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)

Review of the coagulation laboratory records and medical records at Memorial Sloan-Kettering Cancer Center over a three year period (1971--1974) revealed 89 patients with disseminated intravascular coagulation (DIC). The diagnosis of DIC was made if laboratory studies showed evidence of quantitative and qualitative changes in fibrinogen and significant thrombocytopenia. The patients included 19 with leukemia (17 acute), 3 with multiple myeloma, 15 with lymphoma, 46 with metastatic solid tumors, (10 lung, 9 breast, 8 gastrointestinal, 12 genitourinary, 7 miscellaneous) 4 with vascular tumors, and 3 without tumor. Other conditions which might have precipitated or initiated DIC such as gram-negative sepsis, liver impairment, or mucin secreting tumors were present in the majority of patients. Bleeding occurred in 75% of the patients and was fatal in 36%. Thromboembolism occurred in 22.5%. Thirteen percent were asymptomatic. Serum lactic dehydrogenase was elevated in over 75% of the patients at the time of, or subsequent to the occurrence of DIC. Treatment with heparin was helpful in only three of twenty patients. Eighty percent of the patients died within one to over 30 days of the onset of DIC. Post mortem evidence of DIC was present in 18 of 43 autopsies. Results of this study indicate that DIC is a frequent complication of a wide variety of tumors and that its occurrence causes morbidity and mortality in a significant number of patients. Treatment with heparin is of little help unless remission is induced and the precipitating factor(s) are reversed.
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PMID:Disseminated intravascular coagulation: experience in a major cancer center. 17 94

Liver changes and associated host responses were evaluated in four groups of male rats, weighing 300 +/- 20 gm., which received intravenous injection of 2.2 times 10(9) live Escherichia coli. This bolus was given either without additional treatment (group A) or prior to the following regimens: intramuscular injection of gentamicin sulfate, 5 mg. per kg. (group B); intravenous injection of methylprednisolone sodium succinate, 40 mg. per kg. (group C); and intramuscular injection of gentamicin immediately after methylprednisolone sodium succinate treatment (group D). Rats given injections of saline or methylprednisolone sodium succinate served as controls. Survival rates at 10 and 20 hours were 25 per cent and 4 per cent for group A; 44 per cent and 28 per cent for group B; 94 per cent and 70 per cent for group C; 98 per cent and 98 per cent for group D, respectively. In rats of groups A and B, killed at 1, 2, 4, and 6 hours, progressive liver changes included intravascular sequestration of rapidly degranulating leukocytes, fibrinous deposits, and platelet aggregates in sinusoids as well as in spaces of Disse adjacent to subendothelial collagen, and extensive Kupffer cell disruption in association with severe midzonal necrosis. These alterations were accompanied by progressive hypoglycemia and elevations of serum enzymes, glutamic pyruvic transaminase, lactate dehydrogenase, and glutamic oxaloacetic transaminase. Hematologic studies revealed that E. coli bacteremia results in rapid leukopenia and disseminated intravascular coagulation primarily due to activation of the intrinsic coagulation pathway. All above reactions were delayed and markedly reduced in rats treated with methylprednisolone sodium succinate. The results indicate that antibiotic treatment of lethal, Gram-negative bacteremia is effective only in conjunction with early steroid treatment. The protective effects of glucocorticoids on the liver microcirculation and polymorphonuclear leukocytes appear to play a basic role in preventing the early development of disseminated intravascular coagulation, hepatocellular necrosis, and associated major host responses, thereby attenuating lethality of gram-negative septic shock.
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PMID:Glucocorticoid and antibiotic effects on hepatic microcirculation and associated host responses in lethal gram-negative bacteremia. 36 36

Venom from newborn Bothrops asper snakes has higher lethal, hemorrhagic, edema-forming, proteolytic and defibrinating activities than venom from adult B. asper specimens. Electrophoretic analysis confirmed the variation between these venoms. Intramuscular injection of 100 micrograms of venom from newborn specimens in mice induced defibrination, together with moderate increments of serum levels of lactate dehydrogenase, creatine kinase, hemoglobin and total proteins. A conspicuous hemorrhage developed in injected muscle rapidly after envenomation, probably due to a drastic alteration in capillaries and larger blood vessels. Other histological alterations included moderate myonecrosis, lung collapse and prominent renal damage, characterized by tubular necrosis and hyalinization. Polyvalent antivenom effectively neutralized lethal, hemorrhagic and indirect hemolytic activities of newborn B. asper venom, although requiring higher antivenom doses than neutralization of venom from adult B. asper.
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PMID:Pathological and biochemical changes induced in mice after intramuscular injection of venom from newborn specimens of the snake Bothrops asper (Terciopelo). 144 Jun 47

The authors reviewed the case records of 1419 children with acute leukemia and other types of malignant disease involving the bone marrow to define the clinical and laboratory features associated with marrow necrosis as well as the prognostic significance of this complication. Only seven patients were found to have this abnormality: four with newly diagnosed acute lymphoblastic leukemia (ALL), one with relapsed ALL, and two with disseminated neuroblastoma. All patients presented with severe bone pain, bone tenderness, and fever. Levels of serum lactic dehydrogenase were uniformly increased, being especially high in patients with ALL. There was no evidence of severe infection or disseminated intravascular coagulation, complications that have been causally related to marrow necrosis. Four of the five children with ALL remain in complete remission for 10+ to 48+ months. Both patients with neuroblastoma are off therapy, in remission, for 9+ to 15+ months. In contrast to earlier reports, bone marrow necrosis does not appear to confer a poor prognosis in children with malignancy.
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PMID:Bone marrow necrosis in children with malignant disease. 386 Dec 29

Micro-angiopathic haemolytic anaemia is an unusual but well-recognized complication of metastatic adenocarcinoma. A young black man presented with red cell fragmentation, compensated disseminated intravascular coagulation and leuco-erythroblastosis. Metastatic adenocarcinoma of the stomach was suspected but only demonstrated at autopsy. An unusual finding was the elevation of the slow-moving lactate dehydrogenase iso-enzyme (LDH5) level in the plasma which was shown to be produced by metastatic tumour cells recovered from the bone marrow.
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PMID:Micro-angiopathic haemolytic anaemia and an unusual lactate dehydrogenase iso-enzyme pattern in metastatic adenocarcinoma. A case report. 404 83

Sixty-seven cases of eclampsia were managed between August 1977 and July 1980. Routinely acquired laboratory tests of these cases have been analyzed. In addition, the group of patients with eclampsia was compared with a group of 24 healthy pregnant women. There was no significant difference in platelet count, serum fibrinogen, and bilirubin values. The activated partial thromboplastin time was abnormal in 42% of patients with eclampsia. There was no clinical evidence of disseminated intravascular coagulation in any patient. Patients with eclampsia had abnormalities of lactic dehydrogenase, alkaline phosphatase, SGOT, uric acid, BUN, and creatinine. However, in any individual patients there was no single test of great clinical usefulness and no test predictive of maternal or fetal outcome. At present the authors recommend complete blood count (including blood smear and platelet count), clot observation, and serum creatinine tests. Liver function tests are reserved for the patient with upper abdominal pain. Additional tests are recommended if the diagnosis of eclampsia is questionable or if an additional disease process is suspected.
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PMID:Eclampsia II. Clinical significance of laboratory findings. 707 59

A rare isozyme of serum creatine kinase (CK) migrating cathodic to CK-MM on electrophoresis was found in a 30-year-old male with stomach cancer complicated by disseminated intravascular coagulation leading to massive upper gastrointestinal bleeding and marked anemia. Serum CK activity rose to a maximum of 374 U/l without detectable CK-MB isoenzyme. The patient was also characterized by a marked increase in serum lactate dehydrogenase (all isozymes elevated) and by preferential leakage of mitochondrial aspartate aminotransferase and glutamate dehydrogenase, indicating the presence of extensive tissue damage involving mitochondria. Skeletal muscle mitochondria were considered the most likely source of the additional CK isozyme.
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PMID:Cathodic isozyme of serum creatine kinase in a case of stomach cancer complicated by disseminated intravascular coagulation. 744 49

A 43-year-old, bisexual, black man with acquired immunodeficiency syndrome (AIDS), detected by CD4 lymphocyte criteria alone, presented with low-grade fever, chills, malaise, and watery diarrhea of 2 days' duration. Over the next 5 days, he developed a fulminant septicemia-like illness with progressive hypotension, disseminated intravascular coagulation, and very high serum lactic acid dehydrogenase (2,150 U/L) and serum creatine phosphokinase (5,395 U/L) levels, and died. The cause of this illness was not clinically apparent. A bone marrow biopsy performed on the day of his death revealed intracytoplasmic clusters of 3 microns long, oval, basophilic organisms, the exact nature of which was not evident by light microscopy. The diagnosis of disseminated toxoplasmosis (DT) was made only after electron microscopic study of the bone marrow revealed organisms with features typical of Toxoplasma gondii tachyzoites. These features included a multilayered pellicle, a pointed anterior end containing a conoid, up to nine rhoptries, sparse micronemes, and a posterior end containing a nucleus. Some of the organisms had divided by internal budding or endodyogeny. This case illustrates the value of transmission electron microscopy in making the diagnosis of DT.
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PMID:Disseminated toxoplasmosis and acquired immunodeficiency syndrome: diagnosis by transmission electron microscopy. 779 54

All-trans retinoic acid has been used for the treatment of acute promyelocytic leukemia (APL) with encouraging results. However, it has recently been associated with a number of potentially serious complications including the retinoic acid syndrome. We describe two patients with APL who were begun on all-trans retinoic acid therapy (45 mg/m2), but who developed leukocytosis which was treated with hydroxyurea. Both patients demonstrated clinical and laboratory findings of disseminated intravascular coagulation, massive cell lysis manifested by marked increases in serum lactic dehydrogenase, and rapid clinical deterioration. Both patients developed bone marrow necrosis within viable, noninfarcted bone trabeculae. We postulate that the development of bone marrow necrosis in these two patients was not a chance occurrence. Rather, the specific combination of cytotoxic and differentiating agents used in these patients (hydroxyurea with all-trans retinoic acid) caused massive cell lysis and death. The absence of bone marrow necrosis in the setting of induction therapy for APL both with and without all-trans retinoic acid therapy suggests that the addition of hydroxyurea was critical to the development of marrow necrosis. We, therefore, recommend caution in the use of hydroxyurea and all-trans retinoic acid in the treatment of APL.
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PMID:Bone marrow necrosis in two patients with acute promyelocytic leukemia during treatment with all-trans retinoic acid. 760 24

An 8-month-old male infant with severe anemia and thrombocytopenia was brought to our hospital due to fever and pallor. The physical examination on admission showed pale conjunctivae, skin rash, lymphadenopathy and hepatosplenomegaly. Subsequent laboratory studies showed pancytopenia, impaired liver function, elevated lactate dehydrogenase level but without evidence of disseminated intravascular coagulation. Bone marrow aspiration demonstrated increased macrophages and prominent hemophagocytosis. The serological studies revealed a recent infection of human herpesvirus-6 which was confirmed by blood mononuclear cell culture and polymerase chain reaction. This infant was also found to have beta-thalassemia which was confirmed by hemoglobin electrophoresis performed before first transfusion. After treatment with intravenous immunoglobulin and other supportive therapies, the bone marrow abnormalities has completely recovered after 5 days, and the hemogram improved. This report demonstrates the human herpesvirus-6 as the etiology of hemophagocytic syndrome.
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PMID:Human herpesvirus-6 associated hemophagocytic syndrome in beta-thalassemia: report of one case. 860 65


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