Which is better for the management of postpartum perineal pain: Ibuprofen or acetaminophen with codeine?
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Journal Article↗
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A new synthetic codeine substitute: (-)-3-phenoxy-N-methylmorphinan.
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Analgesics↗
[A case of verbal hallucination in codeinism].
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Adult↗
Experience with a urine opiate screening and confirmation cutoff of 2000 ng/mL.
Until recently, most laboratories used an opiate immunoassay screening and confirmation cutoff value of 300 ng/mL for codeine and morphine detection by gas chromatography-mass spectrometry (GC-MS). The cutoff value for opiates was increased to 2000 ng/mL or higher in various laboratories because of concerns that small doses of codeine and foods containing poppy seeds would give a positive opiate-screening result. Workplace drug-testing programs in the U.S. raised the opiate cutoff value to 2000 ng/mL on 30 November 1998. The objective of this study is to describe the results of opiate testing of 8600 urine specimens collected over 24 months with a 2000-ng/mL screening and confirmation (codeine and morphine) cutoff value. Specimens were screened by the EMITdau opiate assay using an in-house 2000-ng/mL morphine calibrator. Presumptive positive findings (N = 621) were analyzed quantitatively by GC-MS for codeine and morphine. One hundred and eighty six urine specimens were positive for codeine and morphine (> 2000 ng/mL), 298 specimens were positive for codeine only (> 2000 ng/mL) and 26 specimens were positive for morphine only (> 2000 ng/mL). All remaining specimens had codeine and morphine values < 2000 ng/mL. The codeine and morphine confirmation rate in this program reduced from 7.1% in 1994-1996 (300-ng/mL cutoff) to 2.1% in 1997-1998 with a 2000-ng/mL cutoff value. The codeine-only confirmation rate lowered from 6.6% (300-ng/mL cutoff) to 3.4% (2000-ng/mL cutoff). It was concluded that increasing opiate screening and codeine and morphine confirmation cutoff values led to > 300% reduction in the confirmed-positive rate for codeine and morphine and a 47% reduction in codeine-only confirmations in a urine drug-testing program where codeine was the major opiate used.
Codeine↗
[Identification of the drugs in the mixture using thin-layer chromatography in sudden poisoning cases].
The problem of acute intoxication has become very urgent now due to a great number of various chemical preparations accumulated during the last decades in the environment. Intoxications with psychotropic drugs and their mixtures form the significant part of the intoxications; there is an increasing tendency of intoxication with several preparations at a time. Amitriptyline and codeine are the preparations, which more frequently can cause intoxication. Fluoxetine is one of the newest and often used antidepressants. Under certain circumstances, like overdose, using all preparations together, long term using or using for suicide, these preparations can be even a cause of death. In such cases amitriptyline, fluoxetine and codeine become the objects of chemical-toxicological analysis. The possibility of the separation and identification of amitriptyline, fluoxetine and codeine in the mixture using thin-layer chromatography was established. Dragendorf reagent, modified by Munje, is most suitable for the spray-distinct of the chromatographic plates for all three substances. Amitriptyline research limit, using this developer, is 0.4 microg, fluoxetine--1.6 microg, codeine--0.8 microg. Most acceptable for separation the components of the mixture are 5 mobile phases: 1. Diethyl acetate-methanol-ammonium hydroxide (concentrated solution) (85:10:5). Amitriptyline, fluoxetine and codeine R(f) medium values respectively are 0.94; 0.63; 0.51. 2. Buthylacetate-methanol-ammonium hydroxide (concentrated solution) (85:10:5). Amitriptyline, fluoxetine and codeine R(f) medium values respectively are 0.65; 0.24; 0.15. 3. Cyclohexane-diethyl acetate-diethyl amine (70:15:15). Amitriptyline, fluoxetine and codeine R(f) medium values respectively are 0.93; 0.75; 0.37. 4. Cyclohexane-buthylacetate-diethyl amine (70:15:15). Amitriptyline, fluoxetine and codeine R(f) medium values respectively are 0.92; 0.51; 0.25. 5. Acetone-1,4-dioxane-ammonium hydroxide (concentrated solution) (30:68:2). Amitriptyline, fluoxetine and codeine R(f) medium values respectively are 0.82; 0.62; 0.42. Recommended methodology for the separation and identification of amitriptyline, fluoxetine and codeine in the mixture using thin-layer chromatography is statistically reliable: when confidence level is 0.95, relative error is less than 0.05; standard deviation is from 0.007 to 0.03. Recommended methodology suits for mixture, extracted from biological liquids, components separation and identification.
Acute Disease↗
Histamine release from isolated rat mast cells: effect of morphine and related drugs and their interaction with compound 48/80.
Morphine, codeine, and pethidine induced histamine release from isolated rat mast cells in the same concentration range. The histamine release induced by morphine and by codeine occurred rapidly, in contrast to the release induced by pethidine. The effect of morphine was reduced by the presence of calcium, enhanced by magnesium, and unaffected by phosphatidyl serine. Pretreatment of the cells with the ionophore A23187 inhibited the response to morphine, indicating a requirement for intracellular calcium. The release induced by morphine and by codeine was inhibited by antimycin A, but the release induced by pethidine was unaffected. The effect of morphine was inhibited by both naloxone and codeine, and naloxone also reduced the release induced by codeine. The effect of pethidine was inhibited by codeine, whereas the influence of naloxone was less pronounced. Preincubation of cells with lower concentrations of morphine reduced the response to a subsequent exposure to morphine. The release induced by compound 48/80 was similarly inhibited after preincubation with morphine as well as after preincubation with codeine and with pethidine. In contrast, preincubation with pethidine enhanced the effect of subsequent incubation with pethidine. Preincubation with low concentrations of compound 48/80 reduced the response to compound 48/80 in the absence of calcium, but was without effect in the presence of calcium. It is suggested that morphine, codeine, pethidine, and naloxone act on common or closely relates sites on the mast cell and that these sites may account for the action of compound 48/80 as well. The results indicate similar mechanisms for the histamine release induced by morphine and by codeine, whereas pethidine clearly has a different mode of action.
Animals↗
Pharmacological studies on dl-glaucine phosphate as an antitussive.
Antitussive effect, toxicity and other related pharmacological properties of dl-1,2,9,10-tetramethoxy-6a,alpha-aporphine phosphate (dl-glaucine phosphate, DL-832) were studied in comparison with those of codeine. Acute toxicity of DL-832 in mice was 2/5 to 7/10 of that of codeine for any routes of i.v., i.p., s.c. and p.o. The antitussive effect as tested by "coughing dog and cat" methods and Domenjoz's method in cats was 1/5 to 4/5 that of codeine, according to the routes administered. Safety margin in antitussive effect was similar to or less than that of codeine. Differing from codeine, levallorphan exerted no influence on the antitussive effect of DL-832. In vitro, DL-832 exerted moderate relaxant actions on normal tone and on contractions induced by histamine and acetylcholine of tracheal muscle. In vivo, it showed a moderate relaxant effect on histamine-induced bronchial constriction. The decrease in the volume of respiratory tract fluid caused by DL-832 was smaller than that by codeine. DL-832 slightly reduced the transportation rate of intratracheal foreign body, although to much lesser extent as compared to codeine. On respiration, blood pressure and heart rate, DL-832 showed depressant effects and moreover it caused changes in ECG. However, all of these effects were similar to and a little weaker than those observed with codeine. DL-832 prolonged hexobarbital sleeping time significantly. Neither analgesic nor anticonvulsant effect was observed. When given in larger doses, DL-832 inhibited intestinal transportation in vivo, although this effect was much weaker than that of codeine. DL-832 showed slight local anesthetic effect.
Anesthetics, Local↗
[UV spectrophotometric research of drug mixture in sudden poisoning cases].
UNLABELLED: The objective of this research--to develop the methodics for analysis of amitriptyline, fluoxetine and codeine in the mixture. RESULTS: The analytical method of amitriptyline, codeine and fluoxetine in the mixture identification and quantitative determination using ultraviolet spectrophotometry was established. Preparations in the mixture can't be separated, because material ultraviolet light peaks are in insufficient distance and therefore cover one another. The maximum of ultraviolet light absorption for amitriptyline is at 217-220 and 238-240 nm; fluoxetine--at 226-228 nm; codeine--at 224-248 and 284-286 nm. Using ultraviolet spectroscopy it's possible to identify amitriptyline, fluoxetine and codeine only after separating mixture components by thin-layer chromatography, the same time executing cleaning of extracts from blood and urine. Using ultraviolet spectroscopy can be identificated at least 0.5 micro g/ml amitriptyline, 1.5 micro g/ml fluoxetine and 1.0 microg/ml codeine. The intervals of the quantitative determination: 5-25 microg/ml amitriptyline; 5-30 microg/ml fluoxetine; 100-300 microg/ml codeine; relative error of the measurement, when confidence level is 95%, is from 0.66 to 1.2% for amitriptyline; from 0.66 to 1.45% for fluoxetine; from 0.33 to 0.88% for codeine. Standard deviation is from 1.15 to 2.08% for amitriptyline; from 1.15 to 2.52% for fluoxetine; from 0.57 to 1.53% for codeine. Molar absorption coefficients for all three preparations in distillated water were determinated. CONCLUSIONS: recommended methodology suits for mixture, extracted from biological liquids, components separation, identification and quantitative determination.
Acute Disease↗
Pharmacokinetics and O-dealkylation of morphine-3-alkyl ethers in the rat. A radioimmunoassay study.
Radioimmunoassay procedures were used to investigate the relationship between the chemical structure and disposition of morphine, codeine, ethylmorphine, t-butylmorphine, and pholcodine. Male Sprague-Dawley rats received po or iv doses of each drug equivalent to 10 mg/kg free base. Blood samples were collected at various times over the 6-hr period after each drug administration, and plasma concentrations of the parent drugs and metabolically produced morphine were determined. A single ethylmorphine antiserum was used for analysis of codeine, ethylmorphine, t-butylmorphine, and pholcodine in separate experiments, whereas a specific morphine antiserum was used in the radioimmunoassay of this compound. The absolute oral bioavailabilities of morphine, codeine, ethylmorphine, and t-butylmorphine all were below 10%, whereas that of pholcodine was over 40%. Terminal half-lives of morphine, codeine, ethylmorphine, and t-butylmorphine after iv administration all were less than 45 min, while that of pholcoline was over 2 hr. Codeine, ethylmorphine, t-butylmorphine, and pholcodine did not appear to undergo conjugation, as evidenced by the similarity between areas under the curve for total (unconjugated plus conjugated) and parent (unconjugated) drugs. Amounts of metabolically produced morphine in rats treated with codeine, ethylmorphine, t-butylmorphine, or pholcodine differed markedly. After oral administration, presystemic O-dealkylation of codeine and ethylmorphine was much greater than that of t-butylmorphine or pholcodine, presumably due to the presence of much bulkier 3-alkyl substituents in the latter compounds. Thus, the ratio of the morphine AUC to that of parent drug after po administration was 1.37 for codeine and 1.60 for ethylmorphine, but only 0.08 for t-butylmorphine and 0.01 for pholcodine.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
A model to evaluate mild analgesics in oral surgery outpatients.
A model was developed to evaluate mild analgesics in an oral surgery outpatient clinic population. On a report form, patients recorded starting pain and then pain intensities, relief responses, and side effects hourly for 3 hr after drug administration. The treatments were randomly allocated to patients on a single-dose-only basis, and the double-blind technique was used. The first of two studies compared codeine 30 mg, aspirin 650 mg, codeine 30 mg with aspirin 650 mg, and placebo in 128 subjects. The second study compared codeine 60 mg, acetaminophen 600 mg, and codeine 60 mg with acetaminophen 600 mg and placebo in 160 subjects. Time-effect curves were generated for both pain relief and pain relief and pain intensity difference (PID). First-hour scores, peak scores, and total scores were statistically analyzed by parametric and nonparametric factorial analysis. Both aspirin 650 mg and acetaminophen 600 mg proved superior to placebo (p less than 0.01) for all measures of effect with both parametric or nonparametric analyses, while codeine 30 mg was not significantly superior to placebo in any analysis. Codeine 60 mg proved significantly superior to placebo for certain measures of effect when analyzed with the nonparametric model. There was no significant interaction between either aspirin or acetaminophen and codeine.
Acetaminophen↗
Effects of ethanol on ethylmorphine metabolism in isolated rat hepatocytes: characterization by means of a multicompartmental model.
Hepatic cytochrome P-450 enzymes mediate at least two important biotransformation pathways of codeine and ethylmorphine starting with either N-demethylation or O-dealkylation, producing polar metabolites which are then subsequently glucuronidated. The present study was designed to characterise the acute effects of ethanol on the metabolism of ethylmorphine and to compare it with the effects on codeine in suspensions of freshly isolated rat hepatocytes. Isolated rat hepatocytes from male Wistar rats were prepared by a collagenase perfusion method. Ethylmorphine, codeine and their metabolites were quantified by HPLC with UV detection. The total ethylmorphine elimination rate was reduced by 12% at 5mM and 38% at 100 mM ethanol. The corresponding percentages for codeine were 16 and 43%. In the presence of ethanol the concentrations of several intermediate and end products of ethylmorphine and codeine changed markedly from the control situation. The experimental data were applied to a mathematical compartmental linear model to estimate the influence of ethanol on the separate reaction rates in the two main metabolic pathways. The ratios between reaction rate constants in the ethylmorphine experiments at 100 and 0 mM ethanol were 0.65 for ethylmorphine-->norethylmorphine, 0.63 for norethylmorphine-->normorphine, 0.56 for ethylmorphine-->morphine, 0.49 for morphine-->normorphine, 0.31 for normorphine-->normorphine-3-glucuronide and 0.49 for morphine-->morphine-3-glucuronide. Almost similar effects of ethanol on codeine metabolism were found. In additional experiments, norethylmorphine or norcodeine (50 microM) was incubated with 5 mM to 100 mM of ethanol and the metabolism of both norethylmorphine and norcodeine was found to be inhibited by ethanol in a concentration-dependent manner. The glucuronidation of morphine and normorphine added in separate experiments was also inhibited by ethanol, from 22 to 36% for morphine-3-glucuronide and 30 to 60% for normorphine-3-glucuronide, respectively, in the presence of 5 mM to 100 mM of ethanol. It was concluded that all steps in the metabolism of ethylmorphine (and codeine) leading to the end products morphine-3-glucuronide and normorphine-3-glucuronide were inhibited by ethanol, and that the glucuronidation process were the ones most affected by ethanol.
Animals↗
Muscle pain perception and sympathetic nerve activity to exercise during opioid modulation.
The purpose of this experiment was to examine the effects of the endogenous opioid system on forearm muscle pain and muscle sympathetic nerve activity (MSNA) during dynamic fatiguing exercise. Twelve college-age men (24 +/- 4 yr) performed graded (1-min stages; 30 contractions/min) handgrip to fatigue 1 h after the ingestion of either 60 mg codeine, 50 mg naltrexone, or placebo. Pain (0-10 scale) and exertion (0-10 and 6-20 scales) intensities were measured during the last 15 s of each minute of exercise and every 15 s during recovery. MSNA was measured continuously from the peroneal nerve in the left leg. Pain threshold occurred earlier [1.8 +/- 1, 2. 2 +/- 1, 2.2 +/- 1 J: codeine, naltrexone, and placebo, respectively] and was associated with a lower rating of perceived exertion (RPE) (2.7 +/- 2, 3.6 +/- 2, 3.8 +/- 2: codeine, naltrexone, and placebo, respectively) in the codeine condition compared with either the naltrexone or placebo conditions. There were no main effects (i.e., drugs) or interaction (i.e., drugs x time) for either forearm muscle pain or RPE during exercise [pain: F (2, 22) = 0.69, P = 0.51]. There was no effect of drug on MSNA, heart rate, or blood pressure during baseline, exercise, or recovery. Peak exercise MSNA responses were 21 +/- 1, 21 +/- 2.0, and 21 +/- 2.0 bursts/30 s for codeine, naltrexone, and placebo conditions, respectively. Peak mean arterial pressure responses were 135 +/- 4, 131 +/- 3, and 132 +/- 4 mmHg for codeine, naltrexone, and placebo conditions, respectively. It is concluded that neither 60 mg codeine nor 50 mg naltrexone has an effect on forearm muscle pain, exertion, or MSNA during high- intensity handgrip to fatigue.
Adolescent↗
Effects of local corticosteroids on acute experimental urticaria.
Corticosteroids are often used in the treatment of acute or chronic urticaria. However, their effects on mastocyte activation as well as on the histamine-induced dermal oedema remain poorly investigated. The aim of the present study was to investigate the effects of corticosteroids (CS) on the development of acute experimental urticaria induced by prick-tests with histamine and codeine. This experimental model corresponds to the common form of urticaria. CS were administered at the site of the histamine and codeine prick tests in order to test for a direct effect on the development of acute urticaria. Two types of experiments were performed: 1) after a 48-hour period of topical CS application on the forearm, 7 healthy volunteers were skin prick-tested with histamine and codeine simultaneously in duplicate, one series in the pretreated area and the other in a non-treated area. 2) six other volunteers were prick-tested with histamine and codeine on their forearm, in duplicate. Immediately after testing, intradermal methyprednisolone was injected at the site of the prick-tests in the last series. Skin wheal and flare responses were measured after 20 mns and statistically compared with and without CS treatment. Whereas short-term CS topical application did not appear to modify cutaneous reactivity to histamine and codeine, local CS injection was associated with a significant increase in the flare induced by histamine and codeine (respectively + 18 +/- 3% and + 38 +/- 3%; P = 0.05). The wheal tended to be increased after injected CS. In conclusion, these results show that CS are neither able to prevent nor to improve experimental urticaria, i.e. wheal and flare, and even increase the histamine and codeine-induced erythema. That a similar result could apply to patients with chronic urticaria and with systemic CS remains to be studied.
Acute Disease↗
Antitussive activity and other related pharmacological properties of d-3-methyl-N-methylmorphinan (AT-17).
Antitussive activity and some other related pharmacological properties of d-3-methyl-N-methylmorphinan were studied. Toxic symptoms in mice and dogs were due to the CNS excitation. Acute toxicity of (AT-17) in mice was slightly (s.c.) or far (p.o.) weaker than that of codeine, but it was three times as toxic as codeine in dogs (i.v.). Antitussive efficacy was about 40% of that of codeine in dogs, whereas 77% as potent as codeine in cats. It showed no relaxing effect on the bronchial muscle of guinea pigs in either normal tone or histamine-induced spasms. It had analgesic effect 1/3 as potent as codeine in mice but it was not antagonized by levallorphan. The prolongation of hexobarbital sleeping time by AT-17 was similar extent to that by codeine. Anti-electroshock effect was half as potent as that of phenobarbital. The inhibitory effect on the transportation of intestinal contents in mice was far weaker than that of codeine. Effect on the respiratory and circulatory systems were also investigated.
Analgesia↗
Effect of terbutaline and bambuterol on immediate-type allergic skin responses and mediator release in human skin.
BACKGROUND: Beta-2 agonists are potent inhibitors of mast cell degranulation in vitro. Intradermally injected they also inhibit mast cell activation in human skin in vivo. To what extent orally administered beta(2)-agonists inhibit mast cell degranulation and allergic skin responses in vivo in daily recommended doses remains unclear. PURPOSE: The main purpose was to study the effects of oral administered terbutaline and bambuterol on allergen- and codeine-induced histamine release and skin responses in intact human skin in vivo. In addition, control studies were carried out with intradermally injected terbutaline. METHODS: Ten allergic subjects were randomized to receive bambuterol (10 mg tablets twice daily), terbutaline (7.5 mg controlled release tablets twice daily) and corresponding placebo for 5 days with a washout phase of 3 days between treatments in a double-blind, double-dummy, cross-over trial. The patients were studied at the fifth day of each regimen, i.e. at day 5, 13, and 21. Allergen- and codeine-induced histamine release was measured by microdialysis technique. Wheal and flare reactions to allergen, codeine, and histamine were measured planimetrically. Measurements were performed in the morning on day 5 on each regimen before medication and for additional 5 h after administration of the morning dose. In a separate series of experiments in another 10 allergic patients, 1-1,000 nM (0.05-50 pmoles) of terbutaline was injected intradermally for measurement of histamine release, prostaglandin D2 (PGD2) synthesis and skin responses. RESULTS: Neither orally administered terbutaline nor bambuterol significantly reduced allergen- or codeine-induced histamine release. Flare reactions to allergen, codeine and histamine remained unaffected which was also the case for the majority of the wheal reactions. In comparison, intradermally injected terbutaline significantly reduced allergen-induced histamine release, PGD(2) synthesis, and skin reactions. Codeine-induced histamine release remained unaffected. Terbutaline significantly reduced flare reactions to codeine and histamine with no effect on wheal reactions. CONCLUSIONS: Terbutaline, in micromolar concentrations, was a potent inhibitor of immediate allergic skin reactions primarily due to inhibition of mast cell degranulation. However orally administered terbutaline, as the active drug itself or released from its pro-drug bambuterol, did not inhibit mast cell activation or allergic skin responses.
Administration, Oral↗
Picenadol in a large multicenter dental pain study.
STUDY OBJECTIVE: To estimate the analgesic dose of picenadol hydrochloride equal to codeine 60 mg in a dental pain model. DESIGN: Randomized, double-blind, parallel, dose-response study. SETTING: Four university-based dental clinics. PATIENTS: Four hundred eight adult patients with moderate or severe pain after extraction of one or more impacted molar teeth plus bone removal. INTERVENTIONS: Patients received orally administered single doses of picenadol 15 and 30 mg, codeine phosphate 30 and 90 mg, or placebo. METHODS: Single oral doses of picenadol 15 and 30 mg, an opioid agonist-antagonist, were compared with codeine 30 and 90 mg and placebo in 408 patients with moderate or severe pain from third molar extraction in a randomized, double-blind, parallel study. Assessments were performed for pain intensity, pain relief, and adverse events for up to 6 hours after drug administration. MAIN RESULTS: Picenadol 30 mg and codeine 90 mg were more effective than placebo based on sum of pain intensity differences, total pain relief, peak pain relief, and duration of analgesia (p < 0.05). Compared with placebo, the frequency of adverse events was highest for patients receiving codeine 90 mg (p < 0.05). No patients discontinued due to adverse events, and all such events resolved spontaneously. CONCLUSIONS: Picenadol 22 mg was estimated to be equianalgesic to codeine 60 mg, and picenadol 30 mg was safe in this dental pain model.
Adult↗
Ibuprofen controlled-release formulation. A clinical trial in dental impaction pain.
This double-blind study compared a controlled-release formulation of ibuprofen 600 mg with three doses of regular ibuprofen 200 mg and three doses of codeine 30 mg. Patients who had dental impaction surgery received the controlled-release ibuprofen, codeine, or regular ibuprofen when postoperative pain reached moderate to severe intensity. At 4 and 8 hours after dose 1, patients who had initially received the controlled-release ibuprofen received a placebo, and those taking ibuprofen and codeine received their second and third doses of those drugs. All doses of study medication or placebo appeared identical for each treatment. Subjects made evaluations hourly for 12 hours in a diary. The controlled-release ibuprofen had a comparable onset to ibuprofen, a higher peak effect, and was significantly more effective than ibuprofen at hour 4; the controlled-release ibuprofen was significantly more effective than codeine for all hourly observations through hour 9. Ibuprofen was significantly better than codeine only through hour 3. The controlled-release ibuprofen had the lowest incidence of side effects and codeine the highest. The single dose of the controlled-release ibuprofen formulation appeared as efficacious as three regular doses of ibuprofen 200 mg over a 12-hour period.
Adult↗
Hair opiates during pain treatment.
Opiates are commonly used for pain treatment, especially for sharp pain like carcinoma pain. Two opiates are generally prescribed in our hospital: morphine and codeine in association with paracetamol. Most of the patients were given oral forms. Incorporation of morphine and codeine in hair of these patients was studied. Opiates testing in hair is performed by gas chromatography-mass spectrometry (GC-MS), using acid hydrolysis in presence of deuterated standards, a three-step liquid extraction and derivatization with BSTFA + TMCS. Results of codeine and morphine content in hair during pain treatment showed no correlation group between dose and concentration of the drug in hair. However, codeine values in hair during pain treatment compared to codeine in the hair of codeine abusers was significantly different (P < 0.0001).
Acetaminophen↗