Original article / research
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2026 |
Month :
January
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15 |
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BO01 - BO06 |
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Spectrum of Biochemical Presentations in Patients with Paraquat Poisoning at a Tertiary Care Hospital in West Bengal, India: A Retrospective Cohort Study
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Ashis Kumar Saha, Ankan Pathak, Prasun Chatterjee
1. Professor and Head, Department of Medicine, Jagannath Gupta Institute of Medical Sciences and Hospital, Kolkata, West Bengal, India.
2. Assistant Professor, Department of Medicine, Jagannath Gupta Institute of Medical Sciences and Hospital, Kolkata, West Bengal, India.
3. Assistant Professor, Department of Medicine, Jagannath Gupta Institute of Medical Sciences and Hospital, Kolkata, West Bengal, India.
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Correspondence
Address :
Ashis Kumar Saha,
P5, Block B, Lake Town, Kolkata, West Bengal, India.
E-mail: asissaha2008@gmail.com
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| | | ABSTRACT |  | : Introduction: Paraquat has been one of the most widely used herbicides in developing countries, particularly in Asia, and is notorious for its extremely high fatality rate due to multi-organ toxicity. In India, most available data are limited to small series or case reports, with very little systematic evidence emerging from Eastern India. Understanding the biochemical spectrum of paraquat poisoning is therefore crucial for guiding early diagnosis, management, and prevention strategies in this vulnerable population.
Aim: To analyse the biochemical spectrum of organ dysfunction in patients with paraquat poisoning admitted to a tertiary care hospital in Eastern India.
Materials and Methods: A retrospective cohort study was conducted at Jagannath Gupta Institute of Medical Sciences and Hospital, West Bengal, India, from November 2023 to July 2025. Twenty-five patients aged 19-45 years with intentional paraquat ingestion were included. Data on demographics, ingested doses of the poison, and liver and renal function tests were collected from the patients. Renal impairments were assessed by measuring serum creatinine at the time of admission and 48 hours later. Hepatic injuries were evaluated using Aspartate Aminotransferase (AST), Alanine Aminotransferase (ALT), and bilirubin levels. Pulse oximetry was performed to measure oxygen saturation. Statistical analysis was conducted using Pearson’s correlation coefficient and p-values.
Results: Most patients (14, 56%) were female, and 21 patients (84%) were aged 20-40 years. Twenty patients (80%) consumed more than 40 grams of paraquat, and 88% presented within six hours of ingestion. Serum creatinine showed a strong positive correlation with the ingested dose at admission (r=0.93) and at 48 hours (r=0.92). Oxygen saturation (SpO2) levels demonstrated a strong negative correlation with the ingested dose (r=-0.91). Correlations of liver enzymes with the ingested dose were weak and non-significant. Male patients had significantly higher creatinine levels.
Conclusion: Paraquat poisoning causes severe renal and moderate hepatic dysfunction, with a high mortality rate. Early intervention is critical, although haemodialysis did not halt renal deterioration. The present study provides region-specific biochemical insights from Eastern India. |
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| Keywords
: Liver dysfunction, Renal failure, Respiratory dysfunction |
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| DOI and Others
: DOI: 10.7860/NJLM/2026/82493.2950
Date of Submission: Aug 04, 2025
Date of Peer Review: Sep 07, 2025
Date of Acceptance: Oct 27, 2025
Date of Publishing: Jan 01, 2026
AUTHOR DECLARATION:
• Financial or Other Competing Interests: None
• Was Ethics Committee Approval obtained for this study? Yes
• Was informed consent obtained from the subjects involved in the study? Yes
• For any images presented appropriate consent has been obtained from the subjects. Yes
PLAGIARISM CHECKING METHODS:
• Plagiarism X-checker: Aug 13, 2025
• Manual Googling: Oct 16, 2025
• iThenticate Software: Oct 25, 2025 (8%)
ETYMOLOGY: Author Origin
EMENDATIONS: 8 |
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INTRODUCTION |
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Paraquat has been one of the most commonly used herbicides in agriculture since 1955, particularly in developing countries such as Thailand (1),(2). In Thailand, the most common cause of acute poisoning is pesticides, followed by herbicides among which glyphosate and paraquat are predominant (3). In Asia-Pacific countries, self-poisoning with paraquat is a leading cause of mortality and morbidity (4),(5).
In India, paraquat poisoning is reported less frequently than pesticide (organophosphate) poisoning; however, it remains an emerging public health concern. Most available literature comprises small case series from Southern India with high case fatality rates, while systematic data from Eastern India are scarce highlighting the need for region-specific studies (6).
Paraquat generates reactive oxygen species through redox cycling, leading to disruption of the mitochondrial electron transport chain. This results in mitochondrial damage, lipid peroxidation, and cellular toxicity involving multiple organs such as the gastrointestinal tract, kidneys, liver, and others (1),(3),(5),(6). Paraquat can be absorbed through the gastrointestinal tract, skin, and inhalation. It has a large volume of distribution (1.2-1.6 L/kg), accumulating mainly in the lungs, kidneys, and liver. Its half-life is approximately 84 hours, and it is excreted through urine (3),(7).
It is a highly toxic compound with a case fatality rate of up to 80%, primarily due to the absence of a specific antidote (8). Ingestion of less than 20 mg/kg causes mild symptoms, while doses exceeding 40 mg/kg can lead to acute multiorgan failure and death within a few hours to days. Ingestion of 20-40 mg/kg typically results in mucosal injury followed by progressive organ failure (9),(10),(11),(12). The highest tissue concentration is found in the lungs (13). Since the first reported case of paraquat poisoning, several studies have been conducted to explore its mechanisms and evaluate combination therapies aimed at modifying its toxicokinetics- either by enhancing elimination or reducing absorption (14),(15),(16).
With the exception of a few large studies from India, there is currently no published literature on paraquat poisoning from Eastern India, and most available data consist of isolated case reports (17),(18).
Therefore, the present study was planned to analyse the biochemical spectrum of organ dysfunction in patients with paraquat poisoning admitted to a tertiary care hospital in Eastern India.
Study Objectives
Renal dysfunction: To assess kidney involvement by monitoring serum creatinine at admission and after 48 hours.
Hepatic dysfunction: To evaluate liver injury through AST, ALT, and bilirubin levels.
Pulmonary dysfunction: To assess lung involvement using pulse oximetry (SpO2).
Dose correlation: To determine the correlation between the ingested dose of paraquat and biochemical derangements.
Sex predilection: To identify any sex-based differences in biochemical presentation.
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Material and Methods |
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This retrospective cohort study was conducted at Jagannath Gupta Institute of Medical Sciences and Hospital, Budge Budge, West Bengal, India, over a period of one year and nine months (November 2023 to July 2025) among patients admitted with intentional paraquat poisoning. The study was approved by the Institutional Ethics Committee (IEC approval no. JIMSH/IEC/2023/11).
Inclusion and Exclusion criteria: Patients aged between 19 and 45 years with a confirmed history of intentional paraquat ingestion were included. Cases with accidental exposure, uncertain diagnosis, or incomplete medical records were excluded.
A total of 25 patients fulfilling the eligibility criteria during the study period were included by complete enumeration, as paraquat poisoning cases are relatively uncommon. No formal sample size calculation was performed due to the retrospective nature of the study.
Study Procedure
An anonymised proforma was used to collect demographic and clinical details, including the dose of paraquat ingested and time to hospital admission.
• Renal involvement was assessed using serum creatinine values at admission and after 48 hours.
• Hepatic dysfunction was evaluated through AST, ALT, and bilirubin levels.
• Pulmonary function was assessed using pulse oximetry (SpO2).
All data were retrieved from medical records and analysed using the Pearson correlation coefficient and p-values to determine associations between the ingested dose and biochemical derangements.
Statistical Analysis
Data analysis was performed using the Statistical Package for the Social Sciences (SPSS) version 31. Results were presented in graphs and tables for clarity. The Pearson correlation coefficient (r) was used to evaluate associations between the ingested dose and biochemical parameters. A p-value <0.05 was considered statistically significant.
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Results |
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The (Table/Fig 1) demonstrates that the majority of patients, 21 (84%), were between 20 and 40 years of age, reflecting the vulnerability of young adults to intentional paraquat ingestion. Females constituted a slight majority (56%), suggesting possible gender-related psychosocial factors in this region. Most patients (80%) consumed more than 40 grams of paraquat, and the vast majority (88%) presented within six hours of ingestion indicating both high-dose exposure and relatively early hospital presentation.
Despite early arrival, severe biochemical derangements were observed: nearly all patients (96%) had elevated serum creatinine, over half had markedly raised AST and ALT, and 44% had SpO2 <80%, indicating significant renal, hepatic, and pulmonary involvement at admission. All patients succumbed within seven days of hospitalisation.
The (Table/Fig 2) demonstrates serum creatinine at admission and after 48 hours was significantly higher in males than females (p=0.04 and p=0.012, respectively). The ingested dose of paraquat was also significantly higher in males (p=0.03), suggesting more rapid and severe acute kidney injury due to higher ingestion doses.
In (Table/Fig 3) the correlation analysis demonstrated a very strong positive correlation between the ingested dose of paraquat and serum creatinine levels, both at admission (r=0.93, p<0.001) and after 48 hours (r=0.92, p<0.001), indicating dose-dependent renal dysfunction.
In contrast, hepatic enzymes (ALT and AST) showed weak and statistically non-significant correlations with the ingested dose, suggesting that hepatic involvement was variable and less directly dose-related. A strong negative correlation was observed between the ingested dose and SpO2 (r=-0.91, p<0.0001), highlighting the severe pulmonary compromise associated with higher doses.
The (Table/Fig 4) demonstrates that the correlation coefficient was 0.94 (p<0.0001), indicating a strong positive correlation between initial serum creatinine and 48-hour values. This suggests progressive renal damage despite haemodialysis.
The (Table/Fig 5) demonstrates the correlation coefficient was 0.47 (p<0.05), suggesting a moderate and statistically significant positive correlation between serum bilirubin and ALT levels.
The (Table/Fig 6) demonstrates that the correlation coefficient was 0.20 (p>0.05), indicating a weak and non-significant positive correlation between serum AST and bilirubin levels.
The (Table/Fig 7) demonstrates that the correlation coefficient was 0.76 (p<0.0001), showing a strong positive correlation between delay in hospital admission and duration of survival after admission. This may be explained by lower ingestion doses in patients who presented later, resulting in relatively prolonged survival.
The (Table/Fig 8) demonstrates that the correlation coefficient was 0.03 (p>0.05), indicating no significant correlation between the ingested dose and survival duration, suggesting that dose alone did not determine survival time.
The (Table/Fig 9) demonstrates that the correlation coefficient was 0.42 (p<0.001), indicating a moderately positive relationship between patient age and serum creatinine at admission.
The (Table/Fig 10) demonstrates that the correlation coefficient was -0.91 (p<0.0001), demonstrating a strong negative correlation between the ingested dose and SpO2 level- indicating that as the ingested dose increased, oxygen saturation decreased.
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Discussion |
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In the present retrospective cohort study from Eastern India, a dose-dependent and strong rise in serum creatinine was observed at admission and at 48 hours, indicating persistent paraquat-associated renal injury despite haemodialysis. A strong inverse correlation between the ingested dose and SpO2 reflected pulmonary compromise, while hepatic enzyme changes showed weak or variable associations. Female predominance and 100% fatality were notable findings. Collectively, these data identify renal dysfunction as the most consistent biochemical hallmark, with pulmonary involvement closely tracking the ingested dose, while hepatic injury appears idiosyncratic and less dose-related.
Paraquat toxicity is driven by redox cycling and Reactive Oxygen Species (ROS) generation, leading to mitochondrial damage and lipid peroxidation. These mechanisms cause multiorgan injury- particularly in the lungs, kidneys, and liver- which aligns with the organ-specific patterns observed in this study (1),(3),(5),(7). Its absorption, distribution, and prolonged elimination kinetics (predominantly involving the lung, kidney, and liver, with a long half-life) explain the progressive tissue injury despite supportive care (3),(7). The high case fatality rate observed in this cohort is consistent with previous studies, underscoring the absence of a specific antidote and the narrow margin between exposure and multiorgan failure (7),(8),(9),(10),(11),(12),(13).
In contrast to earlier Indian studies most of which were limited to small case series, apart from the larger cohorts of Rao R et al., and Ravichandran R et al., (n=55), the present study uniquely provides region-specific biochemical correlation data from Eastern India, based on 25 systematically analysed cases (17),(18). Comparable studies are summarised in (Table/Fig 11) (6),(17),(18),(19),(20),(21),(22),(23),(24). The female predominance noted here contrasts with the male-skewed cohorts reported from southern India, although the age distribution (20-40 years) mirrors previously identified high-risk groups (18). Reported mortality rates from paraquat poisoning vary widely from 22-55% in some studies to as high as 92% in others (17),(21). The findings in the present study lie at the more severe end of this spectrum, highlighting the extreme lethality of paraquat.
The present study also demonstrated that higher ingested doses were associated with elevated serum creatinine and lower oxygen saturation, showing a clear dose-response relationship. These observations corroborate earlier toxicological studies by Kim HJ et al., (7) and the clinical prognostic analyses by Gawarammana IB and Buckley NA (5).
The observation that serum creatinine worsened despite haemodialysis aligns with heterogeneous outcomes reported in the literature on extracorporeal interventions (17). A multicentre study by Yeh YT et al., suggested that haemoperfusion may improve overall survival (25); however, timely initiation appears crucial, with earlier intervention associated with better outcomes (17),(24). The continued renal deterioration in this cohort suggests that delayed or suboptimal timing of haemodialysis is unlikely to reverse established tubular injury.
Adjunctive pharmacologic therapies- such as pulse cyclophosphamide with corticosteroids or antioxidant regimens- have shown variable or context-dependent benefits and require further validation before routine use (11),(16),(26),(27),(28). Operationally, the findings emphasise that ultra-early triage, risk stratification based on ingested dose, and prompt initiation of dialysis or haemoperfusion may improve outcomes in real-world settings (27),(29).
The weak and inconsistent hepatic correlations (ALT/AST/bilirubin vs dose) suggest that hepatic injury is heterogeneous and less dose-deterministic than renal or pulmonary damage. This is consistent with prior reports describing a wide spectrum of hepatic responses from transient enzyme elevations to toxic hepatitis (2),(9),(10),(11). Clinically, this implies that renal and respiratory parameters should serve as the primary indicators for early prognostication, while liver function tests should be interpreted in context rather than as principal severity markers.
For clinicians, the ingested dose at presentation, creatinine trajectory (0-48 hours), and SpO2 trends should guide urgent triage and management decisions. For researchers, these findings underscore the need for prospective studies evaluating time-to-haemoperfusion, standardised antioxidant and immunosuppressive protocols, and the development of practical prognostic tools integrating dose with early renal- pulmonary indices. From a public health perspective, preventive measures and restricted access to paraquat remain critical in rural settings, where intentional self-poisoning is a persistent problem (4),(5).
Limitation(s)
The limitations of this study include a small sample size, retrospective design, and the absence of multivariable adjustment. The initiation and modality of extracorporeal therapies were not standardised, limiting causal inference regarding the efficacy of haemodialysis or haemoperfusion. These limitations highlight the need for prospective, multicentre studies incorporating time-stamped treatment data and adjusted analyses (for age, sex, delay to admission, and ingested dose).
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Conclusion |
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This study from Eastern India demonstrates that paraquat poisoning causes severe renal impairment that correlates strongly with ingested dose, persists despite haemodialysis, and represents the most reliable biochemical predictor of outcome. Pulmonary involvement, reflected by decreasing SpO2, also showed a strong dose-dependent relationship, whereas hepatic dysfunction was less consistent and variable. The young age profile and female predominance underscore the socio-demographic vulnerability of affected rural populations.
These findings suggest that early assessment of ingested dose, along with close renal and pulmonary monitoring, is essential for prognosis. Delayed or non-optimised haemodialysis alone is unlikely to alter disease progression. The extremely high fatality rate observed underscores the urgent need for early triage, preventive strategies, and further evaluation of alternative therapies such as haemoperfusion and antioxidant-immunosuppressive combinations.
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