[Acquired changes in platelet function].
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Biomedical subjects
Publications and source records attributed to J F Lucia.
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A 38-year-old male with proven Takayasu's arteritis presented, in a routine investigation, with thrombocytopenia, prolonged whole blood clotting time and activated partial thromboplastin time. Further studies demonstrated low levels of factor IX caused by a circulating anticoagulant. Immunological studies revealed an IgG (with kappa chains predominance) nature of this. Corticoid therapy decreased but did not suppress the anticoagulant activity. Since similar coagulation abnormalities have been described in collagen diseases, this observation is in support of this etiology to be considered in Takayasu's arteritis.
In four healthy subjects with Factor XII levels equal to or below 50% (selected at random from 100 persons) the release of Kallikrein was studied in order to establish the relationship between the above data and those found in four Hageman trait carriers showing levels of Factor XII above the lowest normal limits. It was found that for similar amounts of Hageman activity three of the carriers showed significantly less release of Kallikrein than the control subjects in whom it was normal. The conclusion was reached that the additional determination of the amount of Kallikrein released may be of value in the detection of carriers of the Hageman trait.
This report describes two people in a family with Hageman trait (homozygotes) (Factor XII = 0.06%). In addition eight family members were studied to evaluate the inheritance of this congenital deficiency. A study of the Kallikrein-Kininogen system induced by the fragments of Factor XII was carried out. It is concluded that the inheritance is as described by Veltkamp and that the Kallikrein release from the prekallikreinogen (Fletcher factor) "in vitro" is related to the amount of Factor XII procoagulant protein.
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