Psoriasis can affect both finger nails and the toe nails (Psoriatic Nails). The percentage of those with psoriasis who have nail involvement is thought to be 50%. For some unknown reason the finger nails are more often involved than toe nails. In most cases people with psoriasis have concurrent nail psoriasis; however, in 5- 10% of cases the nails only may be affected. In one study it was found that the frequency of nail changes in patients with Koebner’s phenomenon was 56%, whereas as in those without Koebner’s phenomenon it was only 29%. Nail psoriasis is approximately 10% more common in males than in females and is positively associated with higher bodyweight.1
Nail psoriasis is characterised clinically by manifestations on the fingernails and toenails. The mean delay of onset for nail dystrophies occurs in individuals with psoriasis between 9 and 11.5 years, explaining the lower prevalence of nail psoriasis in children.2 There may be involvement of only a single nail or of all nails and over time is associated with severe nail destruction or total nail loss.
Clinical Forms of Nail Psoriasis3,4,5
Psoriasis on the Nail Matrix and Plate
Pits or pitting, or dimples – Pitting is the result of the loss of cells from the surface of the nail. (see pictures 1-4 Part 2) Pitting occurs in approximately 70% of psoriatic nails.
Trachyonychia – rough (sandpapered) accentuated linear ridges (longitudinal striations) on the nails
Leukonychia – white nails or milk spots
Beau Lines – deep transverse (side to side) linear depressions, lines or trenches across the nails
Red lunulae – is the white half-moon–shaped area located at the base of fingernails and toenails; it is the only visible part of the nail matrix. The lunula becomes red when the capillaries under the nail are congested.
“Blausen gallery 2014”. Wikiversity Journal of Medicine.
Psoriasis of the Nail Bed
Onycholysis – the separation of the nail plate from the underlying nail bed and hyponychium (commonly known as the “quick”)
Subungal hyperkeratosis – excessive proliferation of the nail bed and hyponychium where a chalk like substance builds up.
Oil spots or salmon patches – these are the only lesions that are exclusive to nail psoriasis; they appear as round or oval yellowish brown/orange coloured areas in the centre of the nail plate
Splinter haemorrhages – small black lines that run from the tip of the nail to the cuticle as the result of the capillaries (very small blood vessels) between the nail and the skin bleeding.
An infection of the skin around the fingernails and toenails usually caused by a bacterial and/or fungal infection.
Acropustulosis – characterised by pustular eruptions beginning in the tips of fingers and toes.
Digits become swollen and malformed.
Psoriatic arthritis initially may present with only a few swollen joints. It is often common for just a single finger or toe to be noticeably swollen. Some people feel stiff when they wake up. As they move around, the stiffness fades. Sausage-like swelling in the fingers or toes (dactylitis), pain in and around the feet and ankles, especially tendinitis in the Achilles tendon or Plantar fasciitis in the sole of the foot and changes to the nails, such as pitting or separation from the nail bed are all indicative of Psoriatic Arthritis. More than 80% of patients with psoriaticarthritis will present with psoriatic nail lesions.
Researchers found that the nail and the enthesis (connective tissue – that directly attaches to the bone, via the distal interphalangeal (DIP) joint extensor tendon) are key players in the pathophysiology of nail psoriasis. Specifically, they found that the extensor tendon, at its enthesis, is able to send superficial fibres, which contribute to the formation of thick tissue surrounding the finger bones. This links the dense fibrous connective tissue from the nail plate to the tissue surrounding the finger bones and indirectly to the extensor tendon. The study suggested that there is an association between the DIP joint arthritis and nail disease due to the close interaction between the nail, joint and its associated tendons and ligaments. This is supported by the fact that although the nail system has no neural component, 50% of patients with nail psoriasis observe mild to severe pain and restricted mobility of the fingers.2
Many patients find that it becomes progressively more and more difficult and painful to use the fingers for gripping cutlery, pens and tools and performing tasks such as buttoning clothes, buttering toast, writing, typing etc., which are actions that we take for granted, become tasks that they can no longer do. As well as daily day to day activities many patients find that psoriatic nails also impact upon their sporting activities such as tennis, golf, swimming etc.
Dogra A.and Kaur Arora A.: Nail Psoriasis: The Journey So Far; Indian J Dermatol. 2014 Jul-Aug; 59(4): 319–333.
Tirant M. et al.; Nail Psoriasis In an Adult Successfully Treated With a Series of Herbal Skin Care Products Family – A Case Report; Journal Of Biological Regulators & Homeostatic Agents; 30, no. 2 (S3), 21-28 (2016)
Sánchez-Regaña M. and Umbert P.; Diagnosis and Management of Nail Psoriasis; Actas Dermosifiliogr. 2008;99:34-43
Ghosal A, Gangopadhyay DN, Chanda M, Das NK. Study of nail changes in psoriasis. Indian J Dermatol. 2004;49:18–21.
Reich K. Approach to managing patients with nail psoriasis. J Eur Acad Dermatol Venereol. 2009;23(Suppl 1):15–21. [PubMed: 19686381]
Psoriasis is one of the most common immune-mediated diseases world-wide. It is a chronic condition that waxes and wanes. Importantly it is not contagious but it can be an extremely painful, disfiguring and disabling condition for which there is no cure.
The exact causes of psoriasis have yet to be determined, however impairment of the immune system and genetics are known to play major roles in its development. When the immune system is somehow triggered it speeds up the growth cycle of skin cells among other immune reactions leading to a thickening of the skin, inflammation and excessive scaling.1
The prevalence of psoriasis in different populations varies between 0 and 12%, with estimates between 2 – 3% in most western populations. The prevalence in the northern most regions of the Russia and Norway ranges between 5–10% of the population and the highest 12% prevalence is found in the arctic population.2 In the U.S., prevalence ranges from 2.2% to 3.15% and the prevalence among African Americans is 1.3%. There is a low prevalence among North American Indians, Asians and Western Africans (0.3%). In Japan it is 0.1-0.2% of the population, in China 0.3% and is virtually undetected in Native South American Indians.3, 4, 5 Estimates of the prevalence of psoriasis in Australia ranges from 2.3% to 6.6% and in the U.K., the range was 1.3% to 2.6%.4,6 In Australia in the indigenous population it occur rarely, with two recent Australian studies reporting small numbers of Indigenous patients in both the urban and rural environment presenting with psoriasis.7
What triggers psoriasis is a complex question and a large number of factors are involved. Genes are important: numerous family studies have provided compelling evidence of a genetic predisposition to psoriasis, although the inheritance pattern remains unclear. The condition will develop in up to 50% of the siblings of persons with psoriasis when both parents are affected, but prevalence falls to 16% when only one parent has psoriasis and falls further to only 8% percent if neither parent is affected.8 Environmental risk factors also play a role: bacterial and viral infections, stress, skin trauma, smoking and obesity have all been associated with the onset and exacerbation of psoriasis.9
The classification of severity is based on several dermatological markers. It often is a combination of a PASI (Psoriasis Area and Severity Index) score and a BSA (Body Surface Area) coverage factor.
A PASI score is used by dermatologist to measure the dermatological markers to determine the severity and extent of psoriasis, especially during a clinical trial. Four body areas, the head, the arms, the torso and the legs, are measured according to redness (erythema), thickness (Induration/Infiltration) and scaling (Desquamation) from 0 to 4. (See Chart)
% coverage of the body affected is also involved in the classification of the severity of psoriasis. The classification of mild psoriasis is made when symptoms affect less than 3% of the body surface. Moderate psoriasis covers 3% – 10% and the classification of severe indicates that symptoms affects more than 10% of the body, also the involvement of the hands, feet, facial, or genital regions, by which, despite involvement of a smaller BSA, the disease may interfere significantly with activities of daily life. This of course does not take into account the emotional impact that the condition has on the sufferer.9
Redness / Erythema
Psoriasis can have a devastating impact on psychological well-being and social functioning, similar to that of cancer, arthritis, hypertension, heart disease, diabetes or depression. Most people with psoriasis suffer feelings of stigmatization because of their highly visible symptoms. This leads to feelings of social discrimination and alienation which compounds the feelings of anxiety and depression.9
Almost 90% of psoriasis sufferers have feelings of shame and embarrassment, 62% feel depressed, 58% suffer from anxiety, 44% feel that they have problems at work with most feeling that they are rejected for promotions, not accepted as part of the work group etc., 42% suffer from a lack of self-confidence due to their self-consciousness and 40% have difficulties in sexual relationships.10
TYPES OF PSORIASIS
Psoriasis has been classified into several different types10, depending upon presentation, including:-
Plaque psoriasis or Psoriasis vulgaris (common type) – comprises approximately 90 percent of cases. Characterized by sharply demarcated erythematous silvery scaling plaques which most commonly occur on the extensor surface of the elbows, knees, scalp, sacral, and groin regions. The lesions are well-defined round or oval plaques that differ in size and in chronic plaque psoriasis that often coalesce to form very large, oddly shaped lesions covering large areas of the body. Other involved areas include the ears, glans penis, perianal region, and sites of repeated trauma.
Scalp psoriasis is plaque psoriasis that is confined to the scalp, nape, forehead, sideburns, ears) the scalp lesions rarely extend > 2 cm beyond the hairline. Compared with plaque psoriasis elsewhere on the body, scalp involvement is frequently asymmetrical.
Guttate psoriasis – numerous small, red or salmon pink, drop-like spots which cover a large portion of the skin. Spots have fine, slivery scale. Lesions are usually located on the trunk, arms and legs. Usually proceeded by a bacterial streptococcal infection (strep throat, chronic tonsillitis) or a viral respiratory infection.
Flexural/intertriginous (Inverse psoriasis) – is located in the skin folds: i.e. armpits, under the breasts, skin folds around the groin and between the buttocks and in the skin fold of the obese. It is particularly subject to irritation from rubbing and sweating because of its location in the skin folds and tender areas. The plaques are thin, have minimal scale and a shiny surface commonly accompanied by secondary fissuring and/or maceration (the softening and breaking down of skin resulting from prolonged exposure to moisture). It is also prone to secondary infections such as tinea and candida.
Palmoplantar psoriasis – presenting as hyperkeratotic (thickened), red or yellowish, scaly plaques on the central palm or weight-bearing areas of the soles. The lesions are well demarcated and often accompanied by painful cracking and fissuring.
Palmoplantar pustulosis (PPP): is characterized by hyperkeratosis and clusters of pustules over the palms, and soles of hands and/or feet. These sterile pustules can remain as discrete pustules or may become confluent, producing lakes of pus which dry out, and the skin subsequently peels off, leaving a glazed, smooth erythematous surface. Quite often new crops of pustules will then appear.
Pustular psoriasis or Generalized Pustular psoriasis (von Zumbusch type) – Pustular psoriasis may be localized clusters of pinhead sized sterile pustules or as in the Generalized presentation – the skin becomes very red and tender and within hours, pinhead-sized pustules appear studding the erythematous back? These painful, sterile pustules may become confluent, producing lakes of pus. Subsequently, the pustules dry out, and the skin peels off, leaving a glazed, smooth erythematous surface on which new crops of pustules may appear. This is usually accompanied by a fever and systemic symptoms e.g. nausea, and may require the patient to be hospitalized.
Erythrodermic psoriasis – characterized by erythema, severe scaling, itching, and pain. This unstable psoriasis may some? times evolve to whole-body involvement that can lead to the inability to maintain homeostatic functions and often requires the patient to be hospitalized.
Nail psoriasis – affecting the nails of the fingers and/or toes, may affect only one or several nails. The most frequent signs of nail psoriasis are pitting and distal onycholysis. Clinical manifestations range from pitting, yellowish discoloration, and paronychia, to subungual hyperkeratosis, onycholysis, and severe onychodystrophy.
Psoriatic arthritis (PsA) a chronic inflammatory joint disease occurs in up to 39 % of patients with psoriasis. This type of arthritis can be slow to develop, with only mild symptoms or it can develop rapidly with extreme pain and characterized by focal bone erosions. PsA can be a severe form of arthritis with prognosis similar to that of rheumatoid arthritis
For more information on each classification of psoriasis refer to posts on each individual type.
Višnja Milavec-Pureti? et al.; Drug Induced Psoriasis; Acta Dermatovenerol Croat 2011;19(1):39-42
Bhalerao A., Bowcock A. M. ; The Genetics of Psoriasis: A Complex Disorder of the Skin and Immune System; Mol. Genet. (1998) 7 (10): 1537-1545 doi:10.1093/hmg/7.10.1537
Kuchekar A.B. et al.; Psoriasis: A comprehensive review; Int. J. of Pharm. & Life Sci. (IJPLS), Vol. 2, Issue 6: June: 2011, 857-877 857
Parisi R et al. Global epidemiology of psoriasis: A systemic review of incidence and prevalence. J Invest Dermatol 2012 Sep 27; [e-pub ahead of print]. (http://dx.doi.org/10.1038/jid.2012.339)
Menter A., Stoff B.; Psoriasis – Chapter 1 History, Epidemiology and Pathogenesis; 2010; Manson Publishing UK.
Parisi R. et al. Global Epidemiology of Psoriasis; Journal of Investigative Dermatology (2013), Volume 133
Heyes C. et al.; Non-infectious skin disease in Indigenous Australians; Australasian Journal of Dermatology (2014) 55, 176–184
Farber, E.M., Nall, L. and Watson, W. (1974) Natural history of psoriasis in 61 twin pairs. Arch. Dermatol., 109, 207–211.
Pelle Stolt, Maglia Rotta; Bringing Psoriasis into the Light; International Federation of Pharmaceutical Manufacturers & Associations; http://www.ifpma.org/fileadmin/content/Publication/2014/Psoriasis_Publication-Web.pdf
Scratching is the natural response to itch (Pruritus) and, by definition, inseparable from it. The act of scratching not only diminishes itch, but it has been found to be rewarding and addictive. The itch-scratch cycle is a complex phenomenon involving sensory, motor and emotional components. The urge to scratch can be remarkably intense because the reward provided by scratching brings such intense relief and may also be associated feelings of pleasure and enjoyment. Recent studies have shown that rating scratching as a pleasurable experience is correlated with the intensity of the underlying itch, both in patients with chronic itch and healthy individuals.1 Various functional brain imaging studies have discovered 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.1,2
The Itch-Scratch-Rash cycle is commonly used to describe this ongoing, never ceasing, always constant itch that makes eczema very different from many other skin condition. Eczema has often been called the “Itch that Rashes” rather than the “Rash that Itches”.3
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, the 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 skin or even severe lichenification (thickening of the skin) and pain.
The Practitioner and Patient need to recognize and address various aspects of itch, including:
(1) Identification and elimination of trigger factors;
(2) Maintaining the skin barrier through emollients – Oil based and Water Based;
(3) Targeting inflammation through topical medications and systemic (oral) medications
(4) Addressing psychological and behavioural components; and
(5) Education – understanding the condition.
The sensation of pruritus can be triggered by endogenous (internal) and exogenous (external) stimuli, which activate specific peripheral nerve endings in the epidermis and dermis layers of the skin.3
Allergies House dust mites, food allergens, air-born contact dermatitis (pollen, etc.), animals (e.g. cat dander), jewellery, certain cosmetic ingredients.
Physical stimuli Temperature: humidity, cold dry air, clothes rubbing on the skin.
Emotional Anxiety/Stress /Anger/ Depression.
How to rate your Itch4
Based on the Eppendorf Itch Questionnaire.
Rate each of the following from 0 to 4
The following describes your Itch………
Worse when Cold
Less when Cold
Worse when Hot
Less when Hot
Feels like ants
Comes in waves
Physical urge to scratch
I only can think of the Itch
When do you feel the need to Itch?
In the Morning
In the Evening
Worse in Bed
After a hot shower
After being outside
After being in the Sun
After Dusting, Sweeping/Vacuuming/ Changing beds
After eating certain foods
How would you describe the need to Scratch?
I find it enjoyable
It is a physical urge
It is compulsive
I forget when I do it
I always want to scratch
I find it satisfying
I find it pleasurable
It hurts but I cannot stop
What action do you take when you feel the urge to scratch?
I scratch with my nails
I scratch with my fingertips
I scratch with my knuckles
I use a pencil/pen/ruler/stick
I use a cold pack
I use a heat pack
I take a cold shower
I take a warm shower
I take a hot shower
I put the air conditioner on
I turn down the ducted heating
I dig my fingernails in
I bite my lip
I scratch until I bleed
I apply pressure
Which areas of the body do you scratch the most?
What distracts you from the urge to scratch?
Company distracts me
Reading a Book
Using a Computer/IPhone/IPad
Listening to music
Applying heat pack
Applying ice pack
Doing something with my hands (hobby)
When you understand your itch, when you itch, what you do when you scratch and what distract you from scratching, you may be able to plan your approach to your itch more methodically and with more control. You may decide that you need to start a meditation or behavioural therapy class to help you control the need to scratch. You may find that you will learn the best times to apply your creams so that you circumvent the urge to scratch e.g. applying creams before gardening or mowing the lawn or doing housework etc.
What can a Patient do to avoid or control the urge to itch?
Scratching is difficult to resist because it gives the mental impression of easing the itch – but this is only for the short-term. Eventually the sensation to itch comes back – even worse that before you 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 if possible.
Gently rub with the back of the fingers, place pressure or gently pinch the area instead of scratching.
Use a cold compress
Parents of children often ask “How can I stop my child from scratching?” And as scratching is an instinctive reaction to itching which can become a compulsive/unconscious habit, that question is not an easy one to answer. Parents can help by keeping their child’s nails short and, especially at night, by covering their hands with cotton mittens.
With older children, it is important that you explain to them how scratching will actually make them feel worse, not better. And that their skin will become redder, more cracked and feel itchier and sorer.
Become aware of any habits of scratching that your or your child may be developing and take especial note as whether it is at a particular time of day, or during a particular activity, such as playing sport or just watching television. If you or the parents of a child become aware of these types of habits then it is important to try to break the habit.
Nonpharmacological Treatments for the Management of Atopic Dermatitis Itch
Cognitive-behavioural methods alter dysfunctional habits by interrupting and altering dysfunctional thought patterns (cognitions) or actions (behaviours) that damage the skin or interfere with dermatologic therapy. e.g. Itch-coping Training Programme or Habit Reversal Training, cognitive-behavioural methods for the reduction of itch and scratching behaviour, including self-monitoring, guidance in skin care and coping skills to manage itch- and scratch-triggering factors, stress-management methods with relaxation techniques and habit reversal. The habit reversal technique teaches patients to recognize the habit of scratching, identify situations that provoke scratching, and train them to develop a competing response practice, for example, a child who unconsciously scratches can be taught to recognize the early signs of the sensation of itch and instead of scratching be taught to clench his/her fists or place his/her hands underneath his/her legs as soon as they feel the sensation of itch.
Biofeedback can enhance the patient’s awareness of tension and help them to relax; improving skin disorders that flare with stress or that have an autonomic nervous system aspect. Biofeedback is a mind-body therapy that uses electronic instruments to assist patients to gain awareness and control over psychophysiological processes. The patient is connected to a machine that measures muscle activity, skin temperature, electrodermal activity, respiration, heart rate, heart rate variability, blood pressure, brain electrical activity, and brain blood flow and visually gives the patient feedback as they go through various “game” like tasks. Chronic itch, which may be somatic, emotional and cognitive, may be treated with therapies that can modulate the autonomic nervous system stress response. Behavioural biofeedback techniques that reduce stress and anxiety have been used to treat chronic pain and itch and could potentially alter the sympathetic over-activity noted in patients with AD.
Hypnosis / Meditation8
With proper training, an individual can intensify this trance state in himself or herself and use this heightened focus to induce mind-body interactions that help alleviate suffering or promote healing. The state of altered consciousness known as a “trance state” may be induced using guided imagery, relaxation, deep breathing, meditation techniques, self-hypnosis or by a trained medical practitioner. Researchers have used relaxation, stress management, direct suggestion for non-scratching behaviour, direct suggestion for skin comfort and coolness, ego strengthening, posthypnotic suggestions, and instruction in self-hypnosis. Their results were statistically significant for reduction in itch, scratching, sleep disturbance, and tension. Reported topical corticosteroid use decreased by 40% at 4 weeks, 50% at 8 weeks, and 60% at 16 weeks. For milder cases of atopic dermatitis, hypnosis along with moisturization can suffice as a primary alternative treatment. For more extensive or resistant atopic dermatitis, hypnosis can be a useful complementary therapy that reduces the amounts required of other conventional treatments.
Read also our Blogs for Psoriasis …. The same techniques can be used for Eczema
Simple Mental/Mind Relaxation Techniques Part 1 – For Psoriasis Patients
Simple Mental/Mind Relaxation Techniques Part 2 – For Psoriasis Patients
Papoiu A. D. P. et al.; Brain’s Reward Circuits Mediate Itch Relief. A Functional MRI Study of Active Scratching; PLOS ONE, www.plosone.org 1 December 2013, Volume 8, Issue 12, e82389
Mochizuki H. et al.; Chapter 23Brain Processing of Itch and Scratching; http://www.ncbi.nlm.nih.gov/books/NBK200933/?report=printable
Hong J. et al.; Management of Itch in Atopic Dermatitis; Seminars in Cutaneous Medicine and Surgery; Elsivier; doi:10.1016/j.sder.2011.05.002; Pg 71-88
Darsow U. et al.; New Aspects of Itch Pathophysiology: Component Analysis of Atopic Itch Using the ‘Eppendorf Itch Questionnaire’; Int Arch Allergy Immunol 2001;124:326–331
Shenefelt PD.; Psychological interventions in the management of common skin conditions; Psychology Research and Behavior Management 2010:3 51–63
Evers Et al.; Effectiveness of a Multidisciplinary Itch-coping Training Programme in Adults with Atopic Dermatitis; Acta Derm Venereol 2009; 89: 57–63
Tran BW. Et al.; Effect of Itch, Scratching and Mental Stress on Autonomic Nervous System Function in Atopic Dermatitis; Acta Derm Venereol 2010; 90: 354–361
Shenefelt PD. ;Hypnosis in Dermatology; Arch Dermatol / VOL 136, MAR 2000
Tobacco smoke contains numerous chemicals that exert inflammatory effects on the human body. Recent studies suggest that cigarette smoking may trigger the development of psoriasis through oxidative, inflammatory and genetic mechanisms. Smoking initiates formation of free radicals that stimulate cell signalling pathways active in psoriasis. Smoking damages the skin by increasing formation of reactive oxygen species (ROS) and decreasing the gene expression of antioxidants. Nicotine also stimulates innate immune cells integral to the pathogenesis of psoriasis. This perpetuates a cycle of chronic inflammation. Smoking also enhances expression of genes known to increase the risk of psoriasis.1,2,5
Research has found that increased smoking intensity corresponds to a higher risk of developing severe psoriasis whilst longer cumulative duration of smoking (pack-years) increases the likelihood of developing psoriasis. The study also demonstrated a graded increase in psoriasis risk with increasing exposure to passive smoke.
In one study, researchers investigated the associations between smoking status, quantity,duration, and cessation and exposure to environmental tobacco smoke and the risk of incident psoriasis in a total population of 185,836 participants from the Nurses’ Health Study (NHS), the Nurses’ Health Study II (NHS II), and Health Professionals’ Follow-up Study (HPFS). They reported that in the NHS, 20% of the cases of incident psoriasis might have been prevented by the elimination of smoking. Similarly, the population-attributable risk was 15% in the NHS II and 19% in the HPFS. For all participants, 17.5% of the incidents of psoriasis were attributable to having ever smoked. Evidence from past association studies seemed to indicate a stronger association between smoking and psoriasis in women than in men.3
Research has also shown that the risk increases with the number of cigarettes smoked daily. Studies have shown that smoking more than 10 cigarettes per day by men who are psoriasis patients may be associated with a more severe expression of disease in their extremities. In addition, smoking among both men and women who are psoriasis patients has been shown to reduce improvement rates and hence difficulty in achieving remission during treatment.4 In a multicentre case-control study of 404 psoriasis patients and 616 controls, the risk for psoriasis was higher in smokers compared with non-smokers, and the association with smoking was stronger and more consistent among women than men. A particularly strong association was also found between smoking more than 15 cigarettes per day and Palmoplantar Pustular Psoriasis (PPP). Several observational and case-control studies have demonstrated up to 94% prevalence of tobacco use in patients with PPP.6
As tobacco smoking also interferes with the bodies immunity by allowing colonization by perio -dontopathic bacteria and by acting as a local irritant, researchers have hypothesized that smoking may act as a trigger or permissive factor of periodontal disease in patients suffering from psoriasis. In order to test this hypothesis, the prevalence and severity of periodontal disease, Researchers assessed a group of smoking and non-smoking psoriasis patients and a group of smoking and non-smoking psoriasis-free controls. In this study it was statistically shown that psoriasis patients who smoke are at an approximately sixfold higher risk of developing severe periodontal disease, as compared to psoriasis patients who do not smoke.7
Another interesting observation was the frequent coexistence of a smoking habit and alcohol consumption in patients with psoriasis. In the literature, alcohol consumption has been described as a factor responsible for triggering psoriasis, but it is said that smoking increases the risk of the onset of the disease. Previous studies have indicated that smokers who drink are twice as likely to develop the disease as non-smokers and non-drinkers.8,9
It is well recognized that stress and anxiety acts in both the initiation and exacerbation of psoriasis. Psychosocial stressors include acute negative life events or chronic strains and have been implicated as risk factors for tobacco use. Psychological stress may influence smoking behaviour (e.g., initiation, maintenance, and relapse) through a number of mechanisms. Specifically, smoking may function as a coping behaviour, whereby nicotine is used to self-medicate in response to stress; it is also possible that exposure to stress may result in diminished self-regulation to control the urge to smoke. Previous observational studies illustrate that acute stressful events and greater exposure to chronic stressors (e.g., related to work, finances, or relationships) are associated with higher smoking prevalence compared to persons who did not experience these stressors.10
So in summary, studies suggest that cigarette smoking may trigger the development of psoriasis through oxidative, inflammatory and genetic mechanisms. Furthermore, smoking is associated with the clinical severity of psoriasis. Smoking also contributes to higher morbidity and mortality from smoking related disorders in these patients. It is, therefore, advisable, if possible to quit smoking, or at the very least, keep your smoking to a minimum, preferably under 10 cigarettes a day. Try to adopt other mechanisms to cope with your stress and anxiety and it is suggested that you read our other blogs on “Simple Physical and Mental Relaxation Techniques”. Using these techniques you may be able to reduce your stress and anxiety levels and this may allow you to cut down on the number of cigarettes you smoke.
Also read our blog “Psoriasis and Alcohol Intake”, “Stress, Anxiety, Depression and Psoriasis”, “Stressed about Psoriasis – Identify Your Stressors and Yours Stress Responses”, “Simple Physical Relaxation Techniques for Psoriasis Patients” and “Simple Mental/Mind Relaxation Techniques Part 1 and Part 2”
Armstrong AW, Armstrong EJ, Fuller EN, et al. Smoking and pathogenesis of psoriasis. Br J Dermatol 2011; 165: 1162-8.
Al-Rubaii A, Al-Ward N, Al-Waiz M. The age of onset of psoriasis and its relationship to smoking habits and stressful life events. Saudi Med J2003; 24:108.
Wenqing Li et al.; Smoking and Risk of Incident Psoriasis Among Women and Men in the United States: A Combined Analysis; American Journal of Epidemiology Advance Access published January 12, 2012; http://aje.oxfordjournals.org/content/early/2012/01/11/aje.kwr325.full.pdf+html
Behnam SM,Behnam SE, Koo JY.; Smoking and psoriasis.; Skinmed. 2005 May-Jun;4(3):174-6.
Armstrong AW, ; Psoriasis and smoking: a systematic review and meta-analysis; British Journal of DermatologyVolume 170, Issue 2, Article first published online: 18 FEB 2014
Freiman A. et al.; Cutaneous Effects of Smoking; Journal of Cutaneous Medicine and Surgery Volume 8 Number 6 December 2004
Antal M. et al.; Smoking as a Permissive Factor of Periodontal Disease in Psoriasis; PLOS ONE | www.plosone.org; March 2014 | Volume 9 | Issue 3 | e92333
Agnieszka B. Owczarczyk-Saczonek , Roman Nowicki; The association between smoking and the prevalence of metabolic syndrome and its components in patients with psoriasis aged 30 to 49 years; Postep Derm Alergol 2015; XXXII (5): 331–336 DOI: 10.5114/pdia.2015.54743
Naldi L, Peli L, Parazzini F. Association of early-stage psoriasis with smoking and male alcohol consumption: evidence from an Italian case-control study. Arch Dermatol1999; 135:1479–84.
Slopen N. et al.; Psychosocial stress and cigarette smoking persistence, cessation, and relapse over 9–10 years: a prospective study of middle-aged adults in the United States; Cancer Causes Control DOI 10.1007/s10552-013-0262-5
Psoriasis is a chronic inflammatory skin disorder and whilst the exact causes of psoriasis have yet to be discovered, the immune system and genetics are known to play major roles in its development. The immune system is somehow mistakenly triggered, which speeds up the growth cycle of skin cells among other immune reactions1.
Researchers show that whether a person develops psoriasis or not may depend on a “trigger”2. These Primary Triggers activate the condition.
Stress – anxiety, depression, psychological illnesses e.g. Post-Traumatic Stress Disorder.
Certain medicines e.g.:- – Anti-malarial– e.g. Doxycycline, chloroquine – Lithium– depression or psychiatric disorders – ACE Inhibitors- High blood pressure medication – Anti-inflammatory medicine – e.g. ibuprofen or Indomethacin – Beta blockers – taken by patients with heart failure – Corticosteroids– Prescribed for a variety of health conditions. Sudden discontinuation of relatively high doses can be a trigger.
Infections –in some people, usually children and young adults, a form of psoriasis called guttate psoriasis develops after a streptococcal throat infection (note: most people who have streptococcal throat infections will not develop psoriasis), upper respiratory infections such as such as streptococcal pharyngitis or sinusitis. People with weakened immune systems; such as HIVpatients, are more susceptible to psoriasis.
There are also a number of Secondary Triggers, and these exacerbate the condition once it has been activated, and will continue to worsen the condition. They are:-
Consumption of alcohol
Weather – exposure to cold
Not all psoriasis sufferers will react to all of the above triggers, so the best thing to do is to record consumption of foods, liquids etc., how you slept, what stresses you were under and any exposure to chemicals and other environmental triggers and at the same time monitor your symptoms e.g. increases itch, irritability, new lesions or worsening of existing lesions etc. Note that some triggers e.g. skin injuries may not show a flare-up up for up to 10 to 14 days after a triggering event, so if you noticed that you were bitten by mosquitos or insects record it with the date and then take note of any subsequent delayed flare ups.
Višnja Milavec-Pureti? et al.; Drug Induced Psoriasis; Acta Dermatovenerol Croat 2011;19(1):39-42
Kuchekar A.B. et al.; Psoriasis: A comprehensive review; Int. J. of Pharm. & Life Sci. (IJPLS), Vol. 2, Issue 6: June: 2011, 857-877 857