[Atypical adenomatous hyperplasia of lung: clinicopathologic study of 8 cases and review of literature].

OBJECTIVE: To study the clinicopathologic and immunohistochemical features of atypical adenomatous hyperplasia (AAH) of lung. METHODS: Eight cases of AAH of lung were studied by light microscopy and immunohistochemical staining for p16, thyroid transcription factor-1 (TTF-1), Ki-67, p53, epidermal growth factor receptor (EGFR) and c-erbB-2. RESULTS: The mean age of the patients was 52 years. The male-to-female ratio was 1:3. Two patients were chronic smokers. The clinical symptoms were relatively non-specific. Three patients had past history of non-pulmonary tumors, while 4 patients had lung adenocarcinoma. CT scan revealed solitary or multifocal hyperdense opacities. Histologically, the lesions ranged from 1 mm to 6 mm in size. Two cases were solitary and 6 cases were multifocal. All were of high-grade lesions. Associated low-grade component was noted in 3 cases. There was no evidence of local recurrence or disease progression in the 7 patients with post-operative follow-up information available (mean duration of follow up = 23 months). Four patients had received chemotherapy as well. Immunohistochemical study showed variable positivity for p16 (5/8), TTF-1 (5/8), Ki-67 (with proliferation index ranging from 1% to 10%), p53 (1/8) and EGFR (1/8). The staining for c-erbB-2 was negative (0/8). Four cases of AAH were associated with pulmonary adenocarcinoma. The adenocarcinoma cells were diffusely positive for TTF-1 (4/4), variably positive for p16 (2/4), Ki-67 (with proliferation index ranging from 2% to 40%), p53 (1/4) and EGFR (3/4), and negative for c-erbB-2 (0/4). CONCLUSIONS: AAH of lung is associated with pulmonary adenocarcinoma. Diagnosis of AAH requires correlation with CT findings and pathologic examination.

Molecular alterations in atypical adenomatous hyperplasia occurring in benign and cancer-bearing lungs.

Atypical adenomatous hyperplasia (AAH) is considered to be a precursor lesion of the lung adenocarcinoma. Several genetic abnormalities have been reported in AAH associated with adenocarcinoma, but little is known about AAH associated with benign lung lesions. To address this we compared the molecular characteristics of AAH present in benign conditions to those coexisting with carcinoma. Seven cases of AAH from resected non-neoplastic lungs (AAH-B) and 12 cases from lungs resected for primary lung carcinoma (AAH-M) were analyzed for loss of heterozygosity (LOH) using 21 polymorphic microsatellite markers situated in proximity to known tumor suppressor genes on chromosomes 3p, 5q, 7p, 9p, 10q, and 17p. Direct DNA sequencing for K-ras mutation was also performed. There was a broad range of LOH in both groups. No LOH was identified in 3 cases (25%) of AAH-M, but all cases of AAH-B showed LOH (P=0.26). Six cases (50%) of AAH-M and 3 cases (43%) of AAH-B showed loss at 1 marker (P=0.99). LOH at 2 or more markers was identified in 3 (25%) cases of AAH-M and 4 (57%) cases of AAH-B (P=0.32). LOH was most frequently detected on chromosomes 3p and 10q in both groups. The difference in overall fractional allelic loss between the 2 groups did not reach statistical significance. K-ras mutations were not identified in either group. Our results showed a significant overlap in LOH patterns between AAH with or without coexistent lung malignancy. Therefore, AAH may represent a smoking induced low-grade neoplastic lesion that may be a precursor lesion of only a subset of invasive lung adenocarcinoma.

Manejo anestésico de una malformación adenoidea quística / Anesthetic management of a cyst adenoid malformation

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A clinicopathological study of resected pulmonary nodules with focal pure ground-glass opacity.

OBJECTIVE: Pulmonary lesions with focal ground-glass opacity (GGO) have been detected increasingly by low-dose helical computed tomography (CT). However, the strategy of treatment for focal pure GGO lesions is still undecided. This study evaluates clinicopathological characteristics of resected pulmonary nodules with focal pure ground-glass opacity. METHODS: Between January 1997 and December 2005, 26 patients (35 lesions) with pure GGO lesions underwent pulmonary resection. The data on patient age, lesion size, pathology, carcinoembryonic antigen (CEA) level and palpability of the tumor in the resected specimen were evaluated. RESULTS: The histological diagnosis was bronchioloalveolar carcinoma (BAC) in 10 patients (12 lesions), atypical adenomatous hyperplasia (AAH) in 15 patients (22 lesions), and focal scar in 1 patient (1 lesion). There were no significant differences in age, sex, tumor size, and CEA level between the patients with BAC, AAH, and focal scar. However, the lesions >10mm in size were all BAC. Palpability of the tumor in the resected specimen was significantly more frequent in BAC cases than in AAH cases (p<0.01). For BAC, lobectomy was performed for four lesions, and limited resection for eight. None of the BACs showed lymphatic or vascular invasion upon pathological examination. At the median follow-up point of 44 months (range: 4-84 months), no recurrences were observed. CONCLUSIONS: BAC and AAH cannot be discriminated by their size. In the resected specimen, BAC lesions are more frequently palpable than AAH lesions. Thoracoscopic surgery is recommended for focal pure GGO after repeated CT even if the GGO lesion is small. Partial resection is a sufficient treatment for pure GGO.

Synchronous pulmonary atypical adenomatous hyperplasia and metastatic osteosarcoma in a young female.

A 17-year-old female underwent metastasectomy of three synchronous lesions in the bilateral lungs under the diagnosis of metastatic osteosarcoma, however, one of them was found to be atypical adenomatous hyperplasia (AAH). Since AAH is very rare among young people, a careful evaluation of high-resolution computed tomographic image is important in determining the operative indications and procedures in patients with multiple metastatic tumors.

A case of multiple atypical adenomatous hyperplasia of the lung detected by computed tomography.

Multiple atypical adenomatous hyperplasia (AAH) of both lungs in a 72-year-old male, detected by computed tomography, is reported. The lesions of the right lung were resected for diagnosis via video-assisted thoracoscopic surgery (VATS). The resected specimen had 22 AAH lesions up to 10 mm in size. For nine of these lesions, the expressions of carcinoembryonic antigen (CEA), c-erbB-2 oncoprotein and p53 gene product were examined by immunohistochemistry and the loss of heterozygosity (LOH) on chromosomes was investigated by polymerase chain reaction analysis. These lesions showed a variety of expressions for CEA, c-erbB-2 and p53 oncoprotein. Three of the nine lesions showed LOH on chromosome 13q, although this was not exhibited in the largest one. These results indicate that each AAH in this case has independent genetic abnormalities and is multicentric.

Malformación adenomatosa quística del pulmón: diagnóstico prenatal / Cystic adenomatoid malformation of the lung: antenatal diagnosis

Presentamos un caso clínico de diagnóstico antenatal de malformación adenomatosa quística del pulmón. Se realiza una revisión de la literatura y se discute el manejo perinatal

[Adenomatoid cystic lung abnormality in adults with associated bronchioloalveolar carcinoma]. / Adenomatoid-zystische Lungenfehlbildung bei Erwachsenen mit assoziiertem bronchioloalveolärem Karzinom.

Lung cysts were observed by chance in the chest radiographs from two women aged 20 and 41. In the surgical specimens the lesions proved to be congenital cystic adenomatoid malformation type 1. The cysts were partially lined by mucous cells. Also near the cysts there were circumscribed tubuloacinar proliferations of mucous cells. In both cases a transition into a bronchioloalveolar carcinoma was seen. Histochemically no sulphomucins could be demonstrated by means of an alcian blue pH 1 reaction in the tumor cells, but was demonstrated in the non-neoplastic cells of the malformation. In both cases CEA was demonstrated in the tumor cells. Some cells in the tubuloacinar proliferations were weakly CEA positive. In one patient the diagnosis of carcinoma was made by intraoperative frozen section and a lobectomy was performed. The other patient had first only a resection of her cystic lesions and had to be reoperated because of the results of the pathological examination. Both patients had no recurrence in the 8 years following the operation. In the literature we found 5 cases of congenital cystic adenomatoid malformation in adults. In 2 cases there was also an associated bronchioloalveolar carcinoma. Several reports exist on the association of different kinds of cystic lung lesions and malignant tumors and their possible pathogenetic relationship. In this paper we draw attention to the development of malignant neoplasia in congenital cystic adenomatoid malformation in adults and its diagnostic problems.