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PubMed1997

Do codeine and caffeine enhance the analgesic effect of aspirin?--A systematic overview.

OBJECTIVE: To assess whether codeine and caffeine enhance the analgesic effect of aspirin in post-operative pain. METHOD: Systematic overview of the literature and meta-analysis of published randomized controlled trials (RCTs). RESULTS: Codeine 60 mg leads to a small increase in the analgesic effect of 650 mg of aspirin when total pain relief score (TOTPAR%) is used as a efficacy end-point. This increased effect was not seen when sum of pain intensity (SPID%) and proportions of patients responding with moderate to excellent pain relief were used as outcome measures. Caffeine did not enhance the analgesic effect of aspirin. CONCLUSION: Codeine 60 mg may produce a small increase in the analgesic effect of aspirin 650 mg. However, this effect is not clinically meaningful. Caffeine has no adjuvant analgesic effect. At over-the-counter (OTC) doses, caffeine and codeine are not useful in aspirin formulations.

Analgesia↗

PubMed1984

Effects of cromolyn on codeine-induced histamine release in vivo.

Cromolyn has been shown to inhibit histamine release from mast cells induced by various stimuli in vitro. However, the local effects of cromolyn on codeine-induced wheal and flare skin reactions are not well understood. Intradermal injection of codeine induced prominent whealing in almost all humans. We studied the effect of local cromolyn injection on codeine-induced skin reactions, histamine release, and ultramicroscopic changes in mast cells in 10 volunteers. The finding in this study showed that injection of a 2% cromolyn solution before or together with the codeine injection does not affect the subsequent skin reactions, histamine release and ultramicroscopic changes of mast cells.

Codeine↗

PubMed1977

Simultaneous determination of codeine and morphine in biological samples by gas chromatography with electron capture detection.

A sensitive gas chromatographic method for the simultaneous determination of codeine and morphine in plasma and brain samples is described. The method involves solvent extraction of the compounds from plasma, derivatization with pentafluoropropionic anhydride and subsequent separation on a 3% OV-17 column. The quantification is performed with electron capture detection. The sensitivity of the method (0.75 ng of morphine and 7.5 ng of codeine in a sample) makes it especially useful for pharmacokinetic investigations. The method was successfully applied to determine the time course of codeine and its metabolite morphine after intravenous administration of codeine to the rat.

Animals↗

PubMed1972

Blood-brain barrier: penetration of morphine, codeine, heroin, and methadone after carotid injection.

Labeled morphine, codeine, heroin, or methadone was injected as a bolus into the common carotid artery of the rat, and the rat was decapitated 15 seconds later. The brain uptake of the drug was calculated by measurement of the brain content of the drug as a percentage of a labeled, highly diffusible reference substance simultaneously injected. The uptake of morphine was below measurability; the uptake of codeine was 24 percent; heroin, 68 percent; and methadone, 42 percent. Brain uptakes of morphine and codeine were also studied after intravenous injection and correlated well with uptakes after carotid injection; the uptake of codeine being nearly complete by 30 seconds. These studies indicate that brain uptake of certain of these drugs is very rapid and that uptake of heroin injected intravenously is probably limited by the regional flow of blood in the brain. The possible relation of this rapid penetration of the blood-brain barrier by heroin to its strongly addictive properties is discussed.

Animals↗

PubMed1978

Double-blind oral analgesic study of butorphanol in musculoskeletal pain: a comparison with codeine and placebo.

Butorphanol tartrate (4 mg and 8 mg) was compared to codeine phosphate (60 mg) and placebo for oral analgesic activity and side-effects employing a double-blind design in ninety-three out-patients suffering from moderate to very severe musculoskeletal pain. The study duration was 72 hours with medication administered every 4 to 6 hours (four times daily) for a total of twelve doses per patient. The results demonstrate that both the 4 mg and 8 mg doses of butorphanol were significantly better (p less than 0.u5) than placebo. While codeine 60 mg also proved active, it appears to be less efficacious than the high dose of butorphanol. The peak effect appeared to be evident in 1 to 2 hours. Butorphanol may be at least seven times more potent than codeine on a milligram basis. Although no serious side-effects were observed, butorphanol appeared to present a greater incidence of side-effects than codeine and placebo in this study.

Adolescent↗

PubMed1991

Differential sensitivity to physical dependence on morphine and codeine in three inbred strains of mice.

The purpose of this experiment is to investigate genetic differences in the development of physical dependence on morphine and codeine in inbred strains of mice, C57BL/6, C3H/He and DBA/2. Mice were treated with morphine- or codeine-admixed food (1, 2 and 3 mg/g of food) for 3 to 9 days. After the termination of drug treatment, the mice were given naloxone (5 mg/kg, s.c.). The incidences of jumping and teeth chattering by naloxone challenge in morphine- and codeine-treated C57BL/6 mice were much greater than those in C3H/He and DBA/2 mice. However, the incidences of other naloxone-precipitated withdrawal signs, such as ptosis and diarrhea, were not different among the three inbred strains of mice. These results indicate that genotype is an important determinant of the degree of most naloxone-precipitated withdrawal signs in morphine- and codeine-treated mice.

Animals↗

PubMed2001

Seizures with intravenous codeine phosphate.

OBJECTIVE: To describe an adverse effect with intravenous codeine in a chid diagnosed with sickle cell anemia. CASE SUMMARY: A seven-year-old boy with sickle cell anemia was admitted to the emergency department with severe pain unresponsive to high doses of oral acetaminophen; subsequently, intravenous codeine phosphate was administered. The patient immediately developed a tonic-clonic seizure, which was treated with intravenous diazepam and naloxone. DISCUSSION: Seizures associated with the intravenous administration of codeine phosphate have not been extensively reported in the literature, and special precautions for using the parenteral route for this drug have been vague and limited. Because of the frequent need for acute pain control in children with sicke cell crisis, they may be exposed to this type of reaction when intravenous narcotics are administered. The need for clear guidelines regarding the drug's appropriate parenteral dosing and administration is essential. CONCLUSIONS: Codeine phosphate-induced seizures are not common. The need for special instructions for its intravenous administration may prevent this type of reaction, especially in patients in need of acute pain control requiring intravenous narcotics.

Analgesics, Opioid↗

PubMedDate not supplied

Slow release polymer-drug systems obtained by moisture promoted polyreactions. 1. Codeine resinate encapsulated in poly(alkyl alpha-cyanoacrylates).

Samples of codeine resinate consisting of a carboxylic cation exchanger (as a polymeric carrier) and codeine (as a drug) were coated with poly(alkyl alpha-cyanoacrylates) by suspending and stirring wet resinate beads in a toluene solution of the monomer. Methyl, ethyl and n-butyl alpha-cyanoacrylates were used as monomers. Each coated material released codeine more slowly than the non-coated. The data obtained confirmed that water promoted the polymerization of alkyl alpha-cyanoacrylates, which proceeded at the surface of the wet resinate beads. The rate of codeine release depended on the type of monomer used for coating, the monomer/resinate feed ratio and the plymerization time.

Analgesics, Opioid↗

PubMed2006

Henoch-Schönlein purpura associated with acetaminophen and codeine.

We report a case of a relapse of Henoch-Schönlein Purpura (HSP) associated with intake of paracetamol (also known as acetaminophene) and codeine. A 69-year-old man presented with fever, gross hematuria, acute renal failure, palpable purpuric skin rash over the legs, feet and arms, arthralgias and abdominal discomfort. 1 week before he had started therapy with co-efferalgan (association of paracetamol and codeine) for cervical arthrosis. Blood test revealed increase in serum creatinine levels (2.6 mg/dl), CRP (375 mg/dl), with no thrombocytopenia or hypocomplementemia. Co-efferalgan was discontinued. Gross hematuria resolved in 2 days, purpuric rash disappeared in 10 days, renal function returned to normal after 2 weeks and abdominal pain and arthralgias improved on the following 2 - 3 weeks. An objective causality assessment in accordance with the Naranjo algorithm, revealed that the adverse drug reaction was probable between paracetamol/codeine and Henoch-Schönlein purpura. To our knowledge, and based on a medline search (up to 2005), we believe that this could be considered the first case of Henoch-Schönlein purpura, associated with intake of paracetamol and codein. Although this event could be considered rare, clinicians should to be aware of possible associations between HUS and the intake of paracetamol and/or codeine to provide an early therapeutic intervention and a close monitoring.

Acetaminophen↗

PubMed2002

Concentrations of unconjugated morphine, codeine and 6-acetylmorphine in urine specimens from suspected drugged drivers.

Concentrations of unconjugated morphine, codeine and 6-acetylmorphine (6-AM), the specific metabolite of heroin, were determined in urine specimens from 339 individuals apprehended for driving under the influence of drugs (DUID) in Sweden. After an initial screening analysis by immunoassay for 5-classes of abused drugs (opiates, cannabinoids, amphetamine analogs, cocaine metabolite and benzodiazepines), all positive specimens were verified by more specific methods. Opiates and other illicit drugs were analyzed by isotope-dilution gas chromatography-mass spectrometry (GC-MS). The limits of quantitation for morphine, codeine and 6-AM in urine were 20 ng/mL. Calibration plots included an upper concentration limit of 1000 ng/mL for each opiate. We identified the heroin metabolite 6-AM in 212 urine specimens (62%) at concentrations ranging from 20 ng/mL to > 1000 ng/mL. The concentration of 6-AM exceeded 1000 ng/mL in 79 cases (37%) and 31 cases (15%) were between 20 and 99 ng/mL. When 6-AM was present in urine the concentration of morphine was above 1000 ng/mL in 196 cases (92%). The concentrations of codeine in these same urine specimens were more evenly distributed with 35% being above 1000 ng/mL and 21% below 100 ng/mL. These results give a clear picture of the concentrations of unconjugated morphine, codeine and 6-acetylmorphine that can be expected in opiate-positive urine specimens from individuals apprehended for DUID after taking heroin.

Automobile Driving↗

PubMed1975

Gas-chromatographic measurement of codeine and norcodeine in human plasma.

A gas-chromatographic method is described for determination of codeine and norcodeine in human plasma. The method is specific, sensitive, and precise. It was developed for use in bioavailability studies of therapeutic doses of codeine sulfate. After ingestion of a 60-mg codeine sulfate tablet, mean peak codeine concentration in plasma was 107 mug/liter at 1.0 hour. No measurable concentration of norcodeine was found in the plasma by this method.

Chromatography, Gas↗

PubMedDate not supplied

Simultaneous determination of codeine and pyridoxine in pharmaceutical preparations by first-derivative spectrofluorimetry.

A method for the simultaneous determination of codeine and pyridoxine was developed, based on the measurement of their native fluorescence signals, by using first-derivative spectrofluorimetry to resolve the mixture. Codeine was measured at lambda(em) = 309 nm, and pyridoxine was measured at lambda(em) = 450 nm. Instrumental parameters were optimized, and the emission spectra were recorded between 275 and 475 nm, at lambda(ex) = 255 nm and excitation and emission slit widths of 2.5 and 10 nm, respectively. Systematic studies on the influence of species usually present along with the analytes (such as caffeine, ascorbic acid, paracetamol, and thiamine) were also performed. The calibration graphs were linear over the ranges of 0.5-7.0 and 0.1-1.0 microg/mL for codeine and pyridoxine, respectively, and the relative standard deviations (n = 10) were about 3%. The method was successfully applied to the determination of codeine and pyridoxine in solutions of synthetic mixtures and in synthetic and semisynthetic pharmaceutical formulations.

Chemistry Techniques, Analytical↗

PubMed1992

Increased urinary morphine, codeine and tetrahydropapaveroline in parkinsonian patient undergoing L-3,4-dihydroxyphenylalanine therapy: a possible biosynthetic pathway of morphine from L-3,4-dihydroxyphenylalanine in humans.

We have identified morphine and codeine in human urine by means of gas chromatography/mass spectrometry. Gas chromatography/mass spectrometry was also used to quantitate the two alkaloids and tetrahydropapaveroline (THP) in urine of both normal subjects and parkinsonian subjects receiving L-dopa therapy. The morphine, codeine and THP levels in healthy nondrinker controls were 2.93 +/- 0.23, 2.01 +/- 0.53 and 6.70 +/- 1.13 pmol/ml (mean +/- S.E.M.), respectively. In contrast, the urinary levels of codeine and THP in L-dopa-treated parkinsonian patients were significantly elevated to 62.20 +/- 17.54 and 31.04 +/- 15.69 pmol/ml, respectively. Some of the parkinsonian patients showed high urinary morphine levels. Morphine excretion was also enhanced in patients complaining of severe pain due to herpes zoster (24.60 +/- 9.51 pmol/ml) but not in patients with severe pain due to cerebral embolus. These alkaloid levels in the urine of abstinent alcoholics were very low. There were significant correlations among these three alkaloid levels in the urine. The results indicate that morphine and codeine are synthesized in the body from L-dopa and/or dopamine, via the THP-related pathway.

Adult↗

PubMed1991

[Pilot study of the metabolism of codeine to morphine and a possible modification by benzodiazepines].

After administration of high-dose codeine we found that in two cases 20-40% of the total morphine-equivalents in the 24-hour urine sample were free morphine. After another 24 hours the proportion of free morphine was up to 70% and after roughly 96 hours even went up to 96%. Although 10% of the administered codeine was eliminated as morphine. In contrast to the values reported in literature we found that even with codeine/morphine ratios greater than 0.5 and morphine concentrations of up to 2000 ng/ml urine one cannot naturally conclude that morphine/diamorphine has been consumed. The short half-life of codeine in serum was 2-4 hours, the final half-life was 9-11 hours. In urine we found a short half-life of 1-6 hours as well as a long half-life of 7-12 hours. When diazepam was administered simultaneously with codeine the expected half-life in serum was up to 1.5 times and in urine 2.5 times. The codeine/morphine ratios were hardly affected so far as evidence goes which they give of preceding drug-intake.

Biotransformation↗

PubMedDate not supplied

Effects of ephedrine and phenylpropanolamine on the antinociceptive effects of morphine and codeine in mice.

The effects of ephedrine and phenylpropanolamine on the antinociceptive activities of morphine and codeine were investigated. Both morphine and codeine exhibited dose-dependent antinociceptive activities in the tail flick test. Ephedrine (5, 10 and 20 mg/kg) and phenylpropanolamine (5, 10 and 20 mg/kg) showed no antinociceptive effect when administered alone. The antinociceptive effects of morphine were enhanced in mice pretreated with ephedrine or phenylpropanolamine. similarly, codeine antinociception was increased in mice pretreated with ephedrine or phenylpropanolamine. In all cases, the ED50 values and single dose comparisons were shifted in the same direction. These effects on the antinociceptive potencies of morphine and codeine were found to be dose-dependent, being statistically significant at the higher dose levels of ephedrine and phenylpropanolamine used in the present study.

Analgesics↗

PubMed1989

[Antitussive effects of Bakumondô-tô and codeine in bronchitic guinea-pigs].

Antitussive effects of Bakumondô-tô and codeine were examined in bronchitic guinea-pigs made by an exposure to SO2. Bakumondô-tô significantly depressed the cough reflex induced by mechanical and chemical stimulations in the bronchitic but not in the normal animals. Repeated administration of Bakumondô-tô significantly suppressed the increased spontaneous discharge of the superior laryngeal nerve in bronchitic animals. On the other hand, the antitussive action of codeine in bronchitic animals was significantly weaker than that in normal animals. Moreover, repeated administrations of codeine significantly potentiated the increased spontaneous discharge of the superior laryngeal nerve. The results suggest that Bakumondô-tô, unlike codeine, has a notable antitussive activity in bronchitic rather than in normal guinea-pigs.

Animals↗

PubMed1988

Antitussive action of the new anilide derivative vadocaine hydrochloride compared with codeine phosphate in four animal models.

Vadocaine hydrochloride (2',4'-dimethyl-6'-methoxy-3-(2-methylpiperidyl) propionanilide hydrochloride, OR K-242-HCl; INN: vadocaine) is a novel antitussive compound structurally resembling local anaesthetics. Its antitussive profile was studied in several animal models. In guinea-pigs, vadocaine reduced by about 70% the cough episodes induced by sulphur dioxide or ammonia. The effective dose was 2.5 mg/kg p.o., and codeine phosphate was less effective. In cats, vadocaine (3 mg/kg i.v.) inhibited by about 80% for 10 min the cough reflex initiated by mechanical irritation of the trachea. When vadocaine was given via the vertebral artery, it was about 10 times more active than by the intravenous route. Codeine was 3 times as active as vadocaine by both routes. This result indicates an important central component in the antitussive action of vadocaine. In another cat model, 5 mg/kg of vadocaine was somewhat weaker than 1 mg/kg of codeine in inhibiting the cough caused by electrical stimulation of the laryngeal nerve (Domenjoz' method). In dogs, both oral and intravenous doses of 6 mg/kg of vadocaine and 2 mg/kg of codeine were approximately equiactive, inhibiting by 60-80% the cough induced by electrical stimulation of the trachea. Concentrations of vadocaine in serum were around 1 microgram/ml during oral administration. By both routes, the antitussive activity (inhibition of cough by 50% or more) lasted at least 2 h. Vadocaine caused local anaesthesia in the guinea-pig wheal preparation at concentrations of 0.25% and 0.5%, and on the guinea-pig cornea at 0.5%. Duration of anaesthesia was longer than that of lidocaine. Vadocaine did not affect the guinea-pig tracheal strip preparation.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Local↗

PubMed1987

Codeine-induced mast cell degranulation in human skin: effect of calcium channel blockers.

Codeine and other opiates can induce immediate type wheal and flare skin reactions. Calcium channel blockers including nifedipine have been shown to inhibit mast cell degranulation in different systems. The oral administration of nifedipine (10 mg) did not affect the size of codeine-induced skin reactions in ten normal volunteers. Mean wheal over flare sizes were 11.7 mm/29.2 mm before nifedipine and 11.5 mm/31.0 mm at peak nifedipine blood levels. Similar observations were made when codeine was injected locally with or without 20 micrograms nifedipine (12.1/29.2 mm and 13.2/29.2 mm, respectively). These data suggest that codeine-induced mast cell degranulation may be mediated by a calcium-independent mechanism. Alternatively, mast cells in the human skin may differ in their reactions to secretagogues when compared with basophils and mast cells from other human tissues or other species.

Adult↗