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Rheumatoid arthritis (RA) is a debilitating, chronic, systemic, autoimmune disease that causes joint pain, swelling, and stiffness. RA patients often experience muscle wasting or loss, known as rheumatoid cachexia, which is believed to be caused by a combination of factors, including chronic inflammation, physical inactivity, oxidative stress, and metabolic changes. This condition leads to a decrease in muscle mass and strength, impacting the patient's quality of life and functional capacity. While there is no standard treatment for rheumatoid cachexia, physical exercise, dietary changes, and medications are recommended to manage the condition and improve muscle strength.
| Characteristics | Values |
|---|---|
| What is it called when rheumatoid arthritis causes muscle loss? | Rheumatoid cachexia or muscle wasting |
| What is rheumatoid cachexia? | A metabolic state that happens when your body loses muscle mass but keeps fat mass |
| What causes rheumatoid cachexia? | Chronic inflammation, lack of physical activity, activation of the nuclear factor kappa-beta pathway, and oxidative stress |
| How common is it? | It is believed to affect about two-thirds of people with rheumatoid arthritis |
| How is it diagnosed? | There is no standard test, but doctors may use imaging tests like CT scans and MRIs, along with measurements of height, weight, and body mass index (BMI) |
| What are the symptoms? | Muscle weakness, decreased strength, and loss of functional capacity |
| What are the treatment options? | Physical exercise, especially a combination of skeletal muscle strength training and aerobic exercise, is currently believed to be the most important countermeasure |
| Are there any dietary recommendations? | Doctors typically recommend a high-protein, low-carbohydrate anti-inflammatory diet, and adding fish oil to your diet may help improve muscle strength |
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What You'll Learn
Rheumatoid cachexia
Rheumatoid arthritis (RA) is an inflammatory joint disease that affects more women than men. It is characterised by joint stiffness, pain, and swelling. RA can lead to a metabolic state called rheumatoid cachexia, or muscle wasting. This condition develops due to chronic inflammation and a lack of physical activity caused by RA.
The loss of muscle mass in people with RA can cause them to appear overweight, even as they experience severe weight loss. This unique presentation of cachexia in RA patients has led experts to classify it as rheumatoid cachexia. There is currently no standard treatment for rheumatoid cachexia, but exercise is believed to be the most effective way to manage the condition. Doctors may also recommend dietary changes, such as a high-protein, low-carbohydrate anti-inflammatory diet, and medications used to treat RA may also help.
To diagnose rheumatoid cachexia, doctors may use dual-energy X-ray absorptiometry (DEXA) to determine the patient's lean body mass, which includes organs, skin, bone, and muscle mass. They may also use imaging tests like CT scans and MRIs, as well as take measurements of height, weight, and body mass index (BMI). While there is no unified list of factors for diagnosing rheumatoid cachexia, doctors generally look for evidence of muscle wasting, increased fat mass, and other indicators of the condition.
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Muscle wasting
Rheumatoid arthritis (RA) is a debilitating, chronic, systemic, autoimmune disease that causes the destruction of joint cartilage and bone. It is characterised by joint stiffness, pain, and swelling, and is accompanied by a loss of body cell mass. This loss of cell mass, known as rheumatoid cachexia, predominates in skeletal muscle but also occurs in the viscera and immune system. Rheumatoid cachexia is a metabolic state that happens when the body loses muscle mass and keeps fat mass. It is believed to affect around two-thirds of people with RA.
RA patients have significantly less muscle mass compared to the general population. The disease is associated with altered body composition, which can result in rheumatoid cachexia. Muscle deterioration in the early stages of the disease can be assessed by quantitative MRI. RA patients often present with low muscle mass and decreased strength.
There are several theories about the causes of muscle wasting in RA. High-grade inflammation has long been proposed as the key driver. However, more recent findings indicate that inflammation alone cannot fully explain the high prevalence of muscle wasting in RA. Other factors, such as nutrition and physical activity, have also been studied. Results indicate that they play a significant role in muscle wasting in RA, but neither of these factors can fully explain the condition.
Oxidative stress is another major mechanism thought to contribute to the development and progression of RA. It has been shown to promote muscle wasting in healthy populations and people with several chronic conditions. All of the aforementioned potential contributors to muscle wasting in RA (i.e., inflammation, nutrition, and physical activity) may promote pro- or anti-oxidative mechanisms.
Insulin resistance is another factor that contributes to muscle wasting in RA. A sedentary lifestyle leads to a reduction in the mitochondrial density of skeletal muscle, resulting in a decreased oxidative capacity of blood-borne fatty acids. This, combined with an increased supply of plasma fatty acids and triglycerides, leads to the accumulation of fatty acid metabolites. Both these fatty acid metabolites and the exposure of the muscle to inflammatory cytokines activate serine kinases, which lead to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and prevent the downstream activation of the insulin signalling cascade, impairing glucose uptake.
Tumour necrosis factor-alpha (TNF-α) and interleukin-1beta are also believed to be central mediators of muscle wasting in RA. They alter the balance between protein degradation and protein synthesis, leading to muscle wasting. TNF-α has also been shown to interfere with insulin receptor signalling.
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Sarcopenia
The rate of muscle loss in sarcopenia is dependent on exercise levels, co-morbidities, nutrition, and other factors. The muscle loss is related to changes in muscle synthesis signalling pathways. The pathologic changes of sarcopenia include a reduction in muscle tissue quality, an increase in fibrosis, changes in muscle metabolism, oxidative stress, and degeneration of the neuromuscular junction. Sarcopenia can cause muscle weakness, loss of stamina, difficulty performing daily activities, slow walking speed, trouble climbing stairs, poor balance, and an increased risk of falls and fractures.
Several factors contribute to the development of sarcopenia, including aging, physical inactivity, obesity, insulin resistance, reduced androgen and growth factor serum concentrations, inadequate protein intake, and a blunted muscle protein synthesis (MPS) response to protein meals or resistance exercise. Additionally, sarcopenia is associated with and may be caused by chronic diseases that negatively affect the musculoskeletal system and physical activity, such as chronic obstructive pulmonary disease (COPD), chronic heart failure (CHF), chronic kidney disease (CKD), diabetes mellitus (DM), human immunodeficiency virus (HIV), and cancer.
Rheumatoid arthritis (RA) is a chronic disease that can lead to a metabolic state called rheumatoid cachexia or muscle wasting. This condition is characterised by muscle loss and the retention of fat mass due to chronic inflammation and lack of physical activity associated with RA. Rheumatoid cachexia may explain why many people with RA also have sarcopenia.
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Oxidative stress
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterised by synovitis and the presence of serum autoantibodies. Skeletal muscle weakness is a common comorbidity that significantly affects the quality of life of patients with RA. While muscle weakness is often attributed to a decrease in muscle mass, or atrophy, studies have shown that this cannot fully explain arthritis-induced muscle weakness. Instead, intramuscular dysfunction appears to be a critical factor underlying the decreased force-generating capacity of patients with arthritis.
Mitochondria, NADPH oxidases (NOX), nitric oxide synthases (NOS), and phospholipases (PLA) have all been associated with increased ROS/RNS production in RA-induced muscle weakness. Brief exposure of skeletal muscle to TNFα, a pro-inflammatory cytokine, has been shown to increase ROS/RNS stress and reduce force generation capacity. In addition, increased circulating levels of TNFα have been shown to induce nNOS activity, which has been linked to muscle weakness in patients with RA. nNOS can produce ROS such as O2− and ONOO−, which may contribute to oxidative damage.
Antioxidants and exercise have been proposed as potential tools to counteract oxidative stress and skeletal muscle weakness in patients with RA. Resistance training and intensive aerobic exercise have been shown to improve body composition and muscle mass without any adverse effects on disease activity.
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Tumor necrosis factor-alpha
Rheumatoid arthritis (RA) can lead to a metabolic state called rheumatoid cachexia, or muscle wasting. This condition arises from chronic inflammation and physical inactivity due to RA. While the exact causes of rheumatoid cachexia are unknown, experts believe that various factors contribute to its development.
In healthy individuals, the body regulates TNF-alpha levels, ensuring that inflammation is triggered only when needed. However, in diseases like rheumatoid arthritis, this regulation can go awry, resulting in excess TNF-alpha and chronic inflammation. This excess TNF-alpha can lead to autoimmune conditions, where the immune system mistakenly attacks healthy body parts, such as joints, causing further inflammation.
TNF-alpha has been associated with muscle wasting and weakness in inflammatory diseases. Studies have shown that TNF-alpha disrupts the differentiation process of muscle cells and promotes catabolism in mature cells, leading to muscle loss. This process is believed to be mediated by reactive oxygen species and nuclear factor-kappaB, which increase ubiquitin/proteasome activity.
Additionally, TNF-alpha has been linked to modulating muscle mass, particularly in pathological diseases such as cancer cachexia and Sarcopenia. High levels of circulating TNF-alpha have been associated with lower muscle mass and strength in older adults. Resistance training and exercise have been shown to influence TNF-alpha levels and their impact on muscle size, architecture, and function.
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Frequently asked questions
Yes, rheumatoid arthritis (RA) can cause muscle loss, also known as muscle wasting or rheumatoid cachexia.
Rheumatoid cachexia is a metabolic state characterised by muscle atrophy, changes in muscle fibre, increased inflammatory biomarkers in the muscle, decreased strength, and the preservation or increase of fat mass.
The exact cause of rheumatoid cachexia is unknown. However, it is believed to be caused by a combination of factors, including chronic inflammation, lack of physical activity, metabolic changes, and oxidative stress.
There is no standard test to diagnose rheumatoid cachexia. Doctors may use imaging tests such as MRI scans and CT scans to identify muscle wasting. They may also measure body mass index and assess levels of malnutrition.
There is currently no standard treatment for rheumatoid cachexia. However, physical exercise, especially a combination of skeletal muscle strength training and aerobic exercise, is believed to be the most important countermeasure. Doctors may also recommend a high-protein, low-carbohydrate anti-inflammatory diet.
