Study of the Ability of Clarithromycin to Induce Oxidative Stress

NCT ID: NCT00707330

Last Updated: 2008-08-11

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Clinical Phase

PHASE1

Total Enrollment

26 participants

Study Classification

INTERVENTIONAL

Study Start Date

2008-05-31

Study Completion Date

2008-07-31

Brief Summary

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The purpose of the study is to examine whether Klacid® (Clarithromycin) will induce oxidative stress (stress from oxygen) in healthy subjects. This is done by measuring the content of a particular substance in the urine sample, which is released when the body is exposed to oxidative stress. In addition, there will also be taken blood samples, which is analysed for another substance that is indicative of oxidative stress.

Detailed Description

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The purpose of the study is to examine whether Klacid® induce oxidative stress in healthy subjects.

Many studies have shown that atherosclerosis can cause acute myocardial infarction (AMI). The development of atherosclerosis is exacerbated by simultaneous infection with Chlamydophila pneumoniae, and its accompanying inflammation. There has been shown a positive association between Chlamydophila pneumoniae antibodies and the incidence of cardiovascular complications, suggesting that Chlamydophila pneumoniae could exacerbate the development of atherosclerosis \[1\]. It has therefore been tried to treat atherosclerotic AMI- patients prophylactically with macrolide antibiotics (which is used to treat Chlamydia infections), to halt development of the atherosclerosis and the accompanying risk of a new acute myocardial infarction.

Two minor studies have demonstrated a positive effect of macrolide-treatment, why a major Danish study of Clarithromycin was implemented \[2-4\]. Clarithromycin treatment was tested against placebo in 4373 atherosclerotic patients who had had an AMI. It appeared that the use of clarithromycin led to an increased cardiovascular mortality, which could not be explained \[4\]. The finding of the study suggests that clarithromycin cannot be used for secondary prophylaxis of cardiovascular complications, but whether clarithromycin can be used for primary prophylaxis is not known.

It has been shown that oxidative stress can participate in the development of cardiovascular complications \[5\], and it could be such an oxidative stress that had led to the increased mortality in the above study. Especially because a recent american study found evidence that bactericidal antibiotics induce oxidative stress in bacteria, leading to cell death \[6\]. This oxidative stress contributes significantly to the impact of the bactericidal antibiotics, which was thought to be primarily attributed to their specific drug/target interactions. The same study also examined erythromycin, from which clarithromycin is a derivate. Erythromycin showed no induction of oxidative stress, but clarithromycin is twice as effective as erythromycin, which could be due to oxidative stress caused by clarithromycin.

This study seeks to clarify a possible mechanism for clarithromycin, by an examination on healthy volunteers without atherosclerosis.

Conditions

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Oxidative Stress

Keywords

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oxidative stress 8-oxo-deoxyguanine 8-oxodG clarithromycin malondialdehyde mda vitamine C ascorbic acid

Study Design

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Allocation Method

RANDOMIZED

Intervention Model

CROSSOVER

Primary Study Purpose

SCREENING

Blinding Strategy

NONE

Study Groups

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1

Subjects randomised to this arm will first be treated with Clarithromycin for a week, then have a 2-week washout, and finally one week of no treatment

Group Type EXPERIMENTAL

Clarithromycin

Intervention Type DRUG

Prolonged release tablet, 500 mg, 1 tablet a day for a week

2

Subjects randomised to this arm will first receive one week of no treatment, then have a 2-week washout, and finally be treated with Clarithromycin for a week

Group Type ACTIVE_COMPARATOR

Clarithromycin

Intervention Type DRUG

Prolonged release tablet, 500 mg, 1 tablet a day for a week

Interventions

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Clarithromycin

Prolonged release tablet, 500 mg, 1 tablet a day for a week

Intervention Type DRUG

Other Intervention Names

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Klacid Uno ATC: J01FA09

Eligibility Criteria

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Inclusion Criteria

* Caucasian
* Non-smoker
* Body mass index (BMI) must be ≥18 and ≤ 30
* Blood pressure must be within the following limits:
* Systolic blood pressure (110 mmHg \> X \< 140 mmHg)
* Diastolic blood pressure (60 mmHg \> Y \< 90 mmHg)
* Normal lipid plasma levels:
* Total cholesterol (≤ 6,0 mmol/l)
* HDL-cholesterol (≥ 0,9 mmol/l)
* LDL-cholesterol (≤ 4,5 mmol/l)
* Triglycerides (0,5-2,2 mmol/l)

Exclusion Criteria

* Smokers
* CRP: \> 10 mg/l
* Prolonged QT interval (defined as QTc \> 450 msec.)
* Severe renal insufficiency (Cpl (creatinine) \> 0100 mmol/l)
* Hereditary galactose intolerance
* A special form of hereditary lactase deficiency (Lapp Lactase deficiency)
* Glucose/galactose malabsorption
* Use of medicines and herbal remedies that affect/is affected by Clarithromycin, or lead to QT prolongation, for example, cisapride, pimozide, terfenadine, ergotamine, dihydroergotamine, fluconazole, ritonavir, carbamazepine, kinidin, disopyramide, lovastatin, simvastatin, warfarin, acenocoumarol, sildenafil, Tadalafil, vardenafil, theophylline, tolterodine, triazolo benzodiazepins, omeprazole, colchinine, digoxin, zidovudine, phenytoin, valproat, atazanavir, itraconazole, saquinavir
* Inborn condition with prolonged QT interval
* The following disorders:
* Coronary artery disease
* Former cardiac arrhythmias
* Severe heart insufficiency
* Non-compensated hypokalemia (defined as Cpl (K) \< 3.2 mmol/ l) and/or hypomagnesemia (defined as Cpl (Mg) \< 0.67 mmol/l)
* Bradycardia ( \< 50 bpm)
* Known allergy to clarithromycin or other macrolides
* Narcotic
* Eating food supplements
Minimum Eligible Age

18 Years

Maximum Eligible Age

35 Years

Eligible Sex

MALE

Accepts Healthy Volunteers

Yes

Sponsors

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Rigshospitalet, Denmark

OTHER

Sponsor Role lead

Responsible Party

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Head of Department of Clinical Parmacology

Principal Investigators

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Henrik E Poulsen, dr. med.

Role: PRINCIPAL_INVESTIGATOR

Head of Department, Department of Clinical Pharmacology, Rigshospitalet

Locations

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Department of Clinical Pharmacology Q, Rigshospitalet, Blegdamsvej 9

Kopenhagen O, , Denmark

Site Status

Countries

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Denmark

References

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Muhlestein JB, Anderson JL. Infectious serology and atherosclerosis: how burdensome is the risk? Circulation. 2003 Jan 21;107(2):220-2. doi: 10.1161/01.cir.0000043909.78380.a0. No abstract available.

Reference Type BACKGROUND
PMID: 12538417 (View on PubMed)

Gupta S, Leatham EW, Carrington D, Mendall MA, Kaski JC, Camm AJ. Elevated Chlamydia pneumoniae antibodies, cardiovascular events, and azithromycin in male survivors of myocardial infarction. Circulation. 1997 Jul 15;96(2):404-7. doi: 10.1161/01.cir.96.2.404.

Reference Type BACKGROUND
PMID: 9244203 (View on PubMed)

Gurfinkel E, Bozovich G, Daroca A, Beck E, Mautner B. Randomised trial of roxithromycin in non-Q-wave coronary syndromes: ROXIS Pilot Study. ROXIS Study Group. Lancet. 1997 Aug 9;350(9075):404-7. doi: 10.1016/s0140-6736(97)07201-2.

Reference Type BACKGROUND
PMID: 9259655 (View on PubMed)

Jespersen CM, Als-Nielsen B, Damgaard M, Hansen JF, Hansen S, Helo OH, Hildebrandt P, Hilden J, Jensen GB, Kastrup J, Kolmos HJ, Kjoller E, Lind I, Nielsen H, Petersen L, Gluud C; CLARICOR Trial Group. Randomised placebo controlled multicentre trial to assess short term clarithromycin for patients with stable coronary heart disease: CLARICOR trial. BMJ. 2006 Jan 7;332(7532):22-7. doi: 10.1136/bmj.38666.653600.55. Epub 2005 Dec 8.

Reference Type BACKGROUND
PMID: 16339220 (View on PubMed)

Dhalla NS, Temsah RM, Netticadan T. Role of oxidative stress in cardiovascular diseases. J Hypertens. 2000 Jun;18(6):655-73. doi: 10.1097/00004872-200018060-00002.

Reference Type BACKGROUND
PMID: 10872549 (View on PubMed)

Kohanski MA, Dwyer DJ, Hayete B, Lawrence CA, Collins JJ. A common mechanism of cellular death induced by bactericidal antibiotics. Cell. 2007 Sep 7;130(5):797-810. doi: 10.1016/j.cell.2007.06.049.

Reference Type BACKGROUND
PMID: 17803904 (View on PubMed)

Other Identifiers

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EudraCT 2008-001299-61

Identifier Type: -

Identifier Source: secondary_id

VEK H-D-2008-026

Identifier Type: -

Identifier Source: secondary_id

DKMA 2612-3720

Identifier Type: -

Identifier Source: secondary_id

Datatilsynet 2008-41-2030

Identifier Type: -

Identifier Source: secondary_id

3-12-1-18-15-23

Identifier Type: -

Identifier Source: org_study_id