5. ●Uv-B (290-320)
●Most of Uv-B is absorbed by the epidermis and
superficial dermis.
●DNA damage and formation of adducts
6. ●Uv-A(320-400)
●Can reach upto mid to lower dermis.
●Uv-A can also produce pyrimidine dimers in DNA
but on a per photon basis it is much less effective.
7. Effects on mast cells
●PUVA treated mast cells have stabilised cell
membranes which l/t decreased release of
histamine.
8. Effects on collagen
●ROI gnerated d/t UVA and PUVA exposure
activate MMP-1----degradation of collagen.
●MMPs are also stimulated as a result of IL-1 and
IL-6 production which is a result of Uva
exposure.
●Sclerotic skin diseases
9. Effects on keratinocytes
●UVB, PUVA, UVA induce acanthosis of
epidermis.
●Accentuation of light scattering by the upper
levels of epidermis.------increase phototherapy
doses progressively so that an equal no of
photons are available for the phototherapy
targets in epidermis and dermis.
●Skin hardening in photosensitivity disorders.
10. Effects on melanocytes
●Uv A exposure causes DNA damage which
stimulates melanocytes because of activation of
DNA repair enzymes.
●In vitiliginous skin the melanocytes in the outer
root sheeth of hair follicle get stimulated
because of the inflammatory mediators released
by keratinocytes.
11. MPD/MED/MTD
MINIMAL PHOTOTOXIC/ERYTHEMA/TANNING
DOSE
MINIMAL DOSE OF PUVA/UVB/UVA1 THAT
PRODUCE A BARELY PERCEPTABLE BUT WELL
DEFINED ERYTHEMA (PUVA/UVB) /PIGMENTATION
(UVA1) WHEN TEMPLATE AREAS OF SKIN ARE
EXPOSED TO INCREASING DOSE OF RADIATION
❑ Previously non exposed skin are irradiated with
increasing dose of radiation ,with rest of body covered
❑Readings are made after 72hrs (PUVA), 24hrs
(UVB/UVA1)
14. Uv-B phototherapy
●2 types of UVB phototherapy : narrowband and
broadband
●NB-UVB : 308-313 nm wavelength
15. ●Psoralen photochemotherapy
●Psoralens are photosensitisers which get activated
upon exposure to UvA radiation.
●Intercalate with DNA and following Uv A exposure
they form a single adduct with DNA and then
become a bifunctional adduct on absorbing a
second photon l/t cross linking of DNA strands.
●Singlet oxygen is also generated----Cox activation.
●
16. UVB Vs PUVA
●UVB does not require psoralen
●Cheaper
●Can be used in pregnancy and childhood
●Does not require post treatment eye protection
●Less carcinogenic
19. DRUGS
NAME TRADE NAME FORMULATIO
N
DOSE
Methoxasalen
(natural)
Oxsoralen
Ultra
8-MOP
Oxsoralen
lotion
10 mg capsule
10 mg/ml
0.4mg/kg – 1 hr
prior to UVA
0.6mg/kg – 2
hr prior to UVA
Trioxsalen
(synthetic)
Trisoralen
Neopsoralen
lotion
5 mg
1%
0.6mg/kg – 2
hr prior to UVA
Bergapten
(5-methoxy
psoralen)
available in
Europe
1.2-1.8mg/kg 2
hr. prior
20. INDICATIONS OF PUVA
● FDA APPROVED
Psoriasis
Vitiligo
Increasing tolerence to
sunlight/enhancing
pigmentation
●OFF LABEL
DERMATOLOGICAL USES
NEOPLASTIC
Mycosis fungoides
Histiocytosis X
PAPULOSQUAMOUS
/DERMATITIS
Atopic dermatitis
Seborrhiec dermatitis
Chronic hand dermatitis
Palmoplanter pustulosis
lichen planus
Parapsoriasis
Pityriasis lichenoides
lymphomatoid papulosis
PHOTOSENSITIVITY
DERMATOSIS
(also used for prevention)
PMLE
Erythropoietic
protoporphyria
Solar urticaria
Chronic actinic dermatitis
21. OTHER PRURITIC
DERMATOSIS
-Dermatographism
-Aquagenic urticaria/pruritis
-Chronic urticaria
-Urticaria pigmentosa
-Polycythemia vera
-Idiopathic pruritis
-Prurigo nodularis
OTHER IMMUNOLOGICAL
CONDITION
-Alopecia areata
-Graft vs. host reaction
-Morphea
-Linear scleroderma
MISCELLANOUS CONDITION
-Grover’s disease
-Ichthyosis linearis
circumflexa
-Scleromyxedema
-Generalized granuloma
annulare
22. ABSOLUTE
●SLE with photosensitivity
●Xeroderma pigmentosum
●Lactation
●History of idiosyncratic reaction to psoralen
●Pemphigus and pemphigoid
RELATIVE
●Photosensitivity or photosensitizing drugs
●Prior exposure to ionizing rays or arsenic
●h/o skin cancer or photo damage
●Pregnancy
●Severe cardiac ,renal, hepatic disease
●Young age (<12 yrs.)
25. ●Based on skin type
●Type------Initial dose(j/cm sq)----dose inc/wk
I .5 .5
II 1 .5
III 1.5 1
IV 2.0 1
V 2.5 1.5
VI 3 1.5
26. TOPICAL PUVA
●8-MOP/TMP – cream, lotion, ointments
●TMP – more phototoxic (30 times) but weaker penetration
Preferred to oral PUVA in conditions
●In patients with hepatic/renal dysfunction/GI disturbances
●In patients with cataract
●In claustrophobic individuals & to permit shorter irradiation
time
●Psoralen drugs interaction
●Disease limited to palms and soles
27. SIDE EFFECTS
SHORT TERM
SIDE EFFECTS
DUE TO
PSORALENS
PHOTOTOXICITY NEW RASH?
Gastrointestinal
disturbance
CNS
symptoms-headache,
dizziness
Bronchoconstriction
Toxic hepatitis
Drug fever
Exanthem
Erythema (M.C.)
Pruritus (M.C.)
Subacute
phototoxicity
Photoonycholysis
Friction blister
Phytophotodermatitis
Koebner
phenomenon
PMLE
Lupus erythematosus
Guttate psoriasis
Seborreic dermatitis
Herpes simplex
NON PHOTOTOXIC REACTIONS CARDIOVASCULAR STRESS,HYPERTRICHOSIS
28. LONG TERM SIDE EFFECTS
CHRONIC
ACTINIC
DAMAGE
Photo ageing in skin
type I-IV
Dryness, wrinkling,
freckling,
telangiectasias,
keratosis partially
reversible after
stopping
PUVA
lentigenes-appears
6-15months after
therapy
OPHTHALMOLOGI
CAL EFFECTS
Data from animal
studies indicate a risk
of premature cataract
but clinical evaluation
suggests no increase
in , even in patients
who neglect careful
eye protection during
long-term PUVA
IMMUNOLOGICAL
CHANGES
Decrease cd4,cd8,
APC function
Impaired IL-2
production
Suppression of
contact and delayed
hypersensitivity
Decrease no. of PMN,
monocytes,
macrophages
29. CARCINOGENESIS
The risk of SCC, but not
of BCC, is significantly
Increased risk for
melanoma – an area of
controversy
✓Dose dependent
✓More in skin type
I/I
✓High risk –past
family history of
skin malignancy or
dysplastic nevi, on
As, cyclosporine,
Mtx, UVB therapy
✓Mutation in p53&p16
✓Defect in DNA repair
mechanism
✓Free radical damage
