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Results for “RADIODERMATITIS”

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At least 829 records · Page 46Linked to original sources
PubMedDate not supplied

Radiation recall dermatitis with cefotetan: a case study.

Radiation recall dermatitis (RRD) is an inflammatory skin reaction that occurs in a previously irradiated body part following drug administration. This phenomenon may occur from days to years following exposure to ionizing radiation. The case of a 54-year-old Caucasian woman who was initially treated with external-beam radiation to the right thoracic region following the diagnosis of a poorly differentiated squamous cell carcinoma of the right lung is reported. She received four cycles of consolidated chemotherapy with docetaxel and carboplatin. Four months later, she was admitted to the hospital for acute cholecystitis and was placed on cefotetan. She developed a tender, erythematous rash on the posterior region of her right thorax 48 hours later. The drug was withdrawn, supportive care was instituted, and the patient subsequently improved. RRD should be suspected in patients who develop an erythematous rash in a previously irradiated region. To our knowledge this entity has not been associated with cefotetan previously.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2006

Interleukin 1beta (IL1B) signaling is a critical component of radiation-induced skin fibrosis.

Interleukin 1 beta (IL1B), a potent pro-inflammatory cytokine, is directly up-regulated by radiation and is known to regulate other inflammation-related molecules, such as the matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs). However, the nature of the interaction of IL1B with MMPs and TIMPs in radiation-induced skin fibrosis is unknown. We examined the response of primary dermal keratinocytes, fibroblasts and endothelial cells to single-fraction radiation (10 Gy) and compared the results to a temporal sequence of histology from irradiated C57BL/6 and IL1R1 knockout mice. These studies showed that keratinocytes are the major IL1-producing cells in vitro and that radiation induces an immediate and chronic elevation in the expression of IL1B mRNA in the skin of C57BL/6 mice. This elevation was principally early and was less pronounced in the IL1R1 knockout strain, which also demonstrated reduced late radiation fibrosis. Radiation also increased expression of MMP mRNA in C57BL/6 mice. Finally, exogenous IL1B protein induced robust endogenous IL1B mRNA expression, along with a brisk increase in MMPs and collagen III, but only in the C57BL/6 mice. In conclusion, these data suggest that IL1B plays a critical role in radiation-induced fibrosis and that the increased MMPs fail to block the IL1-related collagen accumulation.

Animals↗
PubMedDate not supplied

Radiation-recall skin disorders associated with the use of antineoplastic drugs. Pathogenesis, prevalence, and management.

Radiation-recall dermatitis is the occurrence, with subsequent administration of cytotoxic chemotherapy, of an acute inflammatory toxicity in a previously quiescent radiation field. It may occur from days to weeks, and sometimes years, after the radiation therapy. The precise mechanism is unknown. One hypothesis suggests that the initial radiation therapy leads to a depletion of tissue stem cells within the irradiated field and that subsequent cytotoxic chemotherapy exposure causes a 'remembered' reaction among the remaining surviving cells. An alternative proposition suggests that radiation induces heritable mutations within surviving cells, which then produce a subgroup of defective stem cells that are unable to tolerate the second insult of chemotherapy. Recently, ataxia telangiectasia gene mutation and protein kinase deficiency have been associated with patients who have increased susceptibility to severe radiation-induced skin toxicity. Most of the lesions will heal with supportive treatment. Although some reports have noted that radiation-recall dermatitis recurred with subsequent continued administration of the same chemotherapeutic agent, such experience is not universal. At present, a decision as to whether the same chemotherapeutic agent can be continued will usually be determined by the severity of the initial reaction, the chemoresponsiveness of the tumor to this particular agent, the individual patient's wishes, and a clinical judgment that takes into account the availability of alternative therapy.

Antineoplastic Agents↗
PubMed2026

Validation of the Mechanism of Action of Jiedu Shengji Oil in the Treatment of Radiation Dermatitis based on Network Pharmacology and In vivo Experiments.

BACKGROUND: Radiation Dermatitis (RD) is a common complication of radiation therapy, with approximately 90% of patients experiencing moderate to severe radiation dermatitis injury after radiotherapy. Jiedu Shengji oil (JDSJY) is a commonly used herbal topical preparation in our hospital, with remarkable clinical efficacy in treating radiation dermatitis. However, the mechanism of JDSJY in treating RD is unclear. AIMS: The aim of the study is to explore JDSJY's mechanism of action in treating RD through methods, such as network pharmacology and in vivo experiments. METHODS: The active components and disease targets of JDSJY were screened and intersected via network pharmacology for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. The pharmacodynamics of JDSJY was evaluated by establishing a rat model of RD. RESULTS: Network pharmacology showed that the pathway network of JDSJY action involved 64 targets and 6 pathways and might act by targeting key targets, such as C-reactive protein (CRP) and regulating the MAPK signalling pathway. In addition, in vivo experiments showed that JDSJY reduced skin inflammation and inhibited apoptosis, significantly ameliorated mitochondrial damage in keratinocytes, and reduced the levels of antioxidant-related indicators. CONCLUSION: Comprehensive network pharmacology and in vivo experiments revealed that JDSJY's therapeutic efficacy in RD is mediated by ameliorating oxidative stress and maintaining mitochondrial homeostasis in keratinocytes.

Animals↗
PubMed1976

Inherent cellular radiosensitivity of human tumors of varying clinical curability.

It is well known that radiation therapy can be successfully used to cure or control some types of human tumors, while consistently failing in others. This has been ascribed to several factors including differences in the intrinsic sensitivity of the tumor cells and in their ability to recover from radiation damage. In this study, human tumor cells from an osteogenic sarcoma, a glioblastoma, and two medulloblastomas, as well as cells from human skin, were established in tissue culture, and the in vitrox x-ray survival and DNA repair parameters determined. No significant differences in either clonogenic survival or DNA strand rejoining ability could be detected among these human tumors or skin cells, despite the wide variability in their radiocurability in vivo. In addition, skin cell strains derived from patients exhibiting markedly sensitive or resistant skin reactions during fractionated radiotherapy showed no differences in survival characteristics from normal controls. It is therefore suggested that the wide range of radiocurabilities seen among various human tumors cannot be explained on the basis of inherent cellular factors responsible for the survival of tumor cells after x-irradiation.

Adolescent↗
PubMed1977

Preliminary results using twice-a-day fractionation in the radiotherapeutic management of advanced cancers of the head and neck.

Twenty-four cases of advanced T4 cancers of the head and neck were treated using a twice-a-day treatment fractionation delivering a 1,200 rad weekly tumor dose and 7,000 rad total tumor dose in 5 1/2-6 weeks. Acute normal mucosal reactions and skin reactions were plotted weekly and corresponded to reactions observed when delivering 1,000 rad per week in five treatment sessions. Chronic problems have been limited to severe neck fibrosis appearing in three of five patients who underwent a planned neck dissection 6 weeks after the completion of radiotherapy. Local control was observed in 14 of 23 patients (61%) and regional control in 22 of 23 patinets (96%).

Head and Neck Neoplasms↗
PubMed1978

Skin thickness in the therapeutically irradiated breast.

Skin thickening of the breasts of 22 women undergoing excision biopsy of a breast cancer and subsequent radiation therapy to 5,000 rad is considered. The skin thickness of the treated breast returned to normal in 17 of 22 patients studied. Of the 17, nearly 60% returned to normal in 2 years, over 80% in 3 years, and the rest by 4 years. The period of follow-up was less than 4 years in the five patients with residual skin thickening. The alterations in skin thickness are consistent with the histopathologic changes seen in radiation dermatitis.

Breast Neoplasms↗
PubMed2006

[Clinical phase I trial of concurrent chemo-radiotherapy with S-1 for T2NO glottic carcinoma].

We conducted a phase I study to determine a recommended dose (RD) of S-1 for chemo-radiotherapy consisting of S-1+ radiotherapy for T 2 N 0 larynx cancer. The method of administration used to assess the RD was irradiation with 2 Gy/day for 5 days a week until a total dose of 60 Gy, and concomitant administration of S-1 once a day for 2 weeks beginning on the day therapy was started followed by 2 weeks off the drug and 2 weeks on the drug with the dose escalating from S-1 60 mg/body/day (level 1) to 80 mg/body/day (level 2), and then to 100 mg/body/day (level 3). 18 patients were enrolled. 4 patients developed an adverse event of grade 3 radiation dermatitis which became a dose-limiting toxicity (DLT) at level 3. We then concluded that 100 mg/body/day was the maximum tolerated dose (MTD) of S-1 and decided that the RD of S-1 was 80 mg/body/day.

Aged↗