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BACTERIA SKIN COLONIZATION AND INFECTIONS IN PATIENTS WITH ECZEMA

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BACTERIA SKIN COLONIZATION AND INFECTIONS IN PATIENTS WITH ECZEMA

 

CHAPTER ONE

1.1 Background of the study

Relationship between Skin Bacterial Colonization and the Occurrence of Allergen-specific and Non-Allergen-specific Antibodies in Sera of Children with Atopic Eczema/Dermatitis

Syndrome

In this study we investigated skin bacterial colonization,

allergen-specific IgE and antiphospholipid/antinuclear antibodies in 72 children with atopic eczema/dermatitis syndrome (age 2 – 17 years). Bacteria were found on the skin in 41 cases and serological allergen-specific IgE positivity in 37. The different forms of antibodies appeared in the ratio 21/72 (33 antibodies in 21 children).

1.2 Statement of the problem

The occurrence of antiphospholipid antibodies was significantly higher in the patients than in the controls. There were significantly more allergens in the group with bacterial colonization than in the group without colonization.

The SCORAD index showed a significant positive association with the skin colonization. We conclude that there are significant relationships between the occurrence

of Staphylococcus aureus colonization and the levels of inhalant allergen-specific IgE in children with atopic eczema/dermatitis syndrome, and between the occurrence of antiphospholipid IgM positivity and atopic eczema dermatitis syndrome. Key words: antiphospholipid antibody; inhalant allergens; bacterial colonization; Staphylococcus aureus. (Accepted June 26, 2003.)

Atopic eczema/dermatitis syndrome (AEDS) (1) is a chronic cutaneous inflammatory disease that nearly always begins in childhood and follows a remitting/ flaring course that continues throughout life (2 – 4). An

eczematous, severely pruritic disease, AEDS may be

exacerbated by several triggering factors, e.g. allergens,

irritants, seasonal/climate changes and psychic stress.

The disease often moderates with age, but patients

suffer from a life-long skin sensitivity to irritants.

Atopy predisposes patients to various occupational skin

diseases. Most, but not all, individuals with AEDS have

a personal or family history of allergic rhinitis or

asthma (5), along with increased serum IgE antibodies

against inhalant or food allergens (extrinsic type) (6, 7),

or against epithelial antigens (8, 9). The role of IgE

remains obscure, however. The skin bacterial colonization

(as a base of superantigens) and the exogenous

allergens play an important role in the progression of

the clinical status. Antinuclear (ANA) antibodies have

also been observed in an animal model of atopic

dermatitis (10). In addition, the impaired skin barrier,

sweating function (11) and ion content (12) can

contribute to the pathogenesis of AEDS, including

IgE-mediated hypersensitivity against sweat antigen

(13) or epithelial antigens (9). For a better understanding

of the antibody pattern in AEDS (14), we

compared the occurrence of allergen-specific IgE and

antiphospholipid (APL) antibodies, including anticardiolipin

(ACL), and anti-b2-glucoprotein I (Ab2GPI),

as well as ANA antibodies in 72 children with AEDS

from the aspect of bacterial colonization.

1.3 Patients and methods

Seventy-two children (34 boys, 38 girls; mean age 8 years,

range 2 – 17) with atopic eczema/dermatitis syndrome were

included in the study; all were suffering from serious or

medium – severe forms of the disease. The average SCORAD

index (15) was 48.3 (range 24 – 90). The control group

comprised 22 healthy children (10 boys, 12 girls; mean age

8.6 years, range 1.5 – 14). A tampon was used to take samples

from the affected skin for microbiological examination, and

the bacteria were isolated on blood agar medium. The number

of bacteria was determined using a semiquantitative method.

The detection of ANA antibodies was carried out by indirect

immunofluorescence on HEp2 cells. ELISA assays were used

for measuring anticardiolipin and anti-b2-glycoprotein I (16).

Serum total IgE was detected by laser nephelometry. The

allergen-specific IgE was determined by an immunoblot assay

(INTEX Basel). Statistical analysis was performed using

Fisher’s exact test and unpaired t-test and the odds ratio was

calculated.

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