Intralipid Administration Research Articles

Targeting CD3-CD16+CD56+ NK Cells and NK Cell Activity by Intralipid in the Management of Reproductive Failure

Immunological risk factors in recurrent pregnancy loss include autoantibodies, alterations in NK cell number and function, regulatory T cells, the human leukocyte antigen system (HLA), etc., where the treatment options aim to regulate immune dysfunction. Intralipid is a synthetic product traditionally used as a dietary supplement consisting of soybean oil combined with refined egg phospholipids. It has been shown that intralipid exerts physiologic activities, including altering immunological functions, that may benefit patients with certain types of infertility. In this review, we summarize the current state of the art of targeting NK cells and NK cell activity in women with implantation failure or/and recurrent pregnancy loss. We focus on intralipid mechanisms of action and outcomes of clinical trials regarding the efficacy and safety of intralipid infusions in women with reproductive failure. More studies are needed to reveal all the aspects of the safety and effectiveness of intralipid administration in reproductive failure treatment.

POSTER 6Efficacy of intralipid administration to improve in vitro fertilization outcomes

POSTER 6Efficacy of intralipid administration to improve in vitro fertilization outcomes

Intralipid administration in case of a severe venlafaxine overdose in a patient with previous gastric bypass surgery

Intralipid administration in case of a severe venlafaxine overdose in a patient with previous gastric bypass surgery

Efficacy of intralipid administration to improve in vitro fertilization outcomes: A systematic review and meta-analysis

We performed a systematic review and meta-analysis to evaluate whether intralipid administration improved the outcomes of in vitro fertilization. Online databases (PubMed, Cochrane Library, Medline, and Embase) were searched until March 2020. Only randomized controlled trials (RCTs) that assessed the role of intralipid administration during in vitro fertilization were considered. We analyzed the rates of clinical pregnancy and live birth as primary outcomes. Secondary outcomes included the rates of chemical pregnancy, ongoing pregnancy, and missed abortion. We reviewed and assessed the eligibility of 180 studies. Five RCTs including 840 patients (3 RCTs: women with repeated implantation failure, 1 RCT: women with recurrent spontaneous abortion, 1 RCT: women who had experienced implantation failure more than once) met the selection criteria. When compared with the control group, intralipid administration significantly improved the clinical pregnancy rate (risk ratio [RR], 1.48; 95% confidence interval [CI], 1.23–1.79), ongoing pregnancy rate (RR, 1.82; 95% CI, 1.31–2.53), and live birth rate (RR, 1.85; 95% CI, 1.44–2.38). However, intralipid administration had no beneficial effect on the miscarriage rate (RR, 0.75; 95% CI, 0.48–1.17). A funnel plot analysis revealed no publication bias. Our findings suggest that intralipid administration may benefit women undergoing in vitro fertilization, especially those who have experienced repeated implantation failure or recurrent spontaneous abortion. However, larger, well-designed studies are needed to confirm these findings.

Lidocaine Toxicity in a Patient with Liver Cirrhosis Underwent Transcatheter Aortic Valve Implantation

Background: Lidocaine has been commonly used in many clinical settings. Nonetheless, systemic toxicity can be life-threatening and careful attention to dosing, especially among patients with liver dysfunction is important to minimize the risk of toxicity. Objective: The diagnosis of lidocaine toxicity is usually clinical, while rare, but may prove fatal. Methods: Here we discuss 60 years-old man with advanced liver cirrhosis, developed lidocaine-induced cardiovascular and neurotoxicity. Results: Our case study demonstrates a successful treatment of cardiovascular and neurotoxicity with intravenous lipid emulsion in the context of systemic lidocaine toxicity in a liver cirrhosis patient who received lidocaine as a local anesthetic. Conclusions: A high index of suspicion should be maintained for severe toxicity even after subcutaneous administration and prompt intralipid administration may prove lifesaving.

Effect of intralipid administration on calcium therapy in verapamil toxicity.

Lipid emulsions are promising with regard to the treatment of toxicity by agents of high lipophilic nature. Our objective is to investigate the efficacy of intralipid 20% and calcium administration at different times when symptoms of cardiac toxicity occur during verapamil infusion. 24 adult male Spraque-Dawley rats were randomly divided into 4 different groups, the control group, calcium group, calcium following 20% intralipid group and concomitant 20% intralipid and calcium group. Following monitoring under ketamine anesthesia, all groups were administered 37.5 mg kg-1 h-1 verapamil infusion until a 50% decrease occurred in MAPb. At the end of the infusion, verapamil infusion was decreased down to 15 mg kg-1h-1 and the treatment agents predetermined for the groups were administered concomitantly. There is no statistically significant difference between the administration of 20% intralipid synchronized with calcium or as a pretreatment, but both groups provided a higher survival rate when compared to the other groups. The administration of calcium alone in verapamil toxicity is not sufficient; when calcium and 20% intralipid are administered together, there is no difference between the administration of lipid and calcium concomitantly and the administration of lipid prior to calcium (Tab. 1, Fig. 2, Ref. 23).

Effects of soybean lipid infusion on triglyceride and unbound free fatty acid levels in preterm infants

Objective: To determine the plasma triglyceride (TG) and unbound free fatty acid (FFAu) levels in infants treated with increasing dosages of soybean lipid, intralipid (IL), infusion.Study design: TG and FFAu levels were measured in 78 preterm infants (BW 500–2000 g; GA 23–34 weeks) using the fluorescent probe ADIFAB2 and enzymatic method.Results: The infants’ BW was 1266.2 ± 440.7 g and GA 28.8 ± 3.1 weeks. TG levels were 77.4 ± 50 mg/dL, 140.2 ± 188 mg/dL (p < .04 compared to levels during low dose IL infusion) and 135.6 ± 118 mg/dL (p < .004), respectively during increased IL rates. FFAu levels were 17.7 ± 13 nM, 47.3 ± 102.8 nM (p = .07) and 98 ± 234 nM (p = .03). TG levels correlated with IL dose, the rate of IL administration, and FFAu levels. TG and FFAu levels were higher in infants below 28 weeks’ gestationConclusions: Increasing dosage of IL is associated with increasing levels of TG and FFAu, especially in infants below 29 weeks of gestation. The increased level of FFAu suggests inefficient cellular utilization.

Mortalité maternelle liée à l’anesthésie-réanimation. Résultats de l’ENCMM, France 2010–2012

Over the period 2010–2012, maternal mortality linked to anesthesia accounted for 2% of maternal deaths, with no significant change since 2007–2009. Of the 7 maternal deaths analyzed by the expert committee, anesthetic complications were in 5 cases the main cause of death: 4 attributed to direct causes related to anesthetic procedures during childbirth and 1 to indirect cause in connection with an ENT complication during pregnancy. The anesthetic causes of maternal mortality were for the 2010–2012 period: cardiac arrest under spinal anesthesia during caesarean section, local anesthetic intoxication with unsuccessful resuscitation after cardiac arrest without intralipid administration, acute respiratory distress syndrome in the postpartum period after pulmonary aspiration during caesarean section, cardiac arrest during caesarean section under general anesthesia in a context of non-Hodgkin lymphoma with mediastinal syndrome, unsuccessful endotracheal intubation in a context of cellulitis of the oral cavity floor. In two other cases, anesthetic complications were identified as associated causes of death, the primary cause being intracerebral hemorrhage stroke and pulmonary hypertension. In most of the cases analyzed over the period 2010–2012, anesthesia and resuscitation have been involved in the occurrence of maternal deaths, mainly through strategic errors in the management of patients with severe pathology before delivery, as well as through insufficient cardiac resuscitation duration after cardiac arrest.

Abstract 21323: Intralipid Fails to Rescue Bupivacaine-Induced Cardiac Arrest in Pregnant Rats

Background: Pregnant patients routinely get neuraxial anesthesia. Bupivacaine is one of the most commonly used local anesthetics in obstetric anesthesia. Studies have suggested that pregnancy increases Bupivacaine cardiotoxicity. We and others have previously shown that Intralipid (ILP) rescues the heart from Bupivacaine cardiotoxicity in male rats. ILP mediates its cardioprotective effects via glycogen synthase kinase-3b (GSK-3b) phosphorylation. We aimed to investigate Bupivacaine cardiotoxicity and potential for ILP’s rescue in pregnant rats, that has not been studied before. Methods: Late pregnant rats (200-300 g, n=12) at day 20 of pregnancy were used for the study. A group of pregnant rats received Bupivacaine bolus (10 mg/kg, IV over ~20 seconds, n=7) to induce asystole under anesthesia. Resuscitation with ILP 20% (5 ml/kg bolus, and 0.5 ml/kg/min maintenance, n=7) and chest compressions were initiated. The ejection-fraction (EF%), and heart rate (HR) were calculated from echocardiography and EKG at baseline and at 1, 5, and 10 min after ILP treatment. A group of pregnant rats that did not undergo Bupivacaine-induced cardiac arrest and ILP rescue served as sham controls (n=5). Hearts were collected and Western blot was performed to assess GSK-3b phosphorylation. Results: All 7 late pregnant rats developed cardiac arrest a few seconds after Bupivacaine. Interestingly, 6 out of the 7 rats were not rescued with ILP using the same dose as in male rats. In these 6 rats, the average baseline EF and HR were 67.344.47% and 34130.44 bpm. One, five and ten minutes after ILP administration, the EF and HR were 0. Western blots showed that pregnant rats which were not rescued by ILP failed to have GSK-3b activation (pGSK/GSK=0.80±0.51 vs. 1.00±0.56 in late pregnant sham controls; p=0.578). In the late pregnant rat that recovered with ILP, baseline EF and HR (66.302.99% and 31034 bpm), were not different than the rats that did not recover. Conclusions: ILP failed to rescue Bupivacaine-induced cardiac arrest in pregnant rats. This failure of rescue is most likely attributed to the inability of ILP to activate GSK-3b, a known mediator of ILP’s cardioprotection.

Mortalité maternelle liée à l’anesthésie-réanimation. Résultats de l’ENCMM, France 2010–2012

Over the period 2010–2012, maternal mortality linked to anesthesia accounted for 2% of maternal deaths, with no significant change since 2007–2009. Of the 7 maternal deaths analyzed by the expert committee, anesthetic complications were in 5 cases the main cause of death: 4 attributed to direct causes related to anesthetic procedures during childbirth and 1 to indirect cause in connection with an ENT complication during pregnancy. The anesthetic causes of maternal mortality were for the 2010–2012 period: cardiac arrest under spinal anesthesia during caesarean section, local anesthetic intoxication with unsuccessful resuscitation after cardiac arrest without intralipid administration, acute respiratory distress syndrome in the postpartum period after pulmonary aspiration during caesarean section, cardiac arrest during caesarean section under general anesthesia in a context of non-Hodgkin lymphoma with mediastinal syndrome, unsuccessful endotracheal intubation in a context of cellulitis of the oral cavity floor. In two other cases, anesthetic complications were identified as associated causes of death, the primary cause being intracerebral hemorrhage stroke and pulmonary hypertension. In most of the cases analyzed over the period 2010–2012, anesthesia and resuscitation have been involved in the occurrence of maternal deaths, mainly through strategic errors in the management of patients with severe pathology before delivery, as well as through insufficient cardiac resuscitation duration after cardiac arrest.

Effect of Intralipid on the Dose of Ropivacaine or Levobupivacaine Tolerated by Volunteers: A Clinical and Pharmacokinetic Study

(Anesthesiology. 2016;125(3):474–483) On the basis of case reports since 2006 and laboratory studies dating back to 1998, rapid intravenous administration of lipid emulsion—“lipid rescue”—has become standard treatment for local anesthetic systemic toxicity (LAST). Hence, the purpose of this crossover study in volunteers was to determine the effect of Intralipid (Fresenius, Paris, France) administration on the time to neurologic symptoms during local anesthetic systemic toxicity (eg, convulsions; severe arrhythmias).

Lipid emulsion mitigates impaired pulmonary function induced by limb ischemia/reperfusion in rats through attenuation of local cellular injury and the subsequent systemic inflammatory

BackgroundLimb ischemia/reperfusion causes inflammation and elicits oxidative stress that may lead to local tissue damage and remote organ such as lung injury. This study investigates pulmonary function after limb ischemia/reperfusion and the protective effect of a lipid emulsion (Intralipid).MethodsTwenty-four rats were divided into three groups: sham operation group (group S), ischemia/reperfusion group (group IR), and lipid emulsion treatment group (group LE). limb ischemia/reperfusion was induced through occlusion of the infrarenal abdominal aorta for 3 h. The microvascular clamp was removed carefully and reperfusion was provided for 3 h.ResultsThe mean arterial pressure in group LE was higher than group IR during the reperfusion period (P = 0.024). The heart rate of both group LE and IR are significantly higher than group S during the ischemia period(P < 0.001, P < 0.001, respectively). The arterial oxygen pressure of group LE was significantly higher than group IR (P = 0.003), the arterial carbon dioxide pressure of group LE were lower than that of group IR (P = 0.005). The concentration of plasma interleukin-6, tumor necrosis factor-α and malondialdehyde in group LE were significantly lower than group IR (P < 0.001, P = 0.009 and 0.029, respectively). The plasma superoxide dismutase activity in group LE was significantly higher than group IR (P = 0.029). The myeloperoxidase activity in lung tissues of group LE was significantly less than group IR (P = 0.046). Both muscle and lung in group IR were damaged seriously, whereas lipid emulsion (Intralipid) effectively reversed the damage. In summary, Intralipid administration resulted in several beneficial effects as compared to group IR, such as the pulmonary gas exchange and inflammatory.ConclusionsThe ischemic/reperfusion injury of limb muscles with resultant inflammatory damage to lung tissue can be mitigated by administration of a lipid emulsion (Intralipid, 20%, 5 ml/kg). The mechanisms attenuating such a physiological may be attributed to reduction of the degree of limb injury through a decrease in the release of local inflammatory mediators, a reduction of lipid peroxidation, and a blunting of the subsequent remote inflammatory response.

Analysis of the temporal regression of the QRS widening induced by bupivacaine after intralipid administration. Study in an experimental porcine model

ObjectiveThe principal mechanism of cardiac toxicity of bupivacaine relates to the blockade of myocardial sodium channels, which leads to an increase in the QRS duration. Recently, experimental studies suggest that lipid emulsion is effective in reversing bupivacaine cardiac toxicity. We aimed to evaluate the temporal evolution of the QRS widening induced by bupivacaine with the administration of Intralipid. Material and methodsTwelve pigs were anesthetized with intravenous sodium thiopental 5mgkg−1 and sevoflurane 1 MAC (2.6%). Femoral artery and vein were canalized for invasive monitoring, analysis of blood gases and determination of bupivacaine levels. After instrumentation and monitoring, a bupivacaine bolus of 4–6mgkg−1 was administered in order to induce a 150% increase in QRS duration (defined as the toxic point). The pigs were randomized into two groups of six individuals. Intralipid group (IL) received 1.5mLkg−1 of IL over 1min, followed by an infusion of 0.25mLkgmin−1. Control group (C) received the same volume of a saline solution. The electrocardiographic parameters were recorded, and blood samples were taken after bupivacaine and 1, 5, 10 and 30min after Intralipid/saline administration. ResultsBupivacaine (4.33±0.81mg/kg in IL group and 4.66±1.15mg/kg in C group) induced similar electrocardiographic changes in both groups; mean maximal percent increase in QRS interval was 184±62% in IL group, and 230±56% in control group (NS). Lipid administration reversed the QRS widening previously impaired by bupivacaine. After 10min of the administration of IL, the mean QRS interval decreased to 132±56% vs. 15±76% relative to the maximum widening induced by bupivacaine, in IL and C group, respectively. ConclusionIntralipid reversed the lengthening of QRS interval induced by the injection of bupivacaine. Time to normalization of electrocardiographic parameters can last more than 10min. While the phenomena of cardiac toxicity persist, resuscitation measures and adequate monitoring should be continued until adequate heart conduction parameters are restored.

Changes of Total Plasma Triglycerides in Neonates Treated With Intralipid: A Pilot Study.

Dear Editor, The current scientific literature states that Intralipid 10% emulsion has a higher ratio of phospholipids to triglycerides, and contains more lypozomal phospholipids as compared to Intralipid 20% and Intralipid 30%, so it causes higher plasma concentrations of triglycerides, cholesterol and phospholipids (1, 2). It should be noted that serum triglycerides concentration is used as a marker for lipid tolerance and predicting the probability of complications involved with the administration of Intralipid 10%. In view of the fact that Intralipid 10% emulsion is the only currently available Intralipid in Iran, and also used for years, is known to have no significant side effects, we conducted a before and after descriptive, observational study on 20 newborns (10 females and 10 males) hospitalized in NICU of Valiasr hospital, Tehran University of Medical Sciences, that required total intravenous nutrition, and evaluated the effects of Intralipid 10% on neonates’ total plasma triglycerides before TPN and once the dose of Intralipid reached 2.5 g/kg/day. In the first step total plasma triglycerides level was measured. Then continuous daily infusion of Intralipid 10% with 0.5 g/kg/day dose was started increasing daily 0.5 g/kg until enteral nutrition was able to provide approximately 100 to 110 kcal for kg body weight. The outcome was total plasma triglycerides levels higher than 200 mg/dL in newborns receiving intravenous Intralipid 10% nutrition. Heparin was administered routinely with parenteral nutrition; heparin can theoretically release lipase lipoprotein from endothelial cells that may accelerate clearance of lipids from plasma. Total plasma triglycerides was monitored weekly when the Intralipid 10% dosage reached 2.5 g/kg/day and was continued to the end of TPN therapy, or until it reached the maximum level of 150-200 mg/dL, defined in scientific references as the indication for termination of intravenous Intralipid administration. There were no significant differences observed between total plasma triglycerides level before intravenous feeding (62.95 ± 10.46 mg/dL) and after Intralipid terminating dose of 2.5 gr/kg/day (63.15 ± 12.98 mg/dL) (P = 0.9). Also no correlation was observed between birth weight, duration of intravenous feeding and plasma triglycerides level difference (P > 0.005). Viewing the results of this study which has been referred to in detail, we intend to indicate that no significant difference between total plasma triglyceride levels before intravenous feeding and total plasma triglyceride levels after Intralipid 10% dosage has reached 2.5 g/kg/day, was seen (P = 0.9). This study in accordance with previously published studies (3-6) showed that Intralipid 10% is well tolerated by patients and levels of plasma triglycerides did not increase, VLDL and HDL remained in normal range and no significant complication was observed. The last noteworthy point is that the length of infusion can also be an important parameter in modulating possible listed side effects of Intralipid 10% mentioned in other sources. In conclusion, this study showed that in the absence of Intralipid 20% or 30%, the use of Intralipid 10% has not led to high levels of triglycerides in our neonates.

Blood lipids affect rat islet blood flow regulation through β₃-adrenoceptors.

Pancreatic islet blood perfusion varies according to the needs for insulin secretion. We examined the effects of blood lipids on pancreatic islet blood flow in anesthetized rats. Acute administration of Intralipid to anesthetized rats increased both triglycerides and free fatty acids, associated with a simultaneous increase in total pancreatic and islet blood flow. A preceding abdominal vagotomy markedly potentiated this and led acutely to a 10-fold increase in islet blood flow associated with a similar increase in serum insulin concentrations. The islet blood flow and serum insulin response could be largely prevented by pretreatment with propranolol and the selective β₃-adrenergic inhibitor SR-59230A. The nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester prevented the blood flow increase but was less effective in reducing serum insulin. Increased islet blood flow after Intralipid administration was also seen in islet and whole pancreas transplanted rats, i.e., models with different degrees of chronic islet denervation, but the effect was not as pronounced. In isolated vascularly perfused single islets Intralipid dilated islet arterioles, but this was not affected by SR-59230A. Both the sympathetic and parasympathetic nervous system are important for the coordination of islet blood flow and insulin release during hyperlipidemia, with a previously unknown role for β₃-adrenoceptors.

Analysis of the temporal regression of the QRS widening induced by bupivacaine after intralipid administration: study in an experimental porcine model

Analysis of the temporal regression of the QRS widening induced by bupivacaine after intralipid administration: study in an experimental porcine model

Study of the effects of bupivacaine toxicity in transmural dispersion of repolarization and triggered ventricular arrhythmias and its reversion with the intralipid administration. Study in a porcine experimental model

Callejo, D.; De Diego, C.; Zaballos, M.; Sevilla, R.; González, J.; Quintela, O. Author Information

Abstract 330: Intralipid Rescues Delayed Cooling and Restores Contractions in Ischemia-Stunned Heart Cells

Introduction: Cooling is a promising treatment for cardiac arrest. However, delayed cooling (DC) can result in loss of protection against ischemia/reperfusion (I/R) injury. We sought to develop drugs that mimic or augment cooling protection. Intralipid (ILP), a soy-based fat emulsion that is widely used in different clinical setting for parenteral nutrition, has been recently introduced as an antidote against local anesthetic-induced cardiotoxicity. In this study, we utilized a stunned mouse cardiomyocyte model to study the effect of ILP on improving contractile function and its potential role in rescuing abnormal contractility. Methods: Cardiomyocytes, isolated from 1-2-day old C57Bl6/J mice were used. Protocols: 1) Stunning: cells were exposed to 30 min simulated ischemia and 90 min reperfusion followed by 10 min isoproterenol (10 μM). 2) ILP treatment: ILP (0.25%) was administered during 90 min reperfusion. 3) Delayed ILP treatment: ILP was given at 20 min of reperfusion. 4) DC: cooling (32оC) was initiated at 20 min of reperfusion and lasted for 40 min, followed by 30 min re-warming. 5) DC + ILP: ILP was given at start of reperfusion for 90 min in DC. The contraction velocity was measured using Matlab software. Akt phosphorylation was analyzed by Western blot. Results: ILP administration at the onset of reperfusion significantly increased the contraction velocity in stunned cells (66.0 +/- 3.9 % vs. 40.6 +/- 1.7%, P &lt; 0.001) and enhanced the cell response to isoproterenol. The contractile function was not recovered when ILP administration was delayed. Intra-ischemic cooling (IC) improved contractile function that was abolished by DC. Co-treatment of ILP and DC significantly enhanced contractility (43.3 +/- 3.0 % vs. 20.1 +/- 3.9 %, P &lt; 0.01). Akt phosphorylation (p-Akt) was increased by ILP, but decreased when ILP was delayed. Similarly, DC attenuated p-Akt which was increased by ILP+DC. This ILP-induced p-Akt was blocked by API-2, an Akt inhibitor. Conclusion: Our results suggest that optimal ILP treatment improved contractile function and contractile preservation that was mediated by Akt in stunned mouse cardiomyocytes. ILP may serve as a therapeutic agent or adjunct agent to delayed cooling in patients after cardiac arrest.

Lipoprotein X: clinical implications

In this issue of the journal, Stepien et al. describe a case of serum lipoprotein X (Lp-X) in a patient with cholestasis and severe hyperlipidaemia. This abnormal lipoprotein is rich in phospholipid and unesterified cholesterol. The main protein component is albumin within the core and apolipoprotein C upon the surface. Unlike low-density lipoprotein (LDL), Lp-X does not contain apolipoprotein B nor is it removed by the LDL receptor, but Lp-X is cleared by the reticuloendothelial system and the kidneys. Lp-X is about 50 nm in diameter and its major component bile acid is lithocholic. Early studies reported the presence of Lp-X in the serum of patients with cholestasis. The failure of Lp-X to exert feedback inhibition on cholesterol synthesis may contribute to the mechanism of hypercholesterolaemia in obstructive jaundice. However, the presence of serum Lp-X does not facilitate the distinction between intrahepatic and extrahepatic cholestasis. Bile lipoprotein is a precursor of Lp-X and in cholestasis this refluxes into the plasma pool and binds to albumin to form Lp-X. Serum Lp-X usually disappears soon after the cholestasis is relieved. The ratio of plasma bile salts to albumin is important for the integrity of Lp-X and it is catabolized by the action of phospholipase which helps convert lecithin into lysolecithin. In graft versus host disease involving the liver and with cholestasis plasma Lp-X can result in severe hypercholesterolaemia, xanthelasma and cholesteroloma. Lp-X can also be found in cholestasis of pregnancy and primary biliary cirrhosis (PBC). The case presented by Stepien et al. confirms these earlier observations of raised serum Lp-X in cholestasis. Increased serum cholesterol concentrations occur in PBC and this is largely due to the presence of Lp-X, although it is debatable whether this confers increased cardiovascular risk. Indeed, Lp-X may not be atherogenic and data suggest it may have antioxidant LDL activity. Additionally, Lp-X is not significantly taken up by macrophages but is taken up by hepatocytes. Sometimes severe and prolonged cholestasis can result in very high serum Lp-X concentrations resulting in severe hypercholesterolaemia and tendon xanthomata. Complete regression of these xanthomata has been described by treatment with apheresis, which the authors stated should be considered possible first-choice treatment for patients with massive Lp-X accumulation due to cholestasis. Statin therapy may be ineffective in lowering Lp-X. Lecithin-cholesterol acyltransferase (LCAT) is an enzyme responsible for cholesterol esterification in plasma. Lp-X is found in LCAT deficiency which is characterized by low concentrations of high-density lipoprotein (HDL) as well as anaemia, corneal opacities, proteinuria and chronic kidney disease. The Lp-X found in LCAT deficiency may contribute to the renal disease observed in this condition by stimulating monocyte renal infiltration. Proteoglycans have an important role in regulating the uptake of Lp-X into kidney mesangial cells and this mechanism is independent of the scavenger receptor. Guerin et al. reported that in LCAT deficiency the presence of Lp-X is correlated with a progressive change in renal function. In addition to cholestasis and LCAT deficiency, Lp-X may also be found in the plasma after intravenous infusion of Intralipid emulsion such as occurs with total parenteral nutrition. Intralipid administration can elicit an increase in serum total cholesterol (mainly unesterified), phospholipid and LDL. The Lp-X associated with Intralipid infusion seems to occur when phospholipid clearance is exceeded, resulting in phospholipid accumulation with unesterified cholesterol. Pseudohyponatraemia has also been described in some patients with severe hypercholesterolaemia secondary to raised Lp-X. Thus the presence of Lp-X should be considered in pseudohyponatraemia associated with cholestasis. Sivakumar et al. described not only pseudohyponatraemia, but also pseudohypokalaemia and pseudohypochloridaemia in the presence of high concentrations of Lp-X. Various researchers have also found assay bias for serum LDL-cholesterol in the presence of Lp-X. This is an important practical point when it comes to interpreting LDL cholesterol results in severely cholestatic serum samples. Lp-X possesses strong aggregatory properties and can bind to alkaline phosphatase (ALP) producing a Lp-X-ALP complex. This complex may be found in cholestasis; typically that evoked by hepatic malignancy. The Lp-X-ALP complex is also associated with the presence of high-molecular mass ALP and the liver isoenzyme of ALP. Brocklehurst et al. described a stationary band of ALP using starch gel electrophoresis of serum samples from patients with biliary obstruction which was thought to be due to ALP binding to Lp-X. The strong aggregating ability of Lp-X may be important as it can bind and remove free cholesterol from the circulation. There are various assays available for measuring serum Lp-X. Agarose gel electrophoresis utilizes the cathodal

Journal-related Activities and Other Special Activities at the 2012 American Society of Anesthesiologists Annual Meeting

Journal-related Activities and Other Special Activities at the 2012 American Society of Anesthesiologists Annual Meeting