Cleistanthus collinus poisoning: experience at a medical intensive care unit in a tertiary care hospital in south India.

Background & objectives: Ingestion of Cleistanthus collinus causes hypokalemia and cardiac arrhythmias leading to mortality in most cases. We undertook this retrospective study to evaluate the clinical presentation and predictors of outcome in critically ill patients admitted with C. collinus poisoning. Methods: The case records of 56 patients admitted to the medical intensive care unit (MICU) of a tertiary care teaching hospital in south India (2000-2014) with C. collinus poisoning were retrospectively analysed. Results: The mean age of patients was 36.7±13.3 yr; there were 30 males. Salient clinical manifestations included hypokalemia (58%), neutrophilic leucocytosis (48.2%), acute kidney injury (AKI) (42.9%), acute respiratory failure requiring mechanical ventilation (AcRFMv) (32.1%), shock (21.4%); cardiac arrhythmias and neuromuscular weakness (19.6% each); 21 patients (37.5%) had adverse outcome. Longer time-lapsed from consumption to reaching emergency room [median (interquartile range)] (hours) [49 (22-97) vs. 28 (7-56), P=0.038]; higher acute physiology and chronic health evaluation II (APACHE II) score at presentation [14 (8.25-14.75) vs. 2 (0-6) P<0.001]; and presence of the following [odds ratio (95% confidence intervals)] at initial presentation: shock [37.40 (4.29-325.98), P=0.001]; AcRFMv [26.67 (5.86-121.39), P<0.001]; elevated alanine aminotransferase [5.71 (1.30-25.03), P=0.021]; metabolic acidosis [5.48 (1.68-17.89), P=0.005]; acute kidney injury (AKI) [5 (1.55-16.06), P=0.007]; hyponatremia [4.67 (1.25-17.44), P=0.022]; and neutrophilic leucocytosis [3.80 (1.02-14.21), P=0.047] predicted death. A significant (P<0.001) increasing trend in mortality was observed with increasing International Program on Chemical Safety Poisoning Severity Score (IPCS-CSS) grade. Interpretation & conclusions: C. collinus is a lethal poison associated with high mortality for which there is no specific antidote. Careful search and meticulous monitoring of the predictors of death and initiating appropriate corrective measures can be life saving.

Alpha-adrenergic receptor blocking effect of Cleistanthus collinus (Roxb.) Benth. and Hook f. leaf extract on guinea pig isolated smooth muscle preparations.

Aqueous extract of C. collinus leaves inhibited norepinephrine induced contraction in guinea pig vas deferens and aortic strip in a dose-dependent manner. Inhibition of acetylcholine induced contraction in ileum was dose independent. C. collinus extract per se had no effect on isolated guinea pig vas deferens and aortic strip, but inhibited norepinephrine induced contraction in a dose-dependent manner probably by its antagonist action on α-adrenergic receptor. It had inconsistent effect on guinea pig ileum in vitro preparation.

Role of melatonin against oxidative tissue damage induced by Cleistanthus collinus in rat brain.

Background & objectives: The leaves of Cleistanthus collinus, an extremely poisonous plant are consumed for suicidal purposes in various parts of India. The mortality rate is high and there is no antidote. In this study, we attempted to delineate oxidative stress as a possible mechanism of action of C. collinus toxicity in rats and the role of melatonin against injury to brain and heart caused by C. collinus. Methods: Adult Wistar rats (130 -200 g, n = 6 per group) of either sex were used. C. collinus at 8 mg/kg body weight (LD50) was administered orally followed by melatonin 15 mg/kg body weight ip or cysteine 500 mg/kg body weight ip (standard) after 2 h. Malondialdehyde (MDA), reduced glutathione (GSH), glutathione peroxidase and catalase levels in brain, heart and blood were estimated and histopathological examinations (brain and heart) were done. For the survival study, rats were treated with increasing doses of melatonin (5, 10 and 15 mg/kg body weight ip) following a lethal dose of C. collinus (10.5 g/kg body weight orally). Results: The results showed a significant (P<0.05) increase in blood and brain MDA levels and decrease in tissue GSH in the LD50 group. This was accompanied by marked gliosis, spongiform necrosis and lymphocytic inflammatory infiltrates in brain and marked congestion, inflammation and muscle necrosis in heart. Melatonin significantly (P<0.05) reduced lipid peroxidation and reversed the histopathological changes induced by C. collinus in the brain but not in the heart. Interpretation & conclusion: Our results suggest that oxidative mechanisms play an important role in C. collinus induced tissue damage and melatonin, by balancing oxidant-antioxidant status ameliorates oxidative organ injury in brain due to C. collinus toxicity.