Use of homologous platelet gel to manage refractory diabetic lower extremity ulcers: additional experience at a tertiary hospital.

Background: DLEUs are a major cause of morbidity. Appropriate treatment is essential, and newer methods to achieve ulcer healing have been described, including application of PG.

Objective: This study evaluated the effectiveness and safety of homologous PG in patients with chronic noninfected DLEU refractory to standard treatment as well as possible correlations between patient comorbidities and response to treatment.

Chemokine Receptor Expression on Normal Blood CD56(+) NK-Cells Elucidates Cell Partners That Comigrate during the Innate and Adaptive Immune Responses and Identifies a Transitional NK-Cell Population.

Studies of chemokine receptors (CKR) in natural killer- (NK-) cells have already been published, but only a few gave detailed information on its differential expression on blood NK-cell subsets. We report on the expression of the inflammatory and homeostatic CKR on normal blood CD56(+low) CD16(+) and CD56(+high)  CD16(-/+low) NK-cells. Conventional CD56(+low) and CD56(+high) NK-cells present in the normal PB do express CKR for inflammatory cytokines, although with different patterns CD56(+low) NK-cells are mainly CXCR1/CXCR2(+) and CXCR3/CCR5(-/+), whereas mostly CD56(+high) NK-cells are CXCR1/CXCR2(-) and CXCR3/CCR5(+).

Aggressive mature natural killer cell neoplasms: report on a series of 12 European patients with emphasis on flow cytometry based immunophenotype and DNA content of neoplastic natural killer cells.

We report 12 cases of aggressive natural killer (NK) cell neoplasms diagnosed in Portugal, with emphasis on flow cytometry. Ten patients had extranodal NK/T cell lymphoma, nasal type and two had aggressive NK cell leukemia, and seven were men and five were women, with a median age of 50 years. NK cells brightly expressed the CD56 adhesion molecule and CD94 lectin type killer receptor and had an activation-related HLA-DR+ CD45RA+ CD45RO+ immunophenotype, in most cases.

Chemokine receptor repertoire reflects mature T-cell lymphoproliferative disorder clinical presentation.

The World Health Organization classification of mature T-cell lymphoproliferative disorders, combines clinical, morphological and immunophenotypic data. The latter is a major contributor to the classification, as well as to the understanding of the malignant T-cell behavior. The fact that T-cell migration is regulated by chemokines should, in theory, enable us to identify tissue tropism and organ involvement by neoplastic T-cells by monitoring chemokine receptor surface expression.

Clinicobiological, immunophenotypic, and molecular characteristics of monoclonal CD56-/+dim chronic natural killer cell large granular lymphocytosis.

Indolent natural killer (NK) cell lymphoproliferative disorders include a heterogeneous group of patients in whom persistent expansions of mature, typically CD56(+), NK cells in the absence of any clonal marker are present in the peripheral blood. In the present study we report on the clinical, hematological, immunophenotypic, serological, and molecular features of a series of 26 patients with chronic large granular NK cell lymphocytosis, whose NK cells were either CD56(-) or expressed very low levels of CD56 (CD56(-/+dim) NK cells), in the context of an aberrant activation-related mature phenotype and proved to be monoclonal using the human androgen receptor gene polymerase chain reaction-based assay. As normal CD56(+) NK cells, CD56(-/+dim) NK cells were granzyme B(+), CD3(-), TCRalphabeta/gammadelta(-), CD5(-), CD28(-), CD11a(+bright), CD45RA(+bright), CD122(+), and CD25(-) and they showed variable and heterogeneous expression of both CD8 and CD57.

Atopic dermatitis-like non-erythrodermic leukemic variant of CD3(-/+dim) CD4(+) cutaneous T-cell lymphoma preceded by cutaneous papular xanthomatosis.

We report a patient with cutaneous papular xanthomatosis who 4 years later developed a CD3(-/+dim)/CD4(+) T-cell lymphoma. Pruritic xerotic non-erythrodermic skin, eosinophilia and hyper-IgE were present and erroneously classified as atopic dermatitis. Flow cytometry and DNA ploidy analysis of both blood and skin lymphocytes, skin histology and blood T-cell receptor gene rearrangement studies confirmed diagnosis of T-cell lymphoma.

Utility of flow cytometry immunophenotyping and DNA ploidy studies for diagnosis and characterization of blood involvement in CD4+ Sézary's syndrome.

Background And Objectives: The exact immunophenotypic criteria for the identification of Sézary cells in the blood are still poorly defined.

Design And Methods: We analyzed the immunophenotype and DNA cell content of blood T cells in a series of 18 consecutive cases of Sézary's syndrome (SS), 21 normal individuals and 10 patients with reactive erythroderma, and correlated them with molecular and morphological findings.

Results: Phenotypically abnormal CD3+/TCRalphabeta+/CD4+ T cells were found in all SS patients but in none of the reactive erythroderma cases; small diploid, or less frequently hypodiploid Sézary's cells coexisted with large nearly tetraploid Sézary's cells in some cases.

TCRalphabeta+/CD4+ large granular lymphocytosis: a new clonal T-cell lymphoproliferative disorder.

Large granular lymphocyte (LGL) leukemia is a well-recognized disease of mature T-CD8(+) or less frequently natural killer cells; in contrast, monoclonal expansions of CD4(+) T-LGL have only been sporadically reported in the literature. In the present article we have explored throughout a period of 56 months the incidence of monoclonal expansions of CD4(+) T-LGL in a population of 2.2 million inhabitants and analyzed the immunophenotype and the pattern of cytokine production of clonal CD4(+) T cells of a series of 34 consecutive cases.

Non-cytotoxic gamma-delta peripheral T-cell lymphoma affecting the mandibular and parotidal lymph nodes and the skin.

In contrast to the majority of alphabeta peripheral T cell lymphomas (PTCL), which usually originate in lymph nodes and do not express NK-associated molecules, most gammadelta PTCL express a cytotoxic phenotype and originate at extranodal sites. We report a case of a patient with a gamma-delta PTCL who presented with large mandibular and parotidal lymphadenopathy and skin lesions. CD3(+)/TCR-Vdelta1 (+) lymphoma cells did not express the cell surface (CD11b, CD11c, CD16, CD56 and CD57) and cytoplasmic granule molecules (Perforin and Granzyme B) that usually characterize the cytotoxic T-cells, a phenotype that fulfils the criteria for diagnosis of a rare non-cytotoxic variant of a gammadelta T-cell lymphoma.

Immunophenotype and TCR-Vbeta repertoire of peripheral blood T-cells in acute infectious mononucleosis.

Although a number of studies on the phenotypic changes that occur after T-cell activation have already been published, the specific immunophenotypic features of T-lymphocytes and the frequency at which TCR-variable region (TCR-V) restricted T-cell expansions occur "in vivo" during acute viral infection still remains to be established. We report on the immunophenotype and TCR-V repertoire of peripheral blood T-cells from 28 patients with acute infectious mononucleosis. Immunophenotypic studies were performed by flow cytometry using direct immunofluorescence techniques and stain-and-then-lyse sample preparation protocols with three- and four-colour combinations of monoclonal antibodies directed against a large panel of T- and NK-cell associated markers, activation- and adhesion-related molecules and TCR-Vbeta, -Vgamma and -Vdelta families.

Guess what: Chronic 13q14.3+/CD5-/CD23+ lymphocytic leukemia in blood and t(11;14)(q13;q32)+/CD5+/CD23- mantle cell lymphoma in lymph nodes!

We report a case of a patient with two B-cell lymphoproliferative disorders: CD5(-)/CD23(+) B-cell chronic lymphocytic leukemia and CD5(+)/CD23(-) mantle cell lymphoma. These disorders were diagnosed simultaneously based on flow cytometry, immunohistochemistry, fluorescence in situ hybridization, and polymerase chain reaction-based molecular studies. The B-cell lymphocytic leukemia clone predominated in the blood and bone marrow, whereas the mantle cell clone predominated in lymph nodes.

Abnormal NK cell lymphocytosis detected after splenectomy: association with repeated infections, relapsing neutropenia, and persistent polyclonal B-cell proliferation.

We report the case of a boy with hereditary spherocytosis who presented with mild microcytic hypochromic anemia and recurrent leg ulcers that had been present since childhood. Chronic natural killer (NK) cell and B-cell lymphocytosis was detected 1 year after therapeutic splenectomy during investigation of recurrent episodes of neutropenia and persistent lymphocytosis. NK cells proved to be abnormal at immunophenotyping studies, and B-cells were polyclonal and displayed a normal immunophenotype.

The "ex vivo" patterns of CD2/CD7, CD57/CD11c, CD38/CD11b, CD45RA/CD45RO, and CD11a/HLA-DR expression identify acute/early and chronic/late NK-cell activation states.

To define a dynamic sequence of phenotypic changes related to early and late phases of NK-cell activation, we have analyzed by four-color flow cytometry the immunophenotype of normal blood NK-cells from 12 healthy individuals and compared it with those from 15 patients with acute viral infections and 15 patients with either chronic infections or tumors. Although a great interindividual variability was found, nonstimulated CD56(+) NK-cells, present in normal blood samples, usually were CD2(-/+lo), CD7(+hi), HLA-DR(-), CD11b(+), CD38(+), CD11a(+hi), CD45RA(+hi), and CD45RO(-), the expression of CD11c and CD57 being heterogeneous and variable. Recently activated NK-cells, herein corresponding to NK-cells from patients with acute viral infections, displayed a pattern of expression of CD2/CD7 similar to that referred to above, but they typically showed higher levels of CD11a, CD38, and HLA-DR, as well as downregulation of CD11b and CD45RA, accompanied in some cases by coexpression of CD45RO; in addition, these NK-cells were CD11c(+) and CD57(-/+lo).