5 research outputs found
Prolonged lymphocytosis as the first manifestation of Hodgkin-like adult T-cell leukemia/lymphoma
Hodgkin-like ATLL is a rare variant of adult T-cell leukemia/lymphoma (ATLL), a disease caused by human T-cell lymphotropic virus type-1 (HTLV-1). At admission, a 46-year-old female presented with lymphadenomegaly, lymphocytosis, slight elevation of LDH blood level, and acid-alcohol resistant bacilli in sputum and was being treated for pulmonary tuberculosis (Tb). She had lymphocytosis in the previous 20 months. Serology for HTLV-1 was positive. Lymph node was infiltrated by medium-sized lymphocytes with scattered Hodgkin and Reed-Sternberg-like cells CD30+, CS1-4+, and CD79a+. Background cells were CD4+ and CD25+. A clinical diagnosis of favorable chronic ATLL was given. She was treated with chemotherapy but later progressed to acute ATLL and ultimately died. Hodgkin-like ATLL should be considered in the histological differential diagnosis with Hodgkin lymphoma since treatment and prognosis of these diseases are distinct. It is also important to search for HTLV-1 infection in patients with unexplained prolonged lymphocytosis. Keywords: Adult T-cell leukemia/lymphoma, HTLV-1 infection, Pulmonary tuberculosis, Hodgkin-like ATL
Cellular analysis of cutaneous leishmaniasis lymphadenopathy: insights into the early phases of human disease.
Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2014-03-17T17:07:05Z
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Bomfim G Cellular analysis....pdf: 160243 bytes, checksum: 7473c415ca2c57947a0d2f0c249d9e2d (MD5)Made available in DSpace on 2014-03-17T17:07:05Z (GMT). No. of bitstreams: 1
Bomfim G Cellular analysis....pdf: 160243 bytes, checksum: 7473c415ca2c57947a0d2f0c249d9e2d (MD5)
Previous issue date: 2007Hospital Universitário Professor Edgard Santos. Serviço de Imunologia. Salvador, BA, BrasilHospital Universitário Professor Edgard Santos. Serviço de Imunologia. Salvador, BA, BrasilFundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, BrasilFundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, BrasilFundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil / Instituto de Investigação em Imunologia. Instituto do Milênio. Salvador, BA, BrasilFundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil / Instituto de Investigação em Imunologia. Instituto do Milênio. Salvador, BA, BrasilLymphadenopathy is an early clinical sign in cutaneous leishmaniasis (CL), caused by Viannia parasites, and may help to understand the initial host response to these species of Leishmania. We report on characteristics of cells obtained from lymph nodes from cutaneous leishmaniasis patients with lymphadenopathy without ulceration (early phase, N = 21) or lymphadenopathy and ulceration (late phase, N = 29). Early-phase patients exhibited a higher proportion of neutrophils, eosinophils, and CD8+ T cells. Conversely, CD19+ B lymphocytes and plasma cells were more frequently observed in late-phase patients. The signal for IL-10 was significantly higher in late-phase patients; signals for IFN-gamma or IL-4 were similar in both groups. These data reinforce observations of an initial mixed Th1-Th2 profile as well as the early role of the CD8 T cell in cutaneous leishmaniasis. Additionally, there is a chronologic relationship between ulcer development and B-cell increase. IL-10 also increases at a late stage and may be important in limiting tissue damage
ßS-Haplotypes in sickle cell anemia patients from Salvador, Bahia, Northeastern Brazil
Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2012-12-13T17:11:00Z
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Gonçalves, M.S. BS-haplotypes in sickle....pdf: 585067 bytes, checksum: cb0d25b2f356bbb59ad509d85a02d8a8 (MD5)Made available in DSpace on 2012-12-13T17:11:00Z (GMT). No. of bitstreams: 1
Gonçalves, M.S. BS-haplotypes in sickle....pdf: 585067 bytes, checksum: cb0d25b2f356bbb59ad509d85a02d8a8 (MD5)
Previous issue date: 2003Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.Secretaria de Saúde do Estado da Bahia. Fundação Hemocentro da Bahia. Salvador, BA, Brasil.Secretaria de Saúde do Estado da Bahia. Fundação Hemocentro da Bahia. Salvador, BA, Brasil.Hospital Professor Edgar Santos. Salvador, BA, Brasil.Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.Faculdade de Farmácia. Laboratório de Biologia Molecular. Salvador, BA, Brasil.Faculdade de Farmácia. Laboratório de Biologia Molecular. Salvador, BA, Brasil.Universidade Federal da Bahia. Instituto de Matemática. Salvador, BA, Brasil.Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.ßS-Globin haplotypes were studied in 80 (160 ßS chromosomes) sickle
cell disease patients from Salvador, Brazil, a city with a large population
of African origin resulting from the slave trade from Western
Africa, mainly from the Bay of Benin. Hematological and hemoglobin
analyses were carried out by standard methods. The ßS-haplotypes
were determined by PCR and dot-blot techniques. A total of 77
(48.1%) chromosomes were characterized as Central African Republic
(CAR) haplotype, 73 (45.6%) as Benin (BEN), 1 (0.63%) as
Senegal (SEN), and 9 (5.63%) as atypical (Atp). Genotype was CAR/
CAR in 17 (21.3%) patients, BEN/BEN in 17 (21.3%), CAR/BEN in
37 (46.3%), BEN/SEN in 1 (1.25%), BEN/Atp in 1 (1.25%), CAR/Atp
in 6 (7.5%), and Atp/Atp in 1 (1.25%). Hemoglobin concentrations
and hematocrit values did not differ among genotype groups but were
significantly higher in 25 patients presenting percent fetal hemoglobin
(%HbF) ≥10% (P = 0.002 and 0.003, respectively). The median HbF
concentration was 7.54 ± 4.342% for the CAR/CAR genotype, 9.88 ±
3.558% for the BEN/BEN genotype, 8.146 ± 4.631% for the CAR/
BEN genotype, and 4.180 ± 2.250% for the CAR/Atp genotype
(P = 0.02), although 1 CAR/CAR individual presented an HbF concentration
as high as 15%. In view of the ethnic and geographical
origin of this population, we did not expect a Hardy-Weinberg equilibrium
for CAR/CAR and BEN/BEN homozygous haplotypes and a
high proportion of heterozygous CAR/BEN haplotypes since the State
of Bahia historically received more slaves from Western Africa than
from Central Africa
Variation of cytokine patterns related to therapeutic response in diffuse cutaneous leishmaniasis.
Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2015-02-11T17:49:59Z
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Bomfim G Variation....pdf: 147739 bytes, checksum: 7a9c7f1812f8d06b2f66ec0e831c8fdf (MD5)Approved for entry into archive by Ana Maria Fiscina Sampaio ([email protected]) on 2015-02-11T17:50:08Z (GMT) No. of bitstreams: 1
Bomfim G Variation....pdf: 147739 bytes, checksum: 7a9c7f1812f8d06b2f66ec0e831c8fdf (MD5)Approved for entry into archive by Ana Maria Fiscina Sampaio ([email protected]) on 2015-02-11T18:02:08Z (GMT) No. of bitstreams: 1
Bomfim G Variation....pdf: 147739 bytes, checksum: 7a9c7f1812f8d06b2f66ec0e831c8fdf (MD5)Made available in DSpace on 2015-02-11T18:02:08Z (GMT). No. of bitstreams: 1
Bomfim G Variation....pdf: 147739 bytes, checksum: 7a9c7f1812f8d06b2f66ec0e831c8fdf (MD5)
Previous issue date: 1996Universidade Federal da Bahia. Hospital Universitário Professor Edgard Santos. Serviço de Imunologia. Salvador, BA, Brasil.Universidade Federal da Bahia. Hospital Universitário Professor Edgard Santos. Serviço de Imunologia. Salvador, BA, Brasil.Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.Universidade Federal do Maranhão. Faculdade de Medicina. Departamento de Doenças Infecciosas e Parasitárias. São Luis, MA, Brasil.Universidade Federal da Bahia. Hospital Universitário Professor Edgard Santos. Serviço de Imunologia. Salvador, BA, Brasil.Universidade Federal da Bahia. Hospital Universitário Professor Edgard Santos. Serviço de Imunologia. Salvador, BA, Brasil.Diffuse cutaneous leishmaniasis is a rare entity characterized by disseminated cutaneous nodules associated with specific anergy to leishmanial antigens. A low but not absent IFN-gamma expression by cells present in cutaneous lesions has been documented during the active phase of diffuse cutaneous leishmaniasis. In this study we confirm this observation, and extend it by showing a similar pattern in peripheral blood mononuclear cells and the variation of mRNA cytokine expression pattern during different stages of the disease. During active disease, patients did not express mRNA for IFN-gamma, while expressing mRNA for IL-2, IL-4, and IL-10. In contrast, an expression of IFN-gamma and low IL-10 was observed after treatment-induced transient healing of cutaneous lesions. In three patients we have been able to analyze a third PBMC sample obtained after clinical relapse, documenting in all of them decreased IFN-gamma expression with no expression of IL-10. Although there was an association between the appearance of IFN-gamma expression and clinical improvement, with marked expression of IFN-gamma mRNA and decreased expression of mRNA for IL-10 after treatment, this was not sufficient to prevent relapse in these patients. Therefore, it is possible that factors other than the cytokines characteristic of the Th1 and Th2 balance are implicated in the inability of diffuse cutaneous leishmaniasis patients to mount an anti-Leishmania immune response causing clinical improvement