Abstract
Chronic radiation cystitis (CRC) is a consequence of pelvic radiotherapy and affects 5–10% of patients. The pathology of CRC is without curative treatment and is characterized by incontinence, pelvic pain and hematuria, which severely degrades patients’ quality of life. Current management strategies rely primarily on symptomatic measures and have certain limitations. Thanks to a better understanding of the pathophysiology of radiation cystitis, studies targeting key manifestations such as inflammation, neovascularization and cell atrophy have emerged and are promising avenues for future treatment. However, the mechanisms of CRC are still better described in animal models than in human models. Preclinical studies conducted to elucidate the pathophysiology of CRC use distinct models and are most often limited to specific processes, such as fibrosis, vascular damage and inflammation. This review presents a synthesis of experimental studies aimed at improving our understanding of the molecular mechanisms at play and identifying key processes in CRC.
Highlights
With more than 19 million new cases and 9.9 million deaths in 2020, cancer is the second most common cause of death worldwide
Factors related to the patient, as well as to the tumor and treatment, increase the risk of developing chronic radiation cystitis
The symptoms of the chronic phase are the result of a combination of processes that range from the deregulation of urothelium homeostasis, hyperactivation of the endothelium, inflammation, hypoxia, oxidative stress, defect in neuroregulation and fibrosis
Summary
With more than 19 million new cases and 9.9 million deaths in 2020, cancer is the second most common cause of death worldwide. The most common symptoms are proctopathy (5–20%) and radiation-induced cystitis (3.5%) [3]. Patients can experience a wide range of symptoms, from mild pelvic pain to lifethreatening hemorrhagic cystitis weeks, months, or even years after treatment. In its severe form, pain and hemorrhagic cystitis impair patient quality of life, prolong hospitalization and may be life-threatening complications [4]. Despite recovery, patients who have experienced radiation-induced hemorrhagic cystitis have lower overall and event-free survival compared to patients. Treatment is limited managing the etiology of the disease in-depthbecause knowledge of the mechanisms involved, which symptoms and is not requires always effective the causes may be multiple. Based on molecular knowledge from preclinical cystitis studies,inwe present a synthesis the mechanisms involved in volved in radiation-induced order to identify key of effectors.
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