ABSTRACT
Pulmonary nodular lymphoid hyperplasia is an uncommon reactive lymphoproliferative disorder that presents as an asymptomatic lung mass. The histopathologic diagnosis of pulmonary nodular lymphoid hyperplasia may be challenging because of its morphologic overlap with other diseases, such as extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue and immunoglobulin G4-related sclerosing disease. Despite the similarities, there are distinctive morphologic and phenotypic features that allow for the correct diagnosis in the majority of cases. This review aims to discuss the clinicopathologic features of pulmonary nodular lymphoid hyperplasia and contrast them with its histopathologic mimickers.
Subject(s)
Lymphoproliferative Disorders/pathology , Solitary Pulmonary Nodule/pathology , Adult , Aged , Aged, 80 and over , Chromosome Aberrations , Diagnosis, Differential , Female , Humans , Hyperplasia , Immunoglobulin G4-Related Disease/pathology , Lung/pathology , Lymphoma, B-Cell, Marginal Zone/genetics , Lymphoma, B-Cell, Marginal Zone/pathology , Lymphoproliferative Disorders/genetics , Male , Middle Aged , Solitary Pulmonary Nodule/geneticsABSTRACT
Distant metastasis to the jaws, including the maxilla or mandible, is very rare. Although the mandible is the preferred sight of these rare metastases, it is extremely rare for oral cavity malignancies to present as pathological mandibular fractures. Here, we present a case of esophageal adenocarcinoma metastasizing to the mandible, and the first reported case presenting with a pathological mandibular fracture secondary to esophageal adenocarcinoma. We also review the 9 other reported cases of metastatic esophageal adenocarcinoma to either the maxilla or mandible.
ABSTRACT
BACKGROUND: Complement fixation by donor-specific HLA antibodies (DSA) is a primary mechanism for antibody-mediated damage of organ allografts. Using a recently developed kit that measures C1q binding to distinguish complement fixing and nonfixing antibodies, studies showed that C1q + DSAs have a higher risk of rejection and graft loss compared to C1q-DSA. The objective of this study was to assess the ability of the C1q-binding assay to identify clinically significant de novo DSA in renal transplant recipients and to define the properties of DSA that confer C1q binding ability. METHODS: The DSA-positive sera from 34 kidney recipients, 19 with biopsy-proven antibody-mediated rejection (AMR) + and 15 who were AMR-, were assayed in C1q-binding assays (C1q Screen; One Lambda, Inc. Canoga Park, CA). The correlation between C1q-binding activity, presence of AMR, DSA mean fluorescence intensity (MFI) values, and immunoglobulin G isotype was determined. RESULTS: Fifty-three percent (10/19) of sera from AMR+ patients had C1q + DSA, whereas only 13% (2/15) of sera from AMR- patients contained C1q + DSA. C1q + DSA exhibited significantly higher MFI values regardless of whether they were from AMR+ or AMR- patients (16,118 ± 6698 vs 6429 ± 4003; P < 0.0001). C1q + DSA converted to C1q - when diluted to a comparable MFI level as the C1q - DSA from AMR- patients, and some C1q - antibodies converted to C1q + when concentrated to MFI levels comparable to those observed for AMR+/C1q + sera. CONCLUSIONS: The C1q binding activity by de novo DSA in patients with AMR largely reflects differences in antibody strength. The C1q assay does not appear to distinguish functionally distinct DSA with clinical significance.
