Effects of short‐term propofol administration on pancreatic enzymes and triglyceride levels in children

Abstract

SummaryThis prospective, clinical trial evaluated the effects of short-term propofol administration on triglyceride levels and serum pancreatic enzymes in children undergoing sedation for magnetic resonance imaging. Laboratory parameters of 40 children, mean age (SD; range) 67 (66; 4-178) months undergoing short-term sedation were assessed before and 4 h after having received propofol. Mean (SD) propofol loading dose was 2.2 (1.1) mg.kg )1 followed by continuous propofol infusion of 6.9 (0.9) mg.kg )1 .h )1 . Serum lipase levels (p = 0.035) and serum triglyceride levels (p = 0.003) were raised significantly after propofol administration but remained within normal limits. No significant changes in serum pancreatic-amylase levels were seen (p = 0.127). In two (5%) children, pancreatic enzymes and in four (10%) children triglyceride levels were raised above normal limits; however, no child showed clinical symptoms of pancreatitis. We conclude that even short-term propofol administration with standard doses of propofol may have a significant effect on serum triglyceride and pancreatic enzyme levels in children. Little is known about drug-induced pancreatitis, although it is reported to have been caused by over 85 different drugs [1,2]. Drug-induced pancreatitis is a relatively rare disorder, with a prevalence of 1.4% among patients presenting with acute pancreatitis from all causes [1]. Propofol, a sedative-hypnotic agent, is used for sedation as well as for induction of general anaesthesia in children and adults. Propofol is a lipid-based, global central nervous depressant which has a rapid onset of sedation with a dose-related hypnotic effect and a quick and smooth recovery profile. Dose dependent hypotension is the most common complication [3]. Hypertriglyceridaemia is another possible adverse effect [4][5][6][7][8][9][10]. Since its approval in 1989, there have been reports indicating a possible link between the use of propofol and the development of acute pancreatitis [11][12][13][14][15][16][17][18][19]. This was mostly in an intra-or postoperative setting and most of these patients received propofol continuously for several days. Furthermore, in these cases, a number of different drugs were co-administered, thus preventing the establishment of a clear causal link between propofol and the occurrence of acute pancreatitis [12,13,[15][16][17][18][19][20]. Recently, we reported a definite association between short-term propofol administration in an 11-year-old girl and the occurrence of acute pancreatitis [11].The mechanism of propofol-induced pancreatitis remains unknown. Although induction of hypertriglyceridaemia has been described and is therefore a suspected mechanism, it seems unlikely that short-term administration of propofol could raise serum lipid levels as much as to induce pancreatitis. To our knowledge, only one clinical trial (n = 21), focusing on pancreatic function in adult patients under postoperative sedation with propofol, has been published so far and no elevated markers of altered pancreatic ...

A Death Associated with Possible Propofol Infusion Syndrome

“…Serum triglyceride levels also have been reported to rise in these patients with hypertriglyceridemia, lactic acidosis and Brugada-type electrocardiogram changes (coved ST segment elevation in right precordial leads V1-V3) associated. A rise in serum triglycerides may be seen in healthy individuals following propofol infusions who do not subsequently develop any adverse events [6]. This patient also had a rise in the serum triglyceride level, which was evident on hospital day 5.…”

Effects of Propofol and Midazolam Infusions on Serum Lipid and Glucose Levels in Hyperlipidemic Patients Undergoing Coronary Artery Bypass Surgery

“…8,9 Re ports sug gest that pro po fol for mu la ti on, com pri sed of egg-yolk le cit hin con ta i ning 1% soybe an oil, ele va tes se rum li pids, and par ti cu larly TRG. 12,16 In ot her stu di es, no sig ni fi cant in cre a ses ha ve be en ob ser ved. 10,17,18 The go al of our study was to de ter mi ne the risk of ele va ti on in plas ma li pid le vels in pa ti ents with hyper li pi de mi a un der go ing CABG.…”

“…[18][19][20] Low CHL con tent of pro po fol may be re la ted to this fin ding as its ef fect con ti nu es thro ug ho ut pro po fol in fu si on. 16 The non car di ac sur gi cal stu dies sup port the se da ta, sin ce the dec re a se in plas ma Turkiye Klinikleri J Med Sci 2014;34 (2) CHL le vel con ti nu es even in the ab sen ce of the dilu ti o nal ef fect of CPB. [18][19][20] The re sults of our study sho wed that plas ma GLU con cen tra ti on in both gro ups in cre a sed sig nifi cantly du ring sur gery, and con ti nu ed 72 ho urs pos to pe ra ti vely when com pa red to the ba se li ne pre o pe ra ti ve le vel.…”

Mekanik Ventilatördeki Tavşanlarda Propofol İnfüzyonu İle Oluşan Metabolik ve Biokimyasal Değişikliklerde L-Karnitin Tedavisinin Etkileri

“…Asidotik durum ve yüksek serbest yağ asidi seviyelerinin kombinasyonu tripsinojeni aktive eder ve akut pankreatiti başlatabilir (47). Genel olarak hiperlipideminin pankreatite yol açabilmesi için trigliserid seviyelerinin uzun süre 1000-2000 mg/dL'nin üzerinde seyretmesi gerektiğine inanılmakta; propofolün yol açtığı geçici ve ılımlı trigliserid yük-selmesinin pankreatite yol açıp açmayacağı konusu ise hala tartışılmaktadır (48,49). Tavşanlarda yaptığımız çalışmamızda da trigliserid seviyelerinin 2000 mg/dL'nin üzerine çıkması propofol grubunda diğer üç gruba göre amilaz değerlerinin daha yüksek olmasına neden olmuş olabilir.…”