Antithrombin-III deficiency in a Dutch family

Meer, J. van der; Dalen, E. A. Stoepman-Van; Jh, Jansen

doi:10.1136/jcp.26.7.532

Cited by 103 publications

(22 citation statements)

References 13 publications

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“…'4 [16][17][18][19][20][21][22][23][24][25][26][27][28] The family described here, which is to our knowledge the first family with ATIII deficiency identified in the United Kingdom, showed the characteristic association of reduced ATIII concentrations and major episodes of venous thrombosis. As in the families mentioned above, the ATIII deficiency in our family was found on both functional and immnunological assays and therefore probably represented a true reduction in ATIII protein synthesis.…”

Section: Discussionmentioning

confidence: 99%

Familial thrombosis: inherited deficiency of antithrombin III.

Mackie¹,

Bennett²,

Ogston³

et al. 1978

BMJ

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Section: Discussionmentioning

confidence: 99%

Familial thrombosis: inherited deficiency of antithrombin III.

Mackie¹,

Bennett²,

Ogston³

et al. 1978

BMJ

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“…Depressed AT I11 levels caused by hemodilution after surgery or extensive blood loss during parturition might also contribute to the occurrence of thrombosis. From our observations, it seems probable that the reported thrombo-embolic episodes in early pregnancy or after ingestion of synthetic estrogens by patients with hereditary AT I11 deficiency (1,18), are the result of further depressed AT I11 levels by hemodilution. In patients with low-normal AT I11 levels (e.g.…”

Section: G H Weeninketalmentioning

confidence: 70%

“Morning‐After Pill” and Antithrombin III

Weenink

Cate

Kahlé

et al. 1983

Acta Obstet Gynecol Scand

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Plasma antithrombin III (AT III) was studied longitudinally in 15 subjects (13 patients and 2 volunteers), who used the "morning-after pill" (5 mg ethinylestradiol daily for 5 days). The mean decrease in AT III level in the 13 patients was 17% of the pre-treatment value. From additional observations made in 2 of the patients and in the 2 volunteers it is concluded that this decrease is caused by hemodilution due to salt and water retention rather than by a decreased synthesis or increased consumption.

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“…Patients with hereditary deficiency of AT have a marked increased risk of venous thrombotic events and PE (21,114,117,(130)(131)(132)(133). These events typically appear in the mid to late teenage years.…”

Section: Pathological Decreases In Antithrombinmentioning

confidence: 99%

Syndromes of Thrombosis and Hypercoagulability: Congenital and Acquired Thrombophilias

Bick

Kaplan

1998

Clin Appl Thromb Hemost

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This article stresses the common hereditary and acquired blood protein defects associated with thrombosis. The most common of the hereditary defects apear to be APC-R, SPS, antithrombin, protein C, and protein S deficiency, and the most common acquired defects are anticardiolipin antibodies and the lupus anticoagulant (antiphospholipid antibodies). Therefore, these are the defects that should first be looked for in an individual with unexplained thrombosis. If these more common defects are not found, then the rarer defects including HC II, plasminogen or TPA deficiency, dysfibrinogenemia, el evated PAI-1 and hyperhomocysteinemia should be sought. The importance of finding these defects has significant impli cations for therapy of the individual patient and for institutions of family studies to identify, inform, and possibly treat others at risk. It is expected that as knowledge of hemostasis expands, more hereditary and acquired defects, such as elevated lipopro tein (a) or defects of extrinsic (tissue factor) pathway inhibitor (EPI, TFPI), may be associated with enhanced risks of throm bosis. Finally, it must be recalled that a diagnosis of thrombo sis, like that of anemia, is only a generic and partial diagnosis; just as in the anemic patient, the etiology must be clearly de fined. Only in this manner can cost-effective and appropriate therapy for both primary treatment and secondary prevention be designed. In addition, the demonstration of a hereditary defect will allow primary prevention in afflicted family mem bers by allowing the choice of appropriate therapy.

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Antithrombin-III deficiency in a Dutch family

Cited by 103 publications

References 13 publications

Familial thrombosis: inherited deficiency of antithrombin III.

Familial thrombosis: inherited deficiency of antithrombin III.

“Morning‐After Pill” and Antithrombin III

Syndromes of Thrombosis and Hypercoagulability: Congenital and Acquired Thrombophilias

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