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Clinical Importance of Demodex folliculorum in patients receiving phototherapy. Kulac et al, International Journal of Dermatology 2008, 47, 72-77. Introduction.
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Clinical Importance of Demodex folliculorum in patients receiving phototherapy. Kulac et al, International Journal of Dermatology 2008, 47, 72-77
Introduction • Demodex follliculorum is a 0.3mm long, obligate, hair follicle parasite which lives in cluster in the pilosebaceaous duct and has a pathogenic thought role in pityriasis folliculorum, perioral dermatitis, blepharitis, rosacea, eruptions resembling rosacea, and pustular and granulomatous folliculitis. • The density of mites in healthy skin is age dependant and reaches 100% in elderly people.
One of factors responsible for colonization of mites is development of primary or secondary immunosuppression (AIDS…). • Phototherapy is widely used and is thought to act primarily through its immunosuppressive effects. It also increases the amount of skin surface lipids by direct activation of the function of sebaceaous glands.
Materials and methods Selection of patients: • psoriasis and vitiligo from JAN to Feb 2005 • exclusion criteria: previous or actual rosacea, perioral dermatitis, or dermatosis related to D. Folliculorum, immunosuppression, diabetes, the use of antibiotics and sunbathing in the last three months. -24 female and 21 male (45) 36.61 years and 43 sex and matches healthy controls(outpatient dermatology clinic) -sociodemographic, professions, skin types recorded -PUVA or NBUVB dosage and number of treatments recorded.
Phototherapy protocol applied -Waldmann cabinet -dosage 0,5J/cm2 x phototype 3 times a week with increments of 0,5J/cm2 -for PUVA: oral 8-methoxypsoralen 0,6mg/Kg 90 min before exposure -for NBUVB 0,7MED initial dose and increments of 20%.
Sampling method: -standardised “surface” skin biopsy on forehead, cheek and nasal dorsum= non invasive sampling method which involves placing a drop of cyanoacrylic adhesive on a microscope slide, applying the adhesive-bearing surface of the slide to the skin, and removing it gently after it had been allowed to dry. - scotch test removal, clarification with immersion oil and microscope study performed by the same investigator. -Evidence of D folliculorum was defined if 5 or more mites were present per square centimeter.
Clinical findings and clinical demodicinosis types: -In the patient group, the clinical findings (erythema, telangiectasia, follicular tiny papule, follicular tiny pustule, follicular scaling, papule, pustule, nodule and abscess) were recorded. -clinical diagnosis of demodicinosis was done if microscopic evidence was present.
Statistical analysis -mean and SD. -differences were assessed using X2 and Fisher exact tests in nominal variables. -Intergroup D.folliculorum densities were made using the Mann-Whitney U-test and significance was assumed if p smaller then 0.05.
Results • Demodicinosis was detected more frequently in patients receiving phototherapy than in the control group: 13 patients in the phototherapy group and 3 in the control group. • In 8 of the 13 patients, clinical demodicinosis was present. The 5 other didn’t have clinical signs. • In 6 patients ( 2 NBUVB), the clinical picture was pityriasis folliculorum. • In the 2 other patients (1 PUVA), the clinical picture was rosacea. • 1 patient (NBUVB) perioral dermatitis was present but no demodicinosis was present. • 1 patient for PUVA for psoriasis developed sunburn and developed erythema and pustules on the face and demodicinosis was present.
In those 15 patients, no difference in the number of treatments with PUVA (39.58 +/- 30.81, cumulative dose 78.07 +/- 69.82 J/cm2) and NBUVB (48.54 +/- 32.01, CD 171.22 +/- 193.59 J/cm2) -No difference in the skin types -Demodicinosis in 7 of 12 patients with PUVA and 6 of 33 patients in NBUVB -The highest density was found on the cheeks
Discussion • This is the first study relating demodicinosis and phototherapy. Only on case report was available in the literature. • The increase in D folliculorum may have been caused by immunosuppression and enlargement of the sebaceaous glands as a result of phototherapy. • It is also well known that rosacea is exacerbated by sun and heat. • Although the pathogenic relationship between D.folliculorum, rosacea and sunlight is not completely understood, it is possible that increased blood flow in dilated papillary dermal vessels by the effect of solar radiation may provide a favorable environment.
Rosacea is always associated with solar elastosis, and solar degeneration of connective tissue is important in its origin. There is also a seasonal tendency for rosacea to be exacerbated in the spring (sebum production also increases in the summer and after 4 days of UV irradiation)
Immunosuppression, old age, topical and systemic steroids, calcineurin inhibitor usage and diabetes are predisposing factors for demodicinosis. D folliculorum increases in incidence in patients with AIDS, diabetes and hematologic malignancies. (T cell deficiency, decreased CD3+, CD4+, CD8+, CD16+, CD3+/CD20 ratio, 2,5 times increased CD95+ (apoptosis marker) for selection of T and B lymphocyte selection). • the incidence of demodicinosis in patients on phototherapy is similar than in patients with hematologic malignancies.
Conclusion • Immunosuppression and sebaceous gland enlargement from phototherapy can contribute to the development of demodicinosis. The authors believe that demodicinosis should be included in the differential diagnosis of facial eruptions in patients receiving photoherapy. It is therefore recommended to perform a routine surface skin biopsy in that case