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Hemorrhagic Disorders (Hemorrhagic Diathesis)

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456  relevant articles (2 outcomes, 14 trials/studies) found for this Disease

Description: Spontaneous or near spontaneous bleeding caused by a defect in clotting mechanisms (BLOOD COAGULATION DISORDERS) or another abnormality causing a structural flaw in the blood vessels (HEMOSTATIC DISORDERS).

Also Known As:
Hemorrhagic Diathesis; Diatheses, Hemorrhagic; Diathesis, Hemorrhagic; Disorder, Hemorrhagic; Disorders, Hemorrhagic; Hemorrhagic Diatheses; Hemorrhagic Disorder

Relationship Network

Disease Context: Research Results

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Hemic and Lymphatic Diseases
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Hematologic Diseases: 1480
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Hemorrhagic Disorders: 456
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Hemophilia A: 4596
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Disseminated Intravascular Coagulation: 3684
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Idiopathic Thrombocytopenic Purpura: 2858
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von Willebrand Disease: 1650
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Hemophilia B: 1022
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Thrombasthenia: 559
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Essential Thrombocythemia: 538
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Vitamin K Deficiency: 407
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Wiskott-Aldrich Syndrome: 372
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Hypoprothrombinemias: 344
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Bernard-Soulier Syndrome: 263
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Afibrinogenemia: 189
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Factor VII Deficiency: 187
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Factor XI Deficiency: 167
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Factor V Deficiency: 126
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Factor X Deficiency: 107
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Hemostatic Disorders: 106
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Factor XII Deficiency: 105
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Platelet Storage Pool Deficiency: 95
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Factor XIII Deficiency: 94
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Waterhouse-Friderichsen Syndrome: 38

Related Diseases

1. Hemophilia A (Haemophilia)
2. Thrombocytopenia (Thrombopenia)
3. Thrombosis (Thrombus)
4. Neoplasms (Cancer)
5. Liver Cirrhosis (Hepatic Cirrhosis)

Experts

1. Balkan, Can: 1 article (06/2008)
2. Kavakli, Kaan: 1 article (06/2008)
3. Akisü, Mete: 1 article (06/2008)
4. Karapinar, Bülent: 1 article (06/2008)
5. Karapinar, Bulent: 1 article (06/2008)
6. Yilmaz, Deniz: 1 article (06/2008)
7. Akisu, Mete: 1 article (06/2008)
8. Aktaran, Sebnem: 1 article (11/2006)
9. Geyik, Ramazan: 1 article (11/2006)
10. Buyukhatipoglu, Hakan: 1 article (11/2006)

Drugs and Biologics

Drugs and Important Biological Agents (IBA) related to Hemorrhagic Disorders:
1. recombinant FVIIa (rFVIIa)IBA
2. Phenobarbital (Luminal)FDA Link
07/09/1956 - "[Vasoparalytic hemorrhagic diathesis cured by luminal sleep.]"
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3. CollagenIBA
08/13/1990 - "Platelets from a patient with an acquired hemorrhagic disorder had a severely impaired response to collagen, whereas platelet aggregation to other agonists and coagulations tests were normal. "
09/01/2003 - "From 1998-2000, PFA-100 closure time (CT) for epinephrinecollagen (EPI) and ADP-collagen (ADP) cartridges and modified Ivy BTs were performed on outpatients referred for testing for suspected or known hemorrhagic diathesis (n = 346). "
08/01/1993 - "To evaluate the physiologic importance of the different collagen receptors on platelets, we screened 806 patients admitted to the hospital because of hemorrhagic diathesis for eventual laboratory evidence of a pathologic platelet collagen interaction, and found 5 patients with an isolated deficiency in collagen-induced platelet aggregation. "
02/01/1978 - "These studies demonstrated a drug dependent, reversible hemorrhagic diathesis associated with (1) prolongation of bleeding time, (2) decreased platelet aggregation responses to ADP, collagen, and epinephrine, and (3) depleted platelet stores of ADP in the absence of thrombocytopenia. "
12/01/1992 - "This study characterizes a congenital hemorrhagic disorder caused by a platelet function defect with the following features: (1) severely impaired platelet aggregation and fibrinogen or von Willebrand factor (vWF) binding induced by adenosine diphosphate (ADP); (2) defective aggregation, release reaction, and fibrinogen or vWF binding induced by other agonists; (3) normal aggregation and release reaction induced by high concentrations of thrombin or collagen; (4) no further inhibition by ADP scavengers of aggregation, release reaction, and fibrinogen or vWF binding, comparable with those observed for normal platelets in the presence of ADP scavengers; (5) normal membrane glycoprotein (GP) composition and normal binding of the anti-GP IIb/IIIa monoclonal antibody 10E5; (6) no acceleration by ADP of binding of the anti-GP IIb/IIIa monoclonal antibody 7E3; (7) normal platelet-fibrin clot retraction if induced by thrombin or reptilase plus epinephrine, absent if induced by reptilase plus ADP; (8) no inhibition by ADP of the prostaglandin E1-induced increase in platelet cyclic adenosine monophosphate, but normal inhibition by epinephrine; (9) defective mobilization of cytoplasmic Ca2+ by ADP; (10) normal binding of 14C-ADP to fresh platelets, but defective binding of [2-3H]-ADP to formalin-fixed platelets. "
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4. Adenosine Diphosphate (ADP)IBA
09/01/2003 - "From 1998-2000, PFA-100 closure time (CT) for epinephrinecollagen (EPI) and ADP-collagen (ADP) cartridges and modified Ivy BTs were performed on outpatients referred for testing for suspected or known hemorrhagic diathesis (n = 346). "
02/01/1978 - "These studies demonstrated a drug dependent, reversible hemorrhagic diathesis associated with (1) prolongation of bleeding time, (2) decreased platelet aggregation responses to ADP, collagen, and epinephrine, and (3) depleted platelet stores of ADP in the absence of thrombocytopenia. "
12/01/1992 - "This study characterizes a congenital hemorrhagic disorder caused by a platelet function defect with the following features: (1) severely impaired platelet aggregation and fibrinogen or von Willebrand factor (vWF) binding induced by adenosine diphosphate (ADP); (2) defective aggregation, release reaction, and fibrinogen or vWF binding induced by other agonists; (3) normal aggregation and release reaction induced by high concentrations of thrombin or collagen; (4) no further inhibition by ADP scavengers of aggregation, release reaction, and fibrinogen or vWF binding, comparable with those observed for normal platelets in the presence of ADP scavengers; (5) normal membrane glycoprotein (GP) composition and normal binding of the anti-GP IIb/IIIa monoclonal antibody 10E5; (6) no acceleration by ADP of binding of the anti-GP IIb/IIIa monoclonal antibody 7E3; (7) normal platelet-fibrin clot retraction if induced by thrombin or reptilase plus epinephrine, absent if induced by reptilase plus ADP; (8) no inhibition by ADP of the prostaglandin E1-induced increase in platelet cyclic adenosine monophosphate, but normal inhibition by epinephrine; (9) defective mobilization of cytoplasmic Ca2+ by ADP; (10) normal binding of 14C-ADP to fresh platelets, but defective binding of [2-3H]-ADP to formalin-fixed platelets. "
Order ALL the reference details at left...
5. Epinephrine (Adrenaline)FDA LinkGeneric
02/01/1978 - "These studies demonstrated a drug dependent, reversible hemorrhagic diathesis associated with (1) prolongation of bleeding time, (2) decreased platelet aggregation responses to ADP, collagen, and epinephrine, and (3) depleted platelet stores of ADP in the absence of thrombocytopenia. "
12/01/1992 - "This study characterizes a congenital hemorrhagic disorder caused by a platelet function defect with the following features: (1) severely impaired platelet aggregation and fibrinogen or von Willebrand factor (vWF) binding induced by adenosine diphosphate (ADP); (2) defective aggregation, release reaction, and fibrinogen or vWF binding induced by other agonists; (3) normal aggregation and release reaction induced by high concentrations of thrombin or collagen; (4) no further inhibition by ADP scavengers of aggregation, release reaction, and fibrinogen or vWF binding, comparable with those observed for normal platelets in the presence of ADP scavengers; (5) normal membrane glycoprotein (GP) composition and normal binding of the anti-GP IIb/IIIa monoclonal antibody 10E5; (6) no acceleration by ADP of binding of the anti-GP IIb/IIIa monoclonal antibody 7E3; (7) normal platelet-fibrin clot retraction if induced by thrombin or reptilase plus epinephrine, absent if induced by reptilase plus ADP; (8) no inhibition by ADP of the prostaglandin E1-induced increase in platelet cyclic adenosine monophosphate, but normal inhibition by epinephrine; (9) defective mobilization of cytoplasmic Ca2+ by ADP; (10) normal binding of 14C-ADP to fresh platelets, but defective binding of [2-3H]-ADP to formalin-fixed platelets. "
Order ALL the reference details at left...
6. FibrinIBA
7. Fibrinogen (Factor I)IBA
8. Factor XIII (Coagulation Factor XIII)IBA
9. ThrombinIBA
10. von Willebrand FactorIBA
05/01/2005 - "Characterization of a myeloma patient with a life-threatening hemorrhagic diathesis: presence of a lambda dimer protein inhibiting shear-induced platelet aggregation by binding to the A1 domain of von Willebrand factor."
06/22/2002 - "[From gene to disease; from mutations in the Von Willebrand factor gene to hemorrhagic diathesis and thrombocytopenia]"
12/01/1993 - "Synergistic effect of storage pool deficient platelets and low plasma von Willebrand factor on the severity of the hemorrhagic diathesis in Hermansky-Pudlak syndrome."
12/01/1992 - "This study characterizes a congenital hemorrhagic disorder caused by a platelet function defect with the following features: (1) severely impaired platelet aggregation and fibrinogen or von Willebrand factor (vWF) binding induced by adenosine diphosphate (ADP); (2) defective aggregation, release reaction, and fibrinogen or vWF binding induced by other agonists; (3) normal aggregation and release reaction induced by high concentrations of thrombin or collagen; (4) no further inhibition by ADP scavengers of aggregation, release reaction, and fibrinogen or vWF binding, comparable with those observed for normal platelets in the presence of ADP scavengers; (5) normal membrane glycoprotein (GP) composition and normal binding of the anti-GP IIb/IIIa monoclonal antibody 10E5; (6) no acceleration by ADP of binding of the anti-GP IIb/IIIa monoclonal antibody 7E3; (7) normal platelet-fibrin clot retraction if induced by thrombin or reptilase plus epinephrine, absent if induced by reptilase plus ADP; (8) no inhibition by ADP of the prostaglandin E1-induced increase in platelet cyclic adenosine monophosphate, but normal inhibition by epinephrine; (9) defective mobilization of cytoplasmic Ca2+ by ADP; (10) normal binding of 14C-ADP to fresh platelets, but defective binding of [2-3H]-ADP to formalin-fixed platelets. "
Order ALL the reference details at left...

Therapies and Procedures

1. Blood Transfusion (Blood Transfusions)
2. Liver Transplantation
3. Intravenous Injections
4. Splenectomy
5. Tooth Extraction (Tooth Extractions)

Best Treatments:
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