Antithrombin III in critically ill patients

Carvalho, Angelina C. A.; DeMarinis, Sandra; Lynch, Karen E.; Zapol, Warren M.

doi:10.1016/0883-9441(89)90068-3

Cited by 3 publications

(2 citation statements)

References 38 publications

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“…Another possibility to explain PC changes in our septic patients is the release of the monokine, tissue necrosis factor (TNF), in response to endotoxin [31), which may have suppressed transcription of the throm-bomodulin gene in the endothelial cells [32]. The combination of low PC and PS functional activities will add to the low antithrombin I11 (ATIII) levels in our patients [33] and further contribute to their hypercoagulable state.…”

Section: Discussionmentioning

confidence: 96%

Protein S and C alterations in acutely III patients

Sheth

Carvalho

1991

American J Hematol

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Protein C, a potent vitamin K-dependent protein activated by an endothelial cell cofactor, thrombomodulin, has anticoagulant and profibrinolytic activity. Free protein S, a cofactor for protein C, potentiates protein C activity at the endothelial cell surface. Pulmonary thromboemboli are a consistent finding in adult respiratory distress syndrome (ARDS). To determine if protein S or protein C were affected by widespread endothelial cell damage in ARDS, we measured bound and free protein S levels and protein C antigenic and functional levels in 18 patients with acute lung injury, 6 critically ill patients without lung history, and 22 normal subjects. Free (PS:F) and bound (PS:Ag) protein S and protein C antigen (PC:Ag) levels were measured using an enzyme-linked immunoassay and protein C function (PC:Fn) by measuring its anticoagulant activity. We found a significant decrease in bound and free protein S levels of both patient groups in comparison to normal and a shift toward the inactive, bound protein S form. In addition, a significant decrease in free protein S compared to bound protein S in both patient groups was observed. While both PC:Ag and PC:Fn were significantly reduced compared to normal, the PC:Fn was significantly and severely decreased out of proportion to the PC:Ag in both patient groups. There was no difference between those with and without lung injury for both protein S and protein C. Analyzed according to etiology of lung injury, there was no difference in the bound and free protein S, nor in PC:Ag and PC:Fn levels between patients with sepsis and trauma. However, there were significant decreases in both protein S and protein C levels compared with normal subjects. Levels of both PS and PC levels in patients who survived did not differ from those who died. In summary, our data show that both protein S and C are markedly deranged in acutely ill patients who suffered from either sepsis or trauma, and these changes are independent of lung injury. The marked reductions in functional activity of PS and PC may be contributing factors to the thromboembolic complications often observed in these patients.

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Section: Discussionmentioning

confidence: 96%

Protein S and C alterations in acutely III patients

Sheth

Carvalho

1991

American J Hematol

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“…Another factor that plagues trauma patients is the presence of decreased antithrombin III secondary to the release of tissue factors, thus favoring coagulation. [32][33][34][35] The coagulation cascade is further altered in the setting of post-trauma resuscitation with the administration of large volumes of fluid and multiple blood transfusions, thus subjecting the patient to a coagulopathic state.…”

Section: Pathophysiology Of Venous Thrombosismentioning

confidence: 99%

Venous Thromboembolism in Trauma

2003

Semin intervent Radiol

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The rationale of thromboprophylaxis stems from the high incidence of venous thromboembolism (VTE) in hospitalized patients, the clinically silent nature of this entity in a vast majority of patients, and the morbidity and potential mortality that can often be associated with it. There are few specific symptoms associated with deep vein thrombosis (DVT) and VTE, thus making clinical diagnosis unreliable. Making appropriate diagnosis and implementing treatment of DVT prior to a potentially fatal embolic event or the potential sequelae and long-term morbidity of the postphlebitic syndrome is a difficult task in any hospitalized patient. In the setting of trauma, however, diagnosis, prevention, and treatment of DVT and VTE become much more difficult.Objectives: Upon completion of this article, the reader will understand the pathophysiology, diagnosis, and treatment options concerning venous thromboembolic disease. Accreditation: Tufts University School of Medicine (TUSM) is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. TUSM takes responsibility for the content, quality, and scientific integrity of this CME activity. Credit: TUSM designates this educational activity for a maximum of 1 Category 1 credit toward the AMA Physicians Recognition Award. Each physician should claim only those credits that he/she actually spent in the activity.

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