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)

Disseminated intravascular coagulation was induced in kittens by intraperitoneal inoculation of feline infectious peritonitis virus (FIPV). Kittens seronegative to FIPV survived significantly (P less than 0.05) longer than those seropositive to FIPV. Pyrexia, anemia, icterus, hyperbilirubinemia, and elevated concentrations of liver-specific enzymes were detected in the inoculated cats. Lesions induced included disseminated fibrinonecrotic and pyogranulomatous inflammation, hepatic necrosis, and widespread phlebitis and thrombosis. Localization of FIP viral antigen and immunoglobulin G was demonstrated in foci of heptic necrosis by immunofluorescence miroscopy. Lymphopenia, thrombocytopenia, hyperfibrinogenemia, and increased quantities of fibrin-fibrinogen degradation products were present in cats after the onset of clinical illness. Depression of factor VII, VIII, IX, X, XI, and XII plasma activities and prolongation of prothrombin and partial thromboplastin times also developed in infected cats. The accelerated onset of clinical disease and mortality in seropositive kittens vs seronegative kittens and the association of virus and antibody in multiple foci of hepatic necrosis suggest an immune-mediated component is involved in the pathogenesis of this disease.
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PMID:Disseminated intravascular coagulation in experimentally induced feline infectious peritonitis. 625 Apr 26

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

Colony forming unit (CFU) assays were developed for feline granulocyte-macrophage (CFUGM), early erythroid (day 2 CFUE), and late erythroid (day 7 CFUE) colonies in methylcellulose medium. Feline CFUGM and both day 2 and day 7 CFUE were enhanced by feline macrophage conditioned medium and late CFUE often were intimately associated with macrophages. Kittens were inoculated with the Kawakami-Theilen (KT) strain of feline leukemia virus (FeLV) and sequential changes in marrow CFU determined. Erythroid aplasia, characterized by progressive non-regenerative anemia, lymphopenia, and a profound decrease in early and late CFUE but not CFUGM was induced by 3 to 5 weeks after FeLV-KT inoculation. The susceptibility of kittens to FeVL-induced erythroid aplasia was strongly age-related; neonatal kittens were most sensitive and substantial natural resistance developed by 4 weeks of age. The results demonstrate that FeLV-KT infection induced a rapid and selective suppression of erythroid progenitor cells and represents a suitable model of experimentally-induced acquired erythroid aplasia.
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PMID:Feline leukemia virus-induced erythroid aplasia: in vitro hemopoietic culture studies. 627

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

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

A 10-year-old Tennessee Walker gelding, with a history of progressive weight loss, intermittent colic and lethargy, had a slight fever, tachycardia, tachypnea, pallor, ascites and marked ventral edema. Blood analyses revealed anemia, leukocytosis, neutrophilia with a left shift, lymphopenia, monocytosis, hypoproteinemia and a slightly increased SDH level. Abdominocentesis produced red-orange fluid with many RBC and an increased fibrinogen content. Rectal palpation revealed a large mass in the left caudal abdominal quadrant. The animal died shortly after resection of the mass. The histopathologic diagnosis was lymphosarcoma, involving the spleen, liver and lung.
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PMID:Splenic lymphosarcoma in a horse. 654 5

Complete hemograms were evaluated for 57 rats with mononuclear cell leukemia and compared to hemograms obtained from 52 age- and sex-matched nonleukemic rats. All leukemic rats had marked hemolytic anemia and associated spherocytosis, reticulocytosis, anisocytosis, and polychromasia. The anemia varied with the stage of illness and was more severe in rts with advanced leukemia. Death appeared to be related to anemia. There was a marked neutrophilia with left shift, mild lymphopenia, and moderate to severe thrombocytopenia. Atypical mononuclear cells were detected in circulation in all but three rats. Total white blood cell counts ranged from 5.0-370 x 10(3) cells/ml. There was an increase in erythrocyte osmotic fragility with separation into two distinct populations of erythrocytes. Eight of nine rats were Coombs' positive indicating an immune-mediated pathogenesis for the anemia. Hemostasis tests revealed a markedly prolonged prothrombin time, hypofibrinogenemia, slightly increased to normal partial thromboplastin time, and undetected fibrin degradation products. These findings suggest significant liver disease associated with the leukemia.
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PMID:Pathology of the mononuclear cell leukemia of Fischer rats. II. Hematology. 664 39

Nephritis was induced in 300, 18-day-old male Arbor Acre broiler chicks by feeding diets high (42.28%) in protein, high (3.27%) in calcium, containing urea (5%), or deficient in vitamin A. Various hematological parameters were studied at weekly intervals. Normocytic-normochromic anemia, characterized by a decrease in total erythrocyte counts, hemoglobin, packed cell volume, and an increase in erythrocyte sedimentation rate, was evident in the birds kept on diets high in protein, high in calcium, or deficient in vitamin A. Increased total erythrocytes, hemoglobin packed cell volume, and erythrocyte sedimentation rate was observed in birds fed urea. Differential leucocyte counts revealed lymphopenia, heterophilia and monocytosis in birds kept on diets high in protein, containing urea, or deficient in vitamin A. However, lymphocytosis, heteropenia , and monocytosis were recorded in birds fed the high calcium diet.
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PMID:Hematological changes in nephritis in poultry induced by diets high in protein, high in calcium, containing urea, or deficient in vitamin A. 672 70

We have compared risk factors for cavitary histoplasmosis in 62 patients with that manifestation of the infection and in 679 patients with other forms of histoplasmosis, and we have evaluated the clinical and laboratory findings in 45 patients with cavitary histoplasmosis who were cared for at the Indiana University Medical Center hospitals during two large histoplasmosis outbreaks. Chronic obstructive lung disease and old age were the strongest risk factors for cavitary histoplasmosis but male sex, white race and immunosuppression were also important in certain patient groups. Fever, sweats, weight loss, productive cough, anemia, lymphopenia, and alkaline phosphatase elevation were common findings. The patients were occasionally incorrectly treated for presumed class 3 tuberculosis. Cultures were positive in 58% of patients, with sputum samples providing the highest yield (61%). Histoplasmal serologic tests provided useful clues to the diagnosis, positive in over 90% of cases. About one-third of patients recovered spontaneously while another 35% improved following treatment. About 4% developed chronic untreated cavitary histoplasmosis characterized by clinical and roentgenographic exacerbations and remissions. Of the deaths in four patients with untreated disease, one was caused by disseminated histoplasmosis while three died of other causes. Ketoconazole appeared effective in three of seven patients while its effect in three additional patients was uncertain. Toxicity precluded completion of ketoconazole therapy in one patient. Only amphotericin B has been proven to be effective therapy for cavitary histoplasmosis.
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PMID:Cavitary histoplasmosis occurring during two large urban outbreaks. Analysis of clinical, epidemiologic, roentgenographic, and laboratory features. 673 42


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