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PubMedDate not supplied

Acetylcodeine as a urinary marker to differentiate the use of street heroin and pharmaceutical heroin.

Acetylcodeine (ACOD) is a synthesis byproduct present in street heroin but not in pharmaceutical diacetylmorphine (DAM) as used in the Swiss program Heroin-Assisted Treatment for Opiate Dependent Drug Users (HAT). ACOD was evaluated and validated as an urine marker to detect the consumption of street heroin by HAT participants. A gas chromatography-mass spectrometry method allowing the quantitation of ACOD concentrations as low as 0.2 ng/mL urine has been developed. In opiate-naïve subjects, intravenous (i.v.) ACOD showed a plasma elimination half-life of 237 +/- 18 min, urine peak concentrations 2 h after administration, and a detection window of 8 h. Only 0.4 +/- 0.1% was excreted unchanged, with codeine (COD) as the main metabolite. ACOD may be formed by transacetylation when i.v. DAM and oral codeine are co-administered. To avoid false-positive results, the calculation of COD/ACOD ratios is recommended. In a study with 105 HAT participants, 14% of the tested urines were ACOD positive. Only a low correlation was found between the anonymously self-declared consumption of street heroin and the ACOD positive rate.

Acetylation↗
PubMedDate not supplied

Acetylcodeine as a marker of illicit heroin abuse in oral fluid samples.

A method was developed using liquid chromatography linked to atmospheric pressure ionization-tandem mass spectrometry (LC-MS-MS) for the measurement of the opiates, morphine, codeine, 6-monoacetylmorphine (6-MAM), acetylcodeine (AC), and heroin in oral fluid collected from patients attending a substance abuse clinic. Of the 513 oral fluid samples tested, 297 showed detectable concentrations of 1 or more of the opiates and their respective percentage incidence being morphine (97%), codeine (82%), 6-MAM (77%), acetylcodeine (55%), and heroin (45%). A high percentage of these opiate-positive samples (40%) had detectable concentrations of all opiates tested. Significant correlations (p < 0.0001) were found between AC and 6-MAM (r = 0.95), heroin and 6-MAM (r = 0.81), and heroin and AC (r = 0.84). Although none of the subjects in this study were being treated with prescription heroin, nine showed detectable concentrations of heroin with no detectable AC. The mean concentration of heroin in these latter samples was very low compared with samples showing detectable AC (24 vs. 2571 microg/L). Several studies have reported the usefulness of measuring AC in urine for detection of illicit heroin abuse. This study demonstrates that the same marker can also be applied to oral fluid. The additional measurement of heroin in oral fluid is of limited use in monitoring subjects attending a substance abuse clinic.

Biomarkers↗
PubMedDate not supplied

Sudden death of a heroin body packer.

This report documents an unusual case in which the analysis of postmortem specimens from a female heroin body packer revealed phenomenally high concentrations of morphine, 6-monoacetylmorphine (6-MAM), caffeine, and codeine. Several condoms containing white powder had split, emptied their contents into the stomach, and then leaked into the peritoneum through a rupture in the stomach wall. Blood concentrations were: morphine, 120 mg/L; (6-MAM), 184 mg/L; codeine, 1.7 mg/L; and caffeine, 400 mg/L.

Codeine↗
PubMed1996

Analgesic efficacy of the kappa-receptor agonist, enadoline, in dental surgery pain.

To study the analgesic efficacy of enadoline, a selective agonist of the kappa-opioid receptor, a double-blind, randomized comparison was made of enadoline versus placebo and a combination of acetaminophen-codeine in patients with pain after surgical extraction of impacted molar teeth. An initial study involving a comparison of enadoline, a combination, and placebo failed to show any analgesic effect of enadoline. Therefore, a second study with the same design but using higher doses of enadoline was conducted. Despite continued safety and tolerability even at the higher doses, enadoline could not be shown to be superior to placebo. The acetaminophen-codeine combination was significantly more effective than enadoline or placebo. Enadoline did not show analgesic efficacy in this study. Possible reasons for this lack of efficacy are discussed.

Acetaminophen↗
PubMed2001

Effect of apical trephination on postoperative pain and swelling in symptomatic necrotic teeth.

The purpose of this prospective, randomized, blinded study was to determine the effect of apical trephination on postoperative pain and swelling in symptomatic necrotic teeth. Fifty emergency patients participated, and each had a clinical diagnosis of a symptomatic necrotic tooth with associated periapical radiolucency. After endodontic treatment, patients randomly received either an apical trephination or mock trephination procedure. The trephination procedure used a Stabident perforator to provide an initial opening in the cortical bone that was enlarged with files (#25 through #120) and an endodontic spoon. Postoperatively, each patient received: ibuprofen; acetaminophen with codeine (30 mg); and a 7-day diary to record pain, percussion pain, swelling, and number and type of pain medication taken. Results demonstrated the use of an apical trephination procedure did not significantly (p > 0.05) reduce pain, percussion pain, swelling, or number of ibuprofen tablets taken in symptomatic necrotic teeth with periapical radiolucencies. The trephination procedure did significantly (p < 0.05) reduce the use of acetaminophen with codeine overall for the 7 days. In conclusion, because there was not a significant reduction in pain, percussion pain, or swelling we cannot recommend the routine use of an apical trephination procedure, as used in this study, in symptomatic necrotic teeth with radiolucencies.

Acetaminophen↗
PubMed1985

Ultrasound in the diagnosis of sphincter of Oddi spasm.

Biliary colic from spasm of the sphincter of Oddi has been a difficult diagnosis to prove. We describe a patient in whom the diagnosis was arrived at using a pharmacological provocative test employing codeine to reproduce pain and a change in liver and pancreatic serum enzymes, and ultrasound to demonstrate a transient increase in common bile duct diameter. Testing carried out before surgical sphincteroplasty reproduced symptoms, and brought about marked pancreatic and liver enzyme elevation and an increase in common bile duct diameter measured by ultrasound (0.4 to 1.0 cm). Such events did not occur after sphincteroplasty. This case study suggests that codeine may be a useful provocative agent and that ultrasound measurements of changes in common bile duct diameter may provide a useful method in the diagnostic approach to Sphincter of Oddi Spasm.

Acetaminophen↗
PubMed1992

Can NSAIDs cause acute biliary pain with cholestasis?

Two patients had many acute episodes of biliary pain with elevated liver function tests 12-48 h after the last ingestion of nonsteroidal anti-inflammatory drugs (NSAIDs) (including paracetamol) alone or in combination with codeine. One had known intolerance to NSAIDs, but paracetamol had not been previously incriminated in the pathogenesis of the attacks. In this patient the combined use of paracetamol and codeine probably also increased the severity of the episodes. We conclude that in some patients in whom endoscopic cholangiography is normal, biliary pain and abnormal liver function tests could be the result of NSAIDs. A thorough drug history is required in such cases.

Acetaminophen↗
PubMed2002

Recovery after tonsillectomy in adults: a three-week follow-up study.

OBJECTIVE: To evaluate recovery after tonsillectomy and safety and efficacy of ketoprofen in pain treatment after discharge. STUDY DESIGN: A prospective, longitudinal study of 102 patients undergoing tonsillectomy. METHODS: All patients underwent tonsillectomy (or adenotonsillectomy) under general anesthesia. In the hospital, 77 patients received a bolus of 0.5 mg/kg ketoprofen intravenously, followed by a 3-mg/kg continuous infusion over 24 hours, and oxycodone for rescue analgesia. Twenty-five patients received normal saline and oxycodone. At discharge, all patients were prescribed ketoprofen capsules at a dose of 3 to 5 mg/kg per day for postoperative pain control at home, with paracetamol-codeine tablets for rescue analgesia. At home, the patients recorded pain and analgesic consumption each day for the first week after surgery. At 3 weeks, patients recorded the total analgesic requirement, duration of pain, all adverse events during recovery, and return to normal daily activities. RESULTS: No pre-emptive effect of ketoprofen was noticed because there was no significant difference in recovery after discharge between patients who had received ketoprofen or placebo during the first 24 hours after surgery. In the whole study group, the median of pain cessation was 11 days (range, 3-24 days) and the median of analgesic treatment was 12 days (range, 5-25 days). More than 50% of the patients needed 1 to 3 rescue analgesic doses daily during the first week after tonsillectomy. A return back to normal daily activities took place after 12 days (range, 2-24 days). Nine patients needed electrocautery to stop postoperative bleeding. No other serious adverse events occurred. CONCLUSIONS: The main problem after tonsillectomy is significant pain that can last 11 to 12 days after surgery. Ketoprofen combined with paracetamol-codeine provided sufficient analgesia for most patients at home, but because ketoprofen may cause an increase in the secondary hemorrhage rate, it should be prescribed with caution.

Acetaminophen↗
PubMed1997

Correlation of morphine sulfate in blood plasma and saliva in pediatric patients.

This study sought to determine whether saliva concentrations of morphine correlate with plasma levels of morphine in pediatric patients receiving morphine analgesia for severe pain, and to evaluate whether the measurement of saliva morphine concentrations would be a useful, noninvasive, clinical tool to diagnose systemic exposure to morphine. Fifteen pediatric patients were enrolled; for the control group, 18 adult volunteers were recruited. Patients received continuous morphine drips to ameliorate pain caused by a sickle cell vasoocclusive crisis (range, 10-40 micrograms/kg.h). Control subjects were randomized into those receiving acetaminophen with either 8 mg (n = 13) or 30 mg (n = 5) of codeine. All participants fasted at least 2 hours before sample collection. Blood and saliva samples were collected simultaneously. All samples were analyzed by radioimmunoassay for morphine. There was no correlation between saliva and plasma morphine concentrations in either the patients receiving intravenous morphine (r = 0.04, P = 0.89) or in the controls receiving codeine (r = 0.43, P = 0.08). There was no observed difference in the mean counts per minute (CPM) for saliva samples in the pH range 3.96 to 8.06. Saliva concentrations of morphine cannot be used to predict the plasma concentration of morphine in children or adults. However, the concentration of morphine in saliva may be used as a qualitative indicator of systemic exposure to morphine in a subject.

Adolescent↗
PubMedDate not supplied

A review of the efficacy and safety of opioid analgesics post-craniotomy.

--Codeine phosphate is the most commonly used analgesic post-craniotomy. --It is argued, in this paper, that codeine phosphate is an unpredictable pro-drug that does not equate to a safe and effective method of providing analgesia post-craniotomy. --Lack of evidence supporting tramadol's usage and concerns over its interactions and side effects mean its use cannot be advocated. --The traditional justification for withholding morphine in post-craniotomy pain appears to be largely based on anecdotal evidence. --Raising awareness among critical care nurses of the pharmacological properties of the analgesics used is imperative, if post-craniotomy pain is to be adequately treated. --There is an explicit challenge to the neurosurgical community to re-evaluate their pain-management strategies in the post-craniotomy patient.

Analgesics, Opioid↗
PubMed1995

Effects of peripherally and centrally acting analgesics on somato-sensory evoked potentials.

1. The effects of aspirin 1000 mg, paracetamol 1000 mg, codeine 60 mg on somatosensory evoked potentials (SEPs) were measured in a four-way cross-over study. 2. SEPs were elicited by electrical stimulation of the skin overlying the digital nerve at intensities close to pain threshold. 3. Amplitudes and latencies of both early and late SEPs were recorded, as well as first sensory threshold and subjective pain threshold. 4. None of the study medications affected the amplitude or latency of the late SEP components (100-250 ms post-stimulus). The amplitude of early components (15-30 ms post-stimulus) was also unaffected, but aspirin shortened the latency 30 min after ingestion. 5. Sensory detection and pain threshold to electrical skin stimulation were also unaffected by any of the study medications despite subjective central effects with codeine.

Acetaminophen↗
PubMed1990

The influence of furosemide on plasma elimination and urinary excretion of drugs in standardbred horses.

A study of the effects of intravenous administration of either 150 mg or 250 mg of furosemide to standardbred mares pre-treated with other drugs was undertaken to determine whether a unique pattern of drug elimination into urine and from plasma for each compound occurred. Furosemide significantly reduced the plasma concentrations of codeine compared to control 2-6 h after furosemide administration. In contrast, the plasma concentrations of theophylline, phenylbutazone, pentazocine, guaifenesin and flunixin were not markedly altered by furosemide. In the case of acepromazine, clenbuterol and fentanyl, the data generated were insufficient to state with certainty whether or not furosemide affected the plasma concentrations of these three drugs. A significant reduction was noted in the urinary concentrations of guaifenesin, acepromazine, clenbuterol, phenylbutazone, flunixin, fentanyl and pentazocine within 1-4 h of furosemide administration. The urinary concentrations of theophylline remained reduced as long as 8 h after furosemide injection. Furosemide administration to horses pre-treated with codeine resulted in depression of urinary morphine concentrations 2-4 h and 9-12 h after furosemide injection. A lower furosemide dose (150 mg) produced changes in drug urinary excretion and plasma elimination equivalent to the higher dose (250 mg). It is evident that furosemide affects the urinary and plasma concentrations of other co-administered drugs but not in a predictable fashion, which limits the extrapolation of these results to as yet untested drugs.

Acepromazine↗
PubMed1996

Lack of subsensitivity to mizolastine over 8-week treatment.

Mizolastine is a new, nonsedating antihistamine providing satisfactory symptom relief in allergic rhinitis and urticaria. The purpose of this study was to use the wheal and flare skin reactions model to assess the maintenance of the pharmacodynamic effect of mizolastine, administered for 2 months. This double-blind, parallel-group study involved 60 atopic patients randomly allocated, after a 1-week placebo run-in, to once-daily 10 mg mizolastine (n = 29) or placebo (n = 31) groups. Treatment continued for 8 weeks. Prick tests were performed in duplicate with histamine chlorhydrate (10 mg/ml), codeine phosphate (9%), and five increasing concentrations (1-500 reactivity index/ml) of standardized allergen extracts (grass pollen or mites) at days 0, 7, 28, 42, and 56. After 7 days of treatment, inhibition of histamine-induced wheal was -76% and +20%, respectively, with mizolastine and placebo (P = 0.0001), in comparison with baseline; inhibition of flare was -86% and +5%, respectively, with mizolastine and placebo (P = 0.0001). Suppression was maintained to a similar extent throughout the study. Results were consistent between histamine-, codeine-, and allergen-induced tests. Safety was satisfactory in both groups. The study confirms mizolastine as a potent antihistamine which does not induce subsensitivity when taken for 8 weeks, and which can be safely recommended in allergic conditions.

Adolescent↗
PubMed1997

Quantitative measurement of extracellular histamine concentrations in intact human skin in vivo by the microdialysis technique: methodological aspects.

Calculation of recovery is needed in microdialysis studied to calculate absolute concentrations of compounds in the extracellular water space. The purposes of this study were to determine the extracellular concentration of histamine in intact human skin in vivo and to study the validity of absolute histamine measurements during allergic skin reactions. A skin microdialysis technique and two calibration techniques, the no net flux method and the flow rate method, were used to quantify histamine concentrations in resting skin. To validate these techniques, skin glucose concentrations were analysed as well. In addition, the influence of vasodilation and plasma extravasation on recovery was followed after intradermal injection of codeine, a mast-cell secretagogue. As expected, both calibration methods estimated skin glucose concentrations to be identical with venous blood glucose concentrations. However, skin histamine levels could not be calculated by the no net method, because the data did not meet the theoretic assumptions of this method. In contrast, histamine data fitted theoretically with the flow rate method, and skin histamine concentrations of 18.8 +/- 2.8 nM were found to be significantly greater than plasma histamine concentrations of 4.3 +/- 0.7 nM. Within minutes after intradermal injection of codeine, recovery increased significantly in a dose-dependent fashion. Vasodilation per se did not influence recovery. In conclusion, absolute assessment of skin histamine concentrations can be made by microdialysis by the flow rate method. The validity of such an estimate and the theoretic prerequisites for the calculations are discussed. Quantitative measurement of skin histamine levels during allergic reactions cannot be performed since recovery is altered by plasma extravasation after skin challenge.

Adult↗
PubMed1959

Comparative effects of analgesics on pain threshold, respiratory frequency and gastrointestinal propulsion.

In the rat, the ratio of the analgesic to the respiratory depressant potency was the same for morphine, codeine, diamorphine, methadone, dipipanone, piperidylisomethadone, phenadoxone, dextromoramide, and propoxyphene. The relative respiratory depressant activity of pethidine tended to be less, but the difference was not significant. The ratio of the analgesic dose to the dose preventing transport of a charcoal meal in the rat was about the same for morphine, codeine, pethidine, methadone, phenadoxone, dimethylthiambutene, and propoxyphene; the relative activities of these compounds in inhibiting the peristaltic reflex of the isolated guinea-pig ileum were also similar. However, because of differences in the slopes of regression lines in the charcoal meal test, some compounds (for example, morphine) had a greater effect on gastrointestinal propulsion than others (for example, pethidine) when given at moderate analgesic dose levels.In studies of the effects of intracisternal morphine in the rat, effects on the spinal reflex of the tail were to some extent dissociated from effects on the threshold for a squeak response. Further, the delaying of transport of a charcoal meal paralleled depression of respiratory rate, and this is evidence for the participation of a central as well as a peripheral action in the effect of morphine on the gastrointestinal tract. The delay in propulsion was reduced by nalorphine and increased by atropine and two general anaesthetic substances, but was unaffected by a number of other pharmacological agents.

Analgesics↗
PubMed1971

An implanted reservoir of morphine solution for rapid induction of physical dependence in rats.

1. Rats were dosed continuously with morphine hydrochloride by giving a daily dose through tubes connected to small, subcutaneously implanted reservoirs. Morphine was withdrawn by washing out the reservoir with drug vehicle. The daily dose of morphine, or substitute drug received by each rat was determined by difference by estimating the drug remaining in reservoir washings.2. Withdrawal symptoms were more pronounced after 9 days than after 4 days of dosing with morphine.3. Body weight loss, maximal at 24 h, and increased defaecation during the first 7 h were the chief physiological signs of morphine withdrawal. The body weight loss was the result of hypodipsia and anorexia exacerbated by increased defaecation.4. When substituted for morphine in the reservoir, methadone and codeine completely prevented body weight loss and increased defaecation, while pethidine was effective against increased defaecation, but not against 24 h body weight loss. The opiate-antagonist analgesics pentazocine, nalorphine and cyclazocine either had no effect on withdrawal symptoms or increased their severity.5. In morphine dependent rats under continued morphine administration subcutaneous doses of the opiate-antagonists nalorphine, cyclazocine and naloxone all precipitated the withdrawal symptoms of body weight loss and increased defaecation. The weak antagonist pentazocine caused a significantly increased defaecation, but no significant change in body weight, while the opiates pethidine, codeine and methadone had no significant effect on body weight or defaecation.6. The advantages of inducing dependence by this method of dosing are discussed.

Animals↗
PubMed1975

Hyperglycaemia produced by drugs with analgesic properties introduced into the cerebral ventricles of cats.

1 The effects on blood glucose of four substances with analgesic properties (apomorphine, pethidine, codeine and etorphine) and of prostaglandin E(1) were examined in unanaesthetized cats. They were applied by the intraventricular route being either injected into a lateral ventricle or infused into the fourth ventricle through implanted Collison cannulae.2 Apomorphine gave rise to pronounced hyperglycaemia in a dose of 0.75 mg which produced scarcely any hyperglycaemia on intravenous injection. It was more effective on infusion into the fourth ventricle than on injection into a lateral ventricle and was approximately half as potent as morphine in provoking hyperglycaemia.3 Codeine produced no hyperglycaemia in doses of 0.75 and 1.5 mg.4 Pethidine had a weak hyperglycaemic action in doses of 0.75 and 1.5 mg, but the effect was not regularly obtained. Potency of the drug was at most only a third to a sixth that of morphine.5 Etorphine produced strong hyperglycaemia on infusion into the fourth ventricle in a dose of 10 mug. Unlike apomorphine or morphine it was more potent on injection into a lateral ventricle when it produced a strong hyperglycaemic response in doses of 5 or 1 mug, which were subthreshold on infusion into the fourth ventricle. However, this response may have been brought about indirectly as a result of severe asphyxia and of convulsions associated with the injections. On infusion into the fourth ventricle, etorphine was about 75 times as potent as morphine in producing hyperglycaemia.6 Prostaglandin E(1) had no hyperglycaemic action when infused into the fourth ventricle in a dose of 400 ng.

Analgesics↗
PubMed1981

Inhibition of arachidonic acid release as the mechanism by which glucocorticoids inhibit endotoxin-induced diarrhoea.

1 Dexamethasone blocked endotoxin-induced diarrhoea in mice, but not that induced by arachidonic acid or prostaglandin E2. 2 Indomethacin blocked endotoxin and arachidonic acid-induced diarrhoea, but not that induced by prostaglandin E2. 3 Codeine blocked all three forms of diarrhoea. 4 The above data, when considered in relation to literature reports that endotoxin induces prostaglandin synthesis, suggest that dexamethasone blocks diarrhoea by preventing the release of arachidonic acid, the substrate for prostaglandin biosynthesis. 5 The activities of indomethacin and dexamethasone in castor oil diarrhoea support the above conclusion and their inactivity in 5-hydroxytryptophan-induced diarrhoea confirms the absence of 'codeine-like' direct effects on the gut. 6 Other glucocorticoids (hydrocortisone, prednisolone) were also able to block endotoxin diarrhoea, but oestradiol, testosterone and progesterone did not. 7 The inhibitory action of dexamethasone on endotoxin diarrhoea could not be blocked by the protein synthesis inhibitor, cycloheximide, nor by the glucocorticoid receptor antagonist, progesterone. Thus, involvement of glucocorticoid receptor-mediated gene activation could not be demonstrated.

Animals↗