Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenergic activation is known to occur in sepsis and after major surgery or trauma. An elevated serum concentration of adrenaline is followed by lymphocytosis in peripheral blood even in splenectomized patients. The purpose of the present study was to clarify the redistribution of lymphocytes in the tissues during adrenaline infusion. Lymphocytes were isolated from 24 rabbits, labelled with indium-111-tropolone and reinjected into the rabbits. The next day the rabbits were anaesthetized. Eight rabbits received 3 micrograms of adrenaline i.v. followed by 0.2 micrograms/min, eight received 300 micrograms of adrenaline i.v. followed by 20 micrograms/min, while eight received a saline infusion and served as a control group. The activity of labelled cells was imaged with a gamma camera and computer before, during and after adrenaline infusion. The activity of the spleen decreased to 90% and 94% of initial values during low and high doses of adrenaline. The activity of the bone marrow decreased to 91% and 96%, respectively, while the activity of the heart/lung and the liver increased to 107% and 106% with the high dose of adrenaline. In peripheral blood the lymphocytes increased 10%. It is concluded that lymphocytes are redistributed from spleen and bone marrow to peripheral blood, lungs and liver during adrenaline infusion in this animal model.
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PMID:The redistribution of lymphocytes during adrenaline infusion. An in vivo study with radiolabelled cells. 164 46

A 33-year-old man was hospitalized because of thrombocytopenia and severe splenomegaly. On admission 78% of peripheral lymphoid cells were abnormally large, with pale cytoplasm. Flow cytometry of the abnormal lymphocytes showed that they expressed CD 2, CD 3, CD 11, CD 16, and CD 56, but not CD 4 nor CD 8, so they were T-cell large granular lymphocytes (T-LGL). Abnormal lymphocytes obtained from a lymph node expressed CD 2, CD 16, CD 38, and CD 56, but not CD 3, CD 4, and CD 8, so they were natural killer(NK) cells. Splenectomy was performed and the operative specimen showed diffuse infiltration of pleomorphic lymphocytes, probably chronic lymphocytic leukemia cells. After splenectomy, the platelet count returned to normal but the lymphocytosis continued. Two years after discharge, chemotherapy was done because of thrombocytopenia and hepatomegaly. The patient died of disseminated intravascular coagulation arising from sepsis. The differences and similarities between peripheral and lymph-node lymphocytes suggest that LGL and NK cells may be differentiated from the same kind of cell, somewhat differentiated from stem cells.
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PMID:[Chronic lymphocytic leukemia with peripheral T lymphocytes expressing CD 2+, CD 3+, CD 4-, CD 8-, CD 16+, and CD 56+ and lymph-node lymphocytes expressing CD 2+, CD 3-, CD 4-, CD 8-, CD 16+, CD 38+, and CD 56+]. 171 68

We report a patient with the syndrome of large granular lymphocytes in whom the initial clinical features were polyarthritis, hepatosplenomegaly and neutropenia. Relative lymphocytosis was also demonstrated at the expense of a subpopulation with morphology and surface markers characteristic of large granular lymphocytes (CD2+, CD8+, CD16+ and HNK-1+). After 6 months of asymptomatic course, without changes in clinical or laboratory data, the patient died from an acute abdomen with mesenteric ischemia of different likely causes as suggested by necropsy data (multivisceral diffuse infiltrate by large granular lymphocytes, systemic vasculitis and Clostridium sepsis). The association between this syndrome and systemic vasculitis is discussed.
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PMID:[Vasculitis associated with proliferation of large granular lymphocytes]. 225 May 16

Severe hepatotoxicity from phenobarbital occurred in an infant boy who had a complicated illness with chronic bilateral subdural hematomas and sepsis. Skin rash began after 2 weeks of treatment, and signs of hepatocellular failure developed 3 weeks after phenobarbital had been started. Signs of severe liver disease included elevated aminotransferases, conjugated hyperbilirubinemia, significant coagulopathy, hepatosplenomegaly and ascites. Other features of this adverse drug reaction were unremitting fever, leukocytosis with eosinophilia and atypical lymphocytosis, and proteinuria. Sepsis, viral hepatitis, and metabolic liver disease were excluded. The child was on no other medication and had been previously well. In-vitro rechallenge of the patient's lymphocytes with cytochrome P-450 generated metabolites of phenobarbital showed extensive cytotoxicity compared to control. These data support the hypothesis that a defect in drug detoxification was responsible for the child's susceptibility to this drug hepatotoxicity.
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PMID:Phenobarbital hepatotoxicity in an 8-month-old infant. 233 96

A 42-year-old woman was admitted to our hospital because of easy fatigability in Jan. 1976. Laboratory examination revealed severe macrocytic anemia and slight lymphocytosis. She was diagnosed as having pure red cell aplasia (PRCA). She went into hematological remission 6 weeks following 40 mg/day treatment with prednisolone, but the anemia relapsed frequently when the dosage was lessened. She was then treated with 50 mg/day of cyclophosphamide, 50 mg/day of azathioprine, splenectomy, and methylprednisolone pulse therapy, but the recovery from anemia was temporary after each treatment. Since 1984, peripheral lymphocyte counts were 1-30,000/microliters, and reticulocyte counts were 0. She died of sepsis of Listeria in Sep. 1986. Peripheral lymphocytes had large azurophilic granules and an immunophenotype of OKT3+8+11+Ia1+Leu7+.
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PMID:[Chronic T-cell lymphoproliferative disorder associated with pure red cell aplasia]. 249 62

Cell-mediated immunity is not well characterized in very low birth weight infants, and abnormalities may represent a significant vulnerability to infection. This report describes 165 serial studies in 58 infants between 700 and 1300 g birth weight during the first 8 wk of life. Two ml of blood were drawn at 2-wk intervals to measure T cell numbers and subsets and response to phytohemagglutinin (PHA). Overall, lymphocyte proliferation to PHA averaged 17,264 cpm, significantly less than the adult control (23,566 cpm). T cell numbers and subsets were CD3 62% (adult controls 75%), CD4 45% (49%), and CD8 18.6% (27%). Values at birth were lower as all parameters increased for at least the first 4 wk of life: PHA at birth was 15,464 cpm, CD3 48%, CD4 37%, and CD8 13%. Because of the lymphocytosis of premature infants, the absolute numbers of total T cells and subsets were within the normal adult range despite less than 50% of the mononuclear cells at birth being T cells. A study of five infants demonstrated an average of 52% B7+ cells at birth showing that the number of B cells at birth was increased approximately 10-fold over the control number in adults. Clinical correlation showed that the increases in both the % CD8 and the absolute number of CD8+ lymphocytes after birth were correlated with both the occurrence of sepsis and the assessed lymphocyte subsets in a sizeable number of very low birth weight infants serially during the first 8 wk of life including lymphocyte function using isolated mononuclear cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of lymphocyte proliferative response subpopulations in very low birth weight infants and during the first 8 weeks of life. 326 Mar 70

Thymoma has been associated with a variety of autoimmune disorders. We report a case of agranulocytosis and anemia in a 68-year-old woman with a spindle cell thymoma. She was unresponsive to treatment with antibiotics, granulocyte-colony stimulating factor (G-CSF), prednisone, and high-dose intravenous immunoglobulin. Serial bone marrow examinations on this therapy showed progression from a cellular marrow with mild myeloid and erythroid hyperplasia and lymphocytosis, to granulocyte aplasia and severe erythroid hypoplasia. Her serum contained granulocyte-specific antibodies and inhibited the growth in culture of her own marrow cells and marrow cells from a normal donor. An IgG fraction from her serum also inhibited the growth of marrow cells. Although the patient's spindle cell thymoma was surgically removed, she remained neutropenic. She was treated with six plasma exchanges followed by 1,000 milligrams of intravenous cyclophosphamide 2 days after the final plasma exchange and daily G-CSF. Three weeks later her peripheral blood showed marked leukocytosis with pronounced neutrophilia and a left shift. Although her agranulocytosis resolved, she died of fungal sepsis. This case demonstrates that aggressive plasma exchange and immunosuppressive therapy may benefit patients with agranulocytosis associated with thymoma.
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PMID:Immune mediated agranulocytosis and anemia associated with thymoma. 763 79

We review the clinical manifestations and long-term outlook of patients with chronic natural killer (NK) cell lymphocytosis. After reviewing more than 1,500 peripheral blood lymphoid flow cytometry reports and molecular genetics data from patients with suspected large granular lymphocyte (LGL) proliferation, we identified 10 patients (median age at diagnosis, 60 years; range, 35 to 76 years; male:female ratio, 3:2) with persistent (greater than 6 months) increase in phenotypically determined NK cells (CD3-CD16+). Southern blot analysis performed on 9 patients showed no clonal T-cell receptor gene rearrangements. Disease duration was measured from time of initial recognition of LGL or NK cell excess (greater than 40% of the lymphocyte fraction). Clinical data from these 10 patients were compared with those from 68 patients with T-cell LGL (T-LGL) leukemia. Currently, all patients are alive (median disease duration, 5 years; range, 0.8 to 8 years). Associated disease manifestations included pure red blood cell aplasia, recurrent neutropenia, recurrent neutropenic sepsis, and vasculitic syndromes, all of which were responsive to immunosuppressive therapy. No patient had palpable lymphadenopathy or splenomegaly. Compared with the patients with T-LGL leukemia, patients with chronic NK cell leukemia has similar lymphocyte counts, associated conditions, treatment responses, and survival but had less neutropenia and anemia.
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PMID:Chronic natural killer cell lymphocytosis: a descriptive clinical study. 791 84

IL-2 with or without autologous lymphokine-activated killer (LAK) cells, administered early after ABMT for AML may eradicate residual disease and reduce relapses. This paper reports 14 patients who received IL-2 or IL-2 plus LAK cells after ABMT for AML in first relapse or at a later stage, in two separate trials. Patients with AML in first relapse (n = 9), second CR (n = 3) or second relapse (n = 2) underwent ABMT after busulfan (BU), CY and total body irradiation (n = 11) or BU/CY alone (n = 3), with marrow that was (n = 6) or was not (n = 8) purged with 4-HC. In a previously-reported Phase I trial, eight patients received IL-2 (Roche) by continuous infusion at 0.3-3.0 x 10(6) U/m2/day x 5 days and, after 6 days of rest, 0.3 x 10(6) U/m2/day x 10 days. In a subsequent trial, five patients received IL-2 at 3.0 x 10(6) U/m2/day x 5 days, underwent leukapheresis for 3 days and received their LAK cells plus IL-2 (0.3 x 10(6) U/m2/day x 10 days). A sixth patient received only 2 days of IL-2, developed sepsis and died of multiorgan failure. All other patients had mild to moderate toxicity which was reversible. All patients developed neutrophilia, lymphocytosis and thrombocytopenia. IL-2 with or without LAK therapy was initiated 21-91 days (median 51 days) after ABMT. Severe thrombocytopenia (< 10 x 10(9)/l) occurred during the apheresis days.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interleukin-2 with or without lymphokine-activated killer cells as consolidative immunotherapy after autologous bone marrow transplantation for acute myelogenous leukemia. 840 64

Marrow graft failure is a significant cause of morbidity following bone marrow transplantation. A case is reported of marrow graft failure due to neutrophil antibodies. A 13-year-old girl with a large granular lymphocytosis and chronic neutropenia was treated with granulocyte transfusions prior to undergoing a transplant with bone marrow from a partially matched, unrelated donor. Following the transplant, a bone marrow biopsy showed engraftment of donor myeloid cells, but the recipient remained neutropenic. Testing of the serum for neutrophil antibodies found that the recipient's serum had a high-titer neutrophil antibody. Immunoprecipitation studies using the marrow recipient's serum and 125I surface-labeled neutrophils showed that the antibody reacted to the neutrophil-specific antigen NB1. Phenotyping of neutrophils from the marrow donor found that they expressed NB1 antigen, and, in a crossmatch assay, the recipient's serum reacted with donor neutrophils. Despite treatment with granulocyte-macrophage--colony-stimulating factor, the marrow transplant recipient remained neutropenic and died of polymicrobial sepsis and aspergillosis 38 days after the transplant. The presence of high-titer antibodies to neutrophil-specific antigen NB1 in this patient following transplant likely prevented the recovery of her peripheral blood neutrophils and contributed to her death.
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PMID:Prolonged neutropenia resulting from antibodies to neutrophil-specific antigen NB1 following marrow transplantation. 843 Apr 56


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