The effect of a homoeopathic complex in Atopic Dermatitis in children

 

https://ujdigispace.uj.ac.za/bitstream/handle/10210/8324/Olivier.pdf?sequence=1

[Yolande Olivier]

This study aimed to assess the effect of a homoeopathic complex consisting of Graphites 6cH, Histaminum 9cH, Psorinum 6cH and Sulphur 6cH, on atopic dermatitis in children. All the participants of the study received the homoeopathic complex. They were evaluated using the SCORAD index (Scoring of Atopic Dermatitis) and the Children’s Dermatology Life Quality Index.

34 participants who met the inclusion and exclusion criteria were recruited to participate in this pre-test – post-test single group study by means of advertisements placed in and around primary schools in the Gauteng area (with relevant permission given) and in the local newspaper. Participants were also recruited via word of mouth. Once participants were accepted into the study they were allocated into the treatment group which received the homoeopathic complex. The study was done over a four week period. The percentage of the area affected, the intensity of the symptoms, the pruritus and the loss of sleep as well as the quality of life of the participants were evaluated on a weekly basis.

The results revealed that the treatment group showed significant improvements on the percentage of area affected; the intensity of the erythema, oedema, oozing/crusting, excoriation, lichenification and dryness of the atopic dermatitis, as well as itching of the affected area and the degree of sleep loss due to the atopic dermatitis. These improvements occurred in the third and fourth week. This shows that the homoeopathic complex had an effect on reducing the signs and symptoms caused by atopic dermatitis, after two weeks of treatment.

It can be concluded that the homoeopathic complex containing shows potential to have an effect on the signs and symptoms of atopic dermatitis, which warrants further research in this field.

 

INTRODUCTION

Problem Statement

According to the International Study of Asthma and Allergies in Childhood (ISAAC), diseases such as atopic dermatitis, atopic asthma and allergic rhinitis represent major health concerns in many countries (Wahn, 2009). The prevalence of atopic dermatitis has increased significantly

over the past few decades, with highest rates of 45 – 64% occurring amongst preschool children (Butler, 2009), and 40% amongst older children and adults (Manjra, 2005). This increase of prevalence is attributed to environmental factors such as microbial exposure and poor nutrition, which

can lead to atopic dermatitis (Schnopp, 2006). The quality of life of patients suffering from atopic dermatitis and their family members are significantly affected (Manjra, 2005).

Atopic dermatitis is characterized by active skin lesions that are red, flaky, dry and itchy (Fölster-Hols et al., 2007). Atopic dermatitis mostly occurs on the face, scalp and extensor surfaces of extremities in infants. In older children atopic dermatitis commonly occurs in the flexural areas of the body (Schnopp, 2006). The skin usually appears dry and leathery, with hyperpigmented or hypopigmented lesions located in the antecubital and popliteal areas (Porth, 2007).

Pruritus is frequently associated with atopic dermatitis, which leads to scratching and breakdown of the skin barrier; this then allows for entry of environmental allergens and pathogens into the skin and perpetuates chronic skin inflammation (Hauk, 2008).

Atopic dermatitis is thought to occur due to the interplay between susceptible genes, impairment in the function of the skin and gut barriers, aberrant gut microbiota, immunological dysregulations and other environmental factors (Isolauri, 2004). An increase in gut permeability can lead to an increase in the exposure to food antigens (which has been associated with atopic dermatitis) (Sistek et al., 2006).

There is a high prevalence of up to 80% of food allergy being found in infants and young children suffering from atopic dermatitis (Butler, 2009).

Conventional treatment for atopic dermatitis includes antihistamines, topical steroids, antibiotics and systemic steroids, all of which are associated with adverse effects in children (Kalicharan et al., 2005).

 

Homoeopathy is a safe, effective and cost effective way of treating illness by stimulating the body’s own intrinsic healing ability to restore balance (De Schepper, 2007; Lockie, 2006).

Complex prescribing is a method where by single remedies, all of which are indicated for a specific disease, are combined and put into one vehicle. Complexes are used mostly in situations where the physical symptoms outweighs the emotional symptoms, and in such instances a more pragmatic approach may be taken by using combination remedies in low potencies (Lockie, 2006). In this study a complex of remedies was used in the treatment of atopic dermatitis in children.

These remedies included:

Graphites C 6H, indicated for eczema where the skin is rough, hard, itchy and dry (Vermeulen, 2001);

Histaminum C 9H indicated for the inhibition of histamine release that occurs in the body during an allergic reaction (Poitevin, 2006);

Psorinum C 6H indicated for itchy eruptions which occur in the bends of joints, on the scalp and behind the ears (Vermeulen, 2001);

Sulphur C 6H indicated for eczema that is tremendously itchy. Eruptions commonly occur in the hair line, the folds of the skin and the feet (Morrison, 1998).

Homoeopathy may offer a safe and effective alternative treatment for atopic dermatitis, however more research is needed in the field.

Aim of the study

This pre-test - post-test single group research study aimed to assess the effect of a homoeopathic complex consisting of

Graphites C 6H, Histaminum C 9H, Psorinum C 6H, Sulphur C 6H on atopic dermatitis in children.

Evaluated using the SCORAD index (Scoring of Atopic Dermatitis) and the Children’s Dermatology Life Quality Index.

Benefits of the study

This study may show that the homoeopathic complex is effective in reducing the intensity and the frequency of the symptoms of patients who suffer from atopic dermatitis, if positive results are obtained. This would then establish a framework to work within for future larger scale research studies

on the efficacy of the homoeopathic treatment of atopic dermatitis.

 

Atopic dermatitis (atopic eczema) a chronic, relapsing, allergic inflammatory skin disease (Hauk, 2008). The inflammatory response is triggered by the antibody immunoglobulin E (IgE) (Butler, 2009). The body’s predisposition to produce IgE antibodies to allergens is termed atopy (Lang, 2009). People who suffer from atopic dermatitis also stand the risk of developing other IgE mediated diseases such as allergic rhinitis and atopic asthma

and this progression of disease is known as the atopic march (Machinet al., 2004).

Atopic dermatitis can appear as early as the first week after birth and continues into childhood or even into adulthood (Lewis, 1994).

There is a high prevalence of up to 80% of food allergies being found in infants and young children suffering from atopic dermatitis (Butler, 2009).

Older children suffering from atopic dermatitis have been shown to have lower self-esteem, are embarrassed about the state of their skin, lack

self-motivation, and sleep poorly due to the pruritus and inflammation/pain arising from the condition. It has also been shown that children suffering from atopic dermatitis not only do badly at school but they perform poorly at outdoor activities and sports as well (Manjra, 2005).

 

The prevalence of atopic dermatitis has increased significantly over the past few decades, with highest rates of 45 - 64% among preschool children (Butler, 2009), and 40% among older children and adults (Manjra, 2005).

Atopic dermatitis is thought to occur due to the interplay between susceptible genes, impairment in the function of the skin and gut barriers, aberrant gut microbiota, immunological dysregulations and other environmental factors (Isolauri, 2004).

Hereditary factors

Patients who suffer from atopic dermatitis often have a family history of similar conditions (Kumar et al., 2007). It has been shown in certain cases that 60% of adults who suffer from atopic dermatitis have children who developed atopic dermatitis (Wolff and Johnson, 2009).

Skin and gut barrier

If a disruption occurs in the skin barrier transepidermal water loss occurs and dehydration ensues, which causes exacerbation of atopic dermatitis (Wolff and Johnson, 2009). An increasing gut permeability can lead to an increase in the exposure to food antigens (which has been associated with atopic dermatitis) (Sistek et al., 2006). It is estimated that 40% of children suffering from atopic dermatitis have food allergies and experience

flare-ups when they consume milk, eggs, peanuts, soybeans, fish and wheat, all of which are the most common food allergens (Hauk, 2008; Wolff and Johnson, 2009).

Intestinal microflora

The hygiene hypothesis suggests that because of all the advances that have been made with regards to sanitation and our food, microbial exposure has been reduced. Microbial exposure is important, especially from a young age, for the body to develop a proper immune response to different microbes thus decreasing the chances of developing allergies. As a result of the improvements in today’s society, the cell mediated response no longer needs to be as active, and as a result the humoral response becomes over active leaving the patient in a more allergic/atopic state. (Isolauri, 2003). Microbial exposure is also needed to establish a healthy intestinal microflora, which aids in the development of a normal gut barrier, and lessens the likelihood of food allergies developing. The intestinal microflora and gut barrier functions to mount a brief reaction to ingested pathogens and it also ensures hyporesponsiveness to pathogens (Isolauri, 2004). Antibiotics are also known to trigger atopic dermatitis as they decrease the body’s natural intestinal flora allowing for easy access by ingested pathogens into the body (Greene and Harris, 2008).

Immunological dysregulations

Most people with atopic dermatitis have raised eosinophilia and IgE levels, which reflects an increased expression of helper T-cell 2 cytokines. In a patient suffering from atopic dermatitis, the damaged tissue may release autoallergens which in turn could trigger IgE or T-cell mediated responses, thus maintenance of allergic inflammation occurs. Therefore, although IgE responses are triggered by environmental allergens, chronic allergic inflammation in atopic dermatitis could be maintained by endogenous antigens (Wolff and Johnson, 2009).

Environmental factors

There are many environmental factors that exacerbate atopic dermatitis; some of them include the seasons as atopic dermatitis appears to be worse in winter due to the skin being more dehydrated in the winter months. The type of clothing also has an effect especially wool.

Inhalant allergies such as dust mites, pollen and animal dander have also been known to exacerbate atopic dermatitis. The most common things that exacerbate atopic dermatitis include soap, bubble bath, washing detergents, skin moisturizers and chemicals (Wolff and Johnson, 2009).

Pathogenesis of atopic dermatitis

Atopic dermatitis is an immediate (type 1) hypersensitivity allergic reaction. The term, atopy, implies that there is a familial predisposition to

type 1 hypersensitivity reactions (Kumar et al., 2007).

Type 1 hypersensitivity

The type one hypersensitivity reaction is triggered in response to contact to an allergen. This contact activates the helper T-cells 2 (Th2) which  causes the release of cytokine IL-4. IL-4 stimulates the B-cells to release IgE (Kumar et al. , 2007). The IgE then binds to mast cells, which causes a reaction between the bound IgE and the allergen. This reaction destabilizes the mast cells which causes the release of histamine (Greene and Harris, 2008). The release of histamine results in vasodilation, an increase in vascular permeability, smooth muscle contraction and an increase in the  secretion of mucous, all of which form part of the immediate response.

The activation of the mast cells also results in the secretion of several cytokines, which play a role in the late-phase reaction, which is characterized by inflammation and tissue damage (Kumar et al., 2007).

 

Diagnosis

The diagnosis of atopic dermatitis is made by clinical history and the appearance of the skin, and is confirmed by testing for elevated total IgE levels

or specific IgE antibodies to environmental allergens by means of testing for the presence of IgE in the blood.

An IgE reaction to specific allergens can be tested with a skin prick test, immunocap RAST (radioallergsorbent test) or an atopy patch test (Potter, 2008).

The skin prick test consists of introducing a tiny amount of allergen into the skin and then recording the reaction. It involves an intradermal puncture inoculated with an allergen before puncturing the skin. If the skin produces a wheal within 15 minutes (an itchy, red and swollen lesion), it is a positive reaction to that particular allergen. This test is inexpensive and clinically valid; however it cannot be used in patients using antihistamines or any other

immunosuppressive medications. There is also a small risk of anaphylaxis occurring (Allergy UK, 2010; Burns et al., 2004).

The immunocap RAST (radioallergosorbent) test is a blood test which detects specific IgE antibodies to allergens in the blood (Potter, 2008).

This test is more expensive than the skin prick test; it is accurate and gives an objective quantifiable IgE level reading. It can also be used in patients taking allergy medication and there is no risk for anaphylaxis (Burns et al., 2004).

The atopy patch test consists of placing 1cm discs, which are prepared with allergens, on the skin and leaving them for a period of 48 hours. The skin is examined after 48 hours for any redness or swelling, which will indicate a positive reaction (Allergy UK, 2010).

Problems with the atopy patch test is that it can give false-positive reactions, false-negative reactions, unexplained positive reactions and missed allergens from the test (Burns et al., 2004).

Conventional treatment for atopic dermatitis includes antihistamines, topical steroids, antibiotics and systemic steroids (Kalicharan et al., 2005).

Antihistamines block the action of histamine in the body; however they do not stop the interaction between IgE and the antigen. Some of the side-effects may include drowsiness, blurred vision, urine retention and increased heart rate, to name a few (Medterms, 2010).

Antihistamines have great value in alleviating the pruritus associated with atopic dermatitis.

Antihistamines may also be used to control mild symptoms of food allergies (Sweetman, 2009).

Topical steroids are very useful in acute flare-ups as they reduce itchiness and speed up recovery, as they act by suppressing the immune response. These drugs can however cause thinning of the skin, reddening and stretch marks if used over long periods (Lewis, 1994).

Hypopigmentation may also occur with the use of topical steroids. These side effects mainly occur due to the antiproliferative effects on the keratinocytes, and due to the possible interference with the skin flora, which increases the risk of superimposed infections. Topical steroids may also cause systemic side effects but this is all dependent on the chemical structure of the drug, the formulation of the vehicle and the nature of the skin being treated (Sweetman, 2009).

Systemic steroids down regulate pro-inflammatory cytokine production and are very effective in allergic diseases, but have a wide range of adverse effects. Most notably in children they have very serious adverse effects on growth rates and the central nervous system (Davidson, 2006).

By inhibiting the release of various cytokines, systemic steroids have a potent anti-inflammatory effect. Systemic steroids also effect the uptake and excretion of calcium which leads to a decrease in the body’s calcium stores, and thus decreases bone density (Sweetman, 2009).

Antibiotics are prescribed when a bacterial infection, secondary to the atopic inflammation, is suspected. Antibiotics may cause diarrhoea, vomiting,

photosensitivity, auditory and visual hallucinations and will affect the bowel flora, which further increases susceptibility to allergies (Medterms, 2010). Topical antibiotics may be useful where there is a superficial infection of the skin, but applying to large areas of damaged skin is not recommended as

this may lead to systemic toxicity. Antibiotics are only indicated for short-term use as long-term use may lead to bacterial drug resistance (Sweetman, 2009).

Allergic contact dermatitis usually occurs due to local exposure to a substance which the body has been previously exposed to, and the reaction may spread from the initial site of contact. The affected area is very itchy with swelling and vesiculation, with very sharply demarcated borders

(Greene and Harris, 2008).

 

 

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