Context. A significant portion of colorectal biopsies are performed for evaluation of polyps or polypoid lesions. Accurately identifying these lesions will promote better patient care. Objective. Review of the pathology of major colon polyps and polypoid lesions and highlight the most diagnostically useful features and their molecular biology. Data source. Review of recent literature. Conclusions. Polypoid lesions of the colon can be thought of to be under 3 broad categories: syndromic, mesenchymal, and epithelial.
Russell bodies represent a cellular response to overstimulation of plasma cells, leading to the accumulation of abundant, nondegradable, condensed immunoglobulin in dilated rough endoplasmic reticulum cisternae. Russell body gastritis was first described 1998 by Tazawa and Tsutsumi. Since then only 39 cases involving the gastrointestinal tract have been reported in English literature, which include Russell body gastritis, duodenitis, and esophagitis. We report a case of a 44-year-old female with a history of diabetes mellitus, status post kidney and pancreas transplant who presented with multiple episodes of watery diarrhea associated with abdominal pain, nausea, and vomiting. Upper gastroendoscopic examination showed diffuse mild erythema in the gastric body and a clean-based duodenal ulcer. Lower gastroendoscopic examination was normal. Examination of multiple biopsies from duodenal, gastric, terminal ileum, and colonic mucosae revealed numerous plasma cells with abundant eosinophilic granular cytoplasm (Russell bodies) and eccentric nuclei, highlighted by PAS stain and CD 138 plasma cell marker. Helicobacter pylori stains were performed on gastric biopsies and were negative for organisms. To date, there are no cases described in English literature with multifocal Russell body infiltrates in gastrointestinal tract in a single patient including ileum and/or colon. This makes our case the first to be reported with these unique findings; thus, the spectrum of Russell body-associated chronic inflammation of the gastrointestinal tract would be more suitably referred to as "Russell body gastroenterocolitis."
Introduction: Gastric mucosal calcinosis (GMC) is a rare disorder typically encountered incidentally on routine biopsy or autopsy. Patients may present with dyspepsia and gastrointestinal bleeding. Most cases were reported in end-stage renal disease (ESRD) patients. We present a case of GMC in a patient with iatrogenic hypoparathyroidism. Case Report: A 70 year old female with a history of total thyroidectomy complicated by complete hypoparathyroidism at the age of 22, osteoporosis, hypercalciuria, recurrent nephrolithiasis, and chronic kidney disease (CKD) stage 3 presented to the office with chronic epigastric pain. CKD was attributed to nephrocalcinosis in the setting of hypercalciuria. Her pertinent medications included levothyroxine, calcium supplementation (1.8 g/day), calcitriol, vitamin D3, HCTZ, potassium chloride, and alendronate. She denied alcohol use. Physical exam revealed a hemodynamically stable woman of normal weight, with mild epigastric tenderness and guaiac negative stool. Review of lab results over the previous 5 years was notable for chronic hyperphosphatemia (average, 5.6 mg/dL) and frequent episodes of hypocalcemia; blood creatinine level was 1.4 mg/dL. Endoscopy showed pangastric erythema, a sessile gastric polyp, and a superficial ulcer in the gastric body. Biopsies revealed chronic gastritis (negative for H. Pylori), reactive gastropathy, a hyperplastic polyp, and associated patchy interstitial dystrophic calcifications, consistent with GMC (Figure 1).FigureDiscussion: In ESRD, decreased renal phosphorus excretion leads to hyperphosphatemia, secondary hyperparathyroidism, and hypercalcemia. Ca x PO4 product precipitates in tissues with high intracellular pH, such as gastric epithelium, causing GMC. In contrast, our patient had hypoparathyroidism-related hyperphosphatemia with hypocalcemia. Elevated intraluminal and intraepithelial calcium concentration, created by high-dose oral calcium supplementation, could be the cause of elevated Ca x PO4 product formation in the gastric epithelium. Furthermore, chronic inflammation predisposed gastric mucosa to precipitation of calcium salts, consistent with the known mechanism of dystrophic GMC. While many of the reported cases occurred in the setting of hypercalcemia, we described GMC in a patient with post-surgical hypoparathyroidism and hypocalcemia managed with aggressive oral calcium supplementation. The etiology of GMC remains unclear in many cases.
Russell bodies represent a cellular response to overstimulation of plasma cells, leading to accumulation of abundant, nondegradable immunoglobulins.Russell body gastritis was first described in 1998, and since then, 39 cases of the gastrointestinal tract have been reported including Russell body gastritis, duodenitis, and esophagitis.Herein we report an unusual case of a 44-year-old woman post kidney and pancreas transplant, who showed multifocal accumulation of Russell bodies in the upper and lower gastrointestinal tract.She presented with watery diarrhea, nausea, and vomiting, and underwent upper and lower gastroendoscopic examination that demonstrated diffuse mild erythema in the gastric body and a clean based duodenal ulcer.Examination of multiple biopsies from duodenal, gastric, terminal ileum and colonic mucosae revealed numerous monomorphic cells with abundant eosinophilic granular cytoplasm (Russell bodies) and eccentric nuclei, highlighted by PAS stain and CD 138 plasma cell marker.Concomitant expression of kappa and lambda light chain was seen, supporting polyclonal nature of plasma cell infiltrate.Sections of the gastric mucosa revealed patchy intestinal metaplasia.Helicobacter pylori stain was negative for organisms on duodenal and gastric biopsies.She was treated with replacement of fluids and electrolytes and became symptom free, however was subsequently lost to follow-up.She was recently diagnosed with posttransplant lymphoproliferative disorder involving cervical lymph nodes.Including our case, there are 32 reported cases of Russell body gastritis, 5 cases of Russell body duodenitis, and 2 cases of Russell body esophagitis in literature.To date, there are no reported cases of multifocal Russell body infiltrates in gastrointestinal tract in a single patient including ileum and/or colon.This makes our case the first to be reported with these unique findings, and therefore we establish that spectrum of Russell body associated chronic inflammation in the gastrointestinal tract can be extended to "Russell body gastroenterocolitis."
Abstract This is a case report of ascariasis of the common bile duct in a 65-year-old man from Colombia who had undergone prior cholecystectomy. The patient presented with postprandial epigastric pain and a 20-lb weight loss. The laboratory findings were remarkable for peripheral blood eosinophilia. The ultrasound finding was suggestive of periampullary or pancreatic neoplasm. He underwent endoscopic retrograde cholangiopancreatography with endoscopic extraction of a motile, live worm identified as Ascaris lumbricoides. Roundworm infestation should always be suspected in immigrants from endemic areas who present with hepatobiliary symptoms.
Inflammatory fibroid polyps are rare, benign, tumor-like lesions of the gastrointestinal tract.The lesion was first described by Vanek in 1949.Most frequently, they are localized in the gastric antrum, but can develop anywhere in the gastrointestinal tract.In the small intestine, these polyps cause obstruction-intussusception.Most IFPs are polypoid masses smaller than 5 cm, although sizes up to 20 cm have been reported.We report a case of a 56-year-old man with progressive midabdominal pain and tenderness in left lower quadrant.CT scan of abdomen and pelvis revealed an unusual, tubular, elongated mass causing mild partial obstruction and short segment intussusception.The patient underwent exploratory laparotomy and resection of the mass.Gross examination showed a large, solid, tan-white elongated tumor mass protruding into the small bowel lumen on one side and pushing the serosal surface on the other side.The large luminal portion of the protruding tumor measured 15.0 × 5.5 × 4.0 cm, and the extraluminal portion measured 5.5 × 4.0 cm.Total length of the tumor was 20.5 cm.Multiple sections showed a well-demarcated, nonencapsulated, fibrohistiocytic mass composed of widely spaced, bland, spindled and stellate-shaped cells emdedded in a collagenous fibromyxoid stroma with trapped collagen bundles, eosinophils, and few scattered plasma cells with foci of benign lymphoid aggregates.Immunoperoxidase stains were positive for CD34, vimentin, and CD68 (fibrohistiocytic marker) and negative for c-kit (CD117), actin, desmin, and S-100 protein.There was no histologic evidence of malignancy.The histopathologic features and the immunoperoxidase stains were consistent with a benign, nonneoplastic tumor-like mass, consistent with a giant inflammatory fibroid polyp-tumor-like mass (Vanek tumor).Inflammatory fibroid polyp, a rare, benign lesion of the gastrointestinal tract, arises from the submucosa.The lesion described in the present report is the largest inflammatory fibroid polyp reported to date; it occurred in the ileum, heretofore considered a rare location, and had a marked intraluminal and extraluminal component.
Crohn’s disease is a granulomatous systemic illness with extra-intestinal manifestations. Of these extra-intestinal manifestations, lung involvement (0.4%) is the rare manifestation. Bronchopulmonary signs and symptoms are underrecognized, so suspicion should be high when granulomas are seen in lung biopsies. We report the case of a 27-year-old female who presented with bilateral pleuritic chest pain and shortness of breath. Chest X-ray showed left lung masses measuring up to 3.3 cm in the greatest dimension with right mid lung nodular opacity. Given the possibility of metastatic disease, positron emission tomography CT (PET-CT) scan was done, which showed activity in multiple liver lesions and multiple bilateral lung nodules. Both liver and lung biopsies were done, which showed multiple necrotizing and non-necrotizing granulomas. The patient was discharged home on antibiotics and antifungals. Few months later, she presented with loose stools and abdominal pain. CT scan of the abdomen and pelvis showed diffuse colonic wall thickening concerning for colitis. Colonoscopy showed ulcerated mucosa involving multiple parts of the colon. Biopsy of the colon showed mild to moderate acute colitis with submucosal non-necrotizing epithelioid granulomas, consistent with Crohn’s disease.
Schistosomiasis is a parasitic disease caused by blood flukes (trematodes) of the genus Schistosoma.After malaria and intestinal helminthiasis, schistosomiasis is the third most devastating tropical disease in the world, being a major source of morbidity and mortality for developing countries.More than 207 million people are infected, as their agricultural work and recreational activities expose them to infested water.Snails serve as the intermediary agent between mammalian hosts.Schistosomiasis is not usually seen in the United States.We report a case of a 56-year-old man with no significant medical history, who underwent a routine screening colonoscopy.Colonoscopy was remarkable for 2 sessile polyps in the cecum, measuring 0.1 and 0.3 cm in greatest dimension, and multiple petechiae in the rectum.Polyps were removed, and petechiae were biopsied for histologic evaluation.Sections show noncaseating epithelial granulomas with associated eosinophilic infiltrate surrounding Schistosoma mansoni eggs with the characteristic lateral spine.Immunoperoxidase stains demonstrated positivity for S100, confirming the diagnosis of neuroma/Schwann cell hamartoma, and S mansoni eggs were also present here.It is associated with prominent fibrosis and collagen deposits, particularly in the colon and urinary bladder.Symptoms and signs depend on the number and location of eggs trapped in the tissues.Although it has a low mortality rate, schistosomiasis often is a chronic illness that can damage internal organs.Pathology associated with human schistosomiasis is not directly due to the adult worms but rather the large numbers of eggs that become trapped in tissues during egg migration or after embolism in organs such as the liver, spleen, or lungs.In intestinal form, eggs become lodged in the intestinal wall, and the immune response can lead to obstruction of the colon and blood loss.This is the first reported case in which colonic schistosomiasis is associated with cecal neuroma.
