Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Lymphopenia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1995

Steroid resistant nephrotic syndrome associated with spondyloepiphyseal dysplasia, transient ischemic attacks and lymphopenia.

Focal segmental glomerulosclerosis, nephrotic syndrome and chronic renal failure were associated with spondyloepiphyseal dysplasia, growth failure, lymphopenia and transient ischemic attacks leading to severe neurological symptoms in three children. Two boys and one girl developed the full syndrome at the age of 5, 6 and 10 years. Positron emission tomography revealed perfusion defects of both cerebral and cerebellar arteries. A variant of the disease was found in two other children who had a nephrotic syndrome and terminal renal failure with only mild spondyloepiphyseal dysplasia, impaired growth and a normal cerebral function. It is concluded that there may be a close association between focal segmental glomerulosclerosis and spondyloepiphyseal dysplasias.

Brain↗
PubMed1994

[Mechanisms of lymphopenia in HIV infection].

Blood counts of CD4 cells remain the best prognostic factor in patients infected with human immunodeficiency virus (HIV). However, the small number of infected cells contrasts with the importance of lymphocyte depletion. Several mechanisms might explain this depletion including: antibody-dependent cytotoxicity. Twenty to 50% of the antibodies produced in vitro by B lymphocytes are directed against HIV antigens, especially the gp120 and gp41 viral envelope antigen. If this cytotoxicity effect occurs in vivo, it could reduce of lymphocytes carrying the viral genome and partially explain the major lymphopenia in HIV-infected patients. It is not yet known whether the long-term effect of these antibodies is immunoprotective or deleterious, but they may play a protective role at least in the initial stages of the disease. autoimmunity. Sequence homology between the HLA II molecules and the glycoproteins of the viral envelope has been clinically and biologically documented in many manifestations of HIV infection. It has been suggested that alloreactivity, similar to the graft-versus-host reaction could be involved. In addition, programmed cell-death of the CD4 lymphocytes appears to be overactivated in HIV-positive subjects, possibly because the gp120 viral antigen perturbs the CD4-dependent signal for cell death. deleterious effects of cytokines. Tumour necrosis factor, for example, is known to play a role in the regulation of viral replication; it may favour the destruction of contaminated cells but also the initiation of provirus replication and integration into the cell genome. supra-antigens and/or infectious factors. Supra-antigenes, which can link with HLA molecules, are capable of oligoclonal activation without being "processed" in the cell presenting the antigen. This activation might affect cell death. Certain germ toxins could also play a role as cofactors. Cohort studies of asymptomatic HIV patients are needed to improve our understanding of these mechanisms. A therapeutic approach tailored to the stage reached by HIV-infected subjects will then be possible.

AIDS-Related Opportunistic Infections↗
PubMed1996

A flowcytometric study of CD4+ & CD19+ cell lymphopenia in patients with alopecia areata.

Twenty five patients with alopecia areata and 20 healthy controls were studied by flowcytometry employing direct two colour immunofluorescence in erythrocyte lysed whole blood. A significant reduction was observed in helper/inducer (CD4+) lymphocytes (29.4 +/- 7.4 vs 39.45 +/- 8.0, P < 0.01) and B (CD 19+) lymphocytes (11.04 +/- 6.57 vs 15.0 +/- 5.05, P < 0.01) in comparison with healthy controls. Decrease in T-lymphocytes (CD3+) and suppressor/cytotoxic (CD8+) was not significant and activated (HLADR+) lymphocytes and natural killer cells (CD16+ and CD56+) were within normal limits. Our findings suggest a significant T helper (CD4+) and B (CD19+) cell lymphopenia in alopecia areata.

Adolescent↗
PubMed1976

Influenza: response of T-cell lymphopenia to thymosin.

Eighteen volunteers in tow study groups were inoculated with influenza A (H3N2) and their peripheral blood T, B and null cells enumerated at subsequent intervals. Infection with wild-type virus or with a live, attenuated virus vaccine markedly reduced the proportion and absolute number of T-cell rosettes 24 hours after inoculation. T-Cell depression preceded the onset of clinical illness in symptomatic subjects, continued during illness, and returned to normal with recovery. T-cell lymphopenia was most pronounced in volunteers infected with wild-type virus and was accompanied by an increase in null cells. Lymphocytes from six wild-virus recipients with T-cell leukopenia were incubated in vitro with a calfthymus extract (thymosin), significantly increasing the percentage of T rosettes in all six subjects (P less than 0.0001). These data indicate that influenza is accompanied by pronounced quantitative and functional changes in T cells.

Adult↗
PubMed2002

Close link between CD4+ and CD8+ T cell proliferation defects in patients with human immunodeficiency virus disease and relationship to extended periods of CD4+ lymphopenia.

T cell proliferation failure is commonly associated with human immunodeficiency virus (HIV) infection. By examining T cell function on a single-cell basis, we found that CD4(+) T cell proliferation failure was often accompanied by CD8(+) T cell proliferation defects in patients with HIV disease. The defects are characterized by a proportional failure and reduced efficiency of precursor T cell proliferation after stimulation. In this study, patients who historically had low levels of circulating CD4(+) T cells were most likely to demonstrate cellular proliferation failure, regardless of current CD4(+) T cell counts. In contrast, neither historical nor current plasma HIV RNA levels were predictive of proliferation failure. These results suggest that mechanisms of T cell proliferation failure are more complex than can be explained by the direct effects of HIV replication and that therapeutic intervention to avoid prolonged periods of CD4(+) lymphopenia may be desirable for the preservation of immune function in patients with HIV disease.

CD4 Lymphocyte Count↗
PubMed2000

Docetaxel-induced lymphopenia in patients with solid tumors: a prospective phenotypic analysis.

BACKGROUND: The quantitative abnormalities of the different peripheral blood lymphocyte subsets during docetaxel administration were prospectively studied. METHODS: Forty-six chemotherapy-naive patients with solid tumors were treated with docetaxel either in a 3 weekly (n = 33) or weekly (n = 13) schedule. Twenty patients with central nervous system (CNS) metastatic disease as the first clinical presentation of cancer and 35 patients with metastatic colorectal carcinoma treated with chemotherapy were enrolled as controls. The phenotype of peripheral blood lymphocytes was determined by indirect immunofluorescence using appropriate monoclonal antibodies and fluorescent-activated cell sorter analysis. RESULTS: After the administration of the first docetaxel cycle, the absolute number of peripheral blood lymphocytes (P < 0.005), CD3(+) (P < 0.01), CD4(+) (P < 0.01), CD8(+) (P < 0.01), and CD56(+) (P < 0. 01) but not CD20(+) (P < 0.3) cells was significantly decreased compared with the pretreatment values. Further treatment resulted in a further decrease of these lymphocyte subsets including CD20(+) cells (P < 0.01). Similarly, after the administration of the first weekly dose of docetaxel, the absolute number of total lymphocytes, CD3(+), CD4(+), and CD8(+) cells was decreased. The administration of the second weekly docetaxel dose resulted in a further decrease of CD56(+) (P = 0.012) and CD20(+) (P = 0.007) cells. The administration of either high dose corticosteroids in patients with CNS metastases or an irrelevant chemotherapy (CPT-11/5-FU) did not result in similar abnormalities. The discontinuation of docetaxel was associated with a recovery of CD3(+) and CD4(+) lymphocytes within a 3-month period. Eight (17%) patients developed nonneutropenic infections during docetaxel treatment. CONCLUSIONS: Docetaxel has an important but reversible nonspecific lymphopenic effect that seems to be associated with an increased risk for nonneutropenic infections.

Adult↗
PubMed2001

Early death and severe lymphopenia caused by ubiquitous expression of the Rag1 and Rag2 genes in mice.

The recombination activating proteins (RAG1 and RAG2) are essential for V(D)J recombination of immunoglobulin chains. Expression of both genes is lymphocyte-specific and RAG levels are tightly regulated throughout lymphopoiesis and cell cycle. To assess the significance of this pattern of expression, we generated transgenic mice expressing the Rag genes both continuously throughout lymphocyte development and constitutively in most non-lymphoid tissues. The transgenes partially complement an endogenous Rag2 null mutation and lead to a partial block in early B and T lymphopoiesis when introduced on a Rag2 sufficient background. The defect in thymocyte number is restricted to the alpha beta lineage leaving the gamma delta T cell pool intact, while neither IgH phenotypic allelic exclusion nor the kappa/lambda light chain ratio are altered. Finally, the ectopic expression of the Rag genes associates with growth retardation and early death of the animals, a phenotype reminiscent of those reported for mice deficient in double-strand break repair molecules.

Alleles↗
PubMed2003

Early lymphopenia as a risk factor for chemotherapy-induced febrile neutropenia.

Febrile neutropenia (FN) is a frequent complication of cancer chemotherapy, which causes death in 4-21% of patients and worsens the quality of life of patients. As a simple and accurate way of identifying patients who are at risk of FN, a lymphocyte count on post-chemotherapy day 5 was suggested. To confirm the feasibility of this method and to define the incidence of FN among our own patient group, we conducted this prospective study. From September 2001 to February 2002, patients who received cytotoxic chemotherapy at Guro Hospital, Korea University, were enrolled. Blood sampling for a complete blood count was done on the starting day of chemotherapy and on day 3 and day 5 post-chemotherapy. The prospective results of the CBC were compared between the FN group and non-FN group. During the study period, 82 patients were enrolled. The male to female ratio was 52:30, and the median age was 56 years old (range: 14-78). Underlying malignancies were non-Hodgkin's lymphoma (14 patients), stomach cancer (17), breast cancer (11), NSCLC (7), hepatobiliary cancer (10), sarcoma (3), colorectal cancer (3), and others (17). The incidence of FN was 18% (15/82 patients), and ANC at the time of FN was 275 +/- 327/ micro l. Duration of fever was 3.9 +/- 3.5 days. The incidence of FN was significantly higher in patients with lymphocyte counts at day 3 < or = 500/micro l (P = 0.06), day 5 < or = 500/micro l (P = 0.023), day 3 < or = 700/micro l (P = 0.01), and day 5 < or = 700/micro l (P = 0.0001). As a result of a logistic regression test, a day-5 lymphocyte count < or = 700/ micro l was identified as an independent risk factor for FN. In conclusion, a day-5 lymphocyte count <700/micro l was a risk factor for FN. To strengthen our result, we are planning to validate in a larger patient group.

Adolescent↗
PubMed1998

T lymphopenia in genetically obese rats.

Although obese animals are more susceptible to infection, the underlying causes are not fully known. In this study, long-term measurements were made of lymphocyte subsets in peripheral blood, spleen, and thymus in genetically obese Zucker (fa/fa) rats. Blastogenic response of splenocytes to mitogens was also examined. fa/fa rats developed obesity, hyperlipidemia, and hyperinsulinemia after 5 weeks of age. Flow cytometric analysis revealed that T cells in peripheral blood, spleen, and thymus were all reduced significantly in obese rats after 8 weeks of age compared to nonobese (Fa/-) littermates. All T-cell subsets examined, including CD4+ and CD8+ T cells, were similarly reduced in spleen and thymus as well as in peripheral blood with advance in age. In addition, proliferative responses of splenocytes to mitogens were significantly low in obese rats. These results indicate that long-term obesity may reduce the size of the T-cell pool and impair the responsiveness of splenocytes in rats.

Animals↗
PubMed1996

High viral load and CD4 lymphopenia in rhesus and cynomolgus macaques infected by a chimeric primate lentivirus constructed using the env, rev, tat, and vpu genes from HIV-1 Lai.

Chimeric primate lentiviruses composed of SIV and HIV genes may allow the analysis of the role of these discrete HIV genes in viral pathogenesis in macaque monkeys. We have constructed a chimeric virus in which the env, rev, tat, and vpu genes of HIV-1 Lai replace the env, rev, and tat genes of the SIVmac239 genome. This virus, SHIVsbg, replicates efficiently in rhesus (Indian and Chinese subspecies) and cynomolgus monkeys with viral loads in PBMC and lymph nodes of up to one infected cell per 30 cells during the acute phase of the infection. Sera from all monkeys recognize specific HIV-1 glycoproteins. The onset of lymphadenopathy in all animals was concurrent with a depletion of CD4 lymphocytes in peripheral blood. The virulence of this SHIV for rhesus and cynomolgus monkeys therefore closely parallels that of HIV-1 for human in the acute phase of the infection. Changes in the env and vpu genes of a molecular clone of HIV-1 can now be analyzed after passage in nonhuman primate species as the SHIVsbg replicates efficiently. The SHIVsbg-macaque model is an important step in the development of a readily available animal model for HIV-1 vaccine studies.

Animals↗