Platelet function can be abnormally increased, as in association with vascular events, or defective, as in a variety of clinical settings, or display converse phenotypes with increased and decreased platelet responsiveness, as in myeloproliferative neoplasms. Drugs represent the most common cause of platelet dysfunction in our overmedicated society. While aspirin, clopidogrel, prasugrel (or more recently also ticagrelor), and integrin αIIbβ3 receptor antagonists (abciximab, eptifibatide, and tirofiban) are well-known prototypes of antiplatelet drugs, other widely used agents (e.g., nonsteroidal anti-inflammatory drugs, antibiotics, serotonin reuptake inhibitors, and volume expanders) and supplements can also impair platelet function and thus cause or aggravate hemorrhages. Apart from pharmacological agents, certain clinical conditions are often associated with qualitative platelet disorders and a bleeding diathesis. Consequently, in contrast to inherited platelet disorders, acquired platelet function defects are much more frequent in clinical practice and therefore deserve special attention. Their pathogenesis is widespread and heterogeneous with various, sometimes overlapping abnormalities in the same clinical setting. Moreover, acquired platelet dysfunction may occur at any age, and platelet defects can range in severity from mild to life-threatening hemorrhages. Diagnostic work-up of platelet disorders requires meticulous evaluation of medical history, specifically of any drugs interfering with platelet function, careful clinical examination, and a staged laboratory protocol to assess the underlying platelet defect(s). Interpretation of laboratory findings may sometimes be difficult, as reduced platelet responsiveness obtained by in vitro settings may result from “exhausted” platelets due to increased activation in vivo. To identify hyperactive platelets ex vivo, costly procedures are required using flow cytometry in combination with specific monoclonal antibodies. Currently, this approach can be recommended for research purposes only. Platelet dysfunction, sometimes in association with quantitative abnormalities, is present in uremia, liver disease, hematologic disorders, cardiac valvular disease, and extracorporeal settings. Due to their heterogeneity, acquired platelet function disorders will be discussed according to the underlying clinical condition.

Acquired Disorders of Platelet Function

Correspondence to: Univ.-Prof. Dr. Rüdiger E. Scharf, F.A.H.A. rscharf@uni-duesseldorf.de Hämostaseologie 2016; 36: 73–74 Atherosclerosis is an inflammatory disease (1). This statement is no longer news since Russell Ross’ seminal review in 1999. All the more, atherosclerosis does neither represent a mere cholesterol storage disorder of the arterial wall due to passive accumulation of lipids nor is it a bland proliferative process of smooth muscle cells “in response to injury”. In fact, it is now recognized that multiple immune effector mechanisms are implicated in the complex pathogenesis of atherosclerosis, involving mediators of innate and adaptive immunity at various stages of the disease. Consequently, atherogenesis is considered a complex “immune-inflammatory syndrome” (2) characterized by an imbalanced lipid metabolism and a maladaptive immune response, both of which promote and sustain chronic inflammatory processes of the arterial wall (3).

Atherogenesis – tried and tested pieces in the puzzle

Hämostaseologie 2016; 36: 159–160 The human genome consists of about three billion nucleotides or DNA “letters”, forming three-letter codes or “words” and expressing nucleotide sequences or “sentences”. In either way, we are facing a giant number of letters, words, or sentences in genetics and molecular biology. This reminds me of an anecdote of W. A. Mozart’s life. When Emperor Joseph II first listened to The Abduction from the Seraglio, he reportedly said: “My dear Mozart, that is too fine for my ears; there are too many notes.”

Molecular Complexity of the Megakaryocyte-Platelet System in Health and Disease.

Molecular complexity of the megakaryocyte-platelet system in health and disease.

Blood platelets were the focus of recent issues of this Journal (1, 2). Why do these inconspicuous, small cellular fragments, derived from megakaryocytes in the bone marrow, gain so much attention both in clinical settings and basic science? Platelets contribute essentially to survey the integrity of the vascular system by becoming adherent within milliseconds and by forming platelet aggregates at sites of injured endothelial cells or exposed subendothelial matrix structures (3). Overall, platelets play a pivotal role in hemostasis. However, once stimulated, platelets respond uniformly and do not distinguish between traumatic injury and vascular lesions caused by variety of clinical disorders (4). Thus, under pathological conditions, mechanisms otherwise beneficial for hemostasis and vascular integrity may cause occlusive thrombi and, subsequently, acute ischemic syndromes of the heart, brain and other organ systems (5, 6).

Platelet pathology and antiplatelet strategies. Resolved and unresolved issues.

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Platelet pathology and antiplatelet strategies. Resolved and unresolved issues.