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PubMed2026

Prognostic value of lymphopenia in early breast cancer: learnings from the prospective CANTO cohort.

BACKGROUND: Lymphopenia has been associated with poor outcomes in metastatic breast cancer (BC), but its prognostic relevance in early-stage disease remains unclear. This study aimed to evaluate the prognostic value of baseline lymphopenia in patients with non-metastatic BC using data from the prospective French CANTO cohort (NCT01993498). METHODS: 10,854 patients with baseline absolute lymphocyte count (ALC) were analysed. Lymphopenia was defined as ALC < 1.0 × 10⁹ cells/L, measured before any cancer treatment. Relapse-free survival (RFS), overall survival (OS), and treatment-related toxicities were assessed using Kaplan-Meier estimates, piecewise-Cox regression models, and cause-specific hazard analyses considering pre-specified time periods. RESULTS: Baseline lymphopenia was observed in 342 patients (3.1%). It was associated with ECOG performance status > 0, hypoalbuminemia, and prior neoplasia. Lymphopenia correlated with inferior 5-year RFS (89.1% vs. 92.9%) and OS (92.5% vs. 96.4%). In multivariable analyses, lymphopenia was associated with increased risk of early relapse during the first 24 months (HR = 2.11; 95%CI: 1.28-3.48; p = 0.003), but not beyond, and no independent prognostic impact on OS was observed. No significant differences were found in surgical complications or chemotherapy dose intensity, though granulocyte colony-stimulating factor use was higher among lymphopenic patients. CONCLUSION: Baseline lymphopenia is uncommon in early BC but may serve as a marker of early relapse risk. Although it does not independently predict long-term survival, its presence could reflect underlying tumour aggressiveness or patient frailty. These findings support further investigation of lymphocyte subpopulations to refine prognostic stratification in early BC. TRIAL REGISTRATION: Approved by French ethics committee in 2011 (ID-RCB:2011-A01095- 36,11-039 /NCT01993498 [20FEB2012]).

Adult↗

PubMed1992

The role of lymphocyte production and migration in the lymphopenia caused by 2-acetyl-4-tetrahydroxybutyl imidazole.

2-Acetyl-4-tetrahydroxybutyl imidazole (THI), a component of the food colouring ammonia caramel, has been shown to produce a profound and rapid lymphopenia in peripheral blood in the rat. In order to investigate whether the cause of the lymphopenia was due to the reduced production and influx in the circulation, redistribution of lymphocytes into other lymphoid compartments or an increased cell death, THI (1 mg/kg/day) was given in the drinking water for up to 14 days to F344 rats. A profound depletion of lymphocytes after already 1 day was only found in the blood compartment, whereas no such marked and rapid changes were found in the cellularity of other lymphoid compartments. The proportion and absolute number of DNA-synthesizing cells in each lymphoid organ was quantified using an antibody directed against incorporated 5-bromo-2'-deoxyuridine (BrdU), 1 h after a single BrdU injection. Additionally, enumeration and localization of BrdU+ cells was determined at later time points after a single BrdU injection by flow cytometry and immunocytochemistry, in order to examine the distribution and localization of recently formed (BrdU+) lymphocytes. THI treatment had no effect on the proliferation rate and the distribution of newly formed (BrdU+) cells in the lymphoid organs. However, migration studies revealed that THI treatment resulted in an increased percentage of fluorescein-labelled peripheral blood lymphocytes found in the spleen and bone marrow and a decreased percentage in the cervical and mesenteric lymph nodes, 24 h after injection. Collectively these results indicate that the lymphopenia in the peripheral blood compartment after THI treatment, is caused by a rapid sequestration of lymphocytes into the spleen and bone marrow rather than by a reduced lymphocyte production and release into the periphery. The fact that THI also caused lymphopenia in splenectomized rats, indicates that the spleen does not play an active part in the change in migrational behaviour of lymphocytes after THI treatment. Finally, as there was no increase in the absolute number of lymphocytes found in the spleen or bone marrow it seems they are rapidly degraded.

Administration, Oral↗

PubMed1976

Relationship of lymphocytotoxic antibodies to lymphopenia and parameters of disease activity in systemic lupus erythematosus.

Peripheral blood lymphocyte subpopulations determined in 40 patients with systemic lupus erythematosus, revealed significant lymphopenia in comparison to normal controls. The lymphopenia was caused by decreases in the absolute numbers of both T cells and surface immunoglobulin bearing (SIg) cells. There were significant percentage decreases in T cells and normal percentages of SIg cells, resulting in an increased percentage of "null" cells. The lymphopenia was significantly greater in patients considered to have active disease on the basis of clinical parameters, and was strongly correlated with lymphocytotoxic antibodies, DNA antibodies, and hypocomplementemia. The lymphocytotoxic antibodies were reactive with both T and B lymphocytes from normal and ill donors, human organs, and various lymphoblastoid cell lines. In 30 patients who were followed for up to 22 months, the lymphopenia was clearly seen to develop during, but not before, periods of clinical disease activity, independent of changes in therapy.

B-Lymphocytes↗

PubMed1978

Lymphopenia in systemic lupus erythematosus. Clinical, diagnostic, and prognostic significance.

One hundred fifty-eight patients with active, untreated systemic lupus erythematosus (SLE) were studied from the time of diagnosis. Lymphopenia was present in 75%, and another 18% of those patients developed lymphopenia subsequent to disease reactivation. Lymphopenia of less than 1500 cells/microliter occurred more frequently than any of the preliminary criteria for the classification of SLE, and it was the most prevalent initial laboratory abnormality. Lymphocyte counts were significantly lower in lupus than in the other connective tissue diseases except mixed connective tissue disease and polymyositis.

Adolescent↗

PubMed1979

Lymphopenia and lymphocyte transformation in alcoholics.

The basis of peripheral blood lymphopenia observed in patients with chronic alcoholism and liver disease was investigated by examining the effect of sera of these patients on in vitro transformation of normal human peripheral blood lymphocytes. A positive correlation was demonstrated between the serum inhibition of phytohaemagglutinin- and pokeweed mitogen-induced transformation and the degree of lymphopenia. Thus serum factors may contribute to the observed lymphopenia by inhibiting lymphocyte production in vivo.

Alcoholism↗

PubMed1979

Prognostic significance of lymphopenia in sarcoidosis.

During 1959--67, sarcoidosis were diagnosed in a series of 140 patients. All were followed up and 22 developed chronic sarcoidosis. In 134 patients (20 with chronic course) the initial granulocyte, monocyte and lymphocyte counts were known. No differences in granulocyte values were seen between different groups of sarcoidosis patients. Patients with erythema nodosum had significantly increased monocyte levels. Lymphopenia below 1 000/microliter was seen in only 7.5% of the patients. Lymphocyte counts below 1 500 microliter were a common finding, especially in patients developing chronic sarcoidosis. Significantly decreased lymphocyte values were also seen in patients older than 40 years at the time of diagnosis, in patients negative to 10 TU of PPD and in those with a disease requiring treatment with corticosteroids. A correlation was found between initial lymphopenia and less favourable prognosis, 85% of the patients having a very good prognosis. Patients with initial lymphopenia must be carefully followed up. The initial presence of erythema nodosum does not always guarantee a good prognosis.

Adult↗

PubMed1992

Autoantibodies to T and B cell lines detected in serum samples from patients with systemic lupus erythematosus with lymphopenia and hypocomplementaemia.

Antibodies to lymphocytes in serum samples from 88 patients with systemic lupus erythematosus (SLE) and 15 normal control subjects were examined by a cell enzyme linked immunosorbent assay (ELISA) with four human T and B cell lines as antigens. The antibodies reacted with the Wa B cell line and the T cell lines P12 (CD4-, CD8+), Jurkat (CD4-, CD8-), and Hut78 (CD4+, CD8-). Antibody titres in serum samples from patients with SLE were higher than in those from normal control subjects. Titres of antibodies to P12 were correlated with titres of antibodies to Wa, Jurkat, and Hut78 in serum samples from patients with SLE. IgG antibodies to P12 were associated with lymphopenia and reduced haemolytic complement. By thin layer chromatography immunostaining, the antibodies in serum samples from two of 10 patients with SLE with high titres of IgG antibodies to P12 and lymphopenia were shown to react with three monosialoglycosphingolipids and two neutral glycosphingolipids from P12 cells. Antibodies to lymphocytes in serum samples from patients with SLE react with T and B cell lines, recognise a series of cell membrane glycosphingolipids and are associated with the lymphopenia and hypocomplementaemia typical of active disease.

Adult↗

PubMed1977

Lymphopenia caused by cranial irradiation in children receiving craniospinal radiotherapy.

The peripheral blood changes were studied in 67 children who received craniospinal irradiation for posterior fossa tumors. At the completion of a cranial dose of about 3500 rad to the whole brain port, the lymphocytes were reduced to 858/mm3 rom 3084/mm3 preoperatively. The counts of the remaining leukocytes stayed at a level somewhat higher than preoperatively; the eosinophils rose to 288/mm3 from 125/mm3. With the initiation of the spinal field irradiation, which included a large proportion of the total bone marrow, the numbers of all the leukocytes decreased rapidly; the observed leukopenia was mainly secondary to neutropenia. A mechanism that was operating to restore the number of leukocytes became manifest immediately after the completion of radiotherapy, though the number of lymphocytes had not been totally restored to the preoperative level 6 years later. Irradiation of the lymphocytes that circulate through the vascular bed can explain the lymphopenia observed during cranial radiotherapy. Mild leukopenia observed in patients receiving radiotherapy through a relatively small port may be secondary to lymphopenia, and this does not necessarily indicate impaired bone marrow reserves.

Adolescent↗

PubMedDate not supplied

Association of cold-reactive antilymphocyte antibodies with lymphopenia in systemic lupus erythematosus.

In a prospective study 26 of 29 patients with systemic lupus erythematosus had cold-reactive antilymphocyte antibodies cytotoxic for autologous lymphocytes and lymphocytes from normal subjects. The level of antilymphocyte antibodies was highly correlated, by linear regression analysis, with lymphopenia in these patients. The data suggested that both the avidity and the concentration of these antibodies were important determinants in this relationship. A clear association between increased antilymphocyte antibody activity and exacerbation of SLE was demonstrated. Apart from lymphopenia, however, neither type of clinical manifestation nor any particular serologic abnormality appeared to be related to the presence of antilymphocyte antibodies.

Antibodies↗

PubMed1976

Lymphopenia in Sjögren's syndrome with rheumatoid arthritis: relationship to lymphocytotoxic antibodies, cryoglobulinemia, and impaired mitogen responsiveness.

Lymphocyte subpopulation studies in 21 patients with Sjögren's syndrome and rheumatoid arthritis revealed an absolute lymphopenia and a normal percentage of T- and SIg-cells. In one patient, a large percentage of lymphocytes bore both IgG and IgM; after cell trypsinization only IgM was resynthesized. This surface IgM was capable of binding human IgG, suggesting that the presence of multiple classes of immunoglobulins on the surface of these lymphocytes was due to surface rheumatoid factor activity. Profound lymphopenia was associated with high concentrations of cryoglobulins and the presence of lymphocytotoxic antibodies. These antibodies were broadly reactive, causing cytotoxicity of T- and SIg-cells from normal subjects, from viral and lymphoproliferative disease subjects, from different organs, and SIg-cells from human lymphoblastoid cell lines. Lymphocyte transformation after phytohemagglutinin and pokeweed mitogen stimulation was impaired in comparison to normal subjects. Warm washing of the lymphocytes and purification to greater than 80 per cent T-cells did not restore mitogen responsiveness to normal, suggesting that cell coating by an antibody and diminished responder cell number were inadequate explanations for the impaired transformation.

Antibodies↗

PubMed1991

Administration of IL-7 to mice with cyclophosphamide-induced lymphopenia accelerates lymphocyte repopulation.

Lymphopenia was induced in mice by a single injection of cyclophosphamide. IL-7 or a control protein were administered to the mice twice daily and the cellularity and composition of the spleen, lymph node, bone marrow, and thymus were determined at various time points thereafter. In comparison to the control cyclophosphamide-treated mice, animals receiving cyclophosphamide and IL-7 had an accelerated regeneration of splenic and lymph node cellularity. There was no significant difference in the rate of recovery of the bone marrow and thymus of the control and IL-7-treated mice. Assessment of the pre-B cell compartment revealed a dramatic increase in total pre-B cell numbers in the spleen and bone marrow of the IL-7-treated mice as measured by both flow microfluorimetry and a pre-B cell colony-forming assay. This was followed in a few days by a significant increase in surface IgM+B cell numbers to levels above normal values in both the spleen and lymph node. IL-7 administration to cyclophosphamide-treated mice also resulted in an accelerated recovery of peripheral CD4+ and CD8+ cell numbers in the spleen and lymph node. The numbers of CD8+ cells were increased by twofold over normal levels in cyclophosphamide-treated mice receiving IL-7. Myeloid recovery was determined in cyclophosphamide treated mice by assessing the numbers of CFU-granulocyte-macrophage and Mac 1+ cells. There was no significant difference in myeloid recovery between cyclophosphamide-treated mice receiving IL-7 or control protein. These results suggest that administration of IL-7 after chemical-induced lymphopenia may have therapeutic benefits in shortening the period required to achieve normal lymphoid cellularity.

Animals↗

PubMed1977

Prognostic significance of lymphopenia in pulmonary sarcoidosis.

Since BOTTGER (1966, 1969) AND HOFFBRAND (1968) had described the absolute lymphopenia in pulmonary sarcoidosis as a sign of immune deficiency there were several authors who tried to elucidate different problems of sarcoidosis (RACOVEANU et al. 1970, STOJAN et al. 1971, OSODA et al. 1972). One of these problems is the effort to correlate absolute lymphopenia to prognostic parameters. Three controlled therapeutic trials were performed and compared: 59 cases with clinically and histologically proven sarcoidosis with spontaneous regression and 180 cases with different regimens of prednisolone: --a steady increase of the absolute number of lymphocytes in cases without and with treatment is a prognostically good sign, --no increase or even decrease is a poor sign, -- a very low and unchanged number is worst. This seems to confirm--among other things--that course and prognosis of sarcoidosis really may not be affected by time-limited corticotherapy.

Humans↗

PubMed1991

Pneumocystis carinii pneumonia associated with profound lymphopenia and abnormal T-lymphocyte subset ratios during treatment for early-stage breast carcinoma.

Two women with Stage II breast carcinoma treated with lumpectomy followed by breast irradiation and adjuvant chemotherapy developed Pneumocystis carinii pneumonia while receiving cytotoxic chemotherapy. Neither woman had evidence of immunosuppression before therapy. They both had profound lymphopenia, reversed CD4/CD8 ratios, and normal peripheral blood total leukocyte counts at the time of their infections. Both women were seronegative for human immunodeficiency virus type 1 and had no risk factors for such an infection. The patients' CD4 lymphocyte counts increased after chemotherapy for breast carcinoma was discontinued. Thus, it appears that the therapy they received may have caused severe T-lymphocyte mediated immunosuppression.

Adult↗

PubMed1977

Lymphopenia in acute nitrofurantoin pleuropulmonary reactions.

Each of 5 patients with acute nitrofurantoin pleuropulmonary reactions had profound lymphopenia and 4 had eosinophilia developing early in the clinical course after the drug was withdrawn. The 2 patients tested had only one third of the normal numbers of E rosettes (T lymphocytes) in the peripheral blood during recovery. Lymphoblastic transformation tests with purified nitrofurantoin were done in 3 patients and all of them were negative; responses to phytohemagglutinin, concanavalin A, and pokeweed were decreased but still normal. The diagnosis of various nitrofurantoin hypersensitivity reactions relies on clinical data. The mechanisms of these reactions presently remain unclear.

Adult↗

PubMed1991

Neonatal lethality and lymphopenia in mice with a homozygous disruption of the c-abl proto-oncogene.

The c-abl proto-oncogene, which encodes a cytoplasmic protein-tyrosine kinase, is expressed throughout murine gestation and ubiquitously in adult mouse tissues. However, its levels are highest in thymus, spleen, and testes. To examine the in vivo role of c-abl, the gene was disrupted in embryonic stem cells, and the resulting genetically modified cells were used to establish a mouse strain carrying the mutation. Most mice homozygous for the c-abl mutation became runted and died 1 to 2 weeks after birth. In addition, many showed thymic and splenic atrophy and a T and B cell lymphopenia.

Animals↗

PubMed1991

Testosterone induces lymphopenia in turtles.

Owing to the possible role of sex steroids in the immune-neuroendocrine interactions found in lower vertebrates, we attempted to delineate the effect of testosterone propionate on peripheral blood (PB) and the lymphoid organs of the turtle Mauremys caspica. A single intraperitoneal injection of 200 micrograms/g body weight produced thymic involution and intense lymphopenia in the spleen and, less severely, in the PB compartment. It is suggested that lymphocyte redistribution may occur among the various compartments of the body as the main effect of hormone-induced lymphocyte redistribution, although the mechanism in reptiles and mammals is not yet understood.

Animals↗

PubMed1977

Analysis of treatment in childhood leukaemia. III. Independence of lymphopenia induced by irradiation and by chemotherapy.

Lymphopenia induced by treatment for acute lymphoblastic leukaemia is analysed and discussed in relation to the type and incidence of infection occurring in those patients during complete remission. Blood lymphocytes can be placed into three largely independent groups: (1) those lymphocytes susceptible to long-term depletion following irradiation; (2) those lost from the blood during and for a short period after maintenance chemotherapy with methotrexate and 6-mercaptopurine; and (3) the remainder which are not depleted by irradiation or maintenance chemotherapy. The number of cells in each compartment varies from child to child and probably with age but on average is about 1.2 x 10(9)/1. for group 1, 0.7 x 10(9)/1. for group 2 and 0.4 x 10(9)/1. for group 3. Conventional lymphocyte typing crosses these barriers in that: Group 1 consists mainly of E-rosetting cells and cells which show a mitotic response to phytohaemagglutinin; Group 2 also contains E-rosetting cells but contains a major proportion of blood lymphocytes with surface immunoglobulin and essentially all antibody dependent cytotoxic lymphocyte (K-cell) activity; Group 3 comprises E-rosetting cells and a few immunoglobulin-staining cells.

Antimetabolites, Antineoplastic↗

PubMed1975

Acute lymphopenia, stress, and plasma cortisol.

Plasma cortisol levels were determined in 51 children on admission to hospital for a variety of acute illnesses which were associated with a lymphopenia, and again when the lymphocyte count had returned to normal. The ratio cortisol level/lymphocyte count was much higher in the acute phase of the illness than later when the lymphocyte count had returned to normal. It is concluded that the lymphocyte count is a useful means of detecting an acute stress condition, and the time of return of normal plasma cortisol levels.

Acute Disease↗