Psoriasis is
a genetically determined inflammatory and proliferatve disease,
characterized by sharply, well defined plaques covered by silvery
scales that appear mainly on the extensor prominence and scalp.
Psoriasis is
an autoimmune disease .Antigen presented to T helper cells lead to
trigerring secreation of cytokines which initiate proliferation of
keratinocytes and expression of adhesion molecules on the
endothelial cells leading to traction of additional effector T cells
from the circulation .These will lead to more secreation of
cytokines leading to more proliferation of keratinocytes which later
present the clinical features of psoriasis.
Psoriasis is
rare in infants and common in children and young age groups.
Diaper
psoriasis that affects infants is usually classified under infantile
seborrheic dermatitis. It was found that five per cent of infants
and children who develop diaper dermatitis, have the classical
lesions of psoriasis later on.
Pathogenesis
Tumor
necrosis factor–
is a key mediator in
the pathogenesis of psoriasis.
Different
pathological changes that occur in psoriatic lesions are:
Increased
cellular activity in the epidermis due to the rapid proliferation of
the epidermal cells.
Increased
skin scaling.
Epidermal
activity is increased
Increased
vascularity of the dermis.
Increase
protein synthesis rate by the skin.
Psoriatic
reaction is cellular and nuclear in the Malpeghian and granular cell
layer.
Fig. 262. Psoriasis & vitilligo
(Immunologic psoriasis) |
Fig.263. Familial psoriasis |
Etiology
The etiology
of psoriasis is unknown. Psoriasis may be inherited as an autosomal
dominant and may be seen running in some families. Evidence has been
presented for single gene autosomal dominant inheritance with
reduced penetration.
The
abnormality in the classic psoriatic lesions is in the
keratinization cycle since keratinocytes mature more rapidly and
reaches the surface of the skin in a shorter time than normal.
Histopathology
The abnormal
features in the pathogenesis of psoriasis include irregular
epidermal proliferation and increased mitotic figures in
keratinocytes, superficial vascular dilatation and proliferation.
Infiltration of lesions with leukocytes, including neutrophils,
lymphocytes monocytes and macrophages.
The main
histopathological changes are:
Hyperkeratosis
and Parakeratosis.
Epidermal
hyperplasia.
Acanthosis
and papillomatosis.
Marked
infiltrate around dilated capillary loops.
In the
Malpeghian layer, neutrophils may accumulate to form the
characteristic spongiform pustules of Kogoj.
Exacerbating
Factors
Trauma:
Psoriasis at the site of an injury is well known (K“obner‘s
phenomenon). Wide range of injurious local stimuli, including
physical, chemical, electrical, surgical, infective and inflammatory
insults have been recognized to elicit psoriatic lesions or
exacerbate the pre-existing lesions.
Infections:
The role of streptococcal infection, especially in the throat, in
provoking acute guttate psoriasis has long been recognized and this
gives an explanation to the improvement of psoriatic lesions after a
course of antibiotics for treatment infections of tonsillitis or
laryngitis.
Endocrine
factors
The early
report that there are peaks of incidence at puberty and at the
menopause has been supported by more recent findings. Generalized
pustular psoriasis may exacerbate by pregnancy, premenstrual, and by
high dose of estrogen therapy.
Sunlight
Although
sunlight is generally beneficial, a small minority of cases of
psoriasis is provoked by strong flares up during summer time on the
sun exposed areas.
Metabolic
factors
Hypocalcaemia
(e.g. following accidental parathyroidectomy) may precipitate
psoriasis.
Drugs
Lithium,
beta-adrenergic blocking agents, practolol, Clonidine, potassium
iodide, amiodarone, digoxin, the antidepressants, trazodone,
hypolipidaemic agent, penicillin, terfenadine, antimalarials may be
complicated by psoriasiform drug reaction. Withdrawal of systemic
administered corticosteroid, as well as of the potent topical
steroid (clobetasol propionate), is particularly associated with
outbreaks of generalized pustular psoriasis.
Exacerbating
effect due to non-steroid anti-inflammatory drugs such as oral
phenylbutazone, oxyphenbutazone, indomethacin, diclofenac,
meclofenamate and isoprofen is well documented.
Psychogenic
factors
Severe
emotional stress tends to aggravate psoriasis.
Clinical
Manifestations
The lesions
in early infancy and childhood may simulate diaper dermatitis.
Erythema
desquamativum or atopic dermatitis, where differentiation between
these lesions are sometimes not easy. Psoriasis is quite common in
children although congenital psoriasis is very rare.
Children and
teenagers often have the guttate type of psoriasis, while older
patients may present with the other different clinical forms and the
severe types of psoriasis such as erythrodermic and the pustular
types.
Different
Morpholgical Types
Psoriasis
Vulgaris
Skin lesions
The primary
lesions are well- defined scaly papular patches covered by silvery
adherent scales. Scrapping the area with a glass slide leaves a
minute bleeding spot (Auspitz sign), which is diagnostic for
psoriasis.
Fig. 263b. Auzpitz sign
Scrapping
of the silvery scaly lesion of psoriasis by a glass slide will
remove the scales and the epidermis exfoliates leaving minute
bleeding points. This is an important sign for differential
diagnosis of psoriasis from other scaly lesions.
Apart from
the cosmetic problem, psoriasis manifests with minimal symptoms and
the skin lesions are usually non-pruritic.
Fig. 264. Psoriasis Vulgaris
(Erythmatous Patches Covered by
Silvery Scales) |
Fig. 265. Psoriasis of hands & Feet |
The lesions
may have different shapes and patterns; vary from solitary round
lesions simulating discoid eczema, fungal lesions, seborrheic
dermatitis or gyrate plaques or generalized erythrodermic patches.
Fig. 266. Psoriasis Vulgaris |
Fig. 267. Psoriasis of Nails |
Fig. 268. Psoriasis of the scalp & Follicular
lesions of the skin |
Fig. 269. Psoriasis of the scalp |
Mucous
membranes: the
tongue, anogenital area may be involved by psoriasis in the form of
whitish patches.
Nails may
be involved showing transverse ridges or pitting of the nail plate.
Scalp lesions
may extend beyond the hairline and this usually differentiates
psoriasis from seborrheic dermatitis, which have greasy scales.
Psoriatic
arthropathy:
arthropathy is rare and occurs in chronic cases. Psoriasis may be
found concomitant with other skin diseases such as lichen planus,
vitilligo, lupus erythematosus pemphigus and pemhygoid.
Psoriasis in
children
Psoriasis is
quite common in children, although congenital psoriasis is very
rare. The disease appears first in the scalp, where lesions appear
as scaly patches on the scalp and may spread later to involve
different skin sites mainly on the extremities and trunk.
Napkin
psoriasis:
Flexural and
guttate psoriasis is most common in children. Apart from the common
forms, several other patterns of psoriasis occur in childhood. The
disease often first appears on the scalp.
Flexural and
psoriatic intertrigo in children: Interdigital Tinea is uncommon in
children and a toe-cleft intertrigo may be psoriatic. Other flexural
forms also occur.
Infantile
and juvenile pustular psoriasis
Although
this type can affect any age in childhood where in some cases the
onset may begin in the first year. The lesion is usually circinate
or annular. Systemic symptoms are often absent and spontaneous
remissions occur.
Fig.
269b. Infantile psoriasis
( Mis-diagnosed as seborrheic dermatitis)
A history of
an eruption diagnosed as seborrheic dermatitis, napkin dermatitis or
napkin psoriasis is obtained. Fever and toxicity may accompany more
severe forms.
The majority
of children are aged 2 to 10 years old at the time of onset.
Fig. 269 b. Guttate psoriasis
Fig. 269 c. Rupid psoriasis
Guttate
psoriasis
Small
lesions, appearing more or less generally over the body,
particularly in children and young adults, usually after acute
streptococcal infections. The lesions appear as small rounded or
oval patches on the trunk, limbs, scalp and face.
Rupid or
unstable type
This type of
psoriasis is characterized by scaly hyperkeratotic lesions with
concave surfaces, which are unstable and may proceed to pustular, or
erythrodermic type.
Intensive
systemic or topical steroid therapy, hypocalcaemia, acute infection,
over treatment with tar, Dithranol or PUV irradiation and perhaps
severe emotional upset may precipitate this condition.
Erythrodermic
psoriasis
This type of
psoriasis is usually a manifestation of exacerbation of pre-existing
psoriatic lesion as the unstable type. This may follow sensitivity
reaction to different topical applications as tars, anthralin, PUVA,
infections, hypocalcaemia, systemic or topical steroids as
colbetasol used on an extensive body surface for a long period.
|
Fig. 270. Erythrodermic psoriasis
Fig.270b. Erythrodermic psoriasis
|
The
characteristics of the disease are often lost, the whole skin is
involved and there is severe itching (in contrast to other types of
psoriasis, where skin lesions are usually non-itchy). The patient is
febrile and ill. The course is often prolonged where relapses are
frequent and may be fatal.
Fig. 274a. Flexural psoriasis
Follicular
psoriasis: occurs on
the extensor prominence of elbows and knees.
Pustular
psoriasis of Zumbach
This type of
psoriasis is severe, generalized and may be fatal. This is
considered a severe type of psoriasis, due to extensive skin
involvement and usually is accompanied by systemic manifestation
such as hepatitis.
Fig. 271. Pustular psoriasis |
Fig. 272. Erythrodermic & Pustular psoriasis |
Clinical
Features
The onset is
sudden, where iodides and salicylates may act as a triggering
factor. Pus is formed periungual followed by generalized erythema.
Fig. 273. Follicular psoriasis |
Fig. 274. Follicular psoriasis |
Skin
Manifestations
The main
symptoms are pruritus, burning of the skin besides fever; fetid odor
develops due to extensive exfoliation, and oozing. Yellowish dry
crust is formed over a reddish brown shiny surface after drying of
the lesion.
Annular and
other lesions may be seen in acute generalized pustular psoriasis
but are more characteristics of the sub acute or chronic forms of
widespread pustular psoriasis. Lesions begin as discrete areas of
erythema, which become raised and edematous.
Systemic
steroid therapy carries the hazard of disseminated secondary
infections with varicella and other viruses.
Mucous
membrane lesions of
the lips and tongue may lead to superficial ulceration and scaling.
The
prognosis is variable but the disease may terminate spontaneously or
develop into more severe manifestations.
Generalized
pustular psoriasis is well documented in childhood, while
arthropathic psoriasis is rare in children.
Histopathology
of pustular psoriasis:
there is characteristic spongiform pustules in the upper epidermis
lined with swollen epidermal cells and contain polymorph nuclear
leukocytes.
Treatment of
pustular psoriasis:
this type of psoriasis is treated with systemic steroids and ACTH.
Psoriatic
blepharitis and angular stomatitis
The disease
may mimic chronic blepharitis or perleche, usually unilaterally,
with a small plaque of psoriasis on one eyelid extending to the lid
margin or on the cheek at the angle of the mouth.
Psoriasis of
hands and feet: More
extensive chronic lesions may occur with persistent dryness,
hyperkeratosis and fissuring. Pitting of the fingernails may be the
only manifestation for months or even years.
Psoriasis is
usually less severe in summer and worse in winter and this may be
attributed to the beneficial effect of ultraviolet light of the sun.
This phenomenon is clear in cold areas, where sun disappears for
longer time in winter than in the tropical areas.
Acrodermatitis
continua of Hallopeau
Pustular
psoriasis is a disease of middle life. Acrodermatitis may be seen in
children.
The first
lesion starts on a finger or a toe, related usually to a minor
trauma or infection. The skin over the distal phalanx becomes red
scaly and pustules develop.
The nail
folds and nail bed may be involved leading to nail dystrophy. The
proximal edge of the lesion is bordered by a fringe of undermined
epidermis, irregular, often soddens and sometimes proceeded by a
line of vesiculo-pustules. The nail plate may be completely
destroyed.
Bony changes
can occur with osteolysis of the tuft of the distal phalanx. The
free end of the digit may become wasted and tapered, mimicking
scleroderma. In such digits, the circulation may be secondarily
affected so that discomfort is greatest in cold weather.
Acute
Palmoplanter Pustular Psoriasis (Pustular bacterid)
This term
was first used to describe a rare, acute, monomorphic eruption of
sterile pustules occurring on all aspects of the hands and feet. It
begins abruptly so that within a few days large numbers of small 2-4
mm pustules are distributed on the palms, soles, and palmoplanter
aspects of the digits. Sometimes lesions are seen on the dorsa of
the hands and feet.
a)
Fig. 274a,b,c Pustular Psoriasis
b)
c)
The eruption
has a tendency to settle in a few weeks and sometimes only one crop
of pustules develops.
Differential
Diagnosis of Psoriasis
Psoriasis
may simulate different skin diseases
Seborrheic
dermatitis
Sometimes
it is not easily to differentiate seborrheic dermatitis from
psoriasis.
Fig. 274b. Psoriasis of the scalp and the skin
(Silvery and dry scales)
Fig. 274c. Seborrheic dermatitis(Greasy and fine scales, for
D.D )
In
seborrheic dermatitis the lesions are lighter in color, less well
defined and covered with a dull or branny greasy scales.
Eczema at
times develops a psoriasiform appearance, especially on the legs.
Hyperkeratotic eczema of the palms is a common cause of
misdiagnosis.
Lichen
planus
The
violaceous color, glistening surface and presence of oral changes
are usually decisive.
Lichen
simplex can resemble psoriasis closely, particularly on the scalp
and near the elbow. The intensified skin markings, rather ill
defined edge and the marked itching are characteristic.
Pityriasis
lichenoides chronica
Can closely
resemble guttate psoriasis but the lesions are usually less evenly
scattered and have a brownish-red or orange-brown color and are capped
by an opaque, soft, ‘mica-like‘ scale.
Candidiasis
Candida
lesion presents with a glistening, deep red color suggestive of
psoriasis, particularly in the flexures, but scaling tends to be
confined to the edge with small satellite pustules and papules which
are usually evident outside the main area.
Tinea cruris
Has a
well-defined, often polycyclic edge, but Trichophyton rubrum
infections, especially of the palm, cause difficulty in differential
diagnosis. If corticosteroids have been applied, scaling may be
absent, microscopic examination of the scrapings and culture can
settle the diagnosis.
Pityriasis
rubra pilaris
May simulate
psoriasis. The resemblance of pityriasis rubra pilaris may be close,
especially in the erythrodermic phase. The color is generally less
distinct and deeply red, follicular lesions that are apparent and
the horny thickening has a yellowish tinge.
The
psoriasiform lesions of syphilis
May cause
difficulty in differentiation. Other manifestations of syphilis as
condylomata and other signs besides the serological tests for
syphilis help in the differential diagnosis.
Other skin
diseases
Porokeratosis
of Mibelli on the palms and soles, patches of Bowen‘s and
Paget‘s disease and penile erythroplasia may resemble psoriasis,
but the lesions are usually solitary except in chronic arsenical
poisoning. A biopsy may be necessary.
Drug
eruption
This must be
distinguished from psoriasis, particularly the reaction induced by
the beta-blocker (practolol).
Parakeratosis
pustulosa
Is an
eczematous eruption seen in young children and commonly mistaken for
psoriasis, atopic dermatitis or tinea. It affects the skin around
one or more fingernails or toenails, causing subungual
hyperkeratosis and thickening of the free edges of the nail. Scaling
is more marked than pustulation and the lesions have a chronic
course.
Treatment of
Psoriasis
The
physician can treat mild cases of psoriasis. Referral to a
dermatologist may be necessary especially in the following
conditions:
Wide spread
and disseminated lesions.
Exfoliative
lesions and erythrodermic reactions.
Pustular
psoriasis.
Lesions not
responding to the traditional types of medications.
Recurrent
lesions.
-
General
and non-specific measures.
Rest and
mild sedation.
Removal from
a troublesome environment, a holiday or a short stay in hospital may
all help.
Relaxation
in an area where high sunlight exposure is possible, such as the
Dead Sea coast.
Patient
reassurance is very important, convincing him or other contactants
that this type of skin disease is not contagious, can be treated and
needs some patience.
Much care
should be considered in treating psoriasis of infants and young
children, where medications used for adults may cause serious side
effects for these age groups.
-
Tar
therapy
Tar has been
used as topical therapy for more than a century. Goeckerman
popularized its use in psoriasis. Daily application of 2-5% crude
tar, combined with a tar bath and ultraviolet light, has been used.
Scalp
lesions we use an oily preparation of tar that is the oil of cade.
Many
commercial creams, lotions, ointments, gels and shampoos containing
tar extracts are available, which often partially control some cases
of psoriasis but are disappointing in severe disease.
Tar alone is
certainly active in psoriasis as is UVB alone. Coal tar seems to
sensitize the skin to UVA but not to UVB and phototoxicity is of
photodynamic type.
Nevertheless
UVB is more valuable than UVA in conjunction with tar and probably
UVB erythema thresholds prevent UVA exposure sufficient to cause
photosensitization in the Goeckerman regime.
A
combination of 5% crude coal tar and Dithranol was found to be as
effective.
Primary
irritation is uncommon except in unstable psoriasis, and on the
face, genitalia and in the flexures. Allergic contact dermatitis
does occur, but is rare.
Folliculitis
is the commonest side effect.
Reports of
carcinoma in the site of local coal tar treatment is few but may
occur.
Contraindications
of Tar Therapy.
Infants and
young children.
Anogenital
area and axillary folds.
Erythrodermic
or generalized pustular psoriasis.
Pre-existing
folliculitis.
Severe acne.
Sensitivity
to tar and its derivatives.
-
Topical
steroids
It is of
prime importance to begin treatment with mild topical applications
especially in children. If too vigorous successions of therapeutic
procedures are applied, it may be soon found that all effective
methods of treatment have been exhausted.
Mild cases
may need only simple emollients or mild steroid topically as
hydrocortisone ointment.
Combination
of the steroid ointment with salicylic acid or tar, although it can
give good results in older age groups, in children much care should
be kept in mind when prescribing such combinations.
Superior
results with topical steroids occluded by a hydrocolloid dressing as
opposed to plastic film or using (Cordran tape) which is special
tape with fluorinated steroid. This method has also its drawbacks.
Apart from the cutaneous adverse effects, the most potent
preparations or high doses easily suppress plasma cortisol levels,
especially when used for a long period on a wide area of the skin.
This may lead to more absorption of the steroid and more serious
side effects and may induce pustular psoriasis.
N.B.
An amount of
7-g daily clobetasol propionate 0.05% or 0.05% Betamethasone
dipropionate was sufficient to suppress morning plasma cortisol
levels in 20% of patients.
Scalp
lesions need mild steroid lotion and tar shampoos.
Psoriasis of
face and flexural
Much care
should be taken when treating lesions of face, flexural and
genitalia, using only mild steroid, where potent steroids can cause
more complications locally for the delicate skin of such areas.
-
Vitamin
D3 analogues: Calciptrol
(Daivonex) applied once daily to the lesions may give good results
especially, when mild steroid combined with salicylic acid and are
used twice daily.
-
Psoralenes with PUVA or sun light exposurev
Care also
should be considered in using PUVA, PUVB as a line of treatment due
to unwanted side effects and exacerbation of lesions in some
patients where such medications are not indicated for young age
groups less than 12 years of age. Psoralene tablets are taken two
hours before the lesions are exposed to PUVA. The dose of Psoralenes
are adjusted according the weight of patients.
Protect the
eyes by special glasses from the effects of PUVA. If PUVA can‘t be
used, exposure to sunlight which should be in the morning and before
3:00 p.m., where ultraviolet rays decrease after that.
-
Methotroxates:
These drugs
are not used for infants and children due to their hazardous effect
in the young age groups. In adults and older age groups, these may
be used for reluctant, severe psoriasis, which is not responding to
all traditional treatment. Methotroxates should be used under strict
observation and after thorough investigations especially blood count
and liver functions.
-
Other
medications used for psoriasisis:
Clofazimine,
Dapsone and Sulphapyridine are known to enhance neutrophil
phagocytosis and may be helpful in pustular psoriasis.
Infliximab
(3 mg/kg) -(5 mg/kg) is a monoclonal antibody that specifically
binds to tumor necrosis factor-
, blocking its
biologic activity. Infliximab 3-5 mg/kgm. Is well tolerated and can
cause significant improvement of
psoriasis
-
Corticosteroids
Corticosteroids
should be used with extreme caution. Very high doses of prednisolone
followed by an abrupt withdrawal in the treatment of acrodermatitis
continua has precipitated generalized pustular psoriasis.
Small doses
of triamcinolone, in dosage not exceeding 6 mg daily initially and
with maintenance doses of 2-4 mg daily may be effective especially
in severe and erythrodermic lesions.
-
Retinoids
Vitamin A
has long been recognized to have profound effects on epithelial
differentiation and the toxicity of hypervitaminosis A is well
known.
Deficiency
causes cutaneous hyperkeratosis and squamous metaplasia of mucous
membranes.
The term
‘retinoid‘ has been applied to a family of natural and synthetic
analogues of vitamin A.
a.
Isotretinoin
Isotretinoin
was reported to improve generalized pustular psoriasis. Isotretinoin
was also found to be less effective than etretinate in the treatment
of chronic plaque psoriasis.
b.
Etretinate.
Etretinate
has been shown to induce remission in pustular types and appears to
be significantly more effective than PUVA.
In an
attempt to minimize the side-effects associated with long-term, high
dose treatment, clinical improvement was induced with high doses (70
mg etretinate adult dose daily) followed by maintenance of remission
with lower doses (30 mg daily).
c- Acetrtin
( Soriatane) : This is a rettenoid oral drug newly FDA approved for
severe types of psoriasis.It should be taken into consideration all
the precautions and contraindications of its use mainly in child
bearing age groups.
-
Cyclosporin (1-6
mg/kg body weight/day) was found to improve pustular lesions in
adults. Withdrawal of the drug lead to rapid relapse. The side
effects of Cyclosporin need precautions during treatment.
-
Zidovudine (azidothymidine):
AIDS-associated
psoriasis has been reported to clear with oral Zidovudine. This drug
may be the treatment of choice for retinoid-resistant,
AIDS-associated psoriasis, as agents such as methotrexate,
Cyclosporin, PUVA and possibly even topical steroids may be
contra-indicated.
-
Hydroxyurea
Compared
with methotrexate has less side effects as anorexia, nausea and
hepatotoxicity.
Dosage
should rarely exceed 0.5 g thrice daily and sometimes 0.5 g once or
twice daily suffices for maintenance therapy.
-
Fish oil
The
mechanism of action may involve interference with arachidonic acid
metabolism which is one of the major fatty acid components of fish
oil. Fish oil can be used as an adjunctive treatment in psoriasis.
-
Dead Sea
bathing : due to
high salt contents may improve some cases especially if bathing is
followed by sunbathes.
-
Dialysis
and related procedures
Dialysis has
some effect on psoriasis in patients with normal renal function and
that peritoneal dialysis is more effective than haemodialysis,
possibly because substances of higher molecular weight can be
removed in larger quantities.
16-Narrow
band treatment of psoriasis
Narrow-band
UVB Photography
Narrow band laser
treatment for psoriasis and vitilligo has been considered recently
as an effective line of therapy for psoriasis especially cases which
don't respond to the traditional methods of treatment.Although this
type of treatment is expensive,yet it is the line of choice for
those who can afford paying for narrow band costs.
Narrow-band UVB refers to a
specific wavelength of ultraviolet (UV) radiation, 311 to 312 nm.
This range has proved to be the most beneficial component of natural
sunlight for Psoriasis and is promising in the treatment of some
other skin conditions including atopic eczema and vitiligo.
Compared with broadband UVB, in the treatment of psoriasis, Narrow
band UVB treatment has the following features:
* Exposure times are shorter
but of higher intensity.
* The course of treatment is
shorter
* It is more likely to clear
the psoriasis
* Longer periods of
remission occur before the psoriasis reappears
For patients with psoriasis severe enough to require phototherapy,
narrow-band UVB offers efficacy superior to conventional UVB and
appears intrinsically safer than PUVA. However, because it produces
more epidermal damage than wideband UVB, the narrowband treatment
must be used with careful individualization of dosage and patient
monitoring, according to James G. Krueger, MD, PhD.
17- Alefacept is a selective immunomodulator drug
which is recently approved for the treatment of psoriasis. The drug
blocks the effect of the pro-inflammatory cytokine tumor necrosis
factor .
REFERENCES
-
Iselius
L, Williams WR. The mode of inheritance of psoriasis: evidence for
a major gene as well as a multifactorial component and its
implication for genetic counselling. Hum Genet 1984; 68: 73-6.
-
Abel
EA, DiCicco LM, Orenberg EK et al. Drugs in exacerbation of
psoriasis. J Am Acad Dermatol 1986; 15: 1007-22.
-
Abel
EA, Barnes S, Le Vine MJ et al. Psoriasis treatment at the Dead
Sea: second international study tour. J Am Acad Dermatol 1988; 19:
362-4 (letter).
-
Beylot
C, Bioulac P, Grupper C et al. Generalised pustular psoriasis in
infants and children: report of 27 cases. In: Farber EM, Cox AJ,
Jacobs PH, Nall
-
LM,
eds. Psoriasis. Proc 2nd Int Symposium. New York: Yorke Medical
Books, 1977: 171-9.
-
Beylot
C, Puissant A, Bioulac P et al. Particular clinical features of
psoriasis in infants and children. Acta Derm Venereol 1979; 59
(Suppl. 87): 95-7.
-
Beckman
L, Bergdahl K, Cedergren B et al. Genetic markers in psoriasis.
Acta Derm Venereol 1977; 57: 247-51.
-
Arntzen
N, Kavli G, Volden G. Psoriasis provoked by beta-blocking agents.
Acta Derm Venereol 1984; 64: 346-8.
-
Barth
JH, Baker H. Generalized pustular psoriasis precipitated by
trazodone in the treatment of depression. Br J Dermatol 1986; 115:
629-30.
-
Baughman R, Sobel R. Psoriasis, stress and strain. Arch Dermatol
1971; 103: 599-605.
-
Burch
PRJ, Rowell NR. Psoriasis: aetiological aspects. Acta Derm
Venereol 1965; 45: 366-80.
-
Belsito DV, Kechijian P. The role of tar in Goeckerman therapy.
Arch Dermatol 118: 1982; 319-21.
-
Bollag
W. From vitamin A to retinoids: chemical and pharmacological
aspects. In: Orfanos CE, Braun Falco O, Farber EM et al., eds.
Retinoids. Advances in Basic Research and Therapy. Berlin:
Springer-Verlag, 1981: 5-11.
-
Bollag
W. Chemistry and pharmacology of retinoids. In: Farber EM, Cox AJ,
eds. Psoriasis. Proc 3rd Int Symposium. New York: Grune &
Stratton, 1982:175-83.
-
Corbett M. Controlled trials of PUVA and etretinate for psoriasis.
Br J Dermatol 1985; 112: 121-2 (letter).
-
Dobson
RL. The inheritance of psoriasis (editorial). Arch Dermatol 1980;
116: 657.
-
Danno
K, Horio T, Ozaki M et al. Topical 8-methoxypsoralen
photochemotherapy of psoriasis. Br J Dermatol 1983; 108: 519-24.
-
Epstein JH, Farber EM, Nall L et al. Current status of oral PUVA
therapy for psoriasis. J Am Acad Dermatol 1979; 1: 106-17.
-
Krueger GG. Psoriasis; current concepts of its etiology and
pathogenesis. In: Dobson RL, Thiers BH, eds. 1981 Yearbook of
Dermatology. Chicago: Yearbook Medical Publishers, 1981: 13.
-
Farber
EM, Jacobs AH. Infantile psoriasis. Am J Dis Child 1977; 131: 1266
9.
-
Farber
EM, Nall ML. Epidemiology: Natural history and genetics. In:
Roenigk HH, Maibach HI, eds. Psoriasis. New York: Marcel Dekker,
1985: 141-86.
-
Henseler T, Christophers E. Psoriasis of early and late onset:
characterisation of two types of psoriasis vulgaris. J Am Acad
Dermatol 1985; 13: 450-6.
-
Holgate MC. The age-of-onset of psoriasis and the relationship to
parental psoriasis. Br J Dermatol 1975; 92: 443-8.
-
Kavli
G, Frde OH, Arnesen E et al. Psoriasis: familial predisposition
and environmental factors. Br Med J 1985; 291: 999-1000.
-
Jefferson J. Napkin psoriasis. Br J Dermatol 1966; 78: 614-15.
-
Lever
WF, Lever GS, eds. Histopathology of the Skin 6th edn.
Philadelphia: Lippincott, 1983.
-
Mahrle
G. Meyer-Hamme S, Ippen H. Oral treatment of keratinizing
disorders of skin and mucous membraines with etretinate. Arch
Dermatol 1982; 118:97-100
-
Kapp
A, Kemper A, Stop E et al. Detection of circulating immune
complexes in patients with atopic dermatitis and psoriasis. Acta
Derm Venereol 1986; 66: 121- 6.
-
Lerner
MR, Lerner AB. Congenital psoriasis: report of three cases. Arch
Dermatol 1972; 105: 598-601.
-
Pascher F, Wood WS. Erythrodermic psoriasis in children. Arch
Dermatol 1956; 74: 173-6.
-
Wright
N. The cell proliferation kinetics in psoriasis. In: Goldsmith LA,
ed. Biochemistry and Physiology of Skin. Oxford: Oxford
Univer-sity Press, 1983: 203-29.
-
Zachariae H. Epidemiology and genetics. In: Mier PD, van de
Kerkhof PCM, eds. Textbook of Psoriasis. Edinburgh: Churchill
Livingstone, 1986: 4-12.
-
Young
E. The external treatment of psoriasis. Br J Dermatol 1970; 82:
510-15.
Top
|