Splenic abscess caused by Blastomyces dermatitidis.

We have reported a case of fungal splenic abscess caused by Blastomyces dermatitidis. Splenic abscess is an uncommon disorder, and fungus as the causative organism is rare. The diagnosis of splenic abscess can be rapidly made with radionuclide and CT scanning and ultrasonography. Splenectomy with appropriate antifungal chemotherapy is the currently recommended therapy.

Longitudinal study of platelet indices during normal pregnancy.

The purpose of this longitudinal, prospective study was to define platelet indices during normal pregnancy and to compare them to normal nonpregnant values. Indices evaluated included platelet count, mean platelet volume, and platelet distribution width. No significant change occurred in the mean platelet count or mean platelet volume from the second to the third trimester; however, platelet distribution width increased progressively and significantly during this interval (p less than 0.0001). Mean platelet volume versus platelet count showed a significant inverse relationship (p less than 0.0001) and was congruent with normal nonpregnant values. Mean platelet volume versus platelet distribution width exhibited a significant direct relationship (p less than 0.03) that differed remarkably from normal nonpregnant values. These data support the concept of normal pregnancy as a compensated state of progressive platelet consumption. These findings may have important diagnostic and prognostic applications in discerning acute states of platelet consumption superimposed on the compensated consumption of normal pregnancy.

Constitutional hypofibrinogenemia associated with third trimester hemorrhage.

This case of a 31-year-old white woman presenting at 32 weeks gestation with vaginal bleeding supports a possible association between constitutional hypofibrinogenemia and third trimester hemorrhage. Clot based fibrinogen assays were persistently low for the third trimester (patient: 102 to 155 mg per dl; normal range: 400 to 650 mg per dl) and at follow-up, ten months post-partum (patient: 90 mg per dl; normal range 180 to 436 mg per dl); an immunologic fibrinogen level was comparable. The patient gave an unremarkable bleeding history. Of 11 previously reported pregnancies in five hypofibrinogenemic patients, six terminated in placental abruption during the third trimester, two others were complicated by significant post-partum hemorrhage, and one by spontaneous abortion. This case report emphasizes that low functional levels of fibrinogen are potentially disruptive to the integrity of the uteroplacental interface. The pregnant state unmasks and amplifies an otherwise silent to mild hemostatic disorder.

The effect of dextran-40 on platelet adenosine triphosphate release in vitro.

Studies of dextran's effect on platelet function have revealed inconclusive results; some reports have suggested it acts as an aggregating agent, others as an inhibitor to aggregation. This study demonstrates the inhibitory effect of dextran (40,000 MW) on in vitro platelet adenosine triphosphate (ATP) release when stimulated by conventional aggregatory reagents. These data support inhibition of platelet surface phenomena, possibly involving receptor sites, rather than intracellular phenomena as the mechanism of dextran's anti-aggregatory effect. Significant inhibition occurs in vitro at dextran levels approximately twice that normally attained in vivo.

beta-Thromboglobulin and platelet factor 4 levels in a case of acute thrombotic thrombocytopenic purpura.

We have described a case of acute thrombotic thrombocytopenic purpura in which multiple therapeutic methods eventuated in recovery. We suggest that the ratio of the platelet marker proteins beta-thromboglobulin and platelet factor 4 may have value in the assessment of therapy and prognosis in following the clinical course of this disorder of platelets.

Antithrombin III, plasminogen, plasmin, and alpha-2-antiplasmin in donor blood and plasma components.

The functional levels of antithrombin III, plasminogen, plasmin, and alpha-2-antiplasmin were evaluated in sequentially derived fresh frozen plasma, cryoprecipitate, and cryo-poor plasma aliquots from 20 registered blood donors. Antithrombin III is the major plasma inhibitor of the serine proteases of the procoagulant system. Plasminogen, the proenzymatic form of plasmin, is the primary endogenous profibrinolytic moiety; alpha-2-antiplasmin is the principal intermediate acting inhibitor of plasmin. As congenital or acquired deficiencies of antithrombin III and/or plasminogen predispose to thrombosis, and as these agents may be consumed in acute thrombosis, the goal of this investigation was to discern those plasma components which potentially might maximize both antithrombotic and fibrinolytic activities if used therapeutically. Using enzyme specific synthetic substrate methods, it was determined that no spontaneous plasmin activity was evident through phlebotomy or component processing and storage. Analysis of variance showed antithrombin III to be significantly decreased in cryoprecipitate as compared to the other components (p less than 0.0001). Furthermore, the level of antithrombin III or plasminogen in cryo-poor plasma and fresh frozen plasma was not statistically different. Also, the alpha-2-antiplasmin level was not statistically different among the specimen groups. Since fresh frozen plasma and cryo-poor plasma contain comparable total quantities of antithrombin III and plasminogen and as most of the activity of factors I, V, VIII, and XIII is diverted into cryoprecipitate, it is suggested that cryo-poor plasma may be preferable to fresh frozen plasma for the treatment of thrombosis associated with or complicated by antithrombin III and/or plasminogen deficiency.

Diagnostic problems of von Willebrand's disease in a general hospital laboratory.

The expression of variant types of von Willebrand's disease can present an elusive diagnostic problem. Bleeding history of patients can vary greatly, as can the results of tests for the components of the Factor VIII complex. Recent advances in characterizing and measuring the factor VIII complex have greatly improved the diagnosis of the variant forms of von Willebrand's disease. However, some of the less sophisticated procedures, which are more readily available, can still be utilized by the routine general hospital laboratory to identify or suspect the occasional case of von Willebrand's disease. These points are exemplified in this report of seven family members who were studied.