PSORIASIS and COMORBIDITIES – CEREBRAL VASCULAR AND PERIPHERAL ARTERY DISEASE

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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

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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.

 

REFERENCES

  • 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
  • http://www.nhs.uk/conditions/Cerebrovascular-disease/Pages/Definition.aspx
  • 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

PSORIASIS and COMORBIDITIES and INFLAMMATORY BOWEL DISEASE

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WHAT IS COMORBIDITY?

 Comorbidity is a concurrence of multiple diseases or disorders in association with a given disease, in this case, psoriasis.

INCREASED RISK

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

Inflammatory Bowel Disease (IBD) –

Crohn’s Disease

Ulcerative Colitis

Irritable Bowel Syndrome (IBS)

1, 2, 3

Gastro Intestinal (GI) disorders are present in 28% of patients with psoriasis. Common abnormalities in psoriasis patients include changes in the mucous membrane of the duodenum. Psoriasis may cause dermatogenic enteropathy and intestinal inflammation.

Irritable bowel syndrome (IBS) is one of the most common ‘functional’ gastrointestinal disorders accounting for 3% of all primary care consultations, with a strong female predominance. The main features are recurrent abdominal pain and/or discomfort, whose clear relationship to changes in stool frequency or consistency and its relief by defecation implies that they originate in the colon. In addition to these gastrointestinal (GI) symptoms, patients commonly report non-GI symptoms of lassitude, headache, backache, dysmenorrhoea (painful periods/menstruation), and dyspareunia (painful intercourse). Symptoms characteristically wax and wane. IBS patients, in common with other sufferers with functional GI disorders, are more anxious than healthy controls, showing greater anxiety and depression. Many patients believe that stress induces their symptoms.10

Inflammatory Bowel Disease (IBD) are a group of inflammatory conditions in which the body’s own immune system attacks parts of the digestive system. The two major types of IBD are ulcerative colitis (UC) and Crohn’s disease (CD). UC is limited to the colon and/or rectum (normally continuous lesions in the rectum and colon), and affects only the inner lining (mucosal and submucosal layers) of the gut. In contrast, CD can affect any part of the gut from mouth to anus as non-continuous or skip lesions (a majority of cases start in the terminal ileum), and affect the whole thickness of the bowel wall.4

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Within the IBD group is also Microscopic Colitis, an inflammation of the colon that can only be detected with a microscope. There are two types of microscopic colitis – collagenous colitis and lymphocytic colitis. Under a microscope an increase in the number of lymphocytes, a type of white blood cell, can be seen in the epithelium—the layer of cells that lines the colon.15

The two types of colitis affect the colon tissue in slightly different ways:

  • Lymphocytic colitis – The number of lymphocytes is higher, whilst the tissues and lining of the colon are of normal thickness.
  • Collagenous colitis – The layer of collagen, a threadlike protein, underneath the epithelium builds up and becomes thicker than normal.

 The most common symptom of microscopic colitis is chronic, foul smelling, watery, non-bloody diarrhoea. Episodes of diarrhoea may last for weeks, months, or if chronic, even years, however, there may be intermittent periods without diarrhoea. During these periods the patient may even experience bouts of constipation.

Other signs and symptoms of microscopic colitis include15:-

  • A strong urgency to have a bowel movement.
  • Faecal incontinence – accidental passing of stool or fluid from the rectum – especially at night.
  • Pain, cramps, or bloating in the abdomen – that is usually mild but can be incapacitating.
  • Weight loss/gain
  • Nausea – usually without vomiting.
  • Dehydration – as a result from not drinking enough liquids to replace fluids lost through diarrhoea.
IBD SYMPTOMS IBS SYMPTOMS
Frequent and/or Urgent Bowel Movements

Diaorrhea

Bloody Stools

Abdominal Pain & Cramping

Fatigue

Weight Loss

Lack of Appetite

Joint, Skin or Eye Problems

Abdominal Pain & Cramping

Diaorrhea

Bloating

Gas

Mucus in Stools

 

As far back as 1968 studies reported a prevalence of 2-3% of psoriasis in first-degree relatives of patients with CD compared to 0–3% of controls. Later studies found psoriasis in 7–11% of the IBD population compared to 1–2% of general population. In one study, psoriasis was found to be more prevalent in CD (11.2%) than UC (5.7%). 5

In one study5 the Researchers studied the presence and characteristics of psoriasis were recorded and further classified as follows: sebopsoriasis, scalp psoriasis, plaque type psoriasis [trunk, arms], palmo-plantar psoriasis, nail psoriasis, inverse psoriasis, psoriatic arthritis, guttate psoriasis, and pustular psoriasis. Psoriasis that developed after anti-TNF? treatments was also reported. Severity of psoriasis was defined as mild, moderate or severe [not applied to psoriatic arthritis]. The study involved some 251 IBD patients, there were 158 patients with CD [63%] and 93 with UC [37%]. These 251 IBD patients were referred to the dermatologist and psoriasis was detected in 62 [25%], including 36 [58%] with CD and 26 [42%] with UC. The non-IBD group included 62 patients with psoriasis. Mild psoriasis was more frequent in IBD vs non-IBD, whereas moderate and severe psoriasis were more frequent in non-IBD vs IBD. Plaque-type psoriasis was the most common phenotype in both IBD and non-IBD. The frequency of plaque-type, nail psoriasis and psoriatic arthritis was lower in IBD vs non-IBD.

Other researchers analyzed the health records of 174,646 participants from the Nurses’ Health Study (NHS) and NHS II in an effort to also determine whether IBD was associated with specific psoriasis phenotypes. In this study they found 4,400 cases of psoriasis and of these 423 participants had developed CD or UC with a prevalence of psoriasis that was four to six times greater in IBD patients than the estimated prevalence in the general public.6

Several neutralizing anti-TNF agents, such as etanercept and infliximab, have been successfully used to treat autoimmune diseases, including inflammatory bowel disease. However, paradoxically, Infliximab and adalimumab-induced psoriasis in Crohn’s disease has been identified as a side effect of TNF-alpha inhibitor therapy. Researchers reviewed 142 case articles of new-onset psoriasis with infliximab, adalimumab, and etanercept therapy and of these confirmed eighty-one cases of infliximab induced psoriasis.7 In another study the researchers found that the vast majority of the cases (76%) developed psoriasis while on infliximab, and the rest (24%) after switching to adalimumab or certolizumab, indicating that this phenomenon is not drug specific, but rather a pharmacological group effect 12

 In another systematic literature review Researcher reviewed 222 cases. Of the 222 patients, 78.38% were diagnosed with Crohn’s disease, and 48.20% were female. The mean patient age was 26.50 years, and 70.72% of patients had no prior history of psoriasis. Infliximab was the anti-TNF-? therapy that caused the cutaneous reaction in most patients (69.37%). Clinical presentation varied; psoriasis-form lesions were the most common form of psoriasis (55.86%), followed by typical plaque type lesions (20.72%), and pustular-type lesions (3.60%). Six patients (2.70%) concomitantly presented with alopecia, one patient (0.45%) presented with palmoplantar pustulosis, and another patient (0.45%) presented with palmoplantar pustulosis and psoriatic arthritis.9

 Celiac disease is defined as a disease of the small intestine characterized by mucosal inflammation, villous atrophy, and crypt hyperplasia upon exposure to dietary gluten. Several studies have found that psoriasis patients are at an increased risk for celiac disease. A retrospective cohort study compared 25,341 psoriasis patients to over 125,000 matched controls in the U.S. The comparison data showed an odds ratio of 2.2 for the association of psoriasis with celiac disease. They also examined whether patients with celiac disease also have increased risk of psoriasis. A cohort of 28,958 biopsy-confirmed celiac disease patients from Sweden was evaluated for risk of future psoriasis compared to 143,910 age and sex-matched controls. The authors found a positive correlation between celiac disease antibody positivity and an increase in the severity of psoriasis or psoriatic arthritis. Interestingly, in the psoriasis patients, elevated celiac disease antibodies did not necessarily correspond to a biopsy-confirmed diagnosis of celiac disease, suggesting that psoriasis may be associated with gluten “sensitivity” (marked by antibody positivity) but not necessarily fully developed Celiac disease.10

In summary both Psoriasis and IBD and IBS are related inflammatory diseases. The skin and bowel represent both barrier and connection between the inner and the outer sides of the body. On average approximately 25% of patients who experience some form of bowel complaint will be diagnosed with psoriasis. It is also interesting to note that smoking in both IBD/IBS and psoriasis is considered an exacerbating trigger.

REFERENCES

  • 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
  • Huang B.L. et al.; Skin manifestations of inflammatory bowel disease; Frontiers in Physiology; www.frontiersin.org February 2012 | Volume 3 | Article 13 | 1
  • Skroza et al.; Correlations between Psoriasis and Inflammatory Bowel Diseases; Hindawi Publishing Corporation BioMed Research International Volume 2013, Article ID 983902, 8 pages ; http://dx.doi.org/10.1155/2013/983902
  • Lolli E. et al.; Psoriasis Phenotype in Inflammatory Bowel Disease: A Case-Control Prospective Study; Journal of Crohn’s and Colitis, 2015, 699–707 doi:10.1093/ecco-jcc/jjv068 Advanced Access publication April 23, 2015
  • Li W.Q. et al.; Psoriasis, psoriatic arthritis and increased risk of incident Crohn’s disease in US women; Ann Rheum Dis. 2013 July ; 72(7): 1200–1205. doi:10.1136/annrheumdis-2012-202143
  • Famenini S. and Wu J.J.; Infliximab-Induced Psoriasis in Treatment of Crohn’s Disease-Associated Ankylosing Spondylitis: Case Report and Review of 142 Cases; J Drugs Dermatol.2013;12(8):939-943.
  • Denadai R .et al.; REVIEW ARTICLE Induction or exacerbation of psoriatic lesions during anti-TNF-? therapy for inflammatory bowel disease: A systematic literature review based on 222 cases; Journal of Crohn’s and Colitis (2013) 7, 517–524
  • Bhatia B.K. et al.; Diet and Psoriasis: Part 2. Celiac Disease and Role of a Gluten Free Diet; J Am Acad Dermatol. 2014 August ; 71(2): 350–358. doi:10.1016/j.jaad.2014.03.017.
  • Spiller R.C.; Irritable bowel syndrome; Published Online March 14, 2005; British Medical Bulletin 2004; 72: 15–29
  • Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC. Functional bowel disorders. Gastroenterology. 2006 Apr. 130(5):1480-91.
  • Bercik P. et al.; Is irritable bowel syndrome a low-grade inflammatory bowel disease?; Gastroenterol Clin North Am.2005 Jun;34(2):235-45, vi-vii.
  • Gionata Fiorino , Paolo D. Omodei; Psoriasis and Inflammatory Bowel Disease: Two Sides of the Same Coin?; Journal of Crohn’s and Colitis, 2015, 1–2
  • Microscopic colitis. Mayo Clinic website.mayoclinic.org/diseases-conditions/microscopic-colitis/home/ovc-20192308

PSORIASIS and SMOKING

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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 

Smoking

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”

REFERENCES

  • 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

What triggers Psoriasis?

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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.

Possible Primary triggers include:

Koebner Phenomenon Skin Injury e.g. animal bites, burns, electrodesiccation, excoriation, freezing, friction, gunshot wounds, insect bites, lacerations, nail manicuring, Poor fitting shoes, pressure, shaving, surgical grafts, surgical incision, tape stripping, thumb sucking, x-rays, sunburn, tattoos (injury).

……. burned-skin-1556804 FreeImagesmosquito-bite-3-1410910 FreeImagestattoo-in-flame-1187558 FreeImages injury-1182660 FreeImages

Stress anxiety, depression, psychological illnesses e.g. Post-Traumatic Stress Disorder.

Certain medicines e.g.:-pills-1422509 Free Images
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.

Infectionsin 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:-

Triggers

  • Consumption of alcohol
  • Smoking
  • Chemical exposure 
  • Hormones
  • Weather – exposure to cold
  • Adverse foods 

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.

REFERENCES

  1. Višnja Milavec-Pureti? et al.; Drug Induced Psoriasis; Acta Dermatovenerol Croat 2011;19(1):39-42
  2. 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