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)

The effects of recombinant DNA-produced leukocyte interferon (IFLrA) were studied in 37 patients with metastatic cancer who received sequentially escalating doses of 9-86 million units (MU) of IFLrA by im injection twice weekly. The IFLrA was absorbed rapidly and reached a peak serum concentration 6-8 hours after injection. Serum concentration of IFLrA increased proportionately with the dose. The most common side effects included fever, chills, asthenia, anorexia, and weight loss, and leukopenia, granulocytopenia, and lymphopenia occurred frequently. Elevation of serum glutamic-oxaloacetic transaminase was frequent above doses of 50 MU. All side effects were reversible by discontinuation of the drug. Antibodies to IFLrA were detected in 3 patients while on treatment. The presence of antibodies coincided with drastic reduction in serum IFLrA concentration and, in 1 patient, with relapse of disease. Objective tumor responses were documented in patients with lymphomas but not in other groups of patients.
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PMID:Clinical study of recombinant DNA-produced leukocyte interferon (clone A) in a intermittent schedule in cancer patients. 619 33

In specific pathogen-free dogs, clinical signs of experimental canine parvovirus infection were mild, inconsistent and transient. Clinical signs were more pronounced in conventionally-raised dogs, but the severe disease reported in field cases was not reproduced in either group. A pronounced plasma viremia occurred on the 2nd to 4th day post-infection (d.p.i.) in dogs challenged oronasally. Antibody was detectable on the 5th d.p.i. Marked pyrexia was rare, but a significant temperature rise usually coincided with the appearance of antibody and the cessation of viremia. Significant lymphopenia, but not leukopenia, occurred on the 3rd to 7th d.p.i. Virus could be readily isolated from fecal matter on the 3rd to 8th d.p.i.; a few dogs continued to shed virus for up to 12 days. In dogs challenged parenterally, the onset of elevated temperatures, viral shed and antibody production occurred 24-48 hours sooner. Convalescent dogs were no longer contagious for susceptible contact animals 25 days or longer after challenge, although infectious virus persisted in feces for more than 6 months at room temperature. Active giardiasis seemed to exacerbate the clinical syndrome, although treatment with corticosteroids or anti-thymocyte serum did not.
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PMID:Experimental canine parvovirus infection in dogs. 621 33

Six pony foals, free of detectable serum neutralization (SN) antibody against equine herpesvirus type 1 by the standard virus-neutralization (VN) test, were inoculated with equine herpesvirus type 1. The ponies showed typical clinical signs of respiratory tract disease and developed a transient leukopenia, involving lymphocytes as well as neutrophils. The leukopenia reached its lowest point on postinoculation days (PID) 3 to 5 and then returned to base-line values by PID 8 to 10. On quantitation of lymphocyte subpopulations, T and B lymphocytes were decreased during the onset of leukopenia and then recouped during the recovery from leukopenia. However, the proportions of the T and B lymphocytes remained constant during the lymphopenia, ranging from 70% to 80% and 20% to 30%, respectively. The lymphocyte blastogenic response to mitogens increased to peak by PID 2 to 5 and then decreased to base line values or below by PID 7. Mitogen responses of T lymphocyte and mixed lymphocyte preparations were nearly similar. However, the responses of 2 ponies wee somewhat different from the responses of others in that there was an increase in the B lymphocytes in the range of 40% to 50% during the recovery phase of lymphopenia. Also, the 2 ponies' mixed lymphocyte response to mitogens was considerably higher and the T lymphocyte response to mitogen was lower as compared with that of mixed lymphocyte preparation. The importance of these 2 types of responses is discussed.
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PMID:Lymphocytes from ponies experimentally infected with equine herpesvirus 1: subpopulation dynamics and their response to mitogens. 628 78

Acute radiation injury leads to thymic involution, adrenal enlargement, leukopenia, thrombocytopenia, gastrointestinal ulceration, and impaired wound healing. The authors hypothesized that supplemental vitamin A would mitigate these adverse effects in rats exposed to acute whole-body radiation. This hypothesis was based on previous experiments in their laboratory that showed that supplemental vitamin A is thymotropic for normal rodents and lessens the thymic involution, lymphopenia, and adrenal enlargement that follows stress, trauma, and neoplasia, largely obviates the impaired wound healing induced by the radiomimetic drugs streptozotocin and cyclophosphamide, lessens the systemic response (thymic involution, adrenal enlargement, leukopenia, lymphocytopenia) to local radiation, and shifts the median lethal dose (LD50/30) following whole-body radiation to the right. To test their hypothesis, dorsal skin incisions and subcutaneous implantation of polyvinyl alcohol sponges were performed in anesthetized Sprague-Dawley rats at varying times following sham radiation or varying doses of whole-body radiation (175-850 rad). In each experiment, the control diet [which contains about 18,000 IU vit. A/kg chow (3 X the NRC RDA for normal rats)] was supplemented with 150,000 IU vit. A/kg diet beginning at, before, or after sham radiation and wounding or radiation and wounding. The supplemental vitamin A prevented the impaired wound healing and lessened the weight loss, leukopenia, thrombocytopenia, thymic involution, adrenal enlargement, decrease in splenic weight, and gastric ulceration of the radiated (750-850 rad) wounded rats. This was true whether the supplemental vitamin A was begun before (2 or 4 days) or after (1-2 hours to 4 days) radiation and wounding; the supplemental vitamin A was more effective when started before or up to 2 days after radiation and wounding. The authors believe that prevention of the impaired wound healing following radiation by supplemental vitamin A is due to its enhancing the early inflammatory reaction to wounding, including increasing the number of monocytes and macrophages at the wound site; possible effect on modulating collagenase activity; effect on epithelial cell (and possible mesenchymal cell) differentiation; stimulation of immune responsiveness; and lessening of the adverse effects of radiation.
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PMID:Supplemental vitamin A prevents the acute radiation-induced defect in wound healing. 638 75

Hematologic abnormalities were studied prospectively in 38 patients with brucellosis. Anemia was found in 74% of patients, leukopenia in 45%, neutropenia in 21%, lymphopenia in 63%, and thrombocytopenia in 39.5%. Eight patients (21%) were pancytopenic; seven of these individuals also had splenomegaly. Bone marrow hypoplasia was not found. Bleeding complications developed in 26% of patients and were significantly associated with clotting abnormalities (low platelet count, low fibrinogen level, and/or prolongation of thrombin clotting time); i.e., bleeding occurred in approximately 50% of patients with marked clotting abnormalities but in no patients with normal clotting. Determination of fibrinogen levels at different stages of brucellosis led to a redefinition of the normal level for patients with this infection. Patients without clotting abnormalities had fibrinogen levels of 233-711 mg/100 ml (mean, 384 mg/100 ml), whereas patients with thrombocytopenia and prolonged thrombin clotting time had levels of 122-360 mg/100 ml (mean, 216 mg/100 ml; P less than .001) that increased to 233-519 mg/100 (mean, 360 mg/100 ml) when clotting values returned to normal. Lymphopenia was significantly correlated with the severity of clinical manifestations (bleeding and hepatic involvement).
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PMID:Hematologic changes in brucellosis. 648 Nov 87

Observations of 12 patients with AIDS at this institution from March 1981 to April 1984 are reported. Ten patients were homosexuals and two were bisexual. The majority had travelled abroad (USA, Haiti) and reported multiple anonymous sexual contracts. Eleven patients reported symptoms and signs, of 2-12 months' duration, frequently seen in pre-AIDS: fatigue (10), weight loss (10), diarrhea (7), night sweats (5), fever (4), and generalized lymphadenopathy (1). Laboratory studies showed anemia (10), lymphopenia (9), leukopenia (7), decreased T-helper/T-suppressor ratio (10) and cutaneous anergy to multiple skin-test antigens (9). P. carinii pneumonia was diagnosed in three patients, P. carinii pneumonia and Kaposi's sarcoma in one patient and Kaposi's sarcoma in six patients. Another patient had a chronic mucocutaneous infection with herpes simplex and another an intestinal cryptosporidiosis and Kaposi's sarcoma. Alpha-A-interferon was used to treat patients with Kaposi's sarcoma and three patients with limited disease showed a favorable response. Six patients with advanced disease died.
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PMID:[Acquired immune deficiency syndrome in the region of Zurich. Report on 12 cases]. 649 67

Lambs received T-2 toxin at a rate of 0.6 or 0.3 mg/kg body weight per day in a protein reduced diet for 21 days to study the immunological and pathological effects of T-2 toxin in sheep. Blood was collected before T-2 treatment and on days 7, 14 and 21 of the trial for hematological and biochemical examination and for the separation of peripheral blood lymphocytes for the mitogen assay. Myeloid:erythroid ratios were determined from sternal bone marrow samples taken a day before T-2 treatment began, on day 12 and at death (day 22). Lambs treated with 0.6 mg/kg body weight of T-2 toxin daily were leukopenic on day 7 and lymphopenic on days 7 and 14. Also, on day 7, the mitogenic responses of these lambs to the B-cell mitogen, lipopolysaccharide, were significantly depressed and prothrombin times were prolonged. At necropsy, lymphoid atrophy of mesenteric lymph nodes and spleens was most marked in lambs treated with 0.6 mg/kg body weight of T-2 toxin per day. To the authors' knowledge, this is the first report of leukopenia, lymphopenia and lymphoid depletion in ruminants fed T-2 toxin.
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PMID:Experimental T-2 toxicosis in sheep. 664 Apr 13

Staphylococcal enterotoxin A (SEA) administration to monkeys produced an initial lymphocytic leukopenia lasting approximately 24 h. Lymphocytes isolated from blood circulation (PBL) during this stage had normal or decreased [3H]thymidine incorporating activity. After 48 h, however, a significant increase (five- to sixfold) in [3H]thymidine incorporating activity into PBL was apparent. The peak of incorporating activity (seven- to eightfold) was reached 3 to 4 days after SEA administration, followed by a gradual decline, reaching the baseline after 2 weeks. The increased levels of [3H] thymidine incorporation in PBL were concomitant with the conversion of lymphopenia into lymphocytosis, accompanied by the release of many immature cells into the circulation. Lymphocytes isolated 24 h after SEA administration in vivo did not respond to the mitogenic action of SEA in vitro. Lymphocytes isolated at later stages after SEA challenge were fully activated by toxin. From a series of studies, it was concluded that SEA administered to monkeys caused, during the initial 24 h, the removal of a great proportion of lymphocytes from the circulation, followed by the release of new immature cells with augmented DNA synthesis activity. The lymphocytic leukocytosis state declined gradually and reached normal levels between 3 and 4 weeks after the SEA challenge. The biological implications of the hematological changes occurring after SEA challenge in vivo are discussed.
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PMID:In vivo effect of staphylococcal enterotoxin A on peripheral blood lymphocytes. 671 41

The effects of naloxone on the cardiovascular, hematologic and metabolic derangements associated with endotoxic and hemorrhagic shock were studied in unanesthetized horses. In the first of 3 experiments blood glucose and lactate levels, hematocrit, white, red and differential white cell counts, rectal temperature and clinical signs were obtained before and after endotoxin (10 micrograms/Kg) administration in 5 horses. In the second experiment, two groups of 3 horses received either intravenous naloxone (0.04 mg/Kg) or saline, 7 minutes prior to endotoxin. In a third experiment two groups of 4 horses received either saline or naloxone (0.20 mg/Kg) immediately following acute hemorrhage. In the second and third experiments, pulse, mean arterial and right ventricular pressures, and heart rate were also observed. Endotoxin and acute hemorrhage produced hypothermia, leukopenia, lymphopenia, neutropenia, elevations in hematocrit, blood glucose and blood lactate, and clinical signs of shock. Naloxone (0.040 mg/Kg IV) significantly lowered endotoxin-induced increases in right ventricular pressure and heart rate, and at a higher dose (0.20 mg/Kg) antagonized the decrease in pulse and heart rate, and tachycardia observed after acute hemorrhage. These results suggest endogenous opioids are involved in the pathogenesis of shock. Naloxone appeared to attenuate some of the cardiovascular responses associated with shock and thus may be of therapeutic value in shock management.
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PMID:The effects of naloxone on endotoxic and hemorrhagic shock in horses. 673 53

The susceptibility of tumor tissue to therapeutic and smaller doses of chemotherapeutic drugs was assessed on the basis of SH-group inhibition in vitro. As therapeutic dose was decreased, rhythmic changes of tumor susceptibility were observed. In the experiments on tumor-bearing rats, the small dose of chemotherapeutic agent, which in preliminary in vitro experiments proved to be as effective as therapeutic one (1/5 therapeutic dose), was found to cause the same suppression of tumor growth. However, it did not induce leukopenia, lymphopenia, thymus involution or any other manifestations of stress which followed multiple injections of therapeutic doses. The white blood cell and thymus indices in rats, which received the small dose, suggest the development of reactions of training and activation which increase the nonspecific resistance of organism.
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PMID:[Experimental use of antitumor preparations in low doses]. 679 80


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