Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Major infections, such as sepsis and pneumonia, occur in 50-75% of patients following isolated severe head injury. Previous studies have demonstrated that this high incidence of infection following severe head injury may be related to a decrease in helper T-cell activation and function. The present study was designed to investigate the effect of severe head injury on specific subgroups of helper T cells known to enhance or suppress cellular immune function. Specifically, peripheral blood lymphocytes (PBLs) from 10 head-injured patients and 10 matched controls were evaluated following in vitro stimulation with the T-cell mitogen, phytohemagglutinin (PHA). Subsets of helper T cells evaluated included activated helper (CD4+/CD25+) T cells; helper/inducer (CD4+/CDw29+) T cells, which enhance cellular immune activity; and suppressor/inducer (CD4+/CD45R+) T-cells, which induce suppressor (CD8+) T-cells. In addition, the effect of intraventricular fluid (IVF) on PHA-stimulated in vitro CD4 and CD25 expression was investigated to determine whether severe head injury results in the production of mediators within the central nervous system capable of affecting T-cell activation. The results of this study indicate that isolated severe head injury selectively reduces the ability of PHA-stimulated PBLs to express the helper/inducer (CD4+/CDw29+) T-cell (p = 0.023) and activated helper (CD4+/CD25+) T-cell (P = 0.041) phenotypes. There was no significant change in PHA-stimulated CD4 or CD25 expression following incubation of PBLs with intraventricular fluid (IVF) from head-injured patients. The relationship between these changes in specific helper T-cell subpopulations and the infectious complications of severe head injury are discussed.
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PMID:Impairment of helper T-cell function following severe head injury. 137 52

The clinical features and results of laboratory investigations of the first 19 Indian patients with AIDS seen in our hospital are presented. Weight loss, fever, and diarrhea were the most common symptoms. Tuberculosis (TB) was the most common secondary infectious disease; among 13 patients, seven had only pulmonary TB, five had pulmonary and extrapulmonary TB, and one had only extrapulmonary TB. Oropharyngeal candidiasis was found in 11 patients. Other secondary infections were predominantly by virulent bacteria. Opportunistic infections other than candidiasis were infrequent; one patient had cryptococcosis, two had symptomatic cryptosporidiosis, one had noncoagulase-positive staphylococcus septicemia, and one had cytomegalovirus retinitis. Reduced lymphocyte counts (particularly of the CD4 subset), anemia, hypoalbuminemia, hyperglobulinemia, and elevated liver enzyme levels were frequent laboratory findings. Six patients are under follow-up, two are lost to follow-up, and 11 have died. Lymphocyte counts less than 500/mm3 were only seen in those patients who subsequently died. Response to antituberculosis therapy was good in several patients. Thus, the clinical profile of Indian patients with AIDS is not different from the common picture of patients of low socioeconomic and poor hygienic standards; patients presented with TB, undernutrition, and multiple infections. Therefore, a large population of patients with AIDS in India will not be recognized unless they are tested for evidence of HIV infection.
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PMID:Clinical and laboratory profile of AIDS in India. 802 23

The presence of increased levels of suppressor T cells after thermal injury and their relevance remain controversial. It is unclear whether suppressor T cells are the cause or result of sepsis complicating thermal injury. Spleen cells from a standardized murine burn model and sham burn controls were studied and the relationship between the levels of suppressor cytotoxic T cells (CD8, Lyt-2+), helper T cells (CD4, L3T4+), response to concanavalin A (ConA) and to phytohemagglutinin (PHA) and interleukin-2 (IL-2) production was examined. Mortality following infection via cecal ligation and puncture (CLP) of matched controls was also studied. At day 7 postburn, mean ConA (70 +/- 12% of control) and PHA response (58% +/- 5.2% of controls) and IL-2 production (43% +/- 5.4%) were significantly less than sham burn values (100%; p less than 0.05). However, the mean percentage of cells staining with anti-Lyt-2 and anti-L3T4 (9.1 +/- 0.59 and 13.9 +/- 0.65) was similar to the mean percentage in sham burn animals (9.4 +/- 0.65 and 16.6 +/- 1.1). Furthermore, no significant differences were observed between burned mice and controls in helper (17.3% +/- 1.8% burn vs. 21.2% +/- 1.7% sham) or suppressor cell levels (7.8% +/- 1.2% burn vs. 8.6% +/- 0.7% sham) or helper-suppressor ratios on day 10 postburn. Mortality of 20 litter-matched controls subjected to CLP on day 10 postburn was 90%, which was significantly greater than the sham burn mortality of 20%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Suppressor T-cell levels are unreliable indicators of the impaired immune response following thermal injury. 153 80

Ten episodes of musculoskeletal sepsis have been seen in nine patients with HIV infection. Seven patients had AIDS, circulating CD4-positive lymphocyte counts being less than 0.1 x 10(9)/l in six. Septic arthritis recurred in seven patients, osteomyelitis in three and pyomyositis and bursitis each occurred in one patient. Staphylococcus aureus was isolated from four patients, atypical micro-organisms being found in three. Presentation of musculoskeletal infection in this patient group may be atypical but rapid diagnosis is important as early antimicrobial therapy is often successful.
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PMID:Septic bone, joint and muscle lesions associated with human immunodeficiency virus infection. 159

A case is described of an HIV+ man who was successfully treated for Hodgkin's lymphoma, but who later developed non-Hodgkin's lymphoma 3 years later when his immune system became suppressed. The patient was 22 years old when he presented with fever, asthenia, weight loss, and cervical lymphadenopathy. With Hodgkin's lymphoma he also had positive serology for HIV and hepatitis B. He was treated with alternate courses of MOPP and ABVD chemotherapy. In 1990 he again appeared with high fever, progressive cervical, axillary and inguinal lymphadenopathy, with hilar and mediastinal lymph node enlargement on x-ray. CD4 lymphocytes were 577/cubic mm, and the CD4/CD8 ratio was 0.57 (normal 1.8). His cervical lymph node biopsy was classified as non-B non-T large-cell anaplastic lymphoma which was EBV-positive. A Western Blot was positive for small amounts of p24 and p18 antigens. The man was treated with MACOP-B chemotherapy, with some results, but died of sepsis 6 weeks later. The relationships between Hodgkins and non-Hodgkin's lymphoma, the timing of the neoplasm in the course of HIV infection, and the possible re-activation of hepatitis virus were discussed.
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PMID:Non-Hodgkin's lymphoma after prolonged remission of Hodgkin's disease in an HIV-infected patient. 166 42

The immunological and functional consequences of splenectomy in patients with severe trauma are still controversial. In addition to the higher incidence of bacterial infections, including the post-splenectomy sepsis syndrome, alterations of the peripheral blood mononuclear cells (PBM) have been described in patients after splenectomy. We studied the effects of splenectomy in severely injured patients on the number of PBM subsets 30-80 (median 55) months after splenectomy. Compared to a control group of patients with a similar age and a similar severity of trauma there was no significant difference between splenectomized and non-splenectomized patients regarding the absolute and relative numbers of monocytes, B cells, T cells, CD4+ cells, CD8+ cells, NK cells, CD57+/CD8+ cells and CD4+/CD8+ cells. The CD4/CD8 ratios were within the normal range. In two trauma patients without splenectomy the CD57+/CD8+ cells were found to be elevated to 635 and 513 cells/mm3 compared to less than 100 CD57+/CD8+ cells in controls. Except for a slight thrombocytosis in the splenectomized patients (p less than 0.05) the differential cell count showed no difference between both groups. Our data thus suggest that, in a controlled study, splenectomy has little if any effect on peripheral blood mononuclear cell subsets, while severe trauma on its own may have a profound long term effect on T cell subsets in some patients.
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PMID:Posttraumatic splenectomy does not influence human peripheral blood mononuclear cell subsets. 166 82

T lymphocyte subsets were analysed using monoclonal antibodies and flow cytometry to determine whether myocardial infarction and cardiopulmonary resuscitation induce changes in these. Groups of 11 infarct patients and 10 patients with past cardiopulmonary resuscitation were compared with 11 age- and sex-matched controls and 12 sepsis patients. The differences in the CD4/CD8 ratios between the four groups were significant (F = 7.71, P = 0.001). The infarct patients had lower CD4/CD8 ratios (mean +/- s.d. 0.83 +/- 0.43) than the control (2.12 +/- 1.13; P = 0.001) or sepsis cases (1.76 +/- 1.05; P = 0.004), but their ratios did not differ from those of the resuscitation group (0.93 +/- 0.79, P = 0.84). The latter group also had lower ratios than the control (P = 0.003) and sepsis groups (P = 0.013). Most infarct patients had an on admission inverted CD4/CD8 ratio which usually returned to normal in the next 2 days. A permanently low CD4/CD8 ratio may be a poor sign prognostically after both myocardial infarction and resuscitation.
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PMID:Low CD4/CD8 T lymphocyte ratio in acute myocardial infarction. 189 32

Infection remains a major cause of morbidity and mortality in intensive care medicine. The increased susceptibility of the severely injured patient to sepsis and consecutive multiorgan failure has been attributed to abnormalities in cell-mediated immunity. The purpose of our study was to determine changes in the pattern of lymphocyte subpopulations in severely injured patients and to relate these changes to any development of sepsis and to outcome (indirect immunofluorescence with monoclonal antibodies). During 14 months we investigated 28 patients (ages 15-65 years) suffering from severe multisystem trauma (22 cases) or diffuse peritonitis (6 cases), 6 of whom (21.4%) developed sepsis and multiorgan failure; 4 of these 6 septic patients died. According to the clinical data, patients developed sepsis between the 3rd and 6th days after trauma. We therefore defined days 1-3 as the preseptic phase, days 3-6 as the phase of sepsis development, and days 4-10 as the phase of septic disease. In the preseptic phase there was no statistically significant difference in the pattern of the eight lymphocyte subpopulations measured between patients who later developed sepsis and those who did not. During the phase of sepsis development, however, the patients who did develop sepsis showed significantly reduced numbers of CD2-, CD8-, and CD20-positive cells (P = 0.0003; P = 0.009; P = 0.012). The number of helper cells (CD4) was also decreased, but the difference between the two groups failed to reach statistical significance (P = 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lymphocyte subpopulations in patients at risk of sepsis in a surgical intensive care unit]. 224 May 65

A case of large granular lymphocyte (LGL) leukemia with ascites and CNS involvement was reported. A 39-year-old Japanese female was admitted to our hospital in March, 1987 because of high fever. Her clinical and hematological features were characterized by generalized lymphadenopathy, marked hepatosplenomegaly, high serum LDH level (3,257 mU/ml), marked leukocytosis (71,000/microliters) with 74% LGLs and bone marrow infiltration with 57% LGLs. Despite of chemotherapy, ascites, retroperitoneal mass and CNS involvement developed and she died of sepsis after three months. LGLs from the patient's blood, marrow and ascites, stained positively for acid phosphatase. These LGLs were E rossete+ and Fc (IgG) receptor+ and were positive for CD2, OKM1, HLA-DR and Leu11, but were negative for CD1, CD3, CD4, CD8 and Leu7 as well as for terminal deoxynucleotidyl transferase activity. The natural killer activity against K562 target cells was high and was significantly augmented after stimulation by recombinant human interleukin 2. These LGLs also demonstrated normal antibody-dependent cytotoxicity activity. Cytogenetic study on bone marrow cells and ascitic cells revealed clonal chromosomal abnormalities. These clinical, hematological, immunological and cytogenetic findings suggest that this patient had a neoplastic proliferation of natural killer cells.
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PMID:[CD3-, OKM1+, Leu7-, Leu11+ large granular lymphocyte leukemia with ascites and CNS involvement]. 247 53

A varicella infection in a previously healthy young girl was complicated by bacterial sepsis, arthritis, and osteomyelitis in multiple locations. This secondary complication caused by Staphylococcus aureus was associated with a transient defect in granulocyte function and an alteration in the representation of CD4 and CD8 positive lymphocyte subpopulation. The mechanism responsible for secondary bacterial infections following varicella may be due to transient defects in granulocyte function.
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PMID:A transient granulocyte killing defect secondary to a varicella infection. 279 14


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