Photosensitivity and Other Reactions to Sunlight¶
Chapter 64 | Part 2: Cardinal Manifestations and Presentation of Diseases
KEY CLINICAL POINTS¶
- UV radiation (UVR) induces DNA damage, oxidative stress, and immunosuppression, contributing to skin cancer and photodermatoses.
- The Fitzpatrick classification (Table 64-1) categorizes skin phototype based on melanin content and sunburn risk.
- Phototoxicity (non-immunologic) vs. photoallergy (immunologic) are distinct mechanisms of photosensitivity.
- Porphyrias (e.g., PCT, EPP) are inherited metabolic disorders causing cutaneous photosensitivity due to porphyrin accumulation.
- Photoprotection (sunscreen, clothing, avoidance) and phototherapy (NB-UVB, PUVA) are critical for managing photosensitivity.
1. DEFINITION & OVERVIEW¶
Photosensitivity is a cutaneous reaction to sunlight, mediated by chromophores (endogenous/exogenous) absorbing UVR. It encompasses phototoxicity (direct chemical damage) and photoallergy (immune-mediated). UVR also induces immunosuppression, increasing skin cancer risk.
Table 64-1 Skin Type and Sunburn Sensitivity (Fitzpatrick Classification)¶
| TYPE | DESCRIPTION |
|---|---|
| I | Always burn, never tan |
| II | Always burn, sometimes tan |
| III | Sometimes burn, sometimes tan |
| IV | Sometimes burn, always tan |
| V | Never burn, sometimes tan |
| VI | Never burn, always tan |
1.1 UV Radiation and Skin Structure¶
UV-B (290–320 nm) and UV-A (320–400 nm) penetrate skin, with UV-B causing DNA damage and UV-A contributing to photoaging. Melanin (eumelanin vs. pheomelanin) modulates photoprotection. Fitzpatrick classification (Table 64-1) guides sunburn risk assessment.
1.2 Photodynamic Mechanisms¶
UVR activates chromophores (e.g., porphyrins, DNA) to generate reactive oxygen species (ROS) and DNA damage. This leads to erythema, DNA mutations, and immunosuppression, contributing to skin cancer (NMSC, melanoma).
2. EPIDEMIOLOGY¶
UV exposure is a major risk factor for skin cancer (NMSC, melanoma). Fair-skinned individuals (skin types I–III) have higher risk. Porphyrias (e.g., PCT) show geographic variation, with PCT prevalence linked to iron overload and UROD deficiency.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
UV-B induces DNA mutations (e.g., cyclobutane pyrimidine dimers), while UV-A causes oxidative damage and collagen degradation. Porphyrias result from heme synthesis defects, leading to porphyrin accumulation and photosensitivity. Immunosuppression from UVR exacerbates cancer risk.
3.1 DNA Damage and Carcinogenesis¶
UV-B induces DNA mutations (e.g., C → T transitions) in keratinocytes, leading to NMSC. ROS from UVR damage lipids, proteins, and DNA, promoting photoaging and cancer.
3.2 Porphyria Pathogenesis¶
Porphyrias (e.g., PCT, EPP) arise from heme pathway defects. PCT is due to UROD deficiency, while EPP results from ferrochelatase deficiency, causing protoporphyrin accumulation and photosensitivity.
4. CLINICAL FEATURES¶
Acute: sunburn (UV-B), phototoxic eruptions (erythema, blistering). Chronic: photoaging (wrinkling, telangiectasia), actinic keratosis, SCC/BCC. Photoallergic reactions present as pruritic eczema. Porphyrias cause blistering (PCT) or painful burning (EPP).
5. DIFFERENTIAL DIAGNOSIS¶
Differentiate phototoxicity (immediate, sunburn-like) vs. photoallergy (delayed, eczematous). Rule out systemic diseases (e.g., lupus, porphyrias) and drug-induced reactions (e.g., sulfonamides, tetracyclines).
6. INVESTIGATIONS & DIAGNOSIS¶
Phototesting (UV-A/UV-B exposure) identifies photosensitivity. Biopsy confirms porphyrias or photodermatoses. Urinary porphyrin excretion and UROD assays diagnose PCT. Histopathology reveals solar elastosis, actinic keratosis, or SCC.
7. MANAGEMENT & TREATMENT¶
Avoidance of sunlight, photoprotection (broad-spectrum sunscreen, SPF ≥ 30), and drug discontinuation. Phototherapy (NB-UVB, PUVA) for psoriasis/vitiligo. Immunosuppressants (azathioprine) for chronic actinic dermatitis. Afamelanotide for EPP.
Table 64-5 FDA Category I Monographed Sunscreen Active Ingredients¶
| INGREDIENTS | MAXIMUM CONCENTRATION, % |
|---|---|
| p-Aminobenzoic acid (PABA) | 15 |
| INGREDIENTS | MAXIMUM CONCENTRATION, % |
|---|---|
| Avobenzone | 3 |
| Cinoxate | 3 |
| Dioxybenzone (benzophenone-8) | 3 |
| Ecamsule | 15 |
| Homosalate | 15 |
| Octocrylene | 10 |
| Octinoxate | 7.5 |
| Octisalate | 5 |
| Oxybenzone (benzophenone-3) | 6 |
| Padimate O (octyl dimethyl PABA) | 8 |
| Ensulizole | 4 |
| Sulisobenzone (benzophenone-4) | 10 |
| Titanium dioxide | 25 |
| Trolamine salicylate | 12 |
| Zinc oxide | 25 |
7.1 Photoprotection Strategies¶
Use broad-spectrum sunscreen (Table 64-5), wear protective clothing, and avoid midday sun. Water-resistant formulations are recommended for outdoor activities.
7.2 Phototherapy¶
NB-UVB is preferred for psoriasis/vitiligo due to lower skin cancer risk. PUVA (psoralen + UV-A) is effective for cutaneous T-cell lymphoma but carries higher malignancy risk.
8. PROGNOSIS & COMPLICATIONS¶
Chronic UVR exposure increases NMSC and melanoma risk. Porphyrias may lead to scarring or disfigurement. Immunosuppressed patients (e.g., transplant recipients) face heightened skin cancer risk. Persistent light reaction may require long-term photoprotection.
9. SPECIAL CONSIDERATIONS¶
Immunosuppressed patients (e.g., transplant recipients, HIV) are at higher risk for NMSC. Porphyrias require strict sun avoidance. Pregnant patients should avoid tanning beds. Elderly patients need vigilant photoprotection due to increased skin fragility.
10. KEY POINTS & CLINICAL PEARLS¶
- UV-B is a complete carcinogen; UV-A contributes to photoaging.
- Photoprotection is critical for preventing NMSC and melanoma.
- Porphyrias require strict sun avoidance and treatment of underlying metabolic defects.
- Phototherapy (NB-UVB) is safer than PUVA for long-term use.