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  1. 1. 13  Photobiology and Photosensitivity Disorders Jeffrey L. Marx, MDC o n t e n t s13.1  Basic Facts about Ultraviolet Light . . . . . . . . . . . . . . . . 44313.2  Photoimmunology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44413.3  Phototesting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44513.4 Idiopathic Photosensitivity Disorders . . . . . . . . . . . . . . 44613.5  Photosensitivity from Exogenous Agents . . . . . . . . . . 45013.6  Diseases Exacerbated by Sunlight . . . . . . . . . . . . . . . . . 45213.7  Phototherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45313.8  Photochemotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45313.9  Sunscreens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 454 Photobiology and Photosensitivity Disorders  441
  2. 2. Committed to Your Future For practice exam questions and interactive study tools, visit the Dermatology In-Review Online Practice Exam and Study System at DermatologyInReview.com/GaldermaSponsored by
  3. 3. 13.1  BASIC FACTS ABOUT ULTRAVIOLET LIGHT • Wavelengths extend from 10 nanometers (nm) to 400 nm • Subdivided into vacuum UV (10-200 nm), UVC (200-290 nm), UVB (290-320 nm), and UVA (320-400 nm) • UVA is further subdivided into UVAII (320-340 nm) and UVAI (340-400 nm) X-rays Vacuum UV UVC UVB UVA visible light 10 200 290 320 340 400 nm nm nm nm nm nm Figure 13-1. Electromagnetic Radiation: Wavelengths • Ultraviolet C from the sun does not reach the earth’s surface. It is filtered out by the ozone layer • Beyond ultraviolet radiation is visible light (400-760 nm). The blue-violet portion of visible light is near 400 nm. The red portion is at the upper end of the visible spectrum • Beyond visible light is infrared radiation, and beyond infrared are radiowaves • Electromagnetic radiation can also be conceptualized as u TIP energy packets called photons. The energy (E) of photons is a he longer wavelengths of EM T have less energy but penetrate proportional to the frequency (γ) and inversely proportional to more deeply into the skin the wavelength (λ) • Another important formula is: Joules/cm2 = Watts/cm2 x seconds Joules (J) are a measurement of energy dose (fluence) Watts (W) are the power or irradiance of a UV source • For a photobiologic effect to occur, radiation must be absorbed. The absorbing molecule is called a chromophore. The portion of the EM spectrum absorbed by that particular molecule is called its absorption spectrum. The portion of the EM spectrum that produces a particular biologic effect (e.g., erythema, delayed tanning) is called the action spectrum • UVB converts 7-dehydrocholesterol in the skin to previtamin D3, which then thermally isomerizes to form vitamin D3 u TIP • UVB in natural sunlight is the main contributor to erythema. a ltraviolet radiation from the sun U causes several acute effects in the UVB erythema reaches a maximum in 6-24 h. UVB is skin, including photosynthesis of absorbed primarily in the epidermis and characteristically vitamin D, sunburning, immediate produces sunburn (apoptotic) cells on histology pigment darkening, delayed tanning, epidermal thickening, and immuno- • The chromophores involved with UVB erythema are not logic effects clear but appear to involve nucleic acids • UVB is about one thousand times more erythemogenic than UVA and accounts for 80-85% of erythema from sunlight Photobiology and Photosensitivity Disorders  443
  4. 4. • UVA accounts for only 15-20% of sunlight erythema, though there is much more UVA than UVB in sunlight. The erythema from UVA is biphasic with the second peak at 6-24 h. Histologically, there are predominantly lymphocytes around the vascular plexuses of the dermis • As a result of ultraviolet radiation, there is mast cell degranulation and release of histamine and other mast cell products. Certain prostaglandins and interleukins are increased after UV radiation • Immediate pigment darkening fades within minutes after exposure. It is brought on by UVA and visible light. It is caused by photooxidation of preexisting melanin and a redistribution of melanosomes from a perinuclear position into dendrites • Delayed tanning becomes visible about 72 hrs after UVB exposure. UVA contributes to a lesser extent to delayed tanning. Tyrosinase activity and melanocyte numbers increase with delayed tanning • Sunlight also increases the thickness of the epidermis. This is mainly a UVB-induced phenomenon. The thickening increases the tolerance to further sunlight13.2  PHOTOIMMUNOLOGYUV Carcinogenesis • Midrange UVR 280-320 nm more efficient in inducing neoplasia in mice • Long wave UVA, when added to UVB may accelerate carcinogenesisDNA Effects • UVR alters DNA, and UVB is much more efficient than UVA in inducing DNA damage • Cells from patients with AK’s have less DNA repair capacity than controls • UVB is most effective in producing pyrimidine dimers, which may activate oncogenes, particularly in the formation of BCC’s and SCC’s • Dipyrimidine cyclobutane dimers most common (C-T mutation)Suppressor T-cells • Suppressor T-cells induce susceptibility to tumor • These cells appear to arise in UV-irradiated hosts prior to tumors developing, and play a role in carcinogenesisAntigen-Presenting Cells After UVR • Have depressed ability to prime UV-irradiated mice to subcutaneously injected hapten or protein and to applied contact-sensitizing agents • UV-irradiated mice have defective antigen presentation, preventing a normal delayed-type hypersensitivity (DTH) response • Reduction in number of APC’sHuman Studies • There is an increased risk of malignancy in patients undergoing immunosuppressive therapies, with increased frequency of skin cancers (including melanoma) • Renal transplant recipients have 36-fold increased risk of SCCUVR Effects on Contact Dermatitis and DTH • Mice exposed to short-term, high-dose UVR demonstrate decreased splenic APC function • Both DTH and contact hypersensitivity show diminished responses444  2011/2012 Dermatology In-Review l Committed to Your Future
  5. 5. u TIP aSummary UVR in Vitro: • Alters ability of APCs to present antigen • Alters ability of lymphocytes to respond to mitogens or antigen • Alters cytokine production • Induces release of immunosuppressive factors UVR in Vivo: • Induces skin cancers • Alters LC morphology and function • Suppresses the induction of contact hypersensitivity • Suppresses the induction of DTH • Alters cell trafficking • Increases circulating levels of cytokines (IL-1, IL-6, and TNF) • Alters proportions of lymphocyte subtypes in peripheral bloodHypothetical Effects of UVR on Cancer Induction • UVR induces transformation of keratinocytes with expression of tumor-associated antigens • UVR alters APC function, maybe by UVR-induced reduction of antigen-presenting cells and decreased ability of Langerhans cells to present antigen • UVR may cause the release of immunosuppressive factors • Suppressor T-cells are induced13.3  PHOTOTESTINGSkin Types Type I: Always burns, never tans Type II: Usually burns, rarely tans Type III: Rarely burns, usually tans Type IV: Never burns, always tans Types V, VI: Highly pigmented individualsLight Sources for Phototesting and Phototherapy • The most common light sources for phototesting and phototherapy are fluorescent bulbs of various lengths, usually two feet, four feet, or six feet. These are low-pressure mercury vapor lamps with the inner surface of the bulb coated by a specific phosphor • The mercury vapor is excited by the electric current and then emits a line spectrum of 254 nm radiation. The 254 nm radiation is absorbed by the specific phosphor, which emits a continuous spectrum of various wavelengths, depending on the phosphor type. A broadband UVB lamp emits throughout the UVB range and includes some UVA as well • Narrowband UVB lamps emit at 311-312 nm. Those wavelengths have been shown to be considerably more effective for treatment of psoriasis, vitiligo, and other skin disorders • Fluorescent UVA bulbs used for phototesting or PUVA therapy have a peak emission at 352 nm. A major advantage of fluorescent lamps is that there is little warm-up time and a bank or cabinet of bulbs can cover a broad areaPhototesting • Used for suspected photosensitivity patients to determine the offending wavelengths of their disorder and their degree of photosensitivity Photobiology and Photosensitivity Disorders  445
  6. 6. • Unaffected skin of the buttocks, lower back, or ventral forearm is used for Minimal Erythema Dose (MED) testing • Six test squares of increasing UV doses are exposed. The MED is the dose of ultraviolet radiation that produces barely perceptible erythema that completely fills the test square. The MED is read at 24 hrs after delivery of the doses. An additional reading at 15 min after exposure is important when solar urticaria is a consideration • Usually an MEDB, using broadband UVB, and an MEDA, using UVA, are determined on the same day • If photopatch tests are needed to investigate for possible photoallergic contact dermatitis, two sets of the panel of potential photoallergens are applied to the patient’s back on day one. They are then covered with an opaque material. On day 2, one set of photoallergens is uncovered and irradiated with 10 J/cm2 of UVA or one-half of the patient’s MEDA, whichever is less. Those patches are again covered with the opaque material. Readings are done on days 3 and 5 or days 3 and 7. If an irradiated patch is positive, the patient is photoallergic to that product. If both the irradiated and nonirradiated patches are equally reactive, the patient has allergic contact dermatitis to that substance. When an irradiated site shows stronger reactivity than a positive, nonirradiated site, this is interpreted as photoallergic contact dermatitis and allergic contact dermatitis to the same substance • Additional phototesting includes visible light testing. A slide projector can be used as a light source with the infrared radiation (heat) absorbed by a clear container of water in the beam. Repeated MEDs to UVB or UVA, given to the same test site over several days, can be used to reproduce lesions of polymorphous light eruption (PMLE). Alternatively, a single, large dose, consisting of a multiple of the patient’s MEDB or MEDA, can be used to reproduce PMLE13.4  IDIOPATHIC PHOTOSENSITIVITY DISORDERSPolymorphous Light Eruption (PMLE) Figure 13-2. Polymorphous Light Eruption • Most common photodermatosis • Idiopathic disease that usually appears in the first three decades • More common in fair-skinned females. There may be family u TIP a delay of several hours to A history several days is important in • Pathogenesis is unclear but may be related to a type IV distinguishing PMLE from solar hypersensitivity reaction urticaria446  2011/2012 Dermatology In-Review l Committed to Your Future
  7. 7. • Most lesions are erythematous, pruritic papules. The plaque form is less common. Vesicles and an eczematous dermatitis are uncommon. The lesions appear symmetrically on exposed areas, especially the chest and upper extremities, after a delay of several hours to several days. This delay is important in distinguishing the disease from solar urticaria • Same areas are affected year after year. Not all exposed areas show lesions. The lesions appear in the spring or early summer in the northern climates. The condition may improve as the summer progresses • PMLE may occur through windowglass, which filters out UVB Figure 13-3. Repeated UV Doses Evoke Polymorphous Light Eruption at Test Site • The histology of PMLE shows a lymphocytic infiltrate around the superficial and deep vascular plexuses. There may be subepidermal edema. Significant epidermal changes are uncommon • Phototesting reveals a normal MEDB and a normal MEDA. Photopatch tests are negative. Repeated doses to the same skin area of ultraviolet radiation (in some patients, UVB; in more patients, UVA) over a several-day period may reproduce lesions in some of the PMLE patients. Others have produced PMLE lesions with a single, large, multiple MEDB dose or a multiple MEDA dose. One can enhance the chances of eliciting a positive test result if one tests on the areas of clinical involvement • Differential diagnosis of PMLE is lupus erythematosus (LE). Skin biopsy and direct immunofluorescence and blood tests for ANA, anti-SSA, and anti-SSB may aid in distinguishing the two diseases • Most patients have mild disease that can be treated by sun avoidance, especially between 11 a.m. and 3 p.m.; a broad spectrum sunblock containing UVB and UVA blockers; and clothing with a tight weave. Topical steroids are used to treat clinical lesions. For more severe cases, hardening and desensitization can be accomplished with UVB, UVB plus UVA, or PUVA. Antimalarials can be used for resistant cases. A short course of prednisone (20-40 mg) is effective for brief, sunny vacationsActinic Prurigo (AP) • Occurs more frequently in children (girls boys) • May be a distinct entity or may be an HLA-restricted subset of PMLE. It differs from PMLE in the following ways: – Lesions are excoriated papules and nodules that always begin in childhood and often remit in puberty – Lesions occur on all sun-exposed areas Photobiology and Photosensitivity Disorders  447
  8. 8. – Lesions may persist for months, even into the winter – Lesions may occur on non-sun-exposed areas – Outbreaks are not as clearly related to sun exposure – Cheilitis is frequently seen • Evaluation and treatment are similar to PMLE. UVA and UVB can cause lesions • Thalidomide has been very effective for a majority of patientsHereditary PMLE of Native Americans • Similar to actinic prurigo but persists much more frequently into adulthood • Specific HLA types predominate in Native Americans inhabiting certain areas, and 75% of patients have a positive family history • Patients have a papular, excoriated, eczematous dermatitis that occurs predominantly on the face. Cheilitis and conjunctivitis are commonHydroa Vacciniforme (HV) • Rare photosensitivity disorder occurring in childhood • Characterized by umbilicated vesicles on sun-exposed areas. Resolution occurs with crusting followed by pock-like scars • Repeated doses of UVB and UVA can sometimes elicit lesions. Treatment is similar to that discussed with PMLESolar Urticaria (SU) Figure 13-4. Solar Urticaria • Wheals occur on sun-exposed areas • The wheals begin within 10-30 min after exposure and last for about one hour after exposure • The face and hands may not show lesions probably because they are chronically exposed to sun, causing hardening and desensitization • Mediator release during widespread whealing may result in headache, nausea, wheezing, faintness, and syncope • SU is an idiopathic, type I photosensitivity disorder. It usually lasts many years. Rare cases have been associated with erythropoietic protoporphyria (EPP), lupus erythematosus (LE), and with certain drugs. Blood tests for LE and EPP should be performed • Some patients react with wheals to either visible light or UVA or UVB. Others react to both UVA and visible radiation. Some react to both UVB and UVA, and some patients react to UVB, UVA, and visible radiation • Treatment can be difficult. Sun avoidance, protective clothing, and a broad-spectrum sunblock containing titanium dioxide or zinc oxide as one of the ingredients should be used • H-1 antihistamines are of partial benefit448  2011/2012 Dermatology In-Review l Committed to Your Future
  9. 9. • Gradual exposure to UVA or PUVA may desensitize the patient, but there is a risk of evoking the disease with systemic symptomsChronic Actinic Dermatitis (CAD) • Chronic actinic dermatitis includes patients that were previously designated as having persistent light reaction, actinic reticuloid, and photosensitive eczema • Patients are usually middle-aged to elderly males who present with a chronic, eczematous dermatitis in a photodistribution, though there is no history of current exposure to a photosensitizer Figure 13-5. Chronic Actinic Dermatitis • There is relative sparing of the upper lids, behind the ears, under the nose, the submental area, and the finger webs. Some patients show infiltrated, dusky erythematous papules and plaques Figure 13-6. Chronic Actinic Dermatitis • Occasionally, non-sun-exposed areas are involved in CAD patients. Some patients have the condition all year with summer exacerbations • The histology is that of a chronic, eczematous dermatitis, but some patients show histology indistinguishable from mycosis fungoides with atypical mononuclear cells. Circulating Sézary cells have been found in some of those patients • Phototesting is very helpful in diagnosing CAD. The MEDB is markedly diminished, and the MEDB site may show an eczematous or infiltrated appearance. Many of the patients have a lowered MEDA as well and may have a lowered threshold to shorter wavelength visible light in the blue-violet end of the spectrum Photobiology and Photosensitivity Disorders  449
  10. 10. • Many cases of this idiopathic disorder are thought to have begun as photoallergic contact dermatitis or as a drug photosensitivity with broadening of the photosensitivity to include the UVB range. It is unclear why photosensitivity persists u TIP when the photosensitizer is no longer present aome patients may show allergic S • Treatment is difficult and should include strict sun contact dermatitis to the Compositae avoidance, a broad-spectrum sunblock, and protective oleoresins. Positive photopatch tests may be demonstrated to the haloge- clothing. UV-blocking films to cover car and home nated salicylanilides, to musk ambrette, windows can help. Incandescent bulbs with longer or incidentally to sunscreens wavelengths, far from the blue-violet end of the visible spectrum, should be used instead of fluorescent bulbs, which have significant blue-violet radiation. Topical and oral steroids have been used. Oral therapy with azathioprine and cyclosporine have been used. PUVA has also been of help in some patients, though there is the risk of eliciting the disease 13.5  PHOTOSENSITIVITY FROM EXOGENOUS AGENTS • Photosensitivity from exogenous agents requires either a systemic agent, such as a medication, or an external agent, such as a sunscreen or a cosmetic ingredient, plus activating UV radiation, usually UVA • Photosensitivity from systemic and external agents can be divided into phototoxic reactions and photoallergic reactions  •  phototoxic reaction appears as an exaggerated sunburn with erythema and sometimes A blistering, resolving with hyperpigmentation. It is a nonimmunologic reaction that could occur in all individuals given enough of the chemical and enough UVR. It can occur on the first exposure to the chemical and the UVR. Phototoxic reactions that produce damage through reactive oxygen species are called “photodynamic” •  photoallergic reaction is a delayed-type hypersensitivity reaction. It does not occur in all A individuals, and it does not occur on first exposure. A period of sensitization is required. It appears as an eczematous dermatitis in sun-exposed areas. Cross-reactivity to other agents is possible • Topical phototoxicity is most commonly caused by psoralens. Topical 8-methoxypsoralen is used therapeutically to treat psoriasis, localized vitiligo, and hand and foot eczema. Psoralens in certain plants and fruits and vegetables (limes, parsnips, figs, parsley, Bergamot oranges, celery, etc.) can produce phytophotodermatitis when those products are handled and the person, often a bartender, salad chef, or gardener, is exposed to the sun. Another cause of topical photoxicity is tar, used both therapeutically for psoriasis and in roofing materials 450  2011/2012 Dermatology In-Review l Committed to Your Future
  11. 11. • In the past, topical photoallergy has been caused by the halogenated salicylanilides, especially tetrochlorosalicylanilide and tribromosalicylanilide in soaps. Musk ambrette and 6-methyl-coumarin in fragrances have also produced topical photoallergy. These compounds have been removed from marketed products. Jadit, fentichlor, and multifungin are anti-fungal agents used in Australia, the United Kingdom, and Canada. They have produced photoallergic contact dermatitis. PABA, its esters, and non-PABA sunscreen ingredients such as cinnamates, benzophenones, dibenzoylmethanes (Parsol 1789), and homosalate are the most common causes of topical photoallergy. Other reported causes of topical photoallergy are medications such as the phenothiazines, ketoprofen, quinidine, and related compounds. Nurses are the ones most likely affected. Photoallergic contact dermatitis is diagnosed by photopatch testing. Sometimes photoallergic contact dermatitis to sunscreens can be superimposed on another photosensitivity disorder Table 13-1. Phototoxic vs. Photoallergic Reactions Phototoxicity Photoallergy Incidence Relatively high Low Reaction possible on first Yes No exposure Incubation period required after No Yes first exposure Timing of reaction after first Minutes to hours Hours to days exposure Delayed-type hypersensitivity No Yes Cross-reactivity to chemically Rare Common similar agents Clinical appearance Exaggerated sunburn. Eczematous dermatitis, as in Sometimes blisters. Much hyper- allergic contact dermatitis pigmentation Histologic appearance Necrotic keratinocytes, dermal Spongiotic dermatitis with edema, some neutrophils and lymphocytes, macrophages, and occasional lymphocytes occasional eosinophils Causative agents - Furocoumarins - Sunscreens (phytophotodermatitis) - Fragrances (musk ambrette) - Tar (6-methylcoumarin) - Salicylanilides - Handling systemic medication (chlorpromazine etc.)Medication Photosensitivity • Photosensitivity from systemic, exogenous agents is due to administered medications. Some medications such as oral psoralens always produce phototoxic reactions. With most medications, it has been difficult to classify them as phototoxic or photoallergic, so the term medication photosensitivity is more appropriate • Most patients with medication photosensitivity present with diffuse erythema in sun- exposed areas. In some patients, the eruption is eczematous. Covered areas are spared Photobiology and Photosensitivity Disorders  451
  12. 12. •  ther manifestations of medication photosensitivity are: O – Photoonycholysis – quinolones, tetracyclines, psoralens, quinine – Blue-gray pigmentation on sun-exposed areas – amiodarone, chlorpromazine, tricyclic antidepressants. No involvement of sclera, lunulae, mucous membranes, as in argyria – Lichenoid eruption – LP-like lesions (may be confluent) on sun-exposed areas; antimalarials, thiazides, demethylchlortetracycline, fenofibrate, enalapril, quinine, quinidine – Pseudoporphyria – signs of PCT with normal porphyrins; tetracyclines, nalidixic acid, amiodarone, furosemide, ketoprofenMost Common Medications Producing Photosensitivity • Antianxiety drugs: alprazolam, chlordiazepoxide • Anticancer drugs: dacarbazine, 5-FU, vinblastine; methotrexate reactivates UVB- and PUVA- induced erythema • Antidepressants: tricyclics (slate-gray pigment) • Antifungals: griseofulvin • Antimalarials: chloroquine, quinine • Antimicrobials: quinolones, sulfonamides, tetracyclines (doxycycline, the most common) • Antipsychotics: phenothiazines • Cardiac meds: amiodarone, quinidine, enalapril • Diuretics: Lasix (furosemide) (including pseudoporphyria), thiazides • Hypoglycemics: sulfonylureas • Hypolipidemics: fibric acid derivatives • NSAIDs: piroxicam (photoallergy in humans), ibuprofen, naproxen (pseudoporphyria) • Photodynamic therapy agents • Psoralens • Retinoids: isotretinoin and acitretin13.6  DISEASES EXACERBATED BY SUNLIGHTAutoimmune Diseases • Lupus Erythematous (LE) – ­ Systemic LE – Subacute Cutaneous (LE) – Discoid LE • Dermatomyositis • Pemphigus Group • Bullous PemphigoidGenodermatoses • Hailey-Hailey disease (Benign Familial Pemphigus) • Darier’s disease (Keratous Follicularis) • Bloom’s syndrome • Rothmund-Thomson syndrome • Kindler syndrome • Cockayne’s syndrome • Xeroderma Pigmentosum • Trichothiodystrophy • Hartnup disease • Disseminated Superficial Porokeratosis452  2011/2012 Dermatology In-Review l Committed to Your Future
  13. 13. Miscellaneous • Herpes Simplex • Pellagra • Pyridoxine (vitamin B6) deficiency • Grover’s disease (Transient Acantholytic Dermatosis) • Reticular Erythematous Mucinosis Some diseases that normally respond to treatment with ultraviolet radiation may, in otherpatients, be exacerbated by sunlight. These include photosensitive psoriasis and mycosis fungoides.13.7 PHOTOTHERAPY • Narrowband (311-312 nm) UVB is more effective for psoriasis u TIP than broadband UVB; narrowband more closely corresponds a nlike PUVA, narrowband UVB U can be used in pregnancy and to the optimum therapeutic wavelengths for clearing psoriasis. in childhood. It is likely to prove Some studies show narrowband UVB to be as effective as oral less carcinogenic than PUVA PUVA in clearing psoriasis without the necessity of ingesting a photosensitizer and without the need for eye protection • For UVB (broadband or narrowband) therapy, an MEDBB or MEDNB is determined. In our institution, patients on narrowband are begun at 50-60% of their MEDNB and increased by 20% of the previous dose for the next four treatments. If significant erythema occurs, the dose is adjusted downward. Subsequent increments are 10% or less. For broadband UVB, the patients are begun at 50-60% of their MEDBB and increased by 50%, 40%, 30%, and 20% of the previous dose. Thereafter, increments of about 10% are used • Combination therapy with UVB and calcipotriol, anthralin, tazarotene, tar, and emollients may promote faster resolution of plaques. Topical steroids are most helpful for areas where UVB does not reach (e.g., scalp, groin) or when the psoriasis is severely inflamed • Oral agents, especially retinoids, methotrexate, and the newer biologic agents may be added to UVB in extensive, difficult-to-control psoriasis. Combining retinoids with UVB or PUVA (re-UVB or re-PUVA, respectively) augments efficacy, and reduces the doses of either modality necessary for clearing of psoriasis • UVB phototherapy is also effective in treating atopic dermatitis and vitiligo, with narrowband UVB more effective than broadband • UVB has also been effective in patches and thin plaques of cutaneous T-cell lymphoma, PMLE and other photosensitivity disorders, pityriasis lichenoides, pityriasis rosea, idiopathic pruritus, and eosinophilic pustular folliculitis13.8  PHOTOCHEMOTHERAPY • Photochemotherapy involves the ingestion or application of psoralens, usually 8-methoxypsoralen (8-MOP) plus irradiation with ultraviolet A (PUVA). Psoralens intercalate between base pairs of DNA. The psoralens then absorb UVA resulting in monofunctional and bifunctional (cross-link) adducts to pyrimidine bases of DNA. This bonding to DNA results in suppression of DNA synthesis and cell division. This suppression may be the mechanism of action of PUVA in treating psoriasis. Immunologic effects may also play an important role in PUVA treatment of psoriasis and other diseases • The newer, liquid-filled capsules of 8-MOP (Oxsoralen Ultra®) are more rapidly absorbed and reach a higher peak serum level than the old crystalline capsules. A dose of 0.4-0.6 mg/kg of body weight is given of the Oxsoralen Ultra®. After 1-1.5 hours, UVA is given Photobiology and Photosensitivity Disorders  453
  14. 14. • The PUVA bulbs have a peak output in the 350-360 nm range. Besides psoriasis, other diseases responsive to PUVA are: cutaneous T-cell lymphoma, vitiligo, atopic dermatitis, lichen planus, cutaneous mastocytosis, pityriasis lichenoides, lymphomatoid papulosis, generalized granuloma annulare, alopecia areata, morphea, and graft-versus-host disease • PUVA can increase tolerance to sunlight in a variety of photodermatoses including PMLE, solar urticaria, and chronic actinic dermatitis • Acute side effects of PUVA include nausea, vomiting, painful erythema, prolonged itching or stinging, and blisters. Long-term risks of PUVA include photoaging, widespread lentigines, and an increased risk of squamous cell carcinomas. An increased risk of malignant melanoma was observed in a large cohort of PUVA patients •  ecause of the greatly increased risk of squamous cell carcinoma, UVB, preferably narrow- B band, should be used before PUVA is considered and the lifetime number of PUVA treat- ments should be limited. In certain species of animals, an increased risk of cataracts has been documented. Protective eyewear has been advised for PUVA patients during and after treatment. Studies have not shown an increased incidence of cataracts in PUVA patients • Another way to deliver psoralens is by topical application. Bath PUVA has been used and is helpful to eliminate nausea and vomiting, and it avoids the issue of ocular phototoxicity. Localized topical PUVA for psoriasis or eczema of the hands and feet can be effective. The commercial 1% Oxsoralen® solution is usually diluted to 0.1%. Treatments are given every other day. Topical PUVA has also been used for localized vitiligo • Extracorporeal photochemotherapy (photophoresis) can be valuable for erythrodermic CTCL. Little toxicity. It has also been used to prevent organ rejection, treat graft-versus-host disease, and suppress T-cells in rheumatoid arthritis, psoriatic arthritis, SLE, scleroderma, pemphigus • Blood removed from patient’s arm vein. WBC’s plus plasma separated from RBC’s. RBC’s returned to patient. WBC’s irradiated with UVA after 8-MOP has been added. Then WBC’s and plasma returned to patient’s arm13.9  SUNSCREENSPhotodynamic Therapy • Can cause allergic and photoallergic contact dermatitis MEDB with applied sunscreen • SPF= MEDB withouth sunscreen • SPF does not measure UVA protection • Sunscreens divided into chemical blockers, which absorb UVR, and physical blockers, which reflect and scatter UVR • Combine sunscreens with sun avoidance, protective clothing and sunglasses454  2011/2012 Dermatology In-Review l Committed to Your Future
  15. 15. Table 13-2. Sunscreen Ingredients Chemical Absorbers UVB Protection UVA Protection - Avobenzone (parsol 1789) No Yes - Ecamsule No Yes - Cinnamates Yes No - Oxybenzone No Yes - PABA and esters Yes No - Salicylates Yes No - Octocrylene Yes No Physical Blockers - Titanium dioxide Yes Yes - Zinc oxide Yes Yes REF E R E NC E S1 Addo HA et al. A study of compositae plant extract reactions in photosensitivity dermatitis. Photodermatology 1985; 2: 68-79.2. Anderson TF. Light sources in photomedicine. In HW Lim, NA Soter NA, Eds. Clinical Photomedicine. New York: Marcel Dekker, 1993; 37-58.3. Berhanrd JD et al. Ultraviolet A phototherapy in the prophylaxis of solar urticaria. J Am Acad Dermatol 1984; 106: 575-580.4. Bickers DE et al. Hydroa vacciniforme. Arch Dermatol 1978; 114: 1993-1196.5. Birt AR, Davis RA. Hereditary polymorphous light eruption of American Indians. Int J Dermatol 1975; 14: 105-110.6. Boonstra HE, et al. Polymorphous light eruption: A clinical, photobiologic, and follow-up study of 110 patients. J Am Acad Dermatol 2000; 42: 199-207.7. Buchness MR. Photoexacerbated dermatoses. In HW Lim, NA Soter NA, Eds. Clinical Photomedicine. New York: Marcel Dekker, 1993; 269-285.8. Coven TR et al. Narrowband UV-B produces superior clinical and histological resolutio of moderate-to-severe psoriasis in patients compared with broadband UV-B. Arch Dermatol 1997; 133: 1514-1522.9. Dawe RS et al. The natural history of chronic actinic dermatitis. Arch Dermatol 2000; 136: 1215-1220.10. Epstein JH. Polymorphous light eruption. Ann Allergy 1966; 24: 397-405.11. Gilchrest BA et al. The human sunburn reaction:  Histologic and biochemical studies. J Am Acad Dermatol 1981; 5: 411-422.12. Granstein RD. Photoimmunology. In IM Freedberg, IM, et al., Eds. Fitzpatrick’s Dermatology in General Medicine. McGraw Hill, New York, 1999; 1562-73.13. Hann SK et al. Hydroa vacciniforme with unusually severe scar formation: diagnosis by repetitive UVA photo­ testing. J Am Acad Dermatol 1991; 25: 401-403.14. Hawk JLM, Norris PG. Abnormal responses to ultraviolet radiation:  Idiopathic. In IM Freedberg, IM, et al., Eds.. Dermatology in General Medicine. New York: McGraw Hill, 1999; 1573-1589.15. Herd J et al. The use of plastic material for the protection of patients with severe photodermatoses. Br J Dermatol 1973; 88: 283-285.16. Hölze E, et al. Polymorphous light eruption: experimental reproduction of skin lesions. J Am Acad Dermatol 1982; 7: 111-125.17. Horio T. Solar urticaria—idiopathic? Photodermatol Photoimmunol Photomed 2003; 19: 147-154.18. Horio T. Solar urticaria. In HW Lim, NA Soter NA, Eds. Clinical Photomedicine. New York: Marcel Dekker, 1993; 181-192. Photobiology and Photosensitivity Disorders  455
  16. 16. 19. Ive FA et al. “Actinic reticuloid”: a chronic dermotosis associated with severe photosensitivity and the histo- logical resemblance to lymphoma. Br J Dermatol 1969; 81: 469-485.20. Jansen CT. The polymorphic phototest reaction. Arch Dermatol 1982; 118: 638-642.21. Kripke, ML. Carcinogenisis:  Ultraviolet radiation. In Freedberg, IM, et al., eds. Fitzpatrick’s Dermatology in General Medicine. McGraw Hill, New York, 1999; 465-472.22. Lestrani D et al. The clinical features and management of actinic prurigo: A retrospective study. Photodermatol Photoimmunol Photomed 1999; 15: 183-187.23. Lim HW. Abnormal responses to ultraviolet radiation: photosensitivity induced by exogenous agents. In IM Freedberg, IM, et al., Eds.. Dermatology in General Medicine. New York: McGraw Hill, 1999; 1589-1597.24. Lim HW et al. Chronic actinic dermatitis: study of the spectrum of chronic photosensitivity in 12 patients. Arch Dermatol 1990; 126: 317-323.25. Lim HW et al. Chronic actinic dermatitis: an analysis of 51 patients evaluated in the United States and Japan. Arch Dermatol 1994; 130: 1284.26. Ling TC, Givvs NK, Rhodes LE. Treatment of polymorphic light eruption. Photodermatol Photoimmunol Photomed 2003; 19: 217-227.27. Lovell CR et al. Thalidomide in actinic prurigo. Br J Dermatol 1983; 108: 467-470.28. Magnus IA. Dermatological Photobiology. Blackwell Scientific Publications, Oxford, 1976; 7-10.29. Magnus IA et al. Erythropoietic protoporphyria: a new porphyria syndrome with solar urticaria due to proto- porphyria. Lancet 1961; 2: 448-451.30. McGregor JM, Hawk JLM. Acute effects of ultraviolet radiation on the skin. In IM Freedberg, IM, et al., Eds.. Dermatology in General Medicine. New York: McGraw Hill, 1999; 1555-1561.31. Menz J et al. Photopatch testing: a six-year experience. J Am Acad Dermatol 1988; 5: 261.32. Meola T, Soter NA. Photomedicine. In Robins P, ed. Review Notes for the Dermatology Board Exam 2003. Physicians’ Continuing Education Corp., New York, 2003; 97-113.33. Morison WL et al. Oral methoxsalen photochemotherapy of uncommon photodermatoses. Acta Derm Venereol 1979; 59: 366-368.34. Morison WL, Pike RA. Spectral power distributions of radiation sources used in phototherapy and photoche- motherapy. J Am Acad Dermatol 1984; 10: 64-68.35. Norris PG, Hawk JLM. Chronic actinic dermatitis: a unifying concept. Arch Dermatol 1990; 126: 376-378.36. Parrish JA, Jaenicke KF. Action spectrum for the therapy of psoriasis. J Invest Dermatol 1981; 76: 359-364.37. Roelandts R. Photochemotherapy for vitiligo. Photodermatol Photoimmunol Photomed 2003; 19: 1-4.38. Scheen et al. Actinic prurigo. J Am Acad Dermatol 1980; 183-190.39. Serrano G et al. Oxicam-induced photosensitivity. Patch and photopatch testing studies with tenoxicam and piroxicam photoproducts in normal subjects and in piroxicam-droxicam photosensitive patients. J Am Acad Dermatol 1992; 26: 545-551.40. Sisson TRC. Visible light therapy of neonatal hyperbilirubinemia. In Smith CK ed. Photochemical and Photobiological Reviews, Vol. 1. Plenum Press, New York, 1976: 241-268.41. Soter NA. Acute effects of ultraviolet radiation on the skin. Semin Dermatol 1990; 9: 11-15.42. Stern RS et al. Cutaneous squamous-cell carcinoma in patients treated with PUVA. N Engl J Med 1984; 310: 1156-1161.43. Wilkinson DS. Patch test reactions to certain halogenated salicylanilides. Br J Dermatol 1962; 74: 302-306.44. Photoimmunology Summary adapted from Granstein RD. Photoimmunology. In IM Freedberg, IM, et al., Eds. Fitzpatrick’s Dermatology in General Medicine. New York: McGraw Hill, 1999; 1562-1573.45. Most Common Medications Producing Photosensitivity adapted from Lim HW. Abnormal responses to ultra- violet radiation: photosensitivity induced by exogenous agents. In IM Freedberg, IM, et al., Eds.. Dermatology in General Medicine. New York: McGraw Hill, 1999; 1589-1597.46. Sun Protective Agents: Formulations, Effects, and Side Effects . Gasparro FP et al. In Freedberg IM et al., Eds. Fitzpatrick’s Dermatology in General Medicine. New York: McGraw Hill, 2003; 2345.456  2011/2012 Dermatology In-Review l Committed to Your Future
  17. 17. NOTES Photobiology and Photosensitivity Disorders  457
  18. 18. NOTES458  2011/2012 Dermatology In-Review l Committed to Your Future

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