Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

BACKGROUND:Ingestion of organophosphorus (OP) insecticides is associated with acute hyperglycaemia. We conducted a prospective study to determine whether glucose dysregulation on admission associated with ingestion of OP insecticides or other pesticides is sustained to hospital discharge or to 3-12 months later. METHODS:We recruited participants to two similar studies performed in parallel in Anuradhapura, Sri Lanka, and Chittagong, Bangladesh, following hospitalisation for OP insecticide, herbicide or other pesticide self-poisoning. Two-hour 75 g oral glucose tolerance testing (OGTT) was performed after recovery from the acute poisoning, at around the time of discharge. In Sri Lanka, a four time-point OGTT for area-under-the-curve (AUC), C-peptide and homeostatic modelling of insulin resistance (HOMA-IR) was undertaken, repeated after 1 year. In Bangladesh, a 2-h OGTT for glucose was undertaken and repeated after 3 months in participants with initial elevated 2-h glucose. We compared glucose homeostasis by poison group and adjusted findings for age, BMI and sex. FINDINGS:Seventy-three Sri Lankan and 151 Bangladeshi participants were recruited. We observed higher mean [SD] fasting (4.91 [0.74] vs. 4.66 [0.46] mmol/L, p = .003) and 2-h glucose (7.94 [2.54] vs. 6.71 [1.90] mmol/L, p < .0001) in OP-poisoned groups than pyrethroid, carbamate, herbicide or 'other poison' groups at discharge from hospital. In Sri Lanka, HOMA-IR, glucose and C-peptide AUC were higher in OP than carbamate or herbicide groups. Adjusted analyses remained significant except for fasting glucose. Follow-up analysis included 92 participants. There was no significant difference in OGTT results between OP-poisoned and other participants at follow-up (mean [SD] 2-h fasting glucose 4.67 [0.92] vs. 4.82 [0.62], p = .352; 2-h glucose 6.96 [2.31] mmol/L vs. 6.27 [1.86] mmol/L, p = .225). CONCLUSION:We found in this small prospective study that acute OP insecticide poisoning caused acute glucose dysregulation that was sustained to hospital discharge but had recovered by 3-12 months. Acute glucose dysregulation was related to defects in insulin action and secretion. This study did not address long-term risk of diabetes following acute OP insecticide poisoning, but could provide the data for a power calculation for such a study.

Original publication

DOI

10.1080/15563650.2018.1515438

Type

Journal

Clinical toxicology (Philadelphia, Pa.)

Publication Date

04/2019

Volume

57

Pages

254 - 264

Addresses

a University/BHF Centre for Cardiovascular Science, University of Edinburgh , Edinburgh , UK.