PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Coagulation Protein Disorders”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources
PubMed2002

[Thrombophilias associated with cerebral venous thrombosis].

Many coagulation disorders have been associated with cerebral venous thrombosis. These disorders may be primary like protein C and S deficiency, antithrombine III deficiency and activated protein C resistance. Antiphospholipid antibodies represent an acquired disorders of coagulation. A prothrombotic state induced by more common factor including oral contraceptive, pregnancy and puerperium increases the venous thrombosis risk.

3' Untranslated Regions↗
PubMed2004

The nexus between systemic inflammation and disordered coagulation in sepsis.

The innate immune system is designed as an early defense system that recognizes and clears potential microbial invaders. The coagulation system co-evolved with the innate immune system from a common ancestral cellular origin, and these two systems continue to exhibit a remarkable degree of integration in their signaling pathways and regulatory circuits following tissue injury and microbial invasion. Inflammatory mediators generate procoagulant signals and intravascular thrombosis activates multiple components of the innate immune system. The success of recombinant human activated protein C for the treatment of human septic shock is likely attributable to its combined effects as an endogenous anticoagulant and an anti-inflammatory molecule. Further advances in the management of severe infections may accrue with a better understanding of the integral link between coagulation and innate immunity.

Blood Coagulation Disorders↗
PubMed1975

Postoperative problems and management after hepatic resection for blunt injury to the liver.

The postoperative problems and management of 8 patients following right hepatic lobectomy for blunt liver injury are discussed. Multiple injury and in particular chest injury are of importance. Respiratory distress may be insidious in onset and must be anticipated. Most patients require at least temporary positive pressure ventilation. Liver regeneration is rapid and histological evidence of regenerative hyperplasia is present within 3 days of injury. Hypoglycaemia of a degree sufficient to threaten life may occur postoperatively, particularly in the first 48 hours. Jaundice may be a worrying postoperative feature, but the use of T-tube drainage after hepatic lobectomy will enable any possible extrahepatic obstruction to be excluded. Hypoproteinaemia and hypo-albuminaemia occur in the immediate postoperative period, and recovery rapidly follows the peak period of regenerative activity of the liver. Normal levels are regained by the fourth to sixth postoperative weeks. Prophylactic antibiotics have no place in the postoperative management of blunt liver injury. Haemorrhagic diathesis is common after hepatic resection and is of a complex nature. Intravascular coagulation may occur and factor V deficiency is common. The mainstay of treatment is transfusion of fresh blood.

Abdominal Injuries↗
PubMed2005

[Sepsis-associated coagulation disorders].

Coagulation activation with intravascular fibrin formation is a general finding in patients with sepsis. Low coagulation factors may be caused by disseminated intravascular coagulation, as well as by loss of plasma and impaired hepatic synthesis in the course of sepsis. The leading clinical symptom in consumption coagulopathy is bleeding. Therefore, treatment mainly consists of substitution of coagulation factors and platelets. Meningococcal and pneumococcal, as well as some other infections may lead to sepsis-induced purpura fulminans, a condition associated with microvascular thrombosis, necrosis, and haemorrhage. A typical laboratory sign is a very low plasma protein C level. Treatment with protein C concentrate or recombinant activated protein C (Drotrecogin alfa, activated) has been shown to be beneficial in sepsis-induced purpura fulminans. Unfractionated heparin or low molecular weight heparin has been recommended for prophylaxis of venous thrombosis, but there are no clinical studies specifically on patients with sepsis. Antithrombin concentrate is used in patients with antithrombin deficiency treated with heparin for acute venous thrombosis or embolism, extracorporeal circulation procedures or other invasive procedures. There is no indication for general use of antithrombin concentrate in patients with sepsis even in patients with low plasma antithrombin levels. Drotrecogin alfa, activated, is used for treatment of patients with severe sepsis. Its use is not limited to patients with sepsis-induced disseminated intravascular coagulation, although these patients appear to benefit especially from this therapy.

Blood Coagulation Disorders↗