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)

2'-Deoxycoformycin (2'-dCF), a tight-binding inhibitor of adenosine deaminase, was administered to 26 pediatric patients with acute lymphoblastic leukemia in a Phase I study. Doses ranged from 0.25 to 1.0 mg/kg given i.v. for 3 consecutive days. Common toxicity included nausea, vomiting, diarrhea, hepatocellular enzyme elevations, and conjunctivitis. Lymphopenia occurred in all patients. The most serious adverse effects were acute tubular necrosis and central nervous system toxicity, which appeared to be dose related. In addition, two patients given the 0.75-mg/kg dose developed severe hepatic toxicity, although this could not be ascribed definitively to 2'-dCF. Antitumor activity was observed in eight patients, two of whom experienced a complete remission. Inhibition of lymphoblast adenosine deaminase activity was noted in the majority of cases and was observed at all doses. Antileukemic activity occurred at doses of 2'-dCF which were not associated with limiting toxicities. These results suggest that 2'-dCF is active against acute lymphoblastic leukemia and that a starting dose of 0.5 mg/kg/day be utilized in Phase II studies.
Cancer Res 1981 Sep
PMID:Phase I study of 2'-deoxycoformycin in acute lymphoblastic leukemia. 697 90

In six patients with Epstein-Barr virus (EBV) induced infectious mononucleosis (IM) and in two patients with IM-like syndrome, peripheral blood lymphocytes in the acute and convalescent phase were tested for human la-like antigens as well as other cell surface markers. The major population of T lymphocytes in the acute phase showed la-like antigens, as detected by indirect immunofluorescence with heteroantisera, and the number of la-like antigen-positive T lymphocytes decreased with convalescence. The crossabsorption study indicated that the amount of la-like antigen on the surface of IM T cells was less than that of Raji cells.
Blood 1980 Sep
PMID:T lymphocytes expressing human Ia-like antigens in infectious mononucleosis (IM). 699 66

Pretreatment peripheral blood lymphocyte counts have been recorded in 181 consecutive untreated patients with histologically proven Hodgkin's disease and the patients followed prospectively to determine the relationship of lymphopenia to survival. Lymphocyte counts at presentation did not correspond with histology type but were lower in stage 4 disease. Survival in the 77 patients with lymphocyte counts of less than 1.5 X 10(9)/l was 49.7% which was significantly worse (P less than 0.0001) than the 74.2% survival of those with 'normal' counts. This difference was maintained even after adjustment for other acknowledged prognostic variables including sex, age, stage, symptom status, histology type, and response to treatment. The study provides evidence that the lymphocyte count can be used as a meaningful marker in the clinical staging of Hodgkin's disease.
Scand J Haematol 1982 Sep
PMID:Lymphopenia: a bad prognostic factor in Hodgkin's disease. 714 22

Pseudolupus is a syndrome characterized by recurrent fever arthralgia, myalgia, involvement of lung and heart, high sedimentation rate, leukocytosis and lymphopenia. The diagnosis is established by the presence of circulating antimitochondrial antibodies. In 1975 it was found that the disease was due to prolonged treatment with Venocuran, a drug against venous disorders composed of phenopyrazone (pyrazolone derivative), horse-chestnut extract, and Miroton (glycosides extracted from white squill [Urginea maritima], convallaria, oleander and adonis). The drug was then withdrawn. No new cases have come to our attention since then. 15 patients with severe pseudolupus known to us in 1975 have now been followed up. In 6 of the patients all symptoms disappeared within weeks or a few months after withdrawal of the drug. However, the other 9 patients had at least 1 and often 2--3 relapses in the following months to years. In some patients, symptoms remained as long as 4--5 years. Antimitochondrial antibodies persisted in 4 patients for more than 3 years and in 1 patient are still detectable now. The pathomechanism of pseudolupus has not been elucidated.
Schweiz Med Wochenschr 1981 Sep 19
PMID:[Pseudo-(venocuran-)lupus--a minor episode in the history of medicine]. 728 Jun 40

This study describes a series of immunological investigations carried out on a group of 37 HIV-seropositive children, aged 3-4 years, in two different stages of disease defined according to the CDC classification; the Primary stage, an asymptomatic one, showing abnormal immune function (P1-Class, B-Subclass) and the Secondary stage, 6-8 months later, in which patients exhibited non-specific findings, i.e., loss of weight, persistent generalized lymphadenopathy and hepatosplenomegaly, associated with abnormal immune function (P2-Class, A-Subclass). In both stages, immune function was considered 'abnormal' when lymphopenia and a decrease of the CD4/CD8-cell ratio were found. The phenotypes CD16+/56+ (NK) and HLA-DR+/CD3+ (T-activated?)-positive cells, were assessed by flow cytometry, and the following supplementary systemic humoral markers were investigated in homologus serum samples; total HIV(gp)-antibody, HIV(p24)-antibody and p24-antigen presence. If at the primary stage, no significant difference from to the reference values corresponding to the age was noticed, at the Secondary stage the obtained data is presented separately in two subgroups, namely the A-subgroup characterized by the presence of total HIV(gp)-antibody, the presence of HIV(p24)-antibody and the absence of p24-antigenaemia, and the B-subgroup, where total HIV(gp)-antibody was present, HIV(p24)-antibody absent and p24-antigenaemia present. A significant decrease of CD16+/56+ (NK)-cells was found within the two subgroups. As far as HLA-DR+ from CD(3+)-cells was concerned, only those within the B-subgroup showed a high percentage level, compared to the reference values. The importance of the present findings, linked to immune monitoring of HIV infection among children, is discussed.
FEMS Immunol Med Microbiol 1994 Sep
PMID:Changes of blood CD16/CD56 (NK) and HLA-DR/CD3-positive lymphocyte amounts in HIV-infected children, as related to clinical progression and p24-antigen/p24-antibody presence. 752 81

Substantial in vitro evidence suggests that nitric oxide may be a major mediator of interleukin 1 (IL-1) induced pancreatic beta-cell inhibition and destruction in the initial events leading to insulin-dependent diabetes mellitus. Using NG-nitro-L-arginine methyl ester, an inhibitor of both the constitutive and the cytokine inducible forms of nitric oxide synthase, and aminoguanidine, a preferential inhibitor of the inducible form of nitric oxide synthase, we investigated the impact of inhibiting nitric oxide production on food-intake, body weight and temperature, blood glucose, plasma insulin, glucagon, corticosterone and leukocyte- and differential-counts in normal rats injected once daily for 5 days with interleukin 1 beta (IL-1 beta) (0.8 microgram/rat = 4.0 micrograms/kg). Inhibition of both the constitutive and the inducible forms of nitric oxide synthase prevented IL-1 beta-induced fever, hyperglycaemia, hypoinsulinemia, and hyperglucagonemia, and partially prevented lymphopenia and neutrophilia, but had no effect on IL-1 beta-induced anorexia and changes in plasma corticosterone. Preferential inhibition of the inducible form of nitric oxide synthase using two daily injections of 5 mg/rat of aminoguanidine prevented IL-1 beta-induced hyperglycaemia and hypoinsulinaemia, and slightly reduced the pyrogenicity of IL-1 on 3 out of 5 days. Higher doses of aminoguanidine (100 mg/rat) prevented lymphopenia and neutrophilia. We conclude that nitric oxide produced by the inducible form of nitric oxide synthase, mediates the IL-1 beta-induced inhibition of insulin release and that the effect of IL-1 beta on temperature, pancreatic alpha-cells, and leukocyte differential counts seems to be mediated by nitric oxide produced by the constitutive form of nitric oxide synthase.
Cytokine 1994 Sep
PMID:Interleukin 1 beta induces diabetes and fever in normal rats by nitric oxide via induction of different nitric oxide synthases. 753 59

Lifetime follow-up of USTUR Case 246 demonstrated the lack of severe biological effects resulting from his exposure to 241Am. Deterministic effects observed were limited to hematological changes, including lymphopenia and thrombocytopenia. These hematological changes were consistent with those observed in experimental animals following actinide exposure. Cataracts were removed from the left and right eyes at 547 and 1,030 d after the accident, respectively, but were considered to be trauma-induced rather than radiation-induced. No abnormal findings were reported from gross or histological examinations of tissue samples removed at autopsy, other than those resulting from the subject's preexisting cardiovascular disease.
Health Phys 1995 Sep
PMID:Deterministic effects of 241Am exposure in the Hanford Americium accident case. 763 30

Chylothorax in the absence of tumor or trauma is uncommon. Lymphangiomatosis of the bone, although extremely rare, has been associated with chylothorax. The authors describe the case of a 12-year-old boy who presented with a symptomatic left chylothorax associated with lymphangiomatosis of the ribs, scapula, and clavicle. Despite tube thoracostomies and the initiation of total parenteral nutrition, massive losses of chyle persisted, resulting in hypoproteinemia and severe lymphopenia. Control of the chylothorax was achieved by a parietal pleurectomy and application of fibrin glue (Tisseel). In the literature there are 16 cases of chylothorax associated with lymphangiomatosis of the bone. Their presentation, treatment, and outcome are reviewed. Conservative treatments such as dietary manipulations or thoracenteses were rarely successful. Thoracotomy with parietal pleurectomy on the side of the effusion is usually effective in controlling the chylothorax. Lymphangiomatosis should be considered a diagnostic possibility for any child who presents with a chylothorax.
J Pediatr Surg 1994 Sep
PMID:Massive chylothorax associated with lymphangiomatosis of the bone. 780 41

We treated a patient with severe myasthenia gravis with a chimeric (murine/human) anti-CD4 monoclonal antibody (cM-T412) for 7 days and followed the therapeutic effect by standardized muscle function tests, single-fiber electromyography, and immunologic examinations of disease-specific B- and T-cell functions. Clinical and electrophysiologic improvement began within 4 days, lasted for 3 months, and was maximal between days 16 and 58. The CD4+ lymphocytes decreased to a minimum of 80 cells per microliters of peripheral blood, recovered slowly during the first year of follow-up, and did not correlate with changes in disease severity. T-cell stimulation by human acetylcholine receptor was abolished by the treatment but became detectable at the time of worsening of symptoms. The concentration of acetylcholine receptor antibodies in serum was not decreased by the treatment. The results suggest that anti-CD4 antibody administration could be effective in the treatment of severe myasthenia gravis and indicate that acetylcholine receptor-specific T lymphocytes might contribute to the disturbed neuromuscular transmission in the disease.
Neurology 1994 Sep
PMID:Treatment of myasthenia gravis with anti-CD4 antibody: improvement correlates to decreased T-cell autoreactivity. 793 6

Adenosine deaminase (ADA) deficiency is identified here as a cause of adult onset immunodeficiency. Two sisters who noted recurrent, predominantly chest infections in their twenties were found in their thirties to have CD4+ lymphopenia and lymphocyte ADA activity of approximately 5% of the lower limit of normal. Immune function, measured by proliferation of PBMCs in vitro to mitogens and specific Ags, was impaired. Inheritance of a polymorphic marker showed that both patients were heterozygous at the ADA locus. In the paternal allele there was a deletion resulting from homologous recombination between two alu elements that normally flank the first exon and the polymorphic marker. The recombination site was distinct from that in similar deletions described in two infants having severe combined immunodeficiency. This allele is predicted to result in a null phenotype. In the mutant allele inherited from the mother, a C to T transition in a CpG dinucleotide changed the codon for arginine 211, which lies in a conserved sequence close to the active site, to that for cysteine. This mutation has been observed previously in a child in whom the other allele was also a null mutation, but who was diagnosed as having partial ADA deficiency because immune function was apparently normal. The late onset of immunodeficiency in our patients suggests that immune function in children with partial ADA deficiency may deteriorate with time and that ADA deficiency should be regarded as a possible cause of adult onset immune dysfunction of unknown etiology.
J Immunol 1994 Sep 01
PMID:Adult onset immunodeficiency caused by inherited adenosine deaminase deficiency. 805 29


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