ATOPIC DERMATITIS (ECZEMA) AND COMORBIDITIES

blog-link-post-img

Atopic dermatitis (AD), also known as atopic eczema, is a chronic inflammatory disorder that causes significant morbidity and has a wide range of allergic and non-allergic comorbid disorders.

Comorbidity is a concurrence of multiple diseases or disorders in association with a given disease. The patient with AD has an increased risk of developing one or more of a number of other diseases/conditions that share many immunological features with AD.

 CHART 1: Comorbidities Associated with AD

Cutaneous (skin) infections including:-

Bacterial – Staphylococcal   / Impetigo contagiosum

Viral – eczema herpeticum

Fungal

 

Other Skin Conditions:

Vitiligo

Psychological and Psychiatric Disorders – Depression

Anxiety

Attention Deficit/Hyperactivity Disorder (ADHD)

Autistic spectrum disorder (ASD)

Food Allergies/Intolerances Cardiovascular Disease – Arterial hypertension/ Atherosclerosis

Stroke

Prediabetes

Diabetes

Obesity

Fatty Liver

Dyslipidemia (Raised cholesterol)

Allergic conjunctivitis

Cataracts 

Atopic keratoconjunctivitis (AKC) 

Allergic rhinitis

Hayfever

Asthma

Acute upper respiratory infection

Acute pharyngitis

Fatigue, insomnia  

1, 2, 3, 4, 5, 6, 7

Most cases of AD begin in childhood or adolescence, with more than 80% of pediatric patients having persistent symptoms of itch and dry skin in adulthood. The early age of onset and disease chronicity, plus impaired quality of life, secondary to AD weigh heavily on a child’s psychological and behavioural development, with delayed social development throughout life and very high rates of psychological and behavioural disorders and quality-of-life impairment.6 Various studies have consistently indicated an association between AD and ADHD which is independent of environmental exposures and other comorbidities. Particularly infant AD appears to be associated with later development of ADHD symptoms. Sleeping problems due to AD are suggested as playing an important role for the observed association between AD and ADHD. Children with previous or prevalent AD have an approximately 43 % increased risk to be diagnosed with ADHD or to display clinical ADHD symptoms.8

Researchers have found that adults with AD have higher rates of cigarette smoking, consumption of alcoholic, lower rates of exercise, and higher classification of obesity with category II / III consistently indicated in children and adults, hypertension, prediabetes, diabetes, and high cholesterol.6, 7

staph-infection

Bacterial superinfection by staphylococcal aureus is the most common complication in atopic dermatitis and is almost always present in AD flares.  S. aureus is an important human pathogen that causes a variety of  infections ranging from localised skin and soft-tissue infections (SSTIs) to severe necrotising fasciitis and life-threatening infections.7 , 8  S. aureus can be isolatedfrom 55–75% of unaffected AE skin, 85–91% of chronic lichenified lesions and 80–100% of acute exudative skin lesions.9 The correlation between AD severity and colonization with S. aureus has already been well documented, and it is generally known that this colonization is an important mechanism involved in the continued aggravation of the disease in patients.

S. aureus has shown a capacity to develop resistance to antimicrobials that were originally active against the species. In 1961, there were reports of strains that were methicillin resistant, and they were called methicillin-resistant Staphylococcus aureus (MRSA). By 1980, MRSA strains became an endemic problem in hospitals in several countries. Reports on MRSA infections in AD patients have been published since 2005. Some authors suggest that MRSA should be considered when patients with AD present with more intense and generalized erythemas (redness of the skin), and with the predominant location of infection in these patients being the face, and a fetid (fishy) odour present. Studies worldwide suggest that the prevalence of MRSA in the population with AD varies from 0 to 30.8% depending upon the country of research.10

Colonization by streptococcus generally precedes the development of impetignized lesions (by about 10 days). Group A streptococci often colonize the pharynx of asymptomatic people, especially school-age children. In cases of infected atopic dermatitis lesions, a high prevalence of co-infection by staphylococci and streptococci was reported, and these bacteria were present in about 70 to 85% of patients. B-hemolytic streptococci are the main cause of impetigo and are more commonly isolated on the skin of people with AD than on the skin of healthy individuals or of those with other skin diseases.11

Eczema herpeticum (EH) is caused by Herpes simplex virus-1 (HSV-1), Herpes simplex virus-2 (HSV-2), Herpes zoster virus, Coxsackie virus, etc. Also, EH may occur in children who have AD after smallpox vaccination. If corticosteroid therapy is used in these patients because of misdiagnosis, the lesions may worsen. Therefore, if skin lesions or another pre-existing dermatitis is aggravated after varicella (smallpox) infection then EH must be considered and antiviral therapy must be started immediately.11

AD, is an immunoglobulin E (IgE)-mediated disease with a complex etiology (cause) that is accompanied by superficial inflammation and itchy rashes. An association with asthma and Allergic rhinitis (Hayfever) is well documented. Fifty percent of all those with AD develop other allergic symptoms within their first year of life. In the International Study of Asthma and Allergies in Childhood (ISAAC), among the 56 countries, the prevalence of AD in children varied significantly from 0.3% to 20.5% but shows consistent trends in increasing disease prevalence over time. The main risk factors for progression and persistence of asthma are early onset, IgE sensitization, and severity of AD. Approximate 70% of patients with severe AD develop asthma compared with 20-30% of patients with mild AD and approximately 8% in the general population. Epidemiologic studies have consistently demonstrated strong associations between rhinitis and asthma. Recent clinical and basic science evidence indicated that the two diseases share anatomical, physiological, immuno-pathological, and therapeutical factors. Allergic rhinitis is an inflammatory condition affecting nasal mucosal membranes. In sensitized individuals, allergens such as pollens, moulds, and animal dander provoke this allergic response.12, 13

The relationship between food allergy and AD is complex and the presence of food sensitization and allergy earlier in life predicts a prognosis of severe AD. Around 50–70% of children with an early onset of AD are sensitized to one or more allergens. These are mainly food allergens (cow’s milk, hen’s egg and peanuts being the foods most frequently involved). Food allergy is actually much more common in children with AD with studies reporting ranges from 20 to 80% of children being affected.12,13

Allergic conjunctivitis (AC), either seasonal and/or perennial, is one of the most common types of ocular inflammation which causes redness and swelling of the eyes. Estimates vary, but these types of allergy are said to affect at least 15–20% of the population and higher incidences in those with AD. Its pathophysiology also involves a type I IgE-mediated immune reaction triggered by allergens contacting surface of the eye.2 Atopic keratoconjunctivitis (AKC) is a bilateral chronic inflammatory disease of the ocular surface and eyelid. Its pathomechanism involves both a chronic degranulation of the mast cell mediated by IgE, and immune mechanisms mediated by Th1- and Th2-lymphocyte derived cytokines. It is considered the ocular counterpart of AD. Eczematous lesions may be found on the eyelids, or any place on the body. Skin lesions are red and elevated. They often occur in the antecubital (inner elbow) or popliteal (behind the knees) regions. Typically, eczematous lesions are itchy, and scratching them makes them itchier. Ocular findings vary. The eyelid skin may be chemotic (inflamed eyelid) with a fine sandpaper-like texture. There may be mild, or severe, red and swollen eyes.14

If you have any questions please do not hesitate to contact our clinic by either emailing us at info@goodskincare.com.au or message us on our Facebook page https://www.facebook.com/PsoriasisEczemaClinic/

 

 REFERENCES

  • Simpson EL.; Comorbidity in Atopic Dermatitis; Curr Dermatol Rep. 2012 March 1; 1(1): 29–38. doi:10.1007/s13671-011-0003-5
  • Augustin M. et al.; Epidemiology and Comorbidity in Children with Psoriasis and Atopic Eczema; Dermatology 2015;231:35–40 DOI: 10.1159/000381913
  • Deckert S. et al.; Nonallergic comorbidities of atopic eczema: an overview of systematic reviews; Allergy 69 (2014) 37–45 © 2013
  • Ellis CN. et al.; Validation of Expert Opinion in Identifying Comorbidities Associated with Atopic Dermatitis/Eczema; Pharmacoeconomics 2003; 21 (12)
  • Gradman J. et al.; Allergic conjunctivitis in children with asthma, rhinitis and eczema in a secondary outpatient clinic.
  • Silverberg J.I.; Eczema and cardiovascular risk factors in 2 US adult population studies; J Allergy Clin Immunol 2015;135:721-8.
  • Silverberg J.I. and Silverberg N.B.; Atopic Dermatitis: Update on Pathogenesis and Comorbidities
  • Baviera G. et al.; Staphylococcus Aureus And Atopic Dermatitis: Which Came First, The Chicken Or The Egg?; EMJ Dermatol. 2015;3[1]:92-97.
  • Leung DYM.; The role of Staphylococcus aureus in atopic eczema; Acta Derm Venereol 2008; Suppl 216: 21–27
  • Petry V. et al.; Bacterial skin colonization and infections in patients with atopic dermatitis; An Bras Dermatol. 2012;87(5):729-34.
  • Celtik C. et al.; A Life-Threatening Condition In A Child With Chicken Pox: Eczema Herpeticum; Open Journal of Pediatrics 1 (2011) 1-3
  • Tao Zheng et al.; The Atopic March: Progression from Atopic Dermatitis to Allergic Rhinitis and Asthma; Allergy Asthma Immunol Res. 2011 April;3(2):67-73. doi: 10.4168/aair.2011.3.2.67
  • Nutten S.; Atopic Dermatitis: Global Epidemiology and Risk Factors; Ann Nutr Metab 2015;66(suppl 1):8–16
  • La Rosa M. et al.; Allergic conjunctivitis: a comprehensive review of the literature; Italian Journal of Pediatrics 2013, 39:18 http://www.ijponline.net/content/39/1/18

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 CHEMICAL EXPOSURE

blog-20

In this blog we will concentrate on the role of physical contact with chemicals and the effect on psoriasis. For Oral Drug Induced Psoriasis please refer to out blog “PSORIASIS – the Relationship with Drugs”

ROLE OF CONTACT ALLERGENS IN PSORIASIS

Various studies have suggested that hypersensitivity to contact  allergens, namely chemicals, in psoriasis is an important and often underestimated, provocative/exacerbating factor in the manifestation and the course of psoriasis.

Dollarphotoclub_80345209 Chemicals

Recently research has focused on allergic contact dermatitis in psoriasis and results have supported the role of contact allergy in provoking psoriatic lesions on palms and soles. Studies of incidence of contact allergy in patients with palmar and plantar psoriasis report the following results:-

  • Positive patch-tests were found in 39.5% of the psoriatic cases with palmo-plantar involvement therefore indicating a significantly greater hypersensitivity to contact allergen in the group of patients with palmo-plantar psoriatic lesions. Some of the allergens that elicited as positive response were – nickel sulphate, epoxy resin, cobalt chloride, phenylenediamine, paraben mix, detergents, potassium dichromate, nickel sulphate, soap for hands, thiuram mix, neomycin sulfat and nickel.1                                                                                                                                                                                                                                                                              
  • In another study in patients with various presentations of psoriasis vulgaris, the researchers concluded that the result of 68% of patients with a positive patch-test, points to delayed type hypersensitivity to contact allergens as a possibly relevant factor in the presentation or course of psoriasis. The most common allergens were tars, nickel sulphate, perfume and balsam of Peru.2.3                                                                                                                                                                                      
  • In another study, the researchers found 19 patients (25%) with different forms of psoriasis (inverse psoriasis, palmoplantar psoriasis, chronic plaque psoriasis, guttate psoriasis and pustular psoriasis) who had positive patch tests. The most common positive patch-tests were to nickel, fragrance mix, coal tar, colophony and neomycin.4                                                                                                                                                                                                                                                                                 
  • Another study reported allergic disease in 21% of patients tested, but a positive RAST test was obtained in 44%. In chronic plaque-type psoriasis a positive RAST test was significantly more common (58%) than in active psoriasis (22%). Grass pollen and house dust mite were the most prevalent sensitizing allergens, with frequencies of 64% and 53%, respectively in the sensitized subjects. Sensitization increased with age and polysensitization was common. Contact dermatitis was verified with patch tests in 12 men and 20 women, of whom 10 had chronic plaque-type psoriasis and 22 active psoriasis. Tar, nickel sulphate, corticosteroid mixture and thiomersal were the most common allergens. No irritant reactions were seen at the concentrations used.5                             

In some of the studies it was found that when the patients with positive patch-tests avoided the topical products containing the incriminated allergens, they showed improvement in their psoriasis. This strongly suggests that hypersensitivity to contact allergens in psoriasis is a relevant provocative/perpetuating factor in manifestations and the course of psoriasis.1

Other research has suggested that there is a possible interaction between the clinical evolution of psoriasis and the production of the cytokines that intervene in immunoreactions involved in cell-mediated responses and in atopy. The Th1 lymphocytes involved in cell-mediated responses seem to act during the active phase of psoriasis, whereas the Th2 lymphocytes active in atopy are active during the non-active plaque-type phase and, for this reason, are more associated with IgE-mediated allergies. In clinical practice, patients with chronic psoriasis are more likely to develop IgE-mediated diseases, whereas in the active phase they will be more affected by contact dermatitis: the greater application of topical treatments during this phase increases the risk of contact dermatitis.5

Researchers concluded that:-

  • Allergic contact dermatitis has a great role in the provoking and maintenance of the psoriasis lesions.
  • Patch-tests should be included as a routine diagnostic procedure in psoriasis, especially in palmo-plantar psoriasis, in long standing psoriasis and in psoriasis resistant to therapy.
  • Avoidance/elimination of selective previously identified materials/antigens with positive patch-test responses may alleviate and make the treatment of chronic, recalcitrant psoriasis more effective.1

The theory proposed for the most likely cause is thought to be due to skin injury caused by exposure to the chemical/material/antigen and the subsequent initiation of the Koebner effect.

See our blog “Koebner Phenomenon”, blog “Psoriasis and Chemical Exposure to Pollution”, “Psoriasis and Smoking” and “Psoriasis and Alcohol Intake”

REFERENCES

  1. Heule F. et al.; Delayed-type hypersensitivity to contact allergens in psoriasis; Contact Dermatitis; Volume 38,Issue 2, pages 78–82, February 1998
  2. Heule F, Tahapary GJM, Belloc R, Van Joost Th. Delayed-type hypersensitivity to contact allergens in psoriasis: A clinical evaluation. Contact Dermatitis 1998; 38: 78 -82
  3. Binden A. D., Muston H., Beck M. H. (1994): Intolerance and contact allergy to tar and dithranol in psoriasis. Contact Dermatitis. 31: 185–186.
  4. Fleming C. J., Burden A. D. (1997): Contact allergy in psoriasis. Contact Dermatitis. 36: 274–276.
  5. Pigatto P.D.; Atopy and Contact Sensitization in Psoriasis; Acta Derm Venereol 2000; Suppl 211: 19-20
  6. Thappa DM. The isomorphic phenomenon of Koebner. Indian J Dermatol Venereol Leprol 2004;70:187-9