Cases reported "Radiation Injuries"

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1/287. Increased risk of erythema multiforme major with combination anticonvulsant and radiation therapies.

    erythema multiforme major (EMM; stevens-johnson syndrome) is a cutaneous disorder associated with a wide variety of factors including ingestion of drugs such as phenytoin and exposure to intracranial radiation therapy. Based on observations of a 47-year-old black man with brain metastases who developed EMM after combined phenytoin and radiation therapy, we conducted a medline literature search for articles on similar cases from 1966 to the present. Twenty cases were identified that support the hypothesis that EMM is associated with combined phenytoin and radiation therapy. The reaction, or its severity, has no relationship to the phenytoin or radiation therapy dosage, or to the histologic type of brain tumor. Also, EMM has no apparent age or gender predisposition in association with phenytoin-radiation therapy. Thus this is a clinical phenomenon that occurs with unusual frequency in patients with brain tumor who undergo radiation therapy while taking phenytoin. phenytoin and other anticonvulsants such as phenobarbital and carbamazepine induce cytochrome P450 3A and produce oxidative reactive intermediates that may be implicated in hypersensitivity reactions such as EMM. Both carbamazepine and barbiturates have shown cross-sensitivity with phenytoin; furthermore, a case of EMM in a patient receiving carbamazepine and whole brain radiation therapy has been reported. As carbamazepine, valproate, and barbiturates have been associated with EMM, gabapentin may be considered as alternative anticonvulsant therapy when appropriate.
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2/287. Cerebral "radiation necrosis": vascular and glial features.

    Glial and vascular abnormalities in brain, simulating intracranial neoplasia, are described in a patient who received radiation to the pituitary region for treatment of an adenoma, 13 months before death. In addition to the expected changes of cerebral radionecrosis, four interesting features are cited: 1. Diffuse hyperplasia of capillaries in the cerebral cortex with marked endothelial hypertrophy; 2. abundant, large multipolar bizarre cells in the perivascular connective tissues; 3. focal astrocytic proliferation with many cells resembling either Alzheimer type I astrocytes or neoplastic cells, and 4. radiation changes in the non-irradiated brain.
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3/287. dementia following treatment of brain tumors with radiotherapy administered alone or in combination with nitrosourea-based chemotherapy: a clinical and pathological study.

    A retrospective clinical and pathological study of 4 patients who developed the syndrome of radiation induced dementia was performed. All patients fulfilled the following criteria: (1) a history of supratentorial irradiation; (2) no evidence of symptomatic recurrent tumor; (3) no other cause of progressive cerebral dysfunction and dementia. The clinical picture consisted of a progressive "subcortical" dementia occurring 3-12 months after a course of cerebral radiotherapy. Examination revealed early bilateral corticospinal tract involvement in all patients and dopa-resistant Parkinsonian syndrome in two. On CT scan and MRI of the brain, the main features consisted of progressive enlargement of the ventricles associated with a diffuse hypodensity/hyperintensity of the white matter best seen on T2 weighted images on MRI. The course was progressive over 8-48 months in 3 patients while one patient had stabilization of his condition for about 28 years. Treatment with corticosteroids or shunting did not produce sustained improvement and all patients eventually died. Pathological examination revealed diffuse white matter pallor with sparing of the arcuate fibers in all patients. Despite a common pattern on gross examination, microscopic studies revealed a variety of lesions that took two basic forms: (1) a diffuse axonal and myelin loss in the white matter associated with tissue necrosis, particularly multiple small foci of necrosis disseminated in the white matter which appeared different from the usual "radionecrosis"; (2) diffuse spongiosis of the white matter characterized by the presence of vacuoles that displaced the normally-stained myelin sheets and axons. Despite a rather stereotyped clinical and radiological course, the pathological substratum of radiation-induced dementia is not uniform. Whether the different types of white matter lesions represent the spectrum of a single pathological process or indicate that the pathogenesis of this syndrome is multifactorial with different target cells, remains to be seen.
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4/287. radiation-induced localized scleroderma in breast cancer patients.

    radiation-induced scleroderma in breast cancer patients appears to occur in approximately one out of every 500 patients. We report four cases that developed within 3 months of conservative breast surgery and postoperative radiation treatment. The reaction was contained entirely within the treatment field and demonstrated the typical features of this condition where the breast becomes erythematous, violaceous, indurated, retracted, and progressively pigmented. The breast tends to soften and become more comfortable over 1-4 years; however, significant induration, retraction and pigmentary changes remain. There appears to be no predictive factors. radiation-induced scleroderma must be differentiated from cellulitis and recurrent breast cancer.
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5/287. collagen vascular diseases and radiation therapy: a critical review.

    PURPOSE: Although many oncologists have the impression that patients with collagen vascular disease tolerate radiotherapy less well than other patients, until now this was never described in a review article. methods AND RESULTS: The principal objective was to determine whether patients with collagen vascular diseases have a greater risk of severe radiation therapy complications, than those without a collagen vascular disease. However, most of the publications found on this topic are short anecdotal case reports of patients with increased toxicity after radiation. Consequently, the true incidence of these side effects is unknown. CONCLUSIONS: Unless further studies on this subject are reported, each radiation oncologist should be cautious in treating these patients.
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6/287. Delayed radionecrosis of the larynx.

    radiation has been used to treat carcinoma of the larynx for more than 70 years. Radionecrosis is a well-known complication of this modality when treating head and neck neoplasms. It has been described in the temporal bone, midface, mandible, and larynx. Laryngeal radionecrosis is manifested clinically by dysphagia, odynophagia, respiratory obstruction, hoarseness, and recurrent aspiration. The vast majority of patients who develop laryngeal radionecrosis present with these symptoms within 1 year of treatment; however, delayed presentations have been reported up to 25 years after radiotherapy. We present, in a retrospective case analysis, an unusual case of laryngeal radionecrosis in a patient who presented more than 50 years after treatment with radiotherapy for carcinoma of the larynx. The cases of delayed laryngeal necrosis in the literature are presented. This represents the longest interval between treatment and presentation in the literature. The details of the presentation, clinical course, and diagnostic imaging are discussed. The pathogenesis, clinical features, and treatment options for this rare complication are reviewed. Early stage (Chandler I and II) laryngeal radionecrosis may be treated conservatively and often observed. Late stage (Chandler III and IV) cases are medical emergencies, occasionally resulting in significant morbidity or mortality. Aggressive diagnostic and treatment measures must be implemented in these cases to improve outcome. This case represents the longest interval between initial treatment and presentation of osteoradionecrosis in the literature. A structured diagnostic and therapeutic approach is essential in managing this difficult problem.
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7/287. 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.
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8/287. Enhanced accuracy in differential diagnosis of radiation necrosis by positron emission tomography-magnetic resonance imaging coregistration: technical case report.

    OBJECTIVE AND IMPORTANCE: To demonstrate the usefulness of positron emission tomography-magnetic resonance imaging (MRI) coregistration for differentiation of radiation necrosis and recurrent tumor in stereotactic planning. CLINICAL PRESENTATION: T1-weighted MRI scans of a 43-year-old woman revealed a contrast-enhancing lesion 4 years after open removal of a recurrent, right parieto-occipital Grade II oligodendroglioma and subsequent external radiation therapy. The suspected contrast-enhancing lesion revealed only moderate tracer uptake (1.3 times the uptake in the contralateral normal cortex) in a coregistered [11C]methionine positron emission tomographic scan. Approximately 15 mm posterior and mesial to the center of the contrast-enhancing lesion, however, an area of higher tracer uptake was found (1.8 times that of the contralateral normal cortex), which exhibited only very minor contrast enhancement on MRI. TECHNIQUE: The coregistered images were used for planning stereotactic serial biopsies, from the contrast-enhancing lesion as well as from the area with higher methionine uptake. Histological examination demonstrated that the contrast-enhancing lesion with low methionine uptake was necrotic tissue, and the nonenhancing area with high methionine uptake was recurrent tumor. CONCLUSION: High-resolution positron emission tomography and modern coregistration techniques allow differentiation of contrast enhancement and methionine uptake in irradiated brain tissue within small areas. High methionine uptake is typical for recurrent tumor tissue and can be differentiated from minor tracer accumulation resulting from disruption of the blood-brain barrier or macrophage activity within the necrotic area.
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9/287. Complications of total abdominal and spleen irradiation in patients with lymphomas.

    Fifty patients with non-Hodgkin's lymphoma were treated with total abdominal irradiation to a dose of 3000 rad by anterior and posterior fields treated the same day. Fourteen patients developed complications, four with intestinal obstruction due to stenosis and three with total or partial intestinal irradiation damage. These bowel complications were only seen in patients who had previously had a laparotomy. The ways of preventing these complications are discussed. We have studied renal function by means of clinical examination, biologic and radiologic investigations, and scanning in 75 patients who have received splenic irradiation to a dose of 4000 rad. With a mean follow-up time of 36 months, this study has shown that there was no significant change in blood pressure or in biochemical measurements. However, at the 17th month, nephrotomograms demonstrated cortical atrophy of the upper role of the kidney; at the 8th month, low uptake in the irradiated area was seen on 197Hg neohydrine scanning and a decrease in renal plasma flow in the left kidney during dynamic studies with Hippuran.
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10/287. radiation-induced blood-brain barrier damage in astrocytoma: relation to elevated gelatinase B and urokinase.

    Successful management of brain tumors prolongs life, raising the risk of delayed injury secondary to the treatment. radiation therapy, a mainstay of brain tumor treatment, can damage the cerebral blood vessels. Acutely a breakdown of the blood-brain barrier (BBB) may be seen, but fibrosis complicates radiation injury in the chronic phase. matrix metalloproteinases (MMPs) and plasminogen activators are two matrix-degrading proteolytic enzymes, which are induced by radiation. They disrupt the basal lamina around cerebral capillaries and open the BBB. We report a patient with an astrocytoma managed by partial resection and external beam irradiation to maximal tolerable doses. The patient later developed malignant brain edema shortly after stereotactic radiosurgery. Tissue obtained during surgical debulking to control the edema showed very high levels of gelatinase B (92 kDa type IV collagenase) and urokinase-type plasminogen activator (uPA). Tumor cells were absent from the biopsy and subsequent autopsy specimens, but necrosis with fibrosis of the blood vessels was seen. If abnormal matrix enzyme function participates in the expression of radiation injury, then inhibitors to such enzymes may provide one strategy for controlling cerebrovascular damage after therapeutic brain radiation.
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