Logan Steele
Acute myeloid leukaemia (AML) is a haematological malignancy with poor survival odds, particularly in older patients. AML treatment consists of induction and consolidation chemotherapy, followed by potentially curative haematopoietic cell transplantation. These intense treatments are debilitating and increase the risk of mortality. Chemotherapy administration has been shown to directly induce skeletal muscle wasting and dysfunction, which is referred to as myopathy. This can be exacerbated by the effect of chemotherapy on the gastrointestinal tract, which reduces nutrient absorption and increases the risk of infection. As a result, processes that maintain muscle mass and function are compromised, leading to muscle damage and wasting. Cachectic muscle wasting, or cachexia, is associated with both cancer and anticancer chemotherapy. While cachexia is most prevalent in solid tumours, it has also been observed in AML and can have dire consequences. Therefore, it is important to address skeletal muscle mass and cachexia within the AML clinical landscape to improve survivability.
| Characteristics | Values |
|---|---|
| What is AML? | Acute myeloid leukaemia |
| What is muscle wasting? | Loss of muscle mass due to weakening and shrinking of muscles |
| Causes of muscle wasting | Medical conditions, lack of exercise, poor nutrition |
| Diseases associated with muscle wasting | Amyotrophic lateral sclerosis (ALS), muscular dystrophy, multiple sclerosis (MS), spinal muscular atrophy, Guillain-Barre syndrome, carpal tunnel syndrome, spinal cord injury |
| AML and muscle wasting | Skeletal muscle wasting is a consequence of AML and its treatment |
| Factors contributing to muscle wasting in AML | Chemotherapy, disruption of systemic nutrient delivery, cytotoxicity of chemotherapy, multi-organ toxicity |
| Impact of muscle wasting in AML | Increased risk of mortality, morbidity, poor treatment outcomes, reduced quality of life |
| Diagnosis of muscle wasting | Physical examination, blood tests, muscle or nerve biopsy, electromyography (EMG), nerve conduction studies, CT scan, MRI scan |
| Treatment of muscle wasting | Exercise, physical therapy, focused ultrasound therapy, healthy diet |
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What You'll Learn
Chemotherapy-induced cachexia
Cachexia is most prevalent in solid tumours associated with the gastrointestinal (GI) system and lungs. Disruption of systemic nutrient delivery (amino acids and oxygen) is a contributing factor to skeletal muscle wasting. Chemotherapy can independently drive skeletal myopathy and exacerbate cancer-associated myopathy. For haematological cancers such as acute myeloid leukaemia (AML), where intense chemotherapy is the primary treatment, there is a high risk of severe chemotherapy-induced cachexia.
Chemotherapy administration has been shown to directly induce skeletal muscle wasting and dysfunction. This can be exacerbated by the effect of chemotherapy on the gastrointestinal tract (GIT), which compromises the intestinal barrier and reduces nutrient absorption. Chemotherapy also reduces blood cells, causing hypoxia and suppressing the immune response. Consequently, patients experience fatigue and an increased risk of infection.
One strategy to mitigate chemotherapy-induced cachexia is to enhance muscle anabolism or block muscle catabolism. Administration of ghrelin, an endogenous ligand for the growth hormone secretagogue receptor (GHSR)-1a, was shown to protect against cisplatin-induced cachexia by promoting muscle anabolism in experimental animals. Another strategy is to use a mathematical model of chemotherapy-induced muscle wasting to capture the non-linear dose-dependence and explore alternate dosing schedules that preserve lean mass while actively targeting the tumour.
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Cancer-associated myopathy
Risk factors for cancer-associated myopathy include older age (patients older than 45 are at higher risk), a previous personal or family history of cancer, and the presence of certain autoantibodies such as TIF1-gamma or NXP2. Patients with dermatomyositis are at a particularly high risk of developing cancer-associated myopathy, with an estimated 20-30% of patients developing cancer. Polymyositis patients develop cancer at about half the rate of dermatomyositis patients, while those with necrotizing myopathy are also at a higher risk than the general population.
The intense chemotherapy used to treat acute myeloid leukaemia (AML) has been shown to directly induce skeletal muscle wasting and dysfunction, which is referred to as myopathy. This can be exacerbated by the effects of chemotherapy on the gastrointestinal tract, which disrupts nutrient absorption and increases the risk of infection. As a result, patients may experience fatigue and incapacitation. Additionally, cachexia, a life-threatening body wasting syndrome, is observed in AML and can have dire consequences. Cachexia is characterised by weight loss, low body mass index (BMI), and depletion of skeletal muscle mass. While cachexia is more commonly associated with solid tumours, it can also occur in haematological cancers like AML and contribute to muscle wasting.
Optimising treatment and risk management strategies is crucial for improving outcomes for AML patients. Skeletal muscle mass is being considered as an emerging factor in patient risk stratification for AML. By addressing skeletal muscle mass and cachexia within the AML clinical landscape, there is potential to improve the survivability of this disease.
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Muscle mass loss
Muscle wasting, or muscle atrophy, is the loss or thinning of muscle mass due to muscles weakening and shrinking. It can be caused by the disuse of muscles or neurogenic conditions. In the context of acute myeloid leukaemia (AML), muscle wasting is a significant concern with potentially dire clinical consequences.
AML is a haematological malignancy with poor survival odds, particularly in older patients above the age of 65. The standard treatment for AML involves induction and consolidation chemotherapy, which is intense and debilitating. Chemotherapy administration has been identified as a direct contributor to skeletal muscle wasting and dysfunction in AML patients. The cytotoxic nature of chemotherapy increases the risk of multi-organ toxicity and exacerbates the challenges associated with muscle wasting.
One of the mechanisms by which chemotherapy induces muscle wasting in AML is through its impact on the gastrointestinal tract (GIT). Chemotherapy dysregulates motility and compromises the intestinal barrier, leading to reduced nutrient absorption. This disruption of systemic nutrient delivery, particularly amino acids and oxygen, is a contributing factor to skeletal muscle wasting. Additionally, chemotherapy can extirpate blood cells, causing hypoxia and suppressing the immune response, further incapacitating patients.
The severity of muscle wasting in AML is clinically characterised by weight loss, a decrease in body mass index (BMI), and loss of skeletal muscle mass. Skeletal muscle mass is considered a crucial factor in patient risk stratification and predicting patient suitability for AML treatment. The presence of muscle wasting can increase the risk of mortality and negatively impact treatment outcomes.
To address muscle wasting in AML, novel treatment and risk management strategies are essential. Optimising nutrition and incorporating physical therapy or exercise can help mitigate muscle loss. Additionally, patient stratification tools such as the CAchexia SCOre (CASCO) and skeletal muscle index (SMI) can aid in identifying cachexia and myopenia/sarcopenia, respectively, to guide treatment decisions and improve overall survival rates.
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Skeletal muscle wasting
Skeletal muscles are crucial for movement, gestural assistance, metabolic homeostasis, and thermogenesis. They make up approximately 40% of the total body weight and 50% of the total protein. Skeletal muscle wasting, or atrophy, is the wasting or thinning of muscle mass. It is characterised by weakening, shrinking, and decreasing muscle mass and fibre cross-sectional area. It can be caused by the disuse of muscles or neurogenic conditions.
In the context of acute myeloid leukaemia (AML), skeletal muscle wasting is a potential side effect of the intense chemotherapy used to treat the cancer. Chemotherapy has been shown to directly induce skeletal muscle wasting and dysfunction. This is exacerbated by its effects on the gastrointestinal tract (GIT), which disrupt motility and microbiota composition and compromise the intestinal barrier. These symptoms reduce nutrient absorption and increase the risk of infection and inflammation. Ultimately, the processes that maintain muscle mass and function are disrupted, and muscle wasting is accelerated.
Additionally, skeletal muscle wasting in AML may be related to cachexia, a life-threatening body wasting syndrome. Cachexia is associated with both cancer and anticancer chemotherapy. While it is more prevalent in solid tumours, it has been observed in AML patients as well. Cachexia is characterised by weight loss, low body mass index (BMI), and muscle wasting. Skeletal muscle mass loss is considered a critical prognostic factor in cachexia.
The treatment for skeletal muscle wasting depends on the type of atrophy. Disuse atrophy can be treated with regular exercise and improved nutrition. Nutritional support may include working with a dietitian and incorporating nutritional supplements. In cases of neurogenic atrophy, a special type of physical therapy called electrical stimulation can be used to artificially contract the muscles and maintain muscle mass.
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Patient risk stratification
Acute myeloid leukaemia (AML) is a haematological malignancy with poor survival odds, particularly in older patients (over 65 years) in whom it is most prevalent. AML is treated with intense chemotherapy induction regimens, followed by haematopoietic cell transplantation (HCT) to achieve complete remission. While these treatments can be successful in younger patients, their clinical utility is limited in older adults due to the intensity and cytotoxicity of the chemotherapy used, which increases the risk of multi-organ toxicity and mortality.
Cachexia is prevalent in solid tumours associated with the gastrointestinal (GI) system and lungs, and disruption of systemic nutrient delivery (e.g. amino acids and oxygen) is thought to contribute to skeletal muscle wasting. Chemotherapy also plays a significant role in cachexia, as it has been shown to independently drive skeletal myopathy and exacerbate cancer-associated myopathy. In haematological cancers such as AML, where chemotherapy is the primary or only treatment, the risk of severe chemotherapy-induced cachexia is particularly high.
Further stratification strategies are required to improve patient survivability, such as scoring criteria related to skeletal muscle health or the use of cachexia diagnostic tools.
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Frequently asked questions
Muscle wasting, or atrophy, is the loss or thinning of muscle mass due to muscles weakening, shrinking, or becoming damaged. It can be caused by disuse of muscles or neurogenic conditions.
Acute myeloid leukaemia (AML) is a haematological malignancy with poor survival odds, particularly for those over 65. AML treatment consists of intense induction and consolidation chemotherapy, which has been shown to directly induce skeletal muscle wasting and dysfunction. This can be exacerbated by the effect of chemotherapy on the gastrointestinal tract (GIT), which reduces nutrient absorption.
Skeletal muscle mass may be a better predictor of patient suitability for, and outcomes of, AML treatment. Therefore, it is important to pursue novel ideas to optimize current treatment and risk management strategies to improve outcomes for AML patients. One idea is to use patient stratification through the identification of cachexia by the CAchexia SCOre (CASCO) or sarcopenia/obesity by the body mass index (BMI).
