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Results for “Photosensitivity Disorders”

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At least 109 records · Page 6Linked to original sources
PubMed2007

[Dermatitis artefacta presenting as photodermatosis].

Dermatitis artefacta is a form of a self-injury due to psychiatric disorders or internal conflicts. Delayed diagnosis often leads to unnecessary treatments. A 17-year old girl was referred with a putative photodermatosis presenting with erosions on an erythematous base on the face and forearms. The unusual rapid onset of new lesions following phototesting and in particular a reaction induced after a simulated light exposure substantiated the diagnosis of dermatitis artefacta. Faced with the diagnosed the patient admitted she had induced the lesions and was referred for psychiatric care.

Adolescent↗
PubMed2005

Mild skin photosensitivity in cancer patients following injection of Photochlor (2-[1-hexyloxyethyl]-2-devinyl pyropheophorbide-a; HPPH) for photodynamic therapy.

PURPOSE: To measure skin photosensitivity in cancer patients infused with the new second-generation photodynamic sensitizer Photochlor (2-[1-hexyloxyethyl]-2-devinyl pyropheophorbide-a). A major disadvantage of using the clinically approved photosensitizer Photofrin is potentially prolonged and sometimes severe cutaneous phototoxicity. PATIENTS AND METHODS: Forty-eight patients enrolled in Phases 1 and 2 clinical trials underwent two or more exposures to four graded doses (44.4, 66.6, 88.8 or 133.2 J/cm2) of artificial solar-spectrum light (SSL) before and after administration of Photochlor at a dose of 2.5, 3, 4, 5 or 6 mg/m2 . RESULTS: The most severe skin response, experienced by only six of the subjects, was limited to erythema without edema and could only be elicited by exposure to the highest light dose. Conversely, eight subjects had no discernible reaction to SSL at any light dose. For nearly all the patients, the peak skin response was obtained when the interval between sensitizer injection and exposure to SSL was 1 day and, generally, their sensitivity to SSL decreased with increasing sensitizer-light interval. For example, a 2-day sensitizer-SSL interval resulted in less severe reactions than those obtained with the 1-day interval in 79% of the subjects, while 90% of the subjects exposed to SSL 3 days after Photochlor infusion had responses that were less severe than those obtained with either the 1- or 2-day sensitizer-SSL interval. CONCLUSIONS: Photochlor, at clinically effective antitumor doses, causes only mild skin photosensitivity that declines rapidly over a few days.

Dihematoporphyrin Ether↗
PubMed2004

Health hazards associated with curing light in the dental clinic.

The assessment of side effects of substances encountered in odontology by patients and the dental team must include the direct and indirect effects of irradiation emitted from polymerisation devices. The eyes of the lamp operators are at risk from acute and cumulative effects, mainly due to back-reflection of the blue light. Furthermore, phototoxic and photoallergic reactions originating from absorbed radiation in endogenous or exogenous substances accumulated in the operators' eyes and skin (hands) as well as the patients' oral mucosa must also be taken into consideration. Preventive measures include reading the manufacturers' operating instructions for curing devices and using radiation-filtering protection goggles.

Dental Equipment↗
PubMed1991

Hydroa vacciniforme with unusually severe scar formation: diagnosis by repetitive UVA phototesting.

Hydroa vacciniforme is a rare, chronic, photosensitive disorder manifested in childhood by recurrent vesicles that heal with scarring. Reproduction of vesicles with repetitive UVA phototesting may be an important diagnostic aid. Recurrent eruption resulted in severe scarring of the face and a flexion contracture of the finger in our patient. The clinical features and laboratory evaluation of hydroa vacciniforme are reviewed.

Adolescent↗
PubMed1995

Burns induced by plants.

Plants of the family Umbelliferae are known to cause a phytophotodermatitis due to a phototoxic reaction caused by furocoumarin (psoralens) and simultaneous exposure to sunlight. We report four patients with partial skin thickness burns, induced by this phototoxic reaction. One occurred after contact with parsley (Apium petroselinum) and three others after contact with giant hogweed (Heracleum mantegazzianum) and simultaneous exposure to sunlight.

Adolescent↗
PubMed1994

Phototoxicity and photoallergenicity of quinolones in guinea pigs.

Clinical reports indicate that the fluoroquinolone group of antibiotics can induce cutaneous photosensitivity reactions. In the present study, phototoxicity and photoallergenicity of quinolones including nalidixic acid (NA) norfloxacin (NFLX), ofloxacin (OFLX), enoxacin (ENX), ciprofloxacin (CPFX), lomefloxacin (LFLX), and tosufloxacin (TFLX) were experimentally examined in an in vivo system using the guinea pig. Phototoxicity of all quinolones tested was demonstrated after a single, oral administration of the drugs and subsequent exposure to long-wave ultraviolet (UVA) at a dose of 30 J/cm2. The phototoxic potencies were: ENX, LFLX > OFLX > NA, TFLX > NFLX, CPFX. Photoallergic reaction was also induced to LFLX and NA by pretreatment with cyclophosphamide, an immunoadjuvant. No cross-reactions in photoallergy were observed among quinolones. The photo-ingestion test was positive in photoallergically sensitized animals, while the photopatch test was negative. This is the first report which demonstrated experimentally the photoallergenicity of quinolones. Clinical features of the photosensitivity due to quinolones can be explained by the results of the present experiments.

4-Quinolones↗
PubMed2006

Adenovirus mediated transduction of the human DNA polymerase eta cDNA.

Xeroderma pigmentosum (XP) is an autosomal recessive photosensitive disorder with an extremely high incidence of skin cancers. Seven complementation groups, corresponding to seven proteins involved in nucleotide excision repair (NER), are associated with this syndrome. However, in XP variant patients, the disorder is caused by defects in DNA polymerase eta; this error prone polymerase, encoded by POLH, is involved in translesion DNA synthesis (TLS) on DNA templates damaged by ultraviolet light (UV). We constructed a recombinant adenovirus carrying the human POLH cDNA linked to the EGFP reporter gene (AdXPV-EGFP) and infected skin fibroblasts from both XPV and XPA patients. Twenty-four hours after infection, the DNA polymerase eta-EGFP fusion protein was detected by Western blot analysis, demonstrating successful transduction by the adenoviral vector. Protein expression was accompanied by reduction in the high sensitivity of XPV cells to UV, as determined by cell survival and apoptosis-induction assays. Moreover, the pronounced UV-induced inhibition of DNA synthesis in XPV cells and their arrest in S phase were attenuated in AdXPV-EGFP infected cells, confirming that the transduced polymerase was functional. However, over-expression of polymerase eta mediated by AdXPV-EGFP infection did not result in enhancement of cell survival, prevention of apoptosis, or higher rate of nascent DNA strand growth in irradiated XPA cells. These results suggest that TLS by DNA polymerase eta is not a limiting factor for recovery from cellular responses induced by UV in excision-repair deficient fibroblasts.

Adenoviridae↗
PubMed2005

Efficacy of 3 different light doses in the treatment of actinic keratosis with 5-aminolevulinic acid photodynamic therapy: a randomized, observer-blinded, intrapatient, comparison study.

BACKGROUND: Topical 5-aminolevulinic acid-based photodynamic therapy (ALA-PDT) has been established in recent years as an effective treatment for disseminated actinic keratosis (AK). As yet, however, data are lacking to define the optimal light dose for activation of ALA-induced protoporphyrin IX in AK. OBJECTIVE: In the present study our purpose was to compare the efficacy and tolerability of 3 different doses of red light for ALA-PDT of AK. METHODS: Twenty-seven patients with at least 3 clearly definable, mild or moderate AKs on the scalp or face entered the study. After occlusion for 4 hours with 20% ALA, one AK each was irradiated at random with a single dose of 70, 100, or 140 J/cm2. PDT-induced pain was assessed by the patients by means of a visual analog scale that graded pain intensity between 0 and 10. Follow-up examinations were performed 1 and 3 months after PDT. RESULTS: One month after PDT, the rate of complete remission (CR) was 89% for 70 J/cm2, 92% for 100 J/cm2, and 81% for 140 J/cm2. The CR rates at 3 months were 81% for 70 J/cm2, 77% for 100 J/cm2, and 69% for 140 J/cm2. No significant difference in therapeutic efficacy was found among the 3 light doses at either 1 month (P = .36) or 3 months (P = .96) after PDT. The degree of PDT-induced pain during irradiation was substantial and not statistically different (P = .06) for all 3 light doses. LIMITATIONS: The conclusions from this study are limited by the small sample size and only apply to topical ALA-PDT. CONCLUSION: Our results indicate that a red light dose of 70 J/cm2 may be sufficient for effective topical ALA-PDT of disseminated, mild to moderate AK on the face and scalp.

Aminolevulinic Acid↗
PubMed2006

[Photodynamic therapy in dermatology].

Photodynamic therapy (PDT) is a therapeutic modality based on the photooxidation of biological materials induced by a photosensitizer, which selectively locates itself in certain tumorous cells or tissues, so that when illuminated by a light of the right length and at a sufficient dose, these cells are destroyed. In dermatology, PDT with topical 5-aminolevulinic acid or 5-methyl aminolevulinate is very effective in the treatment of actinic keratoses, basal cell carcinomas and Bowen's disease. In addition, very promising results have been obtained in inflammatory pathologies like morphea or sarcoidosis, infections like warts, and cosmetic processes such as photoaging, among others. This article reviews the most significant aspects of PDT in dermatology. First of all, we will review the basic fundamentals of photodynamic treatment. Next, we will outline its clinical applications in dermatology, both in oncological applications and all those dermatological processes in which PDT may play a role in their management. We will also discuss its promising cosmetic application in the treatment of photoaging. We will complete the review with photodiagnosis and the different non-invasive ways to monitor the effectiveness of PDT.

Aminolevulinic Acid↗
PubMed1998

Oxidative damage induced by the fullerene C60 on photosensitization in rat liver microsomes.

We have examined the ability of a commonly used fullerene, C60, to induce oxidative damage on photosensitization using rat liver microsomes as model membranes. When C60 was incorporated into rat liver microsomes in the form of its cyclodextrin complex and exposed to UV or visible light, it induced significant oxidative damage in terms of (1) lipid peroxidation as assayed by thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides and conjugated dienes, and (2) damage to proteins as assessed by protein carbonyls and loss of the membrane-bound enzymes. The oxidative damage induced was both time- and concentration-dependent. C60 plus light-induced lipid peroxidation was significantly inhibited by the quenchers of singlet oxygen ((1)O2), beta-carotene and sodium azide, and deuteration of the buffer-enhanced peroxidation. These observations indicate that C60 is an efficient inducer of peroxidation and is predominantly due to (1)O2. Biological antioxidants such as glutathione, ascorbic acid and alpha-tocopherol significantly differ in their ability to inhibit peroxidation induced by C60. Our studies, hence, indicate that C60, on photosensitization, can induce significant lipid peroxidation and other forms of oxidative damage in biological membranes and that this phenomenon can be greatly modulated by endogenous antioxidants and scavengers of reactive oxygen species.

Animals↗
PubMed1999

Targeting of HIV gp120 by oligonucleotide-photosensitizer conjugates. Light-induced damages.

Some guanine-rich oligonucleotides inhibit HIV infectivity through interaction with the gp120 glycoprotein. Besides, photoinactivation of viruses attracts attention for blood decontamination. The feasibility of targeting a red light-absorbing chlorin-type photosensitizer to gp120 through covalent coupling with 8-mer phosphodiester oligodeoxynucleotides is investigated. Some conjugates inhibit binding of antibodies directed to gp120. Inhibition is significantly increased upon red light activation. The activity of the conjugates correlates with their ability to self-associate, a process strongly favored by the propensity of the hydrophobic chlorin moiety to dimerize. Thus, the photosensitizer moiety both promotes structures with a higher affinity for gp120 and, upon light activation, can induce site-directed damages to the protein.

Amino Acid Sequence↗
PubMed2006

[Incidence of drug-induced photosensitization during phototherapy].

BACKGROUND: Exogenous photosensitization represents one of the adverse effects of phototherapy. However, the impact of potentially photosensitizing drugs on the incidence of photo-induced eruptions during phototherapy is unknown. AIM OF THE STUDY: To determine the incidence of drug photosensitization during phototherapy. PATIENTS AND METHODS: This was a retrospective study of all patients undergoing phototherapy between November 1999 and April 2004 in the Dermatology Department of Caen University Teaching Hospital. Details of all topical or systemic medications taken before or during phototherapy were recorded. Since methoxsalen induces photosensitization, sessions of phototherapy were stratified according to whether methoxsalen was given. Screening was performed for the following clinical signs of drug photosensitization: acute photo-induced, erythematous and/or vesicular eruption, associated with pruritus or burning. RESULTS: In the non-methoxsalen group, use of a potentially photosensitizing drug was found for 29/155 TL01 phototherapy sessions. Drug-induced photosensitization was suspected in 3/29 sessions (10.3%). In the methoxsalen group, a potentially photosensitizing drug was found in 21/118 sessions of PUVA-therapy. Drug-induced photosensitization was suspected in 4/21 sessions (19%). Risk of photo-induced eruption was not associated with photosensitizing drug therapy, TL01 phototherapy or PUVA-therapy. DISCUSSION: Drug photosensitization appears to be rare during phototherapy, regardless of photosensitizing drug intake. It is twice as frequent during PUVA-therapy as during TL01 phototherapy but this difference is not significant.

Adolescent↗
PubMed1983

Hydroa vacciniforme: induction of lesions with ultraviolet A.

Hydroa vacciniforme is a rare photosensitivity disorder with onset in childhood. The distinctive lesion is a vesicle which heals with scarring. We report a case of hydroa vacciniforme in which an abnormal minimal erythema dose to wavelengths of 322 to 370 nm within the ultraviolet A (UVA) range was demonstrated. Vesicles could be induced only with multiple exposures to UVA. Increased tolerance to UVA erythema was induced by multiple UVB exposures, although tanning was poor. Of note were the presence of several halo nevi and a history of the loss of ability to tan. The clinical features and appropriate laboratory evaluation of hydroa vacciniforme are reviewed.

Adult↗
PubMed1999

Augmentation of 12-O-tetradecanoyl 13-phorbol acetate-mediated tumor promoting response by the porphyrin photosensitization of 7,12-dimethyl benz[a]anthracene-initiated murine skin: role of in situ generated reactive oxygen species.

Recently, we have shown that sustained ROS generation by prolonged porphyrin-mediated photosensitization in murine skin acts as a stage I and weak complete tumor promoter. Further to this, in the present study, we show that porphyrin photosensitization of DMBA-initiated murine skin results in the augmentation of TPA-mediated tumor promoting response. The photosensitization increased tumor yield to 15 tumors per mouse as compared to 7.5 tumors per mouse in the group treated with TPA alone. Further, 100% tumor incidence in the TPA-treated photosensitized group occurred at week 11 whereas it occurred at week 19 in the TPA alone treated group. Porphyrin photosensitization slightly decreased the latency period of TPA-mediated tumor formation by 1 week. The TPA-mediated ODC induction (1300% of saline-treated control) has been augmented in the photosensitized group (1950%). However, the amount of [3H]thymidine incorporation was not significantly different in the photosensitized TPA-treated and TPA alone-treated groups. Similarly, TPA treatment in photosensitized animals augmented the depletion of cutaneous glutathione and enhancement of lipid peroxidation. These changes were attenuated in butylated hydroxytoluene-pretreated animals. Our results suggest that cutaneous porphyrin photosensitization augments TPA-mediated tumor promotion in murine skin.

9,10-Dimethyl-1,2-benzanthracene↗