Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia and the associated lung neuroendocrine tumors: clinical experience with a rare entity.

BACKGROUND: Normal adult lungs contain pulmonary neuroendocrine cells (PNECs). PNEC hyperplasia may be either reactive or idiopathic, and the idiopathic type is defined as diffuse idiopathic PNEC hyperplasia (DIPNECH). It is believed that DIPNECH is a neuroendocrine proliferative process associated with carcinoid tumors. The available data regarding this rare condition are very limited. The objective of the current study was to describe the clinical, radiologic, and pathologic characteristics of patients with DIPNECH and the effect of various therapeutic modalities on patient well being. METHODS: The authors retrospectively studied 11 consecutive patients with DIPNECH who were followed at 2 referral centers in Israel between 2000 and 2010. RESULTS: All patients were women, and their median age was 62.8 years. Six patients presented with respiratory symptoms, such as prolonged dyspnea, wheezing, and cough. All patients had carcinoid tumor together with multiple, small pulmonary nodules observed on thoracic high-resolution computerized tomography images. The mean size of the dominant lesion was 19.4 ± 9.6 mm. Nine patients underwent thoracotomy and resection of the dominant lesion. The disease was stable in 5 of 11 patients; in 6 of 10 patients, it progressed, and the patients received treatment with somatostatin analogs, which induced disease stabilization in all patients. Metastatic disease was diagnosed in 3 of 11 patients (36%). All patients were alive at the end of follow-up (mean, 4.63 ± 2.04 years; ongoing). CONCLUSIONS: The association of lung neuroendocrine tumor with multiple nodules in women, together with complains of chronic cough and wheezing, should raise suspicion of DIPNECH. Whenever possible, these patients should undergo surgical excision of the dominant lesion, and somatostatin analogs may be considered for symptomatic or tumor control in patients with progressive disease.

Blood-Brain Barrier Disruption After Cardiopulmonary Bypass: Diagnosis and Correlation to Cognition.

BACKGROUND: Cardiopulmonary bypass (CPB) elicits a systemic inflammatory response that may impair blood-brain barrier (BBB) integrity. BBB disruption can currently be detected by dynamic contrast enhancement magnetic resonance imaging (MRI), reflected by an increase in the permeability constant (Ktrans). We aimed to determine (1) whether CPB induces BBB disruption, (2) duration until BBB disruption resolution, and (3) the obtainable correlation between BBB injury (location and intensity) and neurocognitive dysfunction. METHODS: Seven patients undergoing CPB with coronary artery bypass grafting (CABG) were assigned to serial cerebral designated MRI evaluations, preoperatively and on postoperative day (POD) 1 and 5. Examinations were analyzed for BBB disruption and microemboli using dynamic contrast enhancement MRI and diffusion-weighted imaging methods, respectively. Neuropsychologic tests were performed 1 day preoperatively and on POD 5. RESULTS: A significant local Ktrans increase (0.03 min-1 vs 0.07 min-1, p = 0.033) compatible with BBB disruption was evident in 5 patients (71%) on POD 1. Resolution was observed by POD 5 (mean, 0.012 min-1). The location of the disruption was most prominent in the frontal lobes (400% vs 150% Ktrans levels upsurge, p = 0.05). MRI evidence of microembolization was demonstrated in only 1 patient (14%). The postoperative global cognitive score was reduced in all patients (98.2 ± 12 vs 95.1 ± 11, p = 0.032), predominantly in executive and attention (frontal lobe-related) functions (91.8 ± 13 vs 86.9 ± 12, p = 0.042). The intensity of the dynamic contrast enhancement MRI BBB impairment correlated with the magnitude of cognition reduction (r = 0.69, p = 0.04). CONCLUSIONS: BBB disruption was evident in most patients, primarily in the frontal lobes. The location and intensity of the BBB disruption, rather than the microembolic load, correlated with postoperative neurocognitive dysfunction.

The role of routine bronchoscopy for early detection of bronchial stump recurrence of lung cancer: 1 year post-surgery.

BACKGROUND: Local recurrence after complete resection (R(0)) occur in approximately 20% of patients with stage I disease and in up to 50% with stage III. This study focuses on early detection of stump recurrence by a routine bronchoscopy. METHODS: Prospective analysis 1 year after surgery between April 2006 and April 2008. RESULTS: 104 NSCLC patients (age 69.1+/-9.6 years) participated in the study; 97 underwent lobectomy and 7 pneumonectomy. 61% were stage I, 25% stage II, 10% IIIA, 5% IIIB and 1% stage IV. 66% had N0, 21% had N1 disease, 9% N2 disease and 4% had N3. Bronchoscopy was performed 12.9+/-3.8 months after surgery. Nine percents had stump polyp, 5 (5%) had a suspicious mucosa. Four of the nine polyps were malignant. Nine other patients had squamous metaplasia and two had squamous dysplasia. Malignant stump recurrence was observed in four cases, all had a stump polyp. All had R(0), but two had short (<1.0 cm) tumor-free bronchial margin, two had N1 disease and two N2 disease. Fisher exact analysis showed short bronchus (p=0.003), N2 vs. N0-1 (p=0.012), and N1 vs. N0 (p=0.011) as significant risk factor for stump recurrence. For stump recurrence, one patient underwent completion pneumonectomy and has no evidence for disease (32.2 months), two patients were treated by chemotherapy and one patient died from pneumonia before therapy. CONCLUSION: Routine bronchoscopy 1 year after thoracic resection for NSCLC is justified in patients who are at high risk for local recurrence, i.e. short free bronchial margins and N2/N1 disease.