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)

Seven patients, aged 12 to 19 years, had atypical measles. Prodromal symptoms of fever, malaise, myalgia, headache, nausea, and vomiting were commonly followed by coryza, sore throat, conjunctivitis, photophobia, nonproductive cough, and pleuritic pain. The characteristic rash was erythematous, maculopapular, and progressed frequently to vesicular, petechial, or purpuric lesions. It initially involved palms and soles with subsequent spread to proximal extremities and the trunk, sparing the face. Six of six chest roentgenograms showed infiltrates. Findings not previously described in atypical measles included liver enzyme elevations, thrombocytopenia, disseminated intravascular coagulation, possible transmission among three siblings, and suspected cardiac involvement. Measles complement fixation titers compatible with recent infection were seen in all patients. All patients had previously received killed measles vaccine. A substantial number of persons who are older adolescents or young adults may be at risk of developing atypical measles.
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PMID:Atypical measles in adolescents and young adults. 44 83

Gangrene of an extremity is very uncommon in measles, but we have encountered 3 cases. One patient had a peripheral variety with gangrene of the toes, while the other 2 had major vessel thrombosis. Evidence from the literature is advanced to support the hypothesis that disseminated intravascular coagulation on an immunological basis may be an important precipitating factor. Treatment is briefly discussed.
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PMID:Gangrene of the extremities in measles. 89 66

Simultaneous platelet and fibrinogen survival with 75Se selenomethionine was determined in eight patients with acute infectious hepatitis of intermediate severity. Fibrinogen survival alone was estimated in another nine patients, seven of whom were receiving heparin treatment. Platelet survival was found to be normal (7-9 days) in seven of the 8 patients; it was reduced 4,6 days) only in one patient, who was also affected by measles. Fibrinogen survival was markedly reduced (1-3.7 days) and fibrinogen turnover sharply increased (0.59-2.80 mg/ml/day) in all but one patient, who had thalassaemia major, with normal fibrinogen survival and fibrinogen turnover. Heparin treatment did not affect either platelet survival or fibrinogen turnover. In all patients the coagulation defect was mild and no sign of disseminated intravascular coagulation or of increased fibrinolytic activity could be demonstrated by routine tests. These results are consistent with the hypothesis that in acute infectious hepatitis the decreased survival and increased turnover of fibrinogen might be due to a pathological pathway of defibrination in dependent of thrombin of plasmin.
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PMID:Platelet and fibrinogen survival with 75Se selenomethionine in acute infectious hepatitis. 115 8

Twenty patients with peripheral arteritis due to an infectious disease were studied with the purpose to detect the etiological agent in the vessels belonging to ischemic areas; to establish the relationship between the onset and evolution of the ischemic lesions and the infectious disease; and to verify the appropriateness of the treatment with anticoagulants. Ten patients had meningococal disease with positive blood culture for Neisseria meningitidis. The meningococci were found in vessel walls of ischemic areas. The cutaneous lesions had sudden onset and a rapid evolution. Five patients had pneumonia or gastroenteritis. No microorganisms were detected in the vessel walls of the ischemic areas. The cutaneous necrotic lesions appeared from two to six days after the infectious disease was diagnosed. Therefore, heparinization was considered appropriate to block the extension of the disseminated intravascular coagulation secondary to the vasculitis. Three patients had, probably, post-streptococcal sensibilization arteritis and two post-measles arteritis. No etiological agent was identified in the vessel walls. The necrotic lesions of the extremities appeared from five to 21 days after the clinical course of the infection. The lesions had the complete evolution in a period from one to four days. It was considered appropriate to start the heparinization in the evolutive period of the peripheral lesions in an attempt to reduce the ischemia by the interruption of the intravascular coagulation related to the vasculitis. In heparinized patients in whom the necrotic lesions did not extend completely in the extremities, the evolution to irreversible gangrene and limb loss did not occur.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Arteritis dependent on infective process: the convenience of heparin use]. 184 98

Endothelial injury is important in the pathogenesis of thrombosis, atherosclerosis, disseminated intravascular coagulation, and vasculitis. The ability of several common human viruses to infect cultures of endothelial cells obtained from human umbilical veins or bovine thoracic aorta was demonstrated. Indicators of infection included cytopathology, viral growth curves, and antigen detection by immunofluorescence. Herpes simplex virus type 1, adenovirus type 7, measles virus, and parainfluenza virus type 3 infected both human venous and bovine aorta endothelium. Mumps virus, poliovirus type 1, and echovirus type 9 grew only in human venous cells; coxsackievirus B4 infected only bovine arterial cultures; and cytomegalovirus, influenza A/Victoria/75 (H3N2) virus, and respiratory syncytial virus failed to grow in either cell culture. During replication some viruses caused acute lytic changes; some produced chronic, less destructive alterations; and other induced no apparent cytopathology. The results suggest that viral replication within endothelium may be important in the pathogenesis of viral disease of initiation of vessel-wall injury.
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PMID:Virus infection of endothelial cells. 626 Aug 74

A 58-year-old man was admitted to our hospital with fever, vomiting and disturbance of consciousness after common cold-like symptoms for 2 days. Physical examination showed high fever, moderate hypertension and tachycardia. There were no superficial lymph nodes swelling nor skin rashes. Cerebrospinal fluid (CSF) examination revealed increased protein level (467 mg/dl) and pleocytosis (508 cells/mm3), but no glucose was detected. CSF smear test detected the pneumococcus. Intravenous cefotaxime was administered along with intravenous immunoglobulins and steroid pulse therapy. However, DIC developed, so FOY therapy was started. With these treatments, level of consciousness gradually improved and he became able to eat. At 11th days after the onset, the patient suddenly developed left facial palsy and paresis of the left arm. Head T2-weighted magnetic resonance imaging demonstrated tumor-like hyperintensity signal lesions (28 x 16.6 mm) with ring enhancements in the right frontal lobe. Acute disseminated encephalomyelitis (ADEM) was diagnosed based on MRI and CSF findings, and then additional corticosteroid pulse therapy was administered twice. Herpes simplex virus and herpes zoster virus DNA in the CSF were undetectable by PCR. After 6 days of treatment with corticosteroid pulse therapy, left facial palsy and paresis of the left arm gradually improved and MRI showed the disappearance of tumor-like hyperintense signals. Although ADEM usually develops as a complication after viral infection such as measles, rubella, mumps and herpes zoster, this case suggests that ADEM complication should be considered even after pneumococcal meningoencephalitis.
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PMID:[A case of acute disseminated encephalomyelitis (ADEM) following treatment for pneumococcal meningoencephalitis]. 1934 73