Summary High-dose etoposide (2.0-2.4 g m-2) with granulocyte colony-stimulating factor (G-CSF) is an effective strategy to mobilize perpheral blood progenitor cells (PBPCs), although in some patients this is associated with significant toxicity. Sixty-three patients with malignancy were enrolled into this non-randomized sequential study. The majority (55/63, 870,o) had received at least two prior regimens of chemotherapy. and seven patients had previously failed to mobilize following high-dose cyclophosphamide with G-CSF. Consecutive patient groups received etoposide at three dose levels [2.0 g m-2 (n = 22). 1.8 g m-2 (n = 20) and 1.6 g m-2 (n = 21)] followed by daily G-CSF. Subsequent leukaphereses were assayed for CD34-cell content, with a target total collection of 2.0 x 106 CD34-cells kg-'. Toxicity was assessed by the development of significant mucositis. the requirement for parenteral antibiotics or blood component support and rehospitalization incidence. Ten patients (169o) had less than the minimum target yield collected. Median collections in the three groups were 4.7 (2 g m-2). 5.7 (1.8 g m-2) and 6.5 (1.6 g m-2) x 106 CD34-cells kg-'. Five of the seven patients who had previously failed cyclophosphamide mobilization achieved more than the target yield. Rehospitalization incidence was significantly lower in patients receiving 1.6 g m-2 etoposide than in those receiving 2.0 g m-2 (P = 0.03). These data suggest that high-dose etoposide with G-CSF is an efficient mobilization regimen in the majority of heavily pretreated patients, including those who have previously failed on high-dose cyclophosphamide with G-CSF. An etoposide dose of 1.6 g m-2 appears to be as effective as higher doses but less toxic.

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A 76-year-old man was referred in 2004 for assessment of longstanding dysphagia. His symptoms had changed slightly in that he had been experiencing some regurgitation of food up to 24 hours after a meal. He had first presented in 1984 with a complaint of food sticking on the way down, at the level of the epigastrium, which was intermittent in nature and worse with meat and bread. He had a 15-year history of indigestion at that time and was investigated with a barium meal and a gastroscopy (OGD), both of which were normal. As his symptoms were not progressive or troublesome he was discharged from follow up. He was referred again in 1996 with similar symptoms. The dysphagia had been well controlled by avoiding foods that worsened his symptoms. OGD at that stage proved normal and the patient had settled. He was discharged with a diagnosis of mild motility disorder and advice to re-refer should things change. He attended in 2004 with a change in symptoms – he felt food now seemed to get stuck higher up with regurgitation of contents of previous meals. No worrying symptoms were noted and physical examination was normal. The patient was booked for further OGD and oesophageal manometry to take place on the same day. The OGD was carried out first and it became apparent he had developed a pharyngeal pouch, which was later confirmed on barium swallow (Figure 1). The rest of the examination was normal. He also underwent manometry with the probe being placed over a guidewire. This revealed the presence of incoordination of peristaltic waves with simultaneous pressure rises in the lower oesophagus (Figure 2). It also showed a hypertensive lower oesophageal sphincter (max pressure 53 mmHg) that relaxed appropriately (Figure 3). The patient was referred to the ear, nose and throat surgeons for further management as the pouch was the main contributing factor in the new symptoms. He underwent an uncomplicated endoscopic stapling diverticulotomy with a return to previous level of function.