92: Polymorphic Light Eruption Flashcards
1
Q
What is the most common photodermatosis that typically presents in the spring?
A
Polymorphic light eruption (PMLE) is the most common photodermatosis, particularly among young women in temperate climates.
2
Q
What are the clinical features of PMLE?
A
PMLE presents as a pruritic, erythematous eruption of variable inter-individual morphology, usually papular, on sun-exposed skin areas, occurring within hours to days of exposure, with full resolution in several days.
3
Q
What is the treatment of choice for photohardening in PMLE?
A
The treatment of choice for photohardening in PMLE is broad-spectrum sunscreen use, oral or topical steroids, and prophylactic low-dose immunosuppressive phototherapy.
4
Q
What is the relationship between UV exposure and PMLE lesions?
A
PMLE lesions occur after ultraviolet (UV) exposure, typically within hours to days, and usually resolve fully without scarring after UV exposure ceases.
5
Q
Which sites are usually spared in PMLE?
A
The face and earlobes are usually spared in PMLE.
6
Q
What is the incidence of PMLE in the UK and Australia?
A
The incidence of PMLE is approximately 15% in the UK and 5% in Australia.
7
Q
What is the role of prednisone in the treatment of PMLE?
A
Prednisone is taken initially at the first sign of pruritus in PMLE.
8
Q
What is the significance of a positive family history in PMLE patients?
A
A positive family history is present in approximately 18% of PMLE patients, indicating a potential genetic predisposition.
9
Q
What variant of PMLE has been linked to individuals with darker skin types?
A
The pinpoint papular variant of PMLE has been linked to individuals with darker skin types, particularly in the African American population and dark-skinned individuals in Asia.
10
Q
A patient presents with pruritic, erythematous papules on sun-exposed areas after their first intense sunlight exposure in spring. What is the most likely diagnosis, and what is the underlying pathogenesis?
A
The most likely diagnosis is Polymorphic Light Eruption (PMLE). The underlying pathogenesis involves resistance to UV-induced immune suppression, leading to a delayed-type hypersensitivity reaction against UV-induced antigens.
11
Q
A patient with PMLE reports that their lesions resolve fully within 7-10 days after UV exposure ceases. What does this indicate about the natural course of PMLE?
A
This indicates that PMLE lesions typically resolve fully without scarring over several days, occasionally taking 7-10 days.
12
Q
A patient with PMLE has a history of flares during summer holidays. What phenomenon might explain why their symptoms lessen as summer progresses?
A
The phenomenon is called ‘hardening,’ where repetitive exposures to sunlight lead to skin adaptation, making lesions less likely to occur or less severe.
13
Q
A patient with PMLE is advised to avoid sun exposure and use broad-spectrum sunscreen. Why is broad-spectrum sunscreen particularly important for PMLE patients?
A
Broad-spectrum sunscreen is important because it protects against both UVA and UVB radiation, which are implicated in triggering PMLE.
14
Q
A patient with PMLE is prescribed 20-30 mg of prednisone at the first sign of pruritus. What is the rationale behind this treatment?
A
Prednisone reduces inflammation and alleviates symptoms, providing relief within several days and preventing recurrences during the same exposure period.
15
Q
What is the typical clinical presentation of PMLE?
A
A pruritic, erythematous eruption of variable inter-individual morphology on sun-exposed skin areas.
16
Q
What is the relationship between PMLE and ultraviolet (UV) exposure?
A
PMLE occurs after UV exposure, with lesions appearing within hours to days.
17
Q
Which demographic is most affected by PMLE?
A
Young women in temperate climates.
18
Q
What is the incidence of PMLE in the UK?
A
15%.
19
Q
What is the significance of Langerhans cells in PMLE?
A
Increased number of Langerhans cells are found in PMLE lesions.
20
Q
What is a rare variant of PMLE that occurs on the lower legs?
A
A rare variant of PMLE is not specified in the text, but it is mentioned that there is one.
21
Q
What is the typical duration for lesions to resolve after UV exposure in PMLE?
A
Lesions usually resolve fully within 7 to 10 days after UV exposure ceases.
22
Q
What is the first sign of an impending PMLE eruption?
A
Itching may be noted as the first sign of an impending PMLE eruption.
23
Q
What areas of the body are most affected by PMLE?
A
Particularly sun-exposed areas that are normally covered during winter, such as the upper chest and the extensor aspects of the arms, are most affected.
24
Q
What does the term ‘polymorphous’ refer to in the context of PMLE?
A
The term ‘polymorphous’ describes the variability in lesion morphology observed among different patients with the eruption.
25
What is the most common form of PMLE?
The papular form, characterized by large or small separate or confluent erythematous and edematous papules that may form clusters, is the most common.
26
What are the potential variants of PMLE?
Variants of PMLE include papulovesicular, plaque, localized, juvenile spring eruption, solar purpura, benign summer light eruption, and PMLE sine eruption.
27
What wavebands are most causative in initiating PMLE?
UVA radiation (320 to 400 nm) usually seems more causative than UVB (290 to 320 nm) at initiating PMLE, but lesions can also be induced with UVB alone and sometimes with both waveband ranges.
28
What systemic symptoms may occur in PMLE patients?
Systemic symptoms in PMLE are rare but may include headache, fever, chills, malaise, and nausea.
29
What is the relationship between PMLE and lupus?
PMLE lesions may precede the development of lupus, and progression of PMLE to lupus has been proposed, but long-term follow-up studies have not shown a general increased rate of lupus in PMLE patients.
30
What immunologic aspects are associated with PMLE?
A resistance to UV-induced immune suppression and a subsequent delayed-type hypersensitivity response to UV-modified elements of the skin have been suggested, along with an influx of CD4+ T lymphocytes in early PMLE lesions.
31
A patient with PMLE is found to have increased numbers of Langerhans cells in their lesions. What does this finding suggest about the immune response in PMLE?
This finding suggests a resistance to UV-induced immune suppression and a subsequent delayed-type hypersensitivity response to UV-modified elements in the skin.
32
A patient with PMLE reports that their symptoms worsen after using sunscreen. What could explain this paradoxical reaction?
Some sunscreens preferentially block UVB while transmitting UVA and visible light, which can trigger PMLE if exposure times are lengthened.
33
A patient with PMLE has a history of systemic symptoms like headache and fever after sun exposure. What is the likely cause of these symptoms?
These systemic symptoms may result from UV-induced release of cytokines with pyrogenic activity related to an accompanying sunburn reaction.
34
A patient with PMLE is found to have a history of photosensitive psoriasis. How might PMLE affect their psoriasis symptoms?
PMLE may exacerbate psoriatic lesions due to resistance to UV-induced immune suppression, which would otherwise counteract psoriatic inflammation.
35
A patient with PMLE is found to have a localized variant with erythematous-edematous papules on both elbows. What is this variant called?
This localized variant is called juvenile spring eruption.
36
A patient with PMLE is found to have a rare variant predominantly affecting the lower legs. What is this variant called?
This rare variant is called solar purpura.
37
A patient with PMLE is found to have a history of lupus erythematosus. How might PMLE and lupus be related?
PMLE lesions may precede the development of lupus, and progression of PMLE to lupus has been proposed in some cases.
38
What areas are most affected by PMLE during spring?
Particularly sun-exposed areas that are normally covered during winter, such as the upper chest and the extensor aspects of the arms.
39
What does the term 'polymorphous' refer to in PMLE?
It describes the variability in lesion morphology observed among different patients with the eruption.
40
What is the most common form of PMLE?
The papular form, characterized by large or small separate or confluent erythematous and edematous papules that may form clusters.
41
What is a potential localized subtype of PMLE that affects boys in spring?
Juvenile spring eruption, characterized by pruritic papules and vesicles on their ear helices.
42
What type of radiation is usually more causative in initiating PMLE?
UVA radiation (320 to 400 nm) usually seems more causative than UVB (290 to 320 nm).
43
What effect can sunscreens have on PMLE?
Some patients may note that the use of sunscreens may have a PMLE-enhancing effect if exposure times are lengthened.
44
What are some systemic symptoms that may occur in PMLE?
Headache, fever, chills, malaise, and nausea may occur, although they are rare.
45
What is the relationship between PMLE and lupus?
PMLE lesions may precede the development of lupus, but long-term follow-up studies have not shown a general increased rate of lupus in PMLE patients.
46
What histologic features are associated with early PMLE lesions?
An initial influx of CD4+ T lymphocytes for up to 72 hours, followed by CD8+ T cells in established lesions, consistent with a cellular-mediated immune response.
47
What is the role of UV radiation in the immune response of healthy skin compared to patients with PMLE?
In healthy skin, UV radiation induces an immunosuppressive Th2 micromilieu, leading to the depletion of epidermal Langerhans cells, neutrophilic infiltration, and the release of immunosuppressive cytokines like IL-4 and IL-10. In contrast, patients with PMLE show resistance to UV-induced immune suppression, favoring an immune response to potential UV-induced antigens and exhibiting a Th1 cytokine profile instead.
48
How does PMLE affect the induction of contact hypersensitivity?
Patients with PMLE demonstrate a suppression of contact hypersensitivity following UV exposure, indicating impaired UV-induced tolerance to contact allergens. This contrasts with normal individuals who can develop contact hypersensitivity after UV exposure.
49
What genetic factors are associated with PMLE?
PMLE is indicated to have a polygenic inheritance model. Familial clustering is observed, with a family history of PMLE present in 12% of first-degree relatives of affected individuals. Additionally, a 21% prevalence of photosensitivity was noted among first-degree relatives of PMLE patients.
50
What hormonal factors may influence the incidence of PMLE in women?
Females are described as being relatively resistant to the immunosuppressive effects of UV radiation, requiring more than three times the amount of UV exposure to achieve the same level of immune suppression as men. This may contribute to the higher incidence of PMLE in women. The hormone 17β-estradiol is also suggested to play a role by preventing UV-induced immune suppression.
51
What is the relationship between PMLE and skin cancer prevalence?
Patients with PMLE show a lower prevalence of skin cancer compared to matched controls, suggesting that PMLE may act as a protective condition against skin cancer. This is consistent with the reported resistance to UV-induced immune suppression in PMLE patients.
52
A patient with PMLE has a positive family history of photosensitivity. What percentage of PMLE patients typically report a positive family history?
Approximately 20% of PMLE patients report a positive family history.
53
A patient with PMLE is found to have a Th1 cytokine profile in their lesions. How does this differ from the immune response in healthy UV-exposed skin?
In PMLE, a Th1 cytokine profile is favored, whereas healthy UV-exposed skin exhibits an immunosuppressive Th2 cytokine milieu.
54
A patient with PMLE is found to have abnormal baseline levels of proinflammatory cytokines. How might this contribute to their condition?
Abnormal baseline levels of proinflammatory cytokines, such as IL-1 family members, may create an environment that permits hypersensitivity responses to photoinduced antigens.
55
A patient with PMLE is found to have a genetic deficiency in clearing apoptotic keratinocytes. How might this contribute to their condition?
This deficiency may result in a possible autoantigen source and altered immune function, promoting PMLE.
56
A patient with PMLE is found to have dysregulated expression of antimicrobial peptides like LL-37. How might this contribute to their condition?
Dysregulated expression of antimicrobial peptides may play a role in the failure of immune suppression, contributing to PMLE.
57
A patient with PMLE is found to have a resistance to UV-induced immune suppression. How does this resistance affect their immune response?
This resistance favors immune responses to potential UV-induced antigens, leading to hypersensitivity reactions.
58
A patient with PMLE is undergoing photohardening therapy. How does this therapy restore impaired neutrophil responsiveness?
Photohardening restores impaired neutrophil responsiveness to chemoattractants, reducing PMLE symptoms.
59
A patient with PMLE is found to have increased expression of heat shock protein (HSP65) in their lesions. What does this suggest about the pathogenesis of PMLE?
Increased expression of HSP65 suggests a role for photo-induced antigens in initiating PMLE, similar to autoimmune processes.
60
A patient with PMLE is found to have a familial clustering of photosensitivity. What inheritance model is suggested for PMLE?
A polygenic inheritance model is suggested for PMLE.
61
A patient with PMLE is found to have a higher prevalence of the condition in females. What hormonal factor might explain this gender difference?
The female hormone 17β-estradiol may prevent UV-induced immune suppression by limiting IL-10 release, contributing to the higher prevalence in females.
62
A patient with PMLE is found to have a resistance to UV-induced depletion of Langerhans cells. How does this resistance contribute to their condition?
Resistance to UV-induced depletion of Langerhans cells allows for the persistence of immune responses to photoinduced antigens, contributing to PMLE.
63
What immune response is favored in patients with PMLE after UV exposure?
A Th1 cytokine profile is favored, showing no immunosuppression.
64
How does PMLE affect the induction of contact hypersensitivity?
PMLE shows a resistance to UV-induced immune suppression, impairing the induction of contact hypersensitivity.
65
What is the relationship between PMLE and skin cancer prevalence?
PMLE patients show a trend for decreased skin cancer prevalence compared to matched controls, suggesting a protective condition.
66
What genetic factors are associated with PMLE?
PMLE inheritance is polygenic, with familial clustering evident in first-degree relatives.
67
How do hormonal factors influence PMLE incidence?
Females are described as being relatively resistant to the immunosuppressive effects of UV radiation, requiring more than three times the amount of UV exposure to achieve the same level of immune suppression as men.
68
How do hormonal factors influence PMLE incidence?
Females are more resistant to UV immunosuppression, which may explain the higher incidence of PMLE in women.
69
What role do antimicrobial peptides play in PMLE?
In PMLE, there is greater upregulation and altered expression of antimicrobial peptides, particularly in early stages of lesions.
70
What is the effect of photohardening therapy in PMLE patients?
Photohardening therapy restores impaired UV-induced Langerhans cell depletion and neutrophil influx in PMLE.
71
What is the significance of the 17β-estradiol hormone in PMLE?
17β-estradiol may prevent UV radiation-induced immune suppression by limiting IL-10 release from keratinocytes.
72
What is the impact of microbial elements on PMLE?
Microbial elements may be initial triggers of PMLE, with UV-induced DNA damage to the microbiome involved.
73
What are the diagnostic criteria for polymorphous light eruption (PMLE)?
The diagnostic criteria for PMLE include:
1. **Delayed occurrence** of skin lesions after UV exposure (within hours to days, but not less than 30 minutes).
2. **Persistence** of the skin lesions for several days (up to 10 days).
3. **Monomorphous clinical presentation** on predilection sites.
74
What laboratory tests can help exclude other forms of lupus erythematosus in patients with PMLE?
Laboratory tests that can help exclude other forms of lupus erythematosus in patients with PMLE include:
- **Anti ds-DNA** and **anti-SSA/Ro** or **anti-SSB/La** tests to exclude subacute cutaneous lupus.
- Assessment of **red blood cell protoporphyrins** to exclude erythropoietic protoporphyria.
- **Antinuclear antibody** testing, where 11% of PMLE patients may be positive, but most have insignificant titers of less than 1:160.
75
What histopathological features are characteristic of PMLE?
Histopathological features characteristic of PMLE include:
- Moderate to dense mixed perivascular infiltrate in the upper and mid dermis, predominantly consisting of **T cells**, with neutrophils and infrequent eosinophils.
- **Papillary, dermal, and perivascular edema** with endothelial cell swelling.
- **Epidermal changes** such as spongiosis, occasional dyskeratosis, exocytosis, and basal cell vacuolization (not always present).
76
What is the purpose of phototesting and photoprovocation in diagnosing PMLE?
The purpose of phototesting and photoprovocation in diagnosing PMLE is to:
- Confirm the diagnosis when history and clinical features are not diagnostic.
- Reproduce PMLE lesions in clinical practice, allowing for a subsequent skin biopsy.
- Assess the patient's sensitivity to UV exposure, as PMLE patients do not exhibit abnormal sensitivity to develop erythema upon UV exposure.
77
What are some differential diagnoses for PMLE?
Differential diagnoses for PMLE include:
1. **Mallorca acne**: Characterized by long-persisting acneiform papules on sun-exposed areas.
2. **Prurigo actinica**: Shows prurigo lesions in chronic UV-exposed skin areas, mainly in the face.
3. **Hydroa vacciniforme**: Early onset in childhood with papulovesicular lesions.
4. **Lymphocytic infiltration**: Erythematous plaques, mostly on the face.
5. **Chronic discoid lupus erythematosus**: Can be differentiated by clinical morphology.
6. **Chronic actinic dermatitis**: Eczematous morphology is atypical for PMLE.
78
A patient with PMLE undergoes photoprovocation testing. What is the purpose of this test, and how is it performed?
Photoprovocation testing is performed to reproduce PMLE lesions and confirm the diagnosis. It involves exposing symmetrically located test areas to increasing suberythemal or near-erythemal doses of UVA or UVB radiation for 4-5 days.
79
A patient with PMLE is undergoing photoprovocation testing in early spring. Why is this timing important?
Photoprovocation testing is best performed in early spring to avoid false-negative results due to natural photohardening later in the season.
80
A patient with PMLE is undergoing photoprovocation testing. What percentage of affected subjects typically exhibit sensitivity to UVA, UVB, or both wavebands?
60-90% of affected subjects exhibit sensitivity to UVA, UVB, or both wavebands during photoprovocation testing.
81
A patient with PMLE is undergoing photoprovocation testing. What is the purpose of monitoring negative test areas for several weeks?
Negative test areas are monitored to detect delayed eruptions of possible lupus lesions, which may evolve 10-14 days after provocation.
82
A patient with PMLE is found to have a history of Mallorca acne. How can this condition be differentiated from PMLE?
Mallorca acne is characterized by long-persisting acneiform follicular papules on sun-exposed areas, often linked to the use of oily sunscreen vehicles.
83
A patient with PMLE is undergoing photoprovocation testing. Why might visible light be used in this test?
Visible light may be used to exclude conditions like solar urticaria, which can mimic PMLE.
84
A patient with PMLE is found to have a history of prurigo actinica. How can this condition be differentiated from PMLE?
Prurigo actinica shows prurigo lesions in chronic UV-exposed skin areas, often associated with cheilitis and starting in childhood.
85
A patient with PMLE is found to have a history of hydroa vacciniforme. How can this condition be differentiated from PMLE?
Hydroa vacciniforme is characterized by papulovesicular or bullous hemorrhagic lesions, typically on the face, ears, and dorsum of the hands, with residual scarring.
86
A patient with PMLE is undergoing photoprovocation testing. What is the significance of using previously involved skin for this test?
Using previously involved skin increases the likelihood of reproducing PMLE lesions during photoprovocation testing.
87
What are the diagnostic criteria for PMLE?
Delayed occurrence of skin lesions after UV exposure, persistence of lesions for several days, and monomorphous clinical presentation on predilection sites.
88
What laboratory tests can help exclude other forms of lupus erythematosus in PMLE patients?
Anti ds-DNA and anti-SSA/Ro or anti-SSB/La tests.
89
What is the significance of photoprovocation in diagnosing PMLE?
It is performed to reproduce PMLE lesions in clinical practice, confirming the diagnosis when history and clinical features are not diagnostic.
90
What is the typical histopathological finding in PMLE?
Moderate to dense mixed perivascular infiltrate in the upper and mid dermis, predominantly consisting of T cells, with neutrophils and infrequent eosinophils.
91
What is the role of phototesting in PMLE?
Phototesting can be performed with visible light to exclude solar urticaria.
92
What is Mallorca acne and how is it related to PMLE?
Mallorca acne is characterized by long-persisting acneiform papules on sun-exposed areas and may represent a separate entity from PMLE.
93
What is Prurigo actinica and how does it differ from PMLE?
Prurigo actinica shows prurigo lesions in chronic UV-exposed skin areas, mainly in the face, and has a seasonal character in childhood, unlike PMLE.
94
What is Hydroa vacciniforme and how is it differentiated from PMLE?
Hydroa vacciniforme is characterized by early onset in childhood and intermittent occurrence of papulovesicular or bullous hemorrhagic skin lesions, typically on the face, ears, and dorsum of the hands.
95
What is the typical morphology of skin lesions in chronic actinic dermatitis?
Eczematous morphology, which is atypical for PMLE.
96
What is the typical course and prognosis of PMLE in affected patients?
PMLE is chronic in nature, with a persistent course and a slow tendency to amelioration. In a study with a follow-up of 7 years, 64 of 114 PMLE patients reported diminishing sun sensitivity, and 12 patients had no further sun-precipitated rashes. After an average of 32 years post-onset, 24% of patients were considered cured, 51% reported alleviation of symptoms, and 24% noticed equal or stronger symptoms than before.
97
What are the recommended preventive measures for PMLE?
Preventive measures for PMLE include:
1. Avoiding sun exposure.
2. Using broad-spectrum sunscreens with effective UVA protection.
3. Wearing protective clothing.
98
What medications are used to manage PMLE lesions after eruption?
After the eruption of PMLE lesions, the following medications can be used:
- **Topical steroids** to reduce inflammation and alleviate itch.
- **Oral antihistamines** to shorten the duration of the eruption.
- **Prednisone** (20-30 mg) can be taken at the first sign of pruritus, tapering off as the eruption clears. This treatment may be repeated safely if tolerated.
99
What is photohardening and how is it used in PMLE management?
Photohardening is a preventive approach for individuals with repeated PMLE attacks. It involves:
- **Broadband UVB (290 to 320 nm)**, **narrowband UVB (311 nm)**, or **psoralen plus UVA photochemotherapy** to induce photoadaptation.
- Phototherapy is typically given 2-3 times per week for 4 to 6 weeks.
- Narrowband UVB phototherapy is effective in 70% to 80% of cases and is the treatment of choice due to ease of administration.
100
What are the treatment options for severe PMLE symptoms?
For severe PMLE symptoms, the following treatments are recommended:
- **Azathioprine**, **thalidomide**, or **antimalarials** like chloroquine or hydroxychloroquine, which have immunomodulatory and anti-inflammatory properties.
- Immune suppressive therapy has shown efficacy in reducing the prevalence of PMLE in immunosuppressed individuals.
101
What experimental approaches have been explored for PMLE management?
Experimental approaches for managing PMLE include:
- Oral administration of supplements containing **lycopene**, **beta-carotene**, and **Lactobacillus johnsonii** or extracts from **Polypodium leucotomos**.
- Topical application of **DNA repair enzymes** in after-sun lotions to diminish PMLE symptoms by enhancing removal of UV-induced DNA photoproducts.
102
A patient with PMLE is undergoing photohardening therapy. What are the mechanisms underlying the photohardening effect?
Photohardening works by melanization of the skin, thickening of the stratum corneum, and restoration of immunologic susceptibility, including impaired UV-induced Langerhans cell depletion and neutrophil infiltration.
103
A patient with PMLE is prescribed narrowband UVB phototherapy. Why is this considered the treatment of choice for photohardening?
Narrowband UVB phototherapy is effective in 70-80% of cases and is preferred due to its ease of administration and high efficacy.
104
A patient with PMLE is advised to take oral prednisolone prophylactically before a sunny vacation. What is the purpose of this approach?
Prophylactic oral prednisolone prevents flares by reducing inflammation and immune response before sun exposure.
105
A patient with PMLE is advised to use a sunscreen with high UVA protection. What SPF level and application density are recommended for effective prevention?
An SPF 45 sunscreen with high UVA protection applied at a density of 1 mg/cm² is recommended.
106
A patient with PMLE is undergoing photohardening therapy. What types of phototherapy are effective for this purpose?
Broadband UVB, narrowband UVB (311 nm), and psoralen plus UVA photochemotherapy are effective for photohardening.
107
A patient with PMLE is undergoing photohardening therapy. How does this therapy simulate the natural hardening phenomenon?
Photohardening therapy uses suberythemal doses of UV radiation to induce photoadaptation, mimicking the natural hardening phenomenon.
108
What is the nature of PMLE in most affected patients?
Chronic with a persistent course and a slow tendency to amelioration.
109
What percentage of PMLE patients reported diminishing sun sensitivity in a 7-year study?
64 out of 114 PMLE patients.
110
What is the recommended approach for preventing PMLE?
Avoiding sun exposure and using broad-spectrum sunscreens with effective UVA protection.
111
What medications can be used after the eruption of PMLE lesions?
Topical steroids and occasionally oral antihistamines.
112
What is the purpose of photohardening in PMLE treatment?
To prevent attacks of PMLE through controlled sun exposure.
113
What is the effectiveness of narrowband UVB phototherapy in treating PMLE?
Effective in 70% to 80% of cases.
114
What are some severe treatment options for PMLE?
Azathioprine, thalidomide, or antimalarials like chloroquine or hydroxychloroquine.
115
What role do antioxidants play in PMLE management?
Oral administration of supplements with antioxidant properties may prevent eruption of PMLE.
116
What is the effect of topical application of DNA repair enzymes in PMLE?
It diminished PMLE symptoms in an experimental study.
117
What are the diagnostic criteria for Polymorphic Light Eruption?
1. **Delayed occurrence** of skin lesions after ultraviolet (UV) exposure (within hours to days; but not <30 minutes).
2. **Lesions persist** for several days after exposure (up to 10 days after cessation of UV exposure).
3. **Monomorphous clinical presentation** on sites of predilection (upper chest, extensor arms, with sparing of the face and hands).
118
What factors should be considered when evaluating a patient with lesions despite rigorous avoidance of sunlight?
- **Patient's age at onset**: Childhood, Young adulthood, or Elderly.
- **Presence of pock scars**: Indicates Erythropoietic protoporphyria or Hydroa vacciniforme.
- **History of contact dermatitis** or outdoor hobbies.
- **Excoriations, swallow scars, or dyspigmentation** predominance.
- **Medication history**: Photosensitizing medications may indicate phototoxic or photallergic drug eruption.
119
What are the potential conditions to consider based on the onset and duration of lesions in Polymorphic Light Eruption?
| Onset Duration | Possible Conditions |
|----------------|--------------------|
| Within minutes, resolution within hours | Solar urticaria |
| Within hours to days, resolution within days to weeks | Polymorphic light eruption |
| Within weeks, resolution within weeks | Anetodermal papules, Lupus erythematosus, Mallorca acne |
120
What is the primary condition being diagnosed in the flowchart?
Polymorphic light eruption.
121
What are the diagnostic criteria for polymorphic light eruption?
Delayed occurrence of skin lesions after UV exposure, persistence of lesions for several days, and monomorphous clinical presentation on specific sites.
122
What age groups are considered in the diagnosis of polymorphic light eruption?
Childhood, young adulthood, and elderly.
123
What is a common symptom of polymorphic light eruption after sun exposure?
Painful skin redness and swelling.
124
What should be considered if lesions are present despite rigorous avoidance of sunlight?
Photoexacerbated.
125
What condition is being diagnosed in the flowchart?
Polymorphic light eruption.
126
What should be considered if lesions are present despite rigorous avoidance of sunlight?
Photoexacerbated primary dermatitis.
127
What condition is associated with intermittent occurrence of EM-like rash in the elderly?
Photograggravated erythema multiforme.
128
What is actinic prurigo?
A condition characterized by itching due to sun exposure, often considered in the diagnosis of polymorphic light eruption.
129
What is the significance of the onset and duration of lesions in diagnosing polymorphic light eruption?
It helps differentiate between various skin conditions based on how quickly lesions appear and resolve.
130
What is the relationship between photosensitizing medications and polymorphic light eruption?
Patients taking photosensitizing medications may experience phototoxic or photallergic drug eruptions.
