Actinic Reticuloid

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J Ferguson - One of the best experts on this subject based on the ideXlab platform.

  • The photosensitivity dermatitis and Actinic Reticuloid syndrome: no association with lymphoreticular malignancy.
    The British journal of dermatology, 2006
    Co-Authors: D.j. Bilsland, Iain K. Crombie, J Ferguson
    Abstract:

    Summary In the management of photosensitivity dermatitis/Actinic Reticuloid syndrome (PD/AR) (syn.chronic Actinic dermatitis), a chronic and often severe photodermatosis, there has been concern that patients may be predisposed to the development of lymphoreticular malignancy. A follow-up study of 231 patients with PD/AR who had been investigated at the Photobiology Unit, Ninewells Hospital, Dundee, between 1971 and 1991, was undertaken to determine (i) the incidence and type of malignancies (ii) the causes of any deaths. This information was obtained from three sources: (a) National Cancer Registry data, (b) death certificates, (c) when possible or practical, by casenote review. Thirty-eight malignancies had occurred (in 37 of the 231 patients). Although six of the 38 malignancies were lymphoma registrations, it emerged from a review of casenotes, pathology reports and death certificates that five of the six were incorrect: two were labelled ‘mycosis fungoides’ prior to diagnosis of PD/AR; a case of dermatopathic lymphadenopathy was initially reported as Hodgkin's disease; clerical errors had occurred in two cases. The remaining case was a true B-cell lymphoma. The occurrence of one lymphoreticular malignancy is not significantly different from the number expected in a normal population (0.96), when applying 5-year age-, sex-, and site-specific incidence rates to the cumulative patient years of risk [standardized incidence ratio 1.04 (95% CI 0.03–5.79)]. There was also no significant increase in the risk of non-lymphoma malignancies in the PD/AR subjects. Since diagnosis, 83 patients have died, the majority from cardiorespiratory or cerebrovascular diseases, or the reported malignancies, a pattern expected in an elderly population. This study indicates that PD/AR patients are not at an increased risk of developing lymphoreticular or other malignancies. When the diagnosis is made, specific lymphoma screening measures are not indicated.

  • The photosensitivity dermatitis and Actinic Reticuloid syndrome (chronic Actinic dermatitis) occurring in seven young atopic dermatitis patients
    British Journal of Dermatology, 1998
    Co-Authors: Robert S. Dawe, P. Collins, I. Man, J Ferguson
    Abstract:

    Seven young patients with atopic dermatitis (AD) who presented with a marked photoexposed site dermatitis have been investigated in detail. The results of phototesting, patch testing and other investigations were compatible with the diagnosis of photosensitivity dermatitis/Actinic Reticuloid syndrome (PD/AR) (chronic Actinic dermatitis). It is known that AD patients may have photoaggravation of their dermatitis or exacerbation secondary to a photodermatosis, such as polymorphic light eruption, Actinic prurigo or drug-induced phototoxicity. The patients we describe, however, appear to be an uncommon AD subgroup affected by PD/AR. We recommend that all AD patients who have a history of sunlight-induced exacerbation or marked intolerance of PUVA or ultraviolet B phototherapy should have phototesting and patch testing conducted.

  • cellular sensitivity to oxidative stress in the photosensitivity dermatitis Actinic Reticuloid syndrome
    Journal of Investigative Dermatology, 1994
    Co-Authors: Lee Ann Applegate, J Ferguson, Edgar Frenk, Neil K. Gibbs, B.e. Johnson, Rex M. Tyrrell
    Abstract:

    Skin fibroblasts from certain patients with the photosensitivity dermatitis/Actinic Reticuloid syndrome show enhanced sensitivity to ultraviolet radiation compared to normal fibroblasts. To probe further the link between oxidative damage and this disease, we have obtained a more extensive set of cell lines from patients with a severe form of the disease and examined their sensitivity towards oxidative stress by measuring cell survival following UVA radiation (330-450 nm) or hydrogen peroxide treatment (0.1-2.4 mM). The activation of the stress gene, heme oxygenase, has also been assessed by measuring the accumulation of mRNA after hydrogen peroxide treatment. Our studies have confirmed that a slight ultraviolet sensitivity is a characteristic of photosensitivity dermatitis/Actinic Reticuloid syndrome cell strains and we further demonstrate that these cell lines are particularly sensitive to hydrogen peroxide with up to a three- to fourfold increased sensitivity as compared to normal controls. We also show that certain ataxia telangiectasia strains that are especially sensitive to hydrogen peroxide are also slightly sensitive to ultraviolet radiation. Hydrogen peroxide induces accumulation of mRNA for the oxidant-inducible stress protein, heme oxygenase, with similar kinetics (maximum mRNA accumulation 2-4 h following treatment) and with a similar range of magnitudes in both normal (6.6-20.6 times mRNA increase over basal levels) and photosensitivity dermatitis/Actinic Reticuloid (2.9-12.8 times) skin cells. Because cells from photosensitivity dermatitis/Actinic Reticuloid patients show increased sensitivity towards oxidative stress but show no significant change in oxidant activation of the heme oxygenase gene, we propose that the defect involves a late stage of processing of oxidative damage rather than a compromised free radical scavenging system.

  • Cellular Sensitivity to Oxidative Stress in the Photosensitivity Dermatitis/Actinic Reticuloid Syndrome
    The Journal of investigative dermatology, 1994
    Co-Authors: Lee Ann Applegate, J Ferguson, Edgar Frenk, Neil K. Gibbs, B.e. Johnson, Rex M. Tyrrell
    Abstract:

    Skin fibroblasts from certain patients with the photosensitivity dermatitis/Actinic Reticuloid syndrome show enhanced sensitivity to ultraviolet radiation compared to normal fibroblasts. To probe further the link between oxidative damage and this disease, we have obtained a more extensive set of cell lines from patients with a severe form of the disease and examined their sensitivity towards oxidative stress by measuring cell survival following UVA radiation (330-450 nm) or hydrogen peroxide treatment (0.1-2.4 mM). The activation of the stress gene, heme oxygenase, has also been assessed by measuring the accumulation of mRNA after hydrogen peroxide treatment. Our studies have confirmed that a slight ultraviolet sensitivity is a characteristic of photosensitivity dermatitis/Actinic Reticuloid syndrome cell strains and we further demonstrate that these cell lines are particularly sensitive to hydrogen peroxide with up to a three- to fourfold increased sensitivity as compared to normal controls. We also show that certain ataxia telangiectasia strains that are especially sensitive to hydrogen peroxide are also slightly sensitive to ultraviolet radiation. Hydrogen peroxide induces accumulation of mRNA for the oxidant-inducible stress protein, heme oxygenase, with similar kinetics (maximum mRNA accumulation 2-4 h following treatment) and with a similar range of magnitudes in both normal (6.6-20.6 times mRNA increase over basal levels) and photosensitivity dermatitis/Actinic Reticuloid (2.9-12.8 times) skin cells. Because cells from photosensitivity dermatitis/Actinic Reticuloid patients show increased sensitivity towards oxidative stress but show no significant change in oxidant activation of the heme oxygenase gene, we propose that the defect involves a late stage of processing of oxidative damage rather than a compromised free radical scavenging system.

I. A. Magnus - One of the best experts on this subject based on the ideXlab platform.

  • Oral β carotene therapy in Actinic Reticuloid and solar urticaria
    British Journal of Dermatology, 2006
    Co-Authors: A. Kobza, C.a. Ramsay, I. A. Magnus
    Abstract:

    SUMMARY It is very difficult to find effective, acceptable protective agents for patients who are sensitive to long wave ultraviolet (UV) and visible radiation. It has recently been reported that oral β carotene is a useful photoprotective agent in erythropoietic protoporphyria (EPP) where sensitivity to visible light is important. The action of this drug has therefore been investigated in other diseases where sensitivity to the same part of the spectrum exists. Two patients with Actinic Reticuloid and three with solar urticaria, all sensitive to long wave UV and visible radiation were investigated before, during and after therapy with β carotene. Detailed monochromator tests were carried out and serum carotene and vitamin A levels determined at regular intervals. Therapy was continued from 2 to 12 months. Results showed that there was no objective or subjective evidence of improvement in any of the patients despite high serum carotene levels. Large variations in the dose of radiation required to produce a reaction were seen in all patients and it is essential to take account of this variation when assessing any photoprotective agent. It is possible that the mechanism of photosensitivity in Actinic Reticuloid and solar urticaria is quite different from that in EPP thus explaining the difference in the reported results of β carotene in the last disease.

  • Oral carotene therapy in Actinic Reticuloid and solar urticaria. Failure to demonstrate a photoprotective effect against long wave ultraviolet and visible radiation.
    The British journal of dermatology, 2006
    Co-Authors: A. Kobza, C.a. Ramsay, I. A. Magnus
    Abstract:

    SUMMARY It is very difficult to find effective, acceptable protective agents for patients who are sensitive to long wave ultraviolet (UV) and visible radiation. It has recently been reported that oral β carotene is a useful photoprotective agent in erythropoietic protoporphyria (EPP) where sensitivity to visible light is important. The action of this drug has therefore been investigated in other diseases where sensitivity to the same part of the spectrum exists. Two patients with Actinic Reticuloid and three with solar urticaria, all sensitive to long wave UV and visible radiation were investigated before, during and after therapy with β carotene. Detailed monochromator tests were carried out and serum carotene and vitamin A levels determined at regular intervals. Therapy was continued from 2 to 12 months. Results showed that there was no objective or subjective evidence of improvement in any of the patients despite high serum carotene levels. Large variations in the dose of radiation required to produce a reaction were seen in all patients and it is essential to take account of this variation when assessing any photoprotective agent. It is possible that the mechanism of photosensitivity in Actinic Reticuloid and solar urticaria is quite different from that in EPP thus explaining the difference in the reported results of β carotene in the last disease.

Sarah Rogers - One of the best experts on this subject based on the ideXlab platform.

  • Photosensitivity dermatitis/Actinic Reticuloid syndrome in an Irish population: a review and some unusual features.
    Acta dermato-venereologica, 1995
    Co-Authors: Eugene Healy, Sarah Rogers
    Abstract:

    Nine patients with photosensitivity dermatitis and Actinic Reticuloid syndrome are reported. The rash affected light-exposed skin only in 7 patients and extended to covered sites in 2. Seven were sensitive to UVB, UVA and visible light, one to UVA and one to visible light only. Two patients had significant clinical improvement in spite of both having suffered severe disease previously. Another patient remains exquisitely light-sensitive after 20 years and has developed two squamous cell carcinomas, one of which metastasized to local lymph nodes, and two keratoacanthomas on light-exposed skin.

  • photosensitivity dermatitis Actinic Reticuloid syndrome in an irish population a review and some unusual features
    Acta Dermato-venereologica, 1995
    Co-Authors: Eugene Healy, Sarah Rogers
    Abstract:

    Nine patients with photosensitivity dermatitis and Actinic Reticuloid syndrome are reported. The rash affected light-exposed skin only in 7 patients and extended to covered sites in 2. Seven were sensitive to UVB, UVA and visible light, one to UVA and one to visible light only. Two patients had significant clinical improvement in spite of both having suffered severe disease previously. Another patient remains exquisitely light-sensitive after 20 years and has developed two squamous cell carcinomas, one of which metastasized to local lymph nodes, and two keratoacanthomas on light-exposed skin.

A. Kobza - One of the best experts on this subject based on the ideXlab platform.

  • Oral β carotene therapy in Actinic Reticuloid and solar urticaria
    British Journal of Dermatology, 2006
    Co-Authors: A. Kobza, C.a. Ramsay, I. A. Magnus
    Abstract:

    SUMMARY It is very difficult to find effective, acceptable protective agents for patients who are sensitive to long wave ultraviolet (UV) and visible radiation. It has recently been reported that oral β carotene is a useful photoprotective agent in erythropoietic protoporphyria (EPP) where sensitivity to visible light is important. The action of this drug has therefore been investigated in other diseases where sensitivity to the same part of the spectrum exists. Two patients with Actinic Reticuloid and three with solar urticaria, all sensitive to long wave UV and visible radiation were investigated before, during and after therapy with β carotene. Detailed monochromator tests were carried out and serum carotene and vitamin A levels determined at regular intervals. Therapy was continued from 2 to 12 months. Results showed that there was no objective or subjective evidence of improvement in any of the patients despite high serum carotene levels. Large variations in the dose of radiation required to produce a reaction were seen in all patients and it is essential to take account of this variation when assessing any photoprotective agent. It is possible that the mechanism of photosensitivity in Actinic Reticuloid and solar urticaria is quite different from that in EPP thus explaining the difference in the reported results of β carotene in the last disease.

  • Oral carotene therapy in Actinic Reticuloid and solar urticaria. Failure to demonstrate a photoprotective effect against long wave ultraviolet and visible radiation.
    The British journal of dermatology, 2006
    Co-Authors: A. Kobza, C.a. Ramsay, I. A. Magnus
    Abstract:

    SUMMARY It is very difficult to find effective, acceptable protective agents for patients who are sensitive to long wave ultraviolet (UV) and visible radiation. It has recently been reported that oral β carotene is a useful photoprotective agent in erythropoietic protoporphyria (EPP) where sensitivity to visible light is important. The action of this drug has therefore been investigated in other diseases where sensitivity to the same part of the spectrum exists. Two patients with Actinic Reticuloid and three with solar urticaria, all sensitive to long wave UV and visible radiation were investigated before, during and after therapy with β carotene. Detailed monochromator tests were carried out and serum carotene and vitamin A levels determined at regular intervals. Therapy was continued from 2 to 12 months. Results showed that there was no objective or subjective evidence of improvement in any of the patients despite high serum carotene levels. Large variations in the dose of radiation required to produce a reaction were seen in all patients and it is essential to take account of this variation when assessing any photoprotective agent. It is possible that the mechanism of photosensitivity in Actinic Reticuloid and solar urticaria is quite different from that in EPP thus explaining the difference in the reported results of β carotene in the last disease.

Rex M. Tyrrell - One of the best experts on this subject based on the ideXlab platform.

  • cellular sensitivity to oxidative stress in the photosensitivity dermatitis Actinic Reticuloid syndrome
    Journal of Investigative Dermatology, 1994
    Co-Authors: Lee Ann Applegate, J Ferguson, Edgar Frenk, Neil K. Gibbs, B.e. Johnson, Rex M. Tyrrell
    Abstract:

    Skin fibroblasts from certain patients with the photosensitivity dermatitis/Actinic Reticuloid syndrome show enhanced sensitivity to ultraviolet radiation compared to normal fibroblasts. To probe further the link between oxidative damage and this disease, we have obtained a more extensive set of cell lines from patients with a severe form of the disease and examined their sensitivity towards oxidative stress by measuring cell survival following UVA radiation (330-450 nm) or hydrogen peroxide treatment (0.1-2.4 mM). The activation of the stress gene, heme oxygenase, has also been assessed by measuring the accumulation of mRNA after hydrogen peroxide treatment. Our studies have confirmed that a slight ultraviolet sensitivity is a characteristic of photosensitivity dermatitis/Actinic Reticuloid syndrome cell strains and we further demonstrate that these cell lines are particularly sensitive to hydrogen peroxide with up to a three- to fourfold increased sensitivity as compared to normal controls. We also show that certain ataxia telangiectasia strains that are especially sensitive to hydrogen peroxide are also slightly sensitive to ultraviolet radiation. Hydrogen peroxide induces accumulation of mRNA for the oxidant-inducible stress protein, heme oxygenase, with similar kinetics (maximum mRNA accumulation 2-4 h following treatment) and with a similar range of magnitudes in both normal (6.6-20.6 times mRNA increase over basal levels) and photosensitivity dermatitis/Actinic Reticuloid (2.9-12.8 times) skin cells. Because cells from photosensitivity dermatitis/Actinic Reticuloid patients show increased sensitivity towards oxidative stress but show no significant change in oxidant activation of the heme oxygenase gene, we propose that the defect involves a late stage of processing of oxidative damage rather than a compromised free radical scavenging system.

  • Cellular Sensitivity to Oxidative Stress in the Photosensitivity Dermatitis/Actinic Reticuloid Syndrome
    The Journal of investigative dermatology, 1994
    Co-Authors: Lee Ann Applegate, J Ferguson, Edgar Frenk, Neil K. Gibbs, B.e. Johnson, Rex M. Tyrrell
    Abstract:

    Skin fibroblasts from certain patients with the photosensitivity dermatitis/Actinic Reticuloid syndrome show enhanced sensitivity to ultraviolet radiation compared to normal fibroblasts. To probe further the link between oxidative damage and this disease, we have obtained a more extensive set of cell lines from patients with a severe form of the disease and examined their sensitivity towards oxidative stress by measuring cell survival following UVA radiation (330-450 nm) or hydrogen peroxide treatment (0.1-2.4 mM). The activation of the stress gene, heme oxygenase, has also been assessed by measuring the accumulation of mRNA after hydrogen peroxide treatment. Our studies have confirmed that a slight ultraviolet sensitivity is a characteristic of photosensitivity dermatitis/Actinic Reticuloid syndrome cell strains and we further demonstrate that these cell lines are particularly sensitive to hydrogen peroxide with up to a three- to fourfold increased sensitivity as compared to normal controls. We also show that certain ataxia telangiectasia strains that are especially sensitive to hydrogen peroxide are also slightly sensitive to ultraviolet radiation. Hydrogen peroxide induces accumulation of mRNA for the oxidant-inducible stress protein, heme oxygenase, with similar kinetics (maximum mRNA accumulation 2-4 h following treatment) and with a similar range of magnitudes in both normal (6.6-20.6 times mRNA increase over basal levels) and photosensitivity dermatitis/Actinic Reticuloid (2.9-12.8 times) skin cells. Because cells from photosensitivity dermatitis/Actinic Reticuloid patients show increased sensitivity towards oxidative stress but show no significant change in oxidant activation of the heme oxygenase gene, we propose that the defect involves a late stage of processing of oxidative damage rather than a compromised free radical scavenging system.