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Seborrheic dermatitis
The document provides a comprehensive overview of seborrheic dermatitis, detailing its definition, etiology, risk factors, epidemiology, pathophysiology, and management guidelines. It highlights the condition's clinical symptoms and signs, especially its effects on sebaceous-gland-rich areas of the skin, while offering insight into common treatments and their complications. The document also includes differential diagnoses and emphasizes the importance of patient education and follow-up care.
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Seborrheic dermatitis
- 1. Comprehensive overview of "seborrheicdermatitis” further evidence showing the effectiveness and safety of pimecrolimus Almansouri Daifallah MD
- 2. Outcomes • Terminology: – – – – • • • • • • • • • • • • • • • • • • • Origin: Arabic: French: Synonym: Definition. Etiology Risk factors Epidemiology Pathophysiology Dermatopathology Local Symptoms Systemicsymptoms: Signs Investigation, and DDx, DDx Complications Prognosis Psychological impact Guidelines Priscription table of 1st line medication dose 2 commonest and 2 most serious side effects: Patient education Progression, severity and response assessment methods
- 3. Definition • Seborrhoeic dermatitis(SD) is chronic-recurrent common skin inflammation affect sebaceousgland-rich areas of skin causes scaling. • Dandruff(pityriasis sicca): mildest form of seborrhoeic dermatitis “scaling without inflammation”. • Cradle cap “ ” : is transient form of seborrhoeic dermatitis affecting infants. • SD may be presoriatic stage and may associated with psoraisis and called “seborrhiasis”
- 4. Terminology – Origin: • Seborrhic:adjective from “sebum” and means that the disease particularly affects the sebaceous-gland-rich areas of skin. But not caused by seborrhoea. • Dermatitis: derma: skin, -itis: inflammation. – Arabic: – French: dermatite séborrhéique – Synonym: Dandruff(pityriasis sicca), cradle cap.
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- 6. Etiology • Unknown • Possiblefactors: – ? Malassezia species – ? Immune response: decrease some immunity component. – Genetic; small role.
- 7. Risk factors • HIV;10X and resistant • Neural diseases; Parkinson disease, facial palsy • Neuroleptic medications • Emotional stress
- 8. Epidemiology • % • Twopeaks: infant after 2 wks + 20s -30s. • M>F
- 9. Pathophysiology Genetics: Immune system NB. Theamount of malassezia is not changed. Malassezia species •Helper T cells, phytohemagglutinin and concanavalin stimulation, and antibody titers Malassezia globosa• Malassezia furfur• Malassezia restricta• Malassezia grow and secrete lipases This lipase hydrolyzes sebum TG into > unsaturated fatty acid (non-uniform) > penetrating the skin cause > epidermal hyperprolifration (causes parakeratosis) and inflammation (causes spongiosis) >flakes shedding , loss skin barrier function. RESULT: Inflammation > pruritis. Hyperprolifration> flakes = SD
- 12. Summery of pathophysiology •Malassezia ecosystem and interaction with the epidermis. • Initiation and propagation of inflammation; • Disruption of proliferation and differentiation processes of the epidermis; and • Physical and functional skin barrier disruption.
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- 14. Local symptoms andsigns Symptoms • Pruritus • sensation of tightness “dryness”. • Hair: alopecia and less shine. Aggravated by: winter, dry, indoor, sweating. Signs • Skin: Orange-red “erythema” OR grey white. • Scaling macules: white/ greasy/ yellow orange. • Dryness “sensation of tightness”. • Hair: brittle narrow hair.
- 15. Corona seborrhoica Where? confined toareas of the head and trunk where sebaceous glands are most prominent. Classification: area based
- 16. Classification: Head • Areas: –Scalp, – eyebrows – eyelashes (blepharitis) – beard (follicular orifices)
- 17. Classification: face • Areas: •forehead (“corona seborrhoica”), • nasolabial folds • eye-brows • Glabella
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- 19. Classification: Body Folds Areas: • • • • • • Axillae, Groins, Anogenitalarea, Submammary areas, Umbilicus, Diaper area Description: diffuse, exudative, sharply marinated, brightly erythematous eruption; erosions and fissures common. Tx: Same as other areas but Castellani's paint is very effective
- 20. Management (nice+aad) I. Removecrust: salicylic acid, olive oil, coal tar shampoo. II. Ketoconazole 2% shampoo I. II. III. If failed > Selenium sulphide shampoo 2.5% or ciclopirox 1%. If no compliance > zinc pyrithione shampoo If symptoms subside > continue: once week for 2 weeks. III. Severe itching: potent steroid I. betamethasone valerate 0.1%, II. hydrocortisone butyrate 0.1% III. mometasone furoate 0.1%. Nb. Steroid not applied on bear. IV. F/U not required unless complicated or resistant
- 21. Prescription Medication Route dose salicylic acid shampo o Message forfew Once daily minutes after wetting hair One month Ketoconazol e 2% shampoo shampo o left on for five to Twice/week ten minutes One month Pimecrolimu Cream s 1% fluocinolone shampo acetonide o 0.01% frequency duration Twice daily ≤30 mL 2-4 weeks safe Once daily 2-4 weeks Quick Zinc + B6 retinoic acid Spec Indicati To exclude deficiency orally 1mg/ Kg daily 2 weeks Very severe
- 22. Medication SE Medication Contraindications salicylic acid Sickchild or < 2yr Ketoconazole 2% shampoo Safe for pregnant SE Management Irritation/ burning sensation dryness fluocinolone acetonide 0.01% hypersensitivity to peanuts over-the-counter conditioner TC complications Stop immediately. Very safe, rarely; irritation Subside within 1st day Pregnancy; Cat C Pimecrolimus
- 23. DDx Disease Face Differentiation Smear for bacteria Pitryasisrosea KOH Pitryasis varsicolor Other Response to Rosacea Tx Impetigo Trunk Rosacea KOH Dermatophytosis KOH Mild psoriasis vulgaris Indistinguishable
- 24. Dandruff • Dandruff isdesquamation without inflammation. • Tx: zinc pyrithione shampoo 1 to 2%.
- 25. SD-like lesions • B6or zinc oxide deficiency.
- 26. Follow Up • Responseassessment: • Relapse is prevented by once/ week antifungal shampoo usage.
- 27. Summary • Flaking andpruritus are hallmark of SD.
- 28. References • http://www.pgbeautygroomingscience.com/r ole-of-lipid-metabolism-in-seborrheicdermatitis-dandruff.php • http://www.ncbi.nlm.nih.gov/pubmed?term= 6220754 •http://www.medicaljournals.se/acta/content/ ?doi=10.2340/00015555-1382&html=1
Editor's Notes
- #8 The prevalence has been estimated to be around 35 percent among patients with early HIV infection, and up to 85 percent among patients with AIDS Patients with Parkinson disease often have increased sebum production; in these patients seborrhea and seborrheic dermatitis improve with L-dopa therapyThe reason for the increased susceptibility of patients with HIV infection to seborrheic dermatitis is not known.
- #10 Malassezia hydrolyze human sebum, releasing a mixture of saturated and unsaturated fatty acids. They take up the required saturated FAs, leaving behind unsaturated FAs. The unsaturated FAs penetrate the stratum corneum and due to their non-uniform structure breach the skins barrier function. This barrier breach induces an irritation response, leading to dandruff and seborrheic dermatitis.The Malasseziaspp that have been most commonly associated with SD are M. globosa and M. restricta, both of which are commensal yeasts that require an exogenous source of lipids.
- #14 Spongiosis is mainly intercellular[1] edema (abnormal accumulation of fluid) in the epidermis,[2] and is characteristic of eczematous dermatitis, manifested clinically by intraepidermal vesicles (fluid-containing spaces),
- #22 Pimecrolimus belongs to a family of calcineurin inhibitors that affect T-cell activation, which is a critical step in the cascades inflammation involved in many skin disorders. There is also evidence to suggest that pimecrolimus has direct effects on the release of exogenous IL-2inhibition of pro-inflammatory mediators released from mast cells, such as histamine, serotonin, and B-hexosaminidaseblinded trial of patients with facial SD (N=40), 83 percent of patients achieved complete clearance after two weeks of twice-daily application of pimecrolimus 1% creamThis results in inhibition of T-cell activation, which causes downregulation of the release of proinflammatory cytokines without alteration of fibroblast activity or vasculature proliferation.11–13 Therefore, application of topical pimecrolimus does not cause dermal atrophy or telangiectasia formation.