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)

Cadaver kidneys from donors with DIC appear to have an increased incidence of delayed function and primary nonfunction. These kidneys may be safely transplanted if cortical necrosis is ruled out. Heparin, antiplatelet therapy, and withholding of cyclosporin A therapy in the early post-transplantation period may improve renal function if there is evidence of glomerular capillary thrombosis.
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PMID:Kidney retrieval from cadaver donors with disseminated intravascular coagulopathy. 265 8

Phase I clinical studies of antithrombin III (ATIII) concentrate demonstrated a mean in vivo incremental recovery of functional activity of 1.4 percent per unit/kg administered, an initial 50 percent disappearance time of 22 hours, and a biologic half-life of 3.8 days. Based on these observations, a treatment regimen designed to maintain plasma ATIII levels between 75 and 120 percent of normal has been developed. None of 10 subjects with congenital ATIII deficiency treated prophylactically had evidence of thromboembolism, including four pregnant women at the time of delivery. Five subjects treated for acute thrombosis and/or thromboembolism, four of whom were pregnant, recovered without further thrombotic extension or recurrence. Heparin resistance was reversed in two subjects, both pregnant. Nine subjects with acquired ATIII deficiency also received ATIII treatment for venous or arterial thrombosis or disseminated intravascular coagulation, all with low plasma ATIII levels. Two subjects with disseminated intravascular coagulation demonstrated improvement, one clinically, the other biochemically. All patients with congenital ATIII deficiency survived, but only five of nine with acquired deficiency survived, highlighting the importance in acquired ATIII deficiency of the underlying disease in prognosis. Survival rate was especially poor in subjects with arterial thrombosis in the setting of low plasma ATIII. Administration of ATIII concentrate was well tolerated. None of the subjects who received ATIII concentrate demonstrated evidence of an infectious transmissible agent. These studies demonstrate that it is now feasible to safely replace the deficient protein in congenital ATIII deficiency, either prophylactically or therapeutically.
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PMID:Clinical experience with antithrombin III concentrate in treatment of congenital and acquired deficiency of antithrombin. The Antithrombin III Study Group. 267 72

From 1958 to 1987, 81 cases of pregnancy-related acute renal failure (PR-ARF) were observed (9% of the total number of acute renal failure [ARF] needing dialysis). In the three successive ten-year periods (1958-67, 1968-77, 1978-87) the incidence of PR-ARF fell from 43% to 2.8% with respect to the total number of ARF, and from 1/3,000 to 1/15,000 with respect to the total number of pregnancies. Maternal mortality was high (32%), with 5 cases of death in the last ten years. Irreversible renal damage was recorded in 11.6% of PR-ARF, and, in particular, in 26.3% of cases in preeclampsia-eclampsia (PE-E). Worse maternal and renal prognosis occurred in PE-E complicated by abruptio placentae. Neither disseminated intravascular coagulation (DIC), microangiopathic hemolytic anemia nor prostacyclin imbalance were significantly related to the severity of renal damage. Heparin therapy did not modify DIC evolution and renal outcome and was aggravated by severe hemorrhagic complications. In conclusion, PR-ARF has become a rare, but still critical occurrence, and the most effective measures would be a program of careful prevention.
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PMID:Pregnancy-related acute renal failure. 278 54

A female patient what M3 was seen to incur marked hemorrhagic diathesis during therapy. Heparin infusion was performed to inhibit disseminated intravascular coagulation (DIC). However, oozing from the puncture site of the r-subclavian vein was observed. Her data on coagulation were as follows: AT-3 greater than 100%, fibrinogen 69.0 mg, XIII less than 40%, FPA 2.9 ng/ml and FDP-D dimer 256 ng/ml. The alpha-2-plasmin inhibitor (alpha 2-PI) was 44% and FDP 160 microgram/ml. These results suggested DIC with activated fibrinolysis. Thus, epsilon aminocaproic acid in conjunction with heparin, fibrinogen, and concentrated XIII was administered. The abnormal bleeding improved with an increase of alpha 2-PI and XIII. This clinical response indicated that an activated fibrinolysis and a decreased XIII might have been responsible for provoking the bleeding of the patient.
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PMID:[Antiplasmin drugs and factor XIII concentrates in the treatment of a patient with acute promyelocytic leukemia (M3)]. 281 Jul 83

This paper reports a patient with malignant fibrous histiocytoma of the maxilla who developed DIC during the 12-month observation of the hemostatic course, and a case of squamous cell cancer of the tongue associated with post-operative DIC. The triggers in these 2 cases were malignant tumor, infection, shock and operation. Heparin and aprotinin were administered in both cases. Hemostatic improvement was obtained in case 2, but neither cases were cured. The etiology, diagnosis and treatment of DIC are discussed.
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PMID:Disseminated intravascular coagulation syndrome. 299 55

Antithrombin III (AT III) is known to be the most important inhibitor of serine protease in the coagulation system. In the presence of heparin, AT III is converted from its progressive activity state to an immediate activity state. In disseminated intravascular coagulation (DIC) in the field of obstetrics, the treatment has to be initiated very early. Heparin treatment, on the other hand, is critical since frequently postpartal or postoperative wound bleeding is present. We, therefore, established diagnostic criteria for the early diagnosis of DIC and investigated the clinical efficacy of a therapy with AT III in a well-controlled comparative study versus the injectable synthetic protease inhibitor FOY. The results of the trial showed that the AT III group (92%; n = 24) was significantly (p less than 0.001) superior in clinical efficacy to the FOY group (60%; n = 15). No side effects whatsoever were observed after treatment with AT III concentrate (Behring Institute). From these results, it could be concluded that a single therapy with AT III concentrate can sufficiently control the symptoms of DIC in the field of obstetrics without the risk of increased bleeding.
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PMID:Clinical evaluation of antithrombin III concentrate (BI 6.013) for disseminated intravascular coagulation in obstetrics. Well-controlled multicenter trial. 311 53

The effects of gabexate mesilate on disseminated intravascular coagulation (DIC) accompanying neoplastic diseases or severe infections in ten patients were investigated and compared with those of heparin therapy in ten other patients with DIC. Of 11 patients with DIC (control) who did not receive any anticoagulation therapy for DIC, ten died of pneumonia, DIC secondary to the underlying diseases, or pulmonary edema. Heparin therapy was effective in five patients (50%), while treatment with gabexate was successful in seven patients (70%). Although the therapeutic efficacy of gabexate was not significantly different from that of heparin, in patients in whom bleeding tendencies were observed at the start of the therapy, the former was successful in four (80%) of five patients, while the latter was effective in only one (25%) of four patients treated. The results of this preliminary and nonrandomized study suggest that gabexate is as effective as heparin for the treatment of DIC, and that it may be more successful than heparin in the treatment of DIC accompanied by bleeding diathesis.
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PMID:Gabexate as a therapy for disseminated intravascular coagulation. 313 24

Disseminated intravascular coagulation (DIC), resulting in an acute bleeding diathesis, is always a secondary complication of an underlying disease. Coagulation triggered by the primary process causes consumption of clotting factors and platelets, and ischemic damage secondary to fibrin deposition. Concurrent activation of the fibrinolytic system results in additional clotting factor consumption and the production of fibrin-degradation products (FDP). The combination of decreased clotting factors, FDP, and thrombocytopenia may ultimately culminate in a bleeding diathesis. The balance between the thrombotic and hemorrhagic processes results in a constellation of signs and symptoms. Diagnosis depends on an awareness of predisposing pathologic states and the application of appropriate laboratory tests. Therapy consists of treating the underlying disease and temporizing with an appropriate replacement therapy. Heparin infusion may be of benefit under certain circumstances. The pathogenesis, diagnosis, and treatment of DIC, including new laboratory tests and experimental therapy, are reviewed.
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PMID:Disseminated intravascular coagulation: pathogenesis, diagnosis, and therapy. 330 92

The syndrome of coagulation defects in obstetrics was detected as cause for obstetrical hemorrhage during the 50 years. Some of the etiologic factors like the dead fetus syndrome or the salting out syndrome have vanished. Amniotic fluid embolism is the only syndrome which is clearly associated with disseminated intravascular coagulation. This connection between premature separation is less clear. One concept assumes that the plasma fibrinogen concentration is low because it is consumed in the retroplacental hematoma. Heparin treatment can be fatal if DIC is mistaken with a "loss coagulopathy", which is at present mostly responsible for coagulation defects and obstetrical hemorrhage. This indicates a change in pattern of disease which is due to a better pathophysiologic understanding.
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PMID:[Acute blood coagulation disorders in pregnancy--changing patterns in the disease picture]. 349 59

Eleven of 43 nonimmune patients with falciparum malaria had one or several organ complications: cerebral malaria, acute respiratory failure, acute renal failure, secondary infection, autoimmune haemolysis, spontaneous spleen rupture, and acute pancreatitis. Parasitaemia was 0.1 to 60%. Initial antiparasitic therapy with quinine given parenterally resulted in rapid regression of parasitaemia. An additional schizonticide agent was given depending on parasitic resistance. Supportive therapy comprised intensive-care monitoring including fluid and electrolyte balance and, if necessary, early haemodialysis and (or) endotracheal intubation with PEEP breathing. In one patient with excessive parasitaemia exchange transfusion was performed. Heparin was given only in proven disseminated intravascular coagulation, corticosteroids only in persistent autoimmune haemolysis. All patients survived without suffering permanent defects. Retrospective analysis shows that, apart from rapid specific therapy, supportive treatment of the individual organ complications determines course and prognosis of complicated falciparum malaria.
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PMID:[Complicated malaria tropica: specific and supportive therapy in the imported diseases]. 351 46


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