Tromboplastiinia

Tromboplastiinia is a term used in some medical writings to describe a deficiency or dysfunction of thromboplastin, the tissue factor–phospholipid complex that initiates the extrinsic pathway of blood coagulation. In contemporary English-language practice, the condition is more commonly referred to as thromboplastin deficiency or tissue factor–related coagulation disturbance.

Pathophysiology of thromboplastin involves its role in forming a complex with factor VIIa on phospholipid surfaces, which activates factor X and leads to thrombin generation. When thromboplastin activity is reduced or defective, the extrinsic pathway is impaired, resulting in prolonged prothrombin time (PT) and a propensity for bleeding. The intrinsic pathway (measured by aPTT) may be less affected unless additional factors are involved.

Causes of a thromboplastin-related disorder are rare and can be congenital, involving deficiency of tissue factor or components of the thromboplastin complex. More commonly observed laboratory profiles resembling thromboplastin deficiency arise from conditions that lower factor VII levels or activity, such as vitamin K deficiency, liver disease, or vitamin K antagonist therapy, which can prolong PT. Acquired reductions in tissue-factor–bearing microparticles or other disruptions of the extrinsic pathway can contribute as well.

Clinical features typically include bleeding after injury or mucosal bleeding, with laboratory findings showing an isolated prolongation of PT/INR and a relatively preserved aPTT. Diagnosis requires exclusion of other coagulation abnormalities and, when needed, specific factor assays or mixing studies to assess the extrinsic pathway.

Treatment and prognosis depend on the underlying cause. Addressing the root issue (eg, replenishing vitamin K, treating liver disease, or providing plasma or prothrombin complex concentrates during bleeding) is central. The outlook varies with etiology and the severity of the coagulation disturbance.