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

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