Dr. Sabha Talib Neazee, resident M.D.Dermatology. ppt on phototerapy includes photobiology, photoaging, sunscreens, NBUVB and PUVA therapy. information based on Rooks, IADVL, articles from IJDVL, cancer society. made as a part of curriculum for MD Dermatology.
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Phototherapy. Dr. Sabha Talib Neazee
1.
2. Definitions
• PHOTOTHERAPY: It is a form of treatment for skin conditions involving the
administration of non ionizing radiation (most commonly within the ultraviolet part
of electromagnetic spectrum) in a controlled manner to the skin.
• PHOTOBIOLOGY: It is the study of the effects of UV and VL on living matter.
• PHOTODERMATOLOGY: It is the study of normal as well as abnormal effects of UV
and VL on skin.
• PHOTOSENSITIVITY: Abnormal response to “ordinary “ light exposure
• PHOTOMEDICINE: Study of skin diseases caused by radiation in UV and visible
spectra.
3. TERRESTRIAL RADIATION
• It is the infrared radiation emitted from the atmosphere.
• The following is the list of solar and Terrestrial radiation and their approximate
wavelength range.
1. Ultraviolet- 100 to 400nm
2. Visible - 400 to 700 mm
3. Infrared- > 700nm
4.
5. MEET ULTRAVIOLET
• Radiation with wavelength shorter than light but longer than X ray.
• It have both benign and pernicious impact on the health of living being.
• LET’S CONSIDER THE MOST COMMON TYPES OF UV RAYS.
UVA: 400 to 315nm.
relatively long wavelength
represents close to 95% of the UV Rays
skin aging, wrinkles
damages keratinocytes in basal layer of epidermis=skin cancers
dominant tanning ray
6. UVB-
315-250 nm
Medium wavelength
Only part passes through the
atmosphere
Damages skin cells directly
Main ray that causes sunburn
UVC-
280-100nm
Most harmful
Do not reach earth`s surface
Completely filtered by ozone layer
9. ERYTHEMA
• It is UVR induced inflammation
• Sunburn-common, visible, acute inflammatory response to excessive exposure to UVR
associated with redness
• Wavelength around 300nm is most erythmogenic
• 307.5 causes max burning
10. TANNING
3 tanning process occurs in reaponse to UVR.
1.IMMEDIATE PIGMENT DARKENING- due to immediate photo-oxidation of existing
colourless melanin precursors to UVA and visible radiation.
• Fades within 15 minutes
• Almost undetectable in fair skinned individuals
• Easily observed in skin type 4 or darker.
2.PERSISTENT PIGMENT DARKENING- response to higher UV dose >10jcm2
• Peaks 2 hours post radiation
• Lasts for 1-5 days
• Due to persistent oxidation of melanin precursors.
• End point used to assess UVA protection of sunscreens.
11. 3. MELANOGENESIS OR DELAYED TANNING- facultative pigmentation or
neomelanogenesis
• Stimulation of new melanin synthesis by basal epidermal melanocytes.
• Transported via dendrites to adjacent keratinocytes.
• Redistributed towards skin surface.
* THE ABILITY TO TAN DEPENDS UPON THE SKIN TYPES.
* TAN FADES WHEN THE STRATUM CORNEUM IS SHED OVER SEVERAL WEEKS.
12. IMMUNOMODULATION
1. Effect on antigen presenting cells-depletes the epidermis of langerhan cells
2. Effect on T cells-
a) Stimulates the circulating suppressor T cells-alters the ability of lymphocytes to
respond to mitogens and antigens
b) Suppression of delayed hypersensitivity and contact hypersensitivity- reduction of
tumour rejection – increased incidence of malignancies.
c) Alters the proportion of circulating T cell sub types.
3. Release of inflammatory mediaters-IL-1 and IL-6 which are immunosuppressive and
alter cell trafficking.
4. Other effects-impairment of immunological responses of the epidermal
keratinocytes and lymphocytes
13. IMMUNOMODULATION
1. Effect on antigen presenting cells-depletes the epidermis of langerhan cells
2. Effect on T cells-
a) Stimulates the circulating suppressor T cells-alters the ability of lymphocytes to
respond to mitogens and antigens
b) Suppression of delayed hypersensitivity and contact hypersensitivity- reduction of
tumour rejection – increased incidence of malignancies.
c) Alters the proportion of circulating T cell sub types.
3. Release of inflammatory mediaters-IL-1 and IL-6 which are immunosuppressive and
alter cell trafficking.
4. Other effects-impairment of immunological responses of the epidermal
keratinocytes and lymphocytes
14. DERMAL CANCERS
• Solar UVR exposure associated with actinic keratosis that are indicative of SCC risk
• Non melanoma skin cancers
PHOTOAGING
Definition-process of skin aging which has been accelerated by chronic solar
exposure.
• Also known as DERMATOHELIOSIS.
• Clinically distinct from chronological aging.
15.
16. Lets observe the difference………….
Chronological Aging
• Smooth skin
• Decreased skin thickness
• Fine wrinkles
• Loss of opacity
• Slightly decreased elasticity
• Cancers rare.
Photoaging
• Rubbery
• Increased skin thickness
• Deep and course wrinkles
• Irregular pigmentation
• Dramatically decreased
elasticity
• Cancer seldom
17. SUNSCREENS
Defined as topical formulations that filter and /or scatter UVR.
• In Europe- sunscreens are regulated as cosmetics
• In USA- drug
• In India- still searching……………..
SUN PROTECTION FACTOR: numerical rating system to indicate the degree of
protection provided by a sun care product.
• Defined as ratio of least amount of UV energy required to produce minimal
erythema on sunscreen protected skin to the amount of energy required to produce
the same erythema on unprotected skin.
SPF=MED of photoprotected skin
MED of unprotected skin
Theoretically, a sunscreen with SPF 15 would permit the patient to increase his sun
exposure time fifteen fold before developing sunburn
18. .
CATEGORIZATION SPF
Ultra protection 50+
Very high protection 30-50
High protection 15-25
Medium protection 8-12
Low protection 2-6
RECENT RECOMMENDATIONS FOR SPF CATEGORIZATION
WATER RESISTANT SUNSCREENS: ability of sunscreen to retain its photo protective properties following 2,
20 min intervals or 40 min total of moderate activity in water immersion.
WATER PROOF OR VERY WATER RESISTANT: doubling of aquatic activity time to 4, 20 min activity intervals or
80 min total.
20. PHOTOTHERAPY
• Definition-It is a form of treatment of skin condition involving the administration of
non ionizing radiation in a controlled manner to skin.
HISTORICAL ASPECTS:
• 1400 BC: India- vitiligo patients were given certain plant extracts and exposed to sun.
• 1903: Neils Finsen received Nobel prize for therapeutic results with UV radiation in
lupus vulgaris
• 1974: Parish et al reported useful role of high intensity UVA tubes in combination
with psoralens for psoriasis.
• 1978: Wiskemann introduced irradiation cabins with broad band UVB tubes for
treatment of psoriasis and uremic pruritus.
• 1988: NBUVB phototherapy was introduced by van Weelden et al and Green et al.
22. UVB
• UVB- 280-320 nm
• Full spectrum(BBUVB)- 270-350nm
• Narrow band(NBUVB)- 311-313nm
• NBUVB is now the gold standard
• Advantage- decrease in the erythmogenic wavelength with a 5 fold increase in longer
wavelengths resulting in increased therapeutic effect
• Mechanism of action in Psoriasis- anti-inflammatory, immunosuppressive and cytotoxic.
induction of cis uranic acid
Langerhans cells depletion
Altered antigen presentation
Decreased activity of NK cells
Apoptosis of T lymphocytes and keratinocytes
23. Mechanism of action in vitiligo:
• Stabilization of depigmenting process followed by stimulation of residual follicular
melanocytes.
Stimulates the amelanotic dopa negative melanocytes in the outer hair sheaths
Proliferation
Melanin production
Migration yowards depigmented skin
Mechanism of action in vitiligo:
• Stabilization of depigmenting process followed by stimulation of residual follicular
melanocytes.
Stimulates the amelanotic dopa negative melanocytes in the outer hair sheaths
Proliferation
Melanin production
Perifollicular repigmentation
24. STARTING DOSE- Based on minimal erythema dose in order to reduce the risk of burning on one hand or
under treatment on other.
• Poor correlation with MED and skin types.
• Can be determined by home made templates or by using automatic or UV exposure devices.
MINIMAL ERYTHEMA DOSE: defined as the dose of radiation that produces
minimal, just perceptible erythema at 24hrs post radiation(UK), in other
countries-well defined erythema.
25.
26. STARTING DOSE- 70% or 50% of MED
INCREMENTS- As the skin acclimatizes to UV, by epidermal thickening and pigmentation, it is necessary to
increase the dose.
low increment- 20%
high increment- 40%
FREQUENCY- 2 or 3 times per week.
NO OF EXPOSURE- clearance of psoriasis : 20- 25 increments
- atopic eczema: prolong course
- PLE desensitization : 15 treatments
27. UVA-1
• Long wavelength- 320-400 nm while filtering the erythmogenic UVA and UVB
wavelengths.
• Mechanism of action- penetrates deeper in the dermis
Induces interstitial collagenase and cytokines
Softening of sclerotic skin
Decrease in tumor necrosis factor
Doses – high- >60j/cm2
Medium- 30-60 j/cm2
Low- 10-20 j/cm2
28. PUVA
• Psoralen + UVA.
• Mechanism of action-Psoralen molecule enters the cell nucleus
Gets inserted in nucleic acid bases
UVA
Excited psoralen + pyrimidine base
Photo-adduct
UVA
Links to pyrimidine base
DNA-PSORALEN crosslink
• Inhibits DNA replication, Langerhans cell depletion, immunosuppressive effect on T
lymphocyte functions, mifration and restoration of Th17/regulatory T cells imbalance
in Psoriasis.
29. PSORALENS
• The drug psoralen has no therapeutic effect of its own . Only produces effect when
patient is exposed to UVR.
• Drugs used- Methoxsalen (8-methoxypsoralen)
Bergapten (5-methoxypsoralen)
Unique features of psoralen pharmacology
• Insolubility in water
• Physical formulation influences absorption
• Food reduces absorption
• First pass effect through liver
• Large individual variation in absorption
30. FDA APPROVED INDICATIONS
Psoriasis
Vitiligo
OTHER DERMATOLOGIC USES
Neoplastic
Mycosis fungoides/Sézary syndrome
Histiocytosis X (Langerhans’ cell
histiocytosis)
Papulosquamous/dermatitis
Atopic dermatitis
Seborrheic dermatitis
Chronic hand dermatitis
Palmoplantar pustulosis
Lichen planus
Parapsoriasis
Pityriasis lichenoides
Lymphomatoid papulosis
Photosensitivity dermatoses
Polymorphous light eruption
Erythropoietic protoporphyria
Solar urticaria
Chronic actinic dermatitis
Other pruritic dermatoses
Dermographism
Aquagenic urticaria/pruritus4
Chronic urticaria
Polycythemia vera
Idiopathic pruritus
Urticaria pigmentosa
Prurigo nodularis
Other immunologic dermatoses
Alopecia areata
Graft-versus-host disease
Morphea
Linear scleroderma
32. CONTRAINDICATIONS
Absolute
Pemphigus and pemphigoid
Lupus erythematosus with photosensitivity
Xeroderma pigmentosum
Lactation
History of idiosyncratic reaction to psoralen
compound
Relative
Photosensitivity/photosensitizing medications
Prior exposure to ionizing radiation or arsenic
History or family history of melanoma
History of skin cancer or chronic photodamage
Pregnancy
Severe cardiac, liver or renal disease
Very young age
Pregnancy prescribing status – Category C
33. MINIMAL PHOTOTOXIC DOSE- measured 2 hours ( or 2.5 hours for 5 MOP) after patient has ingested
standard dose of psoralen. Test site read after 72-96 hours.
STARTING DOSE- 40% of MPD for topical PUVA
70% of MPD for oral PUVA
INCREMENTS- 20-% to 40%
FREQUENCY- twice daily as erythema is delayed
EYE PROTECTION- following ingestion of psoralen, patients are required to wear UVA
absorbing glasses before therapy and for atleast 12 hours post therapy. ( children-24 hours)
36. INDICATIONS
• PSORIASIS- most frequent indication. NBUVB can be used in all forms of psoriasis
except generalized pustular and erythmodermic psoriasis for which PUVA can be
considered.
• ATOPIC ECZEMA- UVA1 for acute flares and NBUVB for chronic disease.
• CUTANEOUS T CELL LYMPHOMA- UVB useful for patch stage CTCL. PUVA preferred
for plaque stage. “sanctuary sites” ( flexures) may be the one where disease may
persist
• VITILIGO- NBUVB> PUVA. Photoresponsive areas are face, recent onset, limited
extent, areas containing pigmented hairs and involving non acral sites.
• PMLE- NBUVB=PUVA. But NBUVB have better side effect profile.
• OYHERS- alopecia areata, graft vs host disease,palmoplantar pustulosis, pompholyx
eczema, pruritus, systemic sclerosis, morphoea.
37. ARTIFICIAL UVR????? HOW?????
• Passage of an electric current through mercury vapour enclosed in fluorescent tube.
• Excitation of electrons by mercury
• Excited electrons are absorbed by phosphorous coating on inside of the tube
• Re-emission of radiation of longer wavelengths by the process of fluoresence.
• By changing the phosphorous used ,different spectra in UVA or UVB can be
produced.
EQUIPMENT FOR DELIVERY OF PHOTOTHERAPY-
• whole body cabin
• whole body panels
• Multiutility panels
• Small panel irradiation
• Point sources
40. BALNEOTHERAPY
• Definition- process of delivery of 8 methoxy psoralen or different salt solutions
through bath with a subsequent UVA or UVB irradiation
• Delivery of psoralens by bath prevents systemic side effects associated with oral
PUVA.
• Advantage of shorter and selective photosensitization leading to significantly lower
cumulative UVA exposure.
• Types-
1. Bath PUVA
2. Bathing suit PUVA
3. Soak PUVA
4. Turban PUVA
41. 1. Bath PUVA
Bath tub is filled with 100 liters of warm water.
37.5ml of 1% 8 MOP is added= concentration of 3.75mg/l
Patient soaks the body for 10 min in supine position and 10 min in prone position
Pat dry the skin
Immediately exposed to UVA in a whole body Phototherapy unit
Eyes and genital (males) protected.
Frequency-3 times per week
Duration- 12-15 treatments
Maintenance – for 2-3 months. Twice weekly for 1st month and once weekly.
2. Bathing suit PUVA
2 liters of water+ 1 ml of 1% of 8 MOP =concentration of 3.75mg/l
Bathing suit of fannel material is dipped.
Patient wears suit for 15 min with a raincoat over it to prevent evaporation.
Exposed to UVA
42. 3.Soak PUVA (Basin PUVA)
affected parts are soaked in 3.75mg/ml of 8 MOP
After 30 min, the part is exposed to UVA
Frequency- 3-4 times per week.
Initial UVA dose- 1-2 j/cm2
Increments- 0.5j/cm2
4.Turban PUVA
An absorbent cotton cloth is soaked for 30 seconds in 3.75mg/l solution
Wrapped around the head for 5 min
Repeated 4 times. Total 20 min.
Immediately exposed to UVA.
43. EXTRACORPOREAL PHOTOPHORESIS
• DEFINITION-It is discontinuous leukapheresis procedure that combines
administration of 8-MOP with extracorporeal UVA irradiation to a fraction of
peripheral blood leukocytes.
• It targets the effects of photo chemotherapy directly to circulating pathogenic
leukocytes.
• 3 stages- 1. leukopheresis
2. photo activation
3. reinfusion
• Photo testing not necessary as irradiation occurs outside the body in a machine.
• Std dose is 1-2 j/cm2
• Increments- none
• Frequency-2-3 successive days once a month.
• During 1 treatment session 5%-10% of circulating T cell pool is treated.
• Duration – 6 months
44. ECP – PROPOSED MECHANISMS OF ACTION
• Stimulation of anti-T-cell (tumor cell) immune responses
• Induction of apoptosis of activated (autoreactive) T-cells
FDA approved indications
• Cutaneous T-cell lymphoma
Other dermatologic uses
Autoimmune connective tissue diseases
• Scleroderma
Autoimmune bullous dermatoses
• Pemphigus vulgaris
• Pemphigus foliaceous
• Epidermolysis bullosa acquisita
Graft-versus-host-disease (GVHD)
• Acute GVHD29–32
• Chronic GVHD33–36
• Prevention of GVHD37
Other dermatoses
• Nephrogenic systemic fibrosis38–41
• Oral erosive lichen planus42,43
Contraindications
Absolute
• History idiosyncratic reactions to psoralen compounds
• Pregnancy and lactation
• Severe cardiac disease
Relative
• Poor venous access
• Rapidly progressing disease (such as ‘tumor eruptive CTCL’)
• Hematocrit < 25% (should be transfused with red blood cell
to hematocrit of at least 29%)
• Diastolic blood pressure < 70 mmHg (may need saline
infusion and/or red blood cell transfusion)
• Congestive heart failure
Pregnancy prescribing status – FDA unrated
45.
46. PHOTODYNAMIC THERAPY
• It is a treatment modality involving administration of photosensitizing agents, accumulation
of sensitizer molecules in the target cells followed by selective irradiation of lesion with
visible light.
• MECHANISM OF ACTION- direct cytotoxicity, inflammation and immune host response.
• The mobilization of the host to participate in tumor ablation process is a unique feature of
PDT and is an advantage over conventional anticancer therapy.
• INDICATIONS-
Actinic keratosis
Bowen's disease
Basal cell carcinoma
Squamous cell carcinoma
Kaposi sarcoma
Mycosis fungoides
Malignant melanoma
47. Blue light acne treatment
• It is a non invasive procedure that uses light in the blur wavelength 405-420 nm to
kill the Propionibacterium acnes.
• Approved by FDA for treatment of moderate acne vulgaris or acne vulgaris that has
not responded to any other treatment.
Mechanism of action-
• the porphyrins released by bacteria absorb light of certain wavelwngth and produces
free radical damage that destroys the bacteria.
48.
49. TARGETED PHOTOTHERAPY
• It is application of light therapy directly focused on or targeted at the lesion through
special delivery mechanisms such as fiber optic cables.
• Includes excimer laser (308nm) , intense pulse light systems and non laser ultra violet
light sources.
• ADVANTAGES:
1) Exposure of involved areas only and sparing of uninvolved areas.
2) Quick delivery of energy
3) Shortened duration of treatment
4) Delivery of supererythmogenic doses of energy because uninvolved areas are not
exposed.
5) Easy administration.
50. DISADVANTAGES-
1) Expensive
2) Not adequate to treat extensive areas.
3) Not recommended if lesions occurs over more than 10 % body area.
USES-
1) Vitiligo
2) Psoriasis
3) Oral lichen planus
4) Alopecia areata
5) Atopic dermatitis
6) Mycosis fungoides
7) Lymphomatoid papulosis