Early clinical and neuroradiological worsening after radiotherapy and concomitant temozolomide in patients with glioblastoma: Tumour progression or radionecrosis?

Peca, Carmela; Pacelli, Roberto; Elefante, Andrea; De, Marialaura Del Basso; Vergara, Pierluigi; Mariniello, Giuseppe; Giamundo, A; Maiuri, Francesco

doi:10.1016/j.clineuro.2008.11.003

Cited by 58 publications

(42 citation statements)

References 19 publications

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“…Prior reports have suggested that particular chemotherapeutic agents have interacted with radiation to increase the risk of radiation necrosis [6]. In recent reports, patients with primary malignant astrocytomas treated with temozolomide and radiotherapy have an up to fourfold increase in radiation necrosis compared to patients receiving radiation therapy alone [1,[7][8][9]. Our patient was treated with high dose melphalan which, as an alkylating agent, has a similar mechanism of action and is known to be a radiosensitizer [10,11].…”

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confidence: 66%

Necrosis following skull base irradiation and stem cell transplant for multiple myeloma

et al. 2010

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A 58-year-old Caucasian man with no significant past medical history presented with rapid onset diplopia and blurred vision. Neurological examination revealed bilateral sixth as well as right fourth and fifth cranial nerve palsies, with no other focal neurological deficits. MRI of the head revealed a 6.0 cm 3 4.7 cm 3 3.2 cm soft tissue mass in the sella turcica, replacing most of the clivus and enhancing strongly after gadolinium administration (see Image 1). The radiological differential diagnosis of the tumor included a clival chordoma, an atypical invasive pituitary adenoma, a solitary plasmacytoma or a bone metastasis. Pituitary function testing demonstrated a markedly elevated serum prolactin (1994 ng/dL, normal 3-13 ng/dL), and bromocriptine therapy was initiated. The patient returned 1 month later with anorexia, nausea, fatigue, and new headache. Blood tests revealed renal dysfunction (creatinine 2.34 mg/dL, normal 0.7-1.2 mg/dL) and hypercalcemia (11.96 mg/dL, normal 8.5-10.3 mg/dL), with a decrease in prolactin (411 ng/dL, normal 2.1-17.7 ng/mL). A renal biopsy revealed nonspecific changes, while urine protein electrophoresis showed large free kappa monoclonal peaks. Bone marrow aspirates showed areas with 40-100% plasmocytes. Hemoglobin was 148 g/L (normal 140-180 g/L), b2-microglubulin 6.2 mg/L (normal 0-2.5 mg/L) and albumin 34 g/L (normal 38-50 g/L). A skeletal survey demonstrated multiple lytic lesions. These new findings were diagnostic of kappa light chain myeloma, ISS Stage III. A transsphenoidal debulking of the sellar lesion was performed, revealing a collision tumor consisting of a prolactinoma and a plasmacytoma. Treatment for MM was initiated with thalidomide and dexamethasone, with supportive pamidronate.After surgery, the patient was referred to radiation oncology for consideration of radiation therapy for palliation of worsening cranial nerve deficits. A total of 50.4 Gy in 28 daily fractions was delivered using a multifield intensitymodulated photon plan (1.8 Gy/fraction). The treatment was well tolerated with subtle improvement of the right fifth cranial nerve deficit. On a contrast-enhanced MRI performed 3 months later, the lesion appeared largely necrotic and was decreased in size. Six months after completion of radiation therapy, the patient underwent an autologous stem cell transplant following stem cell mobilization with cyclophosphamide and G-CSF, and melphalan 200 mg/m 2 .One year post radiotherapy, the patient presented with a 10-day history of lethargy, nausea and vomiting, new complete left seventh nerve palsy, decreased hearing on the left side, and a left third nerve deficit. A repeat CT scan revealed an unchanged clival lesion, and a new hypodensity at the left cerebellopontine angle measuring 4.8 cm 3 2.6 cm, compressing the left cerebellar peduncle and 4th ventricle. An MRI showed new high signal intensity on T2 images involving the left side of the medulla, left inferior and middle cerebellar peduncles, left pons, and left cerebral peduncle. The abnormal signal involve...

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confidence: 66%

Necrosis following skull base irradiation and stem cell transplant for multiple myeloma

et al. 2010

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“…Recently, concurrent temozolomide chemotherapy and radiation have become the standard of care for treatment of glioblastoma. Radiation necrosis has been reported at a higher incidence with this protocol (6-13.7%) and with a shorter latency (median 3-6 months) [9]. This may be attributed to the radiosensitizing effect of temozolomide and to the higher degree of endothelial damage inflicted than with single modality therapy.…”

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confidence: 90%

Long-Term Relief of Cerebral Radiation Necrosis Treated with Low-Dose Bevacizumab - a Report of 2 Cases

Hu¹,

Zhao²,

Xu³

et al. 2017

Oncol Res Treat

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Background: Radiation necrosis is 1 of the most significant complications of brain tumor irradiation. The standard treatment for patients with radiation necrosis consists of corticosteroids to reduce the amount of cerebral edema and, if required, cyst drainage. Case Reports: 2 patients with symptomatic radiation necrosis initially unresponsive to steroid treatment were treated with repeated low-dose bevacizumab at 5 mg/kg body weight. Rapid and lasting symptom relief, as well as neuroradiological improvement was seen in both cases. A dramatic rapid magnetic resonance imaging response with decrease in contrast enhancement was found shortly after administering the first dose of bevacizumab. The improvement of perifocal edema was relatively slower than of the reduction of enhancement. Only a slight reduction in size of the involved area could be expected after the first dose of bevacizumab. Further shrinkage was seen after the second and third doses. The individuals reported have been doing well for more than 45 and 22 months, respectively, after the initiation of bevacizumab treatment. Conclusion: Our data add to the literature supporting of the use of bevacizumab as an effective therapeutic agent for radiation necrosis, particularly in cases unresponsive to steroid treatment.

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“…Symptoms depend on the location of tumour and vary among individuals. Without treatment, glioblastoma are usually fatal within a few weeks to several months [1][2][3][4][5][6][7]. Current therapeutic strategies with surgery followed by local radiotherapy and simultaneous as well as adjuvant chemotherapy have increased median life expectancy from 12.1 to 14.6 months [8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

MRI during radiotherapy of glioblastoma

et al. 2016

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Early clinical and neuroradiological worsening after radiotherapy and concomitant temozolomide in patients with glioblastoma: Tumour progression or radionecrosis?

Cited by 58 publications

References 19 publications

Necrosis following skull base irradiation and stem cell transplant for multiple myeloma

Necrosis following skull base irradiation and stem cell transplant for multiple myeloma

Long-Term Relief of Cerebral Radiation Necrosis Treated with Low-Dose Bevacizumab - a Report of 2 Cases

MRI during radiotherapy of glioblastoma

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