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ZusammenfassungRekombinanter Faktor VIIa (rFVIIa) wird über die zugelassenen Indikationen hinaus zunehmend zur Behandlung lebensbedrohlicher Blutungsereignissen bei Versagen der jeweiligen Standardtherapien eingesetzt. Kasuistiken und Fallserien dokumentieren die Wirksamkeit und Sicherheit von rFVIIa zur Blutstillung bei Patienten mit Thrombozytopathien und Thrombozytopenien verschiedener Ursache. Eine Zulassung zur Anwendung von rFVIIa liegt bei Patienten mit Thrombasthenie Glanzmann im Falle eines Refraktärzustandes auf die Transfusion von Thrombozytenkonzentraten vor. rFVIIa-Bolusapplikationen mit Dosierungen zwischen 80 und 120 μg/kg Körpergewicht alle 1,5 bis 3 Stunden werden auch bei Bernard-Soulier-Syndrom, Plättchen- Storage-Pool-Defekten und verschiedenen erworbenen Thrombozytopathien erfolgreich eingesetzt. Bei Thrombasthenie Glanzmann sind zur Gewährleistung einer effektiven Hämostase mindestens drei Bolusgaben notwendig. Bei Thrombozytopenie hat sich bei annähernd der Hälfte der Patienten ein einzelner rFVIIa-Bolus zur Beherrschung sonst unstillbarer Blutungen als ausreichend erwiesen. Dabei kann eine Blutstillung unter rFVIIa auch bei Thrombozytenwerten unter 20 000/μl erreicht werden, wenngleich bei höheren Thrombozytenkonzentrationen eine bessere Wirksamkeit erzielbar ist.

Economizing health care systems has led to industrialized hospitals. The consequences and side effects are substantial and rather promote costs explosion due to the dictated increase in cases and efficiency. Hence, position sensing and change in direction are required. Effective ways to find out of the current crisis are discussed.

ZusammenfassungEs wird ein Überblick über angeborene und erworbene Thrombozytenfunktionsstörungen und ihre Therapiemöglichkeiten gegeben. Angeborene Thrombozytenfunktionsstörungen kommen extrem selten vor, erworbene Störungen hingegen dürften die häufigsten Störungen der Blutstillung sein. Die Aufklärung der den angeborenen Störungen zugrunde liegenden Defekte hat unser Verständnis der Plättchenfunktionen wesentlich verbessert. Erworbene Plättchenfunktionsstörungen werden durch unterschiedlichste Erkrankungen oder Arzneimittel hervorgerufen.

SummaryAcquired haemophilia A (AHA) is caused by autoantibody inhibitors of coagulation factor VIII (FVIII : C). Recent onset of bleeds and isolated prolongation of the activated partial thromboplastin time (aPTT) are characteristic features of the disorder. Reduced FVIII : C activity and a detectable FVIII : C inhibitor in the Bethesda assay confirm the diagnosis. Patients should be referred to expert centres, whenever possible, and invasive procedures with a high risk of bleeding must be avoided, until haemostasis has been secured by adequate therapy.Bypassing agents capable of inducing sufficient thrombin formation in the presence of FVIII : C inhibitors are treatment of choice, including currently available recombinant factor VIIa (NovoSeven™) and activated prothrombin complex concentrate (FEIBA™). These agents represent first line therapy to control acute or severe bleeds. To eradicate inhibitors, immunosuppressive treatment (IST) is indicated in patients with AHA. Glucocorticoids, cytotoxic agents and rituximab are most widely used. However, an ideal IST regimen has not been established so far. Adverse events of IST, including infections as the foremost cause death, are frequent complications in AHA.

Venous thromboembolism (VTE) is associated with high morbidity and mortality. Therefore, effective methods for safe thromboprophylaxis remain an ongoing challenge in daily clinical practice. This is especially true for pregnant women and patients with gynaecological malignancies. Low-molecular weight heparins continue to be agents of choice for pharmacological thromboprophylaxis postoperatively, in pregnant patients at risk, and during the puerperium. However, these drugs can cause bleeds or heparin-induced thrombocytopenia (type II). Based on recent revisions of corresponding guidelines, this article provides an overview of the current state of pharmacological thromboprophylaxis and discusses prevailing problems and unresolved issues.

For many decades, hemostatic and immune defense mechanisms were thought to act independently. More recently, this concept has been revised largely. Thus, it is becoming apparent that platelets, like leukocytes, have multiple functions in innate and adaptive immunity, changing their role from “innocent bystanders” to integral players in inflammatory or infectious processes and immunity (1, 2). For example, platelets express and secrete a variety of pro-inflammatory molecules that can trigger or modulate immune responses (3). Apart from that, up-regulation of plasma components such as distinct adhesive proteins and several coagulation factors in response to inflammatory processes (commonly designated “acute phase reaction”) is a frequent and well-known but less wellunderstood phenomenon. The multiple functions of tissue factor also illustrate the extensive cross talk between inflammation and coagulation. For example, apart from its crucial role in initiating coagulation by activating FVII (4), membrane-bound tissue factor is also capable of signal transduction, thus mediating inflammatory pathways (5). A brief look at the evolution reveals that hemostasis and immune defense have emerged from a “common trunk”. Thus, invertebrates possess circulating cells termed hemocytes that have a dual role: hemocytes protect the host from invading microbes, prevent loss of hemolymph by initiating coagulation upon injury, and mediate wound healing (1, 6). Only at the level of lower vertebrates, immune defense and hemostatic mechanisms are carried out through distinct cell populations, i. e. leukocytes and nucleated thrombocytes, while anucleated platelets are only found in mammals. Recently proposed concepts and designations such as “immuno-thrombosis” (7) or “thrombo-inflammation” (8) are reflecting both the evolutionary nexus and the up-to-date contention of a multifunctional link between hemostasis and the immune system. This theme issue of Hamostaseologie presents several highlights of the GTH Congress 2015 (9, 10) and offers the opportunity to reflect and strengthen a central topic, which was covered in various stateof-the-art lectures at the Dusseldorf conference. Ruggeri and Mendolicchio provide a comprehensive review on the key role of plasma von Willebrand factor (VWF) and its interaction with platelet and endothelial cell receptors or extracellular matrix components during physiological hemostasis and abnormal thrombus formation (11). Specifically, the impact of flow dynamic conditions on the action of VWF after traumatic injury or atherosclerotic plaque rupture is discussed in detail. Complementary to this contribution, Reininger reports on the function of ultra-large VWF multimers that are being formed under abnormally high shear stress and modulated by ADAMTS13-induced proteolytic cleavage. This interaction appears to provide an effective regulatory mechanism to control highly reactive ultra-large VWF multimers (12) . Vogtle et al. summarize recent insights into platelet receptors, including the C-type lectin-like (CLEC) receptor 2, and their role as potential pharmacological tarProf. Rudiger E. Scharf Institut fur Hamostaseologie, Hamo therapie und Transfusionsmedizin, Universitatsklinikum, Heinrich-Heine-Universitat Dusseldorf Fo to : D an ie l S ch um an n

For clinicians, who are not experienced in hemostasis and thrombosis, coagulation and coagulation disorders remain a ‘book of seven seals’ (1). This may be due, at least in part, to the complexity of the hemostatic apparatus and its interaction with inflammatory processes and immune mechanisms, all of which require detailed theoretical knowledge, practical experience, and continuous medical education (CME). More recently, the use of direct oral anticoagulants, which have specific pharmacological targets and pharmacodynamics distinct from those of vitamin K antagonists, heparins, or the pentasaccharide fondaparinux, has created insecurities and concerns among clinicians. Some of these concerns result from the fact that these novel agents with their superior safety profile impact on standard coagulation screening tests (such as prothrombin time and activated partial thromboplastin time) in a way that is different from conventional anticoagulants. This theme issue of Hamostaseologie should facilitate the readers’ access to several acquired coagulation disorders and assist to overcome fundamental problems of understanding hemostasis or, metaphorically spoken, to ‘break some of the seals’ of hemostasis and thrombosis textbooks. As third part in a series of reviews, the current edition also reflects several highlights of the GTH Congress 2015 (2, 3, 4). In his article, Medcalf provides an upto-date view on fibrinolysis, demonstrating that tissue-type plasminogen activator (t-PA)-mediated conversion of plasminogen into plasmin is not solely designed to remove fibrin deposits and blood clots in a self-regulated proteolytic process (5). Importantly, it is shown that t-PA and plasmin have pleotrophic effects and other substrates than fibrin such as prion proteins, amyloid-β, and misfolded or aggregated proteins. Thus, t-PA can act in a nonfibrinolytic (i.e., plasmin-independent) manner and have multiple effects on cerebral functions (e.g., synaptic plasticity, neurotransmission, visual processing, learning and memory). The author therefore concludes that the “original concept for the fibrinolytic system, being focused on fibrin, is a massive understatement” (5). Tiede et al. report on recent advances in the management of acquired hemophilia A (AHA) (6). At an incidence of about 1.3 cases per million people (7), AHA is a rare but challenging bleeding disorder caused by inhibitory autoantibodies against coagulation factor (F) VIII. Apart from hemostatic management to control active bleeding, immunosuppressive treatment is mandatory in AHA to achieve remission. However, the outcome of AHA remains highly variable. Therefore, clinically valid prognostic factors for remission are urgently required. Recently, the GTH-AH (01/2010) study, a multicenter trial conducted under the leadership of Andreas Tiede, has demonstrated for the first time that residual FVIII activity and inhibitor

SummarySpecific membrane glycoproteins (GP) expressed by the megakaryocyte-platelet system, including GPIa-lla, GPIb-V-IX, GPIIb-llla, and GPIV are involved in mediat-ing platelet adhesion to the subendothelial matrix. Among these glycoproteins, GPIIb-llla plays a pivotal role since platelet aggregation is exclusively mediated by this receptor and its interaction with soluble macromolecular proteins. Inherited defects of the GPIIb-llla or GPIb-V-IX receptor complexes are associated with bleeding disorders, known as Glanzmann's thrombasthenia, Bernard-Soulier syndrome, or platelet-type von Willebrand's disease, respectively. Using immuno-chemical and molecular biology techniques, rapid advances in our understanding of the molecular genetic basis of these disorders have been made during the last few years. Moreover, analyses of patients with congenital platelet membrane glycoprotein abnormalities have provided valuable insights into molecular mechanisms that are required for structural and functional integrity, normal biosynthesis of the glycoprotein complexes and coordinated membrane expression of their constituents. The present article reviews the current state of knowledge of the major membrane glycoproteins in health and disease. The spectrum of clinical bleeding manifestations and established diagnostic criteria for each of these dis-orders are summarized. In particular, the variety of molecular defects that have been identified so far and their genetic basis will be discussed.

We have performed a monocenter study on 29 consecutive patients with acquired haemophilia A who were referred for diagnosis and treatment to the Düsseldorf Haemophilia Comprehensive Care Center between March 2001 and February 2010.18 men (age: 44-86 years) and 11 women (age: 20-83 years). For laboratory evaluation, a standardized staged protocol of aPTT, FVIII:C activity and concentration, mixing studies with patient and normal plasma, and quantification of inhibitor titers (Bethesda assay) was used. Diagnostic work-up included elaborate examinations for any underlying disease.In 18 (62%) of the 29 patients with acquired haemophilia A, an underlying disorder was identified, including 9 patients with respiratory diseases (31%), 7 patients with autoimmune disorders (24%), one with malignancy, and one with postpartum state, while in 11 patients (38%) acquired haemophilia A remained idiopathic. Haemotherapy of bleeding, suppression or elimination of the inhibitor, and induction of immunotolerance to endogenous FVIII:C were performed according to a treatment algorithm. Predefined clinical endpoints were control of bleeding, eradication of the inhibitor, complete or partial remission (CR, PR), relapse, or early death (or =30 days). Of the 29 patients in total, 22 individuals achieved CR (76%), three had PR, one relapsed, and three died within 30 days (one of acute myocardial infarction while on antihaemorrhagic treatment, one of sepsis while on immunosuppression due to active acquired haemophilia A, one of lung bleeding in association with pre-existing pulmonary sarcoidosis).This monocenter study demonstrates that control of life-threatening bleeding, eradication of the inhibitor, and induction of tolerance to endogenous FVIII have significantly improved the clinical outcome of acquired haemophilia A. Our data also suggest a shift in underlying disorders associated with acquired haemophilia A, whereby, in comparison to published studies, a relative increase in the proportion of patients with respiratory diseases is present.

Antiplatelet agents and anticoagulants are effective in the prevention and treatment of a variety of thrombotic disorders. Several clinical settings require more intense antithrombotic regimens. These can be provided by combining (i) two antiplatelet drugs, (ii) antiplatelet monotherapy with an anticoagulant, or (iii) anticoagulation with dual antiplatelet treatment (triple therapy). A major side effect of all antithrombotic regimens, however, is the induction of a bleeding diathesis. This is especially true in patients with preexisting haemostatic defects of any kind that may remain compensated, unless platelet function and/or coagulation are not inhibited pharmacologically. To address the dilemma of the "double-edged sword" between thrombosis and bleeding, several strategies are currently under study, including (i) identification of high-risk patients, (ii) stratification of patient subgroups, (iii) individualized decision making, and (iv) administration of "tailor-made" risk-adapted regimens. Nonetheless, prevention and protection from bleeding in patients using antithrombotic agents remain an enduring challenge. For high-risk patients on antiplatelet agents with urgent need of surgery, an algorithm is discussed that allows short-term interruption of oral antithrombotic therapy and i.v. administration of a GPIIb-IIIa receptor antagonist for bridging without increasing perioperative bleeding. When individual patients, using antiplatelet or anticoagulant agents, experience serious or even life-threatening haemorrhages, haemotherapy with platelet units or prothrombin complex concentrates remains an integral part of the clinical management.

Given the high consumption of pharmacological agents in western societies, it is not surprising at all that drugs represent the most common cause of acquired platelet dysfunction. While acetylsalicylic acid, clopigogrel and integrin alphaIIbbeta3 (GPIIb-IIIa) receptor antagonists are well-known as prototypes of antiplatelet drugs, other widely used agents including non-steroidal anti-inflammatory drugs, antibiotics, serotonin reuptake inhibitors, and volume expanders can also impair platelet function and cause or aggravate haemorrhages. Besides pharmacological agents, certain clinical conditions are often associated with qualitative platelet disorders and bleeding diathesis. Consequently, in contrast to inherited platelet disorders, acquired platelet function defects are much more frequent in clinical practice and deserve special attention. Their pathogenesis is widespread and heterogeneous with various, sometimes overlapping abnormalities. Moreover, acquired platelet dysfunctions can occur at any age and range in severity from mild to life-threatening haemorrhages. Due to their heterogeneity, acquired platelet function disorders will be classified and discussed according to the underlying clinical setting or disease.

Apart from on-label indications, recombinant factor VIIa (rFVIIa) is increasingly administered for treatment of life threatening bleeding events when appropriate standard therapy fails. Case reports and short treatment series document the efficacy and safety of rFVIIa to achieve haemostasis in patients with platelet function disorders and thrombocytopenias of various origin. An established on-label indication for the use of rFVIIa is given in patients with Glanzmann thrombasthenia with refractoriness to transfusions of platelet concentrates. Bolus applications of rFVIIa at dosages between 80 and 120 microg/kg body weight every 1.5 to 3 h are also administered successfully in patients with Bernard-Soulier syndrome, platelet storage pool defects, and other acquired platelet function disorders. In patients with Glanzmann thrombasthenia, at least three bolus injections are required to achieve effective haemostasis. In approximately half of the patients with thrombocytopenias, a single bolus of rFVIIa has been shown to be sufficient in managing otherwise untreatable bleeding complications. In these patients, haemostasis was achieved even at platelet counts20,000/microl, although the efficacy of rFVIIa increases at higher platelet concentrations.

Thromboembolic disease remains a leading cause of maternal mortality during pregnancy and the puerperium. Rational and risk-adapted administration of heparin prophylaxis depends on 1. the identification of those women who have an increased risk of thrombosis and 2. the accurate quantification of this risk. In women without prior thrombosis, the presence of a heterozygous factor V Leiden or heterozygous G20210A mutation in the prothrombin gene is associated with a pregnancy-associated thrombotic risk of approximately 1 in 400. Thus, in pregnant carriers of either one of these mutations the risk of venous thromboembolism is low. Therefore, no heparin prophylaxis is recommended. A combination of the two genetic risk factors can increase the risk to a modest level of 1 in 25. In women with a single episode of prior thrombosis associated with a transient risk factor, e.g. surgery or trauma, and no additional genetic risk factor, the probability of a pregnancy-associated thrombosis appears also to be low. However, data are sparse and conflicting. In contrast, in women with a prior idiopathic venous thrombosis who carry an additional hereditary risk factor or who have a positive family history of thrombosis, a high risk (10%) can be expected supporting the indication for active antepartum and postpartum heparin prophylaxis. Despite the remarkable progress in risk stratification, the absolute magnitude of risk and the optimal management in many cases is an issue of ongoing debate.

A survey is given on congenital and acquired platelet functional disorders. Congenital platelet functional disorders are extremely rare. Acquired platelet functional disorders are probably the most frequent disturbances of haemostasis. The knowledge of the defects leading to inherited platelet function disorders much improved our understanding of platelet function in general. Acquired platelet functional disorders are due to various diseases and drugs.

An overview is given on congenital and acquired thrombocytopenias, their pathophysiology, symptoms, diagnosis and therapy with emphasizing heparin-induced thrombocytopenia (HIT) and the thrombotic thrombocytopenic purpura (TTP).

punktlich zum 30. Juni erreichte uns die Nachricht des Schattauer-Verlags: Hamostaseologie hat fur 2010 einen Impact-Faktor erhalten. Die Reaktionen unter den GTH-Vorstandsmitgliedern und in der Schriftleitung waren enthusiastisch und reichten von „super“, „Gratulation“, „phantastisch“ und „IF von 0,78 – unerwartet gut“ bis „kann naturlich noch besser werden!“ Der Anfang ist also gemacht: Ein zartes Pflanzchen ist sichtbar geworden im „Blatterwald“ der wissenschaftlichen Journale. Um bei der Metapher zu bleiben: Die Saat, die unsere Vorganger in der Schriftleitung dieser Zeitschrift, von Prof. Rudolf Marx bis zu Prof. Hans D. Bruhn, gelegt haben, ist aufgegangen. Besonders ihm haben wir zu danken, dass wir so weit gelangt sind. Prof. Bruhn hat das Ziel, fur die Hamo staseologie einen Impact-Faktor zu erreichen, mit Elan und Ausdauer verfolgt. Danken mochten wir auch den Editoren und Autoren der Themenhefte, die mit ihren Arbeiten (und deren Zitation wahrend der Evaluationsphase 2008–2009) substanziell zum Impact-Faktor beigetragen haben. Die acht in jungster Zeit am haufigsten zitierten Arbeiten der Hamostaseologie sind aufgefuhrt ( Seite 150). Nun heist es, das junge Pflanzchen zu pflegen. Dazu sind wir alle aufgerufen. Der Schattauer-Verlag mit seinem Team stellt den Garten. Wir, die Wissenschaftler, mussen das Pflanzchen weiter im Wachstum fordern. Dazu bedarf es wirksamer Nahrstoffe und intensiver Pflege. Erwiesenermasen eignen sich hierfur am besten

Im Februar 2009 hat sich Professor H. D. Bruhn nach nahezu 20-jahriger Tatigkeit im Editorial Board, davon 15 Jahre als Editor-inChief, von seinen Aufgaben zuruckgezogen und uns den Staffelstab fur diese Funktion ubergeben. Seine verdienstvolle und erfolgreiche Arbeit fur unsere Fachzeitschrift ist vom Schattauer-Verlag und von Frau Professorin I. Pabinger, der ersten Vorsitzenden der GTH, gewurdigt worden (Ausgaben 2 und 3 der Hamostaseologie 2009). Wir danken H. D. Bruhn unsererseits sehr fur sein enormes Engagement als Editor. Er ubergibt uns ein gut vorbereitetes Aufgabenfeld: Die Schwerpunkthefte fur 2009 und grosteils 2010 wurden von ihm weitgehend konzeptionell bzw. organisatorisch vorbereitet, was die Weiterfuhrung bzw. Ubernahme der Verantwortlichkeit erleichtert. Herr H. D. Bruhn hinterlasst uns aber auch eine enorme Herausforderung: Nach seiner erfolgreich betriebenen PubMed-Listung der Hamostaseologie steht fur 2010 nun erstmals die Vergabe eines Impact-Faktors fur die Zeitschrift an. Wir wissen alle: Ein Impact-Faktor will erst einmal erreicht, dann aber auch gehalten und – wenn moglich – gar noch gesteigert werden. Es ist wie in der Leichtathletik – hoher, weiter, schneller! Wie beim Hochleistungssport braucht es auch fur eine erfolgreiche, zukunftsorientierte wissenschaftliche Zeitschrift Spitzenkrafte (= Autoren), Manager (= Editoren-Team), einen Trainerstab (= Editorial Board), souverane Schiedsrichter (= Reviewer), gute Organisation (= Verlag) und erst recht fachkundige Zuschauer (= Leser). Nicht vergessen werden durfen die Sponsoren, ohne die weder Sport noch Wissenschaft finanzierbar sind.

ZusammenfassungWir bevorzugen folgendes therapeutisches Vorgehen: Bei Patienten mit gesicherter ITP ist ein Abwarten gerechtfertigt, solange die Thrombozytenwerte mehr als 30000/µl betragen und keine manifesten Blutungen bestehen. Bei Thrombozyten werten unter 30000/µ1 sowie manifesten Blutungen beginnen wir eine PrednisolonTherapie mit initial mindestens 100 mg Prednisolon/die, gefolgt von einer ausschleichenden Dosierung über 6-8 Wochen nach Eintritt der Remission. Beim ersten Rezidiv wird individuell unterschiedlich entweder ein zweiter Therapieversuch mit Prednisolon unternommen oder eine Splenektomie durchgeführt.

ZusammenfassungErworbene Thrombozytenfunktionsstörungen sind außerordentlich häufig und können bei zahlreichen, ganz unterschiedlichen Erkrankungen sowie unter Therapie mit den verschiedenartigsten Medikamenten auftreten. In der Mehrzahl der Fälle handelt es sich um extrinsische Störungen, deren Pathogenese noch weitgehend unklar ist. Vor allem bei malignen Erkrankungen wie akuten und chronischen Leukämien sowie anderen myeloproliferativen und myelodysplastischen Syndromen können sich extrinsische und intrinsische Komponenten zu einem komplizierten Bild überlagern und zu bedrohlicher Blutungsneigung führen. Häufig spielen hierbei Gerinnungsstörungen eine wichtige zusätzliche Rolle.Während in der Diagnostik klinisches Bild, Familienund Eigenanamnese, Blutungszeit und Plättchenzahl sowie der Ausschluß von Gerinnungsstörungen wichtig sind, besteht die Therapie vorwiegend in einer Behandlung der Grunderkrankung oder Absetzen des auslösenden Medikamentes. Nur in seltenen Fällen ist eine Thrombozytensubstitution erforderlich.

ZusammenfassungDie bei chronischen Lebererkrankungen, insbesondere bei Leberzirrhose häufig vorhandene Erniedrigung der peripheren Thrombozytenzahl scheint primär durch das Nebeneinanderbestehen einer Verteilungsstörung zwischen lienalem und zirkulierendem Plättchenpool (mit einer vermehrten Sequestration der Thrombozyten in der Milz) und einer verkürzten Thrombozytenüberlebenszeit (infolge eines gesteigerten Abbaus im Monozyten-Makrophagen-System der Milz) zustande zu kommen. Der immer wieder diskutierte Mechanismus einer schleichenden Verbrauchsko-agulopathie mit intravaskulärem Plättchenabbau und Mikrothrombosierung als Ursache der Thrombozytopenie konnte von uns für Patienten mit schwerer, aber stabiler Leberzirrhose widerlegt werden. Findet man bei schwerer Leberzirrhose trotz lienaler Plättchensequestration und verkürzter Thrombozytenüberlebenszeit normale oder nur gering erniedrigte Thrombozytenzahlen, so kann man davon ausgehen, daß bei diesen Patienten der Plättchenverbrauch durch eine gesteigerte Thrombozytenbildung im Knochenmark kompensiert wird. Mit fortschreitender Dauer und Schwere der chronischen Lebererkrankung scheint jedoch eine sekundäre Bildungsstörung im Knochenmark als eine Ursache für die zunehmende Thrombozytopenie verantwortlich zu sein. Die herabgesetzte Thrombozytopoese läßt sich durch eine unzureichende zyto-plasmatische Ausreifung von Megakaryozyten charakterisieren. Außerdem liegen Hinweise einer zirrhoseinduzierten Stoff Wechselveränderung vor, die zu einer Hemmung der Thrombozytopoese im Knochenmark bzw. zu einer Megakaryozytenreifungsstörung führen könnte. Eine metabolische Störung wie der von uns erbrachte Nachweis eines abnormen Sialinsäurebestandes der Blutplättchen läßt sich auch als eine mögliche Ursache der häufig vorhandenen Thrombozytopathie bei Leberzirrhose interpretieren.