Another family with the factor VII Padua defect is described. The proposita is a 18-year-old female who presented easy bruising and epistaxis. The main laboratory features of the defect are: prolonged prothrombin time, normal partial thromboplastin time, normal Stypven-cephalin clotting time and normal Thrombotest. Factor VII activity is low when assayed using rabbit brain thromboplastin but is normal when assayed using ox brain thromboplastin. The parents of the proposita were consanguineous (first cousins) and were heterozygotes. Other family members were also shown to be heterozygotes for the abnormality. The present patient is not related to the other family with this disorder. The abnormality may be more widespread than originally thought.

A family with a new factor X defect is reported. The proposita is a 56-year-old female. She is asymptomatic and no consanguinity is present between the parents. The main features of the defect are: prolongation of prothrombin time and derivative tests but normal partial thromboplastin time. Factor X was found to be low (about 25–30% of normal) only if tissue thromboplastins were used in the assay system. Chromogenic substrate S-2222 also yielded decreased factor X levels. However, factor X activity was normal with cephalin and cephalin-RVV mixture. Factor X antigen was normal in three immunological systems (electroimmunoassay, an Elisa method and laser nephelometry). Crossed immunoelectrophoresis and antigen-antibody kinetics recorded in a laser nephelometer failed to show major differences from normal factor X. Both sons of the proposita, the father and other family members showed slightly decreased factor X levels and normal factor X antigen and were considered heterozygous for the abnormality. The toponym factor X Padua is proposed to indicate this peculiar abnormality.

A "new" antithrombin III (AT III) abnormality is described in five members of the same family. None of the affected members showed thrombotic manifestations and no consanguinity was present in the family. The main laboratory features were: normal routine clotting tests, slightly decreased AT III activities in all assays carried out in the presence of heparin. In the absence of heparin, antithrombin III activities were instead within normal limitis. Progressive AT III activity and AT III antigen were also normal. Crossed immunoelectrophoresis in the absence of heparin showed a normal pattern both in plasma and serum. In the presence of heparin, the propositi's plasma showed a major, less anodal, abnormal peak and a smaller normal peak. Three peaks were present in the propositi's serum as compared with the two normal ones. This AT III abnormality is different from AT III Padua previously described by us and we propose the toponym of Antithrombin Padua-2 to define this condition.

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Factor VII activity and cross-reacting material was assayed in fresh and deep frozen non-contacted plasma in 43 patients with Hemophilia B belonging to different kindreds. Factor VII activity was found to be slightly decreased (about of 50% normal) in 12 patients, regardless of the thromboplastin used. In an additional patient (hemophilia BM) factor VII was slightly decreased in 1 : 10 diluted plasma but was normal in further diluted plasma. In the remaining 30 patients factor VII activity was normal. No significant variation was found between fresh and deep frozen plasmas. Factor VII antigen or cross-reacting material was normal.