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)

Persistent generalized lymphadenopathy (PGL) is the most frequent AIDS related manifestation in homosexual men. From May 1984 to March 1985, 45 (38%) out of 117 intravenous (iv) drug abusers evaluated had PGL. Thirty-two were males and 13 females (median age 25 years). All patients referred to the frequent sharing of syringes. The median duration of lymphadenopathy was 3 months (range 3-60) with a median number of involved extrainguinal sites of 4 (range 2-7). Systemic symptoms and energy to skin tests were common, whereas splenomegaly and past infections were less frequently encountered. Hypergammaglobulinemia and an inverted T helper/suppressor ratio and lymphopenia were found in 78%, 43%, and 20% of the patients, respectively; the presence of HTLV-III antibodies was demonstrated in 12 (46%) of the 26 tested patients. Histologically, excised lymph nodes from 14 patients exhibited a marked follicular hyperplasia, diffuse plasmacytosis, and a conspicuous capillary proliferation. All patients are followed on a regular basis with clinical examination and laboratory tests; in no case has AIDS or a malignant lymphoma so far developed.
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PMID:Persistent generalized lymphadenopathy: clinical characteristics of a lymphadenopathy syndrome in intravenous drug abusers. 348 71

Monocyte function in rhesus monkeys with simian acquired immune deficiency syndrome (SAIDS) was compared with that in age-matched normal juvenile rhesus monkeys. The functional tests were 1) chemotaxis, 2) phagocytosis of opsonized Candida albicans, 3) killing and/or growth inhibition of Candida albicans, 4) generation of respiratory burst, and 5) monocyte-derived macrophage response (morphology and/or respiratory burst) to stimulating agents such as lymphokines, gamma interferon, endotoxin, and phorbol myristate acetate. The monkeys tested had either clinical SAIDS (alive with lymphadenopathy, splenomegaly, and lymphopenia or neutropenia) or had terminal SAIDS (moribund due to the disease). Responses of monocytes from 14 monkeys with clinical SAIDS were indistinguishable from those of 9 normal juvenile rhesus monkeys, whereas monocytes from 3 monkeys with terminal SAIDS had enhanced phagocytosis and respiratory burst capacity. Chemotaxis, candidacidal/stasis activity, and response to stimulating agents were normal in these terminal cases. Plasma from the SAIDS monkeys was as capable of opsonizing yeasts and of being able to generate chemotactic factors by endotoxin as was control plasma. SAIDS retrovirus (SRV) was detected by co-cultivation of pure monocyte-derived macrophage cultures with Raji cells, an indicator cell line which forms syncytia in the presence of SRV. Four terminal SAIDS cases and one late-stage clinical SAIDS case were virus-positive when the number of macrophages in the cultures ranged from less than 50 to about 500. Terminal SAIDS monocyte-derived macrophages in culture as long as 17 days produced SRV. These data show that in monkeys with SAIDS the major effector functions of monocytes and macrophages involved in host defense are intact (even up until death). Additionally, some of the monocytes are productively infected, and these infected monocytes are viable and adherent in culture.
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PMID:Monocyte function in rhesus monkeys with simian acquired immune deficiency syndrome. 390 21

Cyclophosphamide (Cy; 150 mg/kg) was administered (i.p.) to groups of Sprague-Dawley rats, followed two days later by immunization with ovalbumin (OVA). From that time, cyclosporin A (CsA; 25 mg/kg) or its vehicle was given (p.o.) for a further 13 days. Control animals tested 14 days after immunization, showed strong Arthus-like and modest delayed-type skin reactions to OVA, in contrast to almost total inhibition in animals tested with Cy, CsA or both. Similar effects were observed with respect to serum anti-OVA antibody levels. Despite itself producing lymphopenia, CsA had no additional effect on the lymphocyte depletion caused by Cy. Both drugs, either alone or in combination, caused neutrophilia and monocytosis. An additional eosinophilia due to Cy was prevented by CsA. Cy induced splenomegaly, nodal extramedullary haemopoiesis and increases in both tissue eosinophils and marrow neutrophils. There was also lymphoid depletion in both spleen and lymph nodes which was enhanced by CsA. Thymic lymphoid atrophy was found only when CsA was given. Despite the powerful immunosuppressive properties of both drugs, detailed biochemical and structural analyses showed no other synergistic toxicity, apart from modest hepatic abnormalities. In particular, there was no enhancement of the nephrotoxicity of CsA.
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PMID:Immunosuppressive activity and toxicity of cyclosporin A in rats pretreated with high dose cyclophosphamide. 408 81

The maturing reticulocyte degrades ribosomal RNA to constituent ribonucleoside phosphates. Guanosine ribonucleotides are retained only in small amounts and pyrimidine ribonucleotides only in trace quantities. In the mature erythrocyte more than 97% of total nucleotides are the interconvertible adenosine mono-, di-, and triphosphates. High energy ATP fuels most of the reactions required to sustain viability. Unable to synthesize adenosine phosphates from small precursor molecules, the red cell relies on certain salvage pathways to replenish its losses from the adenosine phosphate pool. The most important of these involve adenosine. Adenylate kinase deficiency, when severe, is associated with nonspherocytic hemolytic anemia. A genetically-determined deficiency of pyrimidine 5'-nucleotidase prevents the normal dephosphorylation of pyrimidine ribonucleotides, and hence is characterized by the unique accumulation of pyrimidine phosphates intracellularly. Other features are chronic hemolytic anemia, splenomegaly, and a profound increase in basophilic stippling on the stained blood film. The syndrome is transmitted as an autosomal recessive disorder. A similar syndrome is found in severe lead poisoning as a consequence of nucleotidase inhibition by lead. An inherited, dominantly transmitted hemolytic anemia associated with low red cell ATP and a 45-70 fold increase in the enzymatic activity of adenosine deaminase has also been documented. The undefined molecular lesion appears to involve overproduction of an entirely normal enzyme protein. Severe deficiency of either of two sequential enzymes of purine metabolism, adenosine deaminase anemia, but by excessive accumulations of deoxyribonucleotides within red cells and lymphocytes. The clinical counterpart of each is a severe immunodeficiency state secondary to lymphopenia and lymphocyte dysfunction. Certain other rare clinical syndromes involving disturbed nucleotide metabolism also are detectable by red cell assay procedures.
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PMID:Erythrocyte disorders of purine and pyrimidine metabolism. 625 19

Clinical and laboratory features have been reviewed in 66 episodes of disseminated histoplasmosis that occurred during two large urban outbreaks in Indianapolis. Immunosuppression, age greater than 54 years, and presence of other serious underlying illnesses predisposed to the disseminated form of the disease; only 21% of patients lacked one of these risk factors. Central nervous system findings, splenomegaly, hepatomegaly, and lymphopenia suggested disseminated disease but were present in only about one-third of patients. Miliary or diffuse pulmonary infiltrates also suggested dissemination and were noted in about one-third of patients, while mediastinal lymphadenopathy was present in only 17%. Histoplasmal serologic tests, positive in 90% of patients, provided useful diagnostic clues. The diagnosis could be confirmed by culture in 88% of patients, and special stains were positive in about two-thirds. Although 10% of patients recovered without treatment, 11 patients (17%) died because of failure to suspect the diagnosis and initiate therapy promptly. Amphotericin B was effective in all patients receiving at least 500 mg, but relapse occurred if the total dose was less than 30 mg/kg. Ketoconazole appeared effective in non-immunosuppressed patients but not in those with underlying immunosuppression; however, a controlled trial comparing ketoconazole and amphotericin B is required to establish the role of this new fungistatic oral agent.
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PMID:Clinical and laboratory features of disseminated histoplasmosis during two large urban outbreaks. 631 46

A syndrome of acquired immunodeficiency has been identified in a group of rhesus monkeys (Macaca mulatta) which died at the California Primate Research Center. Clinical evaluation of these animals revealed that 50% or more had lymphadenopathy, weight loss, and diarrhea. At least 30% had splenomegaly, fever, cutaneous abscesses and/or arthritis/myositis. Two animals had fibrosarcomas. Anemia was seen in 19 animals, lymphopenia in 14, granulocytopenia in four and thrombocytopenia in three. Hepatitis was diagnosed histopathologically in 13. Electrophoresis revealed hypoproteinemia, hypoalbuminemia and hypogammaglobulinemia. Numerous bacterial, protozoal, and viral agents were identified including cytomegalovirus and leukocyte-associated herpesvirus. Pathologic lesions included severe post-reactive depletion of lymphocytes in germinal centers and paracortical regions of lymph nodes. Clinical and pathologic changes indicate an acquired immunodeficiency syndrome which has some similarities to AIDS in humans. This disease in monkeys may provide a model for studying that disease.
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PMID:Clinical features of simian acquired immunodeficiency syndrome (SAIDS) in rhesus monkeys. 632 13

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

Some biologic, hematologic, and immunologic aspects of the growth and metastasis of the MC-2 fibrosarcoma indicated its suitability as a model for the study of lymphogenous metastasis. The tumor was maintained in syngeneic female BALB/c mice by the serial sc passage of 10(5) viable tumor cells. It metastasized macroscopically in all mice to regional lymph nodes (RLN) and to the lungs. Both forward and retrograde node-to-node metastases were found. Tumor growth and metastasis were associated with splenomegaly, thymus atrophy, cachexia, neutrophilia, lymphopenia, and anemia. Tumor excision at various times after inoculation showed that all mice whose tumors were excised when there was histologic evidence of metastasis in all RLN (day 13; mean of tumor wt, 122 mg) died subsequently from metastases, whereas no animals died whose tumors were excised on or before day 8 (mean of tumor wt, 15 mg). The onset of metastasis was seen in some RLN on day 8. All survivors were immune to challenge with 10(5) viable tumor cells, which demonstrated the immunogenicity of the tumor. Concomitant tumor immunity could be demonstrated prior to the onset of metastasis (days 6 and 7) but not early (days 0--2) or late (days 15, 19, and 20) in primary-site tumor growth. The early immune response to the tumor demonstrable as concomitant tumor immunity appeared to be abrogated by the progressive growth and metastasis of the neoplasm. Tumor cells passaged in adult thymectomized, X-irradiated, syngeneic recipients produced larger RLN metastases and smaller primary tumors than those passaged in control mice.
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PMID:Biologic and immunologic studies on a murine model of regional lymph node metastasis. 692 75

We investigated the effects of carrageenans (CAR) on mouse hematopoiesis, one of the many biologic systems affected by these galactan polysaccharides. Mice were injected intravenously with potassium CAR (K+-CAR) or iota CAR (I-CAR) and studied for 7 or 14 days, respectively, thereafter. Treatment with either compound induces anemia, granulocytosis, and early profound thrombocytopenia. Treatment with I-CAR results in an early lymphocytosis, and both compounds induce lymphopenia by 18 h after treatment. Treatment with either CAR compound is associated with an early moderate reduction in the number of nucleated cells and granulocyte/macrophage colony forming cells (CFUGM) per femur. Both compounds induce splenomegaly, and I-CAR treated mice develop hypoplasia of the thymus by 18 h after treatment. The splenomegaly is associated with intense splenic hematopoiesis and an increase in the number of spleen histiocytes; many of the latter are engorged with metachromatically staining material, most likely CAR. There is a sustained increase in the numbers of spleen CFUGM after treatment with either compound; in the case of I-CAR this may be due to proliferation of CFUGM in this organ, perhaps effected by the increased levels of plasma colony stimulating activity. Although it has been suggested that I-CAR is relatively nontoxic, and, therefore, potentially useful for in vivo studies, our observations indicate that it has profound effects on hematopoiesis which must be considered when planning and interpreting in vivo studies using this compound.
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PMID:Effects of carrageenan on the mouse hematopoietic system. 697 Jan 38

In vivo and in vitro T lymphocyte function was studied in 64 patients with X-linked and common "variable" primary hypogammaglobulinaemia. Lymphopenia, splenomegaly, depressed in vitro lymphocyte transformation to mitogens and failure to manifest delayed hypersensitivity skin reactions occurred frequently in the common "variable" group, particularly those with adult onset disease. However, relative circulating T lymphocyte numbers and in vitro lymphocyte transformation in a mixed lymphocyte reaction with the CLA4 lymphoid cell line were normal. Antibody mediated and PHA induced lymphocytotoxicity were also normal. These findings indicate the presence of a generalised lymphocyte defect which is selective for certain T lymphocyte functions. Despite these apparent T lymphocyte defect, none of the patients suffered from the unusual opportunistic parasitic, viral or fungal infections which tend to occur in infants with severe primary defects of both T and B lymphocytes.
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PMID:Cellular immunity in primary hypogammaglobulinaemia: evidence for a generalised lymphocyte defect in some patients with "common" variable hypogammaglobulinaemia. 697 57


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