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Cell & Cellular Life Sciences Journal Research Article 6 min read

Heteroclite and Turgid-Atypical Adenomatous Hyperplasia Lung

Bajaj A*
* Corresponding author
ISSN: 2578-4811  10.23880/cclsj-16000187  Received: November 03, 2023  Published: November 15, 2023
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Keywords
Neoplastic Cells Pulmonary Adenocarcinoma Type II Pneumocytes Stromal Fibrosis
Abstract

Atypical adenomatous hyperplasia emerges as a miniature, localized proliferation of atypical pneumocytes which layer intact alveolar spaces. Atypical adenomatous hyperplasia is contemplated as a precursor lesion to invasive pulmonary adenocarcinoma.

Editorial

Atypical adenomatous hyperplasia emerges as a miniature, localized proliferation of atypical pneumocytes which layer intact alveolar spaces. Atypical adenomatous hyperplasia is contemplated as a precursor lesion to invasive pulmonary adenocarcinoma.

Atypical adenomatous hyperplasia appears as a miniature, localized lesion ≤ 5 millimetre magnitude. Tumefaction appears disparate from alveolar parenchyma and is comprised of proliferation of atypical pneumocytes. Lesion is coated with non-contiguous monolayer of cells whereas circumscribing pulmonary parenchyma appears devoid of prominent inflammatory infiltrate or stromal fibrosis.

The terminology of atypical alveolar epithelial hyperplasia, atypical bronchoalveolar cell hyperplasia, atypical alveolar cell hyperplasia, bronchoalveolar cell adenoma or bronchial adenoma appears obsolete and is not recommended.

Atypical adenomatous hyperplasia lung is frequently discerned as an incidental finding within pulmonary resection specimens. Lesion may concur with female subjects selected for therapeutic surgical resection of pulmonary adenocarcinoma. Alternatively, tumour may be infrequently exemplified within autopsy specimens devoid of pulmonary adenocarcinoma. Atypical adenomatous hyperplasia is categorized as a condition amenable to antecedent morphological detection and a lesion which systematically progresses into pulmonary adenocarcinoma.

Atypical adenomatous hyperplasia may be associated with CYP19A1 genetic polymorphisms. A female predominance is observed. Atypical adenomatous hyperplasia lung is frequently confined to superior pulmonary lobes [1, 2]. Of obscure aetiology, atypical adenomatous hyperplasia lung appears non concurrent with cigarette smoking or tobacco consumption. Neoplastic cells appear clone-specific. Proportionate copy number modifications and genomic mutations appear minimal, in contrast to adenocarcinoma in situ [1, 2]. Atypical adenomatous hyperplasia lung is accompanied by driver mutations within KRAS, EGFR and BRAF genes. However, as lesions appear appropriately alleviated with surgical resection, molecular assessment appears superfluous [2, 3].

Characteristically, tumefaction is discovered incidentally upon evaluation of surgical pathology specimens. Generally, atypical adenomatous hyperplasia appears non detectable upon adoption of cogent imaging techniques. High resolution computerized tomography (CT) may optimally discern enlarged lesions [2, 3].

Upon frozen section, appropriate tumour discernment may be challenging as the lesion is composed of subtle morphological alterations. Besides, lesions demonstrating subtle atypia upon frozen section may be categorized as atypical adenomatous hyperplasia upon evaluation of formalin fixed paraffin embedded sections [2, 3].

Grossly, singular or multifocal, poorly defined, grey/ white, tan or yellow neoplastic zones are observed. Lesion magnitude is ≤5 millimetres and tumefaction is commonly confined to peripheral pulmonary parenchyma, abutting the pleura.

Upon microscopy, atypical adenomatous hyperplasia lung exhibits proliferation of atypical pneumocytes. Constituent cells delineate mild to moderate cellular and nuclear atypia, enhanced cellular magnitude and elevated nucleocytoplasmic ratio. Tumour cells are pervaded with hyperchromatic nuclei and intra-nuclear eosinophilic inclusions. Tumour cells layer intact alveolar spaces wherein atypical cells configure a non-contiguous cellular monolayer [4, 5].

Lesion is constituted of an admixture of club cells and type II pneumocytes. Club cells represent as columnar epithelial cells permeated with eosinophilic cytoplasmic snouts and outpouchings. Type II pneumocytes manifest as cuboidal cells impregnated with finely vacuolated or clear cytoplasm. Characteristically, mitotic figures are minimal (Table 1).

Surrounding pulmonary parenchyma is devoid of significant infiltrate of acute and chronic inflammatory cells or stromal fibrosis (Figures 1 & 2) [4, 5].

Figure 1: Atypical adenomatous hyperplasia demonstrating alveolar spaces lined by columnar epithelial cells incorporated with eosinophilic cytoplasm, enlarged, hyperchromatic nuclei with enhanced nucleocytoplasmic ratio and mild cellular and nuclear atypia. Surrounding pulmonary parenchyma appears unremarkable [6].
Click to enlarge
Figure 1: Atypical adenomatous hyperplasia demonstrating alveolar spaces lined by columnar epithelial cells incorporated with eosinophilic cytoplasm, enlarged, hyperchromatic nuclei with enhanced nucleocytoplasmic ratio and mild cellular and nuclear atypia. Surrounding pulmonary parenchyma appears unremarkable [6].
Figure 2: Atypical adenomatous hyperplasia delineating alveolar spaces lined by columnar epithelial cells permeated with eosinophilic cytoplasm, enlarged, hyperchromatic nuclei with enhanced nucleocytoplasmic ratio and mild cellular and nuclear atypia. Circumscribing pulmonary parenchyma appears mildly inflamed and fibrotic [7].
Click to enlarge
Figure 2: Atypical adenomatous hyperplasia delineating alveolar spaces lined by columnar epithelial cells permeated with eosinophilic cytoplasm, enlarged, hyperchromatic nuclei with enhanced nucleocytoplasmic ratio and mild cellular and nuclear atypia. Circumscribing pulmonary parenchyma appears mildly inflamed and fibrotic [7].

Epithelial Tumours

Papilloma

Squamous cell papilloma NOS

Squamous cell papilloma, inverted

Glandular papilloma

Mixed squamous cell and glandular papilloma Adenoma

Sclerosing pneumocytoma

Alveolar adenoma

Papillary adenoma

Bronchiolar adenoma/ciliated muconodular papillary tumour

Mucinous cystadenoma

Mucous gland adenoma

Precursor glandular lesions

Atypical adenomatous hyperplasia

Adenocarcinoma in situ

Adenocarcinoma in situ, non-mucinous

Adenocarcinoma in situ, mucinous

Adenocarcinoma

Minimally invasive adenocarcinoma

Minimally invasive adenocarcinoma, non-mucinous

Minimally invasive adenocarcinoma, mucinous

Invasive non-mucinous adenocarcinoma

Lepidic adenocarcinoma

Acinar adenocarcinoma

Papillary adenocarcinoma

Micro-papillary adenocarcinoma

Solid adenocarcinoma

Invasive mucinous adenocarcinoma

Mixed invasive mucinous and non-mucinous adenocarcinoma Colloid adenocarcinoma Foetal adenocarcinoma Adenocarcinoma, enteric type Adenocarcinoma NOS Squamous precursor lesions Squamous cell carcinoma in situ Mild squamous dysplasia Moderate squamous dysplasia Severe squamous dysplasia Squamous cell carcinoma Squamous cell carcinoma NOS Squamous cell carcinoma, keratinizing Squamous cell carcinoma, non-keratinizing Basaloid squamous cell carcinoma Lympho-epithelial carcinoma Large cell carcinoma Adenosquamous carcinoma Sarcomatoid carcinoma Pleomorphic carcinoma Giant cell carcinoma Spindle cell carcinoma Pulmonary blastoma Carcinosarcoma Other epithelial tumours NUT carcinoma Thoracic SMARCA4-deficient undifferentiated tumour Salivary gland-type tumours Pleomorphic adenoma Adenoid cystic carcinoma Epithelial-myoepithelial carcinoma Mucoepidermoid carcinoma Hyalinising clear cell carcinoma Myoepithelioma Myoepithelial carcinoma Neuroendocrine tumours of lung Precursor lesion Diffuse idiopathic neuroendocrine cell hyperplasia Neuroendocrine tumours Carcinoid tumour NOS/ neuroendocrine tumour NOS Typical carcinoid/neuroendocrine tumour grade I Atypical carcinoid/neuroendocrine tumour grade II Neuroendocrine carcinomas Small cell carcinoma Combined small cell carcinoma Large cell neuroendocrine carcinoma Combined large cell neuroendocrine carcinoma Tumours of ectopic tissue Melanoma Meningioma Mesenchymal tumours specific to the lung Pulmonary hamartoma Chondroma Diffuse lymphangiomatosis Pleuropulmonary blastoma Intimal sarcoma Congenital peribronchial myofibroblastic tumour Pulmonary myxoid sarcoma with EWSR1-CREB1 fusion PEComatous tumours Lymphangioleiomyomatosis PEComa benign PEComa malignant Haematolymphoid tumours MALT lymphoma Diffuse large B cell lymphoma NOS Lymphomatoid granulomatosis NOS Lymphomatoid granulomatosis, grade I Lymphomatoid granulomatosis, grade II Lymphomatoid granulomatosis, grade III Intravascular large B cell lymphoma Langerhans cell histiocytosis Erdheim-Chester disease NOS: Not otherwise specified Table1: Classification of Lung Tumours World Health Organization 2021 [4].

Atypical adenomatous hyperplasia lung appears immune reactive to thyroid transcription factor-1(TTF1).

Atypical adenomatous hyperplasia lung requires segregation from neoplasms such as non-mucinous adenocarcinoma in situ or reactive pneumocyte hyperplasia [8, 9].

Characteristically, atypical adenomatous hyperplasia is incidentally discovered upon histological examination of pulmonary resection specimens. Appropriate discernment upon miniature core needle biopsy samples or trans- bronchial tissue specimens appears challenging as the entire lesion necessitates precise assessment [8, 9].

Atypical adenomatous hyperplasia lung is devoid of pertinent biochemical and haematological parameters indicative of the lesion. Computerized tomography (CT) exhibits faint, fluid nodules which may assist lesion detection.

Atypical adenomatous hyperplasia can be appropriately managed by surveillance upon computerized tomography (CT). Frequency and duration of surveillance appears contingent to tumour magnitude [8, 9]. Optimally, tumefaction may be subjected by comprehensive surgical eradication.

Prognostic outcomes are superior and incriminated subjects appear alleviated upon adequate extermination of lesion [8, 9].

References

  1. Siddiqui F, Vaqar S, Siddiqui AH (2023) Lung Cancer. Stat Pearls International.
  2. Nguyen C, Larsen NK, Dietz N, Sirineni G, Balters M (2019) Pulmonary Atypical Adenomatous Hyperplasia: Diagnostic and Therapeutic Implications. Cureus 11(11): e6079.
  3. Santore LA, Novotny S, Tseng R, Patel M, Albano D, et al. (2023) Morphologic Severity of Atypia Is Predictive of Lung Cancer Diagnosis. Cancers (Basel) 15(2): 397.
  4. Nicholson AG, Tsao MS, Beasley MB, Borczuk AC, Brambilla E, et al. (2022) The 2021 WHO Classification of Lung Tumors: Impact of Advances Since 2015. Journal of Thoracic Oncology 17(3): 362-387.
  5. Chen J, You L, Dong J (2023) Multiple micromeningiomas coexist with primary lung adenocarcinoma: A case report. Thorac Cancer 14(15): 1398-1400.
  6. Image 1 Courtesy: Wikimedia commons.
  7. Image 2 Courtesy: Libre pathology.
  8. He W, Guo G, Du X, Guo S, Zhuang X (2023) CT imaging indications correlate with the degree of lung adenocarcinoma infiltration. Front Oncol 13: 1108758.
  9. Dai T, Adachi J, Dai Y, Nakano N, Yamato M, et al. (2023) In-depth proteomics reveals the characteristic developmental profiles of early lung adenocarcinoma with epidermal growth factor receptor mutation. Cancer Med 12(9): 10755-10767.
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@article{bajaj2023,
  title   = {Heteroclite and Turgid-Atypical Adenomatous Hyperplasia Lung},
  author  = {Bajaj A},
  journal = {Cell & Cellular Life Sciences Journal},
  year    = {2023},
  volume  = {8},
  number  = {2},
  doi     = {10.23880/cclsj-16000187}
}
Bajaj A (2023). Heteroclite and Turgid-Atypical Adenomatous Hyperplasia Lung. Cell & Cellular Life Sciences Journal, 8(2). https://doi.org/10.23880/cclsj-16000187
TY  - JOUR
TI  - Heteroclite and Turgid-Atypical Adenomatous Hyperplasia Lung
AU  - Bajaj A
JO  - Cell & Cellular Life Sciences Journal
PY  - 2023
VL  - 8
IS  - 2
DO  - 10.23880/cclsj-16000187
ER  -