Lymphocytic gastritis in a patient with dyspepsia.

Lymphocytic gastritis (LG) is uncommon and presents histologically with a nonspecific inflammatory pattern. It is most often associated with celiac disease and Helicobacter pylori gastritis and is rarely associated with other conditions including lymphoma. LG is of clinical importance since its recognition should prompt further clinical evaluation for other disorders.

Aggressive Epstein-Barr virus-negative B-cell post-transplant lymphoproliferative disorder in a hepatitis C-negative liver transplant recipient who received a hepatitis C-positive graft: Implications for D+/R- hepatitis C virus seroconversion.

Post-transplant lymphoproliferative disorder (PTLD) is an uncommon, but well-described complication after liver transplantation. Most recently, Hepatitis C virus (HCV) has been implicated in the development of PTLD. A HCV-negative 62-year-old man with autoimmune hepatitis received a HCV nucleic acid amplification test-positive liver graft from a 73-year-old brain-dead donor (D+/R-). After his recovery from the operation, the patient was treated for HCV and achieved an undetectable viral load. He was readmitted 6 months after transplant with a spontaneous perisplenic hematoma, weight loss, failure to thrive, low-grade fevers, and abnormal liver function tests. He had a rapid clinical deterioration and expired shortly after admission. His liver biopsy demonstrated EBV-negative monomorphic B-cell PTLD. Our case is the first to report an aggressive early-onset EBV-negative monomorphic B-cell PTLD in a HCV D+/R- liver transplant. This case illustrates the paucity of knowledge on HCV seroconversion and its involvement in EBV-negative monomorphic B-cell PTLD development.

PhenoGraph and viSNE facilitate the identification of abnormal T-cell populations in routine clinical flow cytometric data.

BACKGROUND: Flow cytometric identification of neoplastic T-cell populations is complicated by the wide range of phenotypic abnormalities in T-cell neoplasia, and the diverse repertoire of reactive T-cell phenotypes. We evaluated whether a recently described clustering algorithm, PhenoGraph, and dimensionality-reduction algorithm, viSNE, might facilitate the identification of abnormal T-cell populations in routine clinical flow cytometric data. METHODS: We applied PhenoGraph and viSNE to peripheral blood mononuclear cells labeled with a single 8-color T/NK-cell antibody combination. Individual peripheral blood samples containing either a T-cell neoplasm or reactive lymphocytosis were analyzed together with a cohort of 10 normal samples, which established the location and identity of normal mononuclear-cell subsets in viSNE displays. RESULTS: PhenoGraph-derived subpopulations from the normal samples formed regions of phenotypic similarity in the viSNE display describing normal mononuclear-cell subsets, which correlated with those obtained by manual gating (r2 = 0.99, P < 0.0001). In 24 of 24 cases of T-cell neoplasia with an aberrant phenotype, compared with 4 of 17 cases of reactive lymphocytosis (P = 1.4 × 10-7 , Fisher Exact test), PhenoGraph-derived subpopulations originating exclusively from the abnormal sample formed one or more distinct phenotypic regions in the viSNE display, which represented the neoplastic T cells, and reactive T-cell subpopulations not present in the normal cohort, respectively. The numbers of neoplastic T cells identified using PhenoGraph/viSNE correlated with those obtained by manual gating (r2 = 0.99; P < 0.0001). CONCLUSIONS: PhenoGraph and viSNE may facilitate the identification of abnormal T-cell populations in routine clinical flow cytometric data. © 2017 Clinical Cytometry Society.

Kikuchi disease in Connecticut.

Kikuchi disease is a self-limited disorder of unknown etiology characterized by focal painful lymphadenitis, fever, and weight loss that can be mistaken for malignancy. Diagnosis is established by node biopsy. Kikuchi disease is endemic in Asia; 10 cases have been reported in the US to date. We report 3 cases and review other US cases.

Unique pattern of nuclear TdT immunofluorescence distinguishes normal precursor B cells (Hematogones) from lymphoblasts of precursor B-lymphoblastic leukemia.

Normal precursor B cells or hematogones share morphologic and immunophenotypic similarities with lymphoblasts of precursor B-lymphoblastic leukemia. The numbers are often increased and difficult to distinguish in many patients following chemotherapy for precursor B-lymphoblastic leukemia. The purpose of this study was to establish a unique method for differentiating hematogones from lymphoblasts by evaluating the immunofluorescence pattern of nuclear terminal deoxynucleotidyl transferase (TdT) staining in 29 cases of TdT+ acute leukemia and 20 cases with increased numbers of hematogones. All 29 cases of TdT+ acute leukemia demonstrated a finely granular pattern of TdT immunofluorescence that was uniformly distributed in the nucleus, whereas all 20 cases with increased hematogones demonstrated a coarsely granular or speckled pattern of TdT immunofluorescence, which often intensely aligns the nuclear membrane. The nuclear pattern of immunofluorescence using antibodies to TdT is an effective method for distinguishing hematogones from leukemic blasts.

A novel mutation in exon 5 of the ALAS2 gene results in X-linked sideroblastic anemia.

BACKGROUND: Mutations in the erythroid-specific 5-aminolevulinate-synthase gene (ALAS2) have been identified in many cases of X-linked sideroblastic anemia (XLSA). METHODS: A polymerase chain reaction-mediated restriction fragment length polymorphism (RFLP) assay was used. RESULTS: A G527T point mutation was identified. This resulted in a substitution of tyrosine for asparagine at residue 159 (D159Y). This mutation was also identified in the mother of the two probands. Mutations in all three individuals were confirmed by DNA sequencing analysis. CONCLUSIONS: We identified a missense mutation in exon 5 of the ALAS2 gene in two brothers of a consanguineous marriage, who were clinically pyridoxine-responsive.