BThere is hardly any other treatment that is as difficult to adhere to as the fundamental principle of medicine, “Do no harm first”. chemotherapy with classic cell toxins. Despite new treatment concepts such as immune and antibody therapy, it still forms the backbone of oncology – alone or in combination with other drugs. The cytotoxins of chemotherapy prevent cancer cells from growing and multiplying, but they also attack other fast-growing cells in the body – such as the stem cells of the bone marrow, which are necessary for blood formation, or the mucous membrane and hair root cells. Therefore, they harm the patient physically, and also emotionally and socially through their side effects, often with severe long-term consequences.
The side effects also determine the success of chemotherapy because they force a change in treatment depending on their severity. Then either the dose of cell toxins is reduced, the number of treatment cycles is up for grabs, or the therapy is even stopped. This increases the risk that the therapy will not work or will work less well, or that the risk of a relapse will increase. Oncologists are therefore always faced with a difficult decision: what side effects are acceptable when trying to cure or prolong life, and what price does the patient pay for this, even in the long term?
In the journal Nature Reviews Clinical Oncology is now a review paper about some of the most important side effects of classic cytostatic therapy. Gary Lyman from the Fred Hutchinson Cancer Research Center in Seattle and his colleagues make it clear that, despite many advances, it has still not been possible to predict with certainty who will develop which side effects and how the occurrence of these side effects can best be prevented with new concepts and drugs leaves. There are obviously still many unanswered questions about the origin of the individual side effects.
The number of white blood cells often falls
A critical side effect is neutropenia. The number of white blood cells, more precisely: the neutrophilic granulocytes, drops dangerously due to the toxic effect of the cell toxins on blood formation. This leads to a weakening of the immune system. Patients become more susceptible to infections. It becomes particularly critical when an infection actually occurs. Then the neutropenia becomes febrile neutropenia, which requires immediate intervention.
Patients with a high risk of this complication are treated prophylactically with a messenger substance that stimulates the bone marrow to form new white blood cells. However, this messenger also has side effects. The risk of febrile neutropenia is directly related to the severity and duration of the pre-existing neutropenia. But there are other risk factors that have been documented by studies. In addition to previous chemotherapy, this also includes age and gender, concomitant diseases, a poor general condition, the intensity of the chemotherapy, as well as infections and other factors. Physicians expect advances in treatment or prevention from new drugs that have different effects. For example, from those that better protect the blood-forming stem cells from cytotoxins.
The risk of thrombosis is increased
Another critical side effect is venous thromboembolism. A blood clot forms in a deep vein – usually in the leg – which detaches and is flushed into the vascular system. If this blood clot gets into the lungs, it can cause a life-threatening pulmonary embolism. The development of deep vein thrombosis is promoted by three mechanisms. On the one hand, the cancer cells put the blood coagulation in an increased state of alarm. You can also activate this process directly or indirectly. As a result, cancer patients have more thrombosis-triggering stimuli in their blood than people without cancer.
In addition, the penetration of tumor cells into the blood and the reduced mobility of most cancer patients lead to blood congestion in the veins. Chemotherapy and regular blood tests or the insertion of a venous catheter also damage the inner wall of the blood vessels and thus also promote the development of deep vein thrombosis.