Adhäsionsschwäche

Adhäsionsschwäche refers to a condition characterized by a reduced ability of platelets to adhere to the subendothelium of damaged blood vessels. This adhesion is a crucial initial step in the process of hemostasis, the body's mechanism for stopping bleeding. When blood vessels are injured, the exposed subendothelium, particularly components like collagen and von Willebrand factor (vWF), normally triggers platelets to bind to the site. In adhäsionsschwäche, this binding is impaired.

The underlying causes of adhäsionsschwäche can be diverse. It may stem from defects in platelet receptors that interact with the subendothelium, such as the glycoprotein Ib-IX-V complex which binds to vWF, or integrins like GPIIb/IIIa that bind to fibrinogen and vWF. Alternatively, deficiencies or functional abnormalities in plasma proteins like von Willebrand factor itself can lead to impaired platelet adhesion. Certain medications, such as aspirin and other NSAIDs, can also transiently affect platelet function and adhesion.

Clinically, individuals with adhäsionsschwäche may present with a tendency towards bleeding. This can manifest as easy bruising, prolonged bleeding from minor cuts, nosebleeds (epistaxis), or excessive bleeding after surgery or trauma. The severity of symptoms often correlates with the degree of adhesion impairment. Diagnosis typically involves a thorough medical history, physical examination, and laboratory tests, including platelet aggregation studies and assays for specific platelet function defects or plasma protein abnormalities. Treatment strategies depend on the underlying cause and may involve addressing the specific molecular defect, managing contributing factors, or in severe cases, platelet transfusions.