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C J Destache

Publications and source records attributed to C J Destache.

26 records · Page 2Linked to original sources

Impact of a clinical pharmacokinetic service on patients treated with aminoglycosides: a cost-benefit analysis.

In a prospective, randomized study, 75 adults receiving aminoglycosides were followed by a clinical pharmacokinetic service and 70 followed as controls. The two groups were similar in age, gender, height, and APACHE II score. A cost-to-charge ratio was used to derive direct costs of hospitalization and calculate cost-benefit. Excluded from this comparison were patients with incomplete acceptance of pharmacokinetic service recommendations and patients followed by other clinical pharmacists. Pharmacokinetic service patients had shorter hospitalizations (322.67 +/- 270.28 h; controls 442.89 +/- 536.81, p = 0.087) and febrile periods (50.05 +/- 79.38 h; controls 92.23 +/- 122.50, p less than 0.05). More pharmacokinetic service patients had adequate peak levels. Pharmacokinetic service direct costs were lower ($7,102.56 +/- 9,898.19; controls $13,758.64 +/- 22,874.31, p less than 0.05). Calculated direct cost of the service was $85.00/patient. Annual savings for 500 patients is $2,220,540.00.

Amikacin↗

Does accepting pharmacokinetic recommendations impact hospitalization? A cost-benefit analysis.

In a prospective, randomized study, 110 adults receiving aminoglycosides were randomized to follow-up by a clinical pharmacokinetic service (CPS). Of the 110 patients, 35 accepted pharmacokinetic recommendations less than 100% of the time. The two groups were similar in age, sex, height, APACHE II score, and initial creatinine clearance. A cost-to-charge ratio was used to derive direct costs of hospitalization and calculate cost-benefit. Patients whose physicians accepted pharmacokinetic recommendations 100% of the time had shorter hospitalizations (322.67 +/- 270.28 h; CPS less than 100%, 699.54 +/- 806.35; p = 0.001) and febrile periods (50.05 +/- 79.38 h; CPS less than 100%, 120.00 +/- 153.23; p = 0.002). Acceptance of CPS recommendations led to adequate peak levels. Acceptance of CPS recommendations led to lower direct costs ($7,102.56 +/- 9,898.19; CPS less than 100%, $19,629.94 +/- 28,051.89; p less than 0.001). Calculated direct cost of the service was $85/patient.

Aminoglycosides↗

Impact of a clinical pharmacokinetic service on patients treated with aminoglycosides for gram-negative infections.

The present study was a retrospective, case-control design aimed at evaluating whether the clinical pharmacokinetic service (CPS) is cost-effective, as assessed by lengths of hospital stay and aminoglycoside therapy, incidence of a decrease in renal function, and time for resolution of infection as determined by vital signs. Forty-six patients were entered into this study, and were matched by defined criteria. The results of the study demonstrated a six-day difference in hospital stay for the CPS group (p less than 0.05). Length of aminoglycoside therapy was 33 hours shorter for the CPS group. Additionally, the time necessary for resolution of the infection was significantly shorter for this group, as assessed by vital signs returning to normal or baseline. Three patients in each group expired. Two patients in the CPS group and five in the control group developed aminoglycoside-associated increases in serum creatinine. No significant difference was found between the two groups in age, weight, or APACHE II score. Additionally, the two groups were similar with respect to concomitant diseases and concomitant antibiotics used. The approximate cost of the CPS was calculated as $56 per patient. Use of the CPS decreasing hospital stay by six days (mean $1875/patient) would translate to an annual savings of $654,375 in hospital charges, assuming 365 patients received aminoglycoside therapy per year.

Aged↗

Lidocaine-induced second-degree mobitz type II heart block.

Lidocaine-induced atrioventricular (AV) conduction disturbances are an ill-defined phenomenon. Electrophysiological studies in both animal and human subjects have shown that therapeutic doses of lidocaine have no significant effect on AV nodal and His-Purkinje conduction time in the presence of intact AV conduction. Sporadic reports of accelerated AV conduction or complete heart block following lidocaine administration have been published. One case of Mobitz type II heart block has been reported in a patient with a prolonged QTc interval (0.61 sec) who was also receiving prenylamine. Electrophysiological studies designed to evaluate lidocaine's effects on AV conduction present conflicting observations. We report a case of Mobitz type II heart block following therapeutic doses of lidocaine in the absence of acute myocardial infarction or concomitant cardioactive drug administration. This case, in conjunction with other reported data, suggests the occurrence of lidocaine-induced AV block to be unpredictable. Although its occurrence may be infrequent, the severity of these reactions warrants careful selection and monitoring of patients who are to receive lidocaine.

Aged↗

Comparative bioequivalence and efficacy of two sustained-release procainamide formulations in patients with cardiac arrhythmias.

This investigation evaluated the bioequivalence and efficacy of two sustained-release procainamide products. Ten patients with cardiac arrhythmias were randomized to product A (Procan-SR) or product B (Pronestyl-SR). After nine doses of study medication, plasma procainamide and N-acetylprocainamide concentrations were obtained to determine the area under the concentration versus time curve at steady state (AUCSS), mean plasma concentration (CSSav), the observed peak plasma concentration (CSSmax), the observed trough plasma concentration (CSSmin), and the apparent time to achieve CSSmax (tmax). The products were compared on a milligram-equivalent (adjusted) basis. Following completion of blood sampling, patients were crossed-over to the alternate product. There was no washout between treatments. After nine doses of the alternate test medications, blood sampling was repeated. Differences in AUCSS, CSSav, CSSmax, tmax, and intradose peak/trough ratios were not statistically significant. Within-group variability in AUCSS, CSSav CSSmax, and tmax was greater with product B, but this trend did not reach statistical significance. Antiarrhythmic efficacy was not significantly different between the two treatments. Although the greater bioequivalence, lesser variability, and the greater number of tablet dosage sizes would favor product A, patients stabilized on a particular brand of sustained-release procainamide should not be switched to another product without careful monitoring. One patient in this study developed nonsustained ventricular tachycardia with low procainamide plasma concentrations after being switched from product A to product B.

Acecainide↗

Omeprazole: a comprehensive review.

Omeprazole is a member of a new class of substituted benzimidazoles. These agents inhibit the proton pump in the gastric parietal cell, blocking the final step in the gastric acid secretory pathway. Omeprazole has been investigated for the treatment of gastric ulcer, duodenal ulcer, gastroesophageal reflux, and various hypersecretory states. The prolonged inhibition of gastric acid secretion allows for once-daily dosing in patients with peptic ulcer disease and gastroesophageal reflux, and once- or twice-daily dosing in patients with Zollinger-Ellison syndrome. Compared with currently available therapies, omeprazole is well tolerated and demonstrates a more rapid ulcer healing rate. It is superior to conventional therapies in the treatment of Zollinger-Ellison syndrome. Side effects are infrequent when the drug is used for the short-term management of ulcers.

Clinical Trials as Topic↗

Microbiologic effect of bovine cerebrospinal fluid and azithromycin against Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae.

Minimum inhibitory concentrations (MICs) and minimum bactericidal concentrations (MBCs) of azithromycin against reference strains of Streptococcus pneumoniae ATCC 49619, Neisseria meningitidis ATCC 13090, and Haemophilus influenzae ATCC 49247 were determined by the macrodilution broth method with and without 10% bovine cerebrospinal fluid (CSF) supplementation. The MICs and MBCs were within one to two dilutions for N. meningitidis and S. pneumoniae, and no difference was observed for H. influenzae. Time-kill curves demonstrated enhanced killing by azithromycin when 10% bovine CSF was added to media for N. meningitidis. The minimum azithromycin concentration for a greater than 3 log10 reduction in inoculum with bovine CSF was 0.03 microg/ml and without CSF was 0.12 microg/ml, a 3-fold difference. Killing was not significantly different for either H. influenzae nor S. pneumoniae.

Animals↗

Nitric oxide concentrations and cerebrospinal fluid parameters in an experimental animal model of Streptococcus pneumoniae meningitis.

Streptococcus pneumoniae is a common cause of meningitis. Nitric oxide (NO) has been implicated in causing cerebral edema. Modulating NO production in cerebrospinal fluid (CSF) may have a role in the treatment of bacterial meningitis. Experimental S. pneumoniae meningitis was induced in a rabbit model to determine CSF parameters and NO concentrations. An electrochemical probe in the CSF throughout the 7-hour experiment monitored NO concentrations. The animals had S. pneumoniae (10(5)) injected intracisternally and incubated for 1 hour. Cerebrospinal fluid 200-300 microl was obtained by intracisternal puncture at zero, 2, 4, and 7 hours after drug administration to measure glucose, protein, and lactic acid by standard chemical methods. White blood cell count was measured by hemocytometry. Three groups of five animals were used-control (C), ceftriaxone (CTX), and ceftriaxone plus dexamethasone (CTX+D). Ceftriaxone concentrations in CSF were obtained by microdialysis and analyzed by high-performance liquid chromatography. Mean (+/- SEM) CSF white blood cell count was significantly higher at 2 hours in the C group than in the other two groups (C 7307 +/- 1302, CTX 605 +/- 345, CTX+D 730 +/- 43/mm3, p<0.002). Ceftriaxone induced a significant rise in protein at 4 hours compared with the other groups (C 364 +/- 107, CTX 1158 +/- 797, CTX+D 365 +/- 100 mg/dl, p<0.02). Cerebrospinal fluid lactic acid was significantly different at 4 and 7 hours between C and CTX+D groups (4-hr C 8.0 +/- 2.2, CTX+D 2.0 +/- 0.4 mmol/L, p<0.05; 7-hr C 10.2 +/- 2.4, CTX+D 2.8 +/- 0.8 mmol/L, p<0.01). Median NO concentrations were significantly elevated in the control group compared with the other two groups (C 11.7, CTX 6.8, CTX+D 6.5 micro, p<0.02 C vs CTX, p<0.01 C vs CTX+D). Average (+/- SEM) NO concentrations were significantly higher in the C group at 4 hours (18.1 +/- 0.4, CTX 5.8 +/- 1.8 microM, p<0.05; CTX+D 11.5 +/- 4.0 microM, p>0.05), whereas they did not rise significantly until 7 hours in the CTX group (CTX 18.7 +/- 0.7, C 8.9 +/- 0.4 microM, p=0.055; CTX+D 8.1 +/- 2.2 microM, p<0.05). These results indicate that ceftriaxone with or without dexamethasone significantly decreases lactic acid concentrations and white cell penetration into the CSF in an experimental model of S. pneumoniae meningitis. In addition, ceftriaxone induced a significant elevation in CSF protein. Median NO production in the CSF was significantly attenuated by ceftriaxone.

Animals↗