Chapter 25 Inflammatory skin disorders—atopic eczema and psoriasis
AETIOLOGY
Atopic dermatitis (eczema) is most frequently diagnosed in infancy, but may continue through the adult years.1 It involves an inherited tendency towards type 1 hypersensitivity reactions, and as such it is common to also see eczema or other allergic conditions (such as allergic rhinitis and asthma) in an individual’s family history.1 The physiological response to the allergen causes chronic inflammation and requires pathology testing for conclusive diagnosis. In particular, a full blood count to identify elevated eosinophil levels and a serum IgE test are both important, and emphasise the allergenic basis of the disease.1 The presentation of atopic dermatitis may vary depending on the life stage of the individual. Infantile eczema tends to involve lesions that are moist, red, vesicular and covered with crusts. They will tend to occur on the face, neck, buttocks and extensor surfaces of the arms and legs.1 Adults may also present with some moist, red lesions; however, these will mainly be concentrated in flexor regions of the arms and legs. More commonly, adults will present with dry, scaling lesions and with lichenification (thick, leathery patches) in the other areas. Pruritus (itching) is a commonly reported symptom irrelevant of the age.1 Over time affected regions may become more sensitive to irritants such as soaps, fabrics and changes in climate (temperature and humidity).1 These irritants impair skin barrier function by damaging the stratum corneum intercellular bilayers, through either the lipid organisation or removing the lipids overall.2 Interestingly, a recent worldwide prospective cohort study (n = 490,102) found the prevalence of eczema in children in countries such as United Kingdom, New Zealand and Australia is increasing by more than 14% per year.3
In contrast, psoriasis is more likely to present in adolescence, although it also has an as yet undefined familial link. The pathophysiology of psoriasis is generally considered to be unknown.4 It has been mostly linked with increased cellular proliferation and hyperkeratinisation of the dermal layer, and has been described as ‘an autoimmune disease with systemic features’,4 due to the presence of T-cells that remain activated and cause the skin to constantly regenerate.4 Like eczema, psoriasis also begins with small red papules, but lesions eventually develop a silvery plaque (although the basal layer remains red and inflamed). Most commonly, psoriatic lesions are seen on the face, scalp, elbow and knees.1 The key inflammatory markers involved in the development of psoriasis is tumour necrosis factor and interferon-γ.5 Another important intracellular compound is cyclic-AMP (cAMP), which is understood to regulate cellular proliferation, although the precise mechanism and resulting effect on psoriasis are still unclear.6
Another observation that may, over time, assist in the understanding of psoriasis pathophysiology is the comorbidity of psoriasis with other conditions such as obesity, diabetes, heart disease and bowel disorders. It has been hypothesised, based on the known aetiology of the former conditions, that diet and lifestyle may therefore play a role in the development of psoriasis. Furthermore, it has been argued that the connection between bowel disorders and skin may be due to autointoxication through intestinal absorption of microbial antigens.4 However, these hypotheses are still unproven and as such the cause and development of psoriasis require further exploration.
A key consideration in the clinical management of psoriasis and eczema is the potential similarity in presentation and sometimes treatment principles of the two conditions, contrasted by the very different pathophysiological nature. Eczema is an atopic, allergic condition, while psoriasis has autoimmune features. With this in mind, it is important to confirm the accuracy of the diagnosis before initiating a treatment plan (see the box on testing for atopy). Generic autoimmune considerations can be found in Chapter 28 on autoimmunity.
RISK FACTORS
The most important identified risk factor associated with both eczema and psoriasis is heredity; this link is much stronger in atopic eczema. The potential to develop an atopic condition of any kind is much more likely if it is already present within the family.1 Further contributing factors worth considering in eczema rely on the identification of irritants. Common examples include strong detergents, wool, specific allergenic foods
COMMON FOOD ALLERGENS IN ATOPY
Foods commonly identified as allergens in atopic dermatitis include:7
TESTING FOR ATOPY
Testing for allergies in atopic conditions can include the following elements:7
(eggs, dairy, fish and nuts), psychological stress and scratching.1,2 Change in climate can also be an ongoing aggravating factor in eczema.2 Psoriasis has more lifestyle risk factors such as smoking, alcohol consumption, stress and obesity.8
CONVENTIONAL TREATMENT
Conventional management of eczema ideally involves identification of the allergens, and perhaps also any aggravating factors. Beyond this, pharmaceutical treatment relies heavily upon topical glucocorticoids to reduce chronic inflammation, and antihistamine to reduce pruritis.1
Management of psoriasis mostly focuses on interventions to reduce cellular proliferation, including glucocorticoids, tar preparations and ultraviolet light. Severe cases may result in the use of methotrexate.1
KEY TREATMENT PROTOCOLS
Gastrointestinal support
GALT AND THE HYGIENE HYPOTHESIS
The gut-associated lymphoid tissue (GALT) consists of Peyer’s patches, lymphoid nodules and the appendix. To induce an allergenic response from a food-based antigen, such as casein in cow’s milk, the compound must be transported into Peyer’s patches from the intestinal lumen. However, a healthy intestinal cell is lined with epithelial cells constituting a thick layer of glycoproteins. In addition to this, further protection is provided by mucins, digestive enzymes and secretory IgA (sIgA). The process of developing immune reactivity to specific antigens is quite complex and involves many types of immune cells within the GALT, and is explained in more detail in Chapter 28 on autoimmunity. However, it has been suggested that larger particles being processed in the B-cells within the Peyer’s patches may result in the development of T helper 2 cell dominance, while immune response to microbes will stimulate T helper 1 cells (see Figure 25.1).10 If this occurs at an early age, it exacerbates the T helper 2 dominance that naturally occurs during gestation as a way of protecting the developing fetus from maternal immunity, and may contribute to the development of atopy.11 It is upon this understanding that the foundations for the hygiene hypothesis are laid. Initially, the rationale behind the hygiene hypothesis was linked to the epidemiological evidence that individuals in developed countries with improved sanitary practices had higher prevalence of atopic conditions. It was argued that this was due to a lack of provocation of the GALT, resulting in a maintenance of T helper 2 dominance.11 However, more recent researchers now suggest that, although this may be true, the same benefit can be achieved by ensuring exposure to commensal gut microbiota, rather than relying on pathogenic infections to stimulate T helper 1 cells and redress the balance.12
into the circulation from the intestinal lumen. As these are processed and excreted through the skin they contribute to the dermal physiological changes associated with skin conditions.9 For this reason, a focus of naturopathic treatment in eczema and psoriasis is gastrointestinal support to promote healthy permeability, and reduce the absorption of undigested peptides and food antigens.
Dysbiosis and immune function
For example, a recent randomised controlled trial (RCT) has indicated that maternal supplementation with Lactobacillus rhamnosus in the final weeks of gestation and up to 6 months postnatally if breastfeeding, concomitant with ongoing supplementation for the infant up to 2 years old, results in a decreased prevalence of eczema in individuals with a strong family history.13 This may be explained by other research, which found that a similar dose of L. rhamnosus also resulted in a decrease in eczema symptoms.14 The difference in this study was the measurement of objective pathology markers such as C-reactive protein (CRP) and interleukin-6. Interestingly, the levels of CRP were markedly higher in the group given L. rhamnosus than the placebo group. From this, it is suggested that the probiotic bacteria result in an inflammatory response being generated from within the intestinal epithelial cells, contributing to the healing of eczema. As CRP inhibits the production of a range of inflammatory cytokines and chemokines, this may contribute to the explanation. Furthermore, interleukin-6 (also increased in the intervention group) stimulates mucosal protein synthesis and IgA production, thereby reducing intestinal permeability and counteracting elevated IgE levels.14 The rationale behind using probiotics to prevent atopy has been reviewed through a meta-analysis focusing on infants and was found to suggest promising results, although further research is needed.15 However, a recent meta-analysis of the use of probiotics to treat eczema did not yield such positive results and as such the relevance of using probiotics to manage an already established atopic condition may be questioned.16
In conjunction with possible probiotics use, some medicinal herbs may be useful, due to their anti-microbial properties; however, research into this approach for the management of eczema has not been undertaken. In particular, using herbs such as Ocimum basilicum,17 Allium sativum18 and Hydrastis canadensis19 may help to reduce the growth of pathogenic organisms prior to reinoculation with beneficial flora via probiotic supplementation.
Intestinal permeability
Intestinal permeability has been proposed to be an important component within the underlying pathophysiology of atopic conditions such as eczema. The concept of intestinal permeability is structured upon the tight junctions that exist between intestinal cells. These tight junctions are built from a number of membrane proteins. A number of factors proposed to increase intestinal permeability such as oxidative stress and inflammatory cytokines are also linked with atopy. This suggests that the relationship between intestinal permeability and eczema may be bilateral. Similarly, psoriasis has been described as a non-specific manifestation of bowel pathology in which undigested peptides and antigens from food and microbes are absorbed into the intestinal portal system and are eventually transported to the skin for elimination.9 This viewpoint is congruent with the traditional naturopathic approach for skin conditions (see the box on alteratives and depuratives in the previous chapter). For more information on the pathophysiology of intestinal permeability and poor food digestion, see Chapter 5 on food allergy and intolerance.
Probiotics are the most validated approach to managing intestinal permeability in eczema. For example, a probiotic mix (L. rhamnosus 19070-2 and L. reuteri DSM-12246) was found to reduce intestinal hyperpermeability.20 However, the same study also found that there was a direct correlation between the lactulose:mannitol ratio (a measure of intestinal permeability) and the severity of eczema (see the box on birth, breastfeeding and atopy). Another probiotic organism, Saccharomyces boulardii, has also been found to reduce intestinal hyperpermeability.21 However, neither of these treatments has been evaluated for the management of psoriasis.
Another important consideration when addressing intestinal permeability is to ensure the adequate digestion of food and therefore prevent large undigested food particles being absorbed. With this in mind, herbs containing bitter principles are often used to provide vagal stimulation of gastric acid. Such herbs include Gentiana lutea, Andrographis paniculata,Taraxacum officinale and Cynara scolymus.22 A similar effect has also been traditionally achieved through diet, by the ingestion of foods such as dandelion leaves, and lemon juice in warm water. An example of a nutrient which may be useful in this situation is zinc due to its role as a cofactor to carbonic anhydrase.23
Immune modulation
BIRTH, BREASTFEEDING AND ATOPY
Breastfeeding is promoted by the World Health Organization (WHO) as an important factor in infant health.24 WHO recommends exclusive breastfeeding up to 6 months, and nutritionally sound complementary feeding starting from 6 months and continuing up to 2 years old and later if appropriate. One rationale behind this stance is the potential risk associated with feeding infants products other than breast milk in developing atopic conditions, amongst other acute and chronic health risks. Breast milk contains a number of physiological factors that benefit the infant, beyond its nutrient composition, and may be important in preventing atopy. These include a range of immune factors designed to reduce the likelihood of bacterial infection, and epidermal growth factor, which assists in the development of the intestinal lining, thereby improving nutrient absorption and reducing sensitisation to foreign particles.24 Colostrum is also provided to breastfeeding infants in the first few days of life, and provides an immune protection to the infant while it becomes accustomed to the newly developing colony of gut microbiota.24 Inoculation with the strains of microbes that constitute the colony is achieved at birth through vaginal delivery. In contrast, infants birthed through caesarean section have a different profile of microbiota, and an increased risk of atopy, suggesting the composition of flora is vital to healthy immune induction.25 Furthermore, preventative supplementation with probiotics given to women in late stages of pregnancy only benefited infants born through caesarean section.26
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