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)

Both congenital and acquired antithrombin-III (AT-III) deficiencies are amenable to replacement therapy. We describe two antithrombins produced by recombinant DNA techniques from human alpha 1-antitrypsin (alpha 1AT) cDNA in yeast. Alteration of the alpha 1AT active site, replacing methionine 358 with arginine, results in a thrombin inhibition rate similar to that of heparin-activated AT-III. Alteration of two further residues, to give a five-residue sequence identical to AT-III, does not increase this rate further. Neither antithrombin is activated by heparin; both are unglycosylated and have shorter in vivo half-lives (t1/2) than human alpha 1AT. These antithrombins should be suitable for therapeutic replacement of AT-III in cases of congenital deficiency and in conditions associated with acquired AT-III deficiency, such as disseminated intravascular coagulation.
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PMID:Characterization of antithrombins produced by active site mutagenesis of human alpha 1-antitrypsin expressed in yeast. 264 77

In a mature newborn the symptoms of a disseminated HSV infection were evident at the 6th day of life. Later on bleeding occurred as a result of severe consumption coagulopathy. During treatment with Acyclovir the bleeding situation was controlled by fibrinogen replacement. The infant survived and is under normal psychologic and motorical development now. The treatment result is taken for the good virostatic efficacy of Acyclovir. It inhibits the DNA polymerases and therefore the DNA replication within the herpes viruses selectively. This high degree of selectivity is caused by its selective penetration into the infected cells, its faster transformation by the viral thymidine kinase as well as by its stronger affinity for HSV coded polymerase in detail. The diagnosis had been confirmed by detection of herpes viruses within the blister fluid and cerebrospinal fluid as well as by serological findings.
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PMID:[Generalized herpesvirus infection with severe consumption coagulopathy in a newborn infant]. 270 90

Fifty-one patients with different connective tissue diseases in either active or clinically inactive phase were studied to detect the incidence of chronic or subclinical consumption coagulopathy in these forms. Every patient received intravenously 20 mu Ci of [125I] fibrinogen and the clearance of the labeled fibrinogen was evaluated and expressed by the T/2 method. The data confirm the activation of the coagulation system in connective tissue diseases. In patients with S.L.E., enhanced fibrinogen consumption was significantly correlated with disease activity, DNA-binding activity test, serum complement level and an aspecific inflammatory index (serum mucoprotein level). These preliminary data suggest the usefulness of complementary treatment in connective tissue diseases to counteract this specific pathogenetic mechanism.
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PMID:Activation of the coagulation system in connective tissue diseases. A study of [125I] fibrinogen clearance. 745 40

A 45-year-old Japanese male, who had been to the Central African Republic, was admitted to our hospital because of high fever with chills on July 29, 1994. He used chloroquine as a malaria prophylaxis during his stay and for 6 weeks after his return to Japan. On admission, Plasmodium ovale was detected in his blood smears and in the DNA analysis. He was treated successfully with chloroquine (1500 mg over 3 day period) and primaquine (15 mg/day for 14 days beginning day 4). Disappearance of malarial parasites in the peripheral blood smear occurred on the third day and his temperature returned to normal on the 4th day. Interestingly, he had thrombocytopenia and an abnormal grade in fibrin degradation products (FDP) concentration. This led to the suspicion of disseminated intravascular coagulation (DIC). This report indicates the importance of thrombocytopenia which may develop into DIC even though P. ovale malaria infection rarely becomes severe. This is the second report of a P. ovale malaria case in the Central African Republic.
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PMID:[A case of Plasmodium ovale malaria with thrombocytopenia and an abnormality grade in FDP concentration despite the use of chloroquine as a malaria prophylaxis]. 775 55

An apparent increase in the incidence of enterococcal bacteremias from 7 to 48/1000 bacteremias during 1986 to 1991 (p < 0.01) prompted this descriptive clinical and molecular epidemiologic study of 83 episodes occurring in 80 children between 1986 and 1992. Most community-acquired cases were in infants, in comparison with nosocomial episodes (24/26 and 34/57; p < 0.01); many of them were neonates (10/26 and 6/57; p < 0.01). Nosocomial cases were associated with underlying conditions including major surgery 56%, immunosuppression 49%, organ and tissue transplants 30%, and cardiac 32%, pulmonary 25%, renal 21%, and hepatic 21% disorders. Nosocomial episodes developed after a median of 32 days. There were 58 primary and 25 secondary bacteremias. Thirty-two episodes were polymicrobial and 44 organisms were involved. Twenty-six percent of the patients died. In 15%, death was preceded by septic shock, disseminated intravascular coagulation, and polymicrobial bacteremia (p < 0.01). Of 75 isolates, 82% were Enterococcus faecalis and 14% were Enterococcus faecium. Fourteen E. faecalis strains produced hemolysin; none produced beta-lactamase. Three had high-level resistance to gentamicin and 13 to streptomycin; two E. faecium and none of the E. faecalis strains were vancomycin resistant at a low level (p < 0.01) and one was ampicillin resistant. Pulsed-field gel electrophoresis of whole-cell DNA digested with restriction enzymes Sma I and Eag I showed five isolates with a homogeneous pattern, two with another homogeneous pattern, and 68 with distinct heterogeneous patterns. The increase in enterococcal bacteremias was not due to a clonal strain dissemination but to an increase in cases of heterogeneous enterococcal strains. We conclude that enterococcal septicemia is now an important cause of serious morbidity and death in critically ill children.
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PMID:Clinical and molecular epidemiology of enterococcal bacteremia in a pediatric teaching hospital. 807 46

A woman aged 63 presented with septic fever, followed by hepatocellular jaundice. Viral hepatitis was ruled out by serologic tests, but no definite diagnosis could be made. Due to severe disturbance of the plasmatic coagulatory system and a serum bilirubin level above 4 mg/dl, a liver biopsy was not performed. The patient had a persistent septicemia refractory to Imipenem. In spite of intensive care measures, the patient died of disseminated intravascular coagulation and multiorgan failure caused by septic shock. The correct diagnosis of miliary tuberculosis was made only post mortem by histopathological examination of liver specimens and confirmed by detection of Mycobacterium tuberculosis DNA in the patient's liver by polymerase chain reaction.
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PMID:[Miliary tuberculosis of the liver as a cause of septic shock with multi-organ failure]. 816 13

The mitomycin antibiotics, because of their preferential toxicities for hypoxic cells, have significant potential as adjuncts to ionizing radiation in the treatment of solid tumors. To gain information on the mechanism by which these agents exert their cytotoxicities to hypoxic and aerobic cells, the effects of MC, POR and several of their analogs were studied in EMT6 mammary carcinoma cells. The rate of uptake of POR by these cells was directly correlated with the cytotoxicity produced by this agent under both hypoxia and aeration. At equivalent concentrations, uptake of POR into hypoxic cells was more rapid than into aerobic cells. Hypoxic cells also accumulated the antibiotic in concentrations well in excess of that present in the extracellular medium, presumably as a result of reductive activation and covalent binding of POR to cellular structures. Such activation and binding occur to a much lesser degree in aerated cells, resulting in the rapid efflux of POR from these cells when the antibiotic is removed from the extracellular environment. To gain information on the reaction of POR with DNA, mono- and bis-adducts formed in EMT6 cells exposed to this agent were measured. Three major adducts were formed. Two were mono-adducts consisting of deoxyguanosine linked at its N2-position to the C-1 of POR and of 10-decarbamoyl POR. The third was a bis-adduct in which POR was cross-linked to two deoxyguanosines at their N2-positions. More adducts were formed in hypoxia than in air, and more bis-adducts were present in hypoxic cells. Simultaneous exposure of cells to both POR and DIC reduced the total adduct level and a new unknown adduct was formed, primarily under hypoxia. Several mitomycins were evaluated for their capacity to kill EMT6 cells and to produce DNA cross-links in both hypoxia and aeration. The number of cross-links required to produce a given amount of cell kill was similar, regardless of the mitomycin employed or the degree of oxygenation. The findings support the concept that DNA is a critical target in the action of the mitomycins and that cross-linking of the DNA creates an important lesion for cytodestruction.
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PMID:Studies on the mechanism of the cytotoxic action of the mitomycin antibiotics in hypoxic and oxygenated EMT6 cells. 835 15

A 1-year-old boy with Wiskott-Aldrich Syndrome (WAS) who developed malignant lymphoma is described. He showed various complications such as atypical lymphocytosis, disseminated intravascular coagulation (DIC), intracranial hemorrhage, macroamylasemia, and monoclonal gammopathy (immunoglobulin A kappa chain). Epstein-Barr virus (EBV) DNA was detected in the tumor tissue, and the monoclonality of B cells from the tumor tissue was established. EBV-associated lymphoma is frequently observed in immunocompromised patients including those with WAS. The development of macroamylasemia, which is rare in childhood, is discussed in relation to lymphoma and monoclonal gammopathy. This case is unique in that the EBV-associated malignant lymphoma developed at an early age and was accompanied by macroamylasemia.
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PMID:Epstein-Barr virus-associated malignant lymphoma with macroamylasemia and monoclonal gammopathy in a patient with Wiskott-Aldrich syndrome. 902 18

Human parvovirus B19 (HPV-B19) has been known as the etiologic agents of erythema infectiosum in normal childhood, and chronic anemia and thrombocytopenia in immuno-compromised patients. Recently, this virus has been reported as the association with rheumatic manifestation such as rheumatoid arthritis and systemic lupus erythematosus (SLE). We described here a patient whose HPV-B19 infection was mimiking atypical symptoms of SLE at diagnosis, and was persistent because of immuno-suppressive therapy for SLE. A 34-year-old female was admitted to our hospital on 22 June 1995, presenting fever episode and cervical lymph node swelling. Before eighteen months, she was received methyl-predonisolone pulse therapy and plasma exchange by fresh frozen plasma for the treatment of Stevens-Johnson syndrome, and after several weeks these therapy she was suffered from viral infection with lymphadenopathies with a transient appearance of atypical lymphocytes in her peripheral blood smear. On laboratory examination at the present admission, her peripheral blood showed anemia, thrombocytopenia with atypical lymphocytes. Throughout her hospitalization, anti-nuclear antibody (ANA) suspected SLE including anti-DNA and anti-Sm antibody were all negative except of transient week positive ANA screening test. Her physical condition presented poor clinical course with fever elevation, increased ascites and renal dysfunction showing the elevation of CRP and circulating immune-complex (Clq binding method). Her serum was positive for IgM and IgG antibody against VP-1 and VP-2 antigen of HPV-B19 by ELISA in April 1996. And then, HPV-B19 DNA by polymerase chain reaction (PCR) was positive in bone marrow sample in March 1996, and also positive in spleen necropsy at death. We confirmed persistent chronic HPV-B19 infection by measurement of HPV-B19 IgM and IgG antibody by ELISA and HPV-B19 DNA by PCR. The plasmapheresis and administration of intravenous immunoglobulin showed the possible efficacy for her symptom throughout this clinical course. Moreover, bone marrow smear showed the finding of virus-associated hemophagocytic syndrome, and finally, she was died of cervical hemorrhage accompanied with disseminated intravascular coagulation syndrome on July 1996. HPV-B19 infection can present an atypical clinical picture that is highly suggestive of SLE. We suggest that the therapy of steroids and immuno-suppressive agents should be cautious, because these may potentially cause persistent chronic HPV-B19 infection and induced life-threatening clinical course.
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PMID:[Human parvovirus B19 infection mimicking systemic lupus erythematosus: case report]. 931 Dec 85

A fibrinogen variant was identified in a patient with disseminated intravascular coagulation and in one member of her family. Coagulation studies showed marked prolongation of both the thrombin and reptilase times and discrepancy was noted between the levels of plasma fibrinogen, determined by a kinetic vs immunological determination or light scattering assay. Studies on purified fibrinogen revealed an impaired release of fibrinopeptides by thrombin. DNA sequencing revealed a heterozygous A to G point mutation in exon 2 of the A alpha chain, which substituted Arg for His at position 16. This mutation creates a Nla III cleavage site which was used to confirm the mutation.
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PMID:Fibrinogen Poissy I: a new case of the A alpha Arg 16His fibrinogen variant. 939 26


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