naloxone and Pancreatitis

Hemodialysis therapy has been used in the treatment of acute alcohol intoxication for many years, especially acute severe alcohol intoxication.. This study aimed to evaluate whether the combination of conventional treatment and naloxone with hemodialysis has advantages over conventional treatment and naloxone alone in patients with acute severe alcohol intoxication.. After searching 12 databases and 2 clinical trial centers. According to the established inclusion and exclusion criteria, the qualified literatures were screened. The outcome indicators were length of hospital stay, coma time, time of symptom disappearance, the overall complication rate, the incidence of pancreatitis, the incidence of aspiration pneumonia, the incidence of hepatic and renal dysfunction. Analysis was performed using Revman 5.3.. This meta-analysis included 13 studies, including 932 subjects. In the treatment of acute severe alcohol intoxication, the use of hemodialysis on the basis of conventional treatment and naloxone could reduce the length of hospital stay (WMD = -15.16, 95% CI: -17.45 to -12.86, p < 0.001) in hours and (WMD = -4.89, 95% CI: -5.53 to -4.25, p < 0.001) in days; coma time (WMD = -5.43, 95% CI: -6.43 to -4.43, p < 0.001); time of symptom disappearance (WMD = -3.92, 95% CI: -5.37 to -2.47, p < 0.001); the overall complication rate (RR = 0.39, 95% CI: 0.28-0.55, p < 0.001); the incidence of pancreatitis (RR = 0.14, 95% CI: 0.05-0.43, p = 0.0006); the incidence of aspiration pneumonia (RR = 0.15, 95% CI: 0.04-0.66, p = 0.01), and the incidence of hepatic and renal dysfunction (RR = 0.21, 95% CI: 0.06-0.72, p = 0.01).. It can be concluded that compared with the use of conventional treatment and naloxone alone, the use of hemodialysis on the basis of conventional treatment and naloxone for acute severe alcohol intoxication can reduce the length of hospital stay, coma time, time of symptom disappearance, and the incidence of some complications rate. Large scale, multicenter, and well-designed RCTs are needed in the future to prove our conclusions.

Topics: Alcoholic Intoxication; Coma; Humans; Kidney Diseases; Multicenter Studies as Topic; Naloxone; Pancreatitis; Pneumonia, Aspiration; Renal Dialysis

Loperamide is an opioid available over the counter and in prescription form. Loperamide functions as a μ-agonist within the enteric nervous system to slow intestinal motility. Its antidiarrheal properties and primarily peripheral activity make loperamide an important tool in the management of inflammatory bowel disease.. A 42-year-old man was found unconscious in cardiac arrest, and emergency medical personnel restored normal sinus rhythm. Family reported complaints of abdominal pain and that he "went through a lot" of loperamide. In the emergency department, the patient exhibited symptoms consistent with an opioid overdose. Mental status improved after administration of naloxone, an opioid antagonist. An electrocardiogram revealed a prolonged QTc interval, which progressed into Torsades de Pointes rhythm during admission. The patient succumbed from hypoxic brain injury, and there was evidence of acute pancreatitis at autopsy. Loperamide and desmethylloperamide (loperamide metabolite) were detected in blood samples. Cause of death was ruled loperamide toxicity.. Because of reduced central nervous system activity and associated euphoria at therapeutic doses, loperamide abuse is rarely reported. This case demonstrates that an overdose on loperamide can occur in patients seeking symptom alleviation, and may mimic the presentation of opioid overdose.

Topics: Adult; Antidiarrheals; Crohn Disease; Fatal Outcome; Humans; Hypoxia, Brain; Loperamide; Male; Naloxone; Narcotic Antagonists; Opioid-Related Disorders; Pancreatitis

Dog model of acute pancreatitis, induced by intrapancreatoductal injection of fresh trypsin-bile mixture, was used to investigate the effects of naloxone on hemodynamic changes in acute pancreatitis. In the control group, acute pancreatitis was induced and characterized hemodynamically by the decrease in maximum positive and negative dP/dt (+/- dP/dtmax), cardiac output (CO) and cardiac index (CI), and increase in pulmonary vascular resistance (PVR) and systemic vascular resistance (SVP), as well as early reduction of pancreatic blood flow (PBF). In the naloxone treated group, naloxone was given intravenously 10 minutes after the induction of acute pancreatitis (80 micrograms/kg as a bolus + 80 micrograms/kg/h for 3 hours). It was found that naloxone significantly increased PBF and the +/- dP/dtmax effectively prevented the significant decrease in CO, CI and increase in PVR, SVR observed in untreated acute pancreatitis; and significantly reduced the severity of pancreatitis, as assessed by both histological staging and mortality rate. These results suggest that naloxone appears to limit the progression from edematous to hemorrhagic pancreatitis through preserving PBF and improving systemic hemodynamics at the early phase of acute pancreatitis; hence the hypothesis that endogenous opioid peptides may play a role in the pathophysiology of acute pancreatitis.

Topics: Acute Disease; Animals; Bile; Cardiac Output; Dogs; Female; Hemodynamics; Male; Naloxone; Pancreas; Pancreatitis; Regional Blood Flow; Trypsin

120 SD rats were randomly divided into three groups: the sham operation group, the AP (acute pancreatitis) group, the naloxon treated group. AP was induced by intraductal injection of 5% sodium taurocholate solution. Naloxon was given intramuscularly at the dosage of 0.1 g/100 gw immediately after the injection and 90 minutes later. The survival rate and the mean survival time of the rats during 3 days after the induction of AP were determined. The pancreata were sampled for semiquantitative histopathologic evaluation. By using the fractional indicator distribution technique with 86 RB, QP/CO and pancreatic tissue perfusion performed 1 and 6 hours after the induction of AP, the amount of beta-endorphin in the hypothalamus and pituitary was measured 1 and 4 hours after the induction of AP. It was found in the naloxon treated group, the pancreatic blood flow and tissue perfusion was greatly increased, the mortality rate was decreased, and the rats survival time was significantly prolonged. The results suggest that: (1) The hemodynamic changes play an important role in the pathogenesis of AP. (2) Beta-Endorphin may play a role in the pathophysiological process of AP. (3) naloxon has good therapeutic effects on AP.

Topics: Acute Disease; Animals; beta-Endorphin; Female; Male; Naloxone; Pancreas; Pancreatitis; Rats; Rats, Inbred Strains; Regional Blood Flow

The effect of endogenous pituitary and pancreatic beta-endorphins in the physiopathologic factors of acute pancreatitis and the effect of opiate antagonist naloxone in these conditions were studied. Pancreatitis was induced by the injection of 0.5 milligram per kilogram of autologous bile mixed with 10,000 units per kilogram of trypsin into the main duct after ligating the accessory duct. After the induction of acute pancreatitis, plasma beta-endorphin concentrations in systemic and portal blood and cardiovascular function were measured. Ten dogs (control group) were given an intravenous injection of 10 milliliters per kilogram per hour of lactate Ringer's solution one hour before the induction of acute pancreatitis. Six (naloxone group) received an intravenous bolus injection of 2 milligrams per kilogram of naloxone at one hour after the induction of acute pancreatitis and then an intravenous infusion of 2 milligrams per kilogram per hour of naloxone was given under the same conditions as for those in the control group. Beta-endorphin in systemic and portal venous blood in those in the control group increased significantly during the experiments. Beta-endorphin and adrenocorticotropin hormone in systemic venous blood both in the control and naloxone groups increased simultaneously. However, blood pressure, pulse pressure and cardiac output improved quickly after the bolus injection of naloxone and were well maintained during intravenous infusion of naloxone. Also, naloxone improved the survival time from acute pancreatitis and decreased plasma lactate concentrations. Our data show that beta-endorphin, released mainly from the pituitary gland and not from the pancreas, may have an important role in subsequent cardiovascular depression. Also the opiate antagonist naloxone may be effective in the treatment of acute pancreatitis.

Topics: Acute Disease; Adrenocorticotropic Hormone; Animals; beta-Endorphin; Blood Pressure; Cardiac Output; Dogs; Female; Hemodynamics; Lactates; Lactic Acid; Male; Naloxone; Pancreatitis; Portal System

Naloxone, an opiate receptor blocker, has been shown in earlier studies to have positive effect on cardiovascular function in a variety of diseases in which the secretion of endogenous opioid peptides was suspected. In this communication, a dog model of acute pancreatitis (AP) was made by intraductal injection of fresh trypsin-bile mixture, in which the hemodynamic changes were measured, the therapeutic efficacy of naloxone was evaluated. Pancreatitis was characterized by a fall in SAP, CO, dp/dt, an increase in PVR, SVR and the early reduction of pancreatic blood flow (QP). Administration of naloxone produced a significant increase in QP and led to normalization in SAP, CO, dp/dt, PVR and, SVR. In addition, Naloxone significantly reduced the severity and mortality of AP. These results suggest that naloxone appears to limit the progression from edematous to hemorrhagic pancreatitis through preserving QP at the early phase of AP. We propose the hypothesis that endogenous opiates may play a role in the pathophysiology of AP.

Topics: Acute Disease; Animals; Dogs; Hemodynamics; Naloxone; Pancreas; Pancreatitis