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).
Vorwort/Suchen. Zeichen/Abkürzungen. Impressum.