Cancer cachexia is a multi-factorial syndrome, which negatively affects quality of life, responsiveness to chemotherapy, and survival in advanced cancer patients. Our understanding of cachexia has grown greatly in recent years and the roles of many tumor-derived and host-derived compounds have been elucidated as mediators of cancer cachexia. However, cancer cachexia remains an unmet medical need and attempts towards a standard treatment guideline have been unsuccessful. This review covers the diagnosis, assessment, and treatment of cancer cachexia; the elements impeding the formulation of a standard management guideline; and future directions of research for the improvement and standardization of current treatment procedures.

Cancer cachexia: Diagnosis, assessment, and treatment.

About 50% of all patients with cancer eventually develop anorexia/cachexia syndrome, which represents a complex clinical syndrome occurring in several illnesses, including cancer. The syndrome is characterized by systemic inflammation and primarily loss of body fat and body mass. In this review we shortly summarize the pathomechanism of anorexia/cachexia syndrome and list the current pharmacological approaches.

Cachexia in cancer patients

Patients with cancer are at an increased risk for muscle loss via 2 distinct mechanisms: sarcopenia, defined as the age-associated decrease in muscle mass related to changes in muscle synthesis signaling pathways, and/or cachexia, defined as cytokine-mediated degradation of muscle and adipose depots. Both wasting disorders are prevalent; among patients with cancer, 15%-50% are sarcopenic and 25%-80% are cachectic. Muscle mass may be difficult to quantify in overweight/obese individuals. Often, overweight/obese patients with cancer are assumed to be normally nourished when in fact severe muscle depletion may be present. No universally accepted treatment exists for preventing or reversing sarcopenia or cachexia in patients with cancer. Current treatment options are limited to nutrition therapy and exercise, which may lead to difficulties in adherence during cancer treatment. Future treatments may provide pharmaceutical therapy that targets muscle degradation and synthesis pathways. There is a need to determine a multimodal treatment plan for muscle depletion to improve quality of life, survival, and therapy complications in patients with cancer.

Differentiating Sarcopenia and Cachexia Among Patients With Cancer

Cancer cachexia is a multifactorial syndrome characterized by a progressive loss of skeletal muscle mass associated with significant functional impairment. In addition to a loss of skeletal muscle mass and function, many patients with cancer cachexia also experience cardiac atrophy, remodeling, and dysfunction, which in the field of cancer cachexia is described as cardiac cachexia. The cardiac alterations may be due to underlying heart disease, the cancer itself, or problems initiated by the cancer treatment and, unfortunately, remains largely underappreciated by clinicians and basic scientists. Despite recent major advances in the treatment of cancer, little progress has been made in the treatment of cardiac cachexia in cancer, and much of this is due to lack of information regarding the mechanisms. This review focuses on the cardiac atrophy associated with cancer cachexia, describing some of the known mechanisms and discussing the current and future therapeutic strategies to treat this condition. Above all else, improved awareness of the condition and an increased focus on identification of mechanisms and therapeutic targets will facilitate the eventual development of an effective treatment for cardiac atrophy in cancer cachexia.

https://www.physiology.org/doi/pdf/10.1152/ajpheart.00720.2015

The pathogenesis and treatment of cardiac atrophy in cancer cachexia

Background Cancer-associated wasting, termed cancer cachexia, has a profound effect on the morbidity and mortality of cancer patients but remains difficult to recognize and diagnose. While increases in circulating levels of a number of inflammatory cytokines have been associated with cancer cachexia, these associations were generally made in patients with advanced disease and thus may be associated with disease progression rather than directly with the cachexia syndrome. Thus, we sought to assess potential biomarkers of cancer-induced cachexia in patients with earlier stages of disease. Methods A custom multiplex array was used to measure circulating levels of 25 soluble factors from 70 pancreatic cancer patients undergoing attempted tumour resections. A high-sensitivity multiplex was used for increased sensitivity for nine cytokines. Results Resectable pancreatic cancer patients with cachexia had low levels of canonical pro-inflammatory cytokines including interleukin-6 (IL-6), interleukin-1β (IL-1β), interferon-γ (IFN-γ), and tumour necrosis factor (TNF). Even in our more sensitive analysis, these cytokines were not associated with cancer cachexia. Of the 25 circulating factors tested, only monocyte chemoattractant protein-1 (MCP-1) was increased in treatment-naive cachectic patients compared with weight stable patients and identified as a potential biomarker for cancer cachexia. Although circulating levels of leptin and granulocyte-macrophage colony-stimulating factor (GM-CSF) were found to be decreased in the same cohort of treatment-naive cachectic patients, these factors were closely associated with body mass index, limiting their utility as cancer cachexia biomarkers. Conclusions Unlike in advanced disease, it is possible that cachexia in patients with resectable pancreatic cancer is not associated with high levels of classical markers of systemic inflammation. However, cachectic, treatment-naive patients have higher levels of MCP-1, suggesting that MCP-1 may be useful as a biomarker of cancer cachexia.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcsm.12251

Circulating monocyte chemoattractant protein-1 (MCP-1) is associated with cachexia in treatment-naïve pancreatic cancer patients.

Recently, an international consensus diagnostic criterion for cancer cachexia was proposed. The aim of the study is to assess the prevalence of cachexia in patients with advanced cancer and to assess the current status of the diagnosis and management of cancer cachexia. A total of 390 patients with advanced cancer were included. There were 140 patients with cachexia and the prevalence was 35.9%. The prevalence was highest in pancreatic cancer (88.9%), followed by gastric cancer (76.5%) and esophageal cancer (52.9%). Sixty-three patients with cancer cachexia have CT scans available for muscle mass evaluation and 98.4% were sarcopenic. Cachectic patients have a significantly lower overall quality of life and a higher symptom burden. According to oncology physicians, only 33 patients were considered to have cancer cachexia. The false negative rate amounted to 76.4%. The positive rate was related to the body mass index and Eastern Cooperative Oncology Group performance status of the patients. There were few types of pharmacological approaches for cancer cachexia and more than half of cachectic patients did not receive any anticachexia treatment. These results indicate that the prevalence of cachexia in advanced cancer patients was high. However, cancer cachexia was rarely recognized and clinical management for cancer cachexia was very inadequate.

An Epidemiological Survey of Cachexia in Advanced Cancer Patients and Analysis on Its Diagnostic and Treatment Status.

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An Epidemiological Survey of Cachexia in Advanced Cancer Patients and Analysis on Its Diagnostic and Treatment Status.