Psleep: Psoriasis and Sleep
Dermatologists are well aware that sleep is affected in multiple chronic dermatoses which are pruritic or painful. Oftentimes, patients finally come in for treatment due to changes in their sleep. Over the past 20 years, we have seen great medical advancements for the treatment of psoriasis which can safely and effectively control skin, joints, and even improve some of the comorbidities associated with psoriasis. The “invisible” impacts of psoriasis are those not directly seen on examination. These include itch, pain, fatigue and sleep dysfunction, which may be improved by our systemic therapies. However, there is a gap between the patients’ reporting of these experienced invisible impacts and their physician’s assessments of disease severity. In a small study of 102 psoriasis patients, 78% of which were in remission (psoriasis area and severity index [PASI] of 0), nearly 40% of patients were depressed and there was a high percentage of poor sleepers independent of depression severity.1 Therefore, it is important to regularly assess pain, itch, and sleep symptoms to ensure optimal disease control.
Sleep dysfunction is an important comorbidity of psoriasis. Sleep dysfunction is complex and may present as low sleep quality (difficulty maintaining sleep, early awakening), low sleep quantity (insomnia), and daytime dysfunction such as fatigue or sleepiness with reduced energy and motivation—which may affect work, social interactions, and/or family functions. Sleep and skin are intimately related. Sleep dysfunction is seen commonly in patients with psoriasis and has been associated with a higher incidence of obesity, depression, and cardiovascular disease.2 Most adults need 7 to 9 hours of sleep. Decreased sleep is associated with alteration in ghrelin and leptin (neurotransmitters that signal when to eat), increased cortisol levels that contribute to circadian misalignment, thermoregulation, skin pH, and insensible water loss and permeability.3-5 Sleep is immunomodulatory—sleep dysfunction is associated with increased proinflammatory Th1 cytokines.4 Additionally, psoriasis patients have lower melatonin levels and lack a night-time peak.6
Sleep dysfunction is commonly seen in psoriasis patients at levels up to twice the incidence of the general population. Itch and pain are associated with sleep dysfunction. Up to 65% of psoriasis patients itch, and the nocturnal impact of pruritus affects sleep.7 Pruritus may be associated with difficulty falling asleep and nocturnal awakening, which can result in daytime fatigue.8 In one study involving 295 patients with psoriasis in Poland, difficulty falling asleep was reported in 70% of patients and 50% of patients experienced nocturnal awakening, which was most correlated with itch.9 Pruritus follows a circadian rhythm, worsening at night due to lower cortisol levels, impaired barrier function, and dysfunctional thermoregulation. The dysregulation of cytokines, neuropeptides (substance P, somatostatin, and vasoactive intestinal peptide) and thermoregulation may result in impaired sleep induction and nocturnal pruritus.1 The pruritus, depression, and pain symptoms that are present in psoriasis negatively impact sleep duration and sleep architecture by increasing nocturnal awakenings that lead to sleep deprivation.10 Rheumatologists have long been aware that nocturnal awakenings and poor sleep are associated with inflammatory back pain, joint stiffness, and pain.
Psoriasis patients with depression have been found to have an increase in sleep difficulties.11 Depression has been linked to poor sleep, typically insomnia. There is a developing understanding of the bidirectional communication between dermatological and neuropsychological systems. Psoriasis has a demonstrated relationship with depression and anxiety and, likewise, mental stress and suffering has been shown to exacerbate skin conditions.12 Biologics have also been shown to improve depression and mental status in psoriasis patients.13
Sleep dysfunction may contribute to incomplete disease control in psoriasis by potentiating presumably pathogenic patterns of intestinal dysbiosis. The gut microbiome in psoriasis and sleep dysfunction both share an increased Firmicutes to Bacteroidetes ratio and reduced abundance of short chain fatty acid-bacteria—this dysbiosis has been shown to promote systemic inflammation and cardiovascular disease.14 The gut microbiome has a regulatory role with respect to immune activity and the circadian rhythm and thus may play a role in sleep and psoriasis.15
Two sleep disorders associated with psoriasis that should be evaluated by sleep specialists are obstructive sleep apnea (OSA) and restless leg syndrome (RLS).5 Psoriasis patients have an increased risk of OSA (36% to 81% prevalence) and RLS, which may be related to autonomic activation.16 In patients with OSA, continuous positive airway pressure (CPAP) decreases C-reactive protein and IL-6.17 OSA has been associated with cardiovascular disease (CVD) and CPAP may reduce the risk of CVD.18 RLS has a strong relationship to systemic inflammation and is associated with CVD and diabetes mellitus (DM).19,20
Psoriasis is associated with sleep dysfunction and systemic interventions can improve sleep.21 In a small study involving 46 non-anxious and non-depressed patients with psoriasis, psoriatic insomnia was improved after 6 months of systemic treatment of psoriasis.22 Persistent sleep dysfunction is a risk factor for many comorbidities associated with psoriasis, such as CVD, diabetes, depression, and anxiety, as well as impaired quality of life. Chronic sleep impairment is an independent risk factor for myocardial infarction in patients with psoriasis.23
The impacts psoriasis has on an affected individual, their family, and society are numerous. The entire family unit’s sleep quality may be negatively affected when a child has psoriasis.24 Sleep disorders and their associated fatigue create a vicious cycle with anxiety and depression.25 Sleep disturbances are more commonly seen in psoriasis patients who live alone, have comorbidities, and are women. Psoriasis patients who have partners, no itch, no pain, and no comorbidities are less likely to have sleep dysfunction.26 Ideally, systemic psoriasis therapies should control skin, joints, and improve quality and quantity of life. In psoriasis patients, sleep dysfunction leads to worsening skin symptoms, reduced quality of life, and an increased risk of coronary artery disease. Controlling the invisible impacts of psoriasis may be the key to maximizing our patients’ quality of life, reducing morbidity and improving life expectancy.
Annelies Isabelle Johanna Groen works at Mindful Dermatology in Dallas, Texas. Jennifer Clay Cather, MD, is a board-certified dermatologist at Mindful Dermatology in Dallas, Texas, and Medical Director at Modern Research Associates in Dallas, Texas.
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9. Jaworecka K, Rzepko M, Marek-Jozefowicz L, et al. The impact of pruritus on the quality of life and sleep disturbances in patients suffering from different clinical variants of psoriasis. J Clin Med. 2022;11(19):5553.
10. Gowda S, Goldblum OM, McCall WV, et al. Factors affecting sleep quality in patients with psoriasis. J Am Acad Dermatol. 2010;63(1):114-23.
11. Jensen P, Zachariae C, Skov L, et al. Sleep disturbance in psoriasis: a case-controlled study. Br J Dermatol. 2018;179(6):1376-1384.
12. Papa V, Li Pomi F, Borgia F, et al. “Mens Sana in Cute Sana”-a state of the art of mutual etiopathogenetic influence and relevant pathophysiological pathways between skin and mental disorders: an integrated approach to contemporary psychopathological scenarios. Cells. 2023;12(14):1828.
13. Fleming P, Roubille C, Richer V, et al. Effect of biologics on depressive symptoms in patients with psoriasis: a systematic review. J Eur Acad Dermatol Venerol. 2015;29(6): 1063-70.
14. Myers B, Vidhatha R, Nicholas B, et al. Sleep and the gut microbiome in psoriasis: clinical implications for disease progression and the development of cardiometabolic comorbidities. J Psoriasis Psoriatic Arthritis. 2021;6(1):27-37.
15. Li L, Liang T, Jiang T, et al. Gut microbiota: candidates for a novel strategy for ameliorating sleep disorders. Crit Rev Food Sci Nutr. 2023;21:1-17.
16. Gupta MA, Gupta AK. Psoriasis is associated with a higher prevalence of obstructive sleep apnea and restless legs syndrome: a possible indication of autonomic activation in psoriasis. J Clin Sleep Med. 2018; 14(6):1085.
17. Yokoe T, Minoguchi K, Matsuo H et al. Elevated levels of C-reactive protein and interleukin-6 in patients with obstructive sleep apnea syndrome are decreased by nasal continuous positive airway pressure. Circulation. 2003;107(8):1129-34.
18. Marin JM, Carrizo SJ, Vicente E, et al. Long-term cardiovascular outcomes in men with obstructive sleep apnea-hypopnoea with or without treatment with continuous positive pressure: an observational study. Lancet. 2005;365(9464):1046-53.
19. Nowowiejska J, Baran A, Lewoc M, et al. The assessment of risk and predictors of sleep disorders in patients with psoriasis—a questionnaire-based cross-sectional analysis. J Clin Med. 2021; 10: 664-680.
20. Trenkwalder C, Allen R, Hogl B, et al. Comorbidities, treatment, and pathophysiology in restless legs syndrome. Lancet Neurol. 2018;17(11):994-1005.
21. Trovato E, Marruganti C, Valenti A, et al. Association between psoriasis, sleep, and dermatological quality of life: results of a cross sectional study. Ital J Dermatol Venerol. 2023; 158(2):140-148.
22. Vlami K, Pantelidi K, Dalamaga M, et al. Psoriatic insomnia: a subjective and objective sleep evaluation. Acta Derm Venereol. 2023;103:adv00864.
23. Spencer RK, Jin JQ, Elhage KG, et al. Association between poor sleep and myocardial infarction in patients with psoriasis: findings from a cross-sectional study with the National Psoriasis Foundation. Dermatol Ther (Heidelb). 2023;13(11):2903-2909.
24. Horev A, Grinshpun K, Forer E, et al. Pediatric psoriasis negatively influences parental sleep quality. Pediatr Dermatol. 2023; 40(4): 610-614.
25. Skoie IM, Ternowitz T, Jonsson G, et al. Fatigue in psoriasis: a phenomenon to be explored. Br J Dermatol. 2015;172(5):1196-203.
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