Platelets in oncological diseases

Thrombocytosis and paraneoplastic thromboses

Cancer is one of the most important unmodifiable risk factors for venous thromboembolic complications. Tumor growth exerts a systemic effect on the body, frequently manifesting as thrombohemorrhagic syndromes.

A specific manifestation of blood coagulation disorders in cancer patients is Trousseau syndrome—paraneoplastic phlebothrombosis. A key role in its development is played by quantitative changes in blood platelets. When the platelet count pathologically increases and exceeds $320–340 \times 10^9$/L, this inevitably leads to the initiation of blood clotting processes directly in the microvascular bed. This unmodifiable patient-related factor must be considered to assess the risk of recurrence and determine the duration of anticoagulant therapy.

Link between hemostasis and cancer cachexia

Thrombohemorrhagic syndromes and anemias do not develop in isolation, but rather as part of the general paraneoplastic process. Its most frequent manifestation is cachexia, characterized by general weakness and significant weight loss. Systemic exhaustion and hemostatic disorders share common etiopathogenetic roots:

• Action of TNF-α (tumor necrosis factor alpha): This cytokine (formerly called cachectin) is excessively produced by macrophages and monocytes. It directly enhances lipid catabolism, leading to weight loss.
• Tumor intoxication: Breakdown products of both the tumor itself and damaged surrounding tissues enter the bloodstream.
• Chronic blood loss: Recurrent bleeding occurs from disintegrating neoplasm tissue or from vessels eroded (destroyed) by tumor infiltration.
• Competition for substrates and anorexia: The tumor intensively consumes nutrients, while the patient's appetite drops due to tumor endotoxemia and concomitant mental depression.

Combined with neuropsychiatric syndromes (neuropathies, psychoses) and endocrinopathies (impaired hormone production), these factors create a background for severe recurrent thromboses.

Additional risk factors for thrombosis

Although no single factor guarantees a 100% probability of thrombosis, the presence of an oncological disease sharply increases the effect of other triggers. The most important risk factors include:

1. Thrombophilias: Can be genetic (Factor V Leiden mutation, prothrombin mutation) or acquired (antiphospholipid syndrome, antithrombin III, protein C and S deficiency).
2. Obstetric factors: Pregnancy alone increases the risk of thrombosis 6-fold due to slowed blood flow and reduced fibrinolysis. Purulent-septic complications, preeclampsia, and cesarean section (risk increases to 2.2–3.0% vs. 0.08–1.2% in natural childbirth) also make a significant contribution.
3. Concomitant pathology: In addition to oncology, blood clotting is promoted by obesity, hypertension, and rheumatic heart disease.

Clinical presentation in various localization of thrombosis

Blood clotting against the background of thrombocytosis and paraneoplastic reactions can occur in various vascular beds. Specific thrombus localizations produce a characteristic clinical picture:

• Cavernous sinus: Cerebral venous thrombosis manifests as unilateral ptosis and paralysis of cranial nerves III–VI.
• Cortical veins: Isolated thrombosis leads to partial seizures followed by the development of hemiparesis and aphasia.
• Portal vein: In the acute phase, occlusion causes liver infarction, and in the chronic stage, it leads to the formation of portal hypertension.
• Deep veins: Past deep vein phlebothrombosis is dangerous due to the development of post-thrombotic syndrome, which is accompanied by persistent venous outflow impairment and trophic ulcer formation.

Class and exam questions

What else to study on this topic

• Pathogenesis of cancer cachexia and the role of cytokines
• Genetic thrombophilias: Factor V Leiden mutation
• Mechanisms of development of post-thrombotic syndrome
• Types, morphology, and outcomes of thrombi

Other topics in the "Additional Topics" section

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