Background Tuberculosis (TB) is a great mimicker and diagnostic chameleon, and prone to be diagnosed as malignancy. Even though many reports have described the differences between pulmonary TB and lung cancer, the atypical systemic hematogenous disseminated TB (HDTB) is very rare and more confusing in clinical practice. Case presentation A 73-year-old man, HIV-negative, was hospitalized to the local county hospital because of chest pain, low-grade fever, asthenia, anorexia and weight loss for the pasting two months. The CT findings of the two lungs showed multiple round or round-like nodules of different sizes, with clear boundaries and partial fusion. The level of serum CA19–9 was significantly higher than normal, and progressively increased. There were multiple enlarged lymph nodes in the neck, mediastinum, abdominal cavity and pelvic cavity. The symptoms were diagnosed as hematogenous spread of gastrointestinal tumor in the local county hospital. However, when transferred to our provincial hospital, through comprehensive dynamic analysis, this patient was diagnosed as atypical systemic HDTB, no cancer at all. Through routine anti-TB therapy for one year, the patient was recovered very well at the follow-up of half year after withdrawal. Conclusions In the past, most TB misdiagnosis cases involved in single organ and were finally confirmed through invasive examination. This case enriched clinical experiences in the diagnosis of atypical HDTB. We encouraged clinicians to establish a dynamic thinking for diagnosis and treatment and emphasized the value of biopsy and 18F-FDG-PET in distinguishing TB and cancer.

First-generation epithelial growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have markedly improved the treatment of non-small cell lung cancer (non-SCLC) with EGFR-sensitive mutations. However, acquired resistance to these drugs was inevitable. The transformation of lung adenocarcinoma to SCLC following treatment with EGFR-TKIs is a rare phenomenon that contributes to resistance to EGFR-TKIs. The present case concerns a 74-year-old man previously diagnosed with and treated for pneumonia; however, this was later pathologically confirmed as lung adenocarcinoma by transbronchial lung biopsy. Deletion of exon 19 of EGFR was identified by next-generation sequencing technology. The patient improved markedly when treated with gefitinib, but relapsed after 1 year, with markedly increased serum levels of neuron-specific enolase (NSE). Transformation to SCLC was detected by endobronchial ultrasound transbronchial needle aspiration (EBUS-TBNA) re-biopsy, which was negative for the deletion of exon 19 of EGFR. The patient was positive for vimentin expression and refractory to etoposide and cisplatin chemotherapy, and succumbed to the disease 18 months after diagnosis. Transformation of the disease from adenocarcinoma to SCLC may have been due to cancer heterogeneity. Re-biopsy is therefore important in EGFR-TKI-resistant patients for genetic and histological re-evaluation. NSE serum levels may also be useful for detecting early SCLC transformation.

Tuberculosis (TB), is an infectious disease caused by Mycobacterium tuberculosis ( M. tuberculosis ), and presents with high morbidity and mortality. Alveolar macrophages play an important role in TB pathogenesis although there is heterogeneity and functional plasticity. This study aimed to show the characteristics of alveolar macrophages from bronchioalveolar lavage fluid (BALF) in active TB patients. Single-cell RNA sequencing (scRNA-seq) was performed on BALF cells from three patients with active TB and additional scRNA-seq data from three healthy adults were established as controls. Transcriptional profiles were analyzed and compared by differential geneexpression and functional enrichment analysis. We applied pseudo-temporal trajectory analysis to investigate correlations and heterogeneity within alveolar macrophage subclusters. Alveolar macrophages from active TB patients at the single-cell resolution are described. We found that TB patients have higher cellular percentages in five macrophage subclusters. Alveolar macrophage subclusters with increased percentages were involved in inflammatory signaling pathways as well as the basic macrophage functions. The TB-increased alveolar macrophage subclusters might be derived from M1-like polarization state, before switching to an M2-like polarization state with the development of M. tuberculosis infection. Cell-cell communications of alveolar macrophages also increased and enhanced in active TB patients. Overall, our study demonstrated the characteristics of alveolar macrophages from BALF in active TB patients by using scRNA-seq.