Concurrent Administration Of Cimetidine Research Articles

The pharmacokinetics of ziprasidone in healthy volunteers treated with cimetidine or antacid

To evaluate the effects of cimetidine and Maalox(R) (aluminium hydroxide 1.35 g and magnesium hydroxide 1.2 g) on the pharmacokinetics of ziprasidone. Eleven healthy young subjects aged 18-45 years were given single oral doses of ziprasidone 40 mg on three occasions at least 7 days apart. On one occasion ziprasidone was administered alone, on another occasion ziprasidone was co-administered with oral cimetidine 800 mg and on a third occasion ziprasidone was co-administered with oral Maalox(R). The administration of cimetidine increased the ziprasidone AUC(0,infinity) by 6% but there were no statistically significant differences in Cmax, tmax or lambda(z) between the ziprasidone+cimetidine group and the ziprasidone group. The administration of Maalox did not produce any statistically significant differences in AUC(0,infinity), Cmax, tmax or lambda(z) between the ziprasidone+Maalox group and the ziprasidone group. The pharmacokinetics of ziprasidone are not affected by concurrent administration of cimetidine or Maalox. This suggests that other nonspecific inhibitors of cytochrome P450 and antacids are unlikely to alter the pharmacokinetics of ziprasidone.

Cimetidine-induced rise in praziquantel levels in a patient with neurocysticercosis being treated with anticonvulsants.

A patient had neurocysticercosis complicated by a seizure disorder requiring anticonvulsants; previous praziquantel therapy (50 mg/kg/day) had failed to eradicate the disease. In an attempt to inhibit cytochrome P-450 metabolism of praziquantel, cimetidine (1600 mg/day) was coadministered. Before addition of cimetidine, the maximum concentration of praziquantel was 350 ng/mL; concurrent cimetidine administration increased the maximum concentration to 826 ng/mL. The elimination half-life increased from 1.7 h without cimetidine to 3.3 h with cimetidine and the area under the curve for the 12-h sampling period rose from 754 ng.h/mL to 3050 ng.h/mL. Coadministration of cimetidine raises serum praziquantel levels and may be helpful in patients treated concomitantly with praziquantel and anticonvulsants.

Diet and Cimetidine Induce Comparable Changes in Theophylline Metabolism in Normal Subjects K.E. ANDERSON, R.B. MCCLEERY, E.S. VESELL, F.F. VICKERS, A. KAPPAS Hepatology 13:941–946, 1991

This study examines the effects of diet and cimetidine on theophylline metabolism in 12 men. Subjects, all nonsmokers within 15% of their ideal body weight, were 23 to 26 years of age and had no unusual dietary habits. Energy needs were calculated using the Harris‐Benedict equation. Subjects were placed either on a high‐protein, low‐carbohydrate diet (44% of total calories as protein, 35% as carbohydrate, and 21% as fat) or a low‐protein, high‐carbohydrate diet (10% of total calories as protein, 70% as carbohydrate, and 20% as fat) for 15 days on each diet. The order of the dietary periods was reversed in one half of the subjects, and there was a 24‐day washout period between the two dietary periods. Cimetidine (800 mg/d at bedtime) was administered on days 10 to 15 of each dietary period. Aminophylline (3 mg of theophylline base/kg body weight) was administered intravenously as a bolus over 20 to 30 minutes on days 8 and 15 of each dietary period. Blood was withdrawn before and at 1, 2, 4, 6, 8, 12, and 24 hours after the end of the infusion for determination of theophylline plasma levels by high‐pressure liquid chromatography. Theophylline metabolism was studied under four experimental conditions in all 12 subjects. Thus, the effect of: (1) diet change (changing from a high‐progein to a high‐carbohydrate diet), (2) diet change during concurrent cimetidine administration, (3) cimetidine during a high‐protein diet, and (4) the combination of cimetidine and the opposite change in diet (from high carbohydrate to high protein) were examined.Diet change (high protein to high carbohydrate) reduced mean theophylline clearance by 30 ± 10% (p < 0.012). Diet change (high protein to high carbohydrate) during concurrent cimetidine administration, resulted in 23 ± 9% reduction in theophylline clearance (p < 0.016). During a high‐protein diet, cimetidine decreased mean theophylline clearance by 37 ± 5% (p < 0.0009). During a high‐carbohydrate diet, cimetidine decreased theophylline clearance by 30 ± 5% (p < 0.0014). Depending on the direction of change in the protein/carbohydrate ratio, the effects of diet and cimetidine were either additive (theophylline clearance was slower during a high‐carbohydrate diet and cimetidine administration) or counteractive (an increase in the protein/carbohydrate ratio partially counteracts the inhibitory effect of cimetidine).The authors conclude that diet and drugs can have similar effects on hepatic drug metabolism rates in humans. Therefore, during treatment with a drug having a narrow therapeutic index, it would be important to consider not only potential drug‐drug interactions but also drug‐diet interactions. Such interactions could result in either subtherapeutic or excessive drug levels.

Diet and cimetidine induce comparable changes in theophylline metabolism in normal subjects

This study compared the effects of diet and cimetidine on theophylline metabolism and examined interactions between these effects. Twelve men received a high-protein diet for 15 days and at another time a high-carbohydrate diet also for 15 days. Cimetidine, 800 mg daily at bedtime, was administered on days 10 through 15 of each dietary period. Theophylline metabolism was studied after the administration of a single intravenous 3 mg/kg dose on days 8 and 15 of each dietary period. Changing from a high-protein to a high-carbohydrate diet decreased theophylline clearance by about the same extent (30% +/- 10%) as treatment with cimetidine (37% +/- 5% during a high-protein diet and 30% +/- 5% during a high-carbohydrate diet). Cimetidine did not significantly influence the effects of diet on theophylline clearance. Conversely, dietary composition did not influence the degree of inhibition of theophylline metabolism induced by cimetidine. Depending on the direction of the change in protein/carbohydrate ratio, the effects of diet and cimetidine treatment were either additive (theophylline clearance was most prolonged during the high-carbohydrate regimen with concurrent cimetidine administration) or counteractive (increasing the dietary protein/carbohydrate ratio at least partially counteracted the inhibitory effect of cimetidine). In individual subjects, effects of cimetidine on theophylline metabolism were somewhat more consistent than diet-induced changes. The results are further evidence that diet and drugs can have similar effects on hepatic drug metabolism rates in humans. Variations in diet over time and individual differences in responses to diet may provide the potential for considerable instability of drug metabolism rates in free-living subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

The use of cimetidine as a selective inhibitor of dapsone N‐ hydroxylation in man.

1. The N-hydroxylation of dapsone is thought to be responsible for the methaemoglobinaemia and haemolysis associated with this drug. We wished to investigate the effect of concurrent administration of cimetidine (400 mg three times per day) on the disposition of a single dose (100 mg) of dapsone in seven healthy volunteers in order to inhibit selectively N-hydroxylation. 2. The AUC of dapsone (31.0 +/- 7.2 micrograms ml-1 h) was significantly increased (P less than 0.001) in the presence of cimetidine (43.3 +/- 8.8 micrograms ml-1 h). 3. Peak methaemoglobin levels observed after dapsone administration (2.5 +/- 0.6%) were significantly (P less than 0.05) reduced in the presence of cimetidine (0.98 +/- 0.35%). 4. The percentage of the dose excreted in urine as the glucuronide of dapsone hydroxylamine was significantly (P less than 0.05) reduced in the presence of cimetidine (34.2 +/- 9.3 vs 23.1 +/- 4.2%). 5. Concurrent cimetidine therapy might reduce some of the haematological side-effects of dapsone.

Effect of cimetidine and ranitidine on cardiovascular drugs

A compilation of drug interactions between H 2 antagonists and cardiovascular drugs is found in Table I. Cimetidine's potency, lipophilicity, and affinity for binding to the P-450 cytochrome system can probably be attributed to the drug interactions that have been identified with the H 2 antagonists. The mechanism for most cimetidine drug interactions is inhibition of hepatic metabolism. There is conflicting evidence regarding significance of altered liver blood flow for both cimetidine and ranitidine and their influence on other agents. Cimetidine may increase propranolol's blood concentrations and potentiate beta blocking effects through inhibition of hepatic microsomal enzymes and possibly through reduction of hepatic blood flow. Ranitidine has no effect on propranolol. Cimetidine, when administered concurrently with metoprolol, could possibly cause an increase in plasma metoprolol concentrations or bioavailability through inhibition of hepatic P-450 metabolizing enzymes. No effect of cimetidine on metoprolol pharmacodynamics was evident. Ranitidine has no effect on metoprolol pharmacokinetics or pharmacodynamics. Neither H 2 antagonist altered the kinetics or physiologic effects of atenolol. Atenolol is the drug of choice in patients receiving H 2 antagonists, since no interaction has been observed. Metoprolol could probably be used safely in most patients, as no change in pharmacodynamics has been evident. Concurrent administration of cimetidine and nifedipine may result in alterations in heart rate and blood pressure. The mechanism is inhibition of oxidative liver metabolism. Ranitidine has no effect on nifedipine. Studies are needed to investigate the interaction between the H 2 antagonists and diltiazem or verapamil. Cimetidine, given concomitantly with lidocaine, may increase lidocaine concentrations and clinical symptoms of lidocaine toxicity. The mechanism involved is probably a reduction in oxidative drug metabolism or liver blood flow. Ranitidine has no significant effects on lidocaine pharmacokinetics. Cimetidine may increase quinidine levels and symptoms of quinidine toxicity. Additionally, enhanced arrhythmic effects may be observed. The interaction probably caused by an inhibition of hepatic drug metabolism of quinidine by cimetidine would be most significant in patients with liver disease and in the elderly. Ranitidine may enhance quinidine's arrhtthmic effect. Cimetidine can possibly increase procainamide and NAPA serum concentrations, especially in the elderly and in patients with renal dysfunction, predisposing them to adverse side effects. The interaction is mediated by a reduction of tubular secretion of procainamide and NAPA. Conflicting results have been found for ranitidine's influence on procainamide and NAPA. Ranitidine, particularly at higher doses, may alter procainamide and NAPA kinetics. Cimetidine did not alter digoxin pharmacokinetics. Concurrent cimetidine and digoxin administration may possibly increase digoxin serum levels due to altered bioavailability of digoxin tablets. Dosage increases or decreases of cardiovascular drugs usually will not be necessary when H 2 antagonists are administered simultaneously. Patients should be assessed for signs and/or symptoms of adverse or toxic side effects of their cardiac drugs. Monitoring of lidocaine, quinidine, procainamide, NAPA, and digoxin concentrations is recommended to complement clinical judgment and avoid toxicity. Based on the literature, no significant pharmacokinetic clinical effects on cardiac drugs have been noted with ranitidine, while cimetidine may have significant kinetic effects on propranolol, nifedipine, lidocaine, quinidine, procainamide, and NAPA. Since pharmacokinetics, dosing regimens, and cost of cimetidine and ranitidine are comparable, ranitidine is probably the H 2 receptor antagonist of choice to use when concurrent cardiovascular agents are administered. Future investigations will identify other H 2 antagonist-cardiovascular interactions.

Doxepin-Cimetidine Interaction

The influence of concurrent cimetidine administration on the disposition of doxepin was evaluated in 10 healthy volunteers. Each subject ingested 100 mg of doxepin on two different occasions, once while otherwise drug free and once while receiving cimetidine, 300 mg every 6 hours. Doxepin absorptive parameters--time to peak doxepin plasma concentration (2.3, control, vs. 2.4 hours during cimetidine co-administration) and peak concentration achieved (43.3. vs. 55.5 ng/ml)--were not changed during cimetidine administration. Likewise, doxepin elimination half-life was similar in the control state (12.5 hours) and during cimetidine administration (13.2 hours). However, doxepin area under the plasma concentration-time curve (AUC) was increased during concurrent cimetidine administration (533 vs. 695 ng/ml . hour; p less than 0.05), resulting in a trend toward decreased doxepin oral clearance (4404 vs. 3278 ml/min; 0.05 less than p less than 0.1). Relative bioavailability during concurrent cimetidine treatment was 123% of that during the control trial. Desmethyldoxepin AUC was no different between trials (478, control, vs. 433 ng/ml . hour during cimetidine ingestion). Plasma protein binding of doxepin was similar between trials (percent unbound; 10.5, control, vs. 11.2%) and therefore did not influence calculated AUC. These data indicate that doxepin relative bioavailability is increased during concurrent cimetidine administration and suggest that doxepin hepatic extraction is impaired by cimetidine after oral administration. During chronic doxepin therapy, addition of cimetidine to a therapeutic regimen may result in increased doxepin plasma concentration.

Cimetidine alters pethidine disposition in man.

The effect of concurrent cimetidine administration on the disposition of pethidine was investigated in eight healthy male volunteers (18-31 years). The subjects received 70 mg i.v. pethidine HCl doses before and during cimetidine treatment (1200 mg/day p.o.). During cimetidine treatment, pethidine total body clearance (CL) decreased by 22% (0.611 +/- 0.101 [mean +/- s.d.] to 0.474 +/- 0.098 1 kg-1 h, P less than 0.05) and pethidine volume of distribution at steady state (Vss) decreased by 13% (4.79 +/- 0.82 to 4.16 +/- 0.75 l/kg, P less than 0.05). A cimetidine-induced reduction in pethidine oxidation to norpethidine was suggested by a 23% reduction in norpethidine area under the curve from 0 to 24 h (472 +/- 93 to 362 +/- 38 ng ml-1 h, P less than 0.05) and a 29% reduction in peak norpethidine concentration (26.7 +/- 5.3 to 18.9 +/- 1.9 ng/ml, P less than 0.05). There were no significant linear correlations of serum trough cimetidine concentration with percentage reductions in pethidine CL, pethidine Vss, norpethidine AUC (24), or norpethidine peak concentrations. It would appear that the cimetidine-pethidine kinetic interaction may be of sufficient magnitude to be clinically significant. Caution is advised when patients are treated concurrently with these two agents.

Kinetic interactions of nadolol and propranolol with cimetidine.

British Journal of Clinical PharmacologyVolume 17, Issue 4 p. 486-487 Free Access Kinetic interactions of nadolol and propranolol with cimetidine. KL Duchin, KL DuchinSearch for more papers by this authorMA Stern, MA SternSearch for more papers by this authorDA Willard, DA WillardSearch for more papers by this authorDN McKinstry, DN McKinstrySearch for more papers by this author KL Duchin, KL DuchinSearch for more papers by this authorMA Stern, MA SternSearch for more papers by this authorDA Willard, DA WillardSearch for more papers by this authorDN McKinstry, DN McKinstrySearch for more papers by this author First published: April 1984 https://doi.org/10.1111/j.1365-2125.1984.tb02379.xCitations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References Feely, J., Wilkinson, G. R. & Wood, A. J. J. (1981). Reduction of liver blood flow and propranolol metabolism by cimetidine. New Engl. J. Med., 304, 692– 695. Funke, P. T., Malley, M. F., Ivashkiv, E. & Cohen, A. I. (1978). Determinations of serum nadolol levels by GLC-selection monitoring mass spectrometry: comparison with a spectrofluoro-metric method. J. pharm. Sci., 67, 653– 657. Gibaldi, M. & Perrier, D. (1982). Pharmacokinetics. New York: Marcel Dekker, Inc. Kirch, W., Spahn, H., Kohler, H., Ohnhaus, E. E. & Mutschler, E. (1982). Interactions of metoprolol, propranolol, and atenolol with concurrent administration of cimetidine. Klin. Wochenschr., 60, 1401– 1407. Pelkonen, O. & Puurunen, J. (1980). The effect of cimetidine on in vitro and in vivo microsomal drug metabolism in the rat. Biochem. Pharmac., 29, 3075– 3080. Reimann, I. W., Klotz, U., Siems, B. & Frohlich, J. C. (1981). Cimetidine increases steady-state plasma levels of propranolol. Br. J. clin. Pharmac., 12, 785– 790. Shand, D. G., Nuckolls, E. M. & Oates, J. A. (1970). Plasma propranolol levels in adults with observations in four children. Clin. Pharmac. Ther., 11, 112– 120. Citing Literature Volume17, Issue4April 1984Pages 486-487 ReferencesRelatedInformation

Noninteraction of Temazepam and Cimetidine

The possible kinetic interaction of the hypnotic temazepam and the H2-receptor antagonist cimetidine was evaluated. Nine healthy male and female volunteers received a 30-mg oral dose of temazepam on two occasions in random sequence, separated by at least 1 week. On one occasion, temazepam was given in the otherwise drug-free state; on the other, temazepam was given with concurrent administration of cimetidine, 300mg every 6h. Mean pharmacokinetic parameters for temazepam in control versus cimetidine trials were: peak plasma concentration, 560 versus 498 ng/mL; time of peak concentration, 2.0 versus 2.1 h after the dose; volume of distribution, 1.30 versus 1.39 L/kg; elimination half-life, 9.9 versus 11.4h; total clearance, 1.59 versus 1.60 mL/min/kg; free fraction of temazepam in plasma, 4.1 versus 3.8% unbound. Cimetidine has been shown to reduce the metabolic clearance of the benzodiazepines that are biotransformed by oxidative mechanisms. Temazepam, transformed by conjugation, appears unaffected by the coadministration of cimetidine.

The influence of two histamine H2-receptor antagonists, cimetidine and ranitidine, on the plasma levels and clinical effect of nifedipine and metoprolol.

In six healthy volunteers pharmacokinetic and pharmacodynamic interaction of metoprolol and nifedipine with cimetidine and ranitidine was investigated after 1 week of monotherapy with nifedipine and metoprolol and after 1 week each of combined treatment of these drugs with the H2-receptor antagonists. Ranitidine led to a 50% increase in mean peak plasma levels and in the area under the plasma level time curve (AUC) of metoprolol (p less than 0.05) and to an insignificant 30% rise in these parameters of nifedipine (p less than 0.05). Cimetidine increased metoprolol's peak plasma levels of AUC by about 60% (p less than 0.05) and those of nifedipine by 80% (p less than 0.05). Compared to monotherapy with metoprolol beta blocking activity measured by exercise induced tachycardia was not significantly stronger inhibited under the combined treatment of metoprolol with each of the two H2-receptor antagonists. On the other hand the antihypertensive effect of nifedipine was significantly increased during concurrent administration of cimetidine in seven hypertensive patients when compared with monotherapy.

Cimetidine-induced alterations in desipramine plasma concentrations

Concurrent administration of cimetidine for 4 days to eight patients taking maintenance doses of desipramine led to significant elevations of desipramine (P less than 0.001) and its hydroxylated metabolite 2-hydroxydesipramine (P less than 0.001). The mean increase in desipramine plasma levels was 51% and that for 2-hydroxydesipramine was 46%. The present results suggest that tricyclic antidepressant plasma level monitoring might be indicated for certain patients taking concurrent cimetidine and desipramine.

Cimetidine inhibits theophylline clearance in patients with chronic obstructive pulmonary disease: a study using stable isotope methodology during multiple oral dose administration.

1 The effect of concurrent cimetidine administration on the disposition of theophylline was investigated in eight male patients (56-78 years) with chronic obstructive pulmonary disease (COPD). 2 The patients, who were taking oral theophylline preparations chronically (384-1020 mg/day), received a [15N], [13C]-labelled analogue of theophylline (10 mg i.v.) before and during cimetidine treatment (1200 mg/day p.o.). 3 During cimetidine treatment trough levels of theophylline increased 34% (6.4 +/- 0.8 to 8.6 +/- 1.0 micrograms/ml, P less than 0.05), half-life increased 48% (6.5 +/- 0.6 to 9.6 +/- 0.8 h, P less than 0.001), and total plasma clearance decreased 33% (3.88 +/- 0.46 to 2.59 +/- 0.33 l/h, P less than 0.001), without a significant change in volume of distribution or protein binding. 4 The effect of cimetidine on plasma levels of theophylline was maximal within 72 h. Levels returned to control values within 48 h after its discontinuation. 5 Although there was no correlation with mean plasma concentrations of cimetidine, the change in clearance of theophylline correlated with initial clearance values (r = 0.72). 6 Cimetidine reduced the plasma clearance of theophylline in patients with COPD to an extent similar to that reported in healthy volunteers.

Mucosal enzyme activities, with special reference to enzymes implicated in bicarbonate secretion, in the duodenum of rats with cysteamine-induced ulcers.

1. Duodenal mucosa was collected from control rats and from animals which had received cysteamine, cysteamine plus cimetidine or pentagastrin. Animals which received cysteamine with or without cimetidine developed acute duodenal ulcers. Cysteamine treatment resulted in gastric acid hypersecretion, which was largely abolished by concurrent cimetidine administration. 2. Activities of enzymes implicated in bicarbonate secretion, HCO3--activated ATPase, carbonic anhydrase and Na+ + K+-activated ATPase, were measured in the duodenal mucosa of control rats and animals 24 h after subcutaneous administration of cysteamine. Assays of these enzymes in duodenal mucosal homogenates from animals with cysteamine-induced ulcers showed significant decreases in HCO3--activated ATPase and carbonic anhydrase activities compared with controls. 3. Alkaline phosphatase activity also fell significantly in the cysteamine-treated animals, and possibly reflects the HCO3---activated ATPase activity in the brush-border membrane. In contrast, activities of other marker enzymes from the brush-border membrane and from several intracellular organelles were unchanged, indicating an absence of gross organelle pathology in this experimental model. 4. Similar changes in enzyme activity were not caused by treatment with pentagastrin. Administration of cimetidine with the cysteamine did not protect the animals against ulceration, and the activity of HCO3--activated ATPase was persistently decreased. However, the carbonic anhydrase activity was unaltered in this latter group, compared with controls. 5. These findings suggest that in cysteamine-induced duodenal ulceration both gastric acid hypersecretion and impaired duodenal resistance occurs. It is suggested that decreased activities of key enzymes implicated in HCO3--secretion may reflect the biochemical basis for the decreased mucosal resistance.

Accumulation and adverse effects of metoprolol and propranolol after concurrent administration of cimetidine.

Pharmacokinetics of metoprolol, propranolol and atenolol were investigated in six healthy volunteers following 7 days of oral monotherapy with these drugs and after 7 days concurrent administration of each of these betareceptor antagonists with cimetidine. Application of cimetidine did not lead to any interaction with atenolol, whereas mean peak plasma levels of metoprolol were increased by 70%, and those of propranolol by 95% due to concurrent administration of cimetidine (p less than 0.05). The AUC of the two last mentioned beta blockers behaved similarly (p less than 0.05). Measurement of exercise-induced tachycardia on the 6th day of administration showed no differences between monotherapy with the beta blocker and combined treatment with each of them and cimetidine. Except for one volunteer who complained of anxiety, weakness and sweating on the 6th day of cimetidine/metoprolol administration, no adverse effects could be observed during the combination therapy with cimetidine and the beta blockers or in monotherapy with beta blockers.

Interaction of metoprolol, propranolol and atenolol with concurrent administration of cimetidine.

Pharmacokinetics of metoprolol, propranolol, and atenolol were investigated in six healthy volunteers following 7 days of oral monotherapy with these drugs, and after 7 days concurrent administration of each of these betareceptor antagonists with cimetidine. Application of cimetidine did not lead to any interaction with atenolol, whereas mean peak plasma levels of metoprolol were increased by 70%, and those of propranolol by 95% due to concurrent administration of cimetidine (P less than 0.05). The plasma level time curve (AUC) of the two above-mentioned beta blockers behaved similarly (P less than 0.05). Other kinetic parameters of these two drugs were not influenced to a statistically significant extent by cimetidine, despite the tendency for the elimination half-life of metoprolol and propranolol to be prolonged when cimetidine is added. Measurement of exercise-induced tachycardia on the sixth day of administration showed no differences between monotherapy with the beta blockers and combined treatment with each of them together with cimetidine. Apart from one volunteer who complained of anxiety, weakness, and sweating on the sixth day of cimetidine/metoprolol administration, no adverse effects could be observed during the combination therapy with cimetidine and the beta blockers, nor during monotherapy with beta blockers.

Interaction of Metoprolol, Propranolol and Atenolol with Cimetidine

1. Pharmacokinetics of metoprolol, propranolol and atenolol were investigated in six healthy volunteers after 7 days of oral monotherapy with these drugs and after 7 days concurrent administration, with each of these β-adrenoceptor antagonists with cimetidine. 2. Cimetidine did not interact with atenolol, whereas mean peak plasma concentrations of metoprolol were increased by 70%, and those of propranolol by 95% with concurrent administration of cimetidine (P < 0.05). 3. The area under the plasma concentration-time curve for propranolol and metoprolol was similarly increased (P < 0.05).

Concurrent administration of cimetidine and enteric‐coated prednisolone: effect on plasma levels of prednisolone.

British Journal of Clinical PharmacologyVolume 10, Issue 1 p. 87-89 Free Access Concurrent administration of cimetidine and enteric-coated prednisolone: effect on plasma levels of prednisolone. PJ Morrison, PJ MorrisonSearch for more papers by this authorHJ Rogers, HJ RogersSearch for more papers by this authorID Bradbrook, ID BradbrookSearch for more papers by this authorC Parsons, C ParsonsSearch for more papers by this author PJ Morrison, PJ MorrisonSearch for more papers by this authorHJ Rogers, HJ RogersSearch for more papers by this authorID Bradbrook, ID BradbrookSearch for more papers by this authorC Parsons, C ParsonsSearch for more papers by this author First published: July 1980 https://doi.org/10.1111/j.1365-2125.1980.tb00506.xCitations: 15AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat References BODEMAR, G., NORLANDER, B., FRANSSON, L. & WALEN, A. (1979). The absorption of cimetidine before and during maintenance treatment with cimetidine and the influence of a meal on the absorption of cimetidine—studies in patients with peptic ulcer disease. Br. J. clin. Pharmac., 7, 23– 32. BRECKENRIDGE, A.M., CHALLINER, M., MOSSMAN, S., PARK, B.K., SERLIN, M.J., SIBEON, R.G., WILLIAMS, J.R.B. & WILLOUGHBY, J.M.T. (1979). Cimetidine: interaction with warfarin in man. Br. J. clin. Pharmac., 8, 392– 393p. BURLAND, W.L., DUNCAN, W.A.M., HESSELBO, T., MILLS, J.G., SHARPE, P.C., HAGGIE, S.J. & WYLLIE, J.H. (1975). Pharmacological evaluation of cimetidine, a new histamine H2-receptor antagonist, in healthy man. Br. J. clin. Pharmac., 2, 481– 486. CONN, H.O. & BLITZER, B.L. (1976). Nonassociation of adrenocorticosteroid therapy and peptic ulcer. N. Engl. J. Med., 294, 473– 479. FISHER, P., HOUSE, F., INNS, P., MORRISON, P.J., ROGERS, H.J. & BRADBROOK, I.D. (1980). Effect of cimetidine on the absorption of orally administered tetracycline. Br. J. clin. Pharmac., 9, 153– 158. FRIED, J. & ZIETZ, S. (1973). Curve fitting by Spline and Akima methods: possibility of interpolation error and its suppression. Phys. Med. Biol., 18, 550– 558. GIBALDI, M. (1977). Biopharmaceutics and clinical pharmacokinetics, p. 49. Philadelphia: Lea & Febiger. KAMMERER, W.H., FREIBERGER, R.H. & RIVELIS, A.L. (1958). Peptic ulcer in rheumatoid patients on corticosteroid therapy. Arth. Rheum., 1, 122– 141. LEE, D.A.H., TAYLOR, G.M., WALKER, J.G. & JAMES, V.H.T. (1979). The effect of food and tablet formulation on plasma prednisolone levels following administration of enteric-coated tablets. Br. J. clin. Pharmac., 7, 523– 528. MORRISON, P.J., BRADBROOK, I.D. & ROGERS, H.J. (1977). Plasma prednisolone levels from enteric and non-enteric coated tablets estimated by an original technique. Br. J. clin. Pharmac., 4, 597– 603. RANDOLPH, W.C., OSBORNE, V.L., WALKENSTEIN, S.S. & INTOCCIA, A.T. (1977). High pressure liquid chromatographic analysis of cimetidine, a histamine H2-receptor antagonist in blood and urine. J. pharm. Sci., 66, 1148– 1150. STERNBERG, W., KING, C. & TOSKES, P. (1978). Cimetidine inhibits the absorption of protein-bound vitamin B12 but not crystalline vitamin B12. Gastroenterology, 74, 1099. Citing Literature Volume10, Issue1July 1980Pages 87-89 ReferencesRelatedInformation