Liver injury in paraquat poisoning: A retrospective cohort study.

BACKGROUND AND AIMS: Liver injury is one of the common complications of paraquat (PQ) poisoning, but whether the degree of liver injury is related to patient prognosis is still controversial. This study aimed to investigate whether liver injury was a risk factor for death in PQ-poisoned patients. METHODS: We conducted a retrospective cohort study of PQ-poisoned patients from the past 10 years (2011-2020) from a large tertiary academic medical centre in China. PQ-poisoned patients were divided into a normal liver function group (n = 580) and a liver injury group (n = 60). Propensity score matching (PSM) analysis was then performed. RESULTS: A total of 640 patients with PQ poisoning were included in this study. To reduce the impact of bias, dose of PQ, urinary PQ concentration and time from poisoning to hospital admission were matched between the two groups. A 3:1 PSM analysis was performed, ultimately including 240 patients. Compared with the normal liver function group, patients in the liver injury group were older, had a higher R value ([ALT/ULN]/[ALP/ULN]) (p < .001) and had a higher mortality rate. Cox regression analysis showed that there was no significant association between alanine aminotransferase, alkaline phosphatase, total bilirubin levels and hazard of death, but age, PQ dose, creatine kinase isoenzyme, creatine kinase, white blood cell count, neutrophil percentage and lymphocyte percentage were associated with mortality in patients with PQ poisoning. CONCLUSIONS: The occurrence of liver injury within 48 h after PQ poisoning was a risk factor for mortality, and such liver injury was likely of a hepatocellular nature. Age, PQ dose, creatine kinase isoenzyme and white blood cell count were positively correlated with mortality, while creatine kinase, percentage of neutrophils and lymphocytes were inversely correlated.

Mesenchymal stem cell-based therapy for paraquat-induced lung injury.

Paraquat poisoning results in significant pulmonary damage, but current treatments are only minimally effective in repairing the injured lung tissues. Recent research has highlighted the promise of using stem cell therapy, namely mesenchymal stem cells, as a new method for treating paraquat toxicity. These cells have shown effectiveness in decreasing inflammation, apoptosis, and fibrosis in the mice lungs subjected to paraquat. The therapeutic implications of mesenchymal stem cells are believed to arise from their release of bioactive proteins and their capacity to regulate inflammatory responses. However, additional clinical study is required to validate these therapies' efficacy. This review thoroughly explores the pathophysiology of paraquat poisoning and the properties of mesenchymal stem cells. Additionally, it critically assesses the long-term safety and effectiveness of mesenchymal stem cell therapies, which is crucial for developing more dependable and effective treatment protocols. In summary, although mesenchymal stem cells offer promising prospects for treating lung injuries, more investigations are required to optimize their therapeutic promise and ensure their safe clinical application in the context of paraquat poisoning.

Analysis of abnormal expression of signaling pathways in PQ-induced acute lung injury in SD rats based on RNA-seq technology.

Background: Paraquat (PQ) plays an important role in agricultural production due to its highly effective herbicidal effect. However, it has led to multiple organ failure in those who have been poisoned, with damage most notable in the lungs and ultimately leading to death. Because of little research has been performed at the genetic level, and therefore, the specific genetic changes caused by PQ exposure are unclear.Methods: Paraquat poisoning model was constructed in Sprague Dawley (SD) rats, and SD rats were randomly divided into Control group, paraquat (PQ) poisoning group and Anthrahydroquinone-2,6-disulfonate (AH2QDS) treatment group. Then, the data was screened and quality controlled, compared with reference genes, optimized gene structure, enriched at the gene expression level, and finally, signal pathways with significantly different gene enrichment were screened.Results: This review reports on lung tissues from paraquat-intoxicated Sprague Dawley (SD) rats that were subjected to RNA-seq, the differentially expressed genes were mainly enriched in PI3K-AKT, cGMP-PKG, MAPK, Focal adhesion and other signaling pathways.Conclusion: The signaling pathways enriched with these differentially expressed genes are summarized, and the important mechanisms mediated through these pathways in acute lung injury during paraquat poisoning are outlined to identify important targets for AH2QDS treatment of acute lung injury due to paraquat exposure, information that will be used to support a subsequent in-depth study on the mechanism of PQ action.

Management of Paraquat Poisoning-The Way Forward.

How to cite this article: Ahmed A, Prasad A, Bhattacharjee A. Management of Paraquat Poisoning-The Way Forward. Indian J Crit Care Med 2024;28(8):722-723.

Utility of Clinical Variables for Deciding Palliative Care in Paraquat Poisoning: A Retrospective Study.

Background: Patients with paraquat poisoning (PP) have a mortality rate comparable to that of advanced malignancies, yet palliative care is seldom considered in these patients. This audit aimed to identify triggers for early palliative care referral in critically ill patients with PP. Methods: Medical records of patients with PP were audited. Predictors of mortality within 48 hours of hospitalization and 24 hours of intensive care unit (ICU) admission were considered as triggers for palliative care referral. Results: Among 108 patients, 84 complete records were analyzed, and 53 out of 84 (63.1%) expired. Within 48 hours after hospitalization, the lowest oxygen partial pressure in arterial blood to a fraction of inspired oxygen [the ratio of partial pressure of oxygen in arterial blood (PaO2) to the fraction of inspiratory oxygen concentration (FiO2) (PaO2/FiO2)] was the independent predictor of mortality, cut-off ≤ 197; the area under the curve (AUC), 0.924; sensitivity, 97%; specificity, 78%; p <0.001; and 95% confidence interval (CI): 0.878-0.978. Kaplan-Meier survival plot showed that the mean survival time of patients with the lowest PaO2/FiO2, ≤197, was 4.64 days vs 17.20 days with PaO2/FiO2 >197 (log-rank p < 0.001). Sequential organ failure assessment (SOFA) score within 24 hours of ICU admission had a cut-off ≥9; AUC, 0.980; p < 0.001; 95% CI: 0.955-1.000; 91% sensitivity; and 90% specificity for mortality prediction. Out of the total of 84 patients with PP analyzed, there were 11 patients admitted to the high dependency units (13.1%) and 73 patients admitted to the ICU (86.9%). Out of the total of 84 patients of PP in whom data was analyzed, 53 (63.1%) patients required ventilator support. All the 53 patients who required ventilator support due to worsening hypoxemia, eventually expired. Conclusion: The lowest PaO2/FiO2 ≤ 197 within 48 hours of hospitalization, SOFA score ≥9 within 24 hours of ICU admission or need for mechanical ventilation are predictors of mortality in PP patients, who might benefit from early palliative care. How to cite this article: Rao S, Maddani SS, Chaudhuri S, Bhatt MT, Karanth S, Damani A, et al. Utility of Clinical Variables for Deciding Palliative Care in Paraquat Poisoning: A Retrospective Study. Indian J Crit Care Med 2024;28(5):453-460.

Factors associated with refusing hemoperfusion in patients with acute paraquat poisoning.

Background: Paraquat poisoning remains a critical public health issue with no established effective treatment. Hemoperfusion (HP) has been recognized for its potential to remove toxins and is widely employed in several developing countries for managing acute paraquat poisoning cases. However, the reluctance of some patients to undergo this recommended treatment has been observed but not thoroughly investigated. This study aimed to explore the factors associated with the refusal of HP in patients suffering from paraquat intoxication. Materials and Methods: In this retrospective study, data of 358 patients with acute paraquat poisoning were analyzed in Xi'an, China. The outcome of our study was mortality, and the influential factors were age, gender, marital status, educational level, symptoms at presentation, and laboratory findings. A logistic regression model was utilized to explore the independent risk factors. Results: In a total of 358 paraquat-poisoned patients, the significant differences were found between patients who underwent HP and those who did not, particularly regarding mean age (48.02 years vs. 42.32 years; P = 0.01), mental disorders (15.6% vs. 6.1%; P = 0.01), poisoning severity score (2.36 vs. 2.57; P = 0.03), organ failure (10.9% vs. 23.5%; P = 0.02), and mechanical ventilation (18.8% vs. 33.3%; P = 0.02). Patients who refused HP exhibited a higher mortality (20.3% vs. 10.9%; P = 0.03) compared to those who received HP. Age (odds ratio (OR), 1.76; 95% confidence interval (CI): 1.01-3.82; P = 0.01) and history of mental disorders (OR, 2.81; 95% CI: 1.19-6.61; P = 0.02) were identified as significant independent predictors for the refusal of HP. Conclusion: The results of this study showed that elderly individuals and those with a history of mental disorders were independently associated with refusing HP in patients with acute paraquat poisoning.

2-Methoxyestradiol ameliorates paraquat-induced pulmonary fibrosis by inhibiting the TGF-ß1/Smad2/3 signaling pathway.

Paraquat (PQ) is a highly effective and highly toxic herbicide that is highly toxic to both humans and animals. Pulmonary fibrosis is the primary cause of fatality in patients with PQ poisoning, there is no effective drug treatment yet. 2-Methoxyestradiol (2ME) is a natural metabolite of estradiol with anti-tumor, anti-angiogenesis, and anti-proliferative effects. Whether 2ME has the potential to inhibit pulmonary fibrosis induced by PQ is unclear. This study aims to investigate the potential effects and mechanism of 2ME on PQ-induced pulmonary fibrosis. C57BL/6 mice and A549 cells were exposed to PQ to establish pulmonary fibrosis model. In vivo, Hematoxylin and eosin (H&E) staining was utilized to assess the pathological characteristics. Masson's trichrome staining was employed to evaluate the collagen deposition. Western blot and immunohistochemistry were conducted to determine the expressions of fibrosis markers. In vitro, the expressions of epithelial-mesenchymal transition (EMT) markers were detected using western blot and immunofluorescence to evaluated the potential inhibition of PQ-induced EMT by 2ME. And proteins associated with the TGF-ß1/Smad2/3 signaling pathway were measured by western blot in vivo and in vitro. The result found that 2ME can ameliorated PQ-induced pulmonary fibrosis and inhibit the activation of TGF-ß1/Smad2/3 signaling pathway. These findings suggest that 2ME may serve as a potential therapeutic agent for treating PQ-induced pulmonary fibrosis.

Paraquat Poisoning: A Retrospective Study of 55 Patients From a Tertiary Care Center in Southern India.

BACKGROUND: In India the data on paraquat (PQ) poisoning are limited to case reports and small case series. Hence, this study was carried out to understand the clinical features and outcomes of PQ poisoning. We also briefly report the relevant Indian studies on PQ poisoning. MATERIALS AND METHODS: This was a retrospective case record-based study of PQ poisoning victims admitted over a period of 5 years. RESULTS: Of the 55 patients included in this study, the in-hospital mortality rate was 72.7%. Acute kidney injury was the most common manifestation. The use of cyclophosphamide did not affect the clinical outcome. Hemoperfusion (HP) was not done for any patient. Pulmonary edema and acute tubular necrosis were the most common histopathological findings. CONCLUSION: In India, this is one of the most comprehensive studies of PQ toxicity. Hence, we hope that this information would be of use to clinicians who deal with PQ poisoning. HOW TO CITE THIS ARTICLE: Ravichandran R, Amalnath D, Shaha KK, Srinivas BH. Paraquat Poisoning: A Retrospective Study of 55 Patients from a Tertiary Care Center in Southern India. Indian J Crit Care Med 2020;24(3):155-159.

Efficacy of high-dose ambroxol for paraquat poisoning: A meta-analysis of randomized controlled trials.

BACKGROUND: Paraquat (PQ) poisoning is characterized by rapidly progressive acute poisoning with high mortality and no specific antidote. Although some clinical studies have been conducted to investigate the benefits of high-dose ambroxol as an adjuvant treatment for PQ poisoning, the efficacy is controversial. MATERIALS AND METHODS: After searching for relevant articles in English and Chinese databases from 1978 to 2019 according to the keywords (paraquat poisoning/methy viologen/gramoxone, and ambroxol/mucosolvan/Bromhexine), we found seven articles that met our inclusion and exclusion criteria. A meta-analysis was performed using fixed-effects model and random-effects model according to the I 2 value in Stata software (version 15.0). Four outcome indicators (hospital mortality, partial pressure of oxygen (PaO2), oxygenation index (PaO2/FiO2), and survival time of the deceased patients) were of interest to us. RESULTS: The meta-analysis showed that adjuvant treatment with high doses of ambroxol increased PaO2 (weighted mean difference [WMD] = 13.73 [mmHg], 95% confidence interval [CI]: 8.68-18.79, Z = 11.80, P < 0.001), PaO2/FiO2 (WMD = 38.81 [mmHg], 95% CI: 29.85-47.76, Z = 8.49, P = 0.000), and survival time of the deceased patients (WMD = 2.58 [d], 95% CI: 0.97-4.18, Z = 3.15, P = 0.002) compared with usual treatment. Treatment with high doses of ambroxol also appeared to reduce the hospital mortality (relative risk = 0.69, 95% CI: 0.55-0.86, Z = 3.25, P = 0.001). CONCLUSION: This study found that high-dose ambroxol is an effective therapy for PQ poisoning and may reduce the in-hospital mortality.

[The assessment value of urinary NGAL combined with blood NLR in the early prognosis of patients with acute paraquat poisoning].

Objective: To explore the evaluate of neutrophil gelatinase-associated lipocalin (NGAL) , combined with neutrophil/lymphocyte ratio (NLR) in the early prognosis of patients with acute paraquat poisoning (APP) . Methods: In March 2019, 108 APP patients admitted to Emergency Medicine Department of Hebei Medical University from January 2017 to December 2018 were selected as the observation group, 60 healthy people in the same period were see as the control group according to the results of diagnosis and 28-day survival, the observation group was divided into 51 death group and 57 survival group. The correlation between NGAL, NLR and the death of APP patients was analyzed, to explore the value of NGAL and NLR in predicting the death of APP patients. Results: Compared with the Control group, the NGAL and NLR in the observation group were significantly higher (P<0.01) , and the NGAL and NLR in the death group were significantly higher (P<0.05) . The results showed that NGAL and NLR were positively correlated with the death of APP patients on 28th day, and the Correlation Coefficient was 0.456 and 0.638 at 2nd Day (P<0.01) The area under the ROC curve of NGAL, NLR and their combination were 0.764, 0.869 and 0.905, respectively. Conclusion: The combined detection of NGAL and NLR has important clinical significance in the early prediction of 28-day mortality in APP patients.

Ameliorative role of aspirin in paraquat-induced lung toxicity via mitochondrial mechanisms.

Paraquat (PQ) has accounted for numerous suicide attempts in developing countries. Aspirin (ASA) as an adjuvant treatment in PQ poisoning has an ameliorative role. And, it's uncoupling of mitochondrial oxidative phosphorylation role has been well established. The current study aimed at examining the aspirin mechanism on lung mitochondria of rats exposed to PQ. Male rats were randomly allocated in five groups: Control group, PQ group (50 mg/kg; orally, only on the first day), and PQ + ASA (100, 200, and 400 mg/kg; i.p.) groups for 3 weeks. Mitochondrial indices and respiratory chain-complex activities were determined. PQ induced lung interstitial fibrosis; however, ASA (400 mg/kg) led to decrease in this abnormal alteration. In comparison with PQ group, complex II and IV activity, and adenosine triphosphate content in ASA groups had significantly increased; however, reactive oxygen species production, mitochondrial membrane permeabilization, and mitochondrial swelling were significantly reduced. In conclusion, aspirin can alleviate lung injury induced by PQ poisoning by improving mitochondrial dynamics.

Possible involvement of transcriptional activation of nuclear factor erythroid 2-related factor 2 (Nrf2) in the protective effect of caffeic acid on paraquat-induced oxidative damage in Drosophila melanogaster.

Paraquat (PQ) is a widely used herbicide with no antidote which is implicated in the pathogenesis of the Parkinson's disease. The present study then investigated the potential of caffeic acid (CA), a known antioxidant, cardioprotective and neuroprotective molecule to counteract oxidative stress mediated by PQ. In addition, molecular docking was performed to understand the mechanism underlying the inhibitory effect of CA against PQ poisoning. The fruit fly, Drosophila melanogaster, was exposed to PQ (0.44 mg/g of diet) in the absence or presence of CA (0.25, 0.5, 1 and 2 mg/g of died) for 7 days. Data showed that PQ-fed flies had higher incidence of mortality which was associated with mitochondrial dysfunction, increased free Fe(II) content and lipid peroxidation when compared to the control. Co-exposure with CA reduced mortality and markedly attenuated biochemical changes induced by PQ. The mechanism investigated using molecular docking revealed a strong interaction (-6.2 Kcal/mol) of CA with D. melanogaster transcriptional activation of nuclear factor erythroid 2-related factor 2 (Nrf2). This was characterized by the binding of CA to keap-1 domain of Nrf2. Taking together these results indicate the protective effect of CA against PQ-induced oxidative damage in D. melanogaster was likely through its coordination which hinders Nrf2-keap-1 binding leading to an increase of the antioxidant defense system.

Review of a Case of Paraquat Poisoning in a Tertiary Care Rural-based ICU.

Paraquat (1,1'-dimethyl-4, 4'-dipyridylium) is a broad-spectrum liquid herbicide associated with both accidental and intentional ingestion leading to severe and often fatal toxicity.1 Paraquat is actively taken up against a concentration gradient into lung tissue leading to pneumonitis and lung fibrosis. Paraquat also causes renal and liver injury.2 There are few case publications of paraquat poisoning and only few of them have reported that renal failure has ensued before acute respiratory distress syndrome (ARDS). Our patient presented with above lethal dose intake of paraquat containing substance and we did gastric lavage followed by charcoal hemoperfusion and hemodialysis but patient could not be saved despite optimum efforts suggesting the high fatality of this kind of poisoning. HOW TO CITE THIS ARTICLE: Sharma DS, Prajapati AM, Shah DM. Review of a Case of Paraquat Poisoning in a Tertiary Care Rural-based ICU. Indian J Crit Care Med 2019;23(6):284-286. KEY MESSAGES: Acute renal injury with hypoperfusion state due to toxicity at cellular level, redox cycling and intracellular reactive oxidative stress generation may also cause death in early stages in paraquat poisoning despite optimal management.

[Clinical analysis of lower limb thrombosis caused by paraquat poisoning].

Objective: To investigate the causes of peripheral vascular thrombosis in patients with paraquat poisoning. Methods: The patients with paraquat poisoning who were admitted to our department in recent two years were observed to screen out the patients with large vessel thrombosis. The data on toxic exposure history, clinical features, and treatment were collected to analyze the causes of thrombosis in the patients with paraquat poisoning. Results: Three patients had typical lower limb thrombosis. There was one case of right common femoral vein thrombosis, one case of bilateral calf muscle vein thrombosis, and one case of right calf superficial vein thrombosis and right calf muscle vein thrombosis. Conclusions: After paraquat poisoning, the blood is in a hypercoagulable state and prolonged bed rest may increase the risk of thrombosis.

A positive feedback loop promotes HIF-1α stability through miR-210-mediated suppression of RUNX3 in paraquat-induced EMT.

Irreversible pulmonary fibrosis induced by paraquat (PQ) poisoning is the major cause of death in patients with PQ poisoning. The epithelial-mesenchymal transition (EMT) is postulated to be one of the main mechanisms of pulmonary fibrosis. Here, we investigated the role of miR-210 in PQ-induced EMT and its relationship with hypoxia-inducible factor-1α (HIF-1α). Western blotting, immunofluorescence, immunoprecipitation and other methods were used in this study. We found that miR-210 expression was significantly increased after PQ poisoning, and it may be regulated by HIF-1α. Overexpression of miR-210 further increased the HIF-1α protein level and promoted EMT. Moreover, miR-210 knock-down reduced the HIF-1α protein level and decreased the degree of EMT. Runt-related transcription factor-3 (RUNX3), a direct target of miR-210, was inhibited by miR-210 in response to PQ poisoning. RUNX3 increased the hydroxylation ability of prolyl hydroxylase domain-containing protein 2 (PHD2), a key enzyme that promotes HIF-1α degradation. PHD2 immunoprecipitated with RUNX3 and its level changed similarly to that of RUNX3. The expression of the HIF-1α protein was significantly reduced when RUNX3 was overexpressed. HIF-1α protein levels were markedly increased when RUNX3 was silenced. Based on these results, a positive feedback loop may exist between miR-210 and HIF-1α. The mechanism may function through miR-210-mediated repression of RUNX3, which further decreases the hydroxylation activity of PHD2, enhances the stability of HIF-1α, and promotes PQ-induced EMT, aggravating the progression of pulmonary fibrosis. This study further elucidates the mechanism of PQ-induced pulmonary fibrosis and may provide a new perspective for the future development of therapies.

QTc prolongation as a useful prognostic factor in acute paraquat poisoning.

BACKGROUND: Acute paraquat poisoning has a high mortality rate. Several prognostic factors have been proposed to predict the mortality risk of paraquat-poisoned patients. However, these prognostic factors are complex and some require a laboratory. Corrected QT (QTc) has been used as a prognostic factor in several clinical conditions, such as acute organophosphate poisoning. In addition, the measurement can be obtained in a reasonable amount of time. STUDY OBJECTIVES: This study's objective was to investigate whether QTc can predict mortality in paraquat-poisoned patients. METHODS: This was a retrospective study. Potential prognostic factors such as QTc, vital signs at admission, and certain biochemistry variables were analyzed with Cox regression analyses for their ability to predict a patient's survival from paraquat poisoning. RESULTS: Sixty acute paraquat-poisoned patients were admitted to the emergency department during the study period. The QTc of the survival group ranged from 0.35 to 0.48 s, whereas the nonsurvivor group ranged from 0.32 to 0.63 s. The nonsurvivor group contained a higher percentage of patients with QTc prolongation (≥0.45 s) compared with the survivor group (p = 0.04). The hazard ratio of QTc prolongation for a patient's death was found to be 2.47 (95% confidence interval [CI] 1.68-5.67) in patients with a lower potassium level (<3.2 mEq/L) and 3.71 (95% CI 1.53-8.97) in patients with a higher potassium level (≥3.2 mEq/L). In addition, hyperdynamic circulation was observed upon admission of these poisoned patients. CONCLUSION: QTc prolongation is a useful prognostic factor for predicting death in acute paraquat-poisoned patients. Cardiovascular collapse may occur in some paraquat-poisoned patients. Physicians can use QTc as an indicator of a patient's severity of poisoning and mortality risk.

Construction of prognosis prediction model and visualization system of acute paraquat poisoning based on improved machine learning model.

Objective: This study aims to develop a prognosis prediction model and visualization system for acute paraquat poisoning based on an improved machine learning model. Methods: 101 patients with acute paraquat poisoning admitted to 6 hospitals from March 2020 to March 2022 were selected for this study. After expiry of the treatment period (one year of follow-up for survivors and up to the time of death for deceased patients) and they were categorized into the survival group (n = 37) and death group (n = 64). The biochemical indexes of the patients were analyzed, and a prognosis prediction model was constructed using HHO-XGBoost, an improved machine-learning algorithm. Multivariate logistic analysis was used to verify the value of the self-screening features in the model. Results: Seven features were selected in the HHO-XGBoost model, including oral dose, serum creatinine, alanine aminotransferase (ALT), white blood cell (WBC) count, neutrophil count, urea nitrogen level, and thrombin time. Univariate analysis showed statistically significant differences between these features' survival and death groups (P < 0.05). Multivariate logistic analysis identified four features significantly associated with prognosis- serum creatinine level, oral dose, ALT level, and WBC count - indicating their critical significance in predicting outcomes. Conclusion: The HHO-XGBoost model based on machine learning is precious in constructing a prognosis prediction model and visualization system for acute paraquat poisoning, which can help clinical prognosis prediction of patients with paraquat poisoning.

Integrated untargeted and targeted proteomics to unveil plasma prognostic markers for patients with acute paraquat poisoning: A pilot study.

Paraquat (PQ) is a widely used but strongly toxic herbicide, which can induce multiple organ failure. The overall survival rate of the poisoned patients was only 54.4% due to lack of specific antidotes. Besides, the definite pathogenic mechanism of PQ is still not fully understood. In this pilot study, untargeted and targeted proteomics were integrated to explore the expression characteristics of plasma protein in PQ poisoned patients, and identify the differentially expressed proteins between survivors and non-survivors. A total of 494 plasma proteins were detected, and of which 47 were upregulated and 44 were downregulated in PQ poisoned patients compared to healthy controls. Among them, five differential plasma proteins (S100A9, S100A8, MB, ACTB and RAB11FIP3) were further validated by multiple reaction monitoring (MRM)-based targeted proteomic approach, and three of them (S100A9, S100A8 and ACTB) were confirmed to be correlated with PQ poisoning. Meanwhile, 84 dysregulated plasma proteins were identified in non-survivors compared with survivors. Moreover, targeted proteomic and ROC analysis suggested that ACTB had a good performance in predicting the prognosis of PQ poisoned patients. These findings highlighted the value of label-free and mass spectrometry-based proteomics in screening prognostic biomarkers of PQ poisoning and studying the mechanism of PQ toxicity.

Paraquat induced acute kidney and lung injury with a dramatic response to methylprednisolone: A case report.

Background: Paraquat poisoning is one of the leading causes of fatal poisoning in many parts of the world, especially in agricultural countries. Its high toxicity even in small amounts causes rapid damage to multiple organs, especially the kidneys, lungs, and liver, mainly through free radical-mediated injury. As no specific antidote is yet available, early diagnosis and the importance of supportive therapy are critical parts of management. Some evidence suggests a survival benefit from using immunosuppressive drugs. Case report: This case presentation concerns a 15-year-old boy from a village with a history of herbicide poisoning, later confirmed to be paraquat. Despite supportive therapy her condition continued to deteriorate with features of kidney and lung damage. The patient was then treated with methylprednisolone 500 mg daily for 5 days, along with other supportive care, and has made a remarkable recovery. Conclusions: High efficacy as an herbicide, availability and low cost make paraquat an easy-to-encounter poison for suicidal or accidental use. Its high fatality calls for urgent and effective strategies to save lives. Methylprednisolone may play a role in its treatment.

Diagnostic Dilemma in Fatal Paraquat Poisoning: An Autopsy Case Report.

Paraquat is a highly toxic agent used as an herbicide worldwide. Despite its easy and widespread availability, data regarding cases of paraquat poisoning in India is limited. Diagnosis often becomes difficult without a clear history, owing to its rather nonspecific and varying presentation. In the present case, a 22-year-old man was brought with a history of high-grade fever, sore throat, and oral ulcers for around a week. He was symptomatically treated at multiple hospitals and was worked up for suspected diagnoses like diphtheria and influenza (H1N1). Later during treatment, it was revealed that "Paraxzone" was procured online by the patient himself two weeks before the onset of his symptoms. Thence, the treatment regimen was modified following suspicion of paraquat poisoning. However, the delay in diagnosis led to the worsening his condition, and the patient succumbed to death due to pulmonary and renal complications after 16 days of survival. The postmortem examination, supplemented with histopathological evaluation, supported the diagnosis of paraquat poisoning. Paraquat poisoning can mimic a myriad of clinical conditions. Thorough history taking, a high degree of suspicion, and collaborative work with the investigating agency are of paramount importance while dealing with cases of suspected paraquat poisoning in hospital settings.