Numb chin syndrome o neuropatía del nervio mentoniano como primera manifestación de progresión tumoral / Numb chin syndrome

La neuropatía mentoniana o síndrome de Roger es una neuropatía sensitiva que en muchas ocasiones se asocia a una neoplasia subyacente. Presentamos el caso de un paciente cuya progresión tumoral se manifestó en forma de neuropatía mentoniana secundaria a metástasis mandibular

Numb chin or Roger syndrome is a sensory neuropathy that is often associated with an underlying malignancy. We report a case of a patient whose tumor progression manifested as mental neuropathy secondary to mandibular metastasis

[The new classification of lung adenocarcinoma]. / Adenokarzinome der Lunge--die neue Klassifikation.

The new, interdisciplinary IASLC/ATS/ERS classification of lung adenocarcinoma has achieved a considerable impact since its publication in the year 2011. It separates tumours into preinvasive, minimally invasive and invasive subtypes. The preinvasive lesions atypical, adenomatous hyperplasia (AAH) and adenocarcinoma in situ (AIS) together with the minimally invasive adenocarcinoma (MIA), have an excellent prognosis after complete resection with 100 % survival. It enables a reproducible tumour grading by the determination of the predominant histological growth pattern which could be confirmed in several follow-up studies. Thereby the mixed subtype was eliminated which formerly represented about 80 % of all adenocarcinomas. Similarly, the terms bronchioloalveolar adenocarcinoma and bronchioloalveolar tumour growth were eliminated because they represented several distinct entities, specifically the in-situ lesions AAH and ACIS as well as the non-in-situ/invasive tumours like minimally invasive adenocarcinoma, lepidic predominant adenocarcinoma (LPA) and invasive mucinous adenocarcinoma (IMA). Although the classification is based on data from tumour resections it accommodates the fact that most tumours are diagnosed on biopsies and cytological specimens and includes recommendations for an efficient work-up to preserve tissue for molecular testing. Furthermore, the morphological analysis may provide hints for molecular changes including mutations with therapeutic relevance that may enable targeted molecular diagnostics. This review presents essentials facts of the new classification that will be part of the next WHO classification of lung tumors and its follow-up publications.

[Preneoplastic lesions of pulmonary carcinoma]. / Vorläuferläsionen des Lungenkarzinoms.

The World Health Organization (WHO) 2004 classification includes 3 categories of pulmonary preneoplastic lesions, including squamous dysplasia and carcinoma in situ (CIS) for squamous cell carcinoma, atypical adenomatous hyperplasia (AAH) for the majority of adenocarcinomas and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) for carcinoids. The distinction of the 3 grades of squamous dysplasia and CIS is mainly based on the degree by which the basal cell zone is expanded, the degree of cellular atypia and the level of mitoses. The category AAH consists of a proliferation of atypical epithelial cells with Clara cells or type 2 pneumocyte features. They grow along the alveolar septae in a lepidic fashion, sometimes reaching into the terminal bronchioles. In contrast to the newly described adenocarcinoma in situ (AIS), AAH is smaller (≤ 5 mm), has a lower cell density and a lower degree of cellular atypia. The putative cancer stem cells of peripheral adenocarcinomas reside in the bronchioloalveolar duct junction, while those of central squamous cell carcinomas are located in the basal cell compartment of the bronchi. This review provides an overview of the current knowledge on preneoplastic lesions of the lungs and their clinical impact.

Localization of the invadopodia-related proteins actinin-1 and cortactin to matrix-contact-side cytoplasm of cancer cells in surgically resected lung adenocarcinomas.

OBJECTIVES: Actin-associated proteins at cell-matrix-contact sites form invadopodia in cancer cells and participate in migration, matrix degradation and invasion. We investigated an alteration of subcellular localization of invadopodia-related actin-associated proteins, actinin-1 and cortactin, in lung adenocarcinomas, its clinical significance, and its possible regulatory factors. METHODS: Invadopodia-related proteins, actinin-1 and cortactin, were immunohistochemically examined in 90 cases of lung adenocarcinomas. Expression of invadopodia-associated proteins and their possible regulators in lung adenocarcinomas were examined by real-time RT-PCR, database search, and immunohistochemistry. RESULTS: Actinin-1 and cortactin showed matrix-contact-side localization in adenocarcinoma cells, but rarely in normal bronchiolar epithelial cells, alveolar cells, or precursor lesion atypical adenomatous hyperplasia cells. Immunoelectron-microscopic examination of adenocarcinoma cells revealed actinin-1 localization to matrix-contact-side cytoplasm with cytoplasmic protrusions. Matrix-contact-side localization of actinin-1 and cortactin was correlated with tumor stages, lymph node metastasis, vascular permeation, and loss of basement membrane. The tumor-specific survival rate was worse for the group in which matrix-contact-side localization of cortactin was high than for the low group. mRNA of the Rho guanine exchange factor epithelial cell transforming sequence-2 (Ect2) tended to be overexpressed in lung adenocarcinomas and cytoplasmic expression of Ect2 tended to be correlated with matrix-contact-side localization of actinin-1. CONCLUSION: Matrix-contact-side localization of invadopodia-related proteins in the lung adenocarcinoma cells were correlated with invasion, metastasis, and poor prognosis. Ect2 was a possible regulator of matrix-contact-side localization of invadopodia-related proteins.

Epidermal growth factor receptor mutation and p53 overexpression during the multistage progression of small adenocarcinoma of the lung.

INTRODUCTION: A progression model of atypical adenomatous hyperplasia (AAH) to bronchioloalveolar carcinoma (BAC) to invasive adenocarcinoma (ADC) has been proposed. However, the genetic alterations of the AAH-BAC-ADC sequence are not clearly established. We examined the mutation of the epidermal growth factor receptor (EGFR) gene and p53 protein overexpression in the AAH, BAC, and small ADC to understand their role in the pulmonary ADC pathogenesis. METHODS: Twenty AAH, 43 BAC (21 Noguchi type A and 22 type B), and 47 small ADC (Noguchi type C) were enrolled in this study. EGFR mutations at exons 18-21 and p53 protein overexpression were examined by polymerase chain reaction-direct sequencing and immunohistochemistry, respectively. RESULTS: Mutations of the EGFR gene were noted in 45 (40.9%) lesions, which included 7 (35.0%) of AAH, 15 (34.9%) of BAC, and 23 (48.9%) of ADC. Twenty-six (23.6%) of the mutations were detected as exon 19 deletion, 18 (16.4%) as exon 21 point mutation, and 1 (0.9%) as exon 18 point mutation. Overexpression of p53 protein was found in 19 (17.2%) lesions, none of AAH, 4 (9.8%) of BAC, and 15 (31.9%) of ADC. Multivariate analysis showed that p53 overexpression was associated with invasive ADC (P = 0.003). CONCLUSIONS: High frequency and similar incidence of EGFR mutation in AAH, BAC, and ADC support that EGFR gene mutation occurs in the early stage of pulmonary ADC development and tumor initiation from the preneoplastic lung parenchyma to neoplastic conditions. On the contrary, p53 overexpression is a late event during tumor development and plays a role in the progression of the peripheral pulmonary ADC.

[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.

Epidermal growth factor receptor gene mutations in atypical adenomatous hyperplasias of the lung.

Activating epidermal growth factor receptor (EGFR) gene mutations are frequently detected in lung adenocarcinomas, especially adenocarcinomas with a nonmucinous bronchioloalveolar carcinoma component. EGFR-mutated lung adenocarcinomas respond well to EGFR tyrosine kinase inhibitors. We previously found that most (88%) pure nonmucinous bronchioloalveolar carcinomas (adenocarcinoma in situ) already harbor EGFR mutations, indicating that the mutations are an early genetic event in the pathogenesis. We examined 54 atypical adenomatous hyperplasias, precursor lesions of lung adenocarcinomas, obtained from 28 Japanese patients for the hotspot mutations of EGFR exons 19 and 21 and K-ras codon 12. EGFR mutations were observed in 17 of the 54 (32%) atypical adenomatous hyperplasias examined: Ten and seven atypical adenomatous hyperplasias had deletion mutations at exon 19 or point mutations (L858R) at exon 21, respectively. We did not observe apparent histological differences between atypical adenomatous hyperplasias with and without EGFR mutations. K-ras mutation (G12S) was detected in only one atypical adenomatous hyperplasia. As EGFR mutational frequency of atypical adenomatous hyperplasias was much lower than that of nonmucinous bronchioloalveolar carcinomas, we surmise that EGFR-mutated atypical adenomatous hyperplasias, but not atypical adenomatous hyperplasias with wild-type EGFR, are likely to progress to nonmucinous bronchioloalveolar carcinomas.

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.

Genetic relationship among atypical adenomatous hyperplasia, bronchioloalveolar carcinoma and adenocarcinoma of the lung.

Atypical adenomatous hyperplasia (AAH) has been recently defined by WHO as a small lesion, not exceeding 5mm in major axis, composed of slightly enlarged alveolar septa lined by pneumocytes with plump, atypical nuclei. AAH is frequently found in tissue surrounding lung adenocarcinoma and is considered a precursor of this subtype of lung cancer by many Authors. However, the genetic relationship between adenocarcinoma and the associated foci of AAH is not well defined. In particular, it is not clear whether multiple foci of AAH and of adenocarcinoma in the same patients are clonally related to each other or represent independent neoplastic foci. To clarify if AAH and the associated cancer are clonally related, we evaluated the genetic distance between these two lesions in 16 patients, using direct sequencing of mitochondrial DNA (D-loop region). Furthermore, LOH analysis for 7 microsatellites (D3S1478 at 3p21, D3S1300 at 3p14.2, D9S942 at 9p21, D5S346 at 5q21, D17S261 at 17p13.1, D18S46 at 18q21, D19S246 at 19q13.2) was also performed. Our results indicate that, in at least 9 out of 13 informative cases (69.2%), AAH and the associated cancer were not clonally related as they showed a different mutation pattern in the mitochondrial D-loop region. These findings were also in agreement with the LOH data which showed losses in different loci in at least three cases. On the contrary an identical LOH pattern between BAC and AAH was found in one case. Similar but not identical LOH pattern between AAH and related tumors was found in other three cases. Therefore, our results suggest that AAH and the associated cancer are genetically independent in agreement with the concept of cancerization field. Less frequently AAH foci could represent an early spread of cells from the main tumor, rather than a precursor lesion.

Multiple bronchioloalveolar carcinomas in acromegaly: a potential role of insulin-like growth factor I in carcinogenesis.

The molecular pathogenesis of lung cancer, especially multiple and synchronous bronchioloalveolar carcinomas (BACs), is still unknown. Here, we report two cases of multiple BACs associated with acromegaly, and discuss about the possible relationship between these two pathological condition. The first patient was a 52-year-old female with a history of Hardy's surgery for pituitary growth hormone cell adenoma 2 years earlier. The second patient was a 57-year-old female with acromegaly and obstructive sleep apnea syndrome. Both patients were non-smokers and showed a high serum level of insulin-like growth factor I (IGF-I) at the time of admission, even though the level of growth hormone had decreased. High-resolution computed tomography (HRCT) revealed multiple small nodules with pure ground-glass opacity (GGO) in both lungs of the first patient and a small nodule with pure GGO in the right lung of the second one. Partial resection for these tumors were performed under video-assisted thoracoscopic surgery. Resected lung specimens of the first case revealed one papillary adenocarcinoma, seven BACs, and 11 atypical adenomatous hyperplasias (AAHs). The second case showed two foci of BACs. Immunohistochemically, all BACs were strongly positive for IGF-IR which is a specific receptor for IGF-I, and all AAHs were also weakly positive for IGF-IR. Since IGF-I is known as a potent growth factor for normal as well as cancerous cells, it might play an important role for tumorigenesis and/or tumor progression of BACs through its interaction with and/or upregulation of IGF-IR. In addition, much attention should be paid to detect lung lesions in acromegaly with high serum level of IGF-I.

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.

LAT1 expression in normal lung and in atypical adenomatous hyperplasia and adenocarcinoma of the lung.

No previous study has investigated neutral large amino acid transporter type 1 (LAT1) in normal lung cells, or in atypical adenomatous hyperplasia(s) (AAH) and nonmucinous bronchioloalveolar carcinoma(s) (NMBAC) of the lung. The authors examined: (1) the levels of LAT1 mRNA/glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA in 41 normal lung tissues and 34 NMBAC using semiquantitative reverse transcription-polymerase chain reaction; (2) LAT1 mRNA and protein expressions in 35 normal lung tissues, 34 AAH (11 lesions were interpreted as low-grade AAH and 23 as high-grade AAH), and 43 NMBAC using in situ hybridization and immunohistochemistry; and (2) the association of the incidences of LAT1 mRNA and protein expressions with cell proliferation in these lesions. The level of LAT1 mRNA/GAPDH mRNA (1) tended to be higher in NMBAC (12.0+/-8.1) than in normal lung tissues (1.0+/-0.2), and (2) covered a much wider range (from 0 to 276) in NMBAC than in normal lung tissues (from 0 to 5.8), with six NMBAC having values higher than 7.0, while 5.8 was the highest value detected in normal lung tissues. In peripheral normal lung tissues, LAT1 mRNA and protein were detected in bronchial surface epithelial cells and alveolar macrophages (but not in nonciliated bronchiolar epithelial cells, or in alveolar type I or type II cells). In bronchial surface epithelial cells, LAT1 protein appeared to be of a nodular type, which was considered to be a nonfunctional protein pattern. The incidences of positive expressions for LAT1 mRNA and protein were 54.5 and 27.3% in low-grade AAH, 65.2 and 52.2% in high-grade AAH, and 65.1 and 79.1% in NMBAC, respectively. In the case of LAT1 protein expression, significant differences could be shown between total (low-grade plus high-grade) AAH and NMBAC, and between low-grade AAH and NMBAC. Thus, in terms of the incidence of LAT1 protein expression, high-grade AAH appeared intermediate between low-grade AAH and NMBAC. The Ki-67 labeling index (a cell proliferation score) was significantly higher in those AAH and NMBAC that were LTA1-protein-positive than in their LAT1-protein-negative counterparts. In conclusion, LAT1 expression may increase with the upregulation of metabolic activity and cell proliferation in high-grade AAH and NMBAC.

Ultrasmall pulmonary opacities on multidetector-row high-resolution computed tomography: a prospective radiologic-pathologic examination.

OBJECTIVE: To clarify the pathologic findings of ultrasmall pulmonary opacities (5 mm or smaller in diameter) found on multidetector-row high-resolution computed tomography (MD-HRCT). METHODS: Ten lobes in 10 patients were included in this study. Each lobe had a primary lung tumor and was removed surgically. Two thoracic radiologists noted any tiny nonlinear opacity on preoperative MD-HRCT films (1.25-mm thickness) covering the whole lobe. Pathologic findings of detected opacities were evaluated macroscopically and microscopically. RESULTS: Among 139 ultrasmall opacities 5 mm or smaller in diameter, 94 corresponded to normal anatomic structures (partial volume averaging or motion artifact), 36 corresponded to pathologic abnormalities, and 9 were unidentified. Histologic diagnoses of 36 pathologic abnormalities were inflammatory lesions (n = 16), intrapulmonary lymph nodes (IPLN; n = 7), atypical adenomatous hyperplasia (AAH; n = 7), bronchioloalveolar carcinoma (BAC; n = 5), and another neoplastic lesion (n = 1). CONCLUSION: Tiny pulmonary lesions, such as AAHs, BACs, and IPLNs, were identified among ultrasmall opacities found on MD-HRCT.

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.

[Atypical adenomatous hyperplasia and dysplasia in squamous epithelium of the honeycomb lung in outcome of idiopathic fibrosing alveolitis]. / Atipicheskaia adenomatoznaia giperplaziia i displaziia v ploskom épitelii v sotovom legkom v iskhode idiopaticheskogo fibroziruiushchego al'veolita.

Relationships between sclerosis and carcinogenesis in the honeycomb lung were studied in the outcome of two variants of idiopathic fibrosing alveolitis (IFA)-common interstitial pneumonia (CIP) and desquamative interstitial pneumonia (DIP) which may be a background for lung carcinoma development. The material was obtained from 43 patients with the diagnosis of IFA. Immunohistochemically were studied: TNF-alpha (DAKO, Denmark, 1:100), pancytokeratines (Immunotech, Germany, concentration 1:100), Ki67 (DAKO, Denmark, 1:40), TGF-beta (Biosource international, USA, 1:100), CD34 (Novocastra, Great Britain, 1:100), EMA (DAKO, Denmark, 1:100). Differences in morphogenesis of CIP and DIP were found. CIP is characterised by primary pronounced lung interstitium damage with stroma vascularisation already at early stages with secondary involvement of the epithelium with development of adenomatous hyperplasia with or without atypia which is usually observed at the stage of lung honeycomb. Pronounced primary damage of alveolar epithelium as a result of action of activated alveolar macrophages with subsequent proliferation, desquamation and squamous epithelium metaplasia were more typical for DIP. The presence of squamous meta- and dysplasia of the epithelium is characteristic for DIP outcome in the honeycomb lung.

Lung adenocarcinoma associated with atypical adenomatous hyperplasia. A clinicopathological study with special reference to smoking and cancer multiplicity.

Atypical adenomatous hyperplasia (AAH) of the lung has been proposed as a possible precursor lesion of adenocarcinoma of the lung. In the present study, we sought to clarify the clinicopathological characteristics of lung adenocarcinoma cases associated with AAH, with special reference to tobacco smoking and the presence of multiple primary carcinomas of pulmonary and extrapulmonary organs. We examined 123 surgically resected lung adenocarcinomas and conducted histopathological diagnoses for AAH and multiple primary pulmonary carcinomas. Clinicopathological characteristics such as age, sex, smoking index, survival, and the presence of extrapulmonary primary carcinomas were obtained from clinical records, and the associations among these factors were examined statistically. Sixteen lung adenocarcinoma patients had accompanying AAH (the AAH group) and 107 cases did not (the NAAH group). The incidence of primary carcinomas in extrapulmonary organs was higher in the AAH group (37.5%; 6/16) than in the NAAH group (12.5%; 13/107) (P = 0.01). Multiple primary lung cancers tended to be more frequent in the AAH group, but the difference was not statistically significant (P = 0.07). Although there was no difference in tobacco smoking between the two groups, all eight cases with multiple primary lung carcinomas were smokers. Furthermore, multiple primary lung carcinomas were found more frequently in smokers of the AAH group (37.5%; 3/8) than in the smokers of the NAAH group (7.2%; 5/69) (P = 0.04). The results suggested that constitutional or genetic factors might predispose patients to the development of AAH together with extrapulmonary primary carcinomas, and that smoking might contribute to the development of multiple primary lung adenocarcinomas, especially in patients with pre-existing AAH.

[High-resolution CT findings of pulmonary atypical adenomatous hyperplasia of 5 mm or less in diameter].

OBJECTIVE: To clarify the high-resolution CT(HRCT) findings of pulmonary atypical adenomatous hyperplasia (AAH) of 5 mm or less in diameter. MATERIALS AND METHODS: We evaluated the HRCT findings of 43 histopathologically confirmed AAH of 5 mm or less in diameter in 7 patients who underwent lobectomy for pulmonary adenocarcinoma. For comparison, we also examined the HRCT findings of 13 bronchioloalveolar carcinomas (BAC) of the same size from these patients. RESULTS: We identified 36 of 43 AAH and all 13 BAC on HRCT performed with multidetector-row CT. Thirty-five AAH and 11 BAC showed ground-glass opacity without any high-attenuation component. Margins of 20 AAH were well defined, and 16 were ill defined. In BAC, 11 lesions demonstrated well-defined margins, with only 2 showing ill-defined margins. CONCLUSION: Most AAH lesions of 5 mm or less in diameter are identified as ground-glass opacity on HRCT. Detection of minute ground-glass opacity is important in locating AAH on HRCT.

Multiple atypical adenomatous hyperplasia with synchronous multiple primary bronchioloalveolar carcinomas.

We report a case of multiple atypical adenomatous hyperplasia (AAH) associated with synchronous multiple primary bronchioloalveolar carcinomas (BACs). A 58-year-old man was visited for bronchial asthma. A chest computed tomography (CT) scan revealed small, multiple nodules with ground glass attenuation (GGA) throughout both lungs, predominantly in the upper lobes. A high resolution CT (HRCT) scan disclosed well-defined nodules with uniform GGA. Thoracoscopic wedge lung biopsy confirmed the diagnosis. The patient was treated with chemotherapy and had stable disease for two years. It is important to recognize that multiple AAH associated with multiple BACs can present as diffuse, well-defined nodules with uniform GGA on HRCT.

Focal ground-glass opacity detected by low-dose helical CT.

OBJECTIVE: Focal ground-glass opacity (GGO) has been detected increasingly by low-dose helical CT. Although focal GGO suggests in situ neoplastic lesion in the peripheral lung, it remains controversial how to manage these lesions. The purpose of this study was to evaluate the pathologic and radiologic characteristics of focal GGO in order to develop a standard of treatment for these lesions. PATIENTS: Forty-three patients with persistent focal GGO < or = 2 cm in size from January 1998 to September 2000 were studied. Thoracoscopic lung biopsy was performed consecutively for persistent focal GGO following a several-month observation period (mean, 3.7 months). RESULTS: The histologic diagnoses were bronchioloalveolar carcinoma (BAC) in 23 patients, adenocarcinoma with mixed subtypes in 11 patients, and atypical adenomatous hyperplasia (AAH) in 9 patients. None of 34 carcinoma patients had lymph node involvement. All of 17 lesions > or = 1 cm in size were malignant. GGO with solid components on high-resolution CT were highly associated with adenocarcinoma (malignant rate, 93.3%). CONCLUSIONS: Persistent focal GGO after observation for several months was a finding of early adenocarcinoma or its precursor. Especially, lesions > or = 1 cm in size or GGO with solid component were significant signs of malignancy. We concluded lung biopsy should be attempted for persistent focal GGO.