Cutaneous Radiation Syndrome Research Articles

Autologous Adipocyte Derived Stem Cells Favour Healing in a Minipig Model of Cutaneous Radiation Syndrome

Cutaneous radiation syndrome (CRS) is the delayed consequence of localized skin exposure to high doses of ionizing radiation. Here we examined for the first time in a large animal model the therapeutic potential of autologous adipose tissue-derived stroma cells (ASCs). For experiments, Göttingen minipigs were locally gamma irradiated using a 60Co source at the dose of 50 Gy and grafted (n = 5) or not (n = 8). ASCs were cultured in MEM-alpha with 10% fetal calf serum and basic fibroblast growth factor (2 ng.mL−1) and post irradiation were intradermally injected on days 25, 46, 67 and finally between days 95 and 115 (50×106 ASCs each time) into the exposed area. All controls exhibited a clinical evolution with final necrosis (day 91). In grafted pigs an ultimate wound healing was observed in four out of five grafted animals (day 130 +/− 28). Immunohistological analysis of cytokeratin expression showed a complete epidermis recovery. Grafted ASCs accumulated at the dermis/subcutis barrier in which they attracted numerous immune cells, and even an increased vasculature in one pig. Globally this study suggests that local injection of ASCs may represent a useful strategy to mitigate CRS.

Acute radiation syndrome caused by accidental radiation exposure - therapeutic principles.

Fortunately radiation accidents are infrequent occurrences, but since they have the potential of large scale events like the nuclear accidents of Chernobyl and Fukushima, preparatory planning of the medical management of radiation accident victims is very important. Radiation accidents can result in different types of radiation exposure for which the diagnostic and therapeutic measures, as well as the outcomes, differ. The clinical course of acute radiation syndrome depends on the absorbed radiation dose and its distribution. Multi-organ-involvement and multi-organ-failure need be taken into account. The most vulnerable organ system to radiation exposure is the hematopoietic system. In addition to hematopoietic syndrome, radiation induced damage to the skin plays an important role in diagnostics and the treatment of radiation accident victims. The most important therapeutic principles with special reference to hematopoietic syndrome and cutaneous radiation syndrome are reviewed.

Radioprotection by the histone deacetylase inhibitor phenylbutyrate

The histone deacetylase inhibitor (HDAC), phenylbutyrate (PB), is a novel anti-tumor agent. Studies have demonstrated that HDAC inhibitors can suppress cutaneous radiation syndrome and stimulate hematopoiesis. The objective of this study was to test the ability of PB treatment to protect against acute gamma-radiation-induced lethality in the DBA/2 mouse model. A 30-day radiation lethality study was used to assess radioprotective capability of PB. Mechanisms were evaluated using western blots, flow cytometry, and the single-cell gel electrophoresis assay. Western blot studies showed that PB treatment acetylated histones in vivo. For radiation protection studies, prophylactic administration of PB (24 h preradiation; 1-50 mg/kg) provided radioprotection against gamma radiation (8-9.5 Gy) and PB demonstrated a DRF of 1.31 (P = 0.001; 95% confidence interval: 1.27, 1.36). When PB (10 mg/kg) was administered post-radiation (4 h), it also provided significant radioprotection at 8.0 Gy radiation (P = 0.022). PB treatment before radiation was associated with significant elevations in neutrophils and platelets following radiation. Results from single-cell gel electrophoresis of peripheral blood leukocytes demonstrated that PB treatment before radiation can attenuate DNA damage and inhibit radiation-induced apoptosis. These results indicate that an HDAC inhibitor like PB has potential as a radiation protector and that mechanisms of action include attenuation of DNA damage and inhibition of apoptosis.

P035 Adipocyte derived stem cells favour healing in a new minipig model of cutaneous radiation syndrome through reepithelialisation and neoangiogenesis

Adipose-derived stem cells (ASCs) hold promise for bone regeneration but possess inferior osteogenesis potential. Allotransplantation of ASCs engineered with the BMP2/VEGF-expressing baculoviruses into rabbits healed critical-size segmental bone defects. To translate the technology to clinical applications, we aimed to demonstrate massive bone healing in minipigs that more closely mimicked the clinical scenarios, using a new hybrid baculovirus system consisting of BacFLPo expressing the codon-optimized FLP recombinase (FLPo) and the substrate baculovirus harboring the transgene flanked by Frt sequences. Co-transduction of minipig ASCs (pASCs) with BacFLPo and the substrate baculovirus enabled transgene cassette excision, recombination and minicircle formation in ≈73.7% of pASCs, which substantially prolonged the transgene (BMP2 and VEGF) expression to 28 days. When encoding BMP2, the FLPo/Frt-based system augmented the pASCs osteogenesis. Allotransplantation of the BMP2/VEGF-expressing pASCs into minipigs healed massive segmental bone defects (30 mm in length) at the mid-diaphysis of femora, as evaluated by computed tomography, positron emission tomography, histology, immunohistochemical staining and biochemical testing. The defect size was ≈15% of femoral length in minipigs and was equivalent to ≈60–70 mm of femoral defect in humans, thus the healing using pASCs engineered with the FLPo/Frt-based baculovirus represented a remarkable advance for the treatment of massive bone defects.

Multipotent mesenchymal stem cell grafting to treat cutaneous radiation syndrome: Development of a new minipig model

Cutaneous radiation syndrome (CRS) is the delayed consequence of localized skin exposure to high doses of ionizing radiation. Recent grafting of three ionizing radiation-burned patients has suggested the benefit of local bone marrow mesenchymal stem cell (MSC) injection in favor of wound healing and pain control. Here, we have developed a new minipig model of severe CRS to study underlying mechanisms of this cell therapy approach. Göttingen minipigs were locally irradiated using a (60)Co gamma source as follows: ungrafted 50 and 60 Gy (n = 4) and grafted 50 and 60 Gy (n = 3). Bone marrow MSCs were cultured in minimum essential medium with 10% fetal calf serum and basic fibroblast growth factor (2 ng.mL(-1)). Autologous MSCs were intradermally injected twice or three times from days 27 to 96 (range, 99-128.5 × 10(6) MSCs per injection). All animals exhibited a clinical evolution similar to humans after a latency phase of several weeks, including early erythema, hair loss, and dry/moist desquamation followed by necrosis during 81 to 222 days post-ionizing radiation. Skin damage in higher exposed animals appeared slightly earlier. Immunohistology revealed severe skin damage in all animals and rhabdomyolysis in the muscle tissue below the entry area, with the latter being more severe in controls. In grafted animals, MSCs led to local accumulation of lymphocytes at the dermis/subcutis border and improved vascularization. This study establishes a new minipig model that is close to human and allows development of stem cell therapy strategies that can be applied in treatment of human radiation burns.

Présent et futur de la thérapie cellulaire des brûlures

Severe burned patients need definitive and efficient wound coverage. Outcome of massive burns has been improved by using cultured epithelial autografts (CEA). Despite fragility, percentages of success take, cost of treatment and long-term tendency to contracture, this surgical technique has been developed in few burn centres. First improvements were to combine CEA and dermis-like substitute. Cultured skin substitutes provide earlier skin closure and satisfying functional result. These methods have been used successfully in massive burns. Second improvement was to allow skin regeneration by using epidermal stem cells. Stem cells have capacity to differentiate into keratinocytes, to promote wound repair and to regenerate skin appendages. Human mesenchymal stem cells contribute to wound healing and were evaluated in cutaneous radiation syndrome. Skin regeneration and tissue engineering methods remain a complex challenge and offer the possibility of new treatment for injured and burned patients.

Radiation-induced alterations in cytokine production by skin cells

Ionizing radiation exposure of skin results in a cutaneous radiation reaction comprising all pathophysiological reactions and clinical symptoms in irradiated skin. Biological responses of skin occur in a characteristic temporal pattern and mainly depend on radiation quality, dose rate, total dose, and cellular conditions. Immediately after irradiation, production of cytokines by skin cells is initiated and continues as a cascade during all stages of the cutaneous radiation syndrome leading to progressive late symptoms, the predominant of which is fibrosis. Cytokines are important signaling molecules mediating communicative interactions both locally between different cell types within dermal tissues and distantly between organs. Although during recent years much progress has been made in dissecting the complex cytokine network, the role of cytokines in the pathophysiology of the cutaneous radiation reaction is only beginning to be elucidated. Previous studies indicate that the major cytokines in the response of skin cells to ionizing radiation include IL (interleukin)-1, IL-6, tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta, and the chemokines IL-8 and eotaxin. In this paper, existing data on the radiation-induced modulation of cytokine expression by skin cells are reviewed.

Collapse of Skin Antioxidant Status during the Subacute Period of Cutaneous Radiation Syndrome: A Case Report

This case report describes a patient suffering from accidental cutaneous radiation syndrome. Clinical symptoms were characterized by the presence of moist epidermal denudation over approximately 8% of the body surface without signs of necrosis 88 days after radiation exposure. The skin transcriptional profile was obtained and provides a comprehensive overview of the changes in gene expression associated with skin wound healing after irradiation. In particular, our data show a specific set of genes, i.e. SOD1, GPX1, TDX1, TDX2 and HSP60, implicated in the redox control of normal skin repair after radiation exposure, whereas HOX1 and HOX2 were involved in the pathological skin repair. A reduction in the antioxidant capacity of the irradiated tissue concomitant with a progressive establishment of an uncontrolled inflammatory response was noted. Our data corroborate the hypothesis that ROS modulation is a key element of the healing response after cutaneous exposure to radiation and that the collapse of skin antioxidant status interferes directly with wound healing in skin after radiation exposure. Thus a better understanding of the molecular events through which oxidative stress modulates the healing response could result in a more rational therapeutic approach to the pathological process induced after exposure of skin to radiation.

Human mesenchymal stem cells favour healing of the cutaneous radiation syndrome in a xenogenic transplant model

It has been suggested that human mesenchymal stem cells (hMSC) could be used to repair numerous injured tissues. We have studied the potential use of hMSC to limit radiation-induced skin lesions. Immunodeficient NOD/SCID mice were locally irradiated to the leg (30 Gy, dose rate 2.7 Gy/min) using a (60)Co source to induce a severe skin lesion. Cultured bone marrow hMSC were delivered intravenously to the mice. The irradiated skin samples were studied for the presence of the human cells, the severity of the lesions and the healing process. Macroscopic analysis and histology results showed that the lesions were evolving to a less severe degree of radiation dermatitis after hMSC transplant when compared to irradiated non-transplanted controls. Clinical scores for the studied skin parameters of treated mice were significantly improved. A faster healing was observed when compared to untreated mouse. Immunohistology and polymerase chain reaction analysis provided evidence that the human cells were found in the irradiated area. These results suggest a possible use of hMSC for the treatment of the early phase of the cutaneous radiation syndrome. A successful transplant of stem cells and subsequent reduction in radiation-induced complication may open the road to completely new strategies in cutaneous radiation syndrome therapy.

Cutaneous radiation syndrome in multi-organ failure

The likelihood of an individual being exposed to, and thus the probability of cutaneous injury from, nuclear weapons or dispersed nuclear material has, in contrast to post cold war euphoria, considerably increased during the last 13 years. This is in part due to a temporary loss of control of nuclear material, including uncontrolled deployment, and in part to an increasing capability and apparent willingness of terrorist and other criminal groups to use such material for their purposes. A relatively recent danger emerges from the development of so-called robust nuclear earth penetrators (RNEPs) to destroy very deep bunkers, which may be used in future “conventional” wars, and which without doubt will cause contamination with short-range radioactive nuclides, which will primarily affect the skin. In summary, the probability of local cutaneous radiation exposures to extremely high absorbed doses (<60 Gy), with concomitantly survivable bone marrow doses, has increased.

Antitumor histone deacetylase inhibitors suppress cutaneous radiation syndrome: Implications for increasing therapeutic gain in cancer radiotherapy

Radiotherapy is an effective treatment for head and neck, skin, anogenital, and breast cancers. However, radiation-induced skin morbidity limits the therapeutic benefits. A low-toxicity approach to selectively reduce skin morbidity without compromising tumor killing by radiotherapy is needed. We found that the antitumor agents known as histone deacetylase (HDAC) inhibitors (phenylbutyrate, trichostatin A, and valproic acid) could suppress cutaneous radiation syndrome. The effects of HDAC inhibitors in promoting the healing of wounds caused by radiation and in decreasing later skin fibrosis and tumorigenesis were correlated with suppression of the aberrant expression of radiation-induced transforming growth factor beta and tumor necrosis factor alpha. Our findings implicate that the inhibition of HDAC may provide a novel strategy to increase the therapeutic gain in cancer radiotherapy by not only inhibiting tumor growth but also protecting normal tissues.

Management of Cutaneous Radiation Injuries: Diagnostic and Therapeutic Principles of the Cutaneous Radiation Syndrome

The cutaneous symptoms that appear after radiation exposure are caused by a combination of inflammatory processes and alteration of cellular proliferation as a result of a specific pattern of transcriptionally activated proinflammatory cytokines and growth factors. The symptoms follow a time course consisting of prodromal erythema, manifestation, chronic stage, and late stage; these symptoms are referred to as cutaneous radiation syndrome (CRS). The time course depends on several factors such as the applied radiation dose, radiation quality, individual radiation sensitivity, extent of contamination and absorption, and volume of skin exposed. For diagnosis of CRS, the following procedures are used: 7.5 to 20 MHz B-scan sonography, thermography, capillary microscopy, profilometry, nuclear magnetic resonance imaging, bone scintigraphy, and histology. Based on the results of previous experimental and clinical research, pharmacotherapy of CRS can include topical or systemic application of corticosteroids, gamma interferon, pentoxifylline and vitamin E, and superoxide dismutase. The treatment varies according to the stage of CRS. Due to the complexity of the clinical manifestations of radiation disease in most patients, interdisciplinary treatment at specialized centers is necessary. In most cases, dermatologists are asked to provide lifelong therapy and follow-up of the patients.

The cutaneous radiation syndrome: diagnosis and treatment

Accidental exposure to ionising radiation may occur during such catastrophic events as the Chernobyl accident in 1986 or for days and weeks as in Goiania in 1987 and in the military camp during the training of soldiers in Lilo/Georgia in 1997 as well as in medical institutions. The cutaneous symptoms after radiation exposure are based on a combination of inflammatory processes and alteration of cellular proliferation as a result of a specific pattern of transcriptionally activated proinflammatoric cytokines and growth factors. They follow a time course consisting of prodromal erythema, manifestation, chronic stage, late stage and they are referred to as Cutaneous Radiation Syndrome. The time course depends on several factors such as the applied radiation dose, radiation quality, individual radiation sensitivity, the extent of contamination and absorption and volume of the skin. For diagnostics of the cutaneous radiation syndrome the following procedures are used: 7.5 MHz to 20 MHz-B-scan-sonography, thermography, capillary microscopy, profilometry, nuclear magnetic resonance imaging, bone scintigraphy and histology. Based on the results of experimental and clinical research of the last years pharmacotherapy of the cutaneous radiation syndrome includes topic or systemic application of corticosteroids, gamma-interferon, pentoxifylline and vitamin E and superoxide dismutase. The treatment depends on the stage of the cutaneous radiation syndrome. Due to the complexity of the clinical manifestations of radiation disease in most patients an interdisciplinary treatment in specialised centres is necessary. Dermatologists are asked to perform in most cases life-long therapy and follow-up of the patients.

Interferon-gamma in 5 patients with cutaneous radiation syndrome after radiation therapy

Background: Irradiation can cause acute inflammatory responses as well as chronic fibrotic alterations of the skin. Cutaneous radiation fibrosis evokes a complex of therapeutic problems. However, therapeutic options, apart from surgical approaches, are limited. Patients and Methods: Five female patients suffering from severe cutaneous fibrosis were treated with interferon-gamma on a low-dose regimen, 3 × 100 μg/week subcutaneously for 6 months, then once per week for another 6 months. In 4 patients, skin thickness was measured with high-frequency (20 MHz) ultrasound in a clinically well-defined target skin lesion. In 1 patient, nuclear magnetic resonance imaging was performed to quantify the extent of cutaneous radiation fibrosis and to monitor the therapeutic outcome. Results: All patients suffered from radiation-induced cutaneous fibrosis. Additionally, in 1 patient, a fistula, as assessed by lymph vessel scintigraphy, and in another patient a radiation ulcer was diagnosed. In all patients, reduction of radiation-induced fibrosis could be documented. Both fistula and radiation ulcer regressed completely under interferon-gamma therapy. Conclusion: Low-dose interferon-gamma therapy is a new and effective treatment modality for cutaneous radiation fibrosis caused by radiation therapy. The positive impact of interferon-gamma on our patients warrants randomized double-blind trials on therapy of radiation fibrosis.

The outcome of local radiation injuries: 14 years of follow-up after the Chernobyl accident.

The Chernobyl nuclear power plant accident on April 26, 1986 was the largest in the history of the peaceful use of nuclear energy. Of the 237 individuals initially suspected to have been significantly exposed to radiation during or in the immediate aftermath of the accident, the diagnosis of acute radiation sickness (ARS) could be confirmed in 134 cases on the basis of clinical symptoms. Of these, 54 patients suffered from cutaneous radiation syndrome (CRS) to varying degrees. Among the 28 patients who died from the immediate consequences of accidental radiation exposure, acute hemopoietic syndrome due to bone marrow failure was the primary cause of death only in a minority. In 16 of these 28 deaths, the primary cause was attributed to CRS. This report describes the characteristic cutaneous sequelae as well as associated clinical symptoms and diseases of 15 survivors of the Chernobyl accident with severe localized exposure who were systematically followed up by our groups between 1991 and 2000. All patients presented with CRS of varying severity, showing xerosis, cutaneous telangiectasias and subungual splinter hemorrhages, hemangiomas and lymphangiomas, epidermal atrophy, disseminated keratoses, extensive dermal and subcutaneous fibrosis with partial ulcerations, and pigmentary changes including radiation lentigo. Surprisingly, no cutaneous malignancies have been detected so far in those areas that received large radiation exposures and that developed keratoses; however, two patients first presented in 1999 with basal cell carcinomas on the nape of the neck and the right lower eyelid, areas that received lower exposures. During the follow-up period, two patients were lost due to death from myelodysplastic syndrome in 1995 and acute myelogenous leukemia in 1998, respectively. Other radiation-induced diseases such as dry eye syndrome (3/15), radiation cataract (5/15), xerostomia (4/15) and increased FSH levels (7/15) indicating impaired fertility were also documented. This study, which analyzes 14 years in the clinical course of a cohort of patients with a unique exposure pattern, corroborates the requirement for long-term, if not life-long, follow-up not only in atomic bomb survivors, but also after predominantly local radiation exposure.

Accidental radiation exposure and azoospermia.

Seven Georgian male soldiers (19-25 years old) had accidentally been exposed to radiation by Cs-137 between April 1996 and May 1997. No information about the exact time and duration of exposure was available. All patients presented with the subacute stage of Cutaneous Radiation Syndrome with deep painful ulcers on different body sites, predominantly on the legs. Semen analyses showed complete azoospermia in 4 patients, with elevated follicle-stimulating hormone (FSH) in 3 and elevated luteinizing hormone (LH) in 2 of them. One patient had severe oligozoospermia of 7 million sperm per mL, with normal sperm motility and morphology; his FSH and LH levels were elevated. One patient had complete normozoospermia, and the seventh patient had polyzoospermia of 340 million per mL; both of these patients had normal serum hormone levels. Only the patient with oligozoospermia reported a history of delayed testicular descent; his physical examination showed relatively soft and small testicles and a varicocele with considerable reflux. The physical andrological examinations were normal in the other 6 patients. It is very likely that the azoospermia in the 4 patients can be attributed to the radiation accident. In conclusion, it is essential to perform andrological examinations in patients who have been exposed to radiation even if there are only cutaneous injuries detectable, as a high percentage of them can show azoospermia.

The radiation accident in Georgia: Clinical appearance and diagnosis of cutaneous radiation syndrome

Background: Eleven male Georgian soldiers were accidentally exposed to radiation by cesium 137 during their training in a military exercise camp in Lilo, Georgia between November 1996 and May 1997. Objective: The characteristic sequelae of accidental cutaneous irradiation and available diagnostic methods are described. Methods: Magnetic resonance imaging (MRI) of radiation ulcers was performed in all patients; thermography was performed in 2. In 7 patients ulcers and white macules were examined with high-frequency 20 MHz sonography; histologic results were obtained from all patients. Results: Predominant lesions were radiation ulcers in 11 patients and white hairless macules in 7. MRI showed ulcers down to the muscles and an increase of signal intensity in the musculature in 9 cases. The corresponding muscle histology demonstrated vasculitis in 7 patients and necrosis in 2. In 2 patients, MRI signal intensity of the musculature was normal. In 3 patients, 20 MHz sonography showed dermal defects; 1 patient had cutaneous fibrosis. Thermography demonstrated hypothermic zones with extended inflammatory zones adjacent to the radiation ulcers in both patients examined. Conclusion: High-frequency 20 MHz sonography, MRI, and thermography are useful noninvasive methods for diagnosis of the extent of cutaneous radiation syndrome and for therapy planning. (J Am Acad Dermatol 2000;42:453-8.)

NF-κB and AP-1 are responsible for inducibility of the IL-6 promoter by ionizing radiation in HeLa cells

Purpose : To investigate the mechanisms leading to initiation by ionizing radiation of IL-6 transcription in HeLa cells. Materials and methods : HeLa cells were irradiated with X-rays at a dose rate of approximately 1 Gy/min or treated with TPA (100 ng/ml). Transient transfection analysis with truncated IL-6 promoter CAT constructs was used to identify the radiation-sensitive region within the IL-6 promoter/enhancer. Results : For basal expression of the IL-6 gene in unirradiated control cells the presence of the binding site for the nuclear factor kappa B (NF- κB) and the multiple response elements (MRE) were necessary. After deletion of either the activator protein (AP)-1 or the MRE site, radiation-induced IL-6 promoter CAT activity was significantly reduced, whereas after deletion of the NF-kappaB site it was completely abolished. Maximal radiation-induced IL-6 promoter CAT activity was observed when the AP1, NF κB and MRE motifs were present. In electrophoretic mobility shift analyses (EMSA), X-ray-inducible activity was found for NF-kappaB and AP-1 at the MRE constitutive, but no inducible activities were detectable. The nuclear factor IL-6 (NFIL6) element showed no specific radiation-responsive activity. Conclusions : These results demonstrate that NF- κB plays a major role in X-ray-inducible IL-6 expression in HeLa cells. The fact that IL-6 promoter activity was dramatically enhanced in the presence of the MRE and distal AP-1 binding motif is indicative of a cooperative mode of transcriptional activation involving all three transcription factor systems. These data provide new insights into the prodromal events of radiation-induced inflammation of epithelial cells and putatively the cutaneous radiation syndrome.

Histopathological and Cellular Studies of a Case of Cutaneous Radiation Syndrome after Accidental Chronic Exposure to a Cesium Source

This study was designed for the histopathological, cellular and biochemical characterization of a skin lesion removed surgically from a young male several months after accidental exposure to cesium-137, with an emphasis on expression of transforming growth factor beta1 (TGFB1) and tumor necrosis factor alpha (TNFA) and the occurrence of apoptosis. Under a hypertrophic epidermis, a highly inhomogeneous inflammatory dermis was observed, together with fibroblastic proliferation in necrotic areas. Immunostaining revealed overexpression of TGFB1 and TNFA inside the keratinocytes of the hypertrophic epidermis as well as in the cytoplasm of the fibroblasts and connective tissue of the mixed fibrotic and necrotic dermis. Inside this dermis, the TUNEL assay revealed areas containing numerous apoptotic fibroblasts next to areas of normal viable cells. Overexpression of TGFB1 was found in the conditioned medium and cellular fractions of both hypertrophic keratinocytes and fibrotic fibroblasts. This overexpression lasted for at least three passages in tissue culture. The present observations were consistent with the central role of TGFB1 in the determination of chronic radiation-induced damage to the skin and a significant involvement of TNFA. In addition, programmed cell death appeared to take place during the remodeling of the mixed fibrotic and necrotic tissue.

Providing dermatological photographs using the multimedia extension of the international computer database for radiation accident case histories

The World Health Organisation (WHO) Radiation Emergency Medical Preparedness (REMPAN) centres have built up the International Computer Database for Radiation Accident Case Histories (ICDREC) to document the medical treatment of acute radiation syndrome (ARS) patients. Images play an increasing role as complementary information beside text and numerical data in medicine. In particular, retrieval and display of digitised skin photographs serve to improve patient care, medical education and scientific analysis concerning the cutaneous radiation syndrome (CRS). The ICDREC has been built up as a client/server system. Particular focus has been set on using commercial off-the-shelf software components. All the medical data including the multimedia data are stored in a relational database system. The database can be accessed by inexpensive personal computers in the physician's workplace. Retrieval of one photograph via local area network (LAN) requires approximately 3 s. Authorised institutions can access the database via the Internet. The current state of the ICDREC multimedia component is illustrated with the skin lesion treatment of a Chernobyl patient. An example is given on how the workflow in a dermatology department is supported by the ICDREC.