17. Herder GJ, van Tinterent TH, Golding RP et al. Clinical prediction Background: The optimal treatment of large-cell neuroendocrine carcinoma (LCNEC) of the lung remains unclear.Here, our primary objective was to assess the efficacy of cisplatin-etoposide doublet chemotherapy in advanced LCNEC. Accuracy of the pathological diagnosis and treatment toxicity were assessed as secondary objectives.Patients and methods: Prospective, multicentre, single-arm, phase II study with a centralised review of treatmentresponse and pathological data. Patients had untreated performance status (PS) 0/1 stage IV/IIIB LCNEC and received cisplatin (80 mg/m22 d1) and etoposide (100 mg/m22 d1-3) every 21 days. Results: Eighteen centres included 42 patients (mean age, 59 ± 9 years; 69% men; median of four cycles/patient). At least one grade-3/4 toxicity occurred in 59% of patients (neutropaenia, thrombocytopaenia, and anaemia in 32%, 17%, and 12%, respectively). The median progression-free survival (PFS) and overall survival (OS) were 5.2 months (95% confidence interval, CI, 3.1-6.6) and 7.7 months (95% CI, 6.0-9.6), respectively. The centralised pathologist review reclassified 11 of 40 (27.5%) patients: 9 as small-cell lung cancer, 1 as undifferentiated non-small-cell lung cancer, and 1 as atypical carcinoid. Survival data were not significantly changed by excluding the reclassified patients. Conclusions:The pathological diagnosis of LCNEC is difficult. The outcomes of advanced LCNEC treated with cisplatin-etoposide doublets are poor, similar to those of patients with advanced small-cell lung carcinoma (SCLC). Key words: carcinoma, clinical trial phase II, large cell neuroendocrine tumours, small-cell lung cancer introduction Large-cell neuroendocrine carcinoma (LCNEC) of the lung accounts for no more than 1% of all lung cancers. The typical histological features, first described in 1991 [1, 2], include large cells with abundant cytoplasm, a high mitotic rate, extensive necrosis, and a neuroendocrine growth pattern. The World Health Organisation currently classifies LCNEC as a distinct subtype of pulmonary large-cell carcinoma [3] and, therefore, as a subtype of non-small-cell lung carcinoma (NSCLC). However, LCNEC lacks the specific histologic features of NSCLC such as glandular or squamous differentiation, but instead displays evidence of neuroendocrine differentiation reminiscent of small-cell lung carcinoma (SCLC), although the malignant cells in SCLC are smaller, with scant cytoplasm, and invade the tissues in sheets. LCNECLCNEC shares genetic alterations with SCLC [4]. The higher mitotic rates and more extensive necrosis seen in LCNEC and SCLC are in contrast to the lower-grade neuroendocrine tumours, i.e. typical and atypical carcinoids. LCNEC and SCLC also share clinical characteristics including a preponderance of males and smokers and an aggressive clinical course [5][6][7][8][9]. The clinical outcome of LCNEC patients is poor, with overall 5-year survival rates ranging from 15% to 57%. Studies have demonstrated signifi...

Thin-section computed tomography (CT) was performed in 244 patients with infiltrative lung diseases and 29 healthy control subjects to evaluate the frequency, profusion, and diagnostic value of subpleural parenchymal micronodules. These areas of increased attenuation (less than 7 mm in diameter) were analyzed in four groups: coal miners with chest radiographic findings of coal worker's pneumoconiosis (n = 61), coal miners with no radiographic evidence of pneumoconiosis (n = 73), patients with nonoccupational chronic infiltrative lung disease (n = 110), and healthy adults (n = 29). Subpleural parenchymal micronodules were observed with high frequency in pulmonary lymphangitic carcinomatosis, coal worker's pneumoconiosis, and sarcoidosis but were also seen in 14% of control subjects. Predominant sites of lesions were the posterior subpleural areas in the upper lobes. Subpleural parenchymal micronodules have no diagnostic value when observed as an isolated CT finding but may suggest that diagnosis of pneumoconiosis, sarcoidosis, or pulmonary lymphangitic carcinomatosis when observed in association with mild parenchymal lesions.

Twenty cases of cystic adenomatoid malformation of the lung were observed: 2 had died in utero; the diagnosis was made at birth in 13 infants of which 3 were premature. A Bochdalek's hernia had been diagnosed before birth in 2 cases by echo-tomography. The correct antenatal diagnosis had been made in 2 cases. Two infants had no symptoms, 3 were dyspneic, 8 were in respiratory distress and had to be intubated and ventilated. Two had a prune belly syndrome. Eight infants had a thoracotomy during their first week of life. Pulmonary resections concerning those 13 patients comprised 10 lower lobectomies, 1 of which was associated with a lingulectomy, and 2 upper lobectomies, 1 of which was associated with a middle lobe resection. Five patients were diagnosed and operated upon between 10 months and 8 years of age; 4 had recurrent bronchitis and 1 was diagnosed during the treatment of a gastroenteritis. They had 3 lower and 2 upper lobectomies. Recovery was uneventful in all patients except for 1 who was reoperated upon for intestinal obstruction. Antenatal diagnosis of cystic adenomatoid malformation should become standard. The malformation may be mistaken for a pulmonary sequestration or bronchogenic cyst. Differential diagnosis of a congenital hernia is important.

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