Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019087 (hemorrhagic diathesis)
 678 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The main cause of DIC (disseminated intravascular syndrome) is contact of tissue factor with circulating blood. The main symptoms of DIC are bleeding diathesis caused by consumption coagulopathy and organ dysfunction related to circulatory disturbances due to multiple thrombi. However, the symptoms of DIC differ according to degree of fibrinolysis which is characterized by causal disease of DIC. Usually, enhanced fibrinolysis does not cause organ failure but hemorrhagic diathesis, while impaired fibrinolysis does not cause severe bleeding but organ dysfunction. In almost all cases of acute leukemia and in some cases of solid cancer with DIC, hyperfibrinolysis is common. In cases of severe infection with DIC, impaired fibrinolysis due to abnormal elevation of plasminogen activator inhibitor-1 is frequently seen.
 ...
PMID:[Disseminated intravascular coagulation--pathophysiology]. 843 9

DIC is an acquired disorder in which intravascular coagulation may lead to microvascular fibrin formation and a hemorrhagic diathesis. If DIC is acute and severe, fibrin formation may lead to microvascular thrombosis, and consumption of coagulation factors and platelets may result in a hemorrhagic diathesis. Secondary to or simultaneously with coagulation, the fibrinolytic system may be activated, accentuating the bleeding tendency. All the systems involved in DIC, such as coagulation, fibrinolysis, kallikrein-kinin, complement, and possibly other systems are regulated. Coagulation is the central event of DIC. The different coagulation factor derivatives may be generated that can be determined and used as markers for the degree of DIC and for effective control of therapy. Some of the procoagulant and anticoagulant factors are converted in the course of coagulation to their active forms and activation peptides. The active factor is subsequently neutralized by forming a complex with an inhibitor. Hemostatic molecular markers, D-dimer of cross-linked fibrin degradation products (D-dimer), thrombin-antithrombin III complex (TAT), and plasmin-alpha 2-plasmin inhibitor complex (PIC) have all been used for the diagnosis of DIC.
 ...
PMID:[Progress in diagnosis of disseminated intravascular coagulation (DIC)--diagnostic criteria of DIC]. 843 27

A 63-year-old man was evaluated for a lifelong history of bleeding commencing with frequent epistaxis as a child; all previous routine coagulation parameters were within the normal range. The patient's hemorrhagic disorder is characterized predominantly by delayed bleeding at surgical sites. In the resting state, there was no clinical or laboratory evidence of excessive fibrin(ogen)olysis. Bleeding was not caused by disseminated intravascular coagulation, factor XIII deficiency, alpha 2-antiplasmin deficiency, or dysfibrinogenemia. It was found that the patient was deficient in plasma PAI-1 antigen and activity but with approximately half normal antigen and normal activity of platelet PAI-1. The low concentration of plasma PAI-1 was insufficient to neutralize circulating t-PA, resulting in high t-PA activity with normal antigen and causing the hyperfibrinolytic activity observed. Studies on seven family members of the proband indicated autosomal inheritance of plasma PAI-1 deficiency. Studies on this patient emphasize a clear correlation between decreased plasma PAI-1 activity and hyperfibrinolytic bleeding and also emphasize the unique role of plasma PAI-1 in the balance between the coagulation and fibrinolytic mechanisms.
 ...
PMID:Deficiency of plasma plasminogen activator inhibitor 1 results in hyperfibrinolytic bleeding. 848 16

Blood coagulation and rheology were studied with regard to severity of hemorrhagic syndrome and neurological complications in 44 patients with aplastic anemia (AA). Most of these patients appeared to have DIC-syndrome with serious rheological shifts. The patients suffered from hemorrhagic diathesis, nasal and gingival hemorrhages. With AA progression the severity and frequency of hemorrhagic complications increased. Neurological examination revealed in 9 of 12 AA patients organic affections of the nervous system with EEG evidence of bioelectrical shifts. In some patients neurological complications were registered prior to hemorrhagic. Therefore, to diagnose hemorrhagic complications in AA patients it is necessary to assess in details their hemocoagulation, blood rheology and neurological status.
 ...
PMID:[Hemorrhagic and neurological complications in aplastic anemia patients]. 877 61

Some platelet alpha-granule contents were assessed in parallel with other markers of hemostatic imbalance in 50 patients with hepatosplenic schistosomiasis (15 patients with compensated hepatosplenomegaly, 15 patients with advanced hepatic fibrosis and ascites and 20 patients during an acute attack of hematemesis from ruptured esophageal varices). Platelet factor 4 (PF4), beta-thromboglobulin (beta-TG), fibronectin (FN), prothrombin fragment 1 + 2, thrombin-antithrombin (TAT) complexes, fibrin degradation products (FbDP) and D-dimer were assessed in schistosomal patients compared to controls (15 healthy subjects). A significant increase in both thrombin (high TAT and prothrombin fragment 1 + 2 levels) and plasmin (high FbDP and D-dimer levels) generation was detected in decompensated patients establishing the presence of a steady state of low-grade disseminated intravascular coagulation, with and without overt bleeding, in these patients. A decrease in plasma FN concentration was found in diseased groups compared to controls. The reduction in plasma levels of FN paralleled the defective liver function and matched the relative decrease in tissue FN in liver specimens of decompensated patients suggesting that FN levels can be used to evaluate the pathological staging of the disease. A significant increase in beta-TG and PF4 levels was noted in decompensated patients with ascites and/or acute hematemesis compared both to controls and compensated patients reflecting platelet alpha-granule release and consequently increased in vivo platelet activation which may initiate and/or perpetuate the pathophysiological mechanisms of the hemostatic imbalance underlying the hemorrhagic diathesis in hepatosplenic schistosomiasis.
 ...
PMID:Fibronectin, platelet factor 4 and beta-thromboglobulin in endemic hepatosplenic schistosomiasis: relation to acute hematemesis. 909 85

We studied the etiology of subcortical hemorrhage in 55 patients (30 males, 25 females), aged 19-83 years (mean 60 years). CT scan was made in all patients on admission, with the use of intravenous infusion of contrast agent in 35 patients. Cerebral angiography was performed in 37 patients and MRI was performed in 22 patients. Forty-one patients underwent surgery and the other fourteen patients were treated conservatively. The cause of bleeding had been discovered before surgery in 12 cases; 10 arteriovenous malformations and 2 brain tumors. They were discovered by meticulous neuroradiological investigations including cerebral angiography, MRI, dynamic MRI, MRA and enhancing CT. The cause of bleeding was newly discovered after surgery in 7 cases; all of amyloid angiopathy. It remained unknown in the other 22 surgical cases although hypertensive angiopathy was suspected in eleven of them. Among the 14 patients who received conservative therapy, hemorrhagic diathesis including the use of Warfarin and DIC was the cause of bleeding in four cases and the etiology remained unknown in other ten, although hypertensive angiopathy was suspected in eight of them. The 32 patients in whom the etiology remained unknown had been observed as long as 12-120 months (mean, 40 months) and although bleeding has occurred at different locations in two of these patients, there has been no recurrence of bleeding at the same location in any of them. In conclusion, surgery is not indicated to determine the etiology of subcortical hemorrhage when meticulous neuroradiological investigations fail to disclose any vascular or tumorous lesions.
 ...
PMID:[Indications for surgery to determine the etiology of subcortical hemorrhage]. 988 45

Acute disseminated intravascular coagulation (DIC) is a rare complication of aortic aneurysm with or without dissection. We describe an 88-year-old man who presented with severe hemorrhagic diathesis and a pulsating abdominal mass. An abdominal computed tomography (CT) scan revealed a dissecting abdominal aortic aneurysm with thrombus formation, and his coagulation profile showed the features of acute DIC. After he had received blood component therapy, including fresh frozen plasma and cryoprecipitate concentrates, and intravenous heparin infusion (10,000 U/day), the bleeding diathesis and coagulopathy improved. An aneurysmectomy was performed smoothly without excessive bleeding. Coagulation parameters returned to normal after surgery. Dissecting aortic aneurysm should be considered as a possible etiology of acute disseminated intravascular coagulation, even it occurs in rare situations. Surgical intervention is still the main strategy to normalize coagulopathy. Bleeding diathesis must be corrected before surgery in order to prevent massive intraoperative bleeding.
 ...
PMID:Dissecting aortic aneurysm complicated with acute disseminated intravascular coagulation: case report. 1041 24

Acute promyelocytic leukaemia (APL) is characterised by a life-threatening hemorrhagic diathesis which is attributed to a DIC-like coagulopathy. This report describes the problems of childbirth in two patients with untreated APL. It is concluded that caesarean section can be performed without major complications. A prerequisite is an active treatment of the coagulopathy and a close collaboration between the obstetrician and the haematologist.
 ...
PMID:Caesarean section in previously untreated acute promyelocytic leukaemia. Report of two patients. 1081 77

The bleeding syndrome of acute promyelocytic leukemia (APL) is complex and consists of disseminated intravascular coagulation (DIC) and hyperfibrinolysis. Elastase, derived from malignant promyelocytes, is believed to mediate the fibrinogeno- and fibrinolysis by aspecific proteolysis. In this study we measured the role of elastase in fifteen patients with APL by using an assay for elastase degraded fibrin(ogen) and the results were compared with those obtained in patients with sepsis induced DIC. High levels of elastase were observed in sepsis and APL. The levels of fibrinogen and fibrin degradation products were significantly higher in APL patients compared to patients with sepsis induced DIC. Nevertheless, the level of elastase degraded fibrin(ogen) was higher in the sepsis group (635.3 ng/ml, compared to 144.3 ng/ml in APL; p <0.0001). So, the enormous increase in fibrin and fibrinogen degradation products in APL cannot be explained by elastase activity. This study suggests a minor role for elastase mediated proteolysis in the hemorrhagic diathesis in APL patients.
 ...
PMID:Elastase mediated fibrinolysis in acute promyelocytic leukemia. 1089 47

The most impressive clinical feature of acute promyelocytic leukemia (APL) at diagnosis is the presence in 80% to 90% of patients of a severe hemorrhagic syndrome. Recent data favor a fibrinolytic/proteolytic process rather than a disseminated intravascular coagulation as the mechanism mainly responsible for the hemorrhagic diathesis in APL. Morphologically, two main cytologic variants have been Identified: the classical hypergranular APL (M3), which represents the great majority of all APL, and the microgranular variant (M3v), which accounts for about 15% to 20% of all APL. A rare basophilic variant has also been described. With regard to prognosis, it has markedly changed from that of a rapidly fatal acute leukemia to that of a highly curable disease. This revolutionary progress was mainly due to the introduction during the 1990s of all-trans retinoic acid (ATRA) for the treatment of this disease. After the introduction of ATRA, in addition to clinical features such as hyperleukocytosis (white blood cell count > 10 x 10(9)/L) or thrombocytopenia (platelet count < 10 x 10(3)/L) at presentation, immunophenotype markers and polymerase chain reaction status for promyelocytic leukemia/retinoic acid receptor-alpha during follow-up also had an impact on prognosis.
 ...
PMID:Acute promyelocytic leukemia: clinical and morphologic features and prognostic factors. 1117 35


<< Previous 1 2 3 4 5 6 7 Next >>