Stage 4 lung cancer: persistent cough led to diagnosis

This lung cancer diagnosis at a glance

Stage at diagnosis
Stage IV
Subtype
Non-Small Cell Lung Cancer
Biomarkers
KRAS G12C and TP53 R273C; PD-L1 TPS 95%. Other common lung drivers were not detected.
Sex
Male
Spread to
liver, left adrenal gland, lymph nodes, pleural effusion, bones (ribs, vertebrae, iliac bones), left shoulder soft tissue mass
Treatment
immunotherapy, targeted therapy and chemotherapy
Outcome
In Memory

Treatment course, step by step

  1. First-line pemetrexed + cisplatin + recombinant human endostatin was stopped after rash/itching reaction
  2. Second-line liposomal paclitaxel + cisplatin led to stable disease after 3 cycles
  3. Third-line apatinib + sintilimab started July 2021 and improved symptoms, lowered tumor burden, and later produced partial response
  4. Apatinib was interrupted/rechallenged, then changed to anlotinib because of intolerance
  5. ICU supportive care treated immunotherapy-related diabetes/DKA, sepsis, and inflammatory crisis.

What happened, in summary

This 69-year-old man, a former heavy smoker with no prior diabetes, came to care in February 2021 with cough and was diagnosed with Stage IV lung adenocarcinoma. Imaging showed a left lung primary tumor with metastatic disease in the liver, left adrenal gland, lymph nodes, bones, and pleural space. Lung biopsy supported adenocarcinoma, with TTF-1 and pan-CK positivity. Molecular testing found KRAS p.G12C and TP53 p.R273C mutations, while common targetable alterations including EGFR, ALK, ROS1, and MET were not detected. Initial treatment used pemetrexed, cisplatin, and recombinant human endostatin, but a generalized rash and itching led to a switch to liposomal paclitaxel plus cisplatin. After 3 cycles, scans showed stable disease, though fatigue, appetite loss, and shoulder and back pain worsened. A new left shoulder mass was confirmed as metastatic poorly differentiated adenocarcinoma, and PD-L1 testing was strongly positive, with TPS 95%. In July 2021, he began apatinib with sintilimab. This brought symptom relief, tumor-burden reduction, and later a partial response, although apatinib required interruption and later substitution with anlotinib because of intolerance. About 29 months into immunotherapy, he suddenly developed vomiting, diarrhea, loss of consciousness, severe hyperglycemia, profound acidosis, and ketosis consistent with fulminant immune-checkpoint-inhibitor-induced type 1 diabetes and severe diabetic ketoacidosis. Despite ICU-level insulin, fluid, bicarbonate, and anti-infective support, his course was complicated by inflammatory crisis and sepsis. During the crisis, pancreatic autoantibodies were negative, and steroid pulse therapy was avoided because severe ketoacidosis made it unsafe. He died at home shortly after discharge against medical advice.

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This is a lay summary of an account first published by PMC / PubMed Central. Read the original in full

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