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Review Article Review Article Photodynamic therapy in dermatology Chitra S. Nayak Department of Dermatology, BYL Nair Hospital and TN Medial College, Mumbai, India Address for correspondence: Chitra S. Nayak, 302, Arun, 6th Road, Santacruz East, Mumbai - 400055, India. E-mail: [email protected] ABSTRACT Photodynamic therapy is a new modality of therapy being used for the diagnosis and treatment of many tumors. It is now being increasingly used for skin tumors and other dermatological disorders. With its range of application it is certainly the therapy of the future. Its mechanism of action is by the Type II photo-oxidative reaction. The variables are the photosensitizer, the tissue oxygenation and the light source. It has been used to treat various disorders including Bowen’s disease, actinic keratoses, squamous cell carcinomas, basal cell carcinomas, and mycosis fungoides. The side-effects are fortunately mild and transient. Newer photosensitisers like methyl aminolevulinate hold a lot of promise for better therapy. Key Words: Photosensitizer, Light source, Aminolevulinate HISTORY in the target cells followed by selective irradiation of the lesion with visible light. The drug and light are The use of sunlight for the treatment of various skin individually non-toxic, but in combination destroy disorders (heliotherapy) was known to ancient Indians tissues. and Greeks. In the modern era, Oscar Raab, a German medical student first reported the death of Paramecium MECHANISM OF ACTION caudatum (a protozoan) after light exposure in the presence of acridine orange in the year 1900.[1] His The efficacy of PDT depends on all the following professor, von Tappeiner, coined the term mechanisms which are inter-linked: direct cytotoxicity, “photodynamic” to describe oxygen-consuming vascular damage, inflammation and immune host chemical reactions in vivo. Von Tappeiner and Jesionek response.[2] (a dermatologist), in 1904, used topical eosin and visible light to treat skin tumors, condyloma lata and lupus Direct cytotoxicity: In PDT absorption of a light photon vulgaris.[1] by the sensitizer causes its promotion from the ground state to the extremely unstable short lived excited DEFINITION singlet state. The singlet excited photosensitizer emits fluorescence and decays back to the ground state or to Photodynamic therapy (PDT) is a treatment modality the longer lived triplet excited state. Interaction of the involving administration of a photosensitizing triplet sensitizer with surrounding molecules results compound, accumulation of the sensitizer molecules in photo-oxidative reactions (POR) that release singlet How to cite this article: Nayak CS. Photodynamic therapy in dermatology. Indian J Dermatol Venereol Leprol 2005;71:155-60. Received: July, 2004. Accepted: November, 2004. Source of Support: Nil. Conflict of interest: None declared. 155 Indian J Dermatol Venereol Leprol May-June 2005 Vol 71 Issue 3 Nayak CS: Photodynamic therapy in dermatology oxygen resulting in phototoxicity. Lipid peroxidation specific immune cells that appear to be directed against leads to cell membrane defects, which result in cell both strongly and poorly immunogenic cancer types. lysis [Figure 1]. Damage to mitochondria, lysosomes or endoplasmic reticulum occurs depending on the Host immune response: Thus mobilization of the host location of the photosensitizer in the cell. As most to participate in the tumor ablation process is a unique photosensitisers do not localize in the nucleus, nuclear feature of PDT and is an advantage over conventional damage is not an important factor of PDT-mediated anticancer therapy. Use of monoclonal antibody- cytotoxicity. sensitizer conjugates results in greater selectivity and higher complete response rates, enhancing the anti- Vascular injury: Vascular injury is important in tumor tumor properties of PDT. destruction mediated by PDT. Vascular endothelial damage leads to platelet and polymorphonuclear Factors affecting efficacy of PDT leucocyte activation that releases pro-aggregatory The variables in PDT are: agents. These events result in arteriolar constriction, 1. Photosensitizer venular thrombosis and blood flow stasis causing 2. Tissue oxygenation indirect tumor cell kill from nutritional deprivation. 3. Light source Inflammatory response: Degradation of phospholipids Photosensitisers occurring after photo-oxidative damage of cell Photosensitisers that are under various stages of membrane and impairment of vascular functions results investigation for photodynamic therapy are listed in in the release of various inflammatory mediators. This Table 1. An ideal photosensitizer should be chemically leads to accumulation of immune effector cells like pure, have capability of localizing specifically in macrophages and neutrophil granulocytes. neoplastic tissue, should accumulate maximally in Degranulation of neutrophils and release of toxic tumor in short time, and have a short half-life and rapid oxygen radicals, lysosomal enzymes and chemotactic clearance from normal tissues. It should activate at agents contribute to the destruction of the tumor tissue wavelengths with optimal tissue penetration, have a and sustain the damage by attracting further immune high quantum yield for singlet oxygen generation, cells. Establishment of immunological response against should lack dark toxicity and should be effective on the treated malignancy leads to generation of tumor- topical application for dermatological uses. Systemic PDT Initially, after systemic administration, photosensitizing Photon compounds are taken up by most normal and malignant Excited cells, but are retained longer in tumor and rapidly Photosensitiserizer Singlet State proliferating cells. This may be due to increased blood vessel number and permeability and poor lymphatic Type II POR drainage in neoplastic tissue. In fact, many normal Singlet O2 tissues, especially the reticuloendothelial system have greater affinity for photosensitisers than tumor tissue. • Lipid peroxidation • Mitochondrial damage Excited Triplet State • Damage to lysosomes The drug is activated by light corresponding to the • Damage to ER absorption spectrum of the compound. The depth of • DNA damage tissue penetration depends on the wavelength of this absorption spectrum. Light of 630 nm wavelength penetrates 5 mm into tissues while that between 700- 800 nm penetrates to 1-2 cm depth. Light at 850 nm Figure 1: Mechanism of photodynamic therapy within cell does not yield enough energy to produce sufficient Indian J Dermatol Venereol Leprol May-June 2005 Vol 71 Issue 3 156 Nayak CS: Photodynamic therapy in dermatology Table 1: Photosensitizers being clinically investigated for PDT Photosensitizer Wavelength for PDT, nm Indications Route of administration Porfimer sodium (Photofrin) 630 Approved for bladder, esophagus, IV lung cancer. Studies for BCC Tin ethyl etiopurpurin (Purlytin) 660-665 Cutaneous metastases, Kaposi’s IV, lipid emulsion sarcoma, macular degeneration 5-aminolevulinic acid (ALA, Levulan) 635 Actinic keratoses, BCC, CTCL, Topical psoriasis, permanent hair removal Lutetium texaphyrin (Lu- Tex) 720-760 Skin cancer IV ATMPn 640 Psoriasis Topical BPD-MA (Verteporfin) 690 BCC, psoriasis, macular degeneration IV, liposomal formulation m-THPC (Foscan) 650 BCC, head and neck cancer IV, topical Npe6 660-665 Skin cancer IV Talaporfin sodium 640 Carcinoma aerodigestive tract IV photochemical response. is an unstable hydrophilic molecule, has poor penetration depth and consequent requirement of long Hematoporphyrin derivative (HpD) was the first application times, has low tissue selectivity and may systemically studied photosensitizer for clinical PDT. cause porphyrin to accumulate in distant sites Photofrin (porfimer sodium) has enhanced photosensitizing properties and consists of non- Methyl aminolevulinate cream is currently being metallic oligomeric porphyrins viz. a mixture of ethers investigated clinically. Its advantages are that it is a and esters of porphyrin.[1] This is activated at 630 nm. stable lipophilic molecule, has greater and faster At this wavelength there is no penetration beyond 5 penetration as well as a greater selectivity for neoplastic mm, hence lesions may not be effectively treated. The cells and shows no systemic uptake. main disadvantage is cutaneous accumulation and slow clearance from skin leading to long lasting cutaneous Tissue oxygenation photosensitivity, as long as 4-6 weeks. Experimental attempts at improving PDT effectiveness by manipulating tumor oxygen content like subjecting Systemic ALA is used to treat gastrointestinal, the tissue to hyperbaric oxygen have been made. bronchopulmonary and cerebral tumors. ALA-based However, this has no place as yet in clinical PDT. PDT can be potentiated with the use of additive compounds to inhibit or induce certain enzymes of the Light sources heme synthesis pathway.[2] The therapeutic window for PDT is between 600 nm 1. Desferrioxamine enhances ALA-induced and 1200 nm as light of wavelength below 600 nm is protoporphyrin IX (PpIX) accumulation. absorbed by hemoglobin in the tissues and that above 2. Combination of DMSO and EDTA with ALA increased 1200 nm is absorbed by water. Light sources may be PpIX production and enhanced the complete coherent (lasers) or incoherent. Laser beams can be response rate of nodular basal cell carcinomas. launched via fiberoptic cables and delivered into internal tumors via implanted fibers. Topical PDT Topical PDT depends on protoporphyrin IX (PpIX) When porphyrin photosensitisers are used,
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