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Background Pulmonary hypertension (PH) is one of the common complications in chronic obstructive pulmonary disease (COPD). The study aimed to evaluate the predicting ability of N-terminal pro brain natriuretic peptide (NT-pro BNP) in patients with AECOPD-PH and its relationship with the severity of PH. Methods A large retrospective case-controlled study (n = 1072) was performed in the First Affiliated Hospital of Xinjiang Medical University from January 2018 to December 2020, and patients were divided into stable COPD (n = 178), AECOPD (n = 688) and AECOPD-PH group (n = 206). Different statistical models were used to screen for reliable and stable biomarkers. Results In unadjusted analysis and PSM (model 1, 2, 3), red cell distribution width (RDW), total bilirubin (TBIL), and NT-pro BNP were higher in patients with AECOPD-PH than those in AECOPD group. Logistic regression analysis showed, when the range of NT-proBNP was 271–1165 pg/mL (OR: 0.293; 95%CI: 0.184–0.467; P < 0.001) and NT-proBNP > 1165 pg/mL (OR: 0.559; 95%CI: 0.338–0.926; P = 0.024), the morbidity risk of PH in AECOPD patients was increased, so did TBIL. In receiver operating characteristic (ROC) curves, at the cut-off value of NT-proBNP was 175.14 pg/mL, AUC was 0.651 (P < 0.001), which was better than TBIL (AUC: 0.590, P < 0.001). As for the results of rank correlation analysis, NT-proBNP had a weak correlation with severity of PH with AECOPD (rs = 0.299, P = 0.001) and its relative relevance with other biomarkers (RDW was 0.359 and TBIL was 0.238, P < 0.001). Conclusions Our findings suggest that NT-proBNP has a diagnostic efficacy in AECOPD-PH and NT-proBNP has a weak correlation with severity of PH with AECOPD.

Aims: Kupffer cells (KCs) are the liver-resident macrophages and play a leading role in the regulation of liver homeostasis in physiological conditions and in pathology. The study aims to investigate the anti-echinococcosis effect of KCs and the effects of hepatic stellate cells (HSCs) activation in the progression of liver fibrosis in hepatic alveolar echinococcosis (hepatic AE). Methods: Hematoxylin-eosin (H&E) and Masson staining were used to assess the pathological inflammatory changes and collagen deposition, respectively. Immunohistochemistry and qRT-PCR were used to detect the number of aggregates of KCs, the expression of cytokines and activation of HSCs. Results: In the close group, H&E staining showed that the normal lobular structure was destroyed and inflammatory infiltration around the lesion could be observed, and Masson staining showed that blue collagen fibers were clearly deposited near the portal area. IHC showed that KCs surface markers CD68 and CD163, cytokine iNOS and Arg-1 were positively expressed in the vicinity of inflammatory lesions. qRT-PCR indicated that TNF-α, IL-10, and TGF-β1 secreted by KCs were significantly higher than those in the distance group (P < 0.01). It is worth noticing that the expression levels of anti-inflammatory cytokines were slightly higher than that of pro-inflammatory cytokines. Both IHC and qRT-PCR results showed that HSCs activation markers, the expression of α-SMA and Desmin significantly increased. Conclusions: Our research indicates that KCs have immune-protective effect of anti-echinococcosis and promote liver fiber repair, and it also suggests that they have potential therapeutic value for patients with hepatic AE.

The present study aimed to determine the role of the cytokine transforming growth factor-β1 (TGF-β1) in liver fibrosis among patients with hepatic cystic echinococcosis (hepatic CE). Hepatic tissue specimens and serum samples from 30 patients with hepatic CE were collected and TGF-β1 levels were compared between the two groups. The degree of liver fibrosis was assessed by Masson staining. The expression levels of cytokine TGF-β1 in liver tissue and serum were detected by immunohistochemistry and ELISA, respectively. Masson staining of liver lesion tissue in patients with hepatic CE indicated different degrees of fibrosis in the liver and the World Health Organization classification was positively correlated with the severity of liver fibrosis (P<0.05). In addition, the expression of cytokine TGF-β1 was higher in liver lesion tissue specimens compared with that in the adjacent control samples (P<0.05). At the same time, cytokine TGF-β1 in serum specimens of patients was higher than that in the healthy control group (P<0.05). In conclusion, the expression of TGF-β1 is upregulated in patients with hepatic CE, which was closely associated to liver fibrosis. Materials and methods Case source and grouping. A total of 30 patients with hepatic CE admitted to the First Affiliated Hospital of Xinjiang Medical University (Urumqi, China) between July 1, 2013 and June 1, 2017 were enrolled in the present study. The age of the patients ranged from 9 to 74 years (median age, 28 years) and the male-to-female ratio was 12/18. Paired liver lesion tissue and normal tissue were obtained from each patient.