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Biomedical subjects

K Washington

Publications and source records attributed to K Washington.

At least 37 records · Page 2Linked to original sources

Peribiliary vascular plexus in primary sclerosing cholangitis and primary biliary cirrhosis.

The peribiliary vascular plexus plays an important role in physiology of bile flow. Disturbance of the microcirculation may contribute to ductal injury, but little is known about alterations in the vascular supply of small bile ducts in liver disease. Immunoperoxidase stains for vascular endothelium (Ulex europaeus, factor VIII-related antigen, CD34) were used to study the peribiliary vascular plexus in 20 cases of primary sclerosing cholangitis (PSC) and 27 cases of primary biliary cirrhosis (PBC), two diseases characterized by bile duct destruction. Normal liver from 10 autopsy cases of sudden cardiac death was used as a control. Interlobular bile ducts (20- to 80-microm diameter) were identified on AE1/AE3 immunostain; vessels adjacent to the basement membrane of these ducts were counted. Normal interlobular bile ducts had an average of 2.15 vessels per duct (range, 1.68 to 2.71). Few PBC or PSC cases had a normal number of peribiliary vessels. There was a trend toward vasopenia at higher stage, although vascular loss was noted in early stages as well. The pattern of vascular loss was different for the two diseases; in PSC, the periductal capillaries were often preserved but were pushed away from the basement membrane by concentric deposits of collagen. Small residual vessels could be identified within fibrous scars of obliterated bile ducts in PSC. In 4 stage 3 or 4 PSC cases with little bile duct injury, vessel/duct ratio approached normal levels. In PBC, vessels were obliterated in areas of granulomatous inflammation and heavy lymphocytic infiltrate around bile ducts. In conclusion, loss of peribiliary vessels is common in PSC and PBC. Vessel loss is seen in early stages and may contribute an element of ischemia to continued small bile duct loss but is probably secondary to the inflammatory process.

Bile Ducts↗

Gastric graft-versus-host disease: a blinded histologic study.

Acute graft-versus-host disease (GvHD) of the upper gastrointestinal (GI) tract is common after allogeneic bone marrow transplantation (BMT). However, diagnosis cannot be made on clinical presentation and endoscopic findings alone, because these are nonspecific, and histologic confirmation is often desirable. The diagnosis of gastric GvHD is often based on subtle findings with considerable potential for variability in interpretation. Evaluation of the reproducibility of diagnosis and recognition of histologic features of gastric GvHD was based on blinded review of 56 gastric biopsies (24 from patients with allogeneic BMT or unrelated umbilical cord blood transplantation and 32 control biopsies from patients who did not undergo BMT, of whom eight had active GI cytomegalovirus [CMV] infection). Histologic criteria for GvHD were apoptosis and gland destruction, sparse inflammatory infiltrate, and granular eosinophilic debris in dilated glands. Seventeen patients (22 biopsies) were judged to have clinical GvHD on the basis of skin or liver involvement and GI symptoms without other known cause. Eighteen of these 22 gastric biopsies were classified as GvHD by at least two of the three pathologists on initial review. Blinded histologic diagnosis of GvHD had a positive predictive value of 69%, a sensitivity of 82%, and specificity of 76%. False-positive results occurred in CMV gastritis, human immunodeficiency virus (HIV) infection, primary immunodeficiency, and after renal transplantation. Of individual features, granular debris in glands was a specific (94% specificity), but insensitive (41% sensitivity) marker for GvHD. Distinction between GvHD and CMV infection can be difficult, and GvHD can be confused with changes seen in HIV infection and other immunodeficiency states.

Adolescent↗

Expression of cell adhesion molecule CD44 in primary tumors of the liver: an immunohistochemical study.

CD44, a widely distributed integral membrane protein, has been implicated in tumor invasion and metastatic spread in some human carcinomas and lymphomas. In this study, 35 cases of hepatocellular carcinoma from 32 patients (11 cholangiocarcinomas, 9 hepatic adenomas, and 5 cases of focal nodular hyperplasia, a non-neoplastic lesion) were examined by immunohistochemical methods for expression of CD44. The mouse monoclonal antibody A3D8 was used on formalin-fixed, paraffin-embedded tissue; this antibody does not distinguish between standard CD44 and splice variants. Positive membrane staining was seen in 13 of 35 cases of hepatocellular carcinoma (12 of 32 patients), 8 of 11 cases of cholangiocarcinoma, and 1 of 9 cases of hepatic adenoma. The strongest staining for CD44 was seen in two cases of fibrolamellar carcinoma, but CD44 expression was otherwise not related to degree of tumor differentiation. All five cases of focal nodular hyperplasia were negative for CD44. In non-neoplastic liver, hepatocytes were negative; sinusoidal lining cells and portal lymphocytes were positive; bile ducts and proliferating bile ductules were focally positive in some cases. Anatomic stage at time of presentation was similar in both groups of patients, with most patients presenting with stage III or IV disease. A trend towards slightly longer survival in patients whose hepatocellular carcinomas were CD44 negative was noted. These results show that aberrant CD44 expression is present in a subset of hepatocellular carcinomas and in most cholangio-carcinomas. The relationship between CD44 expression and tumor spread is unclear in this group of tumors, but is unlikely to be a simple association between CD44 expression and metastatic potential.

Adenoma, Liver Cell↗

Gastrointestinal pathology in patients with common variable immunodeficiency and X-linked agammaglobulinemia.

Review of the medical records of 43 patients with common variable immunodeficiency (CVID) and 23 patients with X-linked agammaglobulinemia (XLAG) revealed a high incidence of chronic gastrointestinal complaints, most commonly diarrhea. Thirty-eight biopsies, four small-bowel resection specimens, and one autopsy from 10 patients with CVID and one patient with XLAG showed a wide range of abnormalities. A pattern resembling acute graft-versus-host disease, with apoptotic bodies and lymphocytes in crypts, was seen in the stomach (four patients), small bowel (three patients), and colon (three patients). Small-bowel specimens from three CVID patients with malabsorption showed mild to severe villous atrophy. Three CVID patients had Giardia in biopsies. Two cases of small bowel lymphoma associated with nodular lymphoid hyperplasia were identified in CVID patients. One patient's small bowel contained foamy histiocytes in the lamina propria, resembling Whipple's disease or chronic granulomatous disease, with numerous apoptotic bodies in crypts. Ultrastructurally, the histiocytes contained cellular debris. The patient with XLAG had recurrent fissuring necrosis of small bowel resembling Crohn's disease; a patient with CVID had colitis with features similar to ulcerative colitis. Poorly formed granulomas were seen in the stomach (one CVID patient) and the colon (two CVID patients). Lymphocyte populations were dominated by T cells; B cells were scarce except in lymphoid follicles in CVID patients with nodular lymphoid hyperplasia. Patients with CVID and XLAG manifest a spectrum of abnormalities in the gastrointestinal tract, with patterns superficially resembling graft-versus-host disease, inflammatory bowel disease, and Whipple's disease, but often lacking some of the diagnostic features of the diseases. Many of the CVID patients with chronic gastrointestinal complaints (62%) also had evidence of autoimmune phenomena, suggesting that in some patients the inflammatory process in the gastrointestinal tract has an autoimmune component.

Adolescent↗

Endoscopic tattoo agents in the colon. Tissue responses and clinical implications.

Laparoscopic surgery frequently requires tattooing of endoscopically identified sites for localization during surgery. Some tattooing agents cause serious tissue injury, which must be recognized in pathologic examination. Seven surgically resected colons were reviewed after injection with methylene blue or India ink at intervals of 1 day to 7 weeks before surgery. Early reactions to India ink included necrosis, edema, and neutrophilic infiltration in the submucosa and muscularis propria. Vessels were inflamed but without fibrinoid necrosis. Early reactions to methylene blue included ischemic ulceration, necrosis, and eosinophilic infiltration in the submucosa as well as fibrinoid necrosis of vessel walls. In the repair of methylene-blue injury, obliterative intimal fibrosis was seen in vessels. Such changes were absent in the colons injected with India ink. The India ink remained remained visible with the naked eye and microscopically 7 weeks after injection. Methylene blue was not grossly visible 7 days after injection, and only microscopic particles of pigment remained in widely scattered macrophages. In light of these findings, the amount of ink injected should be minimized and the injection site should be completely resected at surgery. Methylene blue is a poor tattoo agent, but its occasional use continues, and pathologists should recognize the resulting reaction.

Adipose Tissue↗

Expression of p53 in adenocarcinoma of the gallbladder and bile ducts.

Point mutation of the p53 tumor suppressor gene appears to be an important event in tumor development and progression, and overexpression of the p53 gene product has been widely studied in a variety of neoplasms. Some point mutations of the p53 gene lead to an increase in half-life in the gene product, which accumulates in the nucleus and can be detected by immunohistochemical means. We studied overexpression of p53 protein in specimens from 12 patients with adenocarcinoma of the gallbladder, two gallbladders with epithelial dysplasia without carcinoma, eight carcinomas of the common bile duct, 13 hilar cholangiocarcinomas, and six peripheral cholangiocarcinomas. The monoclonal antibody Ab-2 (Oncogene Science) was used in conjunction with citrate microwave antigen retrieval. Nuclear staining was scored as positive (graded 1 to 3, depending on number of positive nuclei) or negative. Overexpression of p53 protein was present in 7/12 (58%) gallbladder carcinomas, and was seen more often in moderately or poorly differentiated tumors. Intramucosal carcinoma adjacent to invasive carcinoma was positive in three cases, although fewer cells stained than in the carcinoma. Two cases of low-grade dysplasia not associated with carcinoma were negative. Expression of p53 was not an independent prognostic factor when survival was related to grade and stage of tumor. Three of eight (38%) common bile duct carcinomas and 5/13 (38%) hilar cholangiocarcinomas were positive for p53. Slightly fewer (2/6, 33%) peripheral cholangiocarcinomas were positive. No difference in survival relative to p53 expression was demonstrated.

Adenocarcinoma↗

Anaplastic renal cell carcinoma following neuroblastoma.

Renal cell carcinoma is unusual in children. We report a case of anaplastic renal cell carcinoma arising in a 7-year-old girl following treatment for Stage III neuroblastoma. The renal cell carcinoma has unusual histologic and ultrastructural features, which are discussed. The case is further unusual in that few children with advanced stage neuroblastoma survive long enough to develop second malignant neoplasms.

Anaplasia↗

Secondary tumors of the gastrointestinal tract: surgical pathologic findings and comparison with autopsy survey.

Secondary tumors of the gastrointestinal (GI) tract are unusual but are probably more common than clinically suspected. Comparison of surgical pathologic findings and autopsy experience over a 14-yr period revealed a different spectrum of tumors, which may reflect clinical practice issues and the pathophysiology of individual tumors. Seventy-three surgical resection or biopsy cases with clinically evident secondary tumors were compared with 108 autopsy cases with secondary malignancies involving the GI tract. The most common tumors in surgical specimens were melanoma (22 cases), ovary (11 cases), bladder (eight cases), breast (six cases), and lung (five cases). The most common primary tumors at autopsy were lung (21 cases), gynecologic malignancies (18 cases), breast (14 cases), and pancreas (nine cases). In most cases, routine histologic examination yielded clues to the primary tumor. Metastatic breast carcinoma cases had a high potential for misinterpretation because most metastases consisted of infiltrating strands of pleomorphic cells without gland formation. Signet ring cells were present in most metastases (all six surgical cases and seven of 14 autopsies), regardless of the histologic type of the primary breast carcinoma. The time from diagnosis of the primary tumor to development of GI involvement varied widely, from presentation with GI metastases to more than 30 yr for metastatic malignant melanoma. Survival after development of GI involvement was generally poor, with most patients surviving less than 1 yr. However, long-term palliation may be achieved in a small subset of patients, chiefly those with single small bowel deposits of malignant melanoma or patients with breast carcinoma responsive to tamoxifen.

Adenocarcinoma↗

Tetracycline-induced bile duct paucity and prolonged cholestasis.

Acute self-limited liver disease has been associated with tetracycline use. However, severe prolonged cholestatic hepatitis and bile duct paucity have not been previously attributed to tetracyclines. Hepatitis, characterized by prolonged jaundice, severe pruritus, and moderate increased transaminase values, occurred within 2 months of ingesting tetracyclines in two female patients. Serum bilirubin levels normalized 12 and 34 months after tetracycline ingestion. Liver histology revealed bile duct paucity, severe cholestasis, and minimal necrosis and inflammation. Tetracyclines may infrequently induce bile duct paucity and prolonged, severe, and reversible cholestasis.

Adult↗

Pathology of the pancreas in severe combined immunodeficiency and DiGeorge syndrome: acute graft-versus-host disease and unusual viral infections.

Review of autopsies of 28 children with severe combined immunodeficiency (SCID) or combined immunodeficiency (CID) and three with DiGeorge syndrome showed a high incidence of acute graft-versus-host disease (GVHD) in the pancreas. Acute GVHD (seven cases: four SCID, two CID, and one DiGeorge syndrome) was characterized by lymphocytes around large to medium ducts, damage to ductal epithelium (focal necrosis, reactive nuclear changes, inspissated secretions in duct lumens), and periductal edema. Changes were judged indeterminate but suspicious for GVHD when ductal damage was slight (six cases: three SCID, two CID, and one DiGeorge syndrome). All patients with pancreatic GVHD had received allogeneic bone marrow, fetal liver or thymus transplant, or nonirradiated blood products and had evidence of GVHD in other organs. Immunoperoxidase stain for HLA-DR showed strong-to-moderate staining of duct epithelium in two of four GVHD cases for which blocks were available. This change was nonspecific; weaker staining for HLA-DR was seen in cases with nonspecific abnormalities and in viral pancreatitis. Four cases had histological evidence of viral infection: two had cytomegalovirus pancreatitis, one had patchy parenchymal necrosis caused by adenovirus, and one had giant cell pancreatitis caused by parainfluenza virus. Mild nonspecific changes, such as focal fat necrosis or acinar dilatation, were seen in seven cases. One case had unexplained marked pancreatic atrophy and fibrosis. Acute pancreatic GVHD is not uncommon in autopsies of children with congenital immune deficiencies with GVHD of other organs; however, this finding may not have strong clinical implications in this group of patients. Careful attention to pancreatic ducts is necessary for diagnosis. Unusual viral pancreatitis may also be seen in this group, as well as nonspecific abnormalities.

Bone Marrow Transplantation↗

Expression of the cell adhesion molecule CD44 in gastric adenocarcinomas.

CD44, an integral membrane glycoprotein expressed by many cell types, serves as the principal transmembrane hyaluronate receptor and may be a determinant of metastatic and invasive behavior in carcinomas. The expression of CD44 in 23 gastric adenocarcinoma and 12 peptic ulcer disease (PUD) resection specimens and gastric carcinoma cell lines HS746t and KATO III was examined by immunohistochemistry using the murine monoclonal antibody A3D8 on formalin-fixed, paraffin-embedded tissue or cells. Western blot analysis of whole cell lysates of KATO III and HS746t cells showed protein bands at 85 to 90 kd with KATO III cells expressing an additional band at 145 kd. In normal stomach gastric epithelium was negative. In PUD foveolar epithelium was focally positive, but staining did not correlate with the extent of gastritis. In carcinoma cases intensity of staining was progressively stronger comparing intestinal metaplasia with dysplasia with intramucosal carcinoma. Invasive carcinoma was invariably more strongly positive than dysplasia or intramucosal carcinoma. Twelve adenocarcinomas were weakly positive and 11 were strongly positive. The staining intensity of metastases (12 cases) was the same or weaker than the primary tumor. For the 12 patients whose carcinomas were weakly positive, mean length of survival for the six who died was 23.3 months. Five of the 11 patients whose carcinomas strongly expressed CD44 died within the study period with a mean length of survival of 11.0 months. A key consequence of CD44 overexpression in gastric carcinomas may be development of the invasive phenotype and strong expression may indicate a poorer prognosis.

Adenocarcinoma↗

Tissue culture of epithelium derived from Barrett's oesophagus.

Barrett's oesophagus is a preneoplastic condition in which the squamous mucosa of the oesophagus is replaced by columnar epithelium. Epithelial cells of Barrett's oesophagus were isolated from resected oesophagus specimens by two methods not previously applied to the culture of Barrett's oesophagus cells. These techniques included trypsinisation of small fragments of mucosa, followed by plating in tissue culture dishes, and a direct tissue explant technique. A modified MCDB-153 growth medium was used. Primary trypsin technique cultures were plated on uncoated plastic, or plastic coated with type I collagen, type IV collagen, or fibronectin. Growth on type IV collagen and fibronectin plates was slower but produced less contamination from fibroblasts. By 20-40 days most cultures formed confluent monolayers made up of cells with epithelial morphology. The cells were cytokeratin positive, vimentin negative, and contained alcian blue positive vacuoles, confirming their epithelial origin and suggesting their derivation from Barrett's oesophagus. Electron microscopy showed tonofilaments, microvilli, and desmosomes. Cells proliferated through up to eight subcultures before growth slowed and cells showed senescent changes. This study shows that epithelial cells from Barrett's oesophagus can be grown by comparatively simple tissue culture techniques. These methods can provide sufficient material for a variety of molecular biology and biochemical studies of epithelial cells from Barrett's oesophagus.

Barrett Esophagus↗

Hepatic adenoma: MR characteristics and correlation with pathologic findings.

OBJECTIVE: The purpose of this study was to describe the MR appearance of hepatic adenomas and correlate the MR imaging features with pathologic findings. MATERIALS AND METHODS: MR examinations were performed in 14 patients with 66 hepatic adenomas. The diagnosis of hepatic adenoma was proved pathologically in nine patients (22 lesions). In five other patients (44 lesions), who had type I glycogen storage disease and were known to be at risk for hepatic adenomas, the diagnosis was established by repeated sonographic examinations that showed stability, reduction, or resolution of hepatic tumors. T1- and T2-weighted spin-echo MR images obtained at 1.5 T were retrospectively reviewed for the signal intensity of the lesions relative to liver, the signal pattern, the presence of a capsule, and the presence of hemorrhage. Histopathologic specimens (22 lesions) were reviewed for fat content (graded 0-3), the presence of a capsule, and the presence of hemorrhage. RESULTS: On T1-weighted images, 51 (77%) of 66 lesions were hyperintense, 11 (17%) were hypointense, and four (6%) were isointense with respect to liver. On T2-weighted images, 49 (74%) of 66 lesions were hyperintense, 12 (18%) were isointense, and five (8%) were hypointense. Sixty-one (92%) of 66 lesions were heterogeneous. Eleven (17%) of 66 lesions were hemorrhagic. Of the 22 lesions reviewed histopathologically, 17 were hyperintense on T1-weighted images; 15 of these had a fat content of grade 2 or 3 and two had hemorrhage. All 15 lesions that had a fat content of grade 2 or 3 were hyperintense on T1-weighted images. CONCLUSION: Hepatic adenomas have a variable MR appearance but most often are hyperintense with respect to liver on T1- and T2-weighted images. The high signal intensity often relates to the increased fat content of these lesions.

Adenoma, Liver Cell↗

CT of the liver in patients with metastatic breast carcinoma treated by chemotherapy: findings simulating cirrhosis.

OBJECTIVE: Although the hepatotoxic effects of systemic chemotherapy are well known, CT findings in the liver after systemic chemotherapy have received little attention in the literature. In some patients with breast carcinoma metastatic to the liver who have received chemotherapy, a morphologic pattern develops similar to that associated with cirrhosis. This pattern is characterized by a lobular hepatic contour, segmental volume loss, and enlargement of the caudate lobe. The purpose of this study was to describe the CT appearance of this pseudocirrhosis and to correlate it with pathologic findings. MATERIALS AND METHODS: We reviewed 65 CT examinations of 22 patients with stage IV breast carcinoma with hepatic metastases, who were receiving systemic chemotherapy and for whom abdominal CT scans showed pseudocirrhosis. Nineteen of 22 patients had follow-up CT scans at intervals ranging from 1 to 15 months. Criteria for the diagnosis of pseudocirrhosis included a lobular hepatic contour, segmental volume loss, and enlargement of the caudate lobe. CT findings were correlated with pathologic findings in seven patients. RESULTS: In all patients, CT scans showed retraction of the capsular surface of the liver (15 diffuse, seven focal) with a lobular margin, a finding also seen in advanced cirrhosis. The retraction occurred at the site of subjacent metastases. Findings evolved over 1-3 months. Six of seven patients had pathologic findings suggestive of nodular regenerative hyperplasia. No patients had pathologic evidence of cirrhosis. CONCLUSION: In patients undergoing systemic chemotherapy for breast cancer metastatic to the liver, a pattern may develop that mimics the CT appearance of hepatic cirrhosis. Pathologic findings suggest nodular regenerative hyperplasia as a possible cause.

Adult↗

Pathology of the pancreas in bone marrow transplant patients.

Review of 51 autopsy cases of patients receiving high-dose chemotherapy followed by bone marrow transplantation revealed a high prevalence of pancreatic ductal and acinar changes compared with control groups. Forty-five percent (23 of 51) of bone marrow transplant cases had squamous metaplasia of the pancreatic ducts compared with 10% of randomly selected control cases. Although squamous metaplasia was more common in bone marrow transplant patients receiving chemotherapy, it was not associated with whole body radiation, allogeneic transplantation, or specific drugs. Squamous metaplasia was more common in patients dying 30 days or more after transplantation. Dilatation of the pancreatic acini was present in 78.4% of transplant cases, 35.0% of control cases, and 50.0% of a group of 12 breast cancer patients treated with conventional doses of chemotherapy without bone marrow transplantation. This lesion was associated with uremia. Oncocytic change of the acinar epithelium was present in 52.9% of transplant cases, no control cases, and 41.7% of breast cancer cases. Squamous metaplasia of the pancreas is common in bone marrow transplant patients receiving high-dose chemotherapy and may be a late manifestation of toxic injury to the ducts. A high prevalence of acinar dilatation was associated with terminal uremia. Oncocytic change of acinar epithelium was associated with chemotherapy.

Adult↗

Nodular regenerative hyperplasia in partial hepatectomy specimens.

To investigate possible associations of nodular regenerative hyperplasia (NRH) with antitumor chemotherapy, we reviewed 72 partial hepatic resections (55 with metastatic tumor, 12 hepatocellular carcinomas, and five benign neoplasms). Thirty autopsy livers from adults without malignancies served as controls. Studies included hematoxylin and eosin, reticulin, and trichrome stains and immunostaining for proliferating cell nuclear antigen (PCNA). Five of 72 livers (7%) had NRH. All five patients had received chemotherapy, one by intrahepatic artery infusion. Four had received chemotherapy 2 months or less before undergoing partial hepatectomy. These five cases represented 15% of the 33 patients who received chemotherapy. No NRH was seen in autopsy control livers. In contrast to NRH, multiple hyperplastic foci were seen in 28 of 72 livers (39%). This finding did not correlate with chemotherapy. Two of 30 control livers (7%) showed similar mild regenerative changes. In only one case of NRH was PCNA staining increased over controls. A band of PCNA-positive hepatocytes was seen adjacent to the tumor in 21 cases, suggesting that the presence of tumor may cause a local increase in PCNA expression. Mitoses in hepatocytes and assessment of the thickness of liver cell plates were more sensitive indicators of regeneration than PCNA. Vascular changes, such as sinusoidal fibrosis (11 of 72 cases), thickened hepatic arterioles (13 of 72 cases), and mild thickening of central veins (10 of 72 cases), did not correlate with NRH, hyperplastic foci, or chemotherapy. No cases of hepatoportal sclerosis were identified.

Adenocarcinoma↗

Gastrointestinal cryptococcosis.

Cryptococcal infection of the gastrointestinal (GI) tract is rarely reported, either in disseminated disease or as an isolated finding. We report a case of gastric cryptococcal infection diagnosed by endoscopic biopsy as the initial presentation of the acquired immunodeficiency syndrome (AIDS), and an additional seven cases found by reviewing 23 other autopsy cases of disseminated or pulmonary cryptococcal infection. The patient with gastric cryptococcosis was a 38-year-old man who presented with symptoms of gastroesophageal reflux including odynophagia. Upper GI endoscopy showed Candida esophagitis and gastric nodules. Biopsy of the nodules revealed cryptococcal infection and granulomatous inflammation of the fundic mucosa and submucosa. The patient died 3 weeks later despite anti-fungal therapy. Autopsy revealed widespread cryptococcal infection involving the cecum but not the stomach, suggesting that the gastric lesions resolved with therapy. The sites of infection in the seven other cases were esophagus (three), stomach (one), terminal ileum (one), colon (three), gallbladder (one), and in a focus of Kaposi's sarcoma in the wall of the small bowel (one). Esophageal candidiasis was also present in two of the cases of esophageal cryptococcal infection. Predisposing factors were AIDS (3), hematologic malignancy (3), and corticosteroid therapy (1). In summary, we report a case of gastric cryptococcosis and conclude that cryptococcal infection involves the GI tract more commonly than has been previously reported, with 8/24 (33%) cases positive in our autopsy series. Of clinical significance is the observation that GI cryptococcal infection may be the initial presentation of disseminated disease in the immunocompromised patient, and cryptococcal infection of the esophagus may be found in the setting of esophageal candidiasis.

Acquired Immunodeficiency Syndrome↗