It has been established in recent years that the skin is a direct target of psychological stress via a cascade of hormones, neuropeptides, and neurogenic signals (causing nerve hypersensitivity and inflammation). The skin has been shown to be capable of launching its own local response to stress as well by producing many of the same substances that the brain produces, further enhancing the local effect at the skin level when someone is under acute or prolonged stress. It is no surprise that the skin can perceive and respond to stress similar to the brain and nervous system, since the two systems have evolved from the same germ layer during embryonic development.
The main skin cells (keratinocytes), mast cells (involved in allergy type reactions and inflammation), immune cells, and peripheral nerve endings all will have an effect on various cell behaviour and processes within the skin under stress that can lead to skin disruption, premature ageing and disease development.
The skin is rich in nerve endings, so when an individual is stressed the peripheral nerve endings secrete numerous substances such as Substance P and Nerve growth factor that contribute to hypersensitivity, inflammation, and allergic reactions.
Due to the impact of stress related hormones and peptides, and growth factors on the skin, stress can play a role in the development and exacerbation of skin disorders such as Eczema, Acne, Psoriasis, and Rosacea.
Psychological stress activates the autonomic nervous system to trigger release of catecholamines [e.g. epinephrine and norepinephrine] from the adrenal glands, and in situations of chronic stress corticotrophin releasing hormone [CRH] and ACTH (adrenocorticotropic hormone), mediate a release of glucocorticoids (Cortisol) from the adrenal cortex.
Here is a brief outline of some key stress mediators and the effect that they have on the skin:
Excess levels can cause atrophy and impaired wound healing by interfering with keratinocyte and fibroblast function. Keratinocytes are the primary skin cells that form the epidermis of the skin, and fibroblasts are responsible for collagen and elastin formation.
This manifests as atrophy and thinning of the skin, increased trans-epidermal water loss related to disruption to the skin permeability barrier, and easy bruising with impaired wound healing.
The skin barrier is also negatively impacted by excess cortisol as this effects the lamellar bodies in the skin cells which are responsible for lipid synthesis; the lack of essential lipids weakens the barrier resulting in dry skin, allergies and sensitivity, delayed healing and infections.
Excess glucocorticoids stimulate Insulin production and lead to insulin excess and Insulin resistance. Elevated Insulin stimulates IGF2 (Insulin growth factor) which increases growth of keratinocytes, and stimulates abnormal keratinocyte growth, (exacerbates Psoriasis and Acne) and increases androgens and testosterone release.
This is neuropeptide released in times of stress. Substance P stimulates sebaceous germinative cells and proliferation of sebaceous glands which results in excess oil production and blockage of the oil ducts and the development of acne. Substance P also activates mast cells, increasing histamine release and itch sensation. Substance P induces vascular permeability and inflammation, which aggravates conditions like Eczema and Rosacea.
Corticotropin Releasing Hormone (CRH):
CRH stimulates release of MSH (melanocyte stimulating hormone) causing hyperpigmentation and blotchy skin.
Catecholamines (Adrenaline, Noradrenaline)
Decrease blood perfusion to skin reducing availability of oxygen and nutrients resulting in poor texture and sallow / pallor. Catecholamines have also been shown to cause immune suppression, interfere with DNA repair and contribute to ageing.
While the effects of stress on the skin are only briefly outlined above, it illustrates the significant impact this can have on individuals predisposed to skin conditions. It is therefore imperative to minimise stress where possible in order to avoid any exacerbation of skin disorders.
There are some straight forward tips to reduce stress such as getting a good night’s sleep, exercising and following some simple dietary guidelines (listed below).
Reduce salt intake
Avoid skipping meals
Avoid refined, processed foods.
Avoid high fat foods
Do eat high fibre, low glycaemic index diet
In the following blogs we will present some relaxation techniques that are easy to implement and will have a direct effect in reducing the side effects of stress.
- Dunn, Jeffrey HKoo, John; Psychological Stress and skin aging: A review of possible mechanisms and potential therapies; Dermatology Online Journal 19 (6): 1 University of Colorado, School of
- Medicine, 2 University of California, San Francisco, Department of Dermatology 2013 Permalink: http://escholarship.org/uc/item/3j0766hs
- Jessica M. F. Hall, desAnges Cruser, Alan Podawiltz, Diana I. Mummert, Harlan Jones, Mark E. Mummert; Psychological Stress and the Cutaneous Immune Response: Roles of the HPA Axis and the Sympathetic Nervous System in Atopic Dermatitis and Psoriasis; Dermatology Research and Practice Volume 2012, Article ID 403908, doi:10.1155/2012/403908
- Ying Chen, John Lyga; Brain – Skin Connection: Stress, Inflammation and Skin Aging; Inflammation & Allergy – Drug Targets, 2014, 13, 177-190
- Theoharis C. Theoharides, Jill M. Donelan, Nikoletta Papadopoulou, Jing Cao, Duraisamy Kempuraj, Pio Conti; Mast cells as targets of corticotropin releasing factor and related peptides; TRENDS in Pharmacological Sciences Vol.25 No.11 November 2004
“Water is defined as an essential nutrient because it is required in amounts that exceed the body’s ability to produce it. All biochemical reactions occur in water. It fills the spaces in and between cells and helps form structures of large molecules such as protein and glycogen. Water is also required for digestion, absorption, transportation, dissolving nutrients, elimination of waste products and thermoregulation” (regulation of body temperature) (Kleiner, 1999).
Up to 2 litres of Water is lost daily due to bodily functions, such as perspiration, respiration, urination and defecation.
Diuretic substances in your diet such as caffeinated beverages, alcohol, high sugar and salty foods will increase water loss from the body.
Water requirements range from 8-10 glasses per day depending on diet and physical activity levels. As we age, we have a diminished sense of thirst and tend to drink less fluid, although water is still required. It is therefore important to ensure we drink an adequate amount of water, even in the absence of thirst.
Water can be consumed from drinking pure water as well as from eating certain foods. Depending on diet, up to 50% of your daily water intake can be derived from foods provided they are high in water content such as fruit, salad, soup and vegetables (i.e. iceberg lettuce and cucumber).
How dehydration impacts your skin condition
Key signs of mild to moderate dehydration include increased sensation of pain, thirst, stiffness, headaches, lack of concentration, fatigue and skin problems.
The skin contains approximately 30% water. “Water intake, particularly in individuals with low initial water intake, can improve skin thickness and density and offsets transepidermal water loss (water lost through the skin surface)” (Popkin, Rosenberg & D’Anci, 2010). Hydration improves skin resiliency, elasticity and texture.
The water content in the skin contributes to important functions of the skin such as the development of a healthy skin barrier. The skin barrier guards the skin from microbial infections and infiltration of foreign substances which can cause skin flare ups.
Water deficiency can also lead to impaired skin processes, which can then worsen skin disorders such as dermatitis, psoriasis, acne and rosacea (Rodrigues, Palma, Tavares Marques & Bujan Varela, 2015).
Key tips to keeping hydrated
Create a routine: If you aren’t used to drinking water on a regular basis, start with four glasses of water a day. One glass on rising, one mid-morning, one mid-afternoon and one on retiring. This eliminates 4 out 8 glasses per day. Once you establish this routine, start adding additional glasses of water throughout the day, for example before meals
Convenience: Keep water with you at all times. Keep a refillable water bottle with you at work, in your car, and to take with you when you go on walks etc. Get used to sipping on water as part of your daily routine. Convenience is key, otherwise if it’s out of sight, it’s often out of mind!
Flavour: If you don’t like the taste of water, there are several ways to make it more enticing. Add some fresh herbs like mint, or fresh fruit, or a very small amount of juice (just enough to add a hint of flavour).
Variety: Mix up your water variety and add in some natural sparkling mineral water.
Eat foods high in water content: Eat plenty of fresh fruit and vegetables, in doing so will assist in keeping your body hydrated (this information should not replace any dietary information given by your psoriasis eczema clinic practitioner).
Be aware of cravings: if you are craving salty foods as this can be a signal from the body that you are dehydrated. Try drinking a glass of water before reaching for salty foods.
For more information on the health benefits of water and charts for daily consumption visit: https://www.nrv.gov.au/nutrients/water
- Popkin, B., Rosenberg, I., & D’Anci, K. (2010). Water, Hydration and Health. National Institute of Health, 68(8), 439–458. http://dx.doi.org/doi:10.1111/j.1753-4887.2010.00304.x
- Kleiner, S. (1999). Water. Journal Of The American Dietetic Association, 99(2), 200-206. http://dx.doi.org/10.1016/s0002-8223(99)00048-6
- Rodrigues, L., Palma, L., Tavares Marques, L., & Bujan Varela, J. (2015). Dietary water affects human skin hydration and biomechanics. Clinical, Cosmetic and Investigational Dermatology, 4(411), 413. http://dx.doi.org/10.2147/ccid.s86822
Continuing our series on Psoriasis and Comorbidities
CHART 1: Comorbidities Associated with Psoriasis 1,2,3
|Metabolic Syndrome –
Cerebral Vascular Disease – stroke
Peripheral Artery Disease – PAD
Cerebral Vascular Disease – stroke
A study found that cerebral (brain) vascular disease and peripheral arterial disease was also significantly more likely to be diagnosed in patients with psoriasis than in controls. 1 Cerebral vascular diseases are conditions that are caused by problems that affect the blood supply to the brain. Including:-
- stroke– a serious medical condition where one part of the brain is damaged by a lack of blood supply or bleeding into the brain from a burst blood vessel
- transient ischemic attack (TIA) – a temporary fall in the blood supply to one part of the brain, resulting in brief symptoms similar to stroke
- subarachnoid haemorrhage – a type of stroke where blood leaks out of the brain’s blood vessels on to the surface of the brain
- vascular dementia – persistent impairment in mental ability resulting from stroke or other problems with blood circulation to the brain 2
The results of a study looking at the association between psoriasis and stroke found that patients with severe psoriasis have a 44% increased risk of stroke, a potentially devastating co-morbidity. The risk of stroke in patients with psoriasis could not be explained by both common and rare major risk factors for stroke as identified in routine medical practice, suggesting that psoriasis may be an independent risk factor for stroke. Patients that are classified as having mild psoriasis had a statistically significant increased risk of stroke, however, this association was very modest and of limited clinical significance for the individual patient. The data showed that a patient with mild psoriasis has an excess risk of stroke attributable to psoriasis of 1 in 4115 per year, whereas a patient with severe psoriasis has an excess risk of stroke attributable to psoriasis of 1 in 530 per year. 3
Peripheral Artery Disease – PAD
Peripheral artery disease (PAD) is a narrowing of the peripheral arteries to the legs, stomach, arms, and head which can cause symptomatic claudication (blockage) and may lead to amputation. 1
In patients with psoriasis the diagnosis of peripheral arterial disease was found to be greater than in patients without psoriasis but with dyslipidemia (those with abnormal amount of lipids in the blood) or in smokers.4
Several studies have shown that presence and severity Cerebral vascular diseases (CVD) are related to presence and severity of Carotid Artery Disease (CAD) and PAD. In one study, significant CAD was observed in 25.4% of patients presenting with ischemic stroke. Among this stroke group, patients had a elevenfold likelihood of CAD compared to an age-matched general population. In other studies, PAD has been reported in 20 to 36% of patients with CVD.5
The prevalence of CAD in PAD patients is particularly high. In a systematic review of PAD studies, between 1966?2005, reported that CAD coexisted in 62% of patients when detected using stress tests, and in 90% of patients if the disease was detected by coronary angiography. Another review of the existing literature confirmed these findings, showing that 50% of those presenting with PAD have symptoms of CAD or electrocardiographic abnormalities, 90% have abnormalities on coronary angiography, and 40% have duplex evidence of carotid artery disease.5
A person’s risk also increases if they are over the age of 50 and who 6 : –
- Smoke or used to smoke – If you smoke or have a history of smoking have up to four times greater risk of P.A.D.
- Have diabetes – One in every three people over the age of 50 with diabetes is likely to develop P.A.D. This will be further increased for psoriasis patients with diabetes.
- Have high blood pressure – Also called hypertension, high blood pressure raises the risk of developing plaque in the arteries.
- Have high blood cholesterol – Excess cholesterol and fat in your blood contribute to the formation of plaque in the arteries, reducing or blocking blood flow to your heart, brain, or limbs.
- Have a personal history of vascular disease, heart attack, or stroke. If you have been diagnosed with heart disease, you increase your risk of also developing PAD by 1 in 3.
The signs and symptoms of the disease include 6 :
- Claudication (obstruction of the arteries) – causing fatigue, heaviness, tiredness, cramping in the leg muscles (buttocks, thigh, or calf) that occurs during activity e.g. walking or climbing stairs. This pain or discomfort goes away once the activity is stopped and after resting.
- Experiencing pain in the legs and/or feet that disturbs your sleep.
- Sores or wounds on toes, feet, or legs that heal slowly, poorly, or not at all.
- Colour changes in the skin of the feet, including paleness or purply blueness. The purply blue colouration of psoriasis plaques is especially seen in psoriasis patients who also have diabetes.
- A lower temperature in one leg compared to the other leg.
- Poor nail growth and decreased hair growth on toes and legs.
To improve your general health, mobility, and in order to reduce the risk of heart attack, stroke, and/or amputation it is critical that you reduce any symptoms that you may have of PAD :-
- Quit smoking – Consult with your health care provider to develop an effective cessation plan and ensure you stick to it. This is especially important for psoriasis patients as smoking can be an aggravating trigger for those with chemical sensitivities.
- It is important to lower your high blood pressure, cholesterol, and blood glucose levels. Consult with your health care provider.
- Follow a healthy eating plan. Choose foods that are low in saturated fat, trans fat, and cholesterol. Be sure to increase your vegetable intake especially green vegetables, and those fruits as identified in your consultation with our Psoriasis Eczema Clinic Practitioners.
- Adopt a more physical lifestyle. Aim for 30 minutes of moderate-intensity activity e.g. walking at least 3-4 times per week.
- Reduce your weight – If you are overweight or obese, work with your health care provider to develop a supervised weight loss plan.
- Prodanovich S, Kirsner RS, Kravetz JD, Ma F, Martinez L, Federman DG. Association of Psoriasis with Coronary Artery, Cerebrovascular, and Peripheral Vascular Diseases and Mortality. Arch Dermatol. 2009;145(6):700-703. doi:10.1001/archdermatol.2009.94
- Gelfand JM, Dommasch E, Shin DB, et al. The Risk of Stroke in Patients with Psoriasis. The Journal of investigative dermatology. 2009;129(10):2411-2418. doi:10.1038/jid.2009.112.
- Prodanovich S. et al.; Association of Psoriasis with Coronary Artery, Cerebrovascular, and Peripheral Vascular Diseases and Mortality; Arch Dermatol. 2009;145(6):700-703. doi:10.1001/archdermatol.2009.94
- Shar A.M. et al.; Coronary, Peripheral and Cerebrovascular Disease: a Complex Relationship; Herz 33 · 2008 · Nr. 7 © Urban & Vogel
- NHLBI Diseases and Conditions Index: Peripheral Arterial Disease (P.A.D.) www.nhlbi.nih.gov/health/dci/ Diseases/pad/pad_what.html
WHAT IS COMORBIDITY?
Comorbidity is a concurrence of multiple diseases or disorders in association with a given disease, in this case, psoriasis.
The patient with psoriasis has an increased risk of developing one or more of a number of other diseases/conditions that share many immunological features with psoriasis.
CHART 1: Comorbidities Associated with Psoriasis 1,2,3
|Metabolic Syndrome – Cardiovascular Disease
The immunological abnormalities that lead to the development of psoriasis suggest that these patients may be at increased risk for other diseases associated with an inflammatory state. Research is yet to establish whether other diseases occur as a direct result of the systemic inflammation associated with psoriasis, as a consequence of genetically determined selection, or whether it is possible that the link between psoriasis and Cardiovascular disease and myocardial infarction (MI) may be mediated by other factors beyond inflammation, such as psychological stress, sedentary lifestyle, or possibly poor compliance with management of cardiovascular risk factors.. 4.5
There is increasing evidence to suggest that the immune response, including activated T cells, antigen presenting cells, cytokines, and markers of systemic inflammation such as C-reactive protein, are important to the development of atherosclerosis (hardening and narrowing of the arteries) and ultimately, MI. 2 Research has shown that patients with psoriasis have a higher incidence of MI compared with control patients, with patients who have severe psoriasis as having the highest rate. The risk of MI associated with psoriasis is greatest in younger patients (under the age of 40) with severe psoriasis. This reduces with age but still remains an increased risk even after treatment for traditional cardiovascular risk factors that are associated with aging. 5
Psoriasis is also associated with hypertension (increased blood pressure). In one study researchers examined the association among hypertension, antihypertensive medication use, and risk of incident psoriasis using prospective data from a large cohort of US women. A total of 121,701 participants, of which 2477 participants were diagnosed with psoriasis, were followed for 11 years with 2 yearly questionnaires. Researchers found that a prior history of hypertension was associated with an increased risk of psoriasis among women with hypertension for 6 years or more. Specifically, hypertensive women without medication use and with current medication use were more likely to develop psoriasis compared with women who did not have hypertension. Among the individual antihypertensive drugs, only ?-blockers were associated with an increased risk of psoriasis after regular use for 6 years or more. 6
In a United Kingdom study using a large (7.5 million patients from 415 practices) electronic medical records database (The Health Improvement Network (THIN), a random sample of patients with psoriasis between the ages of 25 and 64 years were identified. The identification parameters were a diagnosis of hypertension; confirmed psoriasis diagnosis and classified psoriasis severity. The severity classification was identified according to the National Psoriasis Foundation classification system 1) mild (limited disease with ?2% BSA affected), moderate (scattered disease with 3%-10% BSA affected), or 2) severe (extensive disease with >10% BSA affected). Blood pressure was compared to the UK National Institute of Health and Care Excellence clinical guidelines, with uncontrolled hypertension being defined as systolic blood pressure of 140 mm Hg or higher or diastolic blood pressure of 90 mm Hg or higher.
All patients with psoriasis who met the inclusion criteria were included in the study, yielding 680, 469, and 173 patients with mild, moderate, and severe psoriasis, respectively. The researchers found a significant positive relationship between psoriasis severity and uncontrolled hypertension independent of potential risk factors for poor blood pressure control. The likelihood of uncontrolled hypertension in patients with vs without psoriasis was greatest among those with moderate and severe skin disease, representing nearly half of the psoriasis patients seen by GPs in the United Kingdom. The findings have important clinical implications, highlighting a need for more effective management of blood pressure in patients with psoriasis, especially those with more extensive skin involvement (i.e. ?3% BSA affected).7
The precise mechanisms that underlie psoriasis and hypertension are unknown. One theory proposed is that adipose (fat) tissue in psoriasis patients serves as a major source of angiotensinogen, which is subsequently converted to angiotensin II. Angiotensin II not only promotes salt retention by kidneys; it also stimulates T-cell proliferation. Angiotensin II also appears to promote inflammation and the development of atherosclerosis. Other theories suggest that increased visceral adipose tissue in psoriasis patients may contribute to hypertension development. Increased visceral adipose tissue may be associated with accumulation of perivascular fat, which can serve as a reservoir for activated effector T cells that promote dysfunction in both hypertension and psoriasis. Or that endothelin-1 may play an important role in the development of hypertension among psoriasis patients. Endothelin-1 is a protein that constricts blood vessels and increase blood pressure, and it is produced by several different cell types including keratinocytes. While the level of endothelin-1 is usually regulated through various mechanisms, their expression appears to be altered in psoriasis patients. 8 The connection between obesity and psoriasis, when taken in light of the above theories, is further strengthened. It is always advisable for those with moderate to severe psoriasis who are overweight to try to lose weight through sensible eating – reducing fast and fatty foods and increasing the intake of vegetables, especially green vegetables.
The development of atherosclerosis and its increased prevalence may be partially explained by the presence of atherosclerotic risk factors, e.g., diabetes, hypertension, obesity, and hyperlipidemia (increased levels of lipids in the blood, including cholesterol and triglycerides) as well as by the chronic inflammatory processes that are commonly observed in psoriasis. 9
Researchers have found that psoriasis patients have impaired endothelial function and greater thickness of the innermost two layers of the wall of the carotid artery which leads to increased arterial stiffness. 9
Atherosclerosis, the underlying process resulting in cardiovascular events, is caused by the build up of atheromatous plaques in the inner layer of the arteries. Atheromatous plaques are an accumulation of degenerative material in the inner layer of an artery wall. The material consists of mostly macrophage cells, or debris, containing lipids, calcium and a variable amount of fibrous connective tissue. The interaction between metabolic abnormalities such as diabetes, high cholesterol etc. and the systemic proinflammatory mechanisms operating involved in psoriasis and psoriatic arthritis may explain the accelerated atherosclerotic process in these patients. Patients with psoriatic disease display abnormalities in the innate and adaptive immune system that result in high serum levels of proinflammatory cytokines that may upregulate cell-mediated immunity, promote inflammatory cell migration through the vascular endothelium (tissue that lines the interior surface of blood vessels), resulting in endothelial dysfunction and thus causing plaque formation and build up. 10
Recent studies clearly demonstrated that inflammation impairs reverse cholesterol transfer (High-density lipoprotein (HDL) cholesterol efflux) in vivo, providing evidence that inflammation impairs HDL function. HDL is a complex lipoprotein particle with a broad variety of functions, exerting atheroprotective activity via effects on the endothelium and by potent anti-inflammatory capabilities. Functional impairment of HDL may contribute to the increased cardiovascular mortality experienced by psoriatic patients. HDL from psoriasis patients and healthy controls was assessed for changed HDL composition. Researchers found that there was a significant reduction in apoA-I levels of HDL from psoriatic patients, whereas levels of apoA-II and proteins involved in acute-phase response, immune response, and endopeptidase /protease inhibition were increased. Psoriatic HDL also contained reduced phospholipid and cholesterol. The researchers found that the compositional alterations impaired the ability of psoriatic HDL to promote cholesterol efflux from macrophages. Importantly, HDL cholesterol efflux capability was more impaired as the psoriasis area and severity increased. 11
Efflux is a mechanism responsible for moving compounds, like cholesterol out of the cells. The efflux process is extremely important because cholesterol overloading, such as occurs in the cells of the arterial walls, leads to the development of atherosclerotic plaque.12
Chronic systemic inflammation associated with psoriasis and psoriatic arthritis induces endothelial dysfunction, altered glucose metabolism, and insulin resistance that plays a significant role in the development of obesity, diabetes mellitus, dyslipidemia (high cholesterol), and cardiovascular disease such as atherosclerosis and myocardial infarction.
Those with moderate to severe psoriasis should ensure that they visit their General Practitioner to have their blood pressure and cholesterol checked and to have an ECG regularly to ensure the health of their heart.
- Arzu K?l?ç, Seray Cakmak; PSORIASIS AND COMORBIDITIES; EMJ Dermatol. 2013;1:78-85.
- Howa Yeung et al.;Psoriasis Severity and the Prevalence of Major Medical Comorbidity – A Population-Based Study; JAMA Dermatol. 2013;149(10):1173-1179. doi:10.1001/jamadermatol.2013.5015
- Aurangabadkar SJ. Comorbidities in psoriasis. Indian J Dermatol Venereol Leprol 2013;79, Suppl S1:10-7
- Elgendy A, Alshawadfy E, Altaweel A, Elsaidi A (2016) Cardiovascular and Metabolic Comorbidities of Psoriasis. Dermatol Case Rep 1: 106.
- Gelfand JM, Neimann AL, Shin DB, Wang X, Margolis DJ, et al. (2006) Risk of myocardial infarction in patients with psoriasis. JAMA 296: 1735-1741.
- Wu S, Han J, Li W, Qureshi AA. Hypertension, Antihypertensive Medication Use, and Risk of Psoriasis.JAMA Dermatol. 2014;150(9):957-963. doi:10.1001/jamadermatol.2013.9957
- Takeshita J, Wang S, Shin DB, et al. Effect of Psoriasis Severity on Hypertension Control: A Population-Based Study in the United Kingdom.JAMA dermatology. 2015;151(2):161-169. doi:10.1001/jamadermatol.2014.2094.
- Wang Armstrong A. et al; Psoriasis and Hypertension Severity: Results from a Case-Control Study; PLoS ONE 6(3):e18227 · March 2011
- Kalkan G , Karada? A.s.:The Association Between Psoriasis and Cardiovascular Diseases: Eur J Gen Med 2013; 10 (Suppl 1):10-16
- Eder L. and Gladman D.D.; Atherosclerosis in psoriatic disease: latest evidence and clinical implications; Ther Adv Musculoskel Dis 2015, Vol. 7(5) 187–195 DOI: 10.1177/ 1759720X15591801
- Holzer M. et al.; Psoriasis alters HDL composition and cholesterol efflux capacity; Journal of Lipid Research Volume 53, 2012
- Phillips M.C.; Molecular Mechanisms of Cellular Cholesterol Efflux; J Biol Chem. 2014 Aug 29; 289(35): 24020–24029.
is an important but underestimated symptom in psoriasis. However, there is limited published research data available on both its prevalence and characteristics. Some studies suggest that its prevalence in psoriasis sufferers, from different parts of the world, ranges from between 70% and 90%. In one Study Researchers found that 83% of psoriatic patients suffered from itching and in 45% of these patients pruritus was a daily occurrence (in 32% “often” and in 13% “always”) 1
Functional brain imaging studies have shown that the itch-scratch cycle in humans can be tracked to specific regions of the brain, including areas related to reward, pain sensation, and addiction.
The Itch-Scratch-Rash cycle is commonly used to describe this ongoing, never ceasing, always constant itch. The itchier a patient feels, the more scratching of the skin that occurs and which ultimately lead to skin damage and the appearance of a red rash. Often, in chronic presentations it becomes a completely unconscious habit and patients are often not even aware that they are scratching. When a patient scratches, their skin becomes inflamed, this inflammation then causes the skin to itch even more, thus making it even harder for the patient to resist the urge to scratch. This vicious circle can become so severe that it causes sleeplessness, irritability, anxiety and stress. In extreme cases it can lead to significant excoriations (open, bloody and deep scratch wounds) on the lesions and the surrounding normal skin. In chronic psoriasis it can even cause severe lichenification (thickening of the skin) and pain.
One study found that itching was the most frequent complaint (64%) among patients hospitalized for psoriasis. A National Psoriasis Foundation USA survey of its members in 2001, reported that for 79% of sufferers – itch was the second most troublesome symptom after scaling. Psoriasis sufferers have indicated that the severity of their itching on a scale from one to 10 VAS scale (from mild, moderate to severe pruritus where scratched plaques bleed). Most described pruritus (itch) as a sensation of stinging (20%) and burning (15%); the intensity reflected by VAS scale was scored as mild only in 13%, moderate in 37% and severe in 33% of those surveyed. 75% percent of itch patients had to scratch until they bled. Itch was also found to be more severe and frequent at night with 50% reporting difficulty in falling asleep. 2, 3
Itching/Scratching can lead to the hypertrophy (enlargement) of cutaneous (skin) nerve endings, which in turn become more sensitive. For those psoriasis sufferers that have as their Primary trigger, flare-ups caused by the “Koebner Phenomenon” (in which skin injury e.g. tattoos, surgical procedures, cuts, insect bites or sunburn etc. elicits a disease response) scratching can continually exacerbate and worsen their condition. The “Koebner Phenomenon” affects between 11% to 75%, depending on various study results. 4
Where constant and vigorous scratching has occurred and plaque scales have been removed, pin point bleeding, known as the Auspitz sign can be observed.
Studies have also shown that in people suffering from depression, and who suffer from itching due to a variety of causes, that there is a correlation between the severity of itchiness and the severity of depression. Itching therefore causes both a real serious physical and psychological suffering, similar to what chronic pain does.5 It has been noted that there is a direct positive relationship between the severity of pruritus and the severity of depression in patients with psoriasis.6 One study revealed that patients with psoriasis, that experienced intense pruritus, also reported significantly higher scores for depression and anxiety, and showed personality traits of somatic anxiety, embitterment, mistrust, and physical trait aggressiveness. It was also noted that approximately 30% of these patients experienced high-level pruritus, when the great majority of patients had very few skin lesions.7
Patients when answering the questions on “what was the aggravating factors of pruritus”, gave the following answers – “when I was stressed out” (35.0%), followed by “in a hot environment” (18.8%), “when sweating” (17.5%), “during a change in the weather” (12.5%), and “in a cold environment” (10.0%). Of these patients, 32.5% complained of itching on the entire body, followed by the scalp and trunk (17.5%), the scalp only (16.3%), and the scalp and extremities (13.8%).8
Scratching, even for adults, is difficult to resist because it does give the impression of easing the itch – but this is only for the short-term. Eventually the sensation to itch comes back – even worse that before the patient scratched.
Basic tips to control the urge to itch:-
- Keep nails short to avoid tearing the skin when scratching.
- Keep cool. Over-heating can trigger the itch. Try to keep your body temperature as constant as you can, wear light layers of cotton clothes.
- Avoid overheated rooms, keep ducted heating to a minimum, and at night keep the bedrooms cold.
- Avoid heavy blankets and doonas – use cotton blankets (hospital style) if possible.
- Gently rub with the back of the fingers, place pressure on the area instead of scratching.
- Use a cold compress
- Aerlyn D. “Treating Itch in Psoriasis.” Dermatology Nursing 18.32006 227-233. 20 Apr. 2008. http://www.medscape.com/viewarticle/541971.
- “Itch Relief.” Psoriasis.org. 9 Nov. 2001. National Psoriasis Foundation. 20 Apr. 2008.
- Prigninao P. et al.; Itch in psoriasis: epidemiology, clinical aspects and treatment options.; Clinical, Cosmetic and Investigational Dermatology 2009:2 9–13
- Sampogna, F. “Prevalence of Symptoms Exerienced by Patients with Different Clinical Types of Psoriasis.”British Journal of Dermatology 151.3 Sep. 2004. 594-599. 20 Apr. 2008. http://www.blackwell-synergy.com/doi/abs/10.1111/j.1365-2133.20.
- Thappa, D.M. “The Isomorphic Phenomenon of Koebner.” Indian Journal of Dermatology, Venereology and Leprology 70.32004 187-189. 23 Apr.2008. http://www.ijdvl.com/text.asp?2004%2F70%2F3%2F187%2F11105.
- Gupta MA.et al. Pruritus in psoriasis. A prospective study of some psychiatric and dermatologic correlates. Arch Dermatol 1988; 124: 1052–1057.
- Remröd C. et al.; Psychological aspects of pruritus in psoriasis; Acta Derm Venereol 2015; 95: 439–443
- Tae-Wook Kim et al.; Clinical Characteristics of Pruritus in Patients with Scalp Psoriasis and Their Relation with Intraepidermal Nerve Fiber Density; Ann Dermatol Vol. 26, No. 6, 2014
also known as flexural or intertriginous psoriasis is a rare form of psoriasis that occurs in the flexural skin folds. Plaque psoriasis is most commonly found on the trunk and extensor surfaces of the body, such as the knees, elbows, sacral (lower back) area, and scalp whereas Inverse psoriasis is found in the folds of the axilla (armpits), submammary (breast) folds, and groin (inguinal) and buttock folds. It can occur in any area where two skin surfaces meet. The inguinal fold is the most commonly affected area, followed by the axilla and the external genitalia. The skin at the inverse body sites differs from skin at extensor sites with less epidermal keratinization (thinner skin) and more sweat glands. The most evident difference between classical plaque-type psoriasis and inverse psoriasis is the lack of, or less, scaling. The lesions are usually well demarcated, erythematous (red), and are often shiny, appear moist, weepy and fissured. The irritation may be increased in inverse psoriasis as a result of the rubbing and sweating involved in the skin folds. 1, 2
Approximately 3–7% of psoriasis patients present with inverse psoriasis and patients with palmar psoriasis have a greater chance of having inverse psoriasis as compared with plaque psoriasis. In one study of 170 psoriasis patients with palmar involvement, 5.3 times more patients had inverse psoriasis than patients with plaque psoriasis. Development of inverse psoriasis has been reported as a paradoxical side effect to treatment with infliximab for Crohn’s disease and hidradenitis suppurativa. Inverse psoriasis has been observed to be more common in the obese population possibly due to the rubbing of the skin folds. 1, 2
Inverse psoriasis affecting the genitalia seems to be underreported and undertreated; and approximately 35% patients with genital psoriasis never speak to their physician about their genital lesions. Nearly 70% of Physicians do not offer treatment for genital lesions. 3
A study on the quality of life and sexual life in 487 patients with genital psoriasis concluded that3:
- patients with genital lesions report even significantly worse quality of life than patients without genital lesions;
- sexual distress and dysfunction are particularly prominent in women;
- sexual distress is especially high when genital skin is affected;
- the attention given to possible sexual problems in the psoriasis population by healthcare professionals is perceived as insufficient by patients.
Results of several questionnaire-based surveys show that involvement of the genital skin region occurs in 29–40% of patients with psoriasis. The genital area may frequently be involved in cases of inverse psoriasis. Of 48 patients with inverse psoriasis, the external genitalia were involved in 38 (79.2%). 4
In another report researchers stated that patients with genital psoriasis have significantly worse quality of life (QoL) scores compared with patients without genital lesions. In addition, numerous patients with psoriasis have sexual dysfunction. Between 25–40% of patients reported a decline of sexual activity since the onset of psoriasis, mainly due to diminished sexual desire, embarrassment of physical appearance and inconvenience caused by scaliness of the skin or topical therapy. Particularly in women with genital psoriasis, sexual distress is higher and sexual function is more significantly impaired compared to those without genital lesions. 4
Inverse psoriasis is often misdiagnosed for bacterial or fungal intertrigo. Intertrigo is inflammation of opposed skin folds caused by skin-on-skin friction that presents as erythematous, macerated (moist, broken, soft skin) plaques. Secondary bacterial and fungal infections are common because the moist, denuded skin provides an ideal environment for growth of microorganisms. Candida is the most common fungal organism associated with intertrigo. Intertriginous candidiasis also presents as well demarcated, erythematous patches but with tell tale satellite papules or pustules at the periphery (around the edges). Candida, Staphylococcus aureus and Malassezia furfur have been shown to colonize psoriatic skin lesions so diagnosis for flexural psoriasis is sometimes not easy. Candida species have been isolated from the skin of 15% of psoriasis patients compared to only 4% in the control group. 5, 6 However, some studies have also suggested that Candida is not commonly found in psoriatic lesions of inverse of genital psoriasis.
Application of topical treatment in the intertriginous areas is considered as treatment under occlusion due to enhanced hydration and increased skin absorption. However, the inverse areas are considered more sensitive and prone to side effects from topical steroids (i.e. due to thinner skin at these locations). 2
- Syed Z. U. and Khachemoune A.; Inverse Psoriasis Case Presentation and Review; Am J Clin Dermatol 2011; 12 (2): 1-4 1175-0561/11/0002-0001/$49.95/0
- Silje Haukali Omland and Robert Gniadecki; Psoriasis inversa: A separate identity or a variant of psoriasis vulgaris?; Clinics in Dermatology (2015) 33, 456–461
- Meeuwi K.A.P. et al.; Genital Psoriasis: A Systematic Literature Review on this Hidden Skin Disease; Acta Derm Venereol 2011; 91: 5–11
- Meeuwis KAP, et al.; Genital Psoriasis Awareness Program: Physical and Psychological Care for Patients with Genital Psoriasis. Acta Derm Venereol. 2015, 95, 211–216
- Wilmer E.N. et al.; Resistant “Candidal Intertrigo” ”: Could Inverse Psoriasis Be the True Culprit?; doi: 10.3122/jabfm.2013.02.120210
- Taheri Sarvtin, et al.;. Evaluation of candidal colonization and specific humoral responses against Candida albicans in patients with psoriasis. International Journal of Dermatology. Dec2014,Vol.53Issue12, pe555-e560. 6p.
Fatigue is a common and often disabling symptom that occurs in patients with chronic inflammatory and autoimmune diseases, cancer, neurological diseases and a number of other conditions in which inflammation and/or cellular stress occurs. Fatigue may be defined as ‘an overwhelming sense of exhaustion, tiredness, languidness, languor, lassitude, and listlessness. It is a subjective feeling which is distinct from weakness, and has a gradual onset. Fatigue can be Acute and/or Chronic (ongoing state of tiredness), that leads to mental or physical exhaustion, or both, and prevents people from functioning within normal boundaries.
There is emerging evidence that points to the innate immune system as an important ‘fatigue generator’, brought on by invading pathogens, autoimmune diseases, cancer or other ‘danger-signals’, as well as cellular stress responses. Many dermatological diseases and conditions demonstrate inflammatory or autoimmune features, suggesting that fatigue can be a common symptom in a number of chronic skin diseases. Also, psoriasis shares common pathways of immune signalling with other inflammatory diseases including psoriatic arthritis and rheumatoid arthritis (RA).1
The reduction of productivity and work capacity caused by fatigue has been studied by industrial psychologists. In these studies, the importance of physical or mental motivational factors has been clearly demonstrated. Real muscular weakness, however, cannot be detected in most individuals who complain about fatigue. The individual affected by fatigue is often unable to handle complex mental problems and tends to be less reasonable. Inferiority complexes may surface. In neurologic and psychiatric departments, anxiety and depression are frequently diagnosed in fatigued patients. 2
In one study stressed psoriasis patients, responding to a comprehensive series of questionnaires had the following physical and psychological symptoms: constant sensation of exhaustion (78.54%); memory problems (72.54%); constant fatigue (70.58%). In another study constant and excessive fatigue and the inability to work occurred in 56.86% (F) and 43.13% (M) of respondents. 3
In one clinical study researchers wanted to determine the relationship between fatigue and disease-related and psychosocial variables in psoriatic arthritis (PsA). They interviewed 499 patients attending the University of Toronto PsA Clinic using a modified fatigue severity scale (mFSS) questionnaire. Results showed that moderate fatigue occurred in 49.5% of PsA patients and severe fatigue in 28.7%. 4
In another clinical study in plaque psoriasis patients, researchers found nearly 50% of psoriasis patients suffered from substantial fatigue. The fatigue severity was also associated with smoking, pain, and depression, but not with psoriasis severity. 5
Because fatigue is a perceived phenomenon, researchers and clinicians rely on subjective measures to indicate the patients’ level of fatigue and impact on their quality of life. It gives an overall picture of the patient and where they are at and plays a roll in determining the need for intervention or effectiveness of treatment. The 9-item Fatigue Severity Scale (FSS) is one of the most commonly used self-report questionnaires to measure fatigue. 6
The FSS questionnaire contains nine statements that attempt to explore severity of fatigue symptoms. Read each statement and circle a number from 1 to 7, depending on how appropriate they felt the statement applied to them over the preceding week. A low value indicates that the statement is not very appropriate whereas a high value indicates agreement (1 disagree to 7 agree).
FSS Questionnaire 7
|During the past week, I have found that:||Score|
Circle closest to how you feel – (1 disagree, 7 agree).
FSS Scoring: Add up the circled numbers and divide by 9. ________
A Fatigue Severity Scale (FSS) score of 4 – defined as the patient is suffering from “Fatigue” and >?5.1 as suffering from “Severe Fatigue”.
Compare results with the following scores:
- People who do not experience fatigue score about 2.8
- People with Lupus score about 4.6
- People with Lyme Disease score about 4.8
- People with fatigue related to Multiple Sclerosis score about 5.1
- People with Chronic Fatigue Syndrome score about 6.1
NOTE: The FSS might have difficulties distinguishing fatigue from depression (the influence of pain may influence scores on the FSS).
For those that have scored 5 or more it is seriously recommended that you see your practitioner and discuss the possibility as to whether you may also be suffering from depression.
- Skoie I.M. et al.; Fatigue in psoriasis: a phenomenon to be explored; British Journal of Dermatology (2015) 172, pp1196–1203
- Carneiro C. et al.; Fatigue in Psoriasis With Arthritis; SKINmed. 2011;9:34–37
- Leovigildo E. S. et al.; Stress level of people with psoriasis at a public hospital; An Bras Dermatol. 2016;91(4):446-54.
- Husted JA, Tom BD, Schentag CT, et al.; Occurrence and correlates of fatigue in psoriatic arthritis Annals of the Rheumatic Diseases 2009;68:1553-1558.
- Skoie I.M. et al.; Fatigue in psoriasis – a controlled study; British Journal of Dermatology; 2017; DOI: 10.1111/bjd.15375
- Valko PO, Bassetti CL, Bloch KE, Held U, Baumann CR. Validation of the Fatigue Severity Scale in a Swiss Cohort. Sleep. 2008;31(11):1601-1607.
- Krupp LB, et al The Fatigue Severity Scale. Application to patients with multiple sclerosis and systemic lupus erythematosus. Arch Neurol 1989; 46:1121– 3.
The patient with psoriasis has an increased risk of developing one or more of a number of other diseases/conditions that share many immunological features with psoriasis.
CHART 1: Comorbidities Associated with Psoriasis
| Renal Disease
Chronic Kidney Disease
1, 2, 3
Numerous case reports have described the coexistence of psoriasis and kidney disease (Glomerulonephritis – acute inflammation of the glomeruli, which are structures in the kidneys that are made up of tiny blood vessels). Various types of kidney disease have been discussed in case studies and clinical research papers, including:-
- IgA nephropathy –
Berger’s disease, is a kidney disease that occurs when an antibody called immunoglobulin A (IgA) lodges in the kidneys causing inflammation.
- Focal segmental glomerulosclerosis –
a rare disease that attacks the kidney’s filtering units (glomeruli) causing serious scarring which leads to permanent kidney damage and even failure.
- Membranous nephropathy –
thickening of a part of the glomerular basement membrane.The glomerular basement membrane is a part of the kidneys that helps filter waste and extra fluid from the blood, and
- Proteinuria –
the presence of excess proteins in the urine.
- Urinary albumin excretion (UAE) –
the presence of excess albumin in the urine.
The exact causative relationship between Psoriasis and kidney disease is unknown; however, over several decades the incidence of the disease occurring in psoriasis patients has been well documented and researched. It has been suggested that given the strong relationship of the metabolic syndrome with psoriasis and kidney disease, it is perhaps not surprising that these diseases may coexist within a psoriasis sufferer. Some mechanisms that have been put forward include immunologic mechanisms such as defects in T cell function as well as increased levels of immune complexes that underlie glomerular injury in psoriasis and tubular injury induced by raised uric acid concentrations in people with psoriasis. When the mechanisms that cause the systemic and kidney/renal disorders are analyzed, the systemic inflammatory process appears to play a fundamental role.1
Immunoglobulin A Nephropathy (IgAN) – is the most common type of glomerular disease in psoriasis patients presenting with hematuria (presence of blood in the urine), a variable degree of proteinuria and occasionally also with a decreased glomerular filtration rate. Several cases of IgAN-accompanied psoriasis have been described in the literature. In one case study of a psoriasis patient with IgAN, the researchers found that the diffuse mesangioproliferative glomerulonephritis was accompanied by vascular nephrosclerosis (hardening of the small blood vessels in the kidneys) and tubulointerstitial nephritis (swelling caused by tubulointerstitial injury) with diffuse fibrosis and tubular atrophy. 2
IgAN is sometimes present in association with seronegative spondyloarthropathies, including psoriatic arthritis. All of the seronegative spondyloarthropathies are associated with mucosal or skin inflammation, which may lead to an increased production of IgA and elevated serum IgA levels. One clinical study found that 14 patients (67%) from a group of 21 patients had evidence of IgA-containing circulating immune complexes at some time in the course of their psoriasis. 2
In a large population based cohort study the risk of moderate to advanced kidney disease in patients with psoriasis was extensively studied. Some 136,529 patients with mild psoriasis and 7354 patients with severe psoriasis based on treatment patterns were compared with 689,702 healthy patients. The researchers reported that “The combined results indicated that, although no association is seen in patients with truly mild disease (less than 2% body surface area affected), as consistent with other previous studies, associations were seen in moderate and severe psoriasis, which are estimated to affect over 20% of patients with psoriasis worldwide. The relative risk of chronic kidney disease was especially increased in younger patients, however, the clinical relevance of the absolute risk of chronic kidney disease attributable to psoriasis increases with age. In patients aged 40-50 with severe disease based on treatment patterns, psoriasis accounts for one extra case of chronic kidney disease per 134 patients per year, and in those aged 50-60, it accounts for one additional case per 62 patients per year.” 3
Urinary albumin excretion (UAE) (Microalbuminuria) is considered to be a marker of glomerular damage and can be used to predict diabetic or hypertensive nephropathy. Early detection of glomerular damage, when it is minimal and/or at a reversible stage is extremely important. Studies performed in patients with psoriasis have found increased UAE in psoriatics compared with healthy controls. Study results have also revealed a significant correlation between UAE and PASI scores (severity of lesions). 4
The researchers strongly recommended that “Closer monitoring for renal insufficiency should be considered for patients with moderate to severe psoriasis (those with 3% or more body surface area affected), and nephrotoxic drugs should be used with caution in this at risk population. 3
Commonly-used drugs which can affect renal function
- Beta blockers – Acebutolol (Sectral), Atenolol (Tenormin); Bisoprolol (Zebeta)
- Vasodilators – hydralazine (Apresoline) and minoxidil (Loniten)
- ACE inhibitors – including Capoten (captopril), Vasotec (enalapril), Prinivil, Zestril (lisinopril), Lotensin (benazepril), Monopril (fosinopril), Altace (ramipril), Accupril (quinapril), Aceon (perindopril), Mavik (trandolapril), Univasc (moexipril)
- Aminoglycosides – including gentamicin, tobramycin, amikacin, streptomycin, neomycin, and paromomycin
- Contrast Dye – used in some diagnostic tests such as MRIs.
- Compound analgesics – NSAIDs (e.g. aspirin, ibuprofen, diclofenac. paracetamol)
- Antiviral agents – including acyclovir (brand name Zovirax)
- Antibiotics – including ciprofloxacin, methicillin, vancomycin, sulfonamides.
- Chemotherapy drugs – including interferons, pamidronate, cisplatin, carboplatin, cyclosporine, tacrolimus, quinine, mitomycin C, bevacizumab; etanercept, methotrexate and anti-thyroid drugs, including propylthiouracil, used to treat overactive thyroid.
Signs and symptoms of chronic kidney disease include:
- high blood pressure
- changes in the amount and number of times urine is passed
- changes in the appearance of your urine (e.g. colour is extremely dark, frothy or foaming urine)
- blood in your urine
- puffiness in your legs, ankles or around your eyes
- pain in your kidney area
- loss of appetite
- difficulty sleeping
- lack of concentration
- shortness of breath
- nausea and vomiting
- bad breath and a metallic taste in your mouth
- muscle cramps
- pins and needles in your fingers or toes.
As you can see these symptoms are very general and may be caused by other illnesses, however, it is extremely important to seek medical advice if you know that you may be susceptible to kidney disease (i.e. runs in the family) or you know that you are taking medication that could cause kidney disease.
- Wan, Joy et al. “Risk of Moderate to Advanced Kidney Disease in Patients with Psoriasis: Population Based Cohort Study.”The BMJ 347 (2013): f5961. PMC. Web. 22 Mar. 2017.
- Zadražil et al.; IgA nephropathy associated with psoriasis vulgaris: a contribution to the entity of “psoriatic nephropathy”; J NEPHROL 2006; 19:382-386
- Wan J. et al.; Risk of moderate to advanced kidney disease in patients with psoriasis: population based cohort study; 2013; 347: f5961., Published online 2013 Oct 15. doi: 10.1136/bmj.f5961; PMCID: PMC3805477
- Dervisoglu E. et al.; The spectrum of renal abnormalities in patients with psoriasis; Int Urol Nephrol; DOI 10.1007/s11255-011-9966-1
The last in our 3 part series addressing psychological and psychiatric disorders associated with psoriasis.
| Psychological and Psychiatric Disorders –
Substance dependence of abuse
1, 2, 3
It is thought that psoriasis has a direct effect on the development of sleep disorders due to the cutaneous (skin) symptoms of the condition. The skin is the primary circadian mediator of core body temperature (CBT), and a decrease in CBT in the late evening is an important mechanism for sleep initiation. Psoriasis has been associated with problems with thermoregulation and researchers have indicated that the reduced ability to dissipate heat is one factor in the inability to initiate sleep. Pruritus (itch) is another contributor to sleep disturbance and it is also regulated by circadian mechanisms. The threshold for pruritus is lowered in the evening due to complex circadian-mediated factors such as lower cortisol levels, decreased epidermal barrier function, and increased distal-to-proximal (distant limbs-to-body centre) gradient in skin temperature. Thus pruritus in psoriasis typically manifests or exacerbates mainly in the evening and worsens at night. 4,5,6
The inflammatory biological mechanism(s) that lead to initiation and exacerbation of psoriasis, also contribute to the development of systemic diseases e.g. depressive disease, hypertension (blood pressure), adverse cardiac events, diabetes, metabolic syndrome and obesity. All of these conditions are known to indirectly give rise to sleep-disordered breathing. The heightened pro-inflammatory state in conditions such as obstructive sleep apnoea syndrome (OSAS) and insomnia could in turn lead to exacerbations of psoriasis.4,5,6
A systematic review of the literature on the relationship between psoriasis, PsA, and formal sleep disorders identified an increased prevalence of OSAS with a 36-81% prevalence in psoriasis versus 2% for women and 4% for men in the general population.4,5 In one study researchers found that some patients with chronic psoriasis and concurrent OSAS showed improvement of their psoriatic lesions while on nasal continuous positive airway pressure (CPAP).6 OSAS leads to severe physical and, possibly, psychological stress to the body, e.g., by hypoxemia (low blood oxygen levels), increased blood pressure, tachycardia (fast or irregular heart rate), sleep fragmentation, reduction of deep sleep, reduction of REM sleep, hypersomnia (excessive sleepiness), and insomnia. It is known that OSAS also dysregulates the function of the patient’s autonomic nervous system and hormone system. It is felt that this might alter the homeostasis of the immune neuroendocrine network in the skin and may cause the initiation of psoriasis in the genetically predisposed individuals.4,5,6
Somatoform Disorders – psychosomatic symptoms
Somatization is the manifestation of psychological distress by the presentation of bodily symptoms such as feeling nausea due to anxiety, stress headaches, falling ill after a trauma and inability to cope with a disease.
Patients with psoriasis exhibit higher scores of hypochondriasis, hysteria, and somatization. As previously exposed hypochondriasis and hysteria may be connected with specific personality traits of patients with psoriasis of late-onset. Psychosomatic factors, namely stressful life events, lack of social support, and attachment insecurity, may explain why patients with psoriasis have greater scores of somatization. Moreover, the presence of depression in psoriasis may modulate itch perception and then exacerbate symptoms of pruritus.7 (Refer to Part 1 of this series) A systematic review of the psychosocial burden of psoriasis found that social stigmatization, high stress levels, physical limitations, depression, employment problems and other psychosocial co-morbidities experienced by patients with psoriasis are not always proportional to, or predicted by, other measurements of disease severity such as body surface area involvement or plaque severity. Some psoriasis patients had, even when their lesions were small and mild, levels of stress and loss of confidence that was not in keeping with the severity of their condition – which leads to the conclusion that they had maladaptive coping mechanisms in play e.g. self blame, blaming parents, social phobia, avoidance behaviours, substance and alcohol abuse etc. 9
Substance – Dependence of Abuse
In our previous blog Psoriasis and Alcohol (ethanol), we stated that patients with psoriasis experience considerable emotional distress, depression and social isolation due to the visibility of skin lesions, especially when the lesions are widespread and severe. Whilst it would be demeaning to state that all psoriasis patients with mild to severe psoriasis suffer from alcoholism, it has been confirmed in several Quality of Life studies that the percentage of psoriasis patients who admit to having a drinking problem may be as high as 32%. Research indicates that men are more likely to use alcohol excessively as a coping mechanism with the psychosocial burden of psoriasis. Consequently they are at a higher risk of developing depression – with the alcohol misuse and psoriasis as underlying causes. 4 Another study indicated that for women, excessive alcohol intake above a certain threshold (?30.0 g/d), may be associated with a significantly increased risk of Psoriatic Arthritis (PsA).5
Alcohol is known to inhibit inflammation and immune responses; however acute and chronic alcohol consumption have opposite effects on inflammatory cell activation. Results indicate that acute alcohol exposure is inhibitory, whereas chronic alcohol exposure leads to an increase in inflammatory cell responses.6
Research has confirmed that alcoholics are more susceptible to infections, as streptococcal infections are trigger factors for psoriasis, this increased susceptibility may be involved in the onset and progress of the disease. It is also known that measurable quantities of ingested ethanol are secreted through human skin. Transdermal ethanol derives from two processes: active secretion by eccrine glands, primarily sweat glands, and passive diffusion through the lipid layers of the skin. Ethanol disrupts the dermal barrier enhancing skin permeability for numerous chemicals and increases the solubility of penetrating chemical compounds.6
Research into the the use of illicit drugs and psoriasis is extremely limited. Methylenedioxymethamphetamine (MDMA), also called Ecstasy, has been reported to initiate Guttate Psoriasis. The researchers theorized that “While MDMA [the main ingredient in ecstasy] is taken for its psychomimetic effect, pharmacologically it increases the level of noradrenaline, serotonin and dopamine by inhibiting the reuptake mechanism. It is known that Patients with psoriasis already have increased levels of noradrenaline.”7 There are also anecdotal stories on support websites where psoriasis sufferers have spoken about the exacerbation of their psoriasis with the use of “meth” (Methamphetamine, Ice). Within our clinic we have had several patients whose psoriasis was initiated and exacerbated by the use of cannabis (street not medicinal), once they ceased the use of cannabis their psoriasis resolved. As long as they did not use cannabis they remained free of any psoriatic lesions.
- Susskind W. and McGuire R.J.: The Emotional Factor in Psoriasis; Scot. med, J., 1959,4:503
- Kessler R. C. et al.; Epidemiology of Anxiety Disorders; M.B. Stein and T. Steckler (eds.), Behavioral Neurobiology of Anxiety and Its Treatment, Current Topics in Behavioral Neurosciences 2, DOI 10.1007/7854_2009_9, # Springer?Verlag Berlin Heidelberg 2009, published online 3 September 2009
- Nasreen S. et al.; Frequency and Magnitude of Anxiety and Depression in Patients with Psoriasis Vulgaris; Journal of the College of Physicians and Surgeons Pakistan 2008, Vol. 18 (7): 397-400
- Brenaut E. et al.; Alcohol consumption and psoriasis: a systematic literature review. J Eur Acad Dermatol Venerol. 2013 Aug;27 Suppl 3:30-5. doi: 10.1111/jdv.12164.
- Shaowei Wu et al.; Alcohol Intake and Risk of Incident Psoriatic Arthritis in Women; J Rheumatol. 2015 May ; 42(5): 835–840. doi:10.3899/jrheum.140808.
- Farkas A, Kemény L.; Psoriasis and alcohol: is cutaneous ethanol one of the missing links?; • British Journal of Dermatology 2010 162, pp711–716
- Tan B., Foley P.; Guttate psoriasis following Ecstasy ingestion; Australasian Journal of Dermatology45(3):167-9 September 2004?