial compartment is diligently inspected in every biopsy, these organisms would almost certainly be missed.
Isosporiasis is among the more common protozoan causes of severe diarrhea in AIDS patients (Figs. 3.316–3.318).190 The Isospora belli organisms are spread via contaminated water or fecal–oral contamination. They localize to the small bowel surface and are exceedingly easy to miss owing to sometimes unremarkable background mucosa and sparsely distributed organisms (Figs. 3.316–3.321). Diagnostic confirmation is facilitated through identification of the oocysts in stool samples or duodenal aspirates.191 Standard therapy consists of trimethoprim–sulfamethoxazole, which is often long term in severely immunocompromised patients.
Cryptosporidia and microsporidia infections can manifest with similar clinical symptoms and are frequent differential considerations, especially on board examinations! Cryptosporidia are small (2 to 5 μm), rounded basophilic structures that attach to the small bowel and pancreatobiliary epithelium (Figs. 3.322–3.326). The organisms can be all too easy to miss on H&E and are best highlighted by Giemsa, silver, or PAS special stains. Microsporidium was recently reclassified from a parasite to a fungus. It is an obligate intracellular organism that is best seen with electron microscopy.
Figure 3.319 Isosporiasis (arrowhead). Oil magnification.
Figure 3.320 Isosporiasis. The Isospora organisms are nested within the duodenal epithelium and have a peripheral clearing (arrowheads) or halo that represents a parasitophorous vacuole only seen during some stages of development.
Figure 3.321 Isosporiasis. The large size of Isospora can help distinguish it from other intracellular protozoa, such as Cyclospora. This Isospora organism is larger than the nucleus of the neighboring enterocyte. Note that the peripheral clearing or halo is still present. Chart review revealed the patient was from Cameroon and presented with diarrhea. He was ultimately determined to have AIDS.
Figure 3.322 Cryptosporidiosis. Cryptosporidiosis is not an infrequent cause of diarrhea in the immunocompromised patient. At low power, the biopsy shows mild villous blunting and crypt hyperplasia. There is neither architectural distortion nor inflammatory injury.
Figure 3.323 Cryptosporidiosis. The histologic “chatter” artifact makes this biopsy difficult, replicating the “real life” issues practicing pathologists routinely face.
Figure 3.324 Cryptosporidiosis. At high power, the characteristic 2 to 5 μm, rounded basophilic structures are seen attached to the small bowel epithelium.
Figure 3.325 Cryptosporidiosis. The organisms are best appreciated at high power, underscoring the difficulty in diagnosis unless “the layers” are diligently inspected in all cases. Although Cryptosporidia are obligate intracellular organisms, they are extracytoplasmic and live within the microvilli of the enterocyte, hence their characteristic surface location.
Figure 3.326 Cryptosporidiosis. The organisms are seen “dancing” on the superficial epithelium. In difficult cases, the organisms can be highlighted by Giemsa, silver, or PAS special stains.
GIARDIA DUODENALIS (GIARDIA LAMBLIA OR GIARDIA INTESTINALIS)
Figure 3.327 Giardiasis. At low power, the duodenal mucosa looks fairly unremarkable, except for the haphazardly arranged luminal debris characteristic of giardiasis. This patient was clinically thought to have an occult malignancy based on the profound weight loss, but all symptoms resolved with Giardiaeradication.
Giardia is the most common intestinal protozoan causing diarrhea in humans (Fig. 3.327).192 Part of the protozoan’s success stems from its ability to infect both the immunocompromised and immunocompetent and its ability to be perpetuated in silent carriers (or asymptomatic patients). This awareness of asymptomatic Giardia infections is important such that one is not misled by a lack of diarrhea&emdash;it happens! Nevertheless, treatment of these asymptomatic cases is critical for prevention of onward spread. The cyst is transmitted via contaminated water or via fecal–oral route, and the flagellated trophozoite adheres to the intestinal epithelium. On duodenal mucosa biopsies, the organisms haphazardly swirl close to the mucosal surface. They can bear such a haphazard arrangement that they can be mistaken for luminal debris to the untrained eye. On closer examination, the trophozoites have been described as clown-faced or pear-shaped based on their peculiar binucleate structure (Figs. 3.328–3.332). Diagnosis can be confirmed with stool smears for the trophozoites or cysts, stool antigen assays, or serologic studies. The only FDA approved treatment is furazolidone (Furoxone),190 although metronidazole is the most common first-line therapy. In the unusual case of recurrent or medically nonresponsive giardiasis, consider the following immunodeficiencies:
Figure 3.328 Giardiasis. On higher power, the Giardia organisms are better visualized (arrowheads). Note that the background mucosa is essentially normal and provides no clues to the infection, making routine inspection for giardiasis critical in every small bowel biopsy. This patient was an avid hiker and likely contracted the organisms by drinking contaminated water or through inadequate hygiene practices.
Figure 3.329 Giardiasis. On highest power, the trophozoites are best seen. Note how the cup-shaped organisms swirl near the duodenal epithelium.
Figure 3.330 Giardiasis. On a busy day, this low power view might seem less than interesting but it underscores that examination of the luminal contents is essential for every biopsy! A bracket highlights the focal collection of Giardia organisms, which are often best appreciated at intermediate power.
Figure 3.331 Giardiasis. This patient had recurrent giardiasis that failed medical management and consequently immunodeficiencies were considered. Although plasma cells were identified, he was ultimately diagnosed with CVID based on abnormal serum immunoglobulin levels. When considering immunodeficiencies related to recurrent giardiasis, it is important to assess for goblet cells and Paneth cells (either can be lost with AIE), plasma cells (up to 67% of those with CVID show a loss of plasma cells), and increased apoptotic bodies (which are a nonspecific feature of various immune-mediated processes).
Figure 3.332 Giardiasis. Higher power shows the cup-shaped forms characteristic of giardiasis.
CHECKLIST: Immunodeficiencies Associated with Giardiasis
IgA Deficiencies
Common Variable Immunodeficiency (CVID)
Autoimmune Enteropathy
IPEX Syndrome (Immunodysregulation, Polyendocrinopathy, Enteropathy, X-Linked Inheritance)
APECED Syndrome (Autoimmune phenomena, Polyendocrinopathy, Candidiasis, and Ectodermal Dystrophy)
X-Linked Agammaglobulinemia
COMMON VARIABLE IMMUNODEFICIENCY
Figure 3.333 Common variable immunodeficiency (CVID). This biopsy originated from a 7-year-old boy with a history of chronic diarrhea. It would be easy to entertain Celiac disease in this case based on the villous blunting, crypt hyperplasia, and intraepithelial lymphocytosis (not appreciated at this power).
Figure 3.334 Common variable immunodeficiency (CVID). Higher power of previous image. At this power, a complete lack of plasma cells is seen. In other fields, prominent apoptotic bodies were also seen, further supporting a pathologic suspicion of CVID. Titration of serum immunoglobulins was diagnostic of CVID and the patient clinically responded to intravenous immunoglobulin administration. Importantly, goblet cells and Paneth cells are seen, making concomitant AIE less likely.
CVID is characterized by hypogammaglobulinemia, a lack of functional plasma cells, impaired response to vaccinations, and chronic infections (including Giardia and bacterial infections) (Figs. 3.333 and 3.334). A lack of plasma cells is helpful, but only seen in two-thirds of cases; identification of plasma cells cannot exclude CVID.144 Therefore, clinicopathologic correlation is essential with titration of serum immunoglobulins serving as an essential component to the diagnosis.
COLLAGENOUS ENTERITIS
Figure 3.335 Collagenous enteritis in a patient with celiac disease. At low power, mild villous blunting and prominent subepithelial collagen are seen. The most common diagnoses linked to collagenous enteritis include collagenous colitis, lymphocytic colitis, and celiac disease. In this case, collagenous enteritis was a manifestation of clinically confirmed celiac disease. The clinical symptoms and histologic changes abated with adherence to a GFD.
Collagenous enteritis can be easily missed at low magnification, particularly since the architectural pattern often remains intact (Fig. 3.335). Remember to spend a moment at higher magnification to routinely inspect all the layers of the small bowel. Doing so may reveal an altered collagen table or otherwise easily missed diagnoses (Figs. 3.336–3.340).
Figure 3.336 Collagenous enteritis in a patient with celiac disease. At higher power, the prominent subepithelial collagen shows an irregular border and contains entrapped capillaries. In addition, moderate villous blunting and a mild prominence of IELs are seen.
Figure 3.337 Collagenous enteritis in a patient with celiac disease.
Figure 3.338 Collagenous enteritis in a patient with collagenous colitis. This case of collagenous enteritis originated from a patient with a history of collagenous colitis and shows a prominent, irregular subepithelial collagen table with entrapped capillaries.
Figure 3.339 Collagenous enteritis in a patient with collagenous colitis.
Figure 3.340 Collagenous enteritis in a patient with collagenous colitis. Prominent entrapped capillaries are seen within the expanded subepithelial collagen table. Note that intraepithelial lymphocytosis can be patchy in collagenous enteritis and is not seen in this field.
SNEAKY NEUROENDOCRINE TUMOR
Figure 3.341 Sneaky neuroendocrine tumor. This biopsy was submitted as a duodenal polyp. At low power, gastric foveolar metaplasia and Brunner gland hyperplasia are seen, findings that could account for the impression of a polyp; however every biopsy deserves closer inspection.
Small bowel biopsies can be treacherous because of all the potential hiding places for sneaky diagnoses (Fig. 3.341). Microscopic neuroendocrine tumors, for example, can be easily obscured by a busy and “abused” small bowel biopsy (Figs. 3.341–3.345) and yet diligent inspection is critical as even microscopic neuroendocrine tumors can behave aggressively. When dealing with a challenging case of crushed and cauterized tissue, consider a chromogranin and synaptophysin immunostain, deeper sections, or ask for a repeat biopsy.
Figure 3.342 Sneaky neuroendocrine tumor. At higher power, the gastric foveolar metaplasia and crushed lymphoid aggregates are better appreciated.
Figure 3.343 Sneaky neuroendocrine tumor. At this power, note the Brunner glands are pushed apart by an expansile process, an alarming finding that deserves close inspection. Brackets highlight pockets of neoplastic cells arranged in nests, suggestive of a neuroendocrine neoplasm. The diagnosis of this sneaky neuroendocrine tumor is particularly challenging in such a busy background.
Figure 3.344 Sneaky neuroendocrine tumor. Higher power. The neoplastic cells (brackets) are poorly preserved, crushed, and could easily be mistaken for crushed lymphocytes if not carefully inspected at higher power.
Figure 3.345 Sneaky neuroendocrine tumor (arc). Alternative field.
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