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Arthritis and its impact on mental health

Introduction:

Arthritis is the medical term for swelling or joint inflammation. It includes more than 100 ailments that have an impact on connective tissues, joints, and surrounding tissues. According to the type of arthritis, specific symptoms can vary, although stiffness and pain in the joints are typically present (1). The most prevalent type of arthritis is osteoarthritis. Other prevalent arthritis related diseases include gout, fibromyalgia, and rheumatoid arthritis (1). Degenerative joint disease or “wear and tear” arthritis are terms used to describe osteoarthritis (OA). Typically, the hands, hips, and knees are affected. When your immune system accidentally attacks healthy cells in your body, as happens in rheumatoid arthritis, also known as RA, inflammation (painful swelling) develops in the affected areas of your body (1). The main area of focus for RA is the joints, frequently several joints at once. The joints of the hand, wrist, and knee are frequently affected by RA. In a RA-affected joint, the inflammation of the joint lining damages the joint tissue. Gout is a typical and painful form of inflammatory arthritis. One joint is typically affected at a point (often the big toe joint) (1). An estimated 58.5 million US individuals (22.7%) every year between 2013 and 2015 reported having ever received a diagnosis of arthritis, rheumatoid arthritis, gout, lupus, or fibromyalgia from a medical professional (1). By 2040, 78 million (26%) US persons 18 and older are anticipated to develop arthritis, according to projections (1).

Factors impacting mental health in arthritis patients

Major psychiatric issues like depression and anxiety can be linked to arthritis through biological and cytokine-related mechanisms as well as the psychological effects of ongoing medical hardship on a patient’s mental health (2). Patient-reported outcomes (PROs) such early morning stiffness (EMS), fatigue, and baseline physical pain have a significant impact on arthritis patients’ quality of life (QoL) (3), contribute to the disease’s high activity, and are also likely to worsen depression. Chronic inflammatory disorders can affect the central nervous system, and psychological stress can affect the immune system (4).

Pain and Fatigue in Arthritis

The National Rheumatoid Arthritis Society (NRAS), a patient-led charity in the UK, conducted the “Invisible Disease: Rheumatoid Arthritis and Chronic Fatigue Survey” in 2014 (5). It found that fatigue is extremely common in RA, with 90% of RA patients reporting it as the primary cause of low mood and depression, 89% reporting chronic fatigue, and 79% never having their level of fatigue assessed (5). Overwhelming exhaustion has been linked to mood changes, self-efficacy, physical function, edema, early morning stiffness (EMS), and elevated levels of ESR or lipopolysaccharide (LPS)-stimulated interleukin-6 (IL-6).

Impact on patient

Patients with RA typically experience tearfulness, irritation, annoyance, anxiety, and despair when discussing how the condition affects their mental health (3). Different symptoms of anxiety and sadness are reported by patients and doctors. The anxiety/depression questionnaires were completed by 1,015 pairs of RA patients and their doctors; accordingly, 38.4%, 9.9%, and 67.1% of cases of anxiety/depression were reported by patients solely, doctors only, and both patients and doctors respectively (6).

Arthritis and depression

Depression is the most prevalent mental health issue linked with arthritis, occurring two times more frequently in people with RA than in the normal public (2). According to a meta-analysis, 16.8% of arthritis patients experience serious depressive disorders, and between 14 and 48% of RA patients experience depression (7). Within the first two years of receiving a diagnosis, 16% of arthritis patients changed occupations, and 33% of arthritis patients quit their jobs (8). The inflammatory mechanism underpinning depression in RA is further supported by the fact that inflammatory arthritis is a risk factor for mental health issues (2). The physiological reaction to stress, including efficient coping mechanisms, is impaired by chronic inflammation (2). Thus, stress is an exacerbating factor that might result in depression (9). The adherence to medical therapy also appears to be reduced by depression (10). This may be accounted for by despondency, a poor cognitive understanding of one’s health, and a lack of confidence in one’s ability to operate while suffering from arthritis (2). Additionally, arthritis patients with depression have worsened pain, exhaustion, and disability coping mechanisms, which results in decreased physical activity and social contact (2). As a result, mental anguish, frustration, and finally depression grow as physical health and function deteriorate (2). These alterations result in poor outcomes, thus it’s critical to address depression to enhance arthritis outcomes and/or lessen elements that lower the efficacy of arthritis treatment (11).

Mechanism of Mental health problems in arthritis

People with arthritis are prone than adults without arthritis to experience symptoms of anxiety or sadness. Over 10 million of the 58.5 million adult arthritis sufferers report having anxiety or depressive symptoms. Younger persons with arthritis (aged 18 to 44) or those with additional chronic diseases are more likely than other individuals with arthritis to experience symptoms of anxiety or sadness (12).
Multifactoral pathophysiology underlies arthritis. Central to the etiology of RA are the pro-inflammatory effects of TNF-a on the function of other cytokines, including IL-1, IL-6, IL-8, and GM-CSF (13). Early in the morning, RA disease activity is worse due to the circadian rhythm of inflammatory cytokines (IL-6, TNF-a), and glucocorticoids (14). T-cell-related RA flares are caused by T cell differentiation, T helper (Th) cells, CD4 cell differentiation, creation of Th1 cells, and release of IFN-c driven by IL-12. Systemic and local inflammation is brought on by IL-23, IL-17A, IL-1, and IL-6 in RA (15).
Numerous theories exist about the mechanisms by which local inflammation, edema, and peripheral cytokines cause extra-articular tissue to undergo brain inflammation. Significantly greater IL-1b, IL-6, and TNF-a concentrations in RA increase the risk of substantial atherogenesis. The secretion of tryptophan metabolites and oxidative stress is enhanced by IL-1 and IFN-alpha, which delays neurogenesis and increases fatigue. Through primary afferent neurons or the endothelial cells of cerebral vessels, where IL-1 acts on macrophage-like cells in the CNS, disrupting neural integrity and making the blood-brain barrier less intact, peripheral inflammation and cytokines IL-1, IL6 and TNF-a transmit signals to the brain. Neurocircuitry dysfunction at the glia can result from chronic inflammation interfering with glutamate neurotransmitters (16). In a short preliminary investigation, neuroinflammation and microglial activation related to systemic inflammation were observed on PET imaging in the cases of systemic inflammation (17).


Depression and Cytokines

The association between depression and inflammation is now better understood because of developments in “immunopsychiatry,” and over the past two or three decades, some have argued that depression is an inflammation-related condition (18). Patients with depression or anxiety were reported to have higher levels of IL-1, IL-6, C-reactive protein, and TNF-alpha in T-cell-mediated inflammation. In RA patients, disruption of the HPA axis by IL-6 may result in anxiety and depression. Additionally, it has been demonstrated that the level of IL-17A is strongly correlated with the degree of depression (19). When CRP levels are high, the ventromedial cortex of the brain is inhibited, which causes anhedonia. CRP is a potential biomarker of disease activity in RA. Increased CSF IL-6 levels are associated with greater suicide attempts, and they play a significant role in the development of depression. Pro-inflammatory cytokines TNF-a, IL-1, Il6, and IFN-a levels, as well as CRP and ESR, are elevated in RA, and these elevated levels of inflammation are thought to act as a “biological scar” that raises the risk of depression (20).

Cognitive Function and Cytokines

In a study by Shin et al., cognitive function scores in 144 arthritis patients were assessed using the American College of Rheumatology neuropsychological battery modified for RA, and the results revealed cognitive impairment in verbal memory, executive function, and visuospatial learning as (20%, 29%, and 18% respectively) (21). A cross-sectional study evaluated the cognitive performance of 60 female RA patients on MTX or bDMARDs using the Montreal Cognitive Assessment (MOCA), and the findings revealed that 60% of RA patients scored MOCA 26 (normal C 26), compared to 49% in the control group (22).

Role of exercise on arthritis patients

  • Engaging in joint-friendly physical exercise helps lessen the pain, functioning, mood, and standard of living associated with arthritis. Low-impact physical activities are less stressful on the body and less likely to cause injuries than high-impact ones. Exercises that are good for your joints include walking, biking, and swimming. Physical activity can also assist patients with arthritis to manage other chronic disorders like diabetes, heart disease, and obesity. It can also prevent the development of arthritis-related disabilities (1).
  • Start slowly while beginning or increasing physical exercise, and give heed to how your body responds to it.
  • Exercises with low impact on the joints, such as brisk walking, cycling, swimming, water aerobics, light gardening, group fitness programs, and dance are examples of low-impact aerobic activities (1).

Conclusion

Both patients and clinicians might benefit from additional observational studies for the early diagnosis of anxiety and depression in arthritis patients utilizing web-based questionnaires. There is a growing corpus of research on anti-rheumatic medications that examines how it affect depression and cognitive performance in arthritis patients. Additional studies are required to distinguish between the affective and physiologic causes of mental health problems in arthritis patients.

References

  1. https://www.cdc.gov/arthritis/types/index.html
  2. Sturgeon J, Finan P, Zautra A. Affective disturbance in rheumatoid arthritis: psychological and diseaserelated pathways. Nat Rev Rheumatol. 2016;12(9): 532–42. https://doi.org/10.1038/nrrheum.2016. 112.
  3. Intriago M, Maldonado G, Cardenas J, Rios C. Quality of life in Ecuadorian patients with established rheumatoid arthritis. Open Access Rheumatol Res Rev. 2019;11:199–205. https://doi.org/10. 2147/OARRR.S216975.
  4. Twigg S, Hensor E, Emery P, Tennant A, Morgan A. Patient-reported outcomes as predictors of change in disease activity and disability in early rheumatoid arthritis: results from the Yorkshire early arthritis register. J Rheumatol. 2017;44(9): 1331–400.
  5. ‘Invisible Disease: Rheumatoid Arthritis and Chronic Fatigue Survey,’’ National Rheumatoid Arthritis Society, 16–22 June 2014. [Online]. Available: https://www.nras.org.uk/invisible-diseaserheumatoid-arthritis-and-chronic-fatigue-survey
  6. Peterson S, Piercy J, Blackburn S, Sullivan E, Karyekar C, Li N. The multifaceted impact of anxiety and depression on patients with rheumatoid arthritis. BMC Rheumatol. 2019
  7. Matcham F, Rayner L, Steer S, Hotopf M. The prevalence of depression in rheumatoid arthritis: a systematic review and meta-analysis. Rheumatology. 2013;52:2136–48
  8. Rezaei F, Doost H, Molavi H. Depression and pain in patients with rheumatoid arthritis: mediating role of illness perception. Egypt Rheumatol. 2014;36(2): 57–64
  9. Straub R, Dhabhar F, Bijlsma J, Cutolo M. How psychological sress via hormones and nerve fibers may exacerbate rheumatoid arthritis. Arthritis Rheum. 2005;52:16–26.
  10. DiMatteo M, Lepper H, Croghan T. Depression is a risk factor for noncompliance with medical treatment: meta-analysis of the effects of anxiety and depression on patient adherence. Arch Intern Med. 2000;160:2101–7
  11. Matcham F, Davies R, Hotopf M, Hyrich K, Norton S, Steer S, Galloway J. The relationship between depression and biologic treatment response in rheumatoid arthritis: an analysis of the British Society for Rheumatology Biologics Register. Rheumatology (Oxford). 2018.
  12. Ba˛k E, Marcisz C, Borodzicz A, Sternal D, Krzemin´ ska S. Comparison of health-related quality of life in patients with rheumatoid arthritis during conventional or conventional plus biological therapy in Poland. Patient Prefer Adherence. 2019;13: 223–31
  13. Brennan F, McInnes I. Evidence that cytokines play. J Clin Invest. 2008;118(11):3537–45.
  14. Spies C, Straub R, Cutolo M, Buttgereit F. Circadian rhythms in rheumatology—a glucocorticoid perspective. Arthritis Res Ther. 2014;16(Suppl 2):S3
  15. Agonia I, Couras J, Cunha A, Andrade A, Macedo J, Sousa-Pinto B. IL-17, IL-21 and IL-22 polymorphisms in rheumatoid arthritis: a systematic review and meta-analysis. Cytokine. 2019
  16. GS Ebrahim Haroon. Inflammation, glutamate, and glia: a trio of trouble in mood disorders. Neuropsychopharmacology. 2017;42(1):193–21515.
  17. Drake C, Boutin H, Jones M, et al. Brain inflammation is induced by co-morbidities and risk factors for stroke. Brain Behav Immun. 2011;25(6): 1113–22.
  18. Miller A. Five things to know about inflammation and depression. Psychiatric Times. 2018;35(4):2018.
  19. Maes M, Van Bockstaele D, Gastel A, Song C, Schotte C, Neels H, DeMeester I, Scharpe S, Janca A. The effects of psychological stress on leukocyte subset distribution in humans: evidence of immune activation. Neuropsychobiology. 1999;39(1):1–9.
  20. Lindqvist D, Janelidze S, Hagell P, Erhardt S, Samuelsson M, Minthon L, Hansson O, Bjo¨rkqvist M, Tra¨skman-Bendz L, Brundin L. Interleukin-6 is elevated in the cerebrospinal fluid of suicide attempters and related to symptom severity. Biol Psychiatry. 2009;66(3):287–92.
  21. Shin S, Katz P, Wallhagen M, Julian L. Cognitive Impairment in Persons With Rheumatoid Arthritis. Arthritis Care Res (Hoboken). 2012;64(8):1144–50.
  22. Ola´h C, Kardos Z, Andrejkovics M, Szarka E, Hodosi K, Domja´n A, Sepsi M, Sas A, Kostya´l L, Fazekas K, Flo´ria´n A, Luka´cs K, Miksi A, Bara´th Z, Kerekes G, Pe´ntek M, Valikovics A, Tama´si L, Bereczki D, Szekanecz Z. Assessment of cognitive function in female rheumatoid arthritis patients: associations with cerebrovascular pathology, depression and anxiety. Rheumatol Int. 2019

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