Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 30-year-old man with recurrent sinopulmonary infections, eventually fatal, was found to have common variable immunodeficiency. In addition to low serum immunoglobulin concentrations he also had lymphopenia and cell-mediated immunodeficiency as shown by cutaneous anergy and a poor lymphocyte response to phytohemagglutinin (PHA) in vitro. However, intradermal injection of PHA produced a vigorous cutaneous response, showing that some cell-mediated responsiveness remained. The responsiveness of his lymphocytes to PHA was restored towards normal (confirmed by chromosome studies) by the addition of a small number of normal leukocytes to cultures; thus a reversible functional defect in his T-lymphocytes was revealed. Experiments indicated that the defect was cellular and not due to serum factors and it was concluded that normal leukocytes restored a missing factor to the patient's T-lymphocytes. Although counts of macrophage precursor cells in the bloodstream were low, thus contributing to the immunodeficiency, this could not have caused the reduced PHA response. Several relatives of this patient had lymphoma; two cousins had common variable immunodeficiency.
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PMID:Reversible dysfunction of T-lymphocytes in common variable immunodeficiency. 14 Jul 58

Myasthenia gravis and lymphoma rarely coexist, but the occurrence of myasthenia shortly after the treatment of a patient with poorly differentiated nodular lymphoma suggested that an immunological disorder may have contributed to the development of both diseases; the fundamental defects in this association may be impaired immunological surveillance and impaired regulation of immune responses to autoantigens. The finding of T-cell immunodeificiency, including profound T-cell lymphopenia, impaired delayed hypersensitivity responses, and failure to a thymus-dependent antibody response to Salmonella adelaide flagellin, is consistent with this hypothesis.
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PMID:Myasthenia gravis and lymphoma. A clinical and immunological association. 31 93

Seventy-one previously untreated patients with non-Hodgkin lymphomas were studied with several readilyvailable tests of immune function: number of peripheral blood lymphocytes, serum immunoglobulins, and delayed hypersensitivity to six recall antigens. The results were correlated to histology (Rappaport classification), stage (Ann Arbor classification), the presence of symptoms, and survival. As a group, 38 patients with diffuse lymphomas exhibited marked impairment in reactivity to five of six antigens (p less than 0.03 to p less than 0.001). In addition, lymphopenia and reduced levels of serum IgA were found in association with diffuse histiocytic lymphoma. Among patients with diffuse lymphoma, lymphocyte number and skin test reactivity tended to be greater in those with localized disease or without constitutional symptoms, and survival was superior for patients free of symptoms (p less than 0.01). As a group, 33 patients with nodular lymphoma had normal numbers of lymphocytes, lower levels of serum IgG and IgA, and significant impairment of reactivity to two antigens (streptokinase-streptodornase and mumps; p less than 0.01); reactivity to three other antigens (Candida albicans, coccidiodin, and tuberculin) was normal. Survival for patients with nodular lymphoma was superior (p less than 0.01) compared to those with diffuse lymphomas. In summary, severe immunodeficiency was found in patients with diffuse lymphoma (particularly diffuse histiocytic lymphoma), and definite but much less severe immunodeficiency was characteristic of patients with nodular lymphoma.
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PMID:Immunodeficiency in patients with non-Hodgkin lymphomas. 31 45

We have looked at the effect of in vivo cortisone acetate treatment on effector cells for antibody-dependent cell-mediated cytotoxicity in mice and rats, using both chicken erythrocytes and the mouse lymphoma cell line AKR.A as target cells, since the AKR.A cell line is susceptible to antibody-dependent cell-mediated cytotoxicity killing only by the lymphoid effector cell, whereas a wide variety of effector cells will lyse chicken erythrocytes in the presence of antibody. The lymphoid K cell, detectable in rat spleen and blood, was unaffected by steroid treatment sufficient to cause lymphopenia, whereas splenic anti-chicken erythrocyte cytotoxicity of whole spleen and of phagocyte-free spleen was depressed in mice and rats. The greatest suppression was seen with nonphagocytic mouse spleen, and may have been in part attributable to steroid-induced redistribution of the effector cell(s), since the cytotoxic capacity of nonphagocytic bone marrow cells was increased by 70% at a time when the activity in spleen was 25% of normal.
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PMID:Effect of cortisone acetate on effector cells for antibody-mediated cytotoxicity in mouse and rat. 61 83

Results are given of investigations of E rosettes in patients with chronic lymphadenosis and malignant lymphoma. The quantity of E rosettes was expressed both as per cents and in absolute numbers calculated from the total amount of lymphocytes in peripheral blood. In the normal controls the percentage of E rosettes was 58% on average while in patients with chronic lymphadenosis it was found to have decreased significantly down to a mean of 6%. However, in absolute values the number of rosette forming lymphocytes was normal and even higher. In the group with malignant lymphoma the percentage decrease was less striking than in those with chronic lymphadenosis, however, the absolute number of rosette forming lymphocytes was always found to be lowered because of evident to considerable lymphopenia. A dynamic study of the observed changes might contribute to a knowledge of the pathophysiology of lymphoproliferative diseases.
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PMID:E rosettes in lymphoproliferative diseases. 108 61

Current knowledge concerning the course of mycosis fungoides and recognized prognostic factors have been reviewed. Those factors with prognostic significance at the time of biopsy diagnosis include age and the clinical findings of skin tumors, ulceration or palpable lymphadenopathy. During the course of disease, the development of skin tumors, ulceration or palpable lymphadenopathy were each associated with a poor prognosis and median survival was only 12 months if all those clinical parameters were present. Patients who developed overt visceral mycosis fungoides rarely survived more than a few months. Lymphocytopenia and the presence of malignant lymphoma in biopsied lymph nodes were also poor prognostic findings. The various modalities of therapy for proven mycosis fungoides were reviewed. Topical therapy and external irradiation were generally of symptomatic benefit only, but two recent studies have shown that aggressive use of topical nitrogen mustard and electron beam therapy are associated with long-term responses in patients with disease confined to the skin. Single agent chemotherapy often resulted in transient responses in advanced and refractory mycosis fungoides. Future approaches to the management of mycosis fungoides have been suggested. These include a thorough review of the histological features, a thorough and systematic pretreatment evaluation and randomized studies of the various treatment modalities including combination therapy in appropriately staged patients.
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PMID:Management of mycosis fungoides--current status and future prospects. 109 Jul 96

Blood findings at diagnosis, in 140 adults with lymphoma, were correlated with bone marrow involvement and survival. An abnormal haemoglobin, leucocyte count or platelet count was found in 57% of patients. Lymphocytopenia occurred in 46%. All patients with thrombocytopenia or neutropenia, 69% with leucopenia and 63% with anaemia had marrow involvement with lymphoma. Marrow involvement in histiocytic and stem cell lymphoma was always associated with anaemia. Marrow involvement in poorly differentiated lymphocytic lymphoma (PDL) was associated with anaemia, thrombocytopenia, leucopenia, lymphocytopenia or lymphoma cells in the blood in 93% of patients. Bone marrow involvement was found in only 13% of patients with normal haematological parameters. In the absence of marrow involvement blood abnormalities at diagnosis did not generally correlate with survival. However, among patients with diffuse PDL who had marrow involvement, anaemia, thrombocytopenia and leucopenia adversely affected survival. Lymphocytopenia did not correlate with survival.
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PMID:Significance of haematological parameters in the non-Hodgkin's malignant lymphomas. 125 24

Sixty-five cases of malignant lymphoma of the nose, paranasal sinuses and hard palate were retrospectively analysed to identify the presence or absence of angiocentric lesions. We observed that the 23 patients with angiocentric lesions had a worse prognosis with a shorter duration of response and also a shorter duration of survival, compared with 42 cases of malignant lymphoma of the same anatomical region but without angiocentric lesions. Patients with angiocentric lymphoma were associated with other bad prognostic factors such as elevated levels of lactic dehydrogenase and beta 2 microglobulin, local bone destruction and lymphopenia. Immunophenotyping studies showed that most patients with angiocentric lesions had T cell lymphomas (18 of 23, 78 per cent). We believe that patients with angiocentric T cell lymphomas of the nose, paranasal sinuses and hard palate represent a distinctive clinico-pathological entity with different clinical presentation and outcome. Patients with angiocentric T cell lymphomas had frequent relapse at extranodal sites and combined therapy should be considered as the initial therapeutic approach.
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PMID:Angiocentric T-cell lymphoma of the nose, paranasal sinuses and hard palate. 139 10

Leukemia inhibitory factor (LIF) is a multi-potential cytokine which has been implicated in the hematopoietic regulatory machinery. For example, we have found that LIF is constitutively expressed in marrow stroma. Other investigators have reported that LIF affects remodeling of bone, and that, in concert with other growth factors, it stimulates hematopoietic stem cell proliferation. Moreover, in vivo animal trials reveal that, at high doses, administration of LIF induces myelosclerosis whereas, at lower doses, megakaryocytosis and thrombocytosis with reduced bone marrow cellularity and marrow lymphopenia are observed. Therefore, the role of LIF in the pathogenesis of myeloproliferative disorders such as myelofibrosis and sclerosis merits investigation. Further, its megakaryocytic stimulatory properties suggest that LIF may be exploitable in the clinic to enhance platelet production.
Leuk Lymphoma 1992 Sep
PMID:The modulatory hematopoietic activities of leukemia inhibitory factor. 149 63

There have been six different phase I trials of Fludara I.V. (fludarabine phosphate) in patients with solid tumors and three different phase I trials of Fludara I.V. in patients with acute leukemia. In addition, one trial of the agent given intraperitoneally has also been published. In patients with solid tumors, the two most often used schedules are a daily bolus schedule of 18 to 25 mg/m2/d for 5 days repeated every 28 days, and a 20 mg/m2 loading dose followed by a 48-hour continuous infusion of the agent at a dose of 25 to 30 mg/m2/d. The dose-limiting toxicity in these studies has been myelosuppression. No dosage or schedule could be recommended for patients with acute leukemia because of the severe neurotoxicity (progressive dementia with blindness leading to coma) noted with doses greater than or equal to 96 mg/m2/d for 5 to 7 days. Other toxicities noted in phase I trials have included somnolence, mild to moderate nausea and vomiting, and a rare and reversible interstitial pneumonitis. Of greatest interest is that a profound lymphopenia has been noted as a side effect of Fludara I.V. That toxicity has proven to be of benefit for patients with chronic lymphocytic leukemia, low-grade lymphoma, and mycosis fungoides, all of which are responsive to Fludara I.V. therapy.
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PMID:Phase I clinical trials with fludarabine phosphate. 169 81


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