Certain medications can inadvertently alter the body’s balance and increase the risk of forming blood clots. This serious side effect can lead to a pulmonary embolism (PE), a life-threatening blockage in the lung’s arteries. Understanding this connection between pharmaceutical agents and clot formation is necessary for patients and healthcare providers. This information raises awareness about the drugs most commonly associated with this risk and the biological reasons behind the phenomenon.
What is a Drug-Induced Pulmonary Embolism?
A pulmonary embolism is a sudden blockage in one of the pulmonary arteries, the blood vessels that carry blood from the heart to the lungs. This obstruction is almost always caused by a blood clot, known as a thrombus, that has traveled from a deeper vein elsewhere in the body, most frequently the legs. This traveling clot is called an embolus, and the condition is often a complication of deep vein thrombosis (DVT). The use of specific medications is a recognized, non-genetic factor that can increase a person’s risk for developing these venous thromboembolisms by disrupting the body’s normal mechanisms for maintaining blood fluidity.
High-Risk Drug Classes
Hormonal therapies represent one of the most widely documented drug classes associated with an elevated risk of blood clots. Combination oral contraceptives, which contain both estrogen and progestin, can increase the risk of venous thromboembolism (VTE) by approximately three to five times compared to non-users. Hormone replacement therapy (HRT) used by postmenopausal women, especially regimens containing estrogen alone or in combination with a progestin, also carries a similar elevated risk. This increased risk is pronounced during the first year of use for both.
Selective Estrogen Receptor Modulators (SERMs), a different class of hormone-related drugs used to treat or prevent breast cancer, also elevate clot risk. Medications such as tamoxifen and raloxifene significantly increase the relative risk of VTE. Tamoxifen users may face a risk of PE that is up to three times higher than that of the general population. This effect is directly related to the drug’s estrogen-like activity in certain tissues.
Several classes of drugs used in cancer treatment are highly prothrombotic, meaning they directly promote clot formation. Erythropoiesis-Stimulating Agents (ESAs), administered to treat anemia in cancer patients, have been shown to increase VTE risk by an average of 75 percent. This increase is tied to the rise in red blood cell count and the subsequent thickening of the blood.
A newer class of cancer treatments, Immune Checkpoint Inhibitors (ICIs), which include agents like nivolumab and pembrolizumab, also significantly raise the risk of VTE. These immunotherapies essentially “rev up” the immune system to fight cancer, but this enhanced immune activity can inadvertently trigger a systemic inflammatory state. This inflammation creates an environment where blood clots form more readily. The risk is often highest in patients with certain cancer types, such as lung cancer and melanoma.
How Medications Trigger Clotting
Clot formation is often explained by a concept called Virchow’s Triad, which describes three broad factors that contribute to thrombosis: damage to the blood vessel lining, sluggish blood flow, and an increased tendency for blood to clot. Medications can influence one or more of these factors. The most common way drugs contribute to pulmonary embolism risk is by inducing hypercoagulability, or making the blood clot too easily.
Hormonal therapies, for example, primarily act by increasing the liver’s production of certain clotting factors, such as Factor VII and Factor X, while simultaneously decreasing the levels of natural anticoagulant proteins. This shift tips the balance toward clot formation and hypercoagulability. The risk is systemic and not localized, which explains why clots can form in the deep veins of the legs.
Chemotherapy and immunotherapy agents contribute to clot formation through a combination of mechanisms. Many chemotherapy drugs cause direct damage to the inner lining of the blood vessel, known as the endothelium. This endothelial injury triggers the body’s repair mechanism, which involves platelet activation and the start of the coagulation cascade, leading to thrombosis.
Cancer treatments can also induce a generalized inflammatory response. This inflammation contributes to hypercoagulability by causing the release of pro-clotting substances and activating platelets. The combination of endothelial injury and a heightened clotting tendency creates a high-risk environment for DVT and subsequent PE.
Recognizing the Warning Signs
Identifying the symptoms of a pulmonary embolism is imperative because the condition can rapidly become life-threatening. The most common warning sign is the sudden onset of shortness of breath, which may occur even while resting. Sharp chest pain is another frequent symptom, often described as pleuritic, meaning it worsens when taking a deep breath, coughing, or bending over. A person with a PE may also experience a rapid or irregular heartbeat as the heart strains to push blood past the blockage in the lungs. A cough that produces bloody or blood-streaked mucus, known as hemoptysis, can also be a sign of the condition.
Other signs can include lightheadedness, dizziness, or fainting, especially in cases of a large clot that significantly impacts blood flow. Swelling, pain, or warmth in one leg, which would indicate a DVT, should also be considered a serious warning sign of a potential or impending PE. If any of these symptoms appear suddenly, seeking immediate medical attention is necessary.