Serial FDG-PET images during CRT show significant increases in SUVpeak for patients in whom RE develops. The changes at week 2 may predict those at risk for the development of grade 3 RE and may be informative for adaptive planning and early intervention.

Insufficiency fractures are recognised consequences of radiotherapy in gynaecological malignancy with reported incidences between 2.7% and 89%. We aimed to determine the incidence and risk factors for insufficiency fractures in patients receiving radical pelvic radiotherapy for uterine and cervical cancer. A case-note review was undertaken of patients treated between January 2007 and December 2008. Insufficiency fractures were identified from radiographs, computed tomography and magnetic resonance images. Chi-squared and Mann-Whitney tests were performed to determine associations between insufficiency fractures and chemotherapy, steroids and age. A total of 285 patients received pelvic radiotherapy, 137 with uterine and 148 with cervical cancer. Mean age was 59 years. A total of 144 patients received chemotherapy, 101 concurrently and 35 adjuvantly. Bone abnormalities affected 67 patients, 33 had pelvic insufficiency fractures, 12 had multiple fractures and 3 patients developed femoral head avascular necrosis. Use of chemotherapy was not associated with development of fractures (P = 0.949). However, cervical cancer patients had a significantly higher incidence of insufficiency fractures (P = 0.018) and bone pain (P = 0.03) compared with uterine cancer patients. This suggests concurrent chemotherapy may be a significant factor in increasing insufficiency fractures and bone morbidity in these patients and highlights a need for further research to identify, prevent and reduce these long-term complications.

A 50-year-old man, previously fit and well, presented to his general practitioner in May 2010 with a 4-week history of intermittent symptoms of parasthesia affecting his lips, slurred speech, and difficulty with mastication. He had dysphagia of solids and reported a weight loss of 9 kg. He had experienced severe occipital headaches, drooping of both eyelids, and fatigue predominantly worse at the end of the day. He was a heavy smoker and worked as a mechanical engineer.Systemic and neurologic examinations were normal apart from presence of bilateral ptosis. Routine laboratory tests were unremarkable apart from grossly elevated antiacetylcholine receptor antibodies of 42.2 nmol/L (range, 0 to 0.2 nmol/L). Computed tomography (CT) and magnetic resonance imaging brain scans were normal, and magnetic resonance angiograms showed normal cerebral vasculature. However, chest radiograph revealed a large right upper lobe soft tissue mass (Fig 1). CT of the chest confirmed an 11-cm mass in the right upper lobe with small right paratracheal nodes. CT guided biopsies from the lung lesion showed necrosis and were inconclusive. Positron emission tomography scan confirmed a large necrotic right upper lobe mass extending to the right hilum, peripherally avid with maximum standardized uptake value of 9.4 (Fig 2). There was no evidence of nodal spread or distant metastasis. Bone marrow examination was normal. There was a multidisciplinary team decision to treat the patient with primary surgery on the basis that this could be an underlying lung cancer or ectopically situated thymoma with associated myasthenia gravis. D I A G N O S I S I N O N C O L O G Y

A 64-year-old male presented to hospital with breathlessness and weight loss. Ultrasound-guided biopsy of supraclavicular lymph node confirmed a diagnosis of small-cell lung cancer. The patient was started on Dexamethasone 8 mg twice daily for symptom control while awaiting urgent oncology assessment. Three days later he was admitted with acute kidney injury and worsening breathlessness. Biochemical changes confirmed tumour lysis syndrome (TLS) that had occurred following steroid therapy. He was given allopurinol followed by rasburicase. His clinical condition continued to worsen and he died of multi-organ failure. To our knowledge, TLS in small-cell lung cancer solely attributed to steroid therapy has not been described before. Due to its rarity, physicians have a very low index of suspicion of TLS in lung cancer when prescribing corticosteroids for palliation of symptoms. Patients with risk factors should be identified and baseline blood tests performed and appropriate prophylaxis commenced.