Lec 5
Alopecia
- It is partial or complete hair loss.
- It may be cicatricial or non-cicatricial
Cicatricial Alopecia:
- It's characterized by presence of scarring and
absence of follicles.
Causes:
1- Physical injuries:
*trauma
*radiation
*burns
2- Infections
*fungal
*bacterial
*protozoal
3- Neoplasms
*basal cell carcinoma
Non-cicatricial Alopecia
- It is characterized by total devoid of hair with
smooth soft skin and absence of scar, or erythema.
- It may be localized or diffuse.
- It may be primary (alopecia areata) or secondary
*Secondary:
a- endocrine: DM, Hypo-or hyperthyroidism,
androgenic alopecia.
b-drugs: cytotoxic drugs, antihyroid, oral
contraceptives
c- systemic: anemia, DM.
Alopecia Areata
Etiology:
*genetic
*autoimmune
Precipitating factors:
*emotional stress
*focal sepsis
Classification
*Alopecia areata monolocularis describes baldness in only
one spot. It may occur anywhere on the head.
*Alopecia areata multilocularis multiple areas of hair loss.
*Alopecia areata barbae may be limited only to the beard
*Alopecia totalis the patient loses all the hair on the scalp
*Alopecia universalis If all body hair, including pubic hair.
Alopecia areata totalis and universalis are rare.
Clinical picture:
Single or multiple, well defined patch totally
devoid of hair with smooth, soft skin.
Treatment:
1- Topical
*corticosteroids: it act by increase blood flow to scalp
*irritant by capsicum or garlic.
2- Systemic
*corticosteroids (in progressive lesion)
*Vitamins (Vit A and zinc)
The duration of therapy about 3 weeks
This disorder has good prognosis and usually spontaneous
recovery occur
Corticosteroids Injections into the scalp. This type of
treatment is repeated on a monthly basis. Results may
take up to a month to be seen.
Androgenic alopecia (genetic)
- Androgen hormone helps in the production of fine
thin hair till follicle loss its activity (no hair on scalp).
Diagnosis:
*Family history
*Presentation (gradual loss of hair)
*Location:
- Male: M pattern, then on vertex, then on side, then
to the back then complete baldness
- Female: around midline, scalp color appears till
sparing hair at front.
Treatment
1- Minoxidil 2% for female, 5% for male, Topically
twice daily, best results after 12 months, if stop
→ hair loss
- Mechanism: it is a vasodilator. Hypothetically, by
widening blood vessels and opening potassium
channels, it allows more oxygen, blood, and
nutrients to the follicle. This may cause follicles
in the telogen phase to shed, which are then
replaced by thicker hairs in a new anagen
phase.
Lab investigations:
Men with androgenic alopecia have:
1-higher levels of 5-alpha-reductase, and higher
levels DHT.
5-alpha-reductase is responsible for converting
free testosterone into DHT
2- Sex hormone binding globulin (SHBG) is lower,
which is responsible for binding testosterone
and preventing its bioavailability and conversion
to DHT
Treatment
-Indication of minoxidil (Hairback lotion®):
Once or twice daily and leave for 4 hours without washing
to help good absorption
- Minoxidil stimulates hair follicles and growth, but does
not reduce DHT or the enzyme responsible for its
accumulation around the hair follicle, 5-alpha reductase,
which is the primary mediator of male pattern baldness
in genetically susceptible individuals. Therefore, when
treatment is stopped, the DHT has its expected effect of
shrinking and ultimately destroying the genetically
predisposed hair follicles.
Side effects:
- Hypertrichosis on skin so avoid contact with face or skin
-Mild hypotension
2- Anti androgenic hormone (oral finasteride)
is not indicated for women and is not recommended in
pregnant women (may be used only by physician
specially in female with hormonal imbalance) Treatment is
effective within 6 to 8 months of treatment.
Side effects include decreased libido, erectile dysfunction,
ejaculatory dysfunction, gynecomastia, and myopathy.
Treatment should be continued as long as positive results
occur.
Dietary Supplement: A dietary supplement, TRX2 (protein),
similar to Minoxidil, TRX2 works by reactivating
potassium channels. The treatment contains L-Carntine-
tartrate, which has been documented to induce hair
growth in humans.
Vitiligo
It's acquired idiopathic leucoderma.
Etiology:
1- Genetic
2- Autoimmune
3- Neurogenic (catecholamine released at the
peripheral nerve endings, results in inhibition of
melanogenesis and destruction of melanocytes).
Clinical picture:
- Symmetrical, asymptomatic milky white
macules of different sizes and shapes.
- Lesions appear first on sun exposure areas e.g.
dorsa of hands, feet, elbow, or areas normally
hyperpigmented e.g genitalia.
- Borders of lesion may be hyperpigmented or
erythematous.
Treatment
1- Systemic
A- Repigmentation
*Psoralen (meladenine ®), orally followed by
exposure to UV (PUVA).
(N.B. Topical psoralens cause severe allergic or
phototoxic reactions)
-Psoralen and ultraviolet A light treatment (PUVA) involves
taking a drug which increases the skin's sensitivity to
ultraviolet light. The skin is then exposed to high doses of
ultraviolet A light. Treatment is required twice a week for
6–12 months or longer.
Narrowband ultraviolet B (UVB) phototherapy is now used
more commonly than PUVA as it is less damaging to the
skin
UVB phototherapy
Treatment can take a few weeks if the spots are on
the neck and face and if they existed not more
than 3 years. If the spots are on the hands and
legs and have been there more than 3 years, it
can take a few months. In a clinic the treatments
are done 2–3 times a week, and at home every
day, which makes the home treatments more
effective.
* Studies have shown that immunomodulator
creams such as tacrolimus ( Elidel and Protopic)
also cause repigmentation in some cases, when
used with UVB narrowband treatments
*Kheilin + UVR
*meladinine precursor (methoxsalen) followed by UV exposure
Duration for 2-4 months (ultrameladinine ®)
*Corticosteroids (to control rapidly progressive vitiligo)
B- Depigmentation (fading the rest of the body)
Hydroquinone cream
2- Other lines of treatment
*Topical steroids
*Topical 5-fluro-uracil
*Topical 20% monobenzyl ether of hydroquinone for residual areas of
hyperpigmentation (bleaching agents).
Side effects of topical steroids:
-Epidermal atrophy (thinning)
-Telangiectasia (prominent surface blood vessels)
- Striae (stretch marks)
Urticaria
- Commonly referred to as hives
- It is may be a response to allergic or non-allergic factors.
- Most cases of hives lasting less than six weeks (acute
urticaria) are the result of an allergic trigger.
Chronic urticaria (hives lasting longer than six weeks) is
rarely due to an allergy (unknown (idiopathic) cause.
-It's characterized by appearance of wheals (raised areas
surrounded by raised base) which resemble stings of nettles.
- This wheels are transient pruritic erythematous edematous
swellings of the dermis and subcutaneous tissues.
- The wheals appear suddenly and resolve
spontaneously within few hours and disappear
without trace within 24 hours of onset, but the
lesions may recur subsequently at the same or
different sites.
- Urticaria may be acute (if the lesions stop to
appear within 2 months of onset) or chronic
(the lesions continue to recur for more than 2
months).
Clinical picture
- It start with acute intense itching followed by
appearance of erythematous whitish edematous
papules, or patches surrounded by red halo which
develop into wheels.
-It occurs at any part but tend to be on the
covered parts of the body.
-The wheals may be few or multiple and may
coalesce together to cover a large area of the
body surface.
- The patent may feel itching, burning, or prickling
sensation.
Pathogenesis
- The urticarial wheals results from dilatation of
the capillaries and small venules lead to
increase capillary permeability, this allow
proteins and fluids to extravasate into the
dermis (wheel).
- Histamine is the most important mediator to
this reaction it's derived from mast cells
present around the capillaries. This process can
be the result of an allergic or nonallergic
reaction, differing in the eliciting mechanism of
histamine release.
Factors provoke urticaria:
1- Allergic factors
A- Exogenous (lead to acute urticaria)
*ingested food: eggs, milk, fish, bananas, chocolates,
tomatoes, spices.
*inhaled substances: pollen dust, perfumes, feather
*injected: penicillin.
*Contact: some clothes, chemicals, or drugs.
Drugs such as: dextroamphetamine , aspirin, ibuprofen,
penicillin, clotrimazole sulfonamides anticonvulsants,
antidiabetic
*Physical agents: cold, heat.
*Exercise, sweating, stress, or any activity leading to a
warming of the core body temperature, such as warm or
hot baths or showers (Histamine is believed to be
discharged in response to stimulation by the
parasympathetic nervous system.)
B- Endogenous
*Parasites, bacterial toxins. (lead to chronic
urticaria)
*Trauma, burns, (lead to acute urticaria)
2- Non-allergic
*Psychogenic
*Insect bites
Treatment
1- Identify the cause by careful history
2- Antihistaminics: orally in chronic urticaria, IM or IV in
acute cases avil®.
3- Systemic corticosteroids only in acute severe resistant
urticaria.
4- Adrenaline (s.c) in acute cases.
5- Mild tranquilizers (if the precipitating factor is psychic
stress or in resistant cases.
6- Local soothing lotions e.g calamine lotion.
Psoriasis
- It's a common genetically determined chronic
disease of the skin
- It’s autoimmune disease that affects the skin. It
occurs when the immune system mistakes the
skin cells as a pathogen, and sends out faulty
signals that speed up the growth cycle of skin
cells.
- The initial lesion is papule, but later (chronic cases)
it's characterized by the presence of sharply
demarcated, dull-red scaly plaques particularly on
extensor skin surface.
Classification
*Non-Pustular psoriasis (chronic stationary psoriasis,
plaque-like psoriasis) is the most common form of
psoriasis. It affects 80 to 90% of people with psoriasis.
Plaque psoriasis typically appears as raised areas of
inflamed skin covered with silvery white scaly skin.
These areas are called plaques.
*Pustular psoriasis appears as raised bumps that are filled
with noninfectious pus (pustules). The skin under and
surrounding the pustules are red and tender. Pustular
psoriasis can be commonly to the hands and feet or
generalized with widespread patches occurring
randomly on any part of the body
*Nail psoriasis: produces a variety of changes in
the appearance of finger and toe nails. These
changes include discoloring under the nail plate,
pitting of the nails, lines going across the nails,
thickening of the skin under the nail
*Guttate psoriasis: is characterized by numerous small,
scaly, red or pink, teardrop-shaped lesions. These
numerous
spots of psoriasis appear over large areas of the body,
primarily the trunk, but also the limbs and scalp.
*Additional types of psoriasis include: psoriatic arthritis,
napkin psoriasis
Etiology
1- Predisposition
Positive genetic basis.
2- Provocation
*Trauma infection
*Endocrine factors Climate
*Light psychogenic
*Drugs
3- Pathogenesis
- 1st theory:
Psoriasis is a disease of defective inhibitors of
epidermal proliferation. Thus it represents excess but
controlled cellular inflammation and proliferation
(fault of epidermis and keratinocytes).
- There is an eight fold shortening in epidermal cell
cycle (8-10 days in psoriasis and 56 – 75 days in
normal skin).
2nd theory (immune-mediated):
In which the excessive reproduction of skin cells
is secondary to factors produced by the
immune system. T cells (which normally
protect the body from infection) become
active, migrate to the dermis and trigger the
release of cytokines (TNF-alfa) which cause
inflammation and rapid production of skin
cells.
Clinical picture
- Initial lesion is papule, dusty red in color,
covered by silvery white scales.
- On scrapping, scales are removed
successively leaving lastly a glistening membrane.
- On removal, multiple bleeding points are
noticed "Auspitz sign"
Sites:
- Scalp
- Flexures
- Penis
- Nails
- Hands and feet
Treatment
- General measures
*Physical and psychological rest.
*General care of health (hospitalization).
*Mild sedation
*Emolients to minimize skin dryness (carbamide
cream)
*Balenotherapy (bathing in water containing salts,
with natural exposure to sun)
*UVB phototherapy (290-320 nm).
- Topical Therapy
*Tar therapy
- it act by ↓ the number and the size of produced
epidermal cell.
- It is less frequently used now due to many
side effects which are:
- increase tendency to sunburn (phototoxicity)
- cancer risk in groin and genital area
- make coloration to skin, cloth, and hair
- cannot be used in inflamed area or before UV
exposure.
* Anthralin paste : antiproliferative activity on
keratinocytes
(ingram regimen: anthraline + tar + UV)
*Keratolytics
-Topical steroids (slow epidermal cell division)
-Salicylic acid ointments
combination of steroids and salicylic acid
(diprosalic®)
Calcipotriol (synthetic derivative of calcitriol or
vitamin D) Cream, oint, scalp solution, It is also available in
combination with the synthetic glucocorticoid
betamethasone as betamethasone/calcipotriol
- It has comparable affinity with calcitriol for the vitamin D
receptor (VDR), The vitamin D receptor is found on the cells
of many different tissues including the thyroid, bone,
kidney, and T cells of the immune system. the binding of
calcipotriol to the VDR modulates the T cells gene
transcription of cell differentiation and proliferation related
genes.
*carbamide (urea): promote hydration and remove excess
keratin in dry skin and increase the action of corticosteroid
If the patient doesn’t respond to topical therapy
and phototherapy:
Systemic therapy
*Acitretin: oral retinoid
(act on retinoid receptors in the keratinocytes to
correct abnormal cell differentiation)
*Corticosteroids (not preferable in routine psoriasis
because clearance occurs, but disease breaks
through again leads to increased incidence of side
effects)
*Methotrexate (suppress cytokines secretion, and
epidermal cell division)
Acute toxic effect: bone marrow suppression and
gastrointestinal bleeding. They can be reversed
by folinic acid rescue (to oppose the folic acid
antagonist of methotrexate) (120mg folinic acid
IV or IM in divided doses over 24 hours
followed by 15 mg/kg orally every 6 hours for 48
hours).
Monitoring of WBC, liver function tests
Interacting drugs: aspirin, NSAIDs, sulfonamides,
and probencid
They increase serum conc and toxicity of
methotrexate
. •
*Cyclosporin A (immunosuppressive agent)
Monitoring of renal functions and blood pressure
regularly, and any rise in creatinine or blood
pressure reversed by decrease in dosage or stop
the drug.
Interacting drugs: NSAIDs, aminoglycosides,
ciprofloxacin.
They increased risk of nephrotoxicity, however,
rifampicin, phenytoin and carbamazepine
decrease plasma conc. of cyclosporine.
*Biological agents: infliximab, etanercept
- They are genetically engineered to block specific
steps in the pathogenesis of psoriasis, targeting
T-cells receptors or the cytokines TNF-α.
