Psoriatic Nails – Part 1

skinconditionsblogcategory

Psoriasis can affect both finger nails and the toe nails (Psoriatic Nails). The percentage of those with psoriasis who have nail involvement is thought to be 50%. For some unknown reason the finger nails are more often involved than toe nails. In most cases people with psoriasis have concurrent nail psoriasis; however, in 5- 10% of cases the nails only may be affected. In one study it was found that the frequency of nail changes in patients with Koebner’s phenomenon was 56%, whereas as in those without Koebner’s phenomenon it was only 29%. Nail psoriasis is approximately 10% more common in males than in females and is positively associated with higher bodyweight.1

Nail psoriasis is characterised clinically by manifestations on the fingernails and toenails. The mean delay of onset for nail dystrophies occurs in individuals with psoriasis between 9 and 11.5 years, explaining the lower prevalence of nail psoriasis in children.2 There may be involvement of only a single nail or of all nails and over time is associated with severe nail destruction or total nail loss.

Clinical Forms of Nail Psoriasis 3,4,5

  1. Psoriasis on the Nail Matrix and Plate
  • Pits or pitting, or dimples – Pitting is the result of the loss of cells from the surface of the nail. (see pictures 1-4 Part 2) Pitting occurs in approximately 70% of psoriatic nails.
  • Trachyonychia – rough (sandpapered) accentuated linear ridges (longitudinal striations) on the nails
  • Leukonychia – white nails or milk spots
  • Beau Lines – deep transverse (side to side) linear depressions, lines or trenches across the nails
  • Red lunulae – is the white half-moon–shaped area located at the base of fingernails and toenails; it is the only visible part of the nail matrix. The lunula becomes red when the capillaries under the nail are congested.

  

Blausen.com staff.

“Blausen gallery 2014”. Wikiversity Journal of Medicine. 

DOI:10.15347/wjm/2014.010. ISSN20018762

  1. Psoriasis of the Nail Bed
  • Onycholysis – the separation of the nail plate from the underlying nail bed and hyponychium (commonly known as the “quick”)
  • Subungal hyperkeratosis – excessive proliferation of the nail bed and hyponychium where a chalk like substance builds up.
  • Oil spots or salmon patches – these are the only lesions that are exclusive to nail psoriasis; they appear as round or oval yellowish brown/orange coloured areas in the centre of the nail plate
  • Splinter haemorrhages – small black lines that run from the tip of the nail to the cuticle as the result of the capillaries (very small blood vessels) between the nail and the skin bleeding.
  1. Paronychia

    An infection of the skin around the fingernails and toenails usually caused by a bacterial and/or fungal infection.

  1. Acropustulosis – characterised by pustular eruptions beginning in the tips of fingers and toes.

          Digits become swollen and malformed.

Psoriatic arthritis initially may present with only a few swollen joints. It is often common for just a single finger or toe to be noticeably swollen. Some people feel stiff when they wake up. As they move around, the stiffness fades. Sausage-like swelling in the fingers or toes (dactylitis), pain in and around the feet and ankles, especially tendinitis in the Achilles tendon or Plantar fasciitis in the sole of the foot and changes to the nails, such as pitting or separation from the nail bed are all indicative of Psoriatic Arthritis. More than 80% of patients with psoriatic arthritis will present with psoriatic nail lesions.

Researchers found that the nail and the enthesis (connective tissue – that directly attaches to the bone, via the distal interphalangeal (DIP) joint extensor tendon) are key players in the pathophysiology of nail psoriasis. Specifically, they found that the extensor tendon, at its enthesis, is able to send superficial fibres, which contribute to the formation of thick tissue surrounding the finger bones. This links the dense fibrous connective tissue from the nail plate to the tissue surrounding the finger bones and indirectly to the extensor tendon. The study suggested that there is an association between the DIP joint arthritis and nail disease due to the close interaction between the nail, joint and its associated tendons and ligaments. This is supported by the fact that although the nail system has no neural component, 50% of patients with nail psoriasis observe mild to severe pain and restricted mobility of the fingers.2

Many patients find that it becomes progressively more and more difficult and painful to use the fingers for gripping cutlery, pens and tools and performing tasks such as buttoning clothes, buttering toast, writing, typing etc., which are actions that we take for granted, become tasks that they can no longer do. As well as daily day to day activities many patients find that psoriatic nails also impact upon their sporting activities such as tennis, golf, swimming etc.

 

REFERENCES

  • Dogra A.and  Kaur Arora A.: Nail Psoriasis: The Journey So Far; Indian J Dermatol. 2014 Jul-Aug; 59(4): 319–333.
  • Tirant M. et al.; Nail Psoriasis In an Adult Successfully Treated With a Series of Herbal Skin Care Products Family – A Case Report; Journal Of Biological Regulators & Homeostatic Agents; 30, no. 2 (S3), 21-28 (2016)
  • Sánchez-Regaña M. and Umbert P.; Diagnosis and Management of Nail Psoriasis; Actas Dermosifiliogr. 2008;99:34-43
  • Ghosal A, Gangopadhyay DN, Chanda M, Das NK. Study of nail changes in psoriasis. Indian J Dermatol. 2004;49:18–21.
  • Reich K. Approach to managing patients with nail psoriasis. J Eur Acad Dermatol Venereol. 2009;23(Suppl 1):15–21. [PubMed: 19686381]

PSORIASIS AND COMORBIDITIES – Occular Inflammation

blog-7

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

Occular Inflammation –

Iritis

Uveitis

Episcleritis

Conjunctivitis

1, 2, 3

Ocular Inflammation

eye  episcleritis eye

Overall, ophthalmological manifestations occur in about 10% of the cases of psoriasis and include blepharitis, conjunctivitis, keratitis, xerophthalmia (a medical condition in which the eye fails to produce tears), corneal abscess, cataract, orbital myositis (inflammation of the eye muscles), symblepharon (adhesion of the eyelid to the eyeball), chorioretinopathy (detachment of the retina), uveitis and ectropion with trichiasis (inwardly growing eyelashes) and madarosis (loss of eyelashes) secondary to eyelid involvement. 1,2

Uveitis

Although the etiology of psoriasis and its association with ocular disease remains unknown, it has been suggested that activated neutrophils in peripheral blood may be responsible for the attacks of anterior uveitis associated with psoriatic arthritis. Uveitis tends to develop more often in patients with arthropathy or psoriasis pustulosa rather than the other forms of psoriasis. Psoriasis patients with uveitis tend to be older than those without psoriasis. 1,2

Uveitis is characterized by an intraocular inflammatory process resulting from various causes. Individual forms of uveitis may be differentiated as a function of the location of the inflammation within the eye, symmetry and continuity of the inflammation, associated complication and distribution of cells along the corneal endothelium. 1,2

schematic diagram of the human eye

The uvea is the mid-portion of the eye. Its anterior portion includes the iris and the ciliary muscle, and its posterior portion consists of the choroid. Anterior uveitis or iritis is the inflammation of the anterior uveal tract. When the adjacent ciliary body is also affected, the process is known as iridocyclitis. Anterior uveitis is four times more common than posterior uveitis.

Uveitis can be divided into four main subgroups according to the etiology of the inflammation – infectious disease, immune-mediated disease, syndromes limited to the eyes or idiopathic forms. Of the patients with uveitis, around 40% of cases are secondary to an immune-mediated disease; around 30% of the cases of uveitis do not fit into any well-defined etiology. 1,2

Uveitis may occur in 7-20% of the patients with psoriasis. In a cross-sectional study researchers found a prevalence of uveitis of 2% in patients with psoriasis irrespective of the severity of the dermatosis. The association between uveitis and chronic plaque psoriasis has also been found, and in these patients uveitis tends to be bilateral affecting both eyes), prolonged and more severe. Uveitis, particularly anterior uveitis, has also been associated with the arthropathic form of the disease and approximately 7% of the patients with psoriatic arthritis may develop uveitis. Some cases of uveitis have been reported to occur even before psoriatic skin disease, and uveitis has been reported as the first presenting sign of Spondyloarthropathies (SpAs – a family of long-term (chronic) diseases of joints) in up to 11.4% of cases. The severity of ocular inflammation does not necessarily correlate with extent of joint findings but may correlate with skin disease. 1,2

Stephen Bafico

Conjunctivitis is a commonly occurring eye condition that can be caused by psoriasis, but it is more commonly due to allergies, bacterial infection, or viral infection. The most common presentation is generalized conjunctival injection with mild photophobia, gritty discomfort, and possible discharge. Thick purulent (pus-like) discharge is a hallmark of bacterial infection and watery discharge is characteristic of viral infections. Increased rates of obstructive meibomian (tarsal – sebaceous gland at the rim of the eyelids) dysfunction were noted in psoriatic patients. Published articles have suggested conjunctivitis prevalence rates in psoriasis patients as high as 64.5%.4

allergicconjunctivitis

Dry eye (Keratoconjunctivitis sicca – Dry Eye Syndrome) has been cited at a prevalence rate of 2.7% of psoriatic arthritis patients. Studies have suggested prevalence rates of dry eyes as high as 18.00% of psoriasis patients.4

 Facial psoriasis can of course present on the eyebrows and on the eyelids.

psoriasis-eye-before psoriasis-eye-after

      Facial Psoriasis – Before                                 Facial Psoriasis – After

When psoriasis affects eyelids or eyelashes, these may become covered with fine plaques and the rims of the eyelids may become red and crusty. If the rims of the eyelids are irritated for long periods of time, the rims of the lids may turn up or down (Ectropion). If the rims turn down, the lashes have a tendency to rub against the surface of the eye and cause further irritation and possibly damage to the surface of the eye.

Psoriatic eye manifestations, uveitis in particular, can lead to serious consequences, including vision loss. It is important at the first sign of occular redness, weeping, blurred vision, for psoriasis sufferers to see their Practitioner immediately, as they may need to be referred to an Ophthalmologist depending upon the severity of the symptoms.

 

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
  • Shiu-chung Au et al.; Psoriatic Eye Manifestations; FALL 2011; psoriasis forum, Vol. 17, No. 3; https://www.psoriasis.org/files/pdfs/forum/Psoriatic-Eye-Manifestations-Forum_Fall_11_WEB.pdf
  • Naiara Abreu de Azevedo Fraga et al.; Psoriasis and uveitis: a literature review; An Bras Dermatol. 2012;87(6):877-83. http://www.scielo.br/pdf/abd/v87n6/v87n6a09.pdf

 

PSORIASIS – Severity and Types

skinconditionsblogcategory

Psoriasis is one of the most common immune-mediated diseases world-wide. It is a chronic condition that waxes and wanes. Importantly it is not contagious but it can be an extremely painful, disfiguring and disabling condition for which there is no cure.

The exact causes of psoriasis have yet to be determined, however impairment of the immune system and genetics are known to play major roles in its development. When the immune system is somehow triggered it speeds up the growth cycle of skin cells among other immune reactions leading to a thickening of the skin, inflammation and excessive scaling.1

The prevalence of psoriasis in different populations varies between 0 and 12%, with estimates between 2 – 3% in most western populations. The prevalence in the northern most regions of the Russia and Norway ranges between 5–10% of the population and the highest 12% prevalence is found in the arctic population.2  In the U.S., prevalence ranges from 2.2% to 3.15% and the prevalence among African Americans is 1.3%. There is a low prevalence among North American Indians, Asians and Western Africans (0.3%). In Japan it is 0.1-0.2% of the population, in China 0.3% and is virtually undetected in Native South American Indians.3, 4, 5 Estimates of the prevalence of psoriasis in Australia ranges from 2.3% to 6.6% and in the U.K., the range was 1.3% to 2.6%.4,6  In Australia in the indigenous population it  occur rarely, with two recent Australian studies reporting small numbers of Indigenous patients in both the urban and rural environment presenting with psoriasis.7

What triggers psoriasis is a complex question and a large number of factors are involved. Genes are important: numerous family studies have provided compelling evidence of a genetic predisposition to psoriasis, although the inheritance pattern remains unclear. The condition will develop in up to 50% of the siblings of persons with psoriasis when both parents are affected, but prevalence falls to 16% when only one parent has psoriasis and falls further to only 8% percent if neither parent is affected.8 Environmental risk factors also play a role: bacterial and viral infections, stress, skin trauma, smoking and obesity have all been associated with the onset and exacerbation of psoriasis.9

The classification of severity is based on several dermatological markers. It often is a combination of a PASI (Psoriasis Area and Severity Index) score and a BSA (Body Surface Area) coverage factor.

A PASI score is used by dermatologist to measure the dermatological markers to determine the severity and extent of psoriasis, especially during a clinical trial. Four body areas, the head, the arms, the torso and the legs, are measured according to redness (erythema), thickness (Induration/Infiltration) and scaling (Desquamation) from 0 to 4. (See Chart)

% coverage of the body affected is also involved in the classification of the severity of psoriasis. The classification of mild psoriasis is made when symptoms affect less than 3% of the body surface. Moderate psoriasis covers 3% – 10% and the classification of severe indicates that symptoms affects more than 10% of the body, also the involvement of the hands, feet, facial, or genital regions, by which, despite involvement of a smaller BSA, the disease may interfere significantly with activities of daily life. This of course does not take into account the emotional impact that the condition has on the sufferer.9

Absent  Mild Moderate Severe Very Severe
Redness / Erythema severe_1

None


Score 1
severe_3
Score 2
severe_4

Score 3

Sev_1
Score 4
Thickness/

Hyperkeratosis

sev_2
None
sev_3
Score 1
Sev_4
Score 2
Sev_5
Score 3
Sev_6
Score 4
Scaling/Desquamation Sev_7
None
Sev_8
Score 1
Sev_9
Score 2
Sev_10
Score 3
Sev_11

Score 4

Sev_12

Psoriasis can have a devastating impact on psychological well-being and social functioning, similar to that of cancer, arthritis, hypertension, heart disease, diabetes or depression. Most people with psoriasis suffer feelings of stigmatization because of their highly visible symptoms. This leads to feelings of social discrimination and alienation which compounds the feelings of anxiety and depression.9

Almost 90% of psoriasis sufferers have feelings of shame and embarrassment, 62% feel depressed, 58% suffer from anxiety, 44% feel that they have problems at work with most feeling that they are rejected for promotions, not accepted as part of the work group etc., 42% suffer from a lack of self-confidence due to their self-consciousness and 40% have difficulties in sexual relationships.10 

TYPES OF PSORIASIS

Psoriasis has been classified into several different types10, depending upon presentation, including:-

  • Plaque psoriasis or Psoriasis vulgaris (common type) – comprises approximately 90 percent of cases. Characterized by sharply demarcated erythematous silvery scaling plaques which most commonly occur on the extensor surface of the elbows, knees, scalp, sacral, and groin regions. The lesions are well-defined round or oval plaques that differ in size and in chronic plaque psoriasis that often coalesce to form very large, oddly shaped lesions covering large areas of the body.  Other involved areas include the ears, glans penis, perianal region, and sites of repeated trauma.
  • Scalp psoriasis is plaque psoriasis that is confined to the scalp, nape, forehead, sideburns, ears) the scalp lesions rarely extend > 2 cm beyond the hairline. Compared with plaque psoriasis elsewhere on the body, scalp involvement is frequently asymmetrical.
  • Guttate psoriasis – numerous small, red or salmon pink, drop-like spots which cover a large portion of the skin. Spots have fine, slivery scale. Lesions are usually located on the trunk, arms and legs. Usually proceeded by a bacterial streptococcal infection (strep throat, chronic tonsillitis) or a viral respiratory infection.
  • Flexural/intertriginous (Inverse psoriasis) – is located in the skin folds: i.e. armpits, under the breasts, skin folds around the groin and between the buttocks and in the skin fold of the obese. It is particularly subject to irritation from rubbing and sweating because of its location in the skin folds and tender areas. The plaques are thin, have minimal scale and a shiny surface commonly accompanied by secondary fissuring and/or maceration (the softening and breaking down of skin resulting from prolonged exposure to moisture). It is also prone to secondary infections such as tinea and candida.
  • Palmoplantar psoriasis – presenting as hyperkeratotic (thickened), red or yellowish, scaly plaques on the central palm or weight-bearing areas of the soles. The lesions are well demarcated and often accompanied by painful cracking and fissuring.
  • Palmoplantar pustulosis (PPP): is characterized by hyperkeratosis and clusters of pustules over the palms, and soles of hands and/or feet. These sterile pustules can remain as discrete pustules or may become confluent, producing lakes of pus which dry out, and the skin subsequently peels off, leaving a glazed, smooth erythematous surface. Quite often new crops of pustules will then appear.
  • Pustular psoriasis or Generalized Pustular psoriasis (von Zumbusch type) – Pustular psoriasis may be localized clusters of pinhead sized sterile pustules or as in the Generalized presentation – the skin becomes very red and tender and within hours, pinhead-sized pustules appear studding the erythematous back? These painful, sterile pustules may become confluent, producing lakes of pus. Subsequently, the pustules dry out, and the skin peels off, leaving a glazed, smooth erythematous surface on which new crops of pustules may appear. This is usually accompanied by a fever and systemic symptoms e.g. nausea, and may require the patient to be hospitalized.
  • Erythrodermic psoriasis – characterized by erythema, severe scaling, itching, and pain. This unstable psoriasis may some? times evolve to whole-body involvement that can lead to the inability to maintain homeostatic functions and often requires the patient to be hospitalized.
  • Nail psoriasis – affecting the nails of the fingers and/or toes, may affect only one or several nails. The most frequent signs of nail psoriasis are pitting and distal onycholysis. Clinical manifestations range from pitting, yellowish discoloration, and paronychia, to subungual hyperkeratosis, onycholysis, and severe onychodystrophy.
  • Psoriatic arthritis (PsA) a chronic inflammatory joint disease occurs in up to 39 % of patients with psoriasis. This type of arthritis can be slow to develop, with only mild symptoms or it can develop rapidly with extreme pain and characterized by focal bone erosions. PsA can be a severe form of arthritis with prognosis similar to that of rheumatoid arthritis

For more information on each classification of psoriasis refer to posts on each individual type.

REFERENCES

  • Višnja Milavec-Pureti?  et al.; Drug Induced Psoriasis; Acta Dermatovenerol Croat 2011;19(1):39-42
  • Bhalerao A., Bowcock A. M. ; The Genetics of Psoriasis: A Complex Disorder of the Skin and Immune System; Mol. Genet. (1998) 7 (10): 1537-1545 doi:10.1093/hmg/7.10.1537
  • Kuchekar A.B. et al.; Psoriasis: A comprehensive review; Int. J. of Pharm. & Life Sci. (IJPLS), Vol. 2, Issue 6: June: 2011, 857-877 857
  • Parisi R et al. Global epidemiology of psoriasis: A systemic review of incidence and prevalence. J Invest Dermatol 2012 Sep 27; [e-pub ahead of print]. (http://dx.doi.org/10.1038/jid.2012.339)
  • Menter A., Stoff B.; Psoriasis – Chapter 1 History, Epidemiology and Pathogenesis; 2010; Manson Publishing UK.
  • Parisi R. et al. Global Epidemiology of Psoriasis; Journal of Investigative Dermatology (2013), Volume 133
  • Heyes C. et al.; Non-infectious skin disease in Indigenous Australians; Australasian Journal of Dermatology (2014) 55, 176–184
  • Farber, E.M., Nall, L. and Watson, W. (1974) Natural history of psoriasis in 61 twin pairs. Arch. Dermatol., 109, 207–211.
  • Pelle Stolt, Maglia Rotta; Bringing Psoriasis into the Light; International Federation of Pharmaceutical Manufacturers & Associations; http://www.ifpma.org/fileadmin/content/Publication/2014/Psoriasis_Publication-Web.pdf
  • https://www.statista.com/statistics/409255/psoriasis-impact-on-individuals-physical-and-social-functioning/
  • Zangeneh F.Z., Shooshtary F.S.; Psoriasis — Types, Causes and Medication – Chapter 1; http://cdn.intechopen.com/pdfs-wm/44173.pdf

PSORIASIS and DIET – Part 1

Integrative Dermatology Blog Image

For many years Dermatologists, General Practitioner’s and many researchers considered that patients who stated that eating certain foods made their psoriasis  worse as being utterly mistaken or delusional. However, over the last several years there has slowly been a change of thought and we are now seeing the results of several recent studies and clinical trials on various nutritional and dietary therapies for psoriasis. And the results have made it clear that diet may influence the health outcome for patients.

A study of some 20,000 eczema and psoriasis patients by the Department of Medical Nutrition, Donau University Krems in Austria, found that the patients showed, besides allergic reactions to foods, an increasing number of pseudo allergic reactions caused by toxic-irritative pollutants (formaldehyde, exhaust particles, food additives, nicotine, wood preservatives, pesticides, heavy metals) which are responsible for the inflammatory process behind the complex symptoms. The Researchers found that 60% of all patients had raised concentrations of circulating immune complexes with food-specific IgE- and IgG responsible for the delayed (Type III) allergic reactions. They found that both in atopic eczema and in psoriasis patients had pseudo allergic  reactions against biogenic amines and had constantly raised serum histamine levels. Previously published results showed significantly reduced DAO activities in  thrombocyte rich plasma of atopic eczema and psoriasis patients explaining their intolerance reactions to histamine, tyramine and octopamine rich foods.1 Diamine oxidase (DAO) is an essential enzyme in the body that breaks down histamine. The body then takes the break-down products (called imidazole compounds) and excretes them through the kidneys into the urine.

Biogenic amines play important role in human body such as: regulation of body and stomach pH, gastric acid secretion, the immune response and cell growth and differentiation. At the same time, amines are important for the growth, renovation and metabolism of every organ in body and are also essential for maintaining the high metabolic activity of the normal functioning and immunological system of the gut. Despite these roles, the consumption of foods with high content of biogenic amines can cause adverse reactions such as nausea, headaches, cardiac palpitation, hot flushes, oral burning, gastric intestinal problems, renal intoxication, rashes and changes in blood pressure. Different biogenic amines can cause different side effects such as: excess tyramine intake could cause hypertension whereas serotonin is a vasoconstrictor. People having deficient natural mechanisms for detoxifying biogenic amines due to genetic defects or due to the intake of antidepressant medicines such as monoamine oxidase inhibitors may experience allergen-type reactions characterized by difficulty in breathing, itching, rash, vomiting, fever and hypertension. 2

Histamine is found in fermented alcoholic beverages, especially wine, champagne and beer,

bacon, salami, luncheon meats and hot dogs,  sour cream, sour milk, buttermilk, sour dough  bread, etc., dried apricots, prunes, dates, figs, raisins, citrus fruits, aged cheese – camembert, brie, blue vein and including goat cheese, walnuts, cashews, and peanuts,  avocados, eggplant, spinach, and tomatoes and smoked fish and certain species of fish: mackerel, tuna, anchovies, sardines.

Psoriasis is considered to be an autoimmune disease and in severe, uncontrollable psoriasis histamine antagonists are of value in reducing disease activity. Histamine formation and release raises the possibility, that histamine is one of the molecules involved in pathogenesis  of autoimmune diseases. 3,5

Tyramine is found in fava beans and tomatoes, broad beans, concentrated yeast extract spreads and bouillons, salamis and mortadella, beer as well as the above foods.

Tyramine, derived from tyrosine, mimics the effects of adrenaline, causing increased heart activity and raising blood pressure. Research has suggested that psychological stress can induce exacerbation of psoriasis. It is further hypothesized that these stress effects on the course and outcome of psoriasis are caused by neuroendocrine modulation of immune functions.4 Excess levels of tyramine releases adrenaline from storage vesicles.4,5 When chronic illness is involved and the body is in a state of chronic stress the adrenal glands begin to work overtime. Over a period of  time the adrenal glands begin to suffer from adrenal fatigue. Impaired adrenal function is associated with the incidence of autoimmune diseases such as skin conditions and arthritis.6

Octopamine is found in green bean, edamame (soybeans), avocados, bananas, pineapple, eggplants, figs, red plums, raspberries, peanuts, Brazil nuts, coconuts, processed meat, yeast as well as the above foods

Octopamine is closely related to the hormone norepinephrine, Researchers studying patients with psoriasis whose psoriasis is associated with increased levels of psychological stress, found that in the psoriasis patients there were significantly increased norepinephrine blood levels compared with non-psoriasis controls. The researchers concluded that there was a positive correlation between the severity of psoriasis and high levels of norepinephrine. 7

There has been a known correlation between Irritable Bowel Diseases such as Crohn’s Disease, Colitis and Irritable Bowel Syndrome (IBS or Leaky Gut), since the 80s. Some researchers have concluded that Psoriasis and IBD are strictly related inflammatory diseases, probably sharing immune-pathogenetic mechanisms. Skin and bowel represent, at the same time, barrier and connection between the inner and the outer sides of the body share similar immune processes which play a key role in maintaining homeostasis and in sustaining pathological processes. 8

 

Solanine is a glyco alkaloid  poison found in species of the nightshade family (solanaceae), e.g. potatoes, tomatoes and eggplant. It can occur naturally in any part of the plant, including the leaves, fruit, and tubers. It is very toxic even in small quantities. Research has shown that the disruption of epithelial barrier integrity is important in the initiation and the cause of inflammatory bowel disease (IBD). Solanine has been found to permeabilize cholesterol-containing membranes, thus leading to the disruption of epithelial barrier integrity. Altered intestinal permeability is believed by some researchers to play a key role in the initiation and propagation of the inflammatory process in conditions other than IBD.9,10  Solanine and related glycoalkaloids are classified as acetylcholinesterase inhibitors leading to increased levels of neurotransmitters which cause prolonged muscle contractions, pain, tenderness, inflammation and stiff body movement. Swollen joints are a clinical manifestation of synovitis and the acute-phase response act as bio marker of pro-inflammatory cytokine production. Solanine may also induce oxidative stress leading to generation of free radicals and alterations in antioxidant and scavengers of oxygen free radicals. 11 There is the potential for solanine to have an adverse effect on psoriatic arthritis. The percentage of arthritic patients who are sensitive to the solanine family of plants might be significantly greater than 10%. A 1982 study published in the Journal of the International Academy of Preventive Medicine demonstrated significant improvements in over 70% of 5,000 (> 3,500) arthritic patients after having eliminated solanine-containing foods from their diets.12

Also read our blog “PSORIASIS and COMORBIDITIES, PSORIASIS and ALCOHOL and PSORIASIS and WATER INTAKE”.

 

REFERENCES

  • Ionescu JG, Constantinescu R, Constantinescu AT; Personalized Anti-Inflammatory Nutrition For Atopic Eczema And Psoriasis Patients; EPMA Journal (2011) 2 (Suppl 1):S157–S165 DOI 10.1007/s13167-011-0118-6
  • Songül ?ahin Ercan, Hüseyin Bozkurt and Çi?dem Soysal ; Significance of Biogenic Amines in Foods and Their Reduction Methods; Journal of Food Science and Engineering 3 (2013) 395-410
  • Nielsen HJ,Hammer JH.; Possible role of histamine in pathogenesis of autoimmune diseases: implications for immunotherapy with histamine-2 receptor antagonists.; Med Hypotheses. 1992 Dec;39(4):349-55.
  • Schmid-Ott G. et al.; Stress-induced endocrine and immunological changes in psoriasis patients and healthy controls. A preliminary study.; Psychother Psychosom.1998;67(1):37-42.
  • Maintz and Novak N.; Histamine and histamine intolerance; Am J Clin Nutr 2007;85:1185–96
  • Physiology of Stress; Chapter 2; http://www.jblearning.com/samples/0763740411/Ch%202_S eaward_Managing%20Stress_5e.pdf
  • Ionescu G,Kiehl R; Increased plasma norepinephrine in psoriasis.; Acta Derm Venereol. 1991;71(2):169-70.
  • 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
  • Patel B. et al.; Potato glycoalkaloids adversely affect intestinal permeability and aggravate inflammatory bowel disease; Volume 8,Issue 5, pages 340–346, September 2002
  • Shah S. Dietary Factors in the Modulation of Inflammatory Bowel Disease Activity.Medscape General Medicine. 2007;9(1):60.
  • Ayad S.K.; Effect of Solanine on Arthritis Symptoms in Postmenopausal Female Albino Rats; Arab Journal of Nuclear Science and Applications, 46(3), (279-285) 2013 27
  • Prousky J. E.; The use of Niacinamide and Solanaceae (Nightshade) Elimination in the Treatment of Osteoarthritis; Journal of Orthomolecular Medicine Vol 30, No 1, 2015

PSORIASIS and SMOKING

skinconditionsblogcategory

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

PSORIASIS and CHEMICAL EXPOSURE to POLLUTION

blog-26

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

PSORIASIS and ALCOHOL INTAKE

lifestyleblogcategoryimage

The course of psoriasis is chronic and over a period of time the condition may be severe and commonly causes emotional problems, which in themselves may lead to relief drinking.1

Psoriasis Alcohol_1Patients with psoriasis experience considerable emotional distress, depression and social isolation due to the visibility of skin lesions, especially when the lesions are widespread and severe. Whilst it would be demeaning to state that all psoriasis patients with mild to severe psoriasis suffer from alcoholism, it has been confirmed in several Quality of Life studies that the percentage of psoriasis patients who admit to having a drinking problem may be as high as 32%. That said, the association between alcohol consumption and increased risk of psoriasis onset and psoriasis worsening has long been suspected.

Alcohol potentially weakens the immune response making psoriasis patients more susceptible to bacterial infections and injuries, which in turn can trigger and exacerbate psoriasis. Case studies have shown a definite connection between high consumption of alcohol and increased severity of psoriasis. Patients with severe psoriasis who misuse alcohol often show improvement after months of abstention or significant reduction in their alcohol intake. Patients who have abstained, improved and then gone on to have a binge drinking session, also experienced more severe flare-ups of their psoriasis upon resumption of drinking.1,2,3 It has also been shown that high alcohol intake is more problematic in the male population than in women.4

Alcohol_1Interestingly in a study of US women, researchers found that the risk for psoriasis varied according to the amount and type of alcoholic beverage consumed. “Non-light beer was the only alcoholic beverage that increased the risk for psoriasis, suggesting that certain non-alcoholic components of beer, which are not found in wine or liquor, may play an important role in new onset psoriasis. One of these components may be the starch-source used in making beer. Beer is one of the few non-distilled alcoholic beverages that use a starch-source for fermentation, which is commonly barley. This differs from wine that uses a fruit-source (grapes) for fermentation. Some types of liquors such as vodka may use a starch-source for fermentation; however these starches are physically separated from the liquor during distillation. Starch sources such as barley contain gluten, which has been shown to be associated with psoriasis. For example, individuals with psoriasis have elevated levels of anti-gliadin antibodies (AgA) and may have a so called ‘latent-gluten sensitivity’ compared to individuals without psoriasis.” 5

This is not to say that other forms of alcohol are then, by default, safe as vodka and other spirits have been shown to increase the severity of psoriasis in other case studies. Alcohol also in general should not be consumed whilst taking various anti-psoriasis medications such as Methotrexate, Cyclosporine, and Acitretin.6

Alcohol also affects the pituitary gland, resulting in reduced secretions of the anti-diuretic hormone that maintains the body’s proper hydration level. More specifically, the kidneys are no longer able to reabsorb sufficient water from your urine, and your body ends up eliminating more water than it absorbs and the person becomes dehydrated. The symptoms of dehydration are fatigue, back and neck pain, increase itch and headaches.

There is still some controversy over safe levels of intake e.g. low and moderate, however, it is still considered prudent to restrict intake whilst on medication. It is certainly recommended for psoriasis patients to reduce or totally restrict alcohol intake, regardless of type, whilst their psoriasis is in a flare up. And when in remission to only consume low to moderate levels of alcohol. All forms of binge drinking should be abstained from.

f you are using alcohol as a crutch to cope with your emotional distress, general stress with work etc. or depression then please seek medical assistance. Also read our blog on “Psoriasis and Water Intake”, “Stress, Anxiety, Depression and Psoriasis” and “Stressed about Psoriasis – Identify Your Stressors and Yours Stress Responses”. Identifying and understanding your stress triggers and finding other ways to cope with your stress and anxiety can help you cut back on your alcohol intake.

REFERENCES

  1. Poikolainen K. Et Al.; Alcohol Intake: A Risk Factor For Psoriasis In Young And Middle Aged Men? ; Bmj Volume 300 24 March 1990
  2. Iva Dediol, Marija Buljan, Danijel Buljan, Vedrana Bulat, Maja Vurnek Živkovi? & Mirna Šitum: Association Of Psoriasis And Alcoholism: Psychodermatological Issue Psychiatria Danubina, 2009; Vol. 21, No. 1, Pp 9–13
  3. Captain G E Vincenti and Dr S M Blunden; Psoriasis and Alcohol Abuse; JR Army Med Corps 1987; 133: 77-78
  4. Zimmerman GM. Alcohol and Psoriasis: A Double Burden.Arch Dermatol.1999;135(12):1541-1542. doi:10.1001/archderm.135.12.1541.
  5. Qureshi AA, Dominguez PL, Choi HK, et al. Alcohol intake and risk of incident psoriasis in US women: a prospective study. Arch Dermatol146(12):1364–9 (2010 Dec).
  6. Vena GA. et al.;The effects of alcohol on the metabolism and toxicology of anti-psoriasis drugs.; Expert Opin. Drug Metab Toxicol. 2012 Aug;8(8):959-72. doi: 10.1517/17425255.2012.691166. Epub 2012 May 17.

 

PSORIASIS – the Relationship with Drugs

researchblogcategoryimage

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 Action Comments
 Beta-blockers  A delayed type hypersensitivity reaction, an immune mediated response and a decrease in intraepidermal cAMP and a consequent increase in peidermal cell turnover Both 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 levels Provokes or induces chronic plaque psoriasis, localized or gnerealized pustular psoriasis and even psoriatic erythroderma.
 Antimalarials  May trigger psoriasis by inhibiting the enzyme transglutaminase Does 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 Medication Symptoms Experienced When Symptoms

First Noticed

  e.g. 15/2  8.00am  Carvedilol   25mg  Blood Pressure New lesions on skin not affecting old lesions 2 weeks after first taking it.
 Or e.g. 15/2  8.00am  Bisoprolol  10mg  Cardiomyopathy Worsening of old lesions After 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

 

Simple Mental/Mind Relaxation Techniques Part 2

lifestyleblogcategoryimage

Are you having trouble controlling your thoughts and finding it difficult to let yourself float in the Full Body Scan Meditation or the Releasing Troubles and Worries Exercise?

simple_mental_part1_5

WELL DON’T WORRY!!!!!!!

Here is a “Thought-Stopping” Exercise that can be used during either the Full Body Scan Meditation or the Releasing Troubles and Worries Exercise or when trying to get to sleep.

In thought-stopping, you would do this exercise FIRST. So lie on a yoga bed for the exercises or in bed to get to sleep.

Think about something that you know is worrying you and will keep you awake …… something troubling you that you will know your mind will churn over and make it difficult to relax or go to sleep.  Force your mind to concentrate on that issue or person e.g. the project at work is in trouble and you know your boss is going to get angry at you and the team. Turn this over in your mind again and again and then suddenly in your mind “Shout Out” STOP!!!!!!. Breath easily and try to relax …… if you feel the issue creeping back into your mind ….. repeat the STOP exercise again and again until your mind releases the thought.

This STOP exercise basically is forcing your brain to recognize when to stop thinking about something …. It abruptly interrupts the thought process and makes the brain shift its focus … this is where the relaxation technique, that you have chosen should now be used.

A number of sites on the internet offer some wonderful guided meditations, and alternative Relaxation Techniques. Below we have listed some of the techniques and their links:-

SAFE HAVEN” – VISUALIZATION – Page 19 http://www.mirecc.va.gov/visn16/docs/Franklin_Relaxation_Therapist_Manual.pdf

QUICK RELAXATION STRATEGIES

https://www.k-state.edu/paccats/Contents/Stress/Quick%20Relaxation%20

Strategies.pdf

 

ABC GUIDED AUDIO MEDITATIONS

http://www.abc.net.au/radionational/programs/lifematters/features/meditation-toolkit/audio-practice/4326674

 

Also read our blog “Stress, Anxiety, Depression and Psoriasis, Stressed about Psoriasis – Identify Your Stressors and Yours Stress Responses, Simple Physical Relaxation Techniques for Psoriasis Patients, Simple Mental/Mind Relaxation Techniques Part 1 – For Psoriasis Patients, Simple Mental/Mind Relaxation

 

REFERENCES

  1. National Center for Health Promotion and Disease Prevention (NCP); Manage Stress Workbook; http://www.prevention.va.gov/mpt/2013/docs/managestressworkbook_dec2013.pdf
  2. Relaxation Techniques for Health: What You Need To Know; National Institutes of Health; U.S. Department of Health and Human Services; https://nccih.nih.gov/sites/nccam.nih.gov/files/Get_The_Facts_Relaxation_Techniques_02-06-2015.pdf
  3. Progressive Muscle Relaxation; http://www.cci.health.wa.gov.au/docs/ACF3944.pdf
  4. Manzoni G.M. et al.; Relaxation training for anxiety: a ten-years systematic review with meta-analysis ; BMC Psychiatry 2008, 8:41 doi:10.1186/1471-244X-8-41
  5. Franklin C.L. et al.: Relaxation Enhancement Therapist Manual; http://www.mirecc.va.gov/visn16/docs/Franklin_Relaxation_Therapist_Manual.pdf