Clinical analysis of pipeline dredging agent poisoning: A case report.

BACKGROUND: Pipeline dredging agents are new household deep cleaning products used to dredge blockages in kitchen and bathroom pipeline caused by grease, hair, vegetable residue, paper cotton fibre, and other organic substances. Pipeline dredging agents are corrosive chemicals that can cause poisoning through corrosive damage to the digestive tract; however, this has not been reported clinically. Therefore, this report emphasises that oral pipeline dredging agent poisoning can cause corrosive damage to the digestive tract and may have serious health consequences. CASE SUMMARY: A 68-year-old man consumed liquor (200 mL) at approximately 13:00 on April 22, 2021. At approximately 16:00, his family found him unresponsive with blackened lips, blood spots in the corners of the mouth, and blood stains on the ground, as well as an empty bottle of a pipeline dredging agent. One hour later, he was admitted to the emergency department of a local hospital. Considering the empty bottle, he was suspected to have sustained severe corrosive damage to the digestive tract and was transferred to our department at 23:15 on April 22, 2021. He developed dysphagia and intermittent fever and experienced difficulty in opening his mouth throughout his hospital stay. The patient's condition gradually stabilised. However, he suddenly developed respiratory failure on day 12, and endotracheal intubation and ventilator-assisted ventilation were performed. However, the patient died after 1.5 h despite emergency rescue efforts. CONCLUSION: Pipeline dredging agents are highly corrosive and may cause corrosive damage to the digestive tract and asphyxia upon consumption.

[Role of store-operated Ca2+ channels in primary hepatocytes under conditions of calcium overload and ethanol-induced injury].

OBJECTIVE: To investigate the role of store-operated calcium channels (SOCs) in primary hepatocytes under conditions of calcium overload and ethanol-induced injury. METHODS: The in vitro model of chronic ethanol-induced hepatocyte injury was established using primary hepatocytes isolated from Sprague-Dawley rats. Ethanol-induced changes (24, 48 and 72 h; 50, 100, 200, 400 and 800 mmol/L) in expression of the SOCs proteins stromal interaction molecule 1 (STIM1) and calcium release-activated calcium channel protein 1 (Oria1) were detected by qualitative PCR analysis (mRNA) and western blotting (protein). The possible role of these two SOCs proteins in the ethanol-induced extracellular calcium influx and related liver cell injury was determined by treating the cell system with various channel blockers (EGTA, La3+, and 2-APB). Cell viability was determined by MTT assay and cytosolic free calcium ion concentration was determined by flow cytometry. RESULTS: After 24 h of exposure to 0 (untreated) to 800 mM/L ethanol, the cell viability was reduced in a concentration-dependent manner. The 400 mmol/L concentration of ethanol decreased cell viability by 57.34% +/- 2.34%. and was chosen for use in subsequent experiments. Compared with the untreated control cells, the ethanol-treated cells showed significantly up-regulated mRNA and protein expression of both STIM1 and Orai1 at all times examined, suggesting that the ethanol-stimulated expression of STIM1 and Orai1 could persist for at least 72 h. The ethanol treatment induced increase in cytoplasmic calcium levels was significantly (and similarly) reduced by co-treatment with any of the three channel blockers. CONCLUSION: Chronic ethanol exposure can increase the expression of STIM1 and Orai1 in primary liver cells, suggesting that ethanol may increase extracellular calcium influx by up-regulating expression of these SOCs protein molecules, ultimately aggravating liver cell damage.

[Clinical studies of dynamic changes on the renal injury indicators of acute paraquat poisoning].

OBJECTIVE: To investigate the clinical significance of dynamic changes of blood urea nitrogen (BUN), serum creatinine (Cr), serum cystatin (Cys C) and urinary protein on renal injury with paraquat poisoning. METHODS: According to the clinical manifestation and curative effect, the clinical information was analyzed retrospectively in 35 cases of acute paraquat poisoning, survival after eight weeks as the standard. Poisoning patients were taken a fasting blood 5 ml and the middle of urinary on the 1st day, 3rd day, 7th day, 14th day, 21st day and 8 weeks after the poisoning. Then the levels of serum BUN, Cr, Cys C and urinary protein were detected by automatic biochemistry analyzer. 30 cases healthy subjects were randomly selected as normal control group, and discharged kidney disease and other diseases of urinary system history. The same laboratory subjects have been done. RESULTS: The level of serum Bun, Cr, Cys C of survival group increased significantly compared with control group within 21 days (P < 0.05). The level of serum BUN, Cr Cys C decreased on the 14th day. The decreased level of serum Cys C was lower than that of serum BUN and Cr. The renal function of 29 cases among 35 cases survival patients recovered on 21st day. The renal function of 31 cases among 35 cases survival patients recovered 8 weeks late. The positive rate of urinary protein of survival patients was high in the early intoxication (76.9%). CONCLUSION: Serum Cys C is sensitive indicator to reveal the kidney injury on paraquat poisoning patients and have higher value of clinical applications in the diagnosis of the kidney injury of paraquat poisoning, which sensitivity is higher than serum BUN and Cr. The kidney injury caused by paraquat poisoning is reversible.

[Changes of serum cytokine caused by acute paraquat poisoning].

OBJECTIVE: To observe the change of cytokine interleukin IL-1 beta, IL-6, IL-10, tumor necrosis factor-alpha (TNF-alpha) occurred in acute paraquat (PQ) poisoning rats and to investigate the mechanism of acute lung injury caused by paraquat (PQ) poisoning. METHODS: All 72 healthy adult Wistar rats were random assigned into normal control groups, paraquat high dose group (120 mg/kg), paraquat middle dose (60 mg/kg) group, paraquat low dose group (30 mg/kg). Three observing periods of time included 8, 24, 72 h and the standards of TNF-alpha, IL-1 beta, IL-6, IL-10 were determined. RESULTS: Every index of the PQ group was significantly higher than that in the NS group at the same period of time (P<0.05 or P<0.01). In the 72 h group, the high dose group was significantly higher than the middle and low dose group (P<0.05), and there was no significantly difference between the middle and low dose group (P>0.05). For the comparison of index in the same dose group, the group of 72 h was much higher than 8 h group and 24 h group (P<0.05), and there was no difference between the 8h group and 24 h group (P>0.05). CONCLUSION: The cytokine may play an important role in paraquat-induced acute lung tissue injury.