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)

Twenty five cattle were infected with T. vivax, 25 with T. congolense, and 25 served as controls. Pathogenic clinical signs of trypanosomal infection were not observed. Secondary bacterial infections were common. Fever, increased heart and respiratory rates, anorexia, and emaciation developed. Elevations in parasitemai and body temperature were positively correlated in the T. vivax group. Infected groups were affected non-uniformly, with some animals in each group remaining asymptomatic and tending to have lower parasitemias. The T. vivax parasitemia was cyclic and the organisms had a genaration time of 7.9 SD 2.5 hours. The first peak of parasitemia in both infections was closely associated with the development of pancytopenia, i.e. anemia, leukopenia, and thrombocytopenia. The bone marrow erythroid response in the T. congolense group was significantly greater thn that in either the T. vivax or control groups. Leukopenia was due to concomitant neutropenia and lymphopenia.
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PMID:Experimental bovine trypanosomiasis (Trypanosoma vivax and T. congolense). I. Sumptomatology and clinical pathology. 54 98

The present article describes the clinical and pathological findings in 5 human immunodeficiency virus (HIV)-infected patients with muscle toxoplasmosis. The patients had marked lymphopenia (5/5), with less than five CD4+ cells/mm3 (3/3), when they developed fever (5/5), and multiorgan failure (5/5), including diffuse encephalitis, pneumonia, pancytopenia, and myopathy. Muscle involvement included weakness and wasting (4/5), myalgias (3/5), and high serum creatine kinase levels (3/3). Serology for toxoplasmosis showed high IgG titers in 3 patients (3/4). Anti-Toxoplasma therapy resulted in complete recovery in 2 patients. Muscle toxoplasmosis was detected by biopsy (3/5) or postmortem evaluation (2/5), and was identified using immunocytochemistry and electron microscopy. Toxoplasma cysts were detected in 0.5 to 4% of muscle fibers close to or remote from necrotic fibers and inflammatory infiltrates. Muscle fibers strongly expressed the major histocompatibility complex class I antigen (2/2) as in polymyositis. We suggest that Toxoplasma gondii should be sought by muscle biopsy in patients who have acquired immunodeficiency syndrome with fever, encephalitis, multiorgan dysfunction, and elevated serum creatine kinase levels of obscure origin.
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PMID:Skeletal muscle toxoplasmosis in patients with acquired immunodeficiency syndrome: a clinical and pathological study. 145 37

To establish an animal model of AIDS, two different "wild" or "adapted" HIV2 Rod and Eho strains were cultivated on monkey cells from different species (baboons, cynomolgus, Rhesus monkeys). Five different available strains were then injected both by intravenous (i.v.) and intracerebral (i.c.) route into ten Rhesus monkeys. Seven animals seroconverted between days 13 and 230. Reverse transcriptase activity in the lymphocyte culture supernatants was detectable in six of the seven animals that seroconverted, and in one animal that remained seronegative. Lymphopenia and a decrease in the CD4+ cell counts were observed in eight animals. One animal, inoculated with HIV2-Rod "wild type," developed a severe cachexia, with dyspnea, and associated neurological symptoms 150 days after inoculation. This animal was sacrificed on day 220. Pathological examination showed typical lesions of actinomycetes infection in the lungs and in the meninges. Another monkey had significant weight loss associated with lymphadenopathies and pancytopenia. These results suggest that in vivo replication of HIV2 in Rhesus monkeys may induce clinical symptoms of immune deficiency. This method is reproducible and may provide a good model for AIDS.
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PMID:Clinical and virological aspects of HIV2 infection in rhesus monkeys. 147 23

Lymphocyte phenotype, bone marrow cellularity, in vitro marrow growth potential, and treatment responses were examined in 22 patients with acquired aplastic anemia who were given anti-thymocyte globulin. Eleven of 22 patients (50 percent) had a significant hematologic response within three months of therapy, confirming the effectiveness of this therapy. Pretreatment fetal hemoglobin concentration, age, sex, severity of pancytopenia, degree of maximal lymphopenia, and total hemolytic complement consumption did not affect response. Patients with severe disease who were treated within 16 weeks after diagnosis had a higher response rate (55 percent) than those treated after 16 weeks (20 percent). In patients with severe disease, a higher pretherapy bone marrow cellularity (p less than 0.001) and presence of granulocyte-macrophage colony growth correlated with response. The actuarial survival of patients with response in the group with severe disease was 100 percent at 12 months as compared with 33 percent in patients without response. Following anti-thymocyte globulin therapy, a reduced number of blood lymphocyte T subpopulations was seen in all patients. At three months after therapy, the patients with response who had severe disease had increased T8-positive cells (+56 percent versus -4 percent for patients without response) and la-positive cells (+32 percent versus -62 percent).
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PMID:Predictive factors for response to anti-thymocyte globulin in acquired aplastic anemia. 387 46

Mononuclear inflammatory infiltrates are characteristic of experimental allergic encephalomyelitis (EAE). Localized EAE was produced in rats in a single day by passive transfer of living lymphoid cells from immunized donors to non-immunized recipients with thermal brain injuries. When the recipients were pretreated with cyclophosphamide 1 or 2 days before cell transfer, neutrophils in the EAE infiltrates notably increased and mononuclear leukocytes decreased. This neutrophilic form of EAE was produced with cells from donors immunized with whole neural tissue or purified myelin basic protein and with adjuvants of different types. This lesion could not be reproduced if the EAE cells were replaced by EAE serum or by irrelevantly immunized cells, or if their activity was foiled by specific "desensitization" or by use of histoincompatible recipients. The 2-day period during which cyclophosphamide prepared recipients for neutrophilic EAE coincided with a transient lymphopenia and relative neutrocytosis caused by the drug. The passive transfer system made it possible for the drug to unbalance the recipient's hemopoietic system without risking adverse effects on the donor cells. The rapid development of the localized form of EAE made it possible to produce lesions before the recipient's transient imbalance gave way to pancytopenia. The new form of EAE may be useful for investigating autoimmune diseases because the neutrophils which indicate the immunologic injury are instantly recognized as reactive recipient cells. Preexisting conventional (mononuclear) EAE prevented subsequent production of neutrophilic infiltrates. This inhibitory effect may be due to local blockade of vessels by mononuclear cells, a concept for which there is evidence. These considerations suggest that the exudation of neutrophils in the new form of EAE may be due to suppression by cyclophosphamide of the mononuclear component of the inflammatory reaction, with loss of its blockading and protective influence on the vessels.
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PMID:A new form of localized allergic encephalomyelitis featuring polymorphonuclear neutrophilic leukocytes. 555 31

A patient with the acquired immune deficiency syndrome experienced pancytopenia during the course of his illness. At the time of maximum depression of the blood cell counts, the hematocrit value was 21%; the WBC count, 1,000/cu mm; and the platelet count, 27,000/cu mm. Lymphopenia was persistent but the number of juvenile neutrophilis was not diminished. Peripheral blood smears were noteworthy for the presence of atypical monocytes with phagocytic vacuoles. Histiocytic hemophagocytophagia was prominent in bone marrow aspirate specimens. Bone marrow biopsy specimens were usually hypocellular and contained collections of atypical lymphocytes and increased reticulin. These hematologic abnormalities are most likely the consequence of persistent viral infection in an immunocompromised host.
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PMID:Acquired immune deficiency syndrome and pancytopenia. 631 79

Blood and marrow specimens were evaluated from 12 patients with the acquired immune deficiency syndrome (AIDS). Ten patients were anemic, eight leukopenic, and three thrombocytopenic. Pancytopenia was present in two patients and subsequently developed in two others. Reticulocyte counts were not increased in the anemic patients. The most common peripheral blood abnormalities were a left shift in the granulocyte series, lymphopenia, atypical lymphocytes, and vacuolated monocytes. Marrow cellularity was increased in five patients and reduced in three. Marrow reticulin was increased in 10 patients; in three of these, marrow could not be obtained by aspiration. Plasma cells were increased in number in every marrow aspirate, and there was a left shift in the myeloid series in most. Aggregates of atypical lymphocytes or a diffuse increase in marrow lymphocytes occurred in seven patients. An increase in histiocytes was observed in seven marrow aspirates; in five of these, the histiocytes were phagocytizing red cells, white cells, and platelets. Necrosis was present in four marrow specimens. These hematologic abnormalities reflect, in part, the presence of systemic infection, inflammation, and the inanition associated with them. However, the high incidence of myelofibrosis, alterations in marrow cellularity, pancytopenia, and hematophagic histiocytosis indicates that the bone marrow is a target organ in AIDS.
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PMID:Hematologic abnormalities in the acquired immune deficiency syndrome. 646 73

A survey of the Western literature of histiocytic medullary reticulosis (malignant histiocytosis) provided 104 case reports with sufficient data from which the presence or absence of an absolute lymphopenia could be ascertained. Of these, 46 (44%) were lymphopenic at presentation or within the subsequent 10 days. A survey of a series of publications containing detailed peripheral leucocyte counts recorded in patients with diseases that, like HMR, may present with, or develop, pancytopenia showed that the incidence of lymphopenia ranged from 14% (Hodgkin's: stages I & II) to 46% (acute myelofibrosis; systemic lupus erythematosus; angio-immunoblastic lymphadenopathy). It was concluded a that HMR should be added to the list of accepted causes of lymphopenia, b that lymphopenia, as an aid to the diagnosis of HMR, will be of limited value, c that when the peripheral leucocyte count of a patient is recorded in a case report, it should be accompanied by a full differential count.
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PMID:Lymphopenia in histiocytic medullary reticulosis. 685 38

We report a case of inadvertent administration of over twice the usual dose of methyl-CCNU. The patient exhibited an early onset of bone marrow suppression. Profound pancytopenia, including lymphopenia, persisted for over seven weeks, Although early recovery started at about five weeks. Permanent marrow damage was indicated by persistent thrombocytopenia and abnormal megakaryocyte morphology at autopsy, some six months after the single exposure to methyl-CCNU. There was no discernible toxicity to lung, liver, or kidneys. The case suggests that the cummulative bone marrow toxicity seen with nitrosoureas is not dose-schedule sensitive. There is also evidence suggesting that high dose nitrosourea therapy affects a bone marrow target population other than the early stem cell target affected by usual doses of these drugs.
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PMID:Toxicity of very high dose nitrosourea administration. 711

Hematologic abnormalities, such as anemia, neutropenia, lymphopenia, and thrombocytopenia, are frequently observed in patients with acquired immunodeficiency syndrome (AIDS). While lymphopenia has been noted in up to 80% of adults, only 50% of children with AIDS are reported to be lymphopenic. We reviewed the blood counts of hospitalized children with AIDS to determine the frequency of lymphopenia and other hematologic abnormalities. Seventy-four children with AIDS (ages 4 months to 9.5 years) were admitted to Kings County Hospital Center (Brooklyn, New York) from January 1990 to March 1991; data consisted of 709 CBCs (range one to 39, median 11) from 176 admissions (range one to 15). In some patients admitted during the study period, charts from previous admissions were reviewed. Anemia (Hb less than than third percentile for age) was noted in 68 of 74 (92%) patients. Leukopenia (WBC less than 4000/mm3) was noted in 32 of 74 (43%) patients. Lymphopenia (lymphocyte counts below normal for age) was seen in 59 of 74 (78%) patients; of these, more than half (31 of 59) had persistently low absolute lymphocyte counts. Thrombocytopenia (platelet count less than 150,000/mm3) was seen in 20 of 74 (27%) and was found in four of eight patients who expired. Pancytopenia was seen in nine of 74 (12%) patients. Progression of hematologic abnormalities with anemia followed by lymphopenia, thrombocytopenia, and finally leukopenia was demonstrated in 22 patients. This review shows a prevalence of hematologic abnormalities that is similar to those of previous reports in children except for a considerably higher prevalence of lymphopenia. As expected, lymphopenia was a marker for disease progression.
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PMID:Prevalence of lymphopenia in children with AIDS. 801 66


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