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

In 36 patients with meningococcal infection a close association between the laboratory evidence of disseminated intravascular coagulation (DIC) and unfavourable prognostic factors was established. Patients with platelet count lessthan 100000/microliter, Normotest lessthan 50% and plasma fibrinogen concentration less than 100 mg/dl had a serious prognosis. No significant differences could be extablished between patients with infection from serogroup A and B meningococci for either laboratory evidence of DIC or prognostic factors.
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PMID:Disseminated intravascular coagulation in patients with meningococcal infection: laboratory diagnosis and prognostic factors. 71 82

Nineteen children, who had been admitted to the Pediatric Hospital of Coimbra with severe meningococcal infection with DIC, were submitted to clinical and radiological examination, an average of 4.2 years after hospitalization, in order to demonstrate late skeletal lesions. Patellar dystrophy, to our knowledge previously unreported, was found in 4 children, all of whom had overlying cutaneous scarring.
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PMID:Late osteoarticular lesions following meningococcemia with disseminated intravascular coagulation. 271 54

During an epidemic of group B meningococcal infection mean values obtained in 96 consecutively affected children showed a reduction in classical pathway function (CH50), normal alternate pathway function (AP50), C4 and factor B levels, and raised C3 levels. CH50, C3 and Factor B were however significantly lower in those children who had a rapid onset of illness, were in shock, had signs of septicaemia, had extensive skin purpura, or who died. The presence of detectable meningococcal antigen by Counter Immuno Electrophoresis (CIE) and laboratory evidence of Disseminated Intravascular Coagulation (DIC) also correlated with lower complement levels. The significant reduction in CH50 and Factor B in the more severely affected patients suggests that activation of both classical and alternate pathways occurs in group B meningococcal infection.
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PMID:Complement abnormalities during an epidemic of group B meningococcal infection in children. 349 93

In 16 patients, 13 with meningococcal infection and 3 suspected to have this infection, 8 patients were found to possess significant higher level of tissue thromboplastin activity of their monocytes isolated from the blood at the admission to the hospital than normal. Five of those 8 patients had an extremely high concentration, greater than 60-300 fold increase, and all these patients died. The exposed tissue thromboplastin activity on the surface of the endotoxin stimulated monocytes is probably the direct inducer of disseminated intravascular coagulation (DIC) in meningococcal infection.
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PMID:Increased tissue thromboplastin activity in monocytes of patients with meningococcal infection: related to an unfavourable prognosis. 684 73

Patients with severe meningococcal infection are characterized by extensive microvascular thrombosis, consumption coagulopathy and secondary hemorrhages. The contribution of the inherited prethrombotic disorders to the severity of the disease course is not established yet. Here, we report on the levels of protein C, protein S, antithrombin and the presence of the factor V Leiden mutation (R506Q) in 50 patients with meningococcal disease, as determined 6 to 58 months after hospital discharge. In addition, we recalled the parents of 16 deceased patients to screen for the mutation in factor V, an abnormality which results in resistance to activated protein C. Among the patients, the prevalence of the genetic risk factors for thrombosis was not higher than expected on the basis of their prevalence in the general population. Moreover, the prevalence of the factor V Leiden mutation was not increased among the parents of the deceased patients. The individual plasma levels of protein C, protein S, and antithrombin did not differ between the patients with or without severe purpura. The present data constitute circumstantial evidence that primary defects in the natural anticoagulant systems do not play a major role in the severity of the disease course. Screening of patients with infectious purpura for inherited thrombotic risk factors is therefore not indicated.
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PMID:Inherited prethrombotic disorders and infectious purpura. 882 83

Meningococcemia and disseminated intravascular coagulation (DIC) have a known association, and they have been identified as a rare cause of osteonecrosis in children. To our knowledge, we report only the second case of an adult with DIC and Neisseria meningitidis infection whose condition was subsequently diagnosed as osteonecrosis. We also review the world medical literature that pertains to osteonecrosis as a sequelae of meningococcal infection associated with DIC.
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PMID:Osteonecrosis following meningococcemia and disseminated intravascular coagulation in an adult: case report and review. 911 99

Meningococcal disease is an infection caused by Neisseria meningitidis, a gram-negative diplococcus that is the leading cause of bacterial meningitis in children and young adults in the United States, with an estimated 2,600 cases reported each year. N. meningitidis infection rates are highest in children 3 to 12 months of age. Four distinct clinical situations are associated with meningococcal infection. The most common is asymptomatic nasopharyngeal colonization. Benign bacteremia is discovered in the absence of classical clinical findings of meningococcemia, but blood cultures are positive for N. meningitidis. Meningitis, the most common pathologic presentation, is associated with fever, headache, and nuchal rigidity. The mortality rate is about 5% in children and 10% to 15% in adults. Meningococcemia, the most severe form of infection, may involve petechial rash, hypotension, and disseminated intravascular coagulation. It is a fulminant condition that can, if untreated, progress from initial symptoms to coma and death in 12 to 48 hours. Spread of these endemic cases can be controlled by administering prophylactic antibiotics to close contacts of patients.
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PMID:Meningococcal disease: recognition, treatment, and prevention. 971

The clinical manifestations and course of meningococcal disease have been well described, but atypical presentations may, if unrecognized, lead to a delay in treatment. We describe here an unusual case of this disease in a 21-y-old woman who presented with an acute rigid abdomen, clinical and laboratory features of sepsis, shock and early DIC with no indication of meningococcal infection. She developed a rapidly spreading purpuric rash, conjunctival haemorrhages, hypotension and tachycardia and a low urine output. Laboratory investigations showed a low platelet count, low haemoglobin and normal WBC. A presumptive diagnosis of meningococcal septicaemia was made and recovery followed treatment with cefotaxime, fluids and inotropes. A fully sensitive Neisseria meningitis Group C, type 2a, subtype NT was isolated from blood cultures, but not from CSF obtained after antibiotic treatment.
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PMID:Acute abdomen as an atypical presentation of meningococcal septicaemia. 1022 2

Mortality of meningococcal septicemia remains high in spite of the improvement of antibiotics treatment and critical care medicine. A 23-year-old male, who had been well until a day earlier, was admitted to the hospital because of a high-grade fever and headache. On the second hospital day, he was still febrile, and it was confirmed that he had disseminated intravascular coagulation. There was no purpuric skin lesion, and a lumbar puncture revealed no abnormality. The condition was complicated by a splenic infarction on the second hospital day, and he suffered a pulmonary infarction on the 8th hospital day. The blood culture was positive for Neisseria meningitidis, making the diagnosis meningococcal septicemia. He was successfully treated with antibiotics and intensive care. Although meningococcocemia in adults is relatively rare in Japan, the disease mortality is still high even in the modern era. Then, once the diagnosis is suspected, it is essential to keep in mind that meningococcal infection requires early recognition of the disease process, prompt initiation of adequate antiinfectious therapy and intensive treatment of multiorgan failure.
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PMID:[Meningococcocemia complicated by disseminated intravascular coagulation, splenic infarction and pulmonary thromboembolism in a young adult: case report]. 1135 26

Tissue factor (TF), the main initiator of blood coagulation, contributes to the manifestation of disseminated intravascular coagulation following septic shock in meningococcal infection. Since a direct relationship between disease severity and lipopolysaccharide (LPS) concentration in the circulation has been shown, we hypothesized that the procoagulant and cytotoxic effects of endotoxin also in vitro were related to its concentration. In vitro studies, however, have frequently used much higher LPS concentrations than those observed in clinical samples. Using elutriation-purified human monocytes, we observed that LPS up to 1000 ng/ml exerted a concentration-dependent increase in TF activity (tenase activity, fibrin formation in plasma). Although there was a dose-dependent increase in TF activity, there was not a concomitant increase in TF expression at LPS concentrations above 1 ng/ml (flow cytometry, Western blotting, TF mRNA). Flow cytometry revealed that this discrepancy between TF activity and TF expression at endotoxin concentrations above 1 ng/ml, coincided with an LPS dose-dependent increase in cell surface phosphatidylserine (PS), considered to promote coagulation. The increased PS expression was associated with an increased number of 7-AAD-positive cells indicating cell death. We conclude that enhancement of monocyte procoagulant activity in vitro by high concentrations of LPS may result from increased PS exposure due to apoptosis and necrosis. Therefore, the LPS concentrations used to examine monocyte procoagulant activity in vitro, should be carefully chosen.
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PMID:Discrepancy between tissue factor activity and tissue factor expression in endotoxin-induced monocytes is associated with apoptosis and necrosis. 1641


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