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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of acute sepsis caused by Gaffkya tetragena in an adult with acquired hypogammaglobulinemia has been described. The Authors pointout the importance that particular conditions of disreactivity and/or of immunodeficiency can play in the acquistion of pathogenicity by Gaffkya tetragena. In the case under discussion a high deficit of IgG and IgA was demonstrable, which had previously caused a long series of infective bacterial diseases.
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PMID:[Acute sepsis caused by "Gaffkya tetragena" in adult with hypogammaglobulinemia (author's transl)]. 1 99

The clinical results obtained with fraction IgGAM are reported. Different types of antibody deficiency syndromes have successfully been treated : 8 cases of Bruton-type agammaglobulinemia. In one of these case a tenacious Pseudomonas infection cleared off during the treatment. Two cases of non sex-linked familial agammaglobulinemia. Three cases of isolated IgM deficiency. Five cases of isolated IgA deficiency. Five cases with Soothill type IgA deficiency associated with high IgE levels. Five cases of septicemia of the new-born. Three cases with acquired agammaglobulinemia and in the premature infant (5 cases). No side-effects nor appearance of anti-IgA antibodies have been observed.
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PMID:[The use of new immunoglobulin preparation, enriched in IgA and IgM (IgGAM)]. 5 7

To define the contribution of aggressive lymphoma treatment to the risk of post-splenectomy septicemia, we investigated the humoral immunity of 44 patients with Hodgkin's disease. Specific antibody against Haemophilus influenzae Type b was significantly reduced (mean, 147 ng per milliliter, P less than 0.01) in patients receiving combined treatment (radiotherapy and chemotherapy), whereas single treatment reduced titers marginally (chemotherapy) or not at all (radiotherapy). Untreated patients had normal values (396 ng per milliliter), and splenectomy was without effect. In some patients who received combined treatment, titers were reduced to levels seen in infants. IgM levels were likewise normal in untreated patients. Chemotherapy, however, significantly reduced IgM levels (P less than 0.025), an effect potentiated by prior splenectomy. IgG, IgA, alternate-pathway activity, C3, C4 and CH50 were all normal or elevated. Aggressive treatment with chemotherapy and radiation impairs humoral defense against encapsulated micro-organisms, and thus magnifies the risk of post-splenectomy septicemia in patients with Hodgkin's disease.
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PMID:Impaired humoral immunity in treated Hodgkin's disease. 30 8

Total hemolytic complement (CH50), conversion of C3 by inulin and cobra venom factor (CoVF), and immunochemical levels of Clq, C4, C2, C3, C5, factor B, properdin, C3b inactivator (KAF), and immunoglobulins (Igs) G, A, and M were measured in the sera of ten patients with abdominal trauma and ten medical patients with septicemia without trauma. Reduction in C3 conversion by CoVF and decrease in the levels of properdin and KAF were demonstrated in the trauma sera. CH50 and the level of C5 were also decreased. Conversion of C3 by inulin and levels of factor B, Clq, C4, C2, and C3 were found to be normal in the patients' sera. Complement levels and activities were found to be normal in the sera of the septic non-trauma patients. A decrease in serum IgM was observed in both patient groups; levels of IgG and IgA were normal. These results indicated that abnormalities of immunoglobulin and of the alternative and classical complement pathways were associated with nonburn trauma. Moreover, the data suggested that consumption of the classical complement pathway associated with septicemia in the thermally injured patient resulted from synergism between the trauma and infection rather than from septicemia per se.
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PMID:Host defense against opportunist microorganisms following trauma. II. Changes in complement and immunoglobulins in patients with abdominal trauma and in septic patients without trauma. 66 70

A factor V inhibitor arose in a 79-year-old man within 1 month of an operation for a fractured leg. Absorption studies with solid-phase antibodies to human immunoglobulins showed the inhibitory activity to be primarily in the IgG class, but also in the IgA class, of immunoglobulins. This is the first report of an IgA immunoglobulin with factor V inhibitory activity. While the inhibitor was present, and at a time when no circulating Factor V activity was detectable, the patient developed septicemia and disseminated intravascular coagulation. The mechanism sustaining disseminated intravascular coagulation despite the absence of circulation factor V activity remains unexplained. The factor V inhibitor disappeared within 5 months of its initial detection. Possible origins of factor V inhibitors are discussed.
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PMID:Factor V antibody and disseminated intravascular coagulation. 67 79

In order to elucidate the pathogenesis of the skin lesions in 'benign gonococcal sepsis' direct immunofluorescence of an early macular lesion and routine histopathology of a mature papulopustular lesion in a patient with septic gonococcal dermatitis have been performed. Histopathology of the mature skin lesion revelaed a pattenr of 'allergic vasculitis'. Direct immunofluorescence showed exclusively deposits of C3 around and within the capillaries and in the basement membrane zone. No specific IgG, IgM, IgA or C4 deposits could be demonstrated. This, together with serological findings and reports from the literature, suggests an important pathogenetic function for complement, activated through the alternative pathway by means of gonococcal endotoxic lipopolysaccharide, in the pathogenesis of the skin lesions in benign gonococcal sepsis.
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PMID:Alternative pathway complement activation:a possible mechanism inducing skin lesions in benign gonococcal spesis. 78 66

The Esch. coli harboured in the gut constitute a reservoir of potential pathogens in the infant and child. The conditions required for these intestinal inhabitants to cause infection are not well understood. The presence of virulence factors such as capsular antigens, especially K1, may be of significance for the ability of Esch. coli to cause neonatal meningitis. The capacity of certain Esch. coli to attach to epithelial cells of mucous membranes may be important for their infective powers in the urinary as well as the intestinal tract. Furthermore, the ability of certain Esch. coli to produce enterotoxins similar to that of V. cholerae is of importance for their capacity to provoke diarrhoea. The importance of the immune defence mechanisms for prevention of these Esch. coli infections is suggested, especially in the form of local immunity provided by secretory IgA antibodies. Such antibodies directed against Esch. coli O and K antigens as well as enterotoxins are present in large amounts in human milk and may be of considerable importance for protection against Esch. coli in the breast-fed baby. Breast feeding may be of special significance until the baby has built up its own local immune defence preventing the micro-organisms from attaching to and invading the intestinal mucous membranes. SIgA antibodies in urine may have a similar protective effect against urinary tract infections. The variable pictures of Esch. coli infections in childhood are striking, ranging from severe sepsis/meningitis or diarrhoea to "asymptomatic" bacteriuria. This variability is obviously closely connected with the presence of various virulence factors and the function of different components of the immune defence.
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PMID:Esch. coli infections in childhood. Significance of bacterial virulence and immune defence. 79 81

Serum opsonic activity for E. coli 075, conversion of C3 by inulin, total hemolytic complement (CH(50)), levels of native C3, factor B, C3b inactivator (KAF), properdin (P), and immunoglobulins (Ig) were determined in 14 patients with burns involving 13% to 91% body surface during 6 to 8 weeks postburn. In the 12 uninfected patients, levels of IgG and IgA were reduced during the first 10 days postburn, and decreased concentrations of P and IgM were demonstrated from three to 6 weeks postburn. C3 conversion was reduced from 10 days to 6 weeks postburn. Levels of C3, factor B, and KAF were normal or elevated for the entire study period. No difference in the occurrence of humoral abnormalities was noted in patients with burns caused by flame, immersion scald, or acid contact. Reduction in C3 conversion and P concentration were the only abnormalities which correlated with increasing burn size. Bacteremia and/or fungemia was documented in the other two patients. In one of these patients, reduction in CH(50) occurred during septicemia due to S. aureus, and in the other, reduction in all measurements of complement was associated with candidemia and Pseudomonas septicemia and occurred prior to the development of shock. Serum opsonic activity was only reduced significantly during sepsis, suggesting that this abnormality occurred as a result rather than a cause of infection. These results indicate that consumption of components of the classical and/or alternative pathways of complement activation may be an important mechanism by which infection is perpetuated in the burn patient. They also emphasize the importance of the clinical management of the burn patient in preventing the development of septic complications.
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PMID:Changes in humoral components of host defense following burn trauma. 87 73

We carried out a study in patients with severe neutropenia from hematologic malignancy and suspected gram-negative sepsis to evaluate the clinical significance of endotoxin concentrations in plasma before and during a therapeutic intervention with a human polyclonal immunoglobulin M (IgM)-enriched immunoglobulin preparation (Pentaglobin; Biotest, Dreieich, Germany). Twenty-one patients with acute leukemia or non-Hodgkin's lymphoma entered the study upon the development of clinical signs of gram-negative sepsis and received the IgM-enriched immunoglobulin preparation every 6 h for 3 days (total dose, 1.3 liter with 7.8 g of IgM, 7.8 g of IgA, and 49.4 g of IgG), in addition to standardized antibiotic treatment. Concentrations of endotoxin and IgM and IgG antibodies against lipid A and Re lipopolysaccharide (LPS) in plasma were determined by a modified chromogenic Limulus amebocyte lysate test and semiquantitative enzyme linked immunosorbent assay, respectively, before each immunoglobulin infusion and during the following 25 days. Seventeen patients were endotoxin positive; in five of these patients, gram-negative infection was confirmed by microbiologic findings. Prior to therapy, endotoxemia correlated significantly with the occurrence of fever, and a quantitative correlation between the endotoxin concentration and body temperature was found during the individual course of infection in 8 of the 17 patients. Overall mortality from endotoxin-positive sepsis was 41% (7 of 17) and 64% (7 of 11) in patients with symptoms of septic shock. Nonsurvivors had significantly higher maximum concentration of endotoxin in plasma compared with those of survivors at the first study day (median of 126 versus 34 pg/ml; P < 0.05) and during the whole septic episode (median of 126 versus 61 pg/ml; P < 0.05). In survivors, immunoglobulin therapy resulted in a significant decrease in endotoxin levels in plasma within the initial 18-h treatment period, from a pretreatment median value of 28 pg/ml to a value of 8 pg/ml (P< 0.05). In the seven patients who died from uncontrollable infection, no effect of therapy on endotoxin levels in plasma was observed. IgM and IgG antibodies against lipid A and Re LPS increased significantly under immunoglobulin treatment, with significant correlations between antibodies against lipid A and Re LPS. These data strongly suggest a prognostic significance of the endotoxin levels in plasma and a potential effect of treatment with a polyclonal IgM-enriched immunoglobulin preparation. Further studies are needed to substantiate these findings and to assess the impact on the clinical course by way of a prospective placebo-controlled clinical trial.
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PMID:Endotoxin concentration in neutropenic patients with suspected gram-negative sepsis: correlation with clinical outcome and determination of anti-endotoxin core antibodies during therapy with polyclonal immunoglobulin M-enriched immunoglobulins. 144 93

Recipients of solid organ allografts require lifelong immunosuppression in order to prevent graft rejection and to maintain graft function. In general, such immunosuppression greatly impairs the cellular immune system, as this level of the immune system is principally responsible for self and non-self recognition. The consequences of allograft transplantation in terms of patient and graft survival when transplants are given to individuals who have a preexisting humoral immune deficiency characterized by a deficiency of the serum levels of one or more of the major Ig classes have not yet been reported. From February 1, 1981 through December 31, 1990, a total of 43 adult patients with a deficiency of 1 or more Ig classes received a ABO-matched liver allograft at this institution. This sample represents 2.5% of a total of 1684 adults transplanted during this interval. These 43 liver graft recipients could be divided into 3 major groups based upon the presence of an IgG, IgM, or IgA deficiency. IgG deficiencies were defined as levels less than 50 mg/dl. Patient and graft survival for the IgA-deficient group was significantly reduced (P less than 0.04 and P less than 0.009, respectively) compared with both the IgG- and IgM-deficient groups. The latter two groups did not differ from controls without an Ig deficiency for these same two endpoints. The major causes of death in the IgA-deficient group were sepsis and opportunistic infection. A third of the deaths in the IgA-deficient group occurred in the perioperative period (first 30 days) while greater than 50% of the deaths occurred within the first 3 months, and all deaths occurred before the first year. Based upon these data, the following conclusions can be made: (1) serum IgA deficiency but not IgG or IgM deficiency is associated with an increased post-OLTx death and graft loss rate; (2) the majority of these deaths are due to sepsis or an opportunistic infection; and (3) most of the deaths occur early. These data suggest that recognition of a deficiency of IgA prior to organ grafting necessitates meticulous attention to the prevention of infection in the immediate perioperative period if patient and graft survival of these patients is to be improved.
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PMID:The association of IgA deficiency but not IgG or IgM deficiency with a reduced patient and graft survival following liver transplantation. 149 40


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