1956
DOI: 10.1111/j.1365-2141.1956.tb06825.x
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Coagulation Defects in a Case of Systemic Lupus Erythematosus with Thrombocytopenia

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Cited by 27 publications
(13 citation statements)
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“…Our study confirms several observations and statements from other in vestigators: (1) the inhibitor does not destroy coagulation factors nor inter mediate products [2]; (2) the inhibitory effect is more marked when weaker concentrations of thromboplastin or phospholipid are used [2,16,21]; (3) some patients also have a true factor II deficiency [2,3,8,17,24], It is shown that the inhibitor activity in our patients is not specifically directed against one or more clotting factors. Since all clotting factor assays are influenced by the inhibitor if the same accelerating phospholipid is used, we are inclined to think that the inhibitor interferes with clotting factor ad sorption on to lipid surfaces [9], probably by covering these up.…”
Section: Discussionsupporting
confidence: 89%
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“…Our study confirms several observations and statements from other in vestigators: (1) the inhibitor does not destroy coagulation factors nor inter mediate products [2]; (2) the inhibitory effect is more marked when weaker concentrations of thromboplastin or phospholipid are used [2,16,21]; (3) some patients also have a true factor II deficiency [2,3,8,17,24], It is shown that the inhibitor activity in our patients is not specifically directed against one or more clotting factors. Since all clotting factor assays are influenced by the inhibitor if the same accelerating phospholipid is used, we are inclined to think that the inhibitor interferes with clotting factor ad sorption on to lipid surfaces [9], probably by covering these up.…”
Section: Discussionsupporting
confidence: 89%
“…Because of the observation of antiplatelet-factor-III activity [17] and the frequently ob served false-positive serological reactions for syphilis [3,5,6,8,14,15,17,19,23], positive cephalin flocculation (Hänger) test [3,5,8,17], and positive direct antiglobulin (Coombs) test [14,15,17] associated with the presence of circulating anticoagulant in these patients, it was generally thought that these phenomena were related to the same immunological complication. F r ic k [8] also found that the blood of a new-born baby from a mother with DLE and a circulating anticoagulant not only contained anticoagulant acti vity of the same type for several weeks after birth, but also abnormal sero logic and turbidimetric tests for a longer period.…”
Section: Introductionmentioning
confidence: 99%
“…However the PT can be utilized to screen for the LA if a weak thromboplastin is used, and this fact forms the basis of the so-called dilute tissue thromboplastin assay (10)(11)(12)(13)(14)(15)(16). In this test the PT of patient and control plasma is performed by using exponential dilutions of tissue thromboplastin.…”
Section: Discussionmentioning
confidence: 99%
“…The type of tissue thromboplastin utilized in the assay does not appear to be a limiting factor, because the abnormality has been observed with dilute rabbit brain (6,lO-14), human brain (15,16), and bovine lung (12) tissue thromboplastins. The marked prolongation of the PT when dilute tissue thromboplastin is utilized appears to be specific for the L A and has not been observed in plasma from patients receiving coumarin compounds, in plasma from patients congenitally deficient in prothrombin, factor VIII, or factor IV, and in plasma containing anti-factor VIII antibody (5,6,11).…”
Section: Discussionmentioning
confidence: 99%
“…17, 18]. The antibodies are mostly directed against the prothrombin activator complex, against factor VIII and against factor IX [1,4,9,13,14,17,18], In such patients se vere bleeding symptoms occur: bleeding in SLE may also be related to thrombocytopenia [1,4], which almost always is associated with the pres ence of antiplatelet antibodies [8,11]. However, some cases with anticoa gulants against factor XI [4,12] and factor XII [4,6,7] have also been reported.…”
mentioning
confidence: 99%