Literature DB >> 1585693

[Acquired antithrombin III deficiency].

G Müller1.   

Abstract

Acquired antithrombin III (AT III) deficiency is based on either decreased activity or synthesis, increased loss or increased consumption. The activity of AT III is decreased in metabolic acidosis, hyperlipoproteinemias and by lipid peroxides. Chronic liver diseases especially liver cirrhosis are associated with very low levels of AT III due to insufficient hepatic synthesis, reduced transcapillary flux ratios, diffuse intravascular coagulation and loss in the ascites. Gastrointestinal loss of AT III may occur in patients with active inflammatory bowel diseases. AT III deficiency is observed in nephrotic syndrome when urinary loss of protein exceeds 5 g/d. During hemodialysis we have not found low AT III levels. Disseminated intravascular coagulation is characterized by activation of the coagulation system and increased consumption of AT III. AT III complexes with activated coagulation factors are subsequently cleared by the reticuloendothelial system.

Entities:  

Mesh:

Substances:

Year:  1992        PMID: 1585693

Source DB:  PubMed          Journal:  Z Gesamte Inn Med        ISSN: 0044-2542


  2 in total

1.  Multiple Retinal Vein Occlusions Associated with Anti-thrombin III Deficiency.

Authors:  Ramin Nourinia; Talie Montahaei; Bahareh Behdad; Ali Aghajani
Journal:  J Ophthalmic Vis Res       Date:  2015 Oct-Dec

2.  GCN2 is required to increase fibroblast growth factor 21 and maintain hepatic triglyceride homeostasis during asparaginase treatment.

Authors:  Gabriel J Wilson; Brittany A Lennox; Pengxiang She; Emily T Mirek; Rana J T Al Baghdadi; Michael E Fusakio; Joseph L Dixon; Gregory C Henderson; Ronald C Wek; Tracy G Anthony
Journal:  Am J Physiol Endocrinol Metab       Date:  2014-12-09       Impact factor: 4.310

  2 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.