Value of prediction model in distinguishing gallbladder adenoma from cholesterol polyp.

BACKGROUND AND AIM: Gallbladder adenomatous polyp is a pre-cancerous neoplasm, and it is difficult to classify from cholesterol polyps before cholecystectomy. The study aimed to clarify the risk characteristics of gallbladder adenomas and establish a prediction model to differentiate gallbladder adenomas from cholesterol polyp lesions. METHODS: From May 2019 to December 2021, the patients underwent cholecystectomy in the Shanghai Eastern Hepatobiliary Surgery Hospital were retrospectively reviewed. According to the permanent pathology test, the patients were divided into adenomas and cholesterol polyps groups. All the included cases received ultrasound equipment examinations before cholecystectomy and their clinical information were completely recorded. Then the patients' baseline characteristics and ultrasound imaging variables were analyzed by logistic regression. Finally, a predictive model for gallbladder adenomas will be established and assessed based on the independent risk factors. RESULTS: A total of 423 cases including 296 cholesterol polyps and 127 gallbladder adenomas were analyzed in detail. Multivariate logistic regression analysis revealed that solitary polyp lesion (OR = 2.954, 95% CI 1.759-4.960, P < 0.001), the maximal diameter of lesions (OR = 1.244, 95% CI 1.169-1.324, P < 0.001), and irregular shape of polyp lesions (OR = 5.549, 95% CI 1.979-15.560, P = 0.001) were the independent predictive factors of gallbladder adenomas. According to the results, regression equation of logit(P) = -3.828 + 1.083*number of gallbladder polyps lesions (GPLs) + 0.218*diameter of GPLs + 1.714*shape of GPLs was established. Area under the curve (AUC) was 0.828 (95% CI 0.782-0.874, P < 0.001). When logit P > 0.204, the sensitivity of estimating adenoma was 79.5%, the specificity of recognizing adenoma was 70.6%, and the whole correct ratio was 73.3%. While the AUC of diameter (10 mm) being a predictive factor in this study was only 0.790 (95% CI 0.741-0.839, P < 0.001). And the sensitivity and specificity of 10 mm as the optimal diagnostic cutoff value to diagnose adenomas were 74.8% and 65.9%, respectively. CONCLUSIONS: The risk factors of solitary polyp lesion, larger diameter, and irregular morphology feature of polyp lesions were significantly related to gallbladder adenomas. And the predictive model established in the study can effectively identify adenomas from cholesterol polyps and help patients to select the optimal treatment protocol.

Association between plasma metal elements and platelet dysfunction in trauma-induced coagulopathy rat model.

BACKGROUND: Disorders of metal elements and platelet dysfunction are common in patients with trauma-induced coagulopathy (TIC). AIM: The aim of this study was to explore the potential role of plasma metal elements in platelet dysfunction in TIC. METHODS: Thirty Sprague-Dawley rats were divided into control, hemorrhage shock (HS) and multiple injury (MI) groups. At timepoints of 0.5 and 3 h after trauma and being documented as HS 0.5 h, HS3 h, MI 0.5 h or MI3 h, blood samples were harvested for inductively coupled plasma mass spectrometer, conventional coagulation function and thromboelastograph. RESULTS: The plasma zinc (Zn), vanadium (V) and cadmium (Ca) decreased initially in HS 0.5 h and recovered slightly in HS3 h, whereas their plasma concentrations continued to decrease from beginning till MI3 h (p < 0.05). In HS, plasma Ca, V and nickel were negatively correlated to the time taken to reach the initial formation (R), whereas R was positively correlated to plasms Zn, V, Ca and selenium in MI (p < 0.05). In MI, plasma Ca was positively correlated to maximum amplitude, and plasma V was positively correlated to platelet count (p < 0.05). CONCLUSION: The plasma concentrations of Zn, V and Ca appeared to contribute to platelet dysfunction in HS 0.5 h, HS3 h, MI 0.5 h and MI3 h, which were trauma type sensitive.

Arachidonic Acid-Dependent Pathway Inhibition in Platelets: its Role in Multiple Injury-Induced Coagulopathy and the Potential Mechanisms.

BACKGROUND: Our previous study demonstrated the types of platelet dysfunction varied at early stage (∼3 h) in trauma-induced coagulopathy (TIC) caused by different types of injuries. And arachidonic acid (AA)-dependent pathway inhibition in platelet seemed to be specific for TIC caused by multiple injury (MI). The aim of this research was to further study AA-dependent pathway inhibition in platelets in a rat model of TIC caused by MI and to explore its potential mechanisms. METHODS: Sprague-Dawley rat model of TIC caused by MI was established. We used thrombelastography with platelet mapping as a measure of platelet function to assess the inhibitory extent of AA-dependent activation pathway. Flow cytometry was used to determine the expression of activation-dependent granular protein P-selectin (CD62P). In addition, the plasma levels of 6-Keto-prostaglandin F1 alpha (6-Keto-PGF1α), Prostaglandin E2, and Thromboxane B2 were assessed by enzyme-linked immuno sorbent assay. RESULTS: The inhibition rate of AA-dependent pathway after injury was significantly higher than that of control. The maximum amplitude decreased in the MI group, compared with that of control. The percentage of CD62P expression in the MI group was remarkably lower than that of control after AA treatment. The plasma concentrations of 6-Keto-PGF1α and PGE2 increased in the MI group. CONCLUSION: Platelets inhibition was observed in TIC caused by MI at early stage after injury, which might be partially attributed to AA-dependent activation pathway dysfunction. The increase of plasma Prostacyclin and PGE2 levels may contribute to the inhibition process.

Study on coagulation profiles and platelet function in trauma-induced coagulopathy caused by three types of injury.

BACKGROUND: Traumatic coagulopathy is a major public health issue globally with undefined mechanisms. We established rat models of hemorrhagic shock (HS), multiple injury (MI) and traumatic brain injury (TBI) to investigate the diversity of traumatic coagulopathy, especially platelet dysfunction. METHODS: Seventy male SD rats were divided randomly into seven groups(n = 10): control, HS30min, HS3h, MI30min, MI3h, TBI30min and TBI3h. Plasma or whole blood was collected for conventional coagulation tests, thromboelastography and platelet mapping. X-ray, 7T magnetic resonance imaging and hematoxylin-eosin staining of injured tissues were conducted to confirm the injuries of rats model. RESULTS: The activated partial thromboplastin time (aPTT) prolonged significantly in HS30min and MI3h groups, compared with those in control (P = 0.0403 and P = 0.0076, respectively). R values decreased in HS30min and HS3h groups, compared with those in control (P < 0.0001 and P < 0.0001, respectively). The maximum amplitude (MA) were 71.8 ± 0.6 mm, 71.9 ± 0.5 mm, 71.8 ± 0.7 mm, 70.0 ± 0.7 mm, 72.6 ± 0.9 mm, 70.4 ± 0.9 mm in HS30min, HS3h, MI30min, MI3h, TBI30min and TBI3h groups respectively, which were lower than those in control (P = 0.0304, P = 0.0205, P = 0.0431, P = 0.0007 and P = 0.0066, respectively). The platelet counts were 539±46 × 109/L, 523±31 × 109/L, 629 ± 18 × 109/L and 636±20 × 109/L in HS30min, HS3h, MI3h and TBI3h groups respectively, which were lower than those in control (P = 0.0040, P = 0.0001, P = 0.0127 and P = 0.0232, respectively). The adenosine diphosphate (ADP) inhibition rate decreased in HS30min group, compared with that in control (P = 0.0355). While, ADP inhibition rate increased in HS3h and TBI3h groups (P = 0.0041 and P = 0.0433 vs. control, respectively). The arachidonic acid (AA) inhibition rate increased in MI30min and MI3h groups, compared with control (P = 0.0029 and P = 0.0185, respectively). CONCLUSION: These results demonstrated that it might be the failure of forming a strong clot instead of the prolonged clot time, which contributed to traumatic coagulopathy. The platelet dysfunctions might contribute to trauma-induced coagulopathy in different ways. The loss of platelets might be the main reason for HS-induced coagulopathy. While, AA-dependent pathway inhibition might account for MI-induced coagulopathy. ADP-dependent pathway inhibition might be the major contributor for TBI-induced coagulopathy.

The Alterations of Copper and Zinc Homeostasis in Acute Appendicitis and the Clinical Significance.

Copper (Cu) and zinc (Zn) are involved in inflammatory process. This study was to investigate the clinical significance of Cu and Zn homeostasis alterations in acute appendicitis (AA). One hundred twenty-two AA patients and 102 healthy controls were enrolled in this study. Of which, 85 patients' appendixes were collected after appendectomy. Another six appendixes from colon cancer patients were collected as tissue controls. The contents of Cu and Zn in serum or appendix were detected, and the Cu to Zn ratio (CZr) was calculated. The concentrations of serum ceruloplasmin (CP), Cu/Zn superoxide dismutase (SOD1), interleukin-6 (IL-6), and interleukin-22 in serum were measured, as well as the activity of CP and SOD1. The serum Zn concentration and SOD1 activity, appendix contents of Cu and Zn significantly decreased in AA patients, compared with those of controls, while serum CZr, concentrations of CP, SOD1, and IL-6, as well as CP activity increased significantly in AA patients. Additionally, serum concentrations of Zn, CP, CZr, or SOD1 activity varied in different pathological types of AA. Indicators such as serum SOD1 activity might serve as predictors for pathological classification before surgery. The serum Zn and CZr may be helpful for diagnosis of pure AA. The Cu and Zn homeostasis was altered in AA patients, which might contribute to inflammatory process of AA.