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Eczema and psoriasis: treatment

in adults and children


Sarajevo School of Science and Technology
Sarajevo Medical School

Student: Lamija Šikalo


Subject: Pharmacology II
Professor: doc. Mirsada Čaušević, PhD
Definition
 Eczema is a nonspecific term for many types of skin
inflammation (dermatitis) and irritation that can have many causes.
 It is characterized by red, itchy and swollen inflammated skin (rash),
that develops fluid-filled bumps that ooze and crust.
 Mostly it is a manifestation of Type I hypersensitivity reactions-
immediate IgE mediated reaction
 When an individual is exposed to an allergen, selected plasma B
cells produce allergen-specific IgE, and for significant levels usually
repeated exposure is needed. Mast cells and basophils create
many pro-inflammatory chemicals
Types of eczema
 There are various types of eczema, and among most common ones are atopic
dermatitis, contact dermatitis and „winter eczema”/xerotic eczema.

An acute recurrent eruption of multiple tiny,


Dyshidrotic Eczema intensely itchy water blisters on the palms, sides
of fingers and soles of the feet.

Localized, chronic thick itchy plaques that


commonly occur on the sides or back of the
Lichen Simplex Chronicus
neck, wrists, ankles, lower legs and inner area of
the thighs.

Multiple, round plaques of eczema that are


Nummular Eczema usually associated with dry skin and occur on the
outer surfaces of the hands, arms and legs.

Yellowish-brown, greasy, scaly patches on the


Seborrheic Eczema
scalp, eyebrows, nose and chest.

A chronic eczema on the inner area of the lower


Stasis Dermatitis
legs and associated with varicose veins.
Fig.1: Seborrheic dermatits (American Fig.2. : Stasis dermatitis
Association of dermatology)
Other causes of eczema
Atopic dermatitis
 It is a complex genetic disease, and genetic defects in the
epidermal barrier protein filaggrin are considered to be the major
cause
 immune-mediated, chronic inflammatory disease
 Stratum corneum of those patients has lower levels of natural
moisturizing factor and also are deicient in extracellular lipids
including ceramides
 Family history of asthma, allergic rhinitis, eczematous dermatitis
 The highest incidence is in children younger than 5
 With infants and toddlers, atopic dermatitis usually starts on the face
or on the elbows and knees, flexor surfaces of the extremities
Atopic dermatitis
 Symptoms: vary, but pruritus is always present
 the predominant lesion is an oozing, crusting, coalescent papule.
 In the acute phase, lesions are red, edematous, scaly patches or
plaques that may be weepy. Occasionally vesicles are present.
 In the chronic phase, scratching and rubbing create skin lesions
that appear dry and lichenified.
Fig.7: Chronic AD,
hyperpigmentation
as a consequence
of repeated
scratching
(AAFP)

Fig.5 :Acute atopic dermatitis in its


weeping, blistering form (AAFP)

Fig.6: AD crusts (AAAAI) Fig.8: Lichenification


(Researchgate)
Treatment
 Regular use of moisturizers and skin emolients
 Topical corticosteroids: Improve itching and redness. In initial phase of
treatment, usually 1% hydrocortisone powder in an ointment is given.
 Immune system suppresors and modulators: Cyclosporine PO is good as
short-term treatment as well as maintenance therapy in both adults and
children
 Antihistamines: they do not have effect on inflammation, but are
recommended before sleep to stop sleep disruption
 Antibiotics: Over 90% of AD skin lesions are found to carry
Staphylococcus, compared to 5% on the skin of healthy people. Topical
or systemic.
 Phototherapy
 Antibiotics used in treatment of AD infections usually include:
 Cephalexin (cephalosporine) tablets
 Penicillin oral solution or tablet
 Clindamycin tablets (Lincosamine/b.-static), sometimes in
combination with penicillin
 trimethoprim/sulfamethoxazole (co-trimoxazole) : IV and PO
 Muciprocin topical treatment or intranasally in bleach bath, since
topical treatments are not very effective in S.aureus infections
Steroids
 There are many types and brands of topical steroids. They are
classified in 4 classes: mild, moderately potent, potent and very
potent. They stop production of pro-inflammatory chemicals (PGs,
leukotriens) and cause vasoconstriction, although they are not cure
 Mild: hydrocortisone, methylprednisolon, prednisolon,
alclometasone dipropionate
 Moderate: desoximethasone, bethasone, flumetasone
 Very potent: clobetasol, Diflucortolone valerate and halcinonide
 The stronger the steroid, the greater risk of side-effects. Be careful!
 Adequate dosage (FTU) to prevent adverse effects, skin thinning
Psoriasis
 Autoimmune condition that can be inherited
 The disease may affect, with varying degrees of severity, people of
all ages.
 Psoriasis triggers T cells to attack healthy skin via cytokines TNF, IL-17
and IL-23, the immune system responds by sending more blood to
the area and making more skin cells and more white blood cells.
 Hyperplasia of keratinocytes forms itchy red raised areas (plaques)
and thick scales.
 Scales may come and go, strep throat, URTI, and stress are
considered as potent triggers
 Appear in skin folds, knees and elbows
Fig.9: Childhood psoriasis (PCDS)
Fig.10: Psoriasis scales (Medical News Today)
Treatment
 Moisturization, skin lotions
 Vitamin D analogues: they act on nuclear receptors of keratinocytes, Langerhans cells
and sebaceous gland cells to modulate transcription. They have anti-proliferative,pro-
differentiation and increasing apoptosis effects on keratinocytes and plaques. PO and
topically
 The main analogues are : Calcitriol, Calcipotriol and Tacalcitol
 Given usually topically in combination with corticosteroids
 Topical retinoids (vitamin A derivatives) help in inflammation
 Salicylic acid
 Phototherapy
References

 British Association of Dermatologists. Patient Information Leaflets (PILs). Atopic eczema.


 Lee-Ellen C. Copstead, PhD, RN. Patophysiology. 5th edition.
 Merck manuals: Atopic dermatitis eczema
 H.P.Rang, J.M. Ritter. Rang and Dale’s Pharmacology.
 Medscape. Atopic dermatitis medication. Author: Brian S Kim, MD, MTR, FAAD; Chief Editor:
William D James, MD
Thank you for
attention!

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