Primary colloid adenocarcinoma of lung: A case report and review of literature

INTRODUCTION

Colloid adenocarcinoma is a rare form of invasive lung cancer distinguished by the accumulation of extracellular mucin, which expands the alveolar spaces and damages the surrounding lung tissue. This uncommon variant accounts for approximately 0.24 percent of all lung cancer cases.^[1] The most frequently reported symptoms include cough, hemoptysis, and chest pain. However, some patients remain asymptomatic, with the condition often discovered during routine health examinations.

On computed tomography (CT) imaging, pulmonary colloid adenocarcinomas typically appear as lobulated tumors with homogeneous low attenuation. Histopathological analysis reveals abundant mucin distending the alveolar spaces, accompanied by the destruction of alveolar walls and lung parenchyma. Neoplastic mucinous columnar epithelial cells partially line the alveolar walls and are seen floating within mucin-filled spaces. These pathological characteristics closely resemble those of cystadenocarcinomas observed in the ovary, breast, and pancreas.^[2-4] Patients with this tumor generally have a favorable prognosis, especially when complete surgical resection is achieved, and no metastasis is present.

Herein, we present a case of colloidal adenocarcinoma of the lung, which was picked up on bronchoscopic biopsy and fine needle aspiration cytology (FNAC) of the cervical lymph node.

CASE REPORT

In the first week of November 2024, a 54-year-old male, with no known comorbidities, presented to the Pulmonary Medicine outpatient department (OPD) of a tertiary care center in Central Kerala, with complaints of progressively worsening shortness of breath and a dry cough of two months' duration. He also reported left-sided dull aching chest pain of two weeks' duration and fever for two days. These symptoms were associated with a significant loss of appetite and a five kg weight loss over two months.

The patient had a history of chronic smoking, consuming approximately 20 bidis per day for 25 years. His occupational history revealed that he worked as a manual laborer in a stone quarry for 15 years, but stopped this work five years ago. There was no past history of pulmonary tuberculosis (PTB), pneumonia, or other significant respiratory illnesses.

On clinical evaluation, the patient’s vital signs were stable, with a SpO₂ of 97 percent on room air. Physical examination revealed palpable, hard lymph nodes in the bilateral supraclavicular regions. Chest auscultation demonstrated decreased breath sounds on the left side, crepitations on the left, and bilateral rhonchi.

Routine blood investigations were within normal limits. A chest X-ray revealed non-homogeneous opacity in the left hilar region [Figure 1].

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Figure 1:

Chest X-ray showing non-homogeneous opacity in the left hilar region The red arrow points towards the non-homogeneous opacity in the left hilar region.

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Subsequently, a contrast-enhanced computed tomography (CECT) of the chest was performed, which showed a minimally enhancing, lobulated, soft-tissue density mass lesion measuring 4.8 × 4.0 × 3.8 cm in the superior segment of the left lower lobe. The mass exhibited internal necrosis and caused an abrupt cut-off of sub-segmental bronchi. It extended to the left hilum, encasing the left interlobar pulmonary artery and its branches. Additionally, there were enlarged mediastinal lymph nodes with bilateral supraclavicular lymph nodes. Imaging identified focal sclerotic areas in the D1 and L1 vertebral bodies and an ill-defined enhancing lesion measuring 10 × 9 mm in the right lobe of the liver, suggestive of metastatic deposits [Figure 2].

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Figure 2:

contrast-enhanced computed tomography (CECT) chest images showing lobulated, minimally enhancing, soft-tissue density mass lesions a) Lung window b) Mediastinal window.

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To further evaluate the left hilar mass, a flexible bronchoscopy (FOB) was performed, revealing mucosal irregularity and narrowing of the airway in the left lower lobe bronchus [Figure 3].

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Figure 3:

Flexible bronchoscopy image showing mucosal irregularity and narrowing of the airway in the left lower lobe bronchus.

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A transbronchial lung biopsy (TBLB) was taken from the abnormal focus and sent for histopathological examination (HPE). HPE revealed a respiratory epithelium lined with infiltrating neoplastic cells arranged in a glandular pattern with abundant signet ring cells. The glands were lined with mucin-laden cuboidal cells showing mild to moderate nuclear pleomorphism, hyperchromatic indented nuclei, and abundant mucinous cytoplasm. Occasional mitotic figures were observed. The stroma showed extracellular mucin deposition and desmoplasia [Figure 4]. These findings were consistent with colloid adenocarcinoma of the lung, a rare morphological variant of lung adenocarcinoma characterized by mucin pools containing well-differentiated adenocarcinoma cells. Further analysis using immunohistochemistry (IHC) marker study demonstrated CK7 diffuse strong positivity, CK20 focal positivity, and tTTF-1 negativity. FNAC of the cervical lymph node was also consistent with metastatic colloid adenocarcinoma.

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Figure 4:

Hematoxylin and eosin staining sections of lung biopsy specimen showing: a) Respiratory epithelium lined with infiltrating neoplastic cells arranged in a glandular pattern [magnification 10x], the red arrow points towards abundant signet ring cell containing mucinous cytoplasm. b) Abundant signet ring cell containing mucinous cytoplasm and stroma with mucin deposition [magnification 40x], the red arrows points towards respiratory epithelium lined with infiltrating neoplastic cells arranged in a glandular pattern.

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Based on the clinical, radiological, and histopathological findings, a diagnosis of primary colloid adenocarcinoma of the lung was established. The patient was subsequently referred to the oncology department for further management, including staging workup and treatment planning.

DISCUSSION

Colloid adenocarcinoma is a rare form of invasive lung cancer distinguished by the accumulation of extracellular mucin, which expands the alveolar spaces and damages the surrounding lung tissue. This uncommon variant accounts for approximately 0.24 percent of all lung cancer cases.^[1] The most frequently reported symptoms include cough, hemoptysis, and chest pain. However, some patients remain asymptomatic, with the condition often discovered during routine health examinations.

On CT imaging, pulmonary colloid adenocarcinomas typically appear as lobulated tumors with homogeneous low attenuation. Histopathological analysis reveals abundant mucin distending the alveolar spaces, accompanied by the destruction of alveolar walls and lung parenchyma. Neoplastic mucinous columnar epithelial cells partially line the alveolar walls and are seen floating within mucin-filled spaces. These pathological characteristics closely resemble those of cystadenocarcinomas observed in the ovary, breast, and pancreas.^[2,3]

According to the World Health Organization (WHO) classification of tumors, colloid adenocarcinoma of the lung is a subtype of adenocarcinoma characterized by abundant mucin pools replacing the air spaces. The tumor cells generally exhibit minimal mitotic activity and lack necrosis. Immunohistochemical staining typically shows strong positivity for CK7. The diagnosis is established through tissue biopsy, which may be obtained via TBLB, video-assisted thoracoscopic surgery (VATS)-guided biopsy, or from resected specimens. In our case, FNAC of the supraclavicular lymph node and TBLB confirmed the diagnosis, and an IHC marker study showed strong positivity for CK7.

The immunoprofile of colloid adenocarcinoma is known to overlap with that of enteric adenocarcinoma or metastatic mucinous adenocarcinoma originating from the gastrointestinal tract.^[4] However, our patient showed no abdominal symptoms, and a CT scan of the abdomen was normal, effectively ruling out metastatic mucinous adenocarcinoma from the gastrointestinal tract. Based on the presence of abundant extracellular mucin pools and sparse tumor cells, we propose that these are characteristic histological features of colloid adenocarcinoma.

If the tumor is localized, recurrence rates may be relatively low, even in cases where the tumor is large. Patients with this tumor generally have a favorable prognosis, especially when complete surgical resection is achieved, and no metastasis is present. According to Russell et al., the estimated five-year survival rate for nine patients with colloid adenocarcinoma of the lung who underwent surgical resection was 51 percent, which is higher compared to other subtypes.^[5]

Due to the rarity of the tumor, long-term prognostic data are limited. The treatment approach for colloid adenocarcinoma should follow the established guidelines for primary lung cancer. Lobectomy or segmentectomy with lymph node dissection is regarded as the preferred treatment option for colloid adenocarcinoma.

CONCLUSION

Colloid adenocarcinoma of the lung is a rare mucin-rich tumor that can resemble other mucinous malignancies, making careful histopathological evaluation essential. This case emphasizes the value of integrating clinical, radiologic, and bronchoscopic findings to achieve an accurate diagnosis. Early recognition of this uncommon entity supports timely treatment planning and may improve overall outcomes.