Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five cases of disseminated meningococcal disease due to serogroup W135 Neisseria meningitidis are presented. The cases ranged in age from 16 months to 23 years, and spanned a clinical spectrum from mild meningitis without rash or evidence of meningococcal septicemia to severe meningoencephalitis with fulminant meningococcemia, disseminated intravascular coagulation, and death. These cases demonstrate that serogroup W135 N meningitidis is fully pathogenic for man and capable of producing the full spectrum of disseminated meningococcal disease associated with other serogroups. Since this serogroup has recently emerged as a significant cause of disease in Europe, attention should be focused on the correct serogroup designation of strains of N meningitidis isolated from clinical material and reported as "nongroupable" by clinical laboratories, so that additional clinical and epidemiologic information may be obtained.
 ...
PMID:Disease due to serogroup W135 Neisseria meningitidis. 11 72

Two patients who developed bilateral renal cortical necrosis as a consequence of Neisseria meningitidis infections are described: 1 patient had meningococcemia and the other had meningococcal meningitis. Both patients developed a Shwartzman-like reaction, disseminated intravascular coagulation and irreversible renal failure. Renal biopsy showed sclerosis of the majority of glomeruli; some glomeruli showed capillary congestion, thrombosis and an increased number of neutrophils; the intralobular arterioles showed thrombotic occlusions.
 ...
PMID:Bilateral renal cortical necrosis in two patients with Neisseria meningitidis sepsis. 180 40

Meningococcal sepsis with cardiovascular manifestations is one of the leading causes of pediatric intensive care admission (14.85%) in our area. We carried out a two phase study over period of 10 years from 1979 to 1988, involving a retrospective analysis of clinical and analytical manifestations in order to determine a prognostic score of the severity of meningococcal infections in our area. A total of 86 cases were studies over a two year period. After establishing the prognostic score, we applied a previously assayed therapeutic protocol, based on the number of criteria of severity, in 170 children selected as having the same criteria. The factors of seriousness considered were: Appearance of the first symptoms less than 12 h. previously, appearance of petechia less than 6 h. previously, hyperthermia, shock at admission, absence of meningitis, fulminating course of purpura and convulsions, leukopenia less than or equal to 5,000 mm3, prothrombin activity less than or equal to 45%, platelets less than or equal to 75,000 mm3, fibrinogen less than or equal to 250 mgrs% and FPD greater than 40 micrograms/ml (p less than or equal to 0.01 (CHI SQUARE]. In the first phase of study, overall mortality was associated with the presence of three criteria, and was highest when more than seven criteria were present. The results indicate that mortality from meningococcal sepsis is linked to fulminating deterioration of hemodynamics and DIC.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Meningococcal sepsis in our area. Study of the disease severity factors and therapeutic management over a 10-year period]. 188 8

It has been recently suggested that an acquired deficiency of proteins C and S could contribute to the pathogenesis of meningococcemic purpura fulminans (PF) in children. Our study was designed to measure the levels of antithrombin III (AT III), protein C, and protein S during adult PF and to determine the effects of an early infusion of high doses of AT III concentrates on clinical and biological alterations of PF. We studied five consecutive adult patients with meningococcemia (type B) and PF. The levels of AT III, protein C (antigen and activity), and protein S (total and free) were measured at admission and 24 h and 1 month later. The treatment included in each case: amoxycillin, dobutamine and high doses of AT III concentrates. All patients survived and were discharged without any sequelae. At admission, biological data were consistent with severely depressed protein C and protein S levels and moderately decreased AT III levels, without any discrepancy between protein C antigen and activity. After 24 h, AT III and protein S levels were within normal ranges, whereas protein C levels were still depressed. These data are consistent with the theory of a particular imbalance in the anticoagulant systems during meningococcemic PF, contrasting with the usual findings observed during septic disseminated intravascular coagulation. The possibility must be considered that high doses of one anticoagulant (AT III concentrates) could compensate for the acute decrease in the other (protein C system).
 ...
PMID:Meningococcemia and purpura fulminans in adults: acute deficiencies of proteins C and S and early treatment with antithrombin III concentrates. 213 71

We have studied the activation state of the fibrinolytic system in 39 patients with systemic meningococcal disease (SMD). Patients defined as having fulminant septicemia (n = 13) with high (greater than 700 ng/L) levels of endotoxin (LPS) in plasma and severe coagulopathy, had significantly lower functional levels of plasminogen (P less than 0.05) and alpha-2-antiplasmin (P less than 0.01) and higher antigen levels of plasminogen activator inhibitor 1 (PAI-1) (P less than 0.01), and fibrin degradation products (FDP) (P less than 0.01), but not of PAI-2 (P greater than 0.1) as compared with less severely ill patients (meningitis and meningococcemia) (n = 25). A positive correlation existed between the admission (maximum) levels of LPS and PAI-1 (r = 0.86, P less than 0.0001). Decreasing admission levels of platelets were associated with increasing levels of PAI-1 (r = -0.55, P less than 0.001). After initiation of treatment with antibiotics and fresh frozen plasma, the PAI-1 levels declined rapidly. PAI-1 levels greater than 360 micrograms/L on admission predicted the development of a severe septic shock combined with renal impairment correctly in 12 of 13 patients (92%). None of 25 patients without multiple organ failure had PAI-1 levels greater than 260 micrograms/L. PAI-1 levels greater than 1850 micrograms/L were associated with 100% fatality. The results suggest that in the early phase of fulminant meningococcal septicemia an extensive plasmin generation occurs. On admission, however, high levels of PAI-1 seem to inhibit the plasmin generation, and thereby promote DIC.
 ...
PMID:Plasminogen activator inhibitor 1 and 2, alpha-2-antiplasmin, plasminogen, and endotoxin levels in systemic meningococcal disease. 231 89

Skin lesions, an important clue to the cause of septicemia, result from five main processes: (1) disseminated intravascular coagulation and coagulopathy; (2) direct vascular invasion and occlusion by bacteria or fungi; (3) immune vasculitis and immune complex formation; (4) emboli from endocarditis; and (5) vascular effects of toxins. Disseminated intravascular coagulation probably plays only a minor role in pathogenesis. Vascular invasion by bacteria may result in a severe inflammatory reaction, as in meningococcemia, or in a minimal reaction, as in ecthyma gangrenosum. Gram-stained smears of scrapings from the base of skin lesions--a frequently neglected procedure--is an important diagnostic adjunct. Skin biopsies are particularly important in the diagnosis of Rocky Mountain spotted fever and infections caused by Candida.
 ...
PMID:Skin clues in the diagnosis of life-threatening infections. 351 82

Late skeletal deformities following meningococcemia associated with disseminated intravascular coagulation are rare. Two basic lesions have been described: epiphyseal avascular necrosis and epiphyseal-metaphyseal defects. These occur primarily in the lower extremities and result in angular deformity and leg length inequality. We recently encountered these lesions in a child 3 years following sepsis. The etiology appears to be acute vascular thrombosis of epiphyseal and metaphyseal vessels mediated through the generalized Shwartzman reaction. An increased incidence of these deformities may be anticipated as more children survive fulminant meningococcemia.
 ...
PMID:Late skeletal deformities following meningococcal sepsis and disseminated intravascular coagulation. 404 19

A method is described for the measurement of soluble thrombin-altered fibrinogen (circulating fibrin) in human plasma. This method is dependent upon the enzymatic incorporation of glycine ethyl ester-(14)C (GEE-(14)C) into circulating fibrin by the action of the fibrin-stabilizing enzyme, factor XIII. The mean incorporation of GEE-(14)C into the fibrinogen of normal human plasma controls was 167 +/-47 dpm/mg fibrinogen. The addition of 0.03 NIH U/ml of thrombin to normal human plasma resulted in a two to threefold increase in the incorporation of GEE-(14)C into the fibrinogen. The addition of plasmin split products of fibrinogen to normal plasma did not increase the incorporation of GEE-(14)C unless these products were also exposed to thrombin. The addition of plasmin split products of a fibrin clot resulted in only minimal increase in the incorporation of GEE-(14)C (57 dpm/mg fibrinogen) at 37.5% concentration. The method was therefore sensitive to thrombin alterations of fibrinogen but insensitive to plasmin alterations of fibrinogen and fibrin.Clinically, the method was found to provide useful information for the diagnosis and treatment of disseminated intravascular coagulation in two patients with meningococcemia, two patients with Rocky Mountain spotted fever, and three patients in whom therapeutic abortions were induced by the injection of hypertonic saline.
 ...
PMID:Detection of intravascular coagulation. 509 9

Partial destruction of the right humeral and right femoral head were discovered in a 30-month-old girl, two years after her recovery from meningococcal septicemia and disseminated intravascular coagulation (DIC). Additional findings were symmetrical epiphyseal-metaphyseal lesions of the lower femora and upper and lower tibiae. The combined skeletal lesions seem to be characteristic sequelae of infantile meningococcemia complicated by DIC. Since this condition is no longer uniformly fatal, the characteristic skeletal dystrophy will be encountered more frequently and should be recognized by radiologists, pediatricians, and orthopedists. The features shared by our patient and the seven previously published cases are presented.
 ...
PMID:Skeletal lesions following meningococcemia and disseminated intravascular coagulation. A recognizable skeletal dystrophy. 682 28

Circulating concentrations of the proinflammatory cytokine leukemia inhibitory factor (LIF) were prospectively determined by radioreceptor competition assay (sensitivity, 1 ng/mL) in 33 subjects with meningococcemia. LIF was detected in the plasma of 13 subjects and was associated with development of septic shock (P < .01), disseminated intravascular coagulation (P < .05), multiorgan failure (P < .05), and death (P < .01). Plasma LIF concentrations were highest (1-1772 ng/mL) at hospital admission and became undetectable within 36 h, and the peak levels correlated inversely with systolic blood pressure (r, -.70, P < .001), peripheral blood leukocyte count (r, -.58, P < .01), and prodromal interval (r, -.60, P < .001). Plasma LIF concentrations > 400 ng/mL were present only in subjects with fatal fulminant infection. LIF concentrations in plasma collected within 12 h of hospital admission correlated with disease severity in patients with meningococcemia. It is likely that LIF participates in the host response to infection, and it may contribute to the pathogenesis of septic shock.
 ...
PMID:Circulating leukemia inhibitory factor levels correlate with disease severity in meningococcemia. 796 17


1 2 3 Next >>