PSORIASIS AND COMORBIDITIES – CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

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Over recent years psoriasis has been classified as a systemic chronic inflammatory disorder and has been linked with several diseases and conditions that are also immune-mediated inflammatory conditions.

Chronic obstructive pulmonary disease (COPD) is characterized by the gradual progression of irreversible airflow obstruction and increased inflammation in the airways and lungs that is generally distinguishable from the inflammation caused by asthma. The symptoms of COPD are shortage of breath, increased risk of bronchitis and emphysema. There are a variety of factors associated with an enhanced chronic inflammatory response have been implicated in the development of COPD, including immune regulation defects, genetic susceptibility, infection, and environmental factors. Smoking being the most important environmental risk factor and key cause. 1, 2

Research has found that increased smoking intensity also corresponds to a higher risk of developing severe psoriasis whilst longer cumulative duration smoking (pack-years) increases the overall likelihood of developing psoriasis. (For more information read on our blog Psoriasis and Smoking). 3

Whilst the exact relationship between psoriasis and COPD remains unclear and controversial among some clinicians, the current research has found consistent association between psoriasis and COPD suggesting a likely pathophysiologic link between the two diseases. The hypothesis of a common cytokine-based pathology, wherein one inflammatory autoimmune disease significantly increased the risk of another, is gradually being accepted.1

COPD in the general population can affect up to 10% across all race types. There appears to be a general consensus that patients with psoriasis are at a greater risk of developing COPD. Preliminary research data has found that the risk to developing COPD by psoriasis patients is increased by between 2.35% and 5.7%. The association between psoriasis and COPD was even stronger in patients with severe psoriasis.  Another study also pointed out that patients >50 years and men were more susceptible to developing COPD.  In another study concentrating only on patients with psoriatic arthritis, COPD was the fifth most frequently found comorbidity, behind only to hypertension, obesity, diabetes, and kidney disease.2, 3

Researchers noted that psoriasis and COPD present shared risk factors such as obesity and physical inactivity, and that both diseases are associated with metabolic syndrome. (Metabolic syndrome includes high blood pressure, high blood sugar, excess body fat around the waist and abnormal cholesterol levels.) These factors could be confounding factors in the association between these two diseases.

Psoriasis patients should of course monitor their blood pressure and sugar serum levels. Controlling one’s weight is also important. If you are concerned about the status of your health please contact your Health Care Practitioner.

And lastly it is recommended that those with psoriasis quit smoking. Not only can smoking trigger and exacerbate psoriasis but it also increases the risk for psoriasis smokers to develop COPD.

You may find these links helpful in your QUIT program:

 

quitline

http://www.quitnow.gov.au/

REFERENCES

  1. Li, Xin et al. “Association between Psoriasis and Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis.” Ed. Alexander V. Alekseyenko. PLoS ONE12 (2015): e0145221.
  2. Dewar M. and Whit Curry JR. J.; Chronic Obstructive Pulmonary Disease: Diagnostic Considerations; American Family Physician; Volume 73, Number 4 U February 15, 2006
  3. Machado-Pinto Jackson, Diniz Michelle dos Santos, Bavoso Nádia Couto. Psoriasis: new comorbidities. An. Bras. Dermatol.  [Internet]. 2016 Feb [cited 2017 Aug 31]; 91 (1): 8-14.

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

comor_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.

 

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

Stress, Anxiety, Depression – Atopic Eczema (AE)/Atopic Dermatitis (AD) and associated Itch

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Atopic dermatitis may be caused by genetic predisposition and environmental conditions, including hereditary factors, allergens, and neurogenous (arising from the nervous system, or from some lesion of the nervous system) and immunological factors. However, the major contributing cause remains unknown. AD may cause psychosocial problems such as anxiety, depression, sleep disorders, emotional excitability, stigmatization, social isolation, and discrimination and on the other hand, all of these factors may also contribute to and exacerbate the symptoms of AD. Of the many factors related to atopic dermatitis, psychological stress is considered to be among the most important.1

 The psychological, physical and social impact of AD is complex and varies among different ages. The relationship of stress, anxiety, depression, not to mention feelings of stigma, shame, embarrassment, and low self-esteem all impact upon a person who is suffering from a skin condition such as AD. Research has confirmed that adults with AD exhibit high levels of anxiety, depression, and emotional excitability. Children with AD also have higher levels of emotional distress and more behavioral problems than healthy children or children with minor skin problems. Psychosocial factors contributed in the form of exacerbating factors in as high as 94% of AD hospitalized patients. Clinically, it has long been appreciated that both acute stress (stressful life events) and chronic psycho-emotional stress can trigger or enhance pruritus.2, 3, 4,5

Pruritus, or itching, is a main symptom of AD and is often one of the first presenting symptoms.

Itching leads to scratching, which leads to and exacerbates the skin lesions.

  • AD has been referred to as the “itch that rashes.”
  • The cycle of itching and scratching is considered an important factor in the maintenance of AD symptoms and is believed to be one of the first symptoms of an impending AD flare.
  • Scratching tends to cause further itching, leading to the so-called “itch-scratch cycle.” 6

Results of one study found that in patients with AD the itching intensity played an important role in determining the patient psychosocial well-being and that a relationship between pruritus and depression was also found.6

 Scratching often begins automatically in association with stress and emotions, and becomes habitual, being performed many times every day. In addition to the psychological factors, such as anger, irritation, impatience, relief, anxiety, etc., many patients say that they somehow find themselves scratching even when they do not feel itchy. Research has identified that habitual scratching is involved in the formation of the lesions of AD. The scratching is patterned, with the rash exhibiting a bilaterally symmetrical distribution over the back and normal skin remaining in the middle where the hands cannot reach, producing a “butterfly” sign. The prominent red face can also be explained by this scratching behavior.4

 This vicious cycle can cause sleeplessness in over 65% of AD sufferers leading to sleep deprivation which leads to tiredness, mood changes and impaired psychosocial functioning of the sufferer and their family, particularly at school and work. Embarrassment, comments, teasing and bullying frequently cause social isolation and may lead to depression or school/work avoidance. The sufferer’s lifestyle is often limited, particularly in respect to clothing, holidays, staying with friends, owning pets, swimming or the ability to play or do sports. For parents caring for a child with eczema, restriction of normal family life, difficulties with complicated treatment regimens causing an increased work load together with disturbed sleep can lead to parental exhaustion and feelings of hopelessness, guilt, anger and depression. And so the whole family is impacted by the condition.5,6,7

Research has suggested that some AD patients might benefit from certain psychological interventions: patients showing psychological characteristics that comprises high depression, low agreeableness and high public self-consciousness would probably benefit from psychological interventions, such as cognitive restructuring, anger management and self-assertiveness training, because these interventions might be able to modulate the extent of the personality characteristics that are associated with induced itch.8

Recent emerging research indicates that mindfulness meditation training may have beneficial effects across a spectrum of health conditions, but the mechanisms linking mindfulness meditation training with health are unknown. One striking feature of the mindfulness training literature to-date is that mindfulness training effects on disease outcomes have been observed in diseases where stress is known to trigger the onset or exacerbation of disease symptoms and pathogenesis (e.g., HIV, psoriasis, depression, pain, chronic inflammation).9   Research has indicated that relaxation techniques appear to be helpful in the treatment of patients suffering from chronic itch in patients that are open to it. And it is becoming a standard recommendation by many Practitioners and hospitals that relaxation training be considered clinically in patients who report that their itch increases during periods of heightened stress.10

The challenge for sufferers of AD is, with the aim of improving their quality of life, to help themselves to find, together with their practitioner, the best personal treatment plan and then sticking to it. The main challenges in the effective management of AD, comes down to patient adherence to the treatment plan and their emotional resilience.

 

References

  • Kwon1 J.A. et al.; Does Stress Increase the Risk of Atopic Dermatitis in Adolescents? Results of the Korea Youth Risk Behavior Web-Based Survey (KYRBWS-VI); PLOS ONE, www.plosone.org; August 2013, Volume 8, Issue 8, e67890
  • Han-Ting Wei et al.; Risk of developing major depression and bipolar disorder among adolescents with atopic diseases: A nationwide longitudinal study in Taiwan; Journal of Affective Disorders 203 (2016) 221–226
  • Buske KIrschbaum Hellhammer et al.,; Endocrine and immune responses to stress in chronic inflammatory skin disorders; 992. 231-240 (2003)
  • Sang Ho Oh et al.; Association of Stress with Symptoms of Atopic Dermatitis; Acta Derm Venereol 2010; 90: 582–588. The Journal of Clinical Investigation; http://www.jci.org; Volume 116, Number 5, May 2006
  • Kamide R.; Atopic Dermatitis: Psychological Care; Journal of the Japan Medical Association (Vol. 126, No. 1, 2001, pages 59–62).
  • Brown T.M. et al.; Assessing Pruritus Among Patients With Atopic Dermatitis: Targeted Literature and Instrument Review; https://www.rtihs.org/sites/default/files/Brown_isporposter_May2012.pdf
  • Lewis-Jones S. Quality of life and childhood atopic dermatitis: the misery of living with childhood eczema. Int J Clin Pract. 2006;60(8):984-992.
  • Schut C. et al.; Personality Traits, Depression and Itch in Patients with Atopic Dermatitis in an Experimental Setting: A Regression Analysis; Acta Derm Venereol 2014; 94: 20–25
  • Creswell J.D. et al.; Brief mindfulness meditation training alters psychological and neuroendocrine responses to social evaluative stress; Psychoneuroendocrinology (2014) 44, 1—12
  • Schut C. et al.; Psychological Interventions in the Treatment of Chronic Itch; Acta Derm Venereol 2015 Preview

PSORIASIS – the Relationship with Viral, Bacterial and Fungal Infections?

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Several viral infections have been associated with the provocation or exacerbation of psoriasis such as strep infections. Psoriasis preceded by herpes simplex virus (HSV) infection has also been reported in the past whilst other less well documented cases of viral induced psoriasis have been reported with Hepatitis B and C. Recently a case of human papilloma virus (HPV) and late onset of psoriasis has been reported. Chikungunya infection, HIV/AIDS, persistent Cytomegalovirus (CMV) infection and varicella zoster virus (VZV) have all been reported as causal and/or aggravating factors. 1,2,3,4,5,6  

The relationship between bacterial infection and the exacerbation of psoriasis is perhaps most clearly demonstrated in guttate psoriasis where there are multiple reports demonstrating that acute exacerbation of guttate psoriasis, in the majority of patients, is preceded by an infection with group A streptococci. Streptococcus pyogenes infection has also been implicated.

Guttate psoriasis is a distinctive acute form of psoriasis that generally occurs in children and young adults. The association between guttate psoriasis and Streptococcus pyogenes is medically well recognized; however, the exact mechanism remains unknown. The streptococcal trigger and genetic background of psoriasis suggest that psoriasis patients may display a particular, genetically determined sensitivity to streptococcal infection. Streptococcal infection has been found exclusively in type I psoriasis patients. (Please refer to our Blog PSORIASIS – Is it all in the family?) In up to 45% of guttate psoriasis cases, Pharyngitis and upper respiratory infections are the most common trigger recorded. Recent studies suggest that continuing, subclinical streptococcal and staphylococcal infections might be responsible not only for the relapse of acute guttate psoriasis but also for a guttate flare of a new episode of chronic plaque psoriasis as 70%of patients with guttate psoriasis go on to develop chronic plaque psoriasis. 7,8.9,10

Activation of T-cells is considered as an important factor in the pathogenesis of psoriasis, since the laboratory studies have shown that the population of T-cells isolated from the skin of patients with psoriasis is capable of stimulating keratinocytes proliferation. Super antigens, including a group of viral or bacterial proteins, can directly bind to major histocompatibility complex (MHC) class II and the V? component of T-cell receptors, and cause T-cells activation. Recently, much attention has been paid to the role of super antigens as triggering factors in the pathogenesis of psoriasis. Super antigens produced by Staphylococcus aureus are among the most lethal toxins. Toxins of this large family trigger an excessive cellular immune response leading to toxic shock. Some examples of staphylococcal super antigens are staphylococcus enterotoxin A, B, and C (SEA, SEB, SEC), toxic shock syndrome toxin-1 (TSST-I) and exfoliative toxin (ET). Staphylococcal super antigens (SAg’s) play role in the pathogenesis of inflammatory skin diseases. Severity of PS is significantly correlated to enterotoxin production of the isolated S. aureus strains. 11

Infectious perianal dermatitis is in fact a group of diverse diseases that are characterised by anal and/or peri-anal inflammation in children and rarely in adults. Perianal streptococcal dermatitis (PSD) generally occurs in children between six months and ten years of age and affects boys more often than girls. Although uncommon, PSD has also been reported as being caused by Staphylococcus aureus.  In one study, the incidence was reported to range from one in 218 to one in 2000 pediatric outpatient visits.14 Signs and symptoms in this study included perianal dermatitis (90%), perianal itching (78%), rectal pain (52%), and blood-streaked stools (35%). Intra-family spread has been reported in 50% of possible cases. Children with streptococcal pharyngitis have a 6% anal carriage rate. PSD develops 24 to 48 hours after acute afebrile pharyngitis. Some cases of perianal streptococcal dermatitis in children may be linked to guttate psoriasis.

A study published in 2014, concluded superantigens and toxins from Candida “…may play various roles in the exacerbation and the persistence of psoriasis.” 60% of the psoriasis patients tested positive for Candida versus 20% of the control group in oral tests and 15% of the psoriasis patients tested positive verses 4% of the control group in skin tests. The link between the exacerbation of psoriasis, and skin and/or gut colonization by Candida albicans was further confirmed in another study in 2015. 12,15

The role of Malassezia species in psoriasis is still undetermined, but several reports have associated the lipophilic yeasts with the development of skin lesions in psoriasis, the lipophilic yeast Malassezia furfur has been implicated in the exacerbation of scalp psoriasis.15

It was found that when cell fragments of Malassezia were topically applied to the skin of psoriatic patients, new psoriatic plaques were induced.15 Research has also reported that there is a significant correlation between the presence of Malassezia yeast and the severity of skin irritation in existing psoriatic plaques.16 These findings suggest that there are several mechanisms by which Malassezia yeasts may contribute to exacerbate psoriasis, but still remains unclear whether these microorganisms are able to initiate the development of psoriasis lesions. Psoriasis is also known to have a strong genetic component. Therefore, research has investigated immune reactions in patients with psoriasis. It has been shown that these individuals have immunological responses to both Malassezia yeasts and to proteins derived from them. T cells reactive to the yeasts have been isolated from lesional skin and it has been demonstrated that antibodies to the yeasts are present in serum taken from patients with psoriasis, but not from control subjects. 17

REFERENCES

  • Jain SP, Gulhane S, Pandey N, Bisne E. Human papilloma virus infection and psoriasis: Did human papilloma virus infection trigger psoriasis?. Indian J Sex Transm Dis 2015;36:201-3
  • Shinichi Imafuku, Reiko Naito, Juichiro Nakayama; Possible association of hepatitis C virus infection with late-onset psoriasis: a hospital-based observational study. ; J Dermatol 2013 Oct 21;40(10):813-8. Epub 2013 Aug 21.
  • Mohamed A.E. et al.; Psoriasis; a new marker for Hepatitis C among Egyptian Patients; Int.J.Curr.Microbiol.App.Sci (2015) 4(6): 761-767
  • Ahmad QM, Sameem F, Shah IH. Prevalence of hepatotrophic viruses b&c in psoriasis -A study from kashmir. Indian J Dermatol 2005;50:200-2
  • Zakaria Mahran and Tarek M. Emran. Prevalence of hepatitis C virus infection in patients with chronic plaque Psoriasis in Damietta Governorate. J Am Sci 2015;11(7):130-133
  • Failla V. et al; Childhood Herpes Zoster-Triggered Guttate Psoriasis; The Open Dermatology Journal, 2012, Volume 6
  • Sigurdardottir S. L. et al.; The association of sore throat and psoriasis might be explained by histologically distinctive tonsils and increased expression of skin-homing molecules by tonsil T cells; British Society for Immunology, Clinical and Experimental Immunology, 174: 139–151
  • Bartenjev I. et al.; Subclinical Microbial Infection in Patients with Chronic Plaque Psoriasis; Acta Derm Venereol 2000; Suppl 211: 17-18.
  • Leung D.Y.M., et al; Evidence for a Streptococcal Superantigen-driven Process in Acute Guttate Psoriasis; The Journal of Clinical Investigation, Inc. Volume 96, November 1995, 2106-2112
  • Weisenseel P. et al.; Streptococcal infection distinguishes different types of psoriasis; Downloaded from http://jmg.bmj.com/ on February 7, 2016 – Published by group.bmj.com
  • Atefi et al.; The Rise of Staphylococcal Super Antigens in Psoriatic Patients: A Case-Control Study; Jundishapur J Microbiol. 2014 May; 7(5): e9912.
  • Taheri Sarvtin,et al.; Evaluation of candidal colonization and specific humoral responses against Candida albicans in patients with International Journal of Dermatology. Dec2014,Vol.53Issue12, pe555-e560. 6p.
  • Fakhrozaman Pezeshkpoor et al.; Prevalence of Candida in saliva and skin lesions of Psoriasis Vulgaris patients; Journal of Mycology Research. Vol 2, No 1, March 2015, Page 9-14
  • Abbas Rasi, Nargess Pour-Heidari; Association between Plaque-Type Psoriasis and Perianal Streptococcal Cellulitis and Review of the Literature – Case Report; Arch Iran Med 2009; 12 (6): 591 – 594
  • Prohi? A.; Psoriasis and Malassezia Yeasts; www.interechopen.com; http://cdn.intechopen.com/pdfs-wm/32471.pdf
  • Baroni A. et al.; Possible role of Malassezia furfur in psoriasis: modulation of TGF-b1, integrin, and HSP70 expression in human keratinocytes and in the skin of psoriasis-affected patients; J Cutan Pathol 2004: 31: 35–42
  • Zomorodian et al.; Malassezia isolated from psoriasis patients; J Cutan Pathol 2008 doi: 10.1111/j.1600-0560.2007.00968.x
  • Gomez-Moyano E, et al. Do Malassezia species play a role in exacerbation of scalp psoriasis?. Journal De Mycologie Médicale (2014), http://dx.doi.org/10.1016/j.mycmed.2013.10.007

PSORIASIS – the Relationship with Drugs

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Cutaneous drug eruptions are one of the most common types of adverse reaction to drug therapy, with an overall incidence rate of 2–3% in hospitalized patients. Almost any medicine can induce skin reactions, and certain drug classes, such as non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics and anti-epileptics have drug eruption rates approaching 1–5%.1

Drug Relationship

Psoriasis & Drugs

Drug ingestion may result in several different responses:-

  1. a) Drugs may trigger the condition in a Patient who is genetically predisposed to psoriasis.
  2. b) Drugs may trigger the condition “de novo”, in a Patient non–predisposed.
  3. c) Drugs may exacerbate existing psoriatic lesions in a Patient.
  4. d) Drugs may trigger a psoriatic flare up in “clinically normal” skin in patients with psoriatic 2

In view of their relationship to psoriasis, therapeutic agents may be classified as follows:

(1)     Drugs with strong reported case evidence for a causal relationship to psoriasis including lithium, beta blockers, and synthetic antimalarial drugs;

(2)     Drugs with a considerable number of studies but insufficient data to support induction  or aggravation of the disease;

(3)     Drugs occasionally reported to be associated with aggravation or induction. 2.3

Drug-provoked psoriasis can be divided into two categories:-

1]       Drug-INDUCED psoriasis – where discontinuation of the causative drug stops the further progression of the disease. This form tends to occur in a “de novo” fashion in patients with no family or previous history of psoriasis. The clinical presentation of   these lesions  may often mimic the pustular variant of psoriasis, often with no nail involvement or associated arthritis. 2

2]       Drug-AGGRAVATED psoriasis – where the disease progresses even after the discontinuation of the offending drug and usually occur in patients with a history of  psoriasis or with a genetic predisposition for the disease. Patients can have exacerbation of pre-existing psoriatic lesions or develop new lesions in previously   uninvolved skin. Histological examination reveals features that are more characteristicof psoriasis vulgaris. 2

These two reactions are not to be confused with “Psoriasiform drug eruption”. This is a broad term that refers to a group of disorders that clinically and/or histologically simulate psoriasis at some point during the course of the disease. This type of eruption is usually associated with seborrheic dermatitis, pityriasis rubra pilaris, secondary syphilis, pityriasis rosea, mycosis fungoides, and some malignancies. 2

Some Drugs that Trigger or Exacerbates Psoriasis

Although a several drugs have been implicated in provoking psoriasis, the strongest evidence is for lithium, beta-blockers, anti-malarials, non-steroidal anti-inflammatory drugs and tetracyclines. In addition, angiotensin-converting enzyme inhibitors, interferons, digoxin, clonidine, carbamazepine, valproic acid, calcium-channel blockers, granulocyte-colony stimulating factor, potassium iodide, ampicillin, penicillin, progesterone, morphine and acetazolamide have been reported to exacerbate psoriasis. 4

 DRUG Mechanism of ActionComments
 Beta-blockers A delayed type hypersensitivity reaction, an immune mediated response and a decrease in intraepidermal cAMP and a consequent increase in peidermal cell turnoverBoth cardioselective and non-cardioselective drugs have been implicated but the frequency is higher with the latter.

Also with topical timolol, reported to induce psoriasis and to transform psoriasis vulgaris (Plaque) into psoriatic erythroderma.

 Lithium      Acts directly by blocking cell differentiation and leading to dysregulation of inflammatory cytokines and indirectly by decreasing cAMP levelsProvokes or induces chronic plaque psoriasis, localized or gnerealized pustular psoriasis and even psoriatic erythroderma.
 Antimalarials May trigger psoriasis by inhibiting the enzyme transglutaminaseDoes not induce psoriasis although they are known to trigger psoriasis in 18% of patients.
 NSAIDs Inhibits the cyclo-oxygenase pathway, leading to accumulation of leukotrienes and hence may exacerbate psoriasis 
 Tetracyclines May provoke psoriasis either by inhibiting cAMP or by inducing Koebner’s phenomenon due to their photosensitizing potential 

It is important for the patient to supply information to their GP or Practitioner as to all medications being used and when the lesions were first noticed, or when they noticed their existing lesions worsening. In some instances the eruption of new lesions may take several weeks or even months to occur, when this happens it may be difficult to determine the exact causal relationship between a drug and an eruption. The following chart may be of assistance in determining if one of your medications may be involved.

 Date Time Medication  Name Dose Reason for MedicationSymptoms ExperiencedWhen Symptoms

First Noticed

  e.g. 15/2 8.00am Carvedilol  25mg Blood PressureNew lesions on skin not affecting old lesions2 weeks after first taking it.
 Or e.g. 15/2 8.00am Bisoprolol 10mg CardiomyopathyWorsening of old lesionsAfter 72 hours, burning red skin, lesions rapidly spread
       
       
       

REFERENCES

  • Lee A. Thomson J.; Drug-induced skin reactions; Adverse Drug Reactions, 2nd edition (ISBN: 0 85369 601 2) Pharmaceutical Press 2006; http://www.pharmpress.com/files/docs/ADRe2Ch05.pdf
  • GRACE K. KIM, DO; b JAMES Q. DEL ROSSO, DO ; Drug-Provoked Psoriasis: Is It Drug Induced or Drug Aggravated? Understanding Pathophysiology and Clinical Relevance; J Clin Aesthetic Dermatol. 2010;3(1):32–38.
  • Milavec-Pureti? V. et al.; Drug Induced Psoriasis; Acta Dermatovenerol Croat; 2011;19(1):39-42
  • Mahajan R, Handa S. Pathophysiology of psoriasis. Indian J Dermatol Venereol Leprol 2013;79, Suppl S1:1-9