Doesciprofloxacin Interact with Cyclosporine?

1994 ◽  
Vol 28 (1) ◽  
pp. 93-96 ◽  
Author(s):  
Lori L. Hoey ◽  
Kathleen D. Lake
Keyword(s):  
Drug Interaction ◽  
Case Reports ◽  
Data Extraction ◽  
Clear Correlation ◽  
Pharmacokinetic Studies ◽  
Review Of The Literature ◽  
Medline Search ◽  
Pharmacokinetic Profiles ◽  
Immune Mediated ◽  
Study Selection

OBJECTIVE: To provide the reader with a review of the literature that evaluates whether a pharmacokinetic or pharmacodynamic drug interaction exists between ciprofloxacin and cyclosporine. DATA SOURCES: A MEDLINE search was used to identify pertinent review articles, pharmacokinetic studies, and case reports. STUDY SELECTION: As both pharmacokinetic trials and case reports were few in number, all available sources were reviewed. DATA EXTRACTION: A few case reports were reviewed; however, data were extracted primarily from prospective human studies involving cyclosporine pharmacokinetic profiles. DATA SYNTHESIS: Ciprofloxacin has been reported to interact with cyclosporine during concomitant use through an interaction with the cytochrome P-450 system or by additive nephrotoxicity. Because ciprofloxacin may be used to treat a variety of infections in transplant recipients who receive cyclosporine, it is important to determine whether an interaction exists. Although cyclosporine is known to cause nephrotoxicity, only a few reports of ciprofloxacin-induced acute renal failure exist, all involving an immune-mediated interstitial nephritis. Four case reports have suggested a possible pharmacokinetic or pharmacodynamic drug interaction between cyclosporine and ciprofloxacin; however, many pharmacokinetic studies have refuted these reports. Several studies performing cyclosporine pharmacokinetic profiles have documented no increased cyclosporine concentrations, thus supporting the premise that ciprofloxacin does not interact with cyclosporine. CONCLUSIONS: Controlled studies involving cyclosporine pharmacokinetic profiles do not support a pharmacokinetic or pharmacodynamic drug interaction between ciprofloxacin and cyclosporine. Although anecdotal case reports have suggested synergistic nephrotoxicity, no clear correlation can be made. Based on our review of the literature, it can be concluded that cyclosporine and ciprofloxacin may be used together safely at the recommended dosages without increased cyclosporine monitoring.

Isoniazid-Associated Psychosis: Case Report and Review of the Literature

1993 ◽  
Vol 27 (2) ◽  
pp. 167-170 ◽  
Author(s):  
Karen A. Pallone ◽  
Morton P. Goldman ◽  
Matthew A. Fuller
Keyword(s):  
Case Report ◽  
English Language ◽  
Case Reports ◽  
Data Extraction ◽  
Data Sources ◽  
Review Of The Literature ◽  
Data Synthesis ◽  
Medline Search ◽  
Study Selection ◽  
Language Literature

Objective To describe a case of isoniazid-associated psychosis and review the incidence of this adverse effect. Data Sources Information about the patient was obtained from the medical chart. A MEDLINE search of the English-language literature published from 1950 to 1992 was conducted and Index Medicus was manually searched for current information. Study Selection All case reports describing isoniazid-associated psychosis were reviewed. Data Extraction Studies were evaluated for the use of isoniazid, symptoms of psychosis, onset of symptoms, and dosage of isoniazid. Data Synthesis The case report is compared with others reported in the literature. The incidence of isoniazid-associated psychosis is rare. Conclusions The mechanism of isoniazid-associated psychosis is uncertain. It appears that isoniazid was associated with the psychosis evident in our patient and in the cases reviewed.

Ifosfamide-Induced Neurotoxicity: A Case Report and Review of the Literature

1992 ◽  
Vol 26 (2) ◽  
pp. 183-187 ◽  
Author(s):  
Lisa J. Miller ◽  
Virginia E. Eaton
Keyword(s):  
Case Reports ◽  
Data Extraction ◽  
Review Of The Literature ◽  
Journal Articles ◽  
Predictive Capability ◽  
Dosage Regimens ◽  
Study Selection ◽  
Study Population ◽  
Pediatric Populations ◽  
Small Study Population

OBJECTIVE: To review published abstracts, journal articles, and case reports for evidence of ifosfamide-induced neurotoxicity in both adult and pediatric populations. DATA SOURCES: Peer-reviewed journal articles (October 1985 through August 1990) obtained through a computer literature search, with subsequent bibliography scanning. STUDY SELECTION: We identified 34 reports that specifically addressed neurotoxicity related to ifosfamide therapy. By consensus of the authors, 8 of these reports were excluded due to a small study population, duplication or age of data. DATA EXTRACTION: Studies were assessed by the first author and verified by the second author. Several colleagues also contributed to the analysis. DATA ANALYSIS: Risk factors and mechanisms behind this potentially fatal neurotoxic reaction remain speculative and, in some cases, contradictory. The predictive capability of a published nomogram is restricted by differences in dosage regimens and encephalopathic classifications. Currently, the best prevention against neurotoxicity is little or no use of concurrent medications that have central nervous system effects. CONCLUSIONS: Further studies should address the influence of other nephrotoxic agents (e.g., cisplatin, aminoglycosides) on the incidence of ifosfamide-induced neurotoxicity.

Rifabutin-Associated Uveitis

1995 ◽  
Vol 29 (11) ◽  
pp. 1149-1155 ◽  
Author(s):  
Alice L Tseng ◽  
Sharon L Walmsley
Keyword(s):  
Adverse Event ◽  
Drug Interactions ◽  
English Language ◽  
Case Reports ◽  
Data Extraction ◽  
Signs And Symptoms ◽  
Medline Search ◽  
Concurrent Therapy ◽  
Study Selection ◽  
Tolerance Study

Objective: To review rifabutin-associated uveitis and discuss the mechanism and potential role of drug interactions with clarithromycin and fluconazole in contributing to this adverse event. Data Sources: A MEDLINE search (1991 through September 1994) of English-language literature using the main MeSH headings “rifabutin” and “uveitis” and the subheadings “adverse effects” and “chemically induced.” Relevant articles also were selected from references of identified articles. Abstracts from recent medical conferences of infectious diseases, pharmacology, and HIV were screened for additional data. Study Selection and Data Extraction: All articles and abstracts reporting uveitis potentially related to rifabutin were considered for inclusion. Fifty-four cases were identified. Pertinent information from the case reports, as judged by the authors, was selected and synthesized for discussion. Data Synthesis: Rifabutin is being prescribed increasingly for the treatment and prophylaxis of Mycobacterium avium complex (MAC) infection in the HIV-infected population. Uveitis was initially thought to be a rare, dose-limited complication of rifabutin therapy. In an early dose-ranging tolerance study, uveitis was associated with daily doses of 1200 mg or more. Because this toxicity appeared to be dose-related, lower dosages (300–600 mg/d) of rifabutin were selected for study in subsequent clinical trials. More recent reports noting the association of uveitis with these lower dosages of rifabutin have raised concerns about the prevalence of this adverse event. In the 54 identified cases, patients presented with symptoms of unilateral or bilateral uveitis from 2 weeks to more than 7 months following initiation of rifabutin therapy. In all reported cases, patients were receiving concurrent therapy with clarithromycin and/or fluconazole, both of which have inhibitory effects on rifabutin metabolism. In most cases, uveitis resolved within 1–2 months following discontinuation of rifabutin with or without administration of topical corticosteroids. Conclusions: Rifabutin is prescribed frequently for the prophylaxis and treatment of MAC infection, especially in patients with HIV. Uveitis is a rare, dose-related toxicity of this therapy. The risk of rifabutin-associated uveitis may be increased in patients receiving concurrent therapy with clarithromycin or fluconazole because of drug interactions. Patients receiving therapy with combinations of any of these agents should be warned about signs and symptoms of uveitis and be monitored closely for the development of rifabutin toxicity. If uveitis develops, rifabutin therapy should be discontinued promptly.

Pharmacotherapy of HIV Dementia

1997 ◽  
Vol 31 (4) ◽  
pp. 457-473 ◽  
Author(s):  
Sarah T Melton ◽  
Cynthia K Kirkwood ◽  
S Nassir Ghaemi
Keyword(s):  
Cognitive Impairment ◽  
Case Reports ◽  
Data Extraction ◽  
Medline Search ◽  
Study Selection ◽  
Pharmacologic Management ◽  
And Behavior ◽  
Pharmacologic Agents ◽  
Hiv 1

Objective To review the clinical presentation and management of cognitive impairment associated with central nervous system HIV type 1 (HIV-1) infection. Data Sources A MEDLINE search pertaining to HIV-related dementia (HIV-D) and pharmacologic management was performed. Additional literature was obtained from reference lists of the identified articles. Study Selection and Data Extraction All clinical trials and case reports evaluating pharmacologic efficacy in terms of clinical response, cerebrospinal fluid (CSF) changes, and neuropathology were considered for inclusion. Selection was not restricted by study design because most information consists of open uncontrolled trials and case reports. Data Synthesis HIV-D is characterized by a triad of disturbances in cognition, motor performance, and behavior in adults. Children present with developmental delay, cognitive impairment, poor brain growth, and other neurologic symptoms. The exact pathophysiologic mechanisms of HIV-D are not known. Numerous pharmacologic agents (e.g., nucleoside reverse transcriptase inhibitors, pentoxifylline, nitroglycerin, memantine, nimodipine, peptide T) are under investigation for management of HIV-D. Zidovudine is the most thoroughly investigated medication, with patients developing HIV-D less frequently and showing improvement on neuropsychological, CSF, and neuropathologic evaluations. Sustained response to zidovudine lasts 6 months to 1 year and optimal response is achieved at higher, but less tolerated, dosages. HIV-D patients frequently have comorbid psychiatric disorders requiring psychopharmacologic agents and are sensitive to the adverse effects of these medications. Conclusions HIV-D is a devastating complication of HIV-1 infection. Zidovudine is the therapy of choice for prevention and management of cognitive impairment in symptomatic HIV-infected patients and patients with AIDS. Recommendations for other medications cannot be made secondary to lack of data. The management of HIV-D may include multiple agents as more data become available regarding combination therapy. Well-designed controlled trials are needed to evaluate the efficacy of established treatments and investigational medications in the management of HIV-D.

Drug-Induced Esophageal Injuries and Dysphagia

2003 ◽  
Vol 37 (11) ◽  
pp. 1675-1684 ◽  
Author(s):  
Jessica L O'Neill ◽  
Tami L Remington
Keyword(s):  
Case Reports ◽  
Data Extraction ◽  
Treatment Strategies ◽  
Esophageal Injury ◽  
Drug Induced ◽  
Medline Search ◽  
Iatrogenic Complications ◽  
Appropriate Treatment ◽  
Study Selection ◽  
Swallowing Dysfunction

OBJECTIVE: To review and analyze medical literature documenting drug-induced esophageal injury and dysphagia and to formulate strategies to enhance pharmacists' prevention, detection, and treatment of these iatrogenic complications. DATA SOURCES: A MEDLINE search (1966–April 2002) was conducted to identify primary and secondary literature using variable combinations of the following search terms: pill-induced, drug-induced, or iatrogenic with esophageal injury, esophageal damage, or dysphagia. Bibliographies were also reviewed to identify additional relevant references. STUDY SELECTION AND DATA EXTRACTION: All case reports, reviews, and clinical studies relating to drug-induced esophageal injury or swallowing dysfunction were evaluated. DATA SYNTHESIS: Drug-induced esophageal injury may be under-recognized. Several drugs have been associated with physical or chemically mediated injuries. Risk factors for injury have been identified and preventive and treatment strategies have been successful in limiting esophageal injury. Drug-induced dysphagia can have serious complications and is most often associated with typical neuroleptics such as haloperidol. CONCLUSIONS: Pharmacists can play a pivotal role in proactively identifying situations where there is a higher likelihood of drug-induced esophageal injury or dysphagia. They can recommend preventive strategies to promote safe medication use, help identify iatrogenic complications when they occur, and assist in formulation of appropriate treatment strategies.

Predicting Inhibitory Drug—Drug Interactions and Evaluating Drug Interaction Reports Using Inhibition Constants

2005 ◽  
Vol 39 (6) ◽  
pp. 1064-1072 ◽  
Author(s):  
Kenneth A Bachmann ◽  
Jeffrey D Lewis
Keyword(s):  
Cytochrome P450 ◽  
Drug Interaction ◽  
Drug Interactions ◽  
Web Sites ◽  
Case Reports ◽  
Data Extraction ◽  
Data Sources ◽  
Study Selection ◽  
Inhibitory Drug

OBJECTIVE: To review the use of inhibitory constants (Ki) determined from in vitro experiments in the prediction of the significance of inhibitory drug—drug interactions (DDIs). DATA SOURCES: Searches of MEDLINE (1966—August 2004) and manual review of journals, conference proceedings, reference textbooks, and Web sites were performed using the key search terms cytochrome P450, drug—drug interaction, inhibition constant, and Ki. STUDY SELECTION AND DATA EXTRACTION: All articles identified from the data sources were evaluated, and information deemed relevant was included for this review. DATA SYNTHESIS: The cytochrome P450 isoenzymes factor prominently in the explanation of numerous DDIs. Although the regulation of these enzymes by one drug can affect the pharmacokinetics of other drugs, the consequences may not necessarily be significant either in terms of pharmacokinetic or clinical outcomes. Yet, many DDI monographs originate as unconfirmed case reports that implicate the influence of one drug on the CYP-mediated metabolism of another, and these often uncorroborated mechanisms can eventually become regarded as dogma. One consequence of this process is the overprediction of potentially important DDIs. The pharmaceutical industry, Food and Drug Administration, and pharmaceutical scientists have developed a strategy for predicting the significance of inhibitory DDIs at the earliest possible stages of drug development based on a new chemical entity's Ki value, determined in vitro. CONCLUSIONS: We suggest that the use of Ki values of drugs purported to behave as CYP inhibitors be incorporated in the assessment of case reports that ascribe DDIs to inhibition of metabolism of one drug by another.

Macrolide Drug Interactions: An Update

2000 ◽  
Vol 34 (4) ◽  
pp. 495-513 ◽  
Author(s):  
Manjunath P Pai ◽  
Danielle M Graci ◽  
Guy W Amsden
Keyword(s):  
Cytochrome P450 ◽  
Drug Interaction ◽  
Drug Interactions ◽  
Case Reports ◽  
Data Extraction ◽  
Depth Information ◽  
Cytochrome P450 Enzyme ◽  
Medline Search ◽  
P450 Enzyme ◽  
Clinically Significant

OBJECTIVE: To describe the current drug interaction profiles for the commonly used macrolides in the US and Europe, and to comment on the clinical impact of these interactions. DATA SOURCES: A MEDLINE search (1975–1998) was performed to identify all pertinent studies, review articles, and case reports. When appropriate information was not available in the literature, data were obtained from the product manufacturers. STUDY SELECTION: All available data were reviewed to provide an unbiased account of possible drug interactions. DATA EXTRACTION: Data for some of the interactions were not available from the literature, but were available from abstracts or company-supplied materials. Although the data were not always explicit, the best attempt was made to deliver pertinent information that clinical practitioners would need to formulate practice opinions. When more in-depth information was supplied in the form of a review or study report, a thorough explanation of pertinent methodology was supplied. DATA SYNTHESIS: Several clinically significant drug interactions have been identified since the approval of erythromycin. These interactions usually were related to the inhibition of the cytochrome P450 enzyme systems, which are responsible for the metabolism of many drugs. The decreased metabolism by the macrolides has in some instances resulted in potentially severe adverse events. The development and marketing of newer macrolides are hoped to improve the drug interaction profile associated with this class. However, this has produced variable success. Some of the newer macrolides demonstrated an interaction profile similar to that of erythromycin; others have shown improved profiles. The most success in avoiding drug interactions related to the inhibition of cytochrome P450 has been through the development of the azalide subclass, of which azithromycin is the first and only to be marketed. Azithromycin has not been demonstrated to inhibit the cytochrome P450 system in studies using a human liver microsome model, and to date has produced none of the classic drug interactions characteristic of the macrolides. CONCLUSIONS: Most of the available data regarding macrolide drug interactions are from studies in healthy volunteers and case reports. These data suggest that clarithromycin appears to have an interaction profile similar to that of erythromycin. Given this similarity, it is important to consider the interaction profile of clarithromycin when using erythromycin. This is especially necessary as funds for further studies of a medication available in generic form (e.g., erythromycin) are limited. Azithromycin has produced few clinically significant interactions with any agent cleared through the cytochrome P450 enzyme system. Although the available data are promising, the final test should come from studies conducted in patients who are taking potentially interacting compounds on a chronic basis.

Interactions between Recreational Drugs and Antiretroviral Agents

2002 ◽  
Vol 36 (10) ◽  
pp. 1598-1613 ◽  
Author(s):  
Tony Antoniou ◽  
Alice Lin-In Tseng
Keyword(s):  
Cytochrome P450 ◽  
Opportunistic Infections ◽  
Case Reports ◽  
Data Extraction ◽  
Case Series ◽  
Opiate Withdrawal ◽  
Pharmacokinetic Studies ◽  
Recreational Drugs ◽  
Medline Search ◽  
Clinically Significant

OBJECTIVE: To summarize existing data regarding potential interactions between recreational drugs and drugs commonly used in the management of HIV-positive patients. DATA SOURCES: Information was obtained via a MEDLINE search (1966–August 2002) using the MeSH headings human immunodeficiency virus, drug interactions, cytochrome P450, medication names commonly prescribed for the management of HIV and related opportunistic infections, and names of commonly used recreational drugs. Abstracts of national and international conferences, review articles, textbooks, and references of all articles were also reviewed. STUDY SELECTION AND DATA EXTRACTION: Literature on pharmacokinetic interactions was considered for inclusion. Pertinent information was selected and summarized for discussion. In the absence of specific data, prediction of potential clinically significant interactions was based on pharmacokinetic and pharmacodynamic properties. RESULTS: All protease inhibitors (PIs) and nonnucleoside reverse transcriptase inhibitors are substrates and potent inhibitors or inducers of the cytochrome P450 system. Many classes of recreational drugs, including benzodiazepines, amphetamines, and opioids, are also metabolized by the liver and can potentially interact with antiretrovirals. Controlled interaction studies are often not available, but clinically significant interactions have been observed in a number of case reports. Overdoses secondary to interactions between the “rave” drugs methylenedioxymethamphetamine (MDMA) or γ-hydroxybutyrate (GHB) and PIs have been reported. PIs, particularly ritonavir, may also inhibit metabolism of amphetamines, ketamine, lysergic acid diethylmide (LSD), and phencyclidine (PCP). Case series and pharmacokinetic studies suggest that nevirapine and efavirenz induce methadone metabolism, which may lead to symptoms of opiate withdrawal. A similar interaction may exist between methadone and the PIs ritonavir and nelfinavir, although the data are less consistent. Opiate metabolism can be inhibited or induced by concomitant PIs, and patients should be monitored for signs of toxicity and/or loss of analgesia. PIs should not be coadministered with midazolam and triazolam, since prolonged sedation may occur. CONCLUSIONS: Interactions between agents commonly prescribed for patients with HIV and recreational drugs can occur, and may be associated with serious clinical consequences. Clinicians should encourage open dialog with their patients on this topic, to avoid compromising antiretroviral efficacy and increasing the risk of drug toxicity.

Macrolides Versus Azalides: A Drug Interaction Update

1995 ◽  
Vol 29 (9) ◽  
pp. 906-917 ◽  
Author(s):  
Guy W Amsden
Keyword(s):  
Drug Interaction ◽  
Drug Interactions ◽  
Case Reports ◽  
Data Extraction ◽  
Membered Ring ◽  
Depth Information ◽  
Variable Effect ◽  
Study Selection ◽  
Variable Success ◽  
Clinically Significant

Objective: To describe the current drug interaction profiles for all approved and investigational macrolide and azalide antimicrobials, and to comment on the clinical impact of these interactions when appropriate. Data Sources: MEDLINE was searched to identify all pertinent studies, review articles, and case reports from 1975 to 1995. When appropriate information was not available in the literature, data were obtained from the product manufacturers. Study Selection: All available data were reviewed to give an unbiased account of possible drug interactions. Data Extraction: Data for some of the interactions were not available from the literature, but were available from abstracts or from company-supplied materials. Although the data were not always entirely explicative, the best attempt was made to deliver the pertinent information that clinical practitioners would need to formulate practice opinions. When more in-depth information was supplied in the form of a review or study report, a thorough explanation of pertinent methodology was supplied. Data Synthesis: Since the introduction of erythromycin into clinical practice, there have been several clinically significant drug interactions identified throughout the literature associated with this drug. These interactions have been caused mostly by inhibition of the CYP3A subclass of hepatic enzymes, thereby decreasing the metabolism of any other agent given concurrently that is also cleared through this mechanism. With the development and marketing of several new macrolides, it was hoped that the drug interaction profile associated with this class would improve. This has been met with variable success. Although some of the extensions of the 14-membered ring macrolides have shown an incidence of interactions equal to that of erythromycin, others have shown improved profiles. In contrast, the 16-membered ring macrolides have demonstrated a much improved, though not absent, interaction profile. The most success in avoiding drug interactions through structure modification has been accomplished with the development of the azalide class, of which azithromycin is the first to be approved for marketing. This agent has to date produced none of the classic drug interactions that most macrolides have demonstrated in patient care. Conclusions: The introduction of new 14- and 16-membered ring macrolides appears to have had a variable effect in modifying the incidence of drug interactions associated with this class. Azithromycin, a member of the new azalide class, has to date produced fewer clinically significant interactions than other azalides with any agent that is cleared through the CYP3A system. Overall, the available data are promising, and the final test should come from conducting studies in patients who are taking potentially interacting compounds on a chronic basis, as most available data are from trials in healthy volunteers.

Mitomycin-Induced Pulmonary Toxicity: Case Report and Review of the Literature

1992 ◽  
Vol 26 (4) ◽  
pp. 481-484 ◽  
Author(s):  
Donna C. Linette ◽  
Karen H. McGee ◽  
James A. McFarland
Keyword(s):  
Pulmonary Toxicity ◽  
English Language ◽  
Case Reports ◽  
Data Extraction ◽  
Vinca Alkaloid ◽  
Corticosteroid Treatment ◽  
Data Synthesis ◽  
Medline Search ◽  
Pulmonary Response ◽  
Study Selection

OBJECTIVE: This report describes a case of mitomycin-induced pulmonary toxicity and reviews the incidence of this adverse effect, reported patterns of toxicity and associated dosages of the drug, and the use of corticosteroids in the management of pulmonary toxicity. DATA SOURCES: Information about our patient was obtained in part from the medical chart; we had also treated him personally in the past. We conducted a MEDLINE search of the English language literature (restricted to human studies) from 1966 to 1991 and manually searched Index Medicus for current information. STUDY SELECTION: All case reports that described pulmonary toxicity possibly associated with mitomycin were reviewed. DATA EXTRACTION: Studies were evaluated for the dosages of mitomycin given to patients, the nature and onset of symptoms, management course, and corticosteroid use. DATA SYNTHESIS: Our case is similar to others described in the literature. The incidence of mitomycin-induced pulmonary toxicity has been reported to range from 2 to 38 percent. Concurrent vinca alkaloid administration may potentiate the risk of an acute pulmonary insult secondary to mitomycin use. The toxicity is usually of slow onset and the average total dosage of drug implicated is 78 mg. A formal evaluation of corticosteroid treatment has not been performed, but various authors have reported success with different regimens. CONCLUSIONS: The incidence of pulmonary toxicity associated with mitomycin is unpredictable, but more likely to occur at higher dosages. Treatment with corticosteroids is encouraged to improve pulmonary response.

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