Multiorgan dysfunction syndrome due to high-dose cantharidin poisoning: A case report.

BACKGROUND: This report delves into the diagnostic and therapeutic journey undertaken by a patient with high-dose cantharidin poisoning and multiorgan dysfunction syndrome (MODS). Particular emphasis is placed on the comprehensive elucidation of the clinical manifestations of high-dose cantharidin poisoning, the intricate path to diagnosis, and the exploration of potential underlying mechanisms. CASE SUMMARY: A patient taking 10 g of cantharidin powder orally subsequently developed MODS. The patient was treated with supportive care, fluid hydration and antibiotics, and hemoperfusion and hemofiltration therapy for 24 h and successfully recovered 8 d after hospital admission. Cantharidin poisoning can cause life-threatening MODS and is rare clinically. This case underscores the challenge in diagnosis and highlights the need for early clinical differentiation to facilitate accurate assessment and prompt intervention. CONCLUSION: This article has reported and analyzed the clinical data, diagnosis, treatment, and prognosis of a case of high-dose cantharidin poisoning resulting in MODS and reviewed the relevant literature to improve the clinical understanding of this rare condition.

Relationship between body fat ratio and inflammatory markers in a Chinese population of adult male smokers.

Objective: To explore the correlation between changes in the body fat ratio (BFR) and peripheral blood inflammatory markers according to smoking status in the adult Chinese male population. Methods: A total of 865 participants (aged 20-70 years) were included. All participants underwent a physical health examination at Xiguzhou Central Hospital between October 2015 and July 2016, including measurements of body mass index (BMI), BFR, white blood cell [WBC] count, and neutrophil-lymphocyte ratio [NLR]. Results: WBCs count and NLR were significantly higher in adult male smokers than in non-smokers (P = 0.00). According to the BFR stratification analysis, WBC count and NLR significantly increased in accordance with BFR (P = 0.00). This finding remained significant after adjusting for relevant confounding factors (P < 0.05). Two-factor stratified analysis of smoking status and BFR showed that WBC count and NLR in the smoking population were higher than in nonsmokers, regardless of BFR. The interaction model showed that BFR and smoking status affected WBC count and NLR changes (P < 0.05). A significant positive correlation was found between WBC count, NLR, and BFR in adult male smokers; however, there was no significant correlation with BMI. There was an interaction between smoking and BFR, both of which synergistically affected changes in inflammatory markers, including WBC count and NLR. Conclusion: WBC count and NLR of smokers with a high BFR were significantly higher than those of nonsmokers with a low BFR. It is important to provide evidence-based medical evidence for social tobacco control and to reduce BFR.

Fanconi syndrome induced by the long-term use of tenofovir disoproxil fumarate: a case report and literature review.

We present the case of a woman of 50 years of age who experienced widespread bone pain along with digestive symptoms, including nausea and vomiting. She had been prescribed tenofovir disoproxil fumarate (TDF) tablets for the treatment of hepatitis B. Laboratory testing revealed low circulating phosphorus and potassium concentrations and acidosis. A whole-body bone scan revealed abnormal bone metabolism. Rheumatologic and urologic conditions were ruled out, and therefore TDF-induced Fanconi syndrome (FS) and related bone pain was diagnosed. After the TDF was discontinued, the patient's symptoms and laboratory indices significantly improved. In this manuscript, we highlight the clinical manifestations of and laboratory test results associated with FS and summarize the cases of TDF-induced FS reported on PubMed between 2013 and 2022 to improve understanding of FS.

Relationship Between Serum Gamma-Glutamyl Transferase Level and Impaired Fasting Glucose Among Chinese Community-Dwelling Adults: A Follow-Up Observation of 6 Years.

Objective: We aimed to investigate the relationship between serum gamma-glutamyl transferase (GGT) and fasting blood glucose (FBG) levels, as well as the cumulative risk of impaired fasting glucose (IFG) regulation in the Chinese adult population after 6 years of follow-up. Methods: A total of 1360 apparently healthy Chinese men and women who completed a community-based health examination survey and did not have IFG in central China in 2010 and 2016 were included in this study. The patients were divided into four groups according to their baseline GGT (in quartiles). The relationship between GGT levels and FBG levels was examined using general linear regression models. The effect of the GGT level on the risk of IFG was analyzed using multivariate logistic regression. The first quartile group of GGT levels was set as the dummy variable in the model, and the odds ratios and 95% confidence intervals of the remaining quartile groups relative to the first quartile group were obtained. Results: After 6 years of follow-up, 16.4% (188/1148) of participants were diagnosed with IFG. The cumulative incidence of IFG in the four groups according to their baseline GGT levels (in quartiles) was 7.7%, 16.1%, 15.8%, and 26.8%, respectively. Based on the Cox multiple regression, the hazard ratio for IFG increased by 28.9% for each unit of increase in the baseline GGT level after adjusting for the confounding factors. The GGT levels of participants in the first quartile were used as the reference group. The relative risks of IFG in the second, third, and fourth quartiles of GGT were 1.70, 1.55, and 2.46, respectively (P = 0.005). Conclusions: GGT was positively associated with the risk of IFG and can be used as an indicator to assess whether a patient may develop prediabetes.

Pancreatic Fat is not significantly correlated with ß-cell Dysfunction in Patients with new-onset Type 2 Diabetes Mellitus using quantitative Computed Tomography.

Objective: Type 2 diabetes mellitus (T2DM) is a chronic condition resulting from insulin resistance and insufficient ß-cell secretion, leading to improper glycaemic regulation. Previous studies have found that excessive fat deposits in organs such as the liver and muscle can cause insulin resistance through lipotoxicity that affects ß-cell function. The relationships between fat deposits in pancreatic tissue, the function of ß-cells, the method of visceral fat evaluation and T2DM have been sought by researchers. This study aims to elucidate the role of pancreatic fat deposits in the development of T2DM using quantitative computed tomography (QCT), especially their effects on islet ß-cell function. Methods: We examined 106 subjects at the onset of T2DM who had undergone abdominal QCT. Estimated pancreatic fat and liver fat were quantified using QCT and calculated. We analysed the correlations with Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) scores and other oral glucose tolerance test-derived parameters that reflect islet function. Furthermore, correlations of estimated pancreatic fat and liver fat with the area under the curve for insulin (AUCINS) and HOMA-IR were assessed with partial correlation analysis and demonstrated by scatter plots. Results: Associations were found between estimated liver fat and HOMA-IR, AUCINS, the modified ß-cell function index (MBCI) and Homeostatic Model Assessment ß (HOMA-ß). However, no significant differences existed between estimated pancreas fat and those parameters. Similarly, after adjustment for sex, age and body mass index, only estimated liver fat was correlated with HOMA-IR and AUCINS. Conclusions: This study suggests no significant correlation between pancreatic fat deposition and ß-cell dysfunction in the early stages of T2DM using QCT as a screening tool. The deposits of fat in the pancreas and the resulting lipotoxicity may play an important role in the late stage of islet cell function dysfunction as the course of T2DM progresses.

Evaluation of the associations of body height with blood pressure and early-stage atherosclerosis in Chinese adults.

Body height has been recently related to the risk of coronary heart disease and metabolic risk factors. However, data are scarce regarding the relationship between body height and early-stage atherosclerotic changes, especially in Chinese individuals. In this study, we aimed to comprehensively examine the associations of body height with early-stage atherosclerosis and blood pressure in Chinese adults. Carotid-femoral pulse wave velocity (cfPWV), carotid-radial pulse wave velocity (crPWV), carotid artery-dorsalis pedis pulse wave velocity (cdPWV), and body height were measured in 5098 men and women. All samples were obtained from a community-based health examination survey in central China. After adjusting for sex, age, weight, fasting glucose level, lipid level, creatinine, and heart rate, low body heights were significantly associated with higher cfPWV, crPWV, and blood pressure (all P for trend <.01), whereas no significant association was found between body height and cdPWV. In addition, we found a significant interaction between prehypertension status and body height in relation to cfPWV, after adjusting for covariates (P for interaction = .0024). The associations were stronger in participants with prehypertension than in those with normal blood pressure. Compared to the group with the tallest stature and normal blood pressure, individuals in the group with the shortest stature and prehypertension had nearly a 2.5 m/s higher cfPWV. These results indicate that short body height was associated with an increased risk of early-stage atherosclerosis in Chinese adults, independent of traditional cardiometabolic risk factors. Prehypertension might modify the association between body height and cfPWV.

SHCBP1 Promotes Papillary Thyroid Carcinoma Carcinogenesis and Progression Through Promoting Formation of Integrin and Collagen and Maintaining Cell Stemness.

Papillary thyroid carcinoma (PTC) is the most common thyroid cancer with a rapidly increasing incidence globally. Bioinformatics analyses suggested that SHCBP1 (SHC SH2 Domain-Binding Protein 1) was significantly up-regulated in PTC tumor tissues, which was further confirmed by immunohistochemical staining and qPCR analyses in Xuzhou cohort. Moreover, the results indicated that the mRNA level of SHCBP1 was negatively associated with patients' disease-free survival rate, and further analysis reveals that patients with high SHCBP1 expression tend to have more lymph node metastasis. Afterward, MTT, colony formation, cell-cycle assay, FACS apoptosis assay, invasion, migration, as well as scratch assay were performed to study the phenotypes change of PTC cells after knocking down SHCBP1. The in vivo subcutaneous tumor model was developed to study the proliferation ability of PTC cells after SHCBP1 knockdown. We show that knock down of SHCBP1 significantly inhibits PTC cell proliferation, cell cycle, invasion and migration in vivo and in vitro. Western blot and qRT-PCR showed that knockdown of SHCBP1 could significantly reduce MYC, KLF4, CD44, ITGA6, ITGB1, ITGB5, and COL4A2 expression at both RNA and protein levels, which indicated that SHCBP1 might be involved in PTC carcinogenesis and progression through targeting formation of integrin and collagen and cell stemness pathways, and can be a potential diagnosis biomarker and therapeutic target for PTC.

Six-year follow-up study on the association between white blood cell count and fasting blood glucose level in Chinese adults: A community-based health examination survey.

BACKGROUND: Pre-diabetes is considered to be an important reversible stage of type 2 diabetes (T2DM); thus, early identification of pre-diabetes may help in the prevention of T2DM. This study aimed to explore the relationship between white blood cell (WBC) counts and the cumulative risk of impaired fasting glucose (IFG) regulation at 6 years. METHODS: A community-based health examination survey was conducted among individuals who were randomly selected from 1300 residents living in China in 2010 to 2016. The participants were divided into four groups according to WBC baseline level. This study initially conducted a cross-sectional analysis of the population who underwent physical examination to explore the relationship between WBC count and FBG levels. Then, a follow-up study was conducted on the population who underwent IFG normal physical examination to explore the relationship between baseline WBC count and changes in FBG levels and the cumulative risk of 6-year IFG. RESULTS: During the 6-year cohort follow-up, 17.2% of the participants developed IFG, and the cumulative incidence rates of IFG in the four groups were 14.7%, 16.3%, 15.8%, and 22.2%. By Cox multiple regression equation the hazard ratio (HR) of the IFG increased by 18.7% for each additional unit of baseline WBC count with no adjustment of any factor. After adjusting factors, HR increased by 8.4%. CONCLUSION: Increased WBC counts are associated with risk of IFG, suggesting chronic inflammation may be involved in the development and progression of IFG.

Effect of vasopressin on hippocampal injury in a rodent model of asphyxial cardiopulmonary arrest.

The effect of vasopressin on the neuronal injury following the restoration of spontaneous circulation (ROSC) in cardiac arrest (CA) is not yet fully understood. The present study was conducted in order to investigate the effect of vasopressin alone, or in combination with epinephrine, on the ROSC and hippocampal injury in a rat model of asphyxial CA. Asphyxial CA was induced in 144 rats by clamping the tracheal tube, and animals were allocated equally into the following three groups: Treatment with vasopressin (0.8 U/kg); epinephrine (0.2 mg/kg); or vasopressin (0.8 U/kg) plus epinephrine (0.2 mg/kg). An additional 48 rats underwent a sham surgical procedure without asphyxial CA and cardiopulmonary resuscitation. Hippocampal tissue was harvested at 1, 3, 6 and 12 h post-ROSC, and the levels of p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) p65 were determined using immunohistochemistry. In comparison with rats treated with epinephrine alone, higher ROSC success rates were observed in rats treated with vasopressin, or vasopressin plus epinephrine. In addition, treatment with vasopressin attenuated hippocampal injury and reduced hippocampal p38 MAPK and NF-κB expression more efficiently compared with epinephrine alone. In conclusion, treatment with vasopressin exhibits a protective effect in patients experiencing CA, and this may be attributed to the inhibition of p38 MAPK and NF-κB expression.

Prognostic Value of Plasma Visfatin Level for Chinese Patients with Severe Carbon Monoxide Poisoning.

BACKGROUND: This prospective observatory study was designed to investigate whether plasma visfatin might serve as a marker of prognosis in patients with severe carbon monoxide (CO) poisoning. METHODS: A total of 52 consecutive patients with severe CO poisoning and 52 gender- and age- matched healthy subjects were enrolled in the study, and their plasma visfatin levels were determined using an enzyme-linked immunosorbent assay. The clinical outcomes, including in-hospital mortality, 6-month mortality, and poor outcome (Glasgow Outcome Scale score of 1 - 3), were recorded. RESULTS: Plasma visfatin levels were statistically significantly higher in patients than in healthy controls (97.4 ± 28.0 ng/mL vs. 12.1 ± 3.7 ng/mL; p < 0.001). Multivariate logistic regression analysis showed that plasma visfatin level was an independent prognostic predictor of in-hospital mortality [odds ratio (OR), 1.214; 95% confidence interval (CI), 1.103 - 1.425; p < 0.001], 6-month mortality (OR, 1.269; 95% CI, 1.085 - 1.534; p < 0.001), and 6-month poor outcome (OR, 1.302; 95% CI, 1.023 - 1.520; p < 0.001). Moreover, receiver operating characteristic curves showed that plasma visfatin level had high predictive value for in-hospital mortality [area under curve (AUC), 0.931; 95% CI, 0.832 - 1.000], 6-month mortality (AUC, 0.894; 95% CI, 0.801 - 0.987), and 6-month poor outcome (AUC, 0.886; 95% CI, 0.796 - 0.977). CONCLUSIONS: Plasma visfatin levels are significantly higher in patients with severe CO poisoning and could be a useful biomarker to predict short- and long-term clinical outcome after severe CO poisoning.

Neuroprotective effects of erythropoietin in patients with carbon monoxide poisoning.

The purpose of this study was to evaluate the efficacy of erythropoietin (EPO) for treating patients with carbon monoxide (CO) poisoning. We conducted a randomized, prospective study of 103 patients with CO poisoning in two groups: an EPO group (n = 54; patients received EPO) and a placebo group (n = 49; patients received normal saline). The study endpoints were the functional outcome at day 30 (the Barthel index and neurologic sequelae), National Institutes of Health Stroke Scale (NIHSS) score, and the levels of S-100ß. At 18 days, the NIHSS score improved significantly and S-100ß levels significantly decreased in patients in the EPO group. At 30 days, patients in the EPO group had a superior Barthel index and fewer patients had delayed neurologic sequelae (DNS). This study demonstrated that early administration of EPO to patients with CO poisoning improved neurological outcomes and reduced the incidence of DNS.