Introduction: Hashimoto's thyroiditis is a common autoimmune thyroid disease; however, pulmonary involvement is a rare manifestation. Lymphocytic interstitial pneumonitis is commonly associated with autoimmune diseases, but its association with Hashimoto's thyroiditis remains poorly understood. Case: A 63-year-old male with prior diagnosis of Hashimoto's thyroiditis presented with recurrent massive pleural effusion and progressive dyspnea. He also experienced fatigue, cold intolerance, and constipation. Physical examination revealed facial puffiness, diffuse goiter, and dry skin. Thyroid function tests performed 6 months before admission confirmed overt hypothyroidism (thyroidstimulating hormone [TSH] 80.30 µIU/mL, free thyroxine 4 [FT4] 0.46 ng/dL). One month prior to admission, laboratory findings showed subclinical hypothyroidism (TSH 9.09 µIU/mL, FT4 1.42 ng/dL). Despite levothyroxine treatment TSH levels remained elevated at 21.8 µIU/mL during admission. Anti-thyroid peroxidase antibodies were positive (13.95 IU/mL). Repeated thoracentesis revealed exudative pleural effusion with lymphocytic predominance and no evidence of malignancy in cytological examination. Infectious etiologies and malignancy were ruled out. Thyroid ultrasonography demonstrated diffuse hypoechoic enlargement of the thyroid gland. Chest radiography showed massive unilateral pleural effusion, while thoracic computed tomography revealed ground-glass opacities with a reticulogranular pattern and interlobular septal thickening, accompanied by multiple thin-walled cysts, highly suggestive of lymphocytic interstitial pneumonitis. Thyroid immunohistochemical analysis was performed (CD 20, CD 3, CD 10, CD 138, Ki 67, BCL 2, BCL 6, Thyroglobulin, MUM 1, Cyclin D1), consistent with lymphocytic thyroiditis. Significant clinical and laboratory improvement was achieved after combined treatment with levothyroxine and corticosteroid. Conclusion This case underscores the importance of considering autoimmune-related lymphocytic interstitial pneumonitis in patients with Hashimoto's thyroiditis who present with unexplained recurrent pleural effusion after exclusion of more common etiologies, such as infection and malignancy. Early recognition may lead to favorable improvement.
Lung Diseases, Interstitial ; Pleural Effusion ; Thyroiditis

With the increasing utilization of cancer therapy, the incidence of lung injury associated with these treatments continues to rise. The recognition of pulmonary toxicity related to cancer therapy has become increasingly critical, for which interstitial lung disease (ILD) is a common cause of mortality. Cancer therapy-related ILD (CT-ILD) can result from a variety of treatments including chemotherapy, targeted therapy, immune checkpoint inhibitors, antibody-drug conjugates, and radiotherapy. CT-ILD may progress rapidly and even be life-threatening; therefore, prompt diagnosis and timely treatment are crucial for effective management. This review aims to provide valuable information on the risk factors associated with CT-ILD; elucidate its underlying mechanisms; discuss its clinical features, imaging, and histological manifestations; and emphasize the clinical-related views of its diagnosis. In addition, this review provides an overview of grading, typing, and staging treatment strategies used for the management of CT-ILD.
Humans ; Lung Diseases, Interstitial/diagnosis* ; Neoplasms/therapy* ; Risk Factors ; Immune Checkpoint Inhibitors/adverse effects* ; Antineoplastic Agents/therapeutic use*

Lung cancer is the cancer with the highest incidence and mortality rate worldwide. In addition to the diversified treatment and prolonged lifespan in view of the development of medical technology, the side effect of medicine should not be ignored. Drug-induced interstitial lung disease (DI-ILD) is also commonly encountered during this process, and ILD triggered by the treatment of lung cancer characterized by the inflammation and scarring of lung tissue after the antitumor treatment in lung cancer leads to a poor prognosis and high mortality. The diagnosis and treatment of ILD caused by anti-lung cancer agents remains challenging in clinical settings and requires joint efforts from multidisciplinary team (MDT). This review systematically updates the epidemiology, molecular pathogenesis, genomics/genetics study, diagnosis and treatment of ILD related to anti-lung cancer agents. By the integration of the latest evidences, the paper offers clinical work references for early diagnosis of ILD related to anti-lung cancer agents to enhance the survival and quality of life of the lung cancer patients.
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Humans ; Lung Diseases, Interstitial/therapy* ; Lung Neoplasms/drug therapy* ; Antineoplastic Agents/therapeutic use*

Both carcinoembryonic antigen and CA19-9 are considered as predictive markers of intestinal cancer recurrence and metastasis.In addition,CA19-9 elevation is considered as a predictive marker of connective tissue disease-related interstitial lung disease.The incidence of oxaliplatin and capecitabine-associated interstitial lung disease is low,and there is no report about CA19-9 as a predictive marker of oxaliplatin and capecitabine-associated interstitial lung disease.This paper reports a case of interstitial lung disease with CA19-9 elevation caused by oxaliplatin and capecitabine adjuvant therapy for ileocecal carcinoma.The change trend of serum carcinoembryonic antigen in this patient was consistent with tumor recurrence and metastasis,and that of serum CA19-9 was consistent with the severity of interstitial lung disease.Therefore,CA19-9 elevation after intestinal cancer surgery does not necessarily indicate the tumor recurrence and metastasis,and attention should be paid to the possibility of oxaliplatin and capecitabine-associated interstitial lung disease.
Humans ; CA-19-9 Antigen/blood* ; Capecitabine ; Cecal Neoplasms/drug therapy* ; Chemotherapy, Adjuvant ; Deoxycytidine/administration & dosage* ; Fluorouracil/administration & dosage* ; Lung Diseases, Interstitial/blood* ; Organoplatinum Compounds/administration & dosage* ; Oxaliplatin

INTRODUCTION: Exposure to chemical agents in salon products, such as ammonia and formaldehyde, poses significant respiratory health risks for hairdressers. This study aimed to assess the prevalence of Diffuse Parenchymal Lung Disease Patterns (DPLD) observed in chest X-rays of hairdressers in the National Capital Region and to document their reported respiratory symptoms. METHODS: An analytical, cross-sectional study was conducted involving 100 hairdressers who underwent plain chest X ray examinations to identify any of the 12 recognized DPLD patterns. Participants also accomplished a self administered questionnaire detailing their demographic information, working conditions, health histories and current respiratory symptoms. RESULTS: Thirty nine percent of participants showed DPLD patterns on chest X-rays, primarily fine reticular opacities (69.23%) and coarse reticular opacities (25.64%). Positive associations (RR>1) were linked to over five years of work, lack of PPE, daily exposure to hair iron steam, respiratory symptoms, and salon vapor exposure of exceeding five hours daily. Symptoms reported included shortness of breath (27%) and throat irritation (15%). Logistic regression confirmed a significant link between DPLD and positive respiratory symptoms. CONCLUSION This study highlights the risk of structural lung abnormalities and respiratory symptoms among hairdressers, emphasizing the need for improved workplace safety, consistent PPE use and routine medical screenings to reduce occupational health risks.
Human ; Lung diseases, interstitial

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease characterized by progressive lung fibrogenesis and histological features of usual interstitial pneumonia. IPF has a poor prognosis and presents a spectrum of disease courses ranging from slow evolving disease to rapid deterioration; thus, a differential diagnosis remains challenging. Several biomarkers have been identified to achieve a differential diagnosis; however, comprehensive reviews are lacking. This review summarizes over 100 biomarkers which can be divided into six categories according to their functions: differentially expressed biomarkers in the IPF compared to healthy controls; biomarkers distinguishing IPF from other types of interstitial lung disease; biomarkers differentiating acute exacerbation of IPF from stable disease; biomarkers predicting disease progression; biomarkers related to disease severity; and biomarkers related to treatment. Specimen used for the diagnosis of IPF included serum, bronchoalveolar lavage fluid, lung tissue, and sputum. IPF-specific biomarkers are of great clinical value for the differential diagnosis of IPF. Currently, the physiological measurements used to evaluate the occurrence of acute exacerbation, disease progression, and disease severity have limitations. Combining physiological measurements with biomarkers may increase the accuracy and sensitivity of diagnosis and disease evaluation of IPF. Most biomarkers described in this review are not routinely used in clinical practice. Future large-scale multicenter studies are required to design and validate suitable biomarker panels that have diagnostic utility for IPF.
Humans ; Idiopathic Pulmonary Fibrosis/diagnosis* ; Biomarkers ; Lung Diseases, Interstitial ; Lung ; Bronchoalveolar Lavage Fluid ; Disease Progression ; Prognosis

The patient is a female infant, 4 months and 9 days old, who was admitted to the hospital due to recurrent fever, cough, and hepatomegaly for over a month. The patient was a healthy full-term infant with a normal birth history. At 2 months and 22 days after birth, she developed recurrent fever, cough, and respiratory distress. Chest imaging revealed diffuse bilateral lung lesions, and fiberoptic bronchoscopy showed interstitial changes in both lungs. These suggested the presence of interstitial lung disease. The patient also presented with hepatomegaly, anemia, hyperlipidemia, hypothyroidism, and malnutrition. Genetic testing indicated compound heterozygous variations in the MARS1 gene. This mutation can cause interstitial lung and liver disease, which is a severe rare disorder that typically manifests in infancy or early childhood. It is inherited in an autosomal recessive manner and characterized by early-onset respiratory insufficiency and liver disease in infants or young children. Since its first reported case in 2013, as of June 2023, only 38 related cases have been reported worldwide. This article reports the multidisciplinary diagnosis and treatment of interstitial lung and liver disease in an infant caused by MARS1 gene mutation.
Female ; Humans ; Infant ; Cough ; Hepatomegaly/pathology* ; Liver Diseases ; Lung/pathology* ; Lung Diseases, Interstitial/pathology* ; Mutation

A 54-year-old, non-smoking woman was diagnosed as stage ⅣB adenocarcinoma with widespread bone metastasis (cT4N2M1c) in the First Affiliated Hospital, Zhejiang University School of Medicine. Immunohistochemistry result showed the presence of anaplastic lymphoma kinase (ALK) gene rearrangement; next-generation sequencing (NGS) indicated EML4-ALK fusion (E6:A20) with concurrent CCDC148-ALK (C1:A20), PKDCC-ALK (Pintergenic:A20)and VIT-ALK (V15:A20) fusions. After 32 weeks of alectinib treatment, the patient complained cough and exertional chest distress but had no sign of infection. Computed tomography (CT) showed bilateral diffuse ground glass opacities, suggesting a diagnosis of alectinib-related interstitial lung disease (ILD). Following corticosteroid treatment and discontinuation of alectinib, clinical presentations and CT scan gradually improved, but the primary lung lesions enlarged during the regular follow-up. The administration of crizotinib was then initiated and the disease was stable for 25 months without recurrence of primary lung lesions and ILD.
Female ; Humans ; Middle Aged ; Carcinoma, Non-Small-Cell Lung/drug therapy* ; Crizotinib/therapeutic use* ; Lung Neoplasms/drug therapy* ; Anaplastic Lymphoma Kinase/therapeutic use* ; Lung Diseases, Interstitial/diagnosis*

Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease, the cause is not yet clear. Pathological manifestations are abnormal repair changes resulting from sustained lung injury. Macrophages have been identified as playing a key role in IPF pathogenesis. In different local microenvironments, macrophages can exhibit either classically activated (M1) or alternately activated (M2) phenotypes. M1 plays a key role in promoting inflammatory response and is involved in the process of causing alveolar tissue injury. M2 is involved in wound healing and stopping lung inflammation. Previous studies have shown that activation of 5-hydroxytryptamine (5-HT) signaling is enhanced in pulmonary fibrosis and that 5-HT receptors play an important role in the observed pro-fibrotic effects. As a multifunctional signaling molecule, 5-HT is closely related to lung macrophage polarization, early lung tissue injury, abnormal proliferation and repair, and late extracellular matrix (ECM) deposition. This article reviewed the role of 5-HT and M2 macrophages in the pathogenesis of IPF and the possible regulatory mechanism of 5-HT, in order to provide a reference for further research.
Humans ; Serotonin ; Macrophages ; Lung Diseases, Interstitial/pathology* ; Lung/pathology* ; Idiopathic Pulmonary Fibrosis ; Fibrosis

Humans ; Child ; Lung Diseases, Interstitial/diagnosis* ; Lung/pathology* ; Biopsy/methods* ; Bronchoscopy/methods*