Drug-Induced Esophageal Injuries and Dysphagia

2003 ◽  
Vol 37 (11) ◽  
pp. 1675-1684 ◽  
Author(s):  
Jessica L O'Neill ◽  
Tami L Remington

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.

2018 ◽  
Vol 52 (7) ◽  
pp. 662-672 ◽  
Author(s):  
Edna Patatanian ◽  
Melanie K. Claborn

Objective: To review the literature on drug-induced restless legs syndrome (DI-RLS). Data Sources: The review included a search for English-language literature from 1966 to December 2017 in the MEDLINE, PubMed, and Ovid databases using the following search terms: restless legs syndrome (RLS), periodic limb movement, adverse effects, and drug-induced. In addition, background articles on the pathophysiology, etiology, and epidemiology of RLS were retrieved. Bibliographies of relevant articles were reviewed for additional citations. Study Selection and Data Extraction: All case reports, case series, and review articles of DI-RLS were identified and analyzed. There were only a small number of controlled clinical trials, and most data were from case reports and case series. Results: Several drugs and drug classes have been implicated in DI-RLS, with antidepressants, antipsychotics, and antiepileptics having the most evidence. In addition, RLS may be linked with a number of disorders or underlying predisposing factors as well. Conclusions: The prevalence of RLS is variable and ranges from 3% to 19% in the general population. There are many predisposing factors to RLS, but an emerging body of evidence suggests that there is an association between numerous drugs and RLS.


1993 ◽  
Vol 27 (2) ◽  
pp. 167-170 ◽  
Author(s):  
Karen A. Pallone ◽  
Morton P. Goldman ◽  
Matthew A. Fuller

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.


2011 ◽  
Vol 45 (10) ◽  
pp. 1297-1301 ◽  
Author(s):  
Edna Patatanian ◽  
Nancy Toedter Williams

Objective: To review the current literature on drug-induced yawning. Data Sources: Literature was accessed through MEDLINE/PubMed (1996-July 2011), International Pharmaceutical Abstracts (1997-July 2011), and EMBASE, using the search terms yawning, drug-induced yawning, and adverse drug reactions. Study Selection and Data Extraction: Relevant clinical trials and case reports were selected and included to present background information. Bibliographies of all relevant articles were reviewed for additional citations. Data Synthesis: Yawning is a common stereotype behavior with unknown physiologic function that occurs in most vertebrates and humans as early as 15 weeks of intrauterine life. Yawning Is under the control of several neurotransmitters and neuropeptides, Including dopamine, serotonin, oxytocin, and acetylcholine. Among drugs, antidepressants, opioids, dopaminergic agents, benzodiazepines, and induction agents are the main pharmacologic classes associated with yawning. Conclusions: Yawning is rarely a serious adverse reaction and is not frequently listed in the drug summary. Most available data are based on case reports, small studies, and older literature. Clinicians should be aware of the agents commonly triggering this behavior.


1995 ◽  
Vol 29 (11) ◽  
pp. 1149-1155 ◽  
Author(s):  
Alice L Tseng ◽  
Sharon L Walmsley

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.


1997 ◽  
Vol 31 (4) ◽  
pp. 457-473 ◽  
Author(s):  
Sarah T Melton ◽  
Cynthia K Kirkwood ◽  
S Nassir Ghaemi

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.


1993 ◽  
Vol 27 (5) ◽  
pp. 622-633 ◽  
Author(s):  
Edward A. Hartshorn ◽  
Murray P. Ducharme ◽  
Maureen Smythe ◽  
Greg Strohs

OBJECTIVE: To provide a comprehensive review of drug-induced alterations in serum creatinine concentrations (SCrs). DATA SOURCES: Information was obtained from a MEDLINE search, reference lists from articles identified in the search, review articles, and abstracts. STUDY SELECTION: Emphasis was placed on clinical studies of direct relevance to clinical practitioners. DATA EXTRACTION: Literature was assessed for its methodology, results, discussion, and conclusion. DATA SYNTHESIS: Two analytical systems to assay SCr are commonly employed in clinical practice—the Jaffé-based and enzymatic methods. Several drugs have been reported to interfere with SCr results obtained with both analytical systems by producing assay interference. In addition, trimethoprim, cimetidine, and salicylates produce elevations in the SCr by altering the normal elimination pathways of creatinine. Phenacemide has been reported to increase creatinine elimination, but the mechanism of this effect is unknown. CONCLUSIONS: Pharmacists should recognize the clinical significance of drug-induced interference with SCr and propose alternative methods of determining concentrations in selected patients.


1992 ◽  
Vol 26 (4) ◽  
pp. 481-484 ◽  
Author(s):  
Donna C. Linette ◽  
Karen H. McGee ◽  
James A. McFarland

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.


1996 ◽  
Vol 30 (5) ◽  
pp. 527-533 ◽  
Author(s):  
Thomas M Brown ◽  
Brian P Skop ◽  
Thomas R Mareth

OBJECTIVE: TO review the symptoms, pathophysiology, and treatment of the serotonin syndrome (SS). DATA SOURCES: A MEDLINE search (1957–1995) of the English-language literature pertaining to the SS was performed. Additional literature was obtained from reference lists of pertinent articles identified through the search. STUDY SELECTION AND DATA EXTRACTION: All articles were considered for possible inclusion in the review. Pertinent information, as judged by the authors, was selected for discussion. DATA SYNTHESIS: The SS, an occasionally fatal disorder, is characterized by symptoms such as mental status changes, seizures, myoclonus, and blood dyscrasias. Both the central and peripheral serotonergic systems and several serotonin receptor types are involved in the symptomatology of the SS. The pathogenesis of SS may be due to endogenous as well as iatrogenic deficits in peripheral serotonin metabolism, a stimulus for release of serotonin, and interactions with other neurotransmitter systems. Lorazepam, serotonin-blockers, and nitroglycerin have been used successfully to treat SS. CONCLUSIONS: The SS is increasingly recognized and reported in the literature. Clinical and basic science research have increased our understanding of the pathophysiology, conditions, and agents that may predispose to the development of the syndrome. Newer treatment strategies are discussed.


2000 ◽  
Vol 34 (4) ◽  
pp. 479-482 ◽  
Author(s):  
Jennifer J Menke ◽  
Jodi R Heins

OBJECTIVE: To describe a case of epididymo-orchitis that developed four years after treatment with intravesical bacillus Calmette–Guérin (BCG) and to review the incidence of this adverse effect. DATA SOURCES: Information about the patient was obtained from the medical chart. A MEDLINE search of English-language literature (from January 1976 to April 1999) was conducted. STUDY SELECTION: All case reports of BCG-related epididymo-orchitis were evaluated. Review articles describing complications of BCG therapy for bladder cancer and the prevention and treatment of these complications were reviewed. DATA EXTRACTION: Studies were evaluated for reports of BCG-related epididymo-orchitis and its treatment. DATA SYNTHESIS: Our case report is compared with others reported in the literature. The incidence of BCG-associated epididymo-orchitis is rare. CONCLUSIONS: Epididymo-orchitis should be considered as a late complication of BCG therapy for bladder cancer. Proper patient selection may help decrease the risk of complications from BCG therapy.


1994 ◽  
Vol 28 (1) ◽  
pp. 93-96 ◽  
Author(s):  
Lori L. Hoey ◽  
Kathleen D. Lake

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.


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