Itch + Psoriasis

skinconditionsblogcategory

Itch (Pruritus)

is an important but underestimated symptom in psoriasis. However, there is limited published research data available on both its prevalence and characteristics. Some studies suggest that its prevalence in psoriasis sufferers, from different parts of the world, ranges from between 70% and 90%. In one Study Researchers found that 83% of psoriatic patients suffered from itching and in 45% of these patients pruritus was a daily occurrence (in 32% “often” and in 13% “always”) 1

Functional brain imaging studies have shown that the itch-scratch cycle in humans can be tracked to specific regions of the brain, including areas related to reward, pain sensation, and addiction.

The Itch-Scratch-Rash cycle is commonly used to describe this ongoing, never ceasing, always constant itch. The itchier a patient feels, the more scratching of the skin that occurs and which ultimately lead to skin damage and the appearance of a red rash. Often, in chronic presentations it becomes a completely unconscious habit and patients are often not even aware that they are scratching. When a patient scratches, their skin becomes inflamed, this inflammation then causes the skin to itch even more, thus making it even harder for the patient to resist the urge to scratch. This vicious circle can become so severe that it causes sleeplessness, irritability, anxiety and stress. In extreme cases it can lead to significant excoriations (open, bloody and deep scratch wounds) on the lesions and the surrounding normal skin. In chronic psoriasis it can even cause severe lichenification (thickening of the skin) and pain.

One study found that itching was the most frequent complaint (64%) among patients hospitalized for psoriasis. A National Psoriasis Foundation USA survey of its members in 2001, reported that for 79% of sufferers – itch was the second most troublesome symptom after scaling. Psoriasis sufferers have indicated that the severity of their itching on a scale from one to 10 VAS scale (from mild, moderate to severe pruritus where scratched plaques bleed). Most described pruritus (itch) as a sensation of stinging (20%) and burning (15%); the intensity reflected by VAS scale was scored as mild only in 13%, moderate in 37% and severe in 33% of those surveyed. 75% percent of itch patients had to scratch until they bled. Itch was also found to be more severe and frequent at night with 50% reporting difficulty in falling asleep. 2, 3

Itching/Scratching can lead to the hypertrophy (enlargement) of cutaneous (skin) nerve endings, which in turn become more sensitive. For those psoriasis sufferers that have as their Primary trigger, flare-ups caused by the “Koebner Phenomenon” (in which skin injury e.g. tattoos, surgical procedures, cuts, insect bites or sunburn etc. elicits a disease response) scratching can continually exacerbate and worsen their condition. The “Koebner Phenomenon” affects between 11% to 75%, depending on various study results. 4

Where constant and vigorous scratching has occurred and plaque scales have been removed, pin point bleeding, known as the Auspitz sign can be observed.

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Studies have also shown that in people suffering from depression, and who suffer from itching due to a variety of causes, that there is a correlation between the severity of itchiness and the severity of depression. Itching therefore causes both a real serious physical and psychological suffering, similar to what chronic pain does.5 It has been noted that there is a direct positive relationship between the severity of pruritus and the severity of depression in patients with psoriasis.6 One study revealed that patients with psoriasis, that experienced intense pruritus, also reported significantly higher scores for depression and anxiety, and showed personality traits of somatic anxiety, embitterment, mistrust, and physical trait aggressiveness. It was also noted that approximately 30% of these patients experienced high-level pruritus, when the great majority of patients had very few skin lesions.7

Patients when answering the questions on “what was the aggravating factors of pruritus”, gave the following answers –  “when I was stressed out” (35.0%), followed by “in a hot environment” (18.8%), “when sweating” (17.5%), “during a change in the weather” (12.5%), and “in a cold environment” (10.0%). Of these patients, 32.5% complained of itching on the entire body, followed by the scalp and trunk (17.5%), the scalp only (16.3%), and the scalp and extremities (13.8%).8

Scratching, even for adults, is difficult to resist because it does give the impression of easing the itch – but this is only for the short-term. Eventually the sensation to itch comes back – even worse that before the patient scratched.

Basic tips to control the urge to itch:- 

  • Keep nails short to avoid tearing the skin when scratching. 
  • Keep cool. Over-heating can trigger the itch. Try to keep your body temperature as constant as you can, wear light layers of cotton clothes.
  • Avoid overheated rooms, keep ducted heating to a minimum, and at night keep the bedrooms cold.
  • Avoid heavy blankets and doonas – use cotton blankets (hospital style) if possible. 
  • Gently rub with the back of the fingers, place pressure on the area instead of scratching. 
  • Use a cold compress 

it_2

REFERENCES:

  1. Aerlyn D. “Treating Itch in Psoriasis.” Dermatology Nursing 18.32006 227-233. 20 Apr. 2008. http://www.medscape.com/viewarticle/541971.
  2. “Itch Relief.” Psoriasis.org. 9 Nov. 2001. National Psoriasis Foundation. 20 Apr. 2008.
    http://www.psoriasis.org/news/stories/2001/20011109_itch.php.
  3. Prigninao P. et al.; Itch in psoriasis: epidemiology, clinical aspects and treatment options.; Clinical, Cosmetic and Investigational Dermatology 2009:2 9–13
  4. Sampogna, F. “Prevalence of Symptoms Exerienced by Patients with Different Clinical Types of Psoriasis.”British Journal of Dermatology 151.3 Sep. 2004. 594-599. 20 Apr. 2008. http://www.blackwell-synergy.com/doi/abs/10.1111/j.1365-2133.20.
  5. Thappa, D.M. “The Isomorphic Phenomenon of Koebner.” Indian Journal of Dermatology, Venereology and Leprology 70.32004 187-189. 23 Apr.2008. http://www.ijdvl.com/text.asp?2004%2F70%2F3%2F187%2F11105.
  6. Gupta MA.et al. Pruritus in psoriasis. A prospective study of some psychiatric and dermatologic correlates. Arch Dermatol 1988; 124: 1052–1057.
  7. Remröd C. et al.; Psychological aspects of pruritus in psoriasis; Acta Derm Venereol 2015; 95: 439–443
  8. Tae-Wook Kim et al.; Clinical Characteristics of Pruritus in Patients with Scalp Psoriasis and Their Relation with Intraepidermal Nerve Fiber Density; Ann Dermatol Vol. 26, No. 6, 2014

PSORIASIS and CHEMICAL EXPOSURE to POLLUTION

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Human beings are continuously exposed to environmental pollutants. Because of its critical location, the skin is a major interface between the body and the environment and provides a biological barrier against an array of chemical and physical environmental pollutants. The skin can be defined as our first defense against the environment because of its constant exposure to oxidants, including ultraviolet (UV) radiation and other environmental pollutants such as diesel fuel exhaust, cigarette smoke (CS), halogenated hydrocarbons, heavy metals, and ozone (O3). The exposure to environmental pro-oxidant agents leads to the formation of reactive oxygen species (ROS) and the generation of bioactive molecules that can damage skin cells.1

 The skin is a potential target for oxidative injury, as it is continuously exposed to UV radiation and other environmental stresses generating reactive oxygen species (ROS). ROS mediated oxidative damage involves a vast number of biological molecules since it causes lipid peroxidation, DNA modification, and secretion of inflammatory cytokines.2 ROS induced oxidation of polyunsaturated fatty acids results in the metabolization of the lipid peroxidation into malondialdehyde (MDA). Lipids are structural components of cell membranes, critical in the formation of the permeability barrier of cells, whilst MDA is used as a biomarker of lipid peroxidation.2,3

pollution-in-the-city-1445561-1599x1066

Alterations that disturb the skin barrier function in either stratum corneum lipid metabolism or protein components of the corneocytes are involved in the development of various mild or severe skin diseases, including erythema, oedema, hyperplasia, “sunburn cell” formation, skin aging, contact dermatitis, atopic dermatitis, psoriasis, and skin cancers.1

The mechanism by which environmental insults exert a detrimental effect the skin barrier function is through the generation of oxidative stress, which overwhelms the skin’s defenses by quickly depleting the enzymatic (glutathione peroxidase, glutathione reductase, superoxide dismutase, catalase) and nonenzymatic (vitamin E, vitamin C, and glutathione) antioxidant capacity, thus leading to deleterious effects.1 The enzymes, including glutathione peroxidase, superoxide dismutase (SOD) and catalase (CAT) decrease the concentration of the most harmful oxidants, hence an inadequate antioxidant protection or excess ROS production generates oxidative stress and contributes to the development of cutaneous diseases and disorders.

Increased capacity for chemotaxis (the directional movement of cells in response to chemical stimuli), adhesion (the interaction of a cell with a neighbouring cell or with the underlying extracellular matrix, via specialized multi-protein adhesive structures) and increased ROS production in neutrophils, keratinocytes and fibroblasts of the skin matrix, have been reported in patients with psoriasis. Research results have shown that increased oxidative stress in these patients, as demonstrated by the high plasma malondialdehyde (MDA) levels and compromised levels of the antioxidant defense enzymes, have been observed even at the time of diagnosis itself. Other reports have suggested that, fibroblasts in the lesion-free skin of psoriasis patients have shown signs of increased oxidative damage even before the formation of the characteristic psoriatic plaque/lesions which may indicate the involvement of abnormal immune reactions leading to the onset of the disease.2

Sun UV rays, Ozone (O3 – the primary constituent of smog), cigarette smoke (CS) exposure, and pollutants, in addition to the natural process of aging, contribute to the generation of free radicals and reactive oxygen species (ROS) that interact with lipid-rich plasma membrane and initiate the so-called lipid peroxidation reaction cascade. The progressive depletion of antioxidant content in the stratum corneum leads to the cascade of effects which result in an active cellular response in the deepest layers of the skin. ROS is known to stimulate the release of pro-inflammatory mediators from a variety of skin cells. Skin inflammation, in turn, leads to skin infiltration by activated neutrophils and other phagocytic cells that generate further free radicals (both reactive oxygen and nitrogen species), thus establishing a vicious circle.1

 There is no doubt that the skin is continuously and simultaneously exposed to several oxidative stressors, and these can have additive, if not synergistic, effects. Whilst UV ray therapy has been proven to be an effective treatment for psoriasis and there is certainly anecdotal information that indicates sun exposure also improves psoriatic lesions, there has been little or no research on the effects of combined UV and O3 on the inducement and or exacerbation of psoriasis.  While environmental UV radiation penetrates into the epidermis (UV-B) or into the dermis (UV-A) and is known to induce the release of tissue-degrading enzymes, O3 oxidizes biological systems only at the surface. Therefore, because O3 and UV cooperatively damage subcutaneous (SC) components they exert an additive effect in cutaneous tissues. Research results have suggested that UV irradiation has been shown to compromise the skin barrier and simultaneous exposure to O3 may enhance this phenomenon by perturbing SC lipid constituents that are known to be critical determinants of the barrier function. It has been proposed that the by-products of O3-induced lipid oxidation penetrate the outer skin barrier and cause effects on constituents of the deeper epidermis that can lead to activation of transcription factors, such as Nuclear factor kappa B (NF-?B), which regulates a variety of proinflammatory cytokines. NF-?B is a protein transcription factor that orchestrates inflammation and other complex biological processes. It is a key regulatory element in a variety of immune and inflammatory pathways, in cellular proliferation and differentiation and in apoptosis. Therefore NF-?B is a crucial mediator involved in the pathogenesis of psoriasis.1,3,4,6

It has been theorized that responses to air pollutants may be age related, and several recent studies have shown that skin responses to pollutants are modulated by age. The free radical theory of aging is supported by finding that oxidative damage to biomolecules accumulates and increases with age. In aging skin, the process oxidative damage involves not only proteins, lipids and DNA but also is linked with alteration of the collagenous extracellular matrix in the dermis. The extensive research in the aging process of human skin found that levels of MMP-1 increased with age and contributed to fragmentation and disorganization of collagen fibers in the dermis. Researchers have also found that both a contact of fibroblasts with collagen fibers and collagen cross-links of collagen fibers are strongly reduced in aged skin (80% and 75%, respectively). Despite a large body of knowledge a detailed molecular mechanism of the skin aging is not fully recognized.1,5

Further research is required to determine exactly how air pollutants can induce and/or exacerbate psoriasis and other skin conditions. However one theory proposed for the most likely cause is thought to be due to skin injury caused by exposure to the chemical pollutant and the subsequent initiation of the Koebner effect.

See our blog “Koebner Phenomenon”, “Psoriasis and Chemical Exposure” and “Psoriasis and Smoking”

References

  • Valacchi et al.; Cancer Cutaneous responses to environmental stressors ; Annals Of The New York Academy Of Sciences;  Issue: Nutrition and Physical Activity in Aging, Obesity, and Cancer; Ann. N.Y. Acad. Sci. ISSN 0077-8923; https://www.semanticscholar.org/paper/Cutaneous-responses-to-environmental-stressors-Acad-Sci/09cdc1c7eda0a59cce84c65631d380a180cc4f1b/pdf
  • Ayala A. et al.; Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal; Oxidative Medicine and Cellular Longevity Volume 2014, Article ID 360438, 31 pages; file:///C:/Documents%20and%20Settings/marg/My%20Documents/Downloads/360438.pdf
  • Kadam P. et al.; Role of Oxidative Stress in Various Stages of Psoriasis; Ind J Clin Biochem (Oct-Dec 2010) 25(4):388–392; file:///C:/Documents%20and%20Settings/marg/My%20Documents/Downloads/12291_2010_Article_43.pdf
  • Goldminz AM. Et al.; NF-?B: an essential transcription factor in psoriasis.; J Dermatol Sci.2013 Feb;69(2):89-94. doi: 10.1016/j.jdermsci.2012.11.002. Epub 2012 Nov 14.
  • Kruk J., Duchnik E.; Oxidative Stress and Skin Diseases: Possible Role of Physical Activity; Asian Pacific Journal of Cancer Prevention, Vol 15, 2014
  • Burke KE,Wei H.; Synergistic damage by UVA radiation and pollutants.; Toxicol Ind Health May/June 2009 25: (4-5): 219-224

What triggers Psoriasis?

skinconditionsblogcategory

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

What is the Koebner Phenomenon?

The Koebner phenomenon was first described by Heinrich Koebner (1838-1904), one of the outstanding dermatologists of the 19th century. His initial observations and studies resulted from having seen patients who had developed psoriasis at sites of excoriations, horse bites, and tattoos and he first published his findings in 1876. However, the definition has been extended to include lesions developed after trauma in people with no pre-existing dermatosis. Several other skin diseases e.g. lichen planus, vitiligo and Darier disease, can also present with Koebner phenomenon. Koebner phenomenon occurs in about 25% of people with psoriasis after various traumatic injuries, but this may be much higher as patients may not recognize the original traumatic episode (e.g. insect bite) and therefore the Koebner effect may go unreported. 1

Koebner response may follow:
(1)     mechanical or thermal trauma – due to animal bites, burns, electrodessication, 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). 2

Bellybutton PsoriasisTattoo psoriasisPsoriasis after surgery

         Psoriasis after Belly Ring Piercing                                          Psoriasis after a Tattoo                                       After removal of Benign Growth

 

(2)  dermatoses – skin conditions e.g. carbuncles/furuncles (boils and/or cysts), dermatitis, dermatitis herpetiformis, dermatophytosis,          diaper dermatitis secondary to Candida infection, eczema, epidermal inclusion cyst, folliculitis, herpes simplex, herpes zoster,                   lichen planus, lymphangitis, measles, miliaria, perianal neuro   dermatitis, pityriasis rosea, psoriasis, scabies, seborrheic dermatitis,              varicella, vitiligo. 2

Psoriasis after Herpes Zoster

                  Psoriasis after herpes Zoster     

    

(3)     allergic or irritant reactions – following Bacillus Calmette–Guérin (BCG) vaccination (tuberculosis), tuberculin skin test, hair                   spray, hair tints, influenza   vaccination, photosensitivity, positive patch testing, scratch skin test, tattoos (allergic reaction to ink),                 urticaria 2 , and

(4)     therapy – such as Grenz ray therapy – “ultrasoft” or “soft” radiation, roentgen radiation therapy, iodine application, ultraviolet light            (PUVA). 2

Psoriatic lesions usually form within 10-20 days of the wounding event (but may range from 3 days to 2 years). However, it usually coincides with the duration of the wound healing phase. This strongly suggests that skin in predisposed individuals may continue to develop normally right up until the substantial triggering skin trauma. 3,4

 

REFERENCES

  • Arias-Santiago A. et al.; The Koebner phenomenon: psoriasis in tattoos; CMAJ, April 16, 2013, 185(7)
  • Thappa DM. The isomorphic phenomenon of Koebner. Indian J Dermatol Venereol Leprol 2004;70:187-9
  • Matovi? L. et al.; The Koebner phenomenon, a prognostic sign of PUVA therapy effectiveness in patients with     psoriasis vulgaris–yes or no?; Med Pregl. 1999 Nov-Dec;52(11-12):437-40.
  • Chee Ren Ivan Lam et al.; Wound Repair Studies Reveal New Insights to Psoriasis; http://www.intechopen.com/