Mediastinal parathyroid carcinoma: a case report and review of the literature.

BACKGROUND: Parathyroid carcinoma (PC) is an uncommon cause of primary hyperparathyroidism (PHPT) and particularly rare in the mediastinum. Herein, we present a case of mediastinal PC and conduct a related literature review. CASE PRESENTATION: We described a case of a 50-year-old female patient with PHPT due to mediastinal PC. She was initially admitted to a local hospital in her hometown with hypercalcemia and high blood concentrations of PTH (parathyroid hormone). The patient underwent neck parathyroidectomy and pathological examination suggested parathyroid adenoma. Although the overproduction of serum calcium and PTH declined after the surgery, calcium and PTH increased again one month later, so the patient was transferred to our hospital. A 99mTc-sestamibi scan revealed an ectopic finding in the mediastinum, which was also indicated on the CT image. After removing the mediastinal mass, the metabolism of calcium and PTH quickly reverted to normal and the pathologic features of the mass were consistent with PC. By reviewing the related literature, we noticed that only scattered reports were published before 1982, and those were not included in the present review due to their differences with current radiological examination and treatment methods. After excluding outdated studies, we summarized and analyzed 20 reports of isolated mediastinal PC and concluded that. Parathyroidectomy remains the only curative treatment for the disease. Furthermore, the success of treatment directly depends on accurate preoperative localization. CONCLUSION: With this study, we emphasize the importance of accurate preoperative diagnosis of mediastinal PC and improve clinicians' understanding of the disease.

Nesfatin-1, a novel energy-regulating peptide, alleviates pulmonary fibrosis by blocking TGF-ß1/Smad pathway in an AMPKα-dependent manner.

Pulmonary fibrosis is a chronic progressive disease which steadily causes a critical public health concern. Nesfatin-1, a novel energy-regulating peptide discovered in 2006, could increase the level of AMPK phosphorylation. Previous studies have unveiled that Nesfatin-1 possessed many pharmacological effects including anti-inflammation, anti-oxidative stress, anti-fibrosis, and the regulation of lipid metabolism. Here, we investigated the impact of Nesfatin-1 on pulmonary fibrosis. Male C57BL/6J mice were intraperitoneally injected with Nesfatin-1 (10 µg·kg-1·day-1) for 21 days since mice were intratracheally administrated with bleomycin (BLM) (2 U/kg). Primary murine lung fibroblasts were stimulated with TGF-ß1 (10 ng/ml) for 48 h. The results showed that Nesfatin-1 treatment significantly improved pulmonary function and decreased the production of collagen in BLM-treated mice. Meantime, Nesfatin-1 treatment also inhibited oxidative stress and inflammation in lung tissues from BLM-treated mice. Mechanically, Nesfatin-1 blocked the activation of TGF-ß1/Smad2/3 signaling pathway in lung tissues challenged with BLM. In addition, we found that Nesfatin-1 enhanced the phosphorylation of AMPKα during pulmonary fibrosis. However, pharmacological inhibition or genetic deletion of AMPKα could both offset the pulmonary protection mediated by Nesfatin-1 during pulmonary fibrosis. Our experimental results firstly show Nesfatin-1 might serve as a novel treatment or adjuvant against pulmonary fibrosis by blocking TGF-ß1/Smad pathway in an AMPKα-dependent manner.

Placenta­derived mesenchymal stem cells ameliorate lipopolysaccharide­induced inflammation in RAW264.7 cells and acute lung injury in rats.

Acute lung injury (ALI) is a severe lung syndrome with high morbidity and mortality, due to its complex mechanism and lack of effective therapy. The use of placenta­derived mesenchymal stem cells (pMSCs) has provided novel insight into treatment options of ALI. The effects of pMSCs on lipopolysaccharide (LPS)­induced inflammation were studied using a co­culture protocol with LPS­stimulated RAW264.7 cells. An LPS­induced ALI Sprague­Dawley rat model was developed by intravenously injecting 7.5 mg/kg LPS, and intratracheal instillation of 1x105 pMSCs was performed after administration of LPS to investigate the therapeutic potential of these cells. pMSCs ameliorated LPS­induced ALI, as suggested by downregulated pro­inflammatory cytokine tumor necrosis factor­α and increased anti­inflammatory cytokine interleukin­10 in both cell and animal models. Moreover, the protein and leukocyte cells in bronchoalveolar lavage fluid decreased at a rapid rate after treatment with pMSCs. Histopathology demonstrated that pMSCs alleviated the infiltration of inflammatory cells, pulmonary hyperemia and hemorrhage, and interstitial edema. In addition, pMSC reduced the LPS­induced expression of C­X­C motif chemokine ligand 12 in RAW264.7 macrophages and in lung tissue of ALI rats. This demonstrated that pMSCs are therapeutically effective in LPS­induced ALI.

MicroRNA­375 prevents TGF­ß­dependent transdifferentiation of lung fibroblasts via the MAP2K6/P38 pathway.

Transdifferentiation of lung fibroblasts to myofibroblasts is a crucial pathophysiological process in pulmonary fibrosis. MicroRNA­375 (miR­375) was initially identified as a tumor­suppressive factor, and its expression was negatively associated with the severity of lung cancer; however, its role and potential mechanism in myofibroblast transdifferentiation and pulmonary fibrosis remain unclear. In the present study, human lung fibroblasts were stimulated with transforming growth factor­ß (TGF­ß) to induce myofibroblast transdifferentiation. A mimic and inhibitor of miR­375, and their negative controls, were used to overexpress or suppress miR­375 in lung fibroblasts, respectively. The mRNA expression levels of fibrotic markers, and protein expression of α­smooth muscle actin and periostin, were subsequently detected by reverse transcription­quantitative PCR and western blotting, to assess myofibroblast transdifferentiation. miR­375 was markedly upregulated in human lung fibroblasts after TGF­ß stimulation. The miR­375 mimic alleviated, whereas the miR­375 inhibitor aggravated TGF­ß­dependent transdifferentiation of lung fibroblasts. Mechanistically, miR­375 prevented myofibroblast transdifferentiation and collagen synthesis by blocking the P38 mitogen­activated protein kinases (P38) pathway, and P38 suppression abrogated the deleterious effect of the miR­375 inhibitor on myofibroblast transdifferentiation. Furthermore, the present study revealed that mitogen­activated protein kinase kinase 6 was involved in P38 inactivation by miR­375. In conclusion, miR­375 was implicated in modulating TGF­ß­dependent transdifferentiation of lung fibroblasts, and targeting miR­375 expression may help to develop therapeutic approaches for treating pulmonary fibrosis.

Pulmonary pathology of early-phase COVID-19 pneumonia in a patient with a benign lung lesion.

AIMS: An ongoing outbreak of 2019 novel coronavirus (CoV) disease (COVID-19), caused by severe acute respiratory syndrome (SARS) CoV-2, has been spreading in multiple countries. One of the reasons for the rapid spread is that the virus can be transmitted from infected individuals without symptoms. Revealing the pathological features of early-phase COVID-19 pneumonia is important for understanding of its pathogenesis. The aim of this study was to explore the pulmonary pathology of early-phase COVID-19 pneumonia in a patient with a benign lung lesion. METHODS AND RESULTS: We analysed the pathological changes in lung tissue from a 55-year-old female patient with early-phase SARS-CoV-2 infection. In this case, right lower lobectomy was performed for a benign pulmonary nodule. Detailed clinical, laboratory and radiological data were also examined. This patient was confirmed to have preoperative SARS-CoV-2 infection by the use of real-time reverse transcription polymerase chain reaction and RNA in-situ hybridisation on surgically removed lung tissues. Histologically, COVID-19 pneumonia was characterised by exudative inflammation. The closer to the visceral pleura, the more severe the exudation of monocytes and lymphocytes. Perivascular inflammatory infiltration, intra-alveolar multinucleated giant cells, pneumocyte hyperplasia and intracytoplasmic viral-like inclusion bodies were seen. However, fibrinous exudate and hyaline membrane formation, which were typical pulmonary features of SARS pneumonia, were not evident in this case. Immunohistochemical staining results showed an abnormal accumulation of CD4+ helper T lymphocytes and CD163+ M2 macrophages in the lung tissue. CONCLUSION: The results highlighted the pulmonary pathological changes of early-phase SARS-CoV-2 infection, and suggested a role of immune dysfunction in the pathogenesis of COVID-19 pneumonia.

GDF-15 prevents lipopolysaccharide-mediated acute lung injury via upregulating SIRT1.

Inflammation and oxidative stress were involved in alveolar epithelial cells (AECs) damage and contributed to the progression of acute lung injury (ALI). Growth differentiation factor-15 (GDF-15) was reported to have important roles in pulmonary diseases, yet its role in AECs damage and ALI remains elusive. Herein, we found that GDF-15 was upregulated upon LPS stimulation in murine lungs and human AECs. GDF-15 treatment prevented, whereas Gdf-15 silence aggravated LPS-induced inflammation, oxidative stress and apoptosis. Moreover, we determined that GDF-15 alleviated AECs damage and ALI via upregulating SIRT1, and SIRT1 suppression completely abrogated the beneficial effects of GDF-15 in vivo and in vitro. GDF-15 protected against LPS-triggered AECs damage and ALI via upregulating SIRT1, and GDF-15 might be a valuable therapeutic candidate for treating ALI.

Colon Interposition for Corrosive Esophageal Stricture: Single Institution Experience with 119 Cases.

The colon is an alternative graft organ for esophageal reconstruction. The present study reviewed our experience with the colon interposition for esophageal replacement following corrosive ingestion, to evaluate the outcomes of colon interposition based on our surgical experience. The clinical data of 119 patients who underwent colon interposition for esophageal replacement from January 2005 to March 2017 were retrospectively analyzed. The routes of the colon interposition were retrosternal in 119 (100%). The median operative time was 390 min (range: 290-610 min) and the median blood loss was 615 mL (range: 270-2500 mL). Of these 119 patients, the cervical anastomosis was performed at the hypopharynx (n=20, 16.8%), the larynx (n=3, 2.5%), and the cervical esophagus (n=96, 80.7%). Five patients experienced cervical anastomotic leakage (4 cases for esophagus-colon, and one for hypopharynx-colon). One patient experienced wound infection of the abdominal wall. Three patients had injury of recurrent laryngeal nerve and hoarseness. Three patients had stress ulcer with bleeding and treated with octreotide. Two patients suffered from incomplete intestinal obstruction. The postoperative follow-up was made for 12 months in all patients and all of them were alive. In conclusion, The colon is well-suited for esophageal reconstruction. The selection of the colon graft should be flexible and be based on the inspection of blood supply and the length needed. We must therefore make every effort to reduce the number of postoperative complications, and improve the quality of life for patients.

Knockdown of Sfrp4 attenuates apoptosis to protect against myocardial ischemia/reperfusion injury.

Secreted frizzled-related protein (Sfrp) 4 is a protein that involve in cardiac development and several cardiovascular diseases. However, the effect of Sfrp4 in mediating myocardial ischemia/reperfusion injury remains unknown. In this work, adenoviral (Ad)-shSfrp4 adenoviruses was used to knockdown of Sfrp4 in myocardium to examine the role of Sfrp4 in mediating myocardial I/R injury. Knockdown of Sfrp4 in mice attenuated myocardial I/R injury, as indicated by the decrease levels of lactate dehydrogenase and creatine kinase, and increment of ventricular function following I/R injury. Besides, knockdown of Sfrp4 led to a reduction in Bax, active caspase 3, and increase Bcl-2 and c-Myc in cardiac tissue. Knockdown of Sfrp4 lost its protection against I/R injury in mice infected with Ad-dn-AKT. In conclusion, knockdown of Sfrp4 in myocardium attenuated myocardial ischemia and reperfusion injury by AKT signaling pathway.

Downregulation of lysyl oxidase-like 4 LOXL4 by miR-135a-5p promotes lung cancer progression in vitro and in vivo.

Aberrant microRNAs are widely identified in multiple cancers, including lung cancer. miR-135a-5p can function as a significant tumor regulator in diverse cancers via impacting multiple genes in oncogenic pathways. Nevertheless, the biological role of miR-135a-5p in lung cancer is poorly known. Here, we investigated its function in lung cancer. As exhibited, miR-135a-5p was elevated in lung cancer cells in contrast to BEAS-2B cells. Then, we inhibited miR-135a-5p expression by transfecting LV-anti-miR-135a-5p into lung cancer cells. As displayed, miR-135a-5p was obviously reduced in A549 and H1299 cells. Knockdown of miR-135a-5p repressed lung cancer cell growth and cell proliferation. Meanwhile, cell colony formation capacity was depressed, cell apoptosis was enhanced and cell cycle progression was blocked in G1 phase by inhibition of miR-135a-5p in vitro. Additionally, the migration and invasion of A549 and H1299 cells was strongly depressed by LV-anti-miR-135a-5p. For another, by using informatics analysis, lysyl oxidase-like 4 (LOXL4) was speculated as the downstream target of miR-135a-5p. We validated their direct correlation and moreover, overexpression of miR-135a-5p restrained LOXL4 levels in lung cancer cells. Subsequently, we proved that miR-135a-5p promoted lung cancer development via targeting LOXL4 by carrying out the in vivo assays. Taken these together, our study revealed miR-135a-5p might be indicated as a perspective for lung cancer via targeting LOXL4.

Changes in Palm Temperature as Predictor of Long-term Cure of Sympathicotomy for Palmar hyperhidrosis?

OBJECTIVES: To investigate the long-term relationship between intraoperative temperature changes of the palm, treatment effects and compensatory hyperhidrosis (CH). METHODS: We retrospectively analyzed the data of 41 patients with palmar hyperhidrosis who underwent bilateral endoscopic sympathicotomy 3 to 6 years ago. Before and after the operation, changes in ipsilateral palm temperature were monitored and recorded to evaluate the curative effect of the sympathicotomy. RESULTS: All operations were performed successfully. Concerning cure, there was no statistically significant difference between patients with different maximum temperature (Tmax) values (p = 0.455). There was a very weak correlation between postoperative palm temperature (34.309 ± 1.377°C) (p = 0.049; correlation coefficient - 0.218). The T3 + T4 sympathicotomies had a higher Tmax (p = 0.000). The incidence and degree of CH had no relationship with Tmax in the left (p = 0.266 and p = 0.168, respectively) or the right hand (p = 0.640 and p = 0.824, respectively). CONCLUSIONS: Temperature change has a relationship with surgery, but it cannot directly predict the long-term curative effect of a sympathicotomy or the occurrence of CH. Additional studies are required.

Predictive value of the thymofatty specimen weight index in outcomes of extended thymectomy due to non-thymomatous myasthenia gravis.

OBJECTIVES: To evaluate the predictive value of the intraoperative thymofatty specimen weight (TFSW) index on predicting the prognosis of extended thymectomy (ET) for non-thymomatous myasthenia gravis. METHODS: This is a prospective non-interventional study in which patients who underwent ET between January 2012 and June 2015 were enrolled. Resected thymus and surrounding adipose tissues were weighed using an electronic scale intraoperatively and adjusted to the body surface area (BSA) to calculate the TFSW index. The primary end point was defined as complete stable remission (CSR) according to the Myasthenia Gravis Foundation of America (MGFA) guidelines. RESULTS: One hundred and eighteen patients who completed postoperative follow-up were included in this study. After a mean follow-up period of 44 months, 68 (57.6%) patients reached clinical CSR. The MGFA class, histopathology and TFSW index were associated with a postoperative CSR in univariate analysis. When the Cox hazard multiple regression model was used, the TFSW index was found to be an independent predictor for CSR (hazard ratio 2.056; 95% confidence interval 1.182-3.576). Based on ROC analysis, an optimal TFSW index cut-off value (35.9 g/m2) with the highest sensitivity and specificity was determined. CONCLUSIONS: The TFSW index is an important independent predictor for mid-term CSR after ET in non-thymomatous myasthenia gravis patients. During the ET surgery, every effort should be made to take a tissue specimen with a TFSW index more than 35.9 g/m2.

CXCR4 is involved in CD133-induced EMT in non-small cell lung cancer.

Metastasis is the major cause of death in patients with non-small cell lung cancer (NSCLC), and epithelial-mesenchymal transition (EMT) has been observed to be one of the key regulators of metastasis in certain cancers as it confers an invasive phenotype. CD133 is a widely used cancer stem cell (CSC) marker, and CD133-positive cancer cells are thought to be tumor-initiating cells with CSC characteristics, while CXCR4, a stromal-derived-factor-1 specific chemokine receptor, is highly expressed in NSCLC tissues and participates in cancer progression by regulating cell anti-apoptosis. We previously demonstrated that CXCR4 promotes NSCLC chemoresistance by upregulating CYP1B1, however, the relationship of CD133, CXCR4 and EMT processes in NSCLC metastasis are unclear. In this study, we detected a CD133 and CXCR4 high expression in tissue specimens from 64 NSCLC patients by immunohistochemistry, of which CD133 and CXCR4 were found to be positively associated with metastatic NSCLC patients. CD133 was found to promote NSCLC tumorigenesis and mediated the expression of CXCR4. Furthermore, CD133/CXCR4 co-expression was found to be an independent prognostic factor as shown by univariate and multivariate Cox regression analysis, and was observed to regulate the expression of EMT-related molecules and transcriptional factors in NSCLC. In addition, our results showed that E-cadherin and Vimentin were simultaneously downregulated and upregulated, in CD133+CXCR4+ A549 cells, respectively. While E-cadherin was upregulated and Vimentin was downregulated in metastatic NSCLC patients. Vimentin expression was also observed to have a positive correlation with CD133/CXCR4 co-expression in NSCLC patients and survival analysis results suggested that Vimentin high expression might be significantly associated with poor survival rates of the patients. Thus, these results suggest that the CD133/CXCR4/EMT axis may be a prognostic marker and may provide novel targets for combinational therapies in the treatment of NSCLC.

CXCR4 promotes cisplatin-resistance of non-small cell lung cancer in a CYP1B1-dependent manner.

Chemoresistance is the main cause of treatment failure and high mortality in advanced lung cancer. Cisplatin, an important chemotherapeutic agent for lung cancer, has been observed to show enormously reduced chemotherapeutic efficacy owing to the development of chemoresistance. CXCR4, a stromal-derived-factor-1 specific chemokine receptor, is highly expressed in non-small cell lung cancer (NSCLC) tissues and participates in cancer progression by regulating cell growth, apoptosis or invasion. In this study, we therefore investigated whether CXCR4 plays a role in the cisplatin associated resistance in NSCLC. We detected the expression of CXCR4 in tissue specimens from 64 NSCLC patients by immunohistochemistry. Cisplatin-resistant NSCLC cells A549/DDP and its parental A549 cells were employed in this study. RNA interference was performed to silence the CXCR4. The influence of CXCR4 on tumor cell chemoresistance, apoptosis and growth, as well as the relationship between CXCR4 and the expression of cytochrome p450 associated molecule CYP1B1 in NSCLC were evaluated. Finally, we found CXCR4 was significantly highly expressed in cisplatin-resistant NSCLC patients and the A549/DDP cell line. CXCR4 inhibition by siRNA reversed chemoresistance and decreased tumor cell proliferation. Bioinformatics analysis showed that the expression of CYP1B1 had a positive correlation with CXCR4, the CYP1B1 silencing significantly decreased CXCR4 expression levels and cisplatin resistance. Immunohistochemistry also verified that CYP1B1 was upregulated in NSCLC tissues of cisplatin-resistant patients. In conclusion, our results indicate that overexpression of CXCR4 in NSCLC promotes cisplatin resistance via CXCR4-mediated CYP1B1 upregulation. Thus, it can be used as a potential therapeutic target in NSCLC chemoresistance patients and be used as a clinical predictor of cisplatin response.

Effect of CXCL12/CXCR4 on increasing the metastatic potential of non-small cell lung cancer in vitro is inhibited through the downregulation of CXCR4 chemokine receptor expression.

Lung cancer ranks as the most common type of cancer in males worldwide. Although great advances have been achieved in chemotherapy and radiotherapy, the long-term survival rate of lung cancer patients has not improved significantly. Dissemination of lung cancer in the thoracic cavity and metastatic spread to the liver, bone and brain are characteristic of non-small cell lung cancer (NSCLC), constituting the primary source of morbidity and mortality in lung cancer. Increasing evidence also indicates that the CXC chemokine receptor 4 (CXCR4)/chemokine CXC motif ligand 12 (CXCL12) chemokine axis is important for the cell invasion and migration of lung cancer. CXCR4 is a G protein-coupled receptor with a major role in lymphocyte homing. Its ligand, CXCL12, is secreted by target organs and functions as a highly efficient chemotactic factor for T cells, monocytes, pre-B cells, dendritic cells and myeloid bone marrow-derived cells. In the current study, recombinant CXCR4-specific small interfering RNA-pBSilence1.1 plasmids were constructed and transfected into the A549 NSCLC cell line in vitro. Reverse transcription polymerase chain reaction and western blotting revealed that CXCR4 was downregulated in transfected cells compared with control cells. The results of MTT and Transwell migration assays indicated that the specific downregulation of CXCR4 inhibited cell growth, invasiveness and migration. Thus, siRNA targeting of CXCR4 may effectively inhibit the effect of CXCL12/CXCR4 on increasing the metastatic potential of NSCLC.

Ivor-Lewis esophagectomy for esophageal cancer after distal gastrectomy.

We report the use of gastric remnant for esophageal substitution after distal gastrectomy in a 53-year-old man with esophageal cancer. This patient had a 4-month history of progressive dysphagia for solid food. An upper gastrointestinal endoscopy showed a 7.0 cm bulge tumor in the middle-lower esophagus, wherein the upper margin was located 28 cm from the dental arcade. Computed tomography (CT) of the chest revealed wall thickening in the middle-lower esophagus. In this case, radical en bloc esophagectomy with a two-field lymph node dissection was performed in the upper abdomen and mediastinum via a posterolateral right thoracotomy through the fifth intercostal space. Esophagogastric anastomosis was performed mechanically in the apex of the chest using a circular stapler. The gastric remnant was used for reconstruction of the esophago-gastrostomy and placed in the right thoracic cavity. The patient was discharged on the 12th postoperative day without complications. The gastric remnant may be used for reconstruction in patients with esophageal cancer as a substitute organ after distal gastrectomy.

VATS right upper lobectomy.

Standard thoracotomy has been considered as the classic approach and only choice for the diagnosis and treatment of certain thoracic diseases especially in patients with peripheral lung cancer. Video-assisted thoracic surgery (VATS) is a new minimally invasive thoracic surgery through small incisions in the intercostal muscle of chest wall by using modern camera technology, high-tech equipment and surgical instrument. Consequently, VATS has become the preferred main method for peripheral lung cancer in the last two decades. The aim of the present paper is to describe and discuss the operative techniques of VATS for right upper lobectomy (RUL).

Esophageal reconstruction with remnant stomach: a case report and review of literature.

The number of patients developing esophageal cancer after gastrectomy has increased. However, gastric remnant is very rarely used for reconstruction in esophageal cancer surgery because of the risk of anastomotic leakage resulting from insufficient blood flow. We present a case of esophageal cancer using gastric remnant for esophageal substitution after distal gastrectomy in a 57-year-old man who presented with a 1-month history of mild dysphagia and a background history of alcohol abuse. Gastroscopy showed a 1.2 cm × 1.0 cm bulge tumor of the lower third esophagus with the upper margin located 39 cm from the dental arcade. Computed tomography of the chest showed lower third esophageal wall thickening. The patient underwent en bloc radical esophagectomy with a two-field lymph node dissection of the upper abdomen and mediastinum via a left-sided posterolateral thoracotomy through the seventh intercostal space. The upper end of the esophagus was resected 5 cm above the tumor. The gastric remnant was used for reconstruction of the esophago-gastrostomy and placed in the left thoracic cavity. The patient started a liquid diet on postoperative day 8 and was discharged on the 10(th) postoperative day without complications. In this report, we demonstrate that the gastric remnant may be used for reconstruction in patients with esophageal cancer as a substitute organ after distal gastrectomy.

Surgical treatment of synchronous gastric and esophageal carcinoma: case report and review of literature.

A 65-year-old man was admitted to our hospital because of advanced esophageal squamous cell carcinoma located on the left posterior wall of the lower thoracic esophagus and gastric adenocarcinoma in the antrum. Esophagectomy and distal gastrectomy with two-field lymph node dissection (mediastinum and abdomen) were performed via a left-sided abdominothoracic incision. The remnant gastric was pulled up successfully with the blood supply maintained by the left gastric vessel. He was discharged on the 13th postoperative day without any complications.

[Etiology and treatment of non-thoracotraumatic pneumomediastinum].

OBJECTIVE: To investigate the etiological factors, pathogenesis, and treatment of pneumomediastinum not caused by thoracic injury and chest operation. METHODS: 56 patients with non-thoracotraumatic pneumomediastinum were divided into 3 groups according to etiology: idiopathic pneumomediastinum (n = 37), descending pneumomediastinum (n = 11) and ascending pneumomediastinum (n = 8). All of 56 patients received symptomatic treatment by mediastinotomy and etiological treatment on the basis of different primary affection of mouth, throat, neck, bronchus, colon etc. RESULTS: Complete recovery was observed in 45 patients and partial recovery was found in 5 patients. The causes of death in 6 patients were serious pulmonary infection with respiratory failure, descending necrotizing mediastinitis with multi-organ failure and colonic perforation with septicopyemia. CONCLUSION: Most non-thoracotraumatic pneumomediastinum are secondary to the underlying diseases, the mechanisms of its pathogenesis include lung interstitium path (idiopathic), oropharyngeal and cervical interspace path (descending), and extraperitoneal space path (ascending). The treatment should be focused on dealing with primary diseases as well as symptomatic treatment by mediastinotomy.