Tigecycline-related pancreatitis: a review of spontaneous adverse event reports.

Tigecycline-related pancreatitis: a review of spontaneous adverse event reports.

Jan 2013

Okon E, Engell C, van Manen R, Brown J.

Source

Beth Israel Medical Center, Newark, New Jersey , the Netherlands.

Abstract

Keywords:

• tigecycline;
• pancreatitis;
• tetracycline;
• antimicrobials;

• adverse drug reaction

• 
  

STUDY OBJECTIVE:

To provide clinicians with an understanding of the comparative occurrence of tigecycline and pancreatitis, and to provide any clinically relevant characteristics that may be useful in identifying the patients at risk.

DESIGN:

Retrospective cohort study.

DATA SOURCE:

Spontaneous reports in the United States Food and Drug Administration (FDA) Adverse Event Reporting System (AERS) database generated between January 1997 and December 2010.

PATIENTS:

Sixty-two patients who experienced pancreatitis while receiving tigecycline therapy.

MEASUREMENTS AND MAIN RESULTS:

Disproportionality analysis with Bayesia
n correction methodology was used to compare tigecycline with all other agents listed in the AERS. Disproportionality analysis uses an adverse event relative reporting ratio (RRR) to compare the occurrence of a specific adverse event with an index drug of interest to the occurrence of the same adverse event with similar agents or with all other FDA-approved prescription drugs. The value was considered meaningful if the 5th percentile of the distribution of the RRR (RRR(05) ) was 2 or greater. Our review identified 62 potential cases of tigecyline-related pancreatitis. An RRR(05) score of 10.4, 10.38, and 2.87 was determined for tigecycline-related pancreatitis compared with all other agents, systemic antibiotics, and select tetracyclines listed in the AERS, respectively. In addition, a sex-based RRR(05) score was higher in women versus men (14.432 vs 3.125) when tigecycline was compared with all agents in the AERS.

CONCLUSION:

Our analysis suggests a quantitative signal between tigecycline use and pancreatitis; however, given the limitations of our study, a cause-and-effect relationship cannot be inferred. Thus, additional rigorous scientific analyses are warranted to explore these findings.

Wiley OnLine

Documentation of vancomycin-resistant Staphylococcus aureus (VRSA) among children with atopic dermatitis in the Qassim region, Saudi Arabia.

Sept 2012

Alzolibani AA, Al Robaee AA, Al Shobaili HA, Bilal JA, Issa Ahmad M, Bin Saif G.

Source

Department of Dermatology, College of Medicine, Qassim University, Buraydah 51477, Saudi Arabia. azolibani@yahoo.com.

Abstract

INTRODUCTION:

Staphylococcus aureus is known as a common pathogen in atopic dermatitis. A methicillin-resistant S. aureus strain with reduced susceptibility to vancomycin (VISA/VRSA) is increasing worldwide. The aims of this study were to evaluate the antibiotic-susceptibility pattern of S. aureus isolated from children with atopic dermatitis and to identify the occurrence of resistance to glycopeptide antibiotics.

METHODS:

Swabs were collected from atopic dermatitis skin lesions of 80 children being treated at dermatology clinics whose ages ranged from 6 months to 15 years in the period from March 2009 to February 2010. Isolates were studied with an antibiogram for an antibiotic-susceptibility test. The selected antibiotics were the usually administered antimicrobials at dermatological clinics in Buraydah (Qassim, Saudi Arabia). Results were determined as minimal inhibitory concentration (MIC) using the Vitek system.

RESULTS:

Thirty S. aureus isolates showed resistance to streptomycin (100%), benzylpenicillin and ampicillin (96.7%), and oxacillin (90%). S. aureus resistance to trimethoprim/sulfamethoxazole, tigecycline, and vancomycin was 63.3%, 83.3%, and 53.3%, respectively. Resistance to linezolid was less, at 5.7%.

CONCLUSIONS:

Strains of MRSA with decreasing susceptibility to vancomycin were documented in the Qassim region of Saudi Arabia. Other studies will be required on VISA/VRSA strains concerning phenotypic and genotypic characterization.

PubMed

Effects of tigecycline, linezolid and vancomycin on biofilms of viridans streptococci isolates from patients with endocarditis.

Effects of tigecycline, linezolid and vancomycin on biofilms of viridans streptococci isolates from patients with endocarditis.

Int J Artif Organs. 2007 Sep

Presterl E, Lassnigg A, Eder M, Reichmann S, Hirschl AM, Graninger W.
Department of Medicine I, Division of Infectious Diseases and Tropical Medicine, Medical University of Vienna, Vienna - Austria and Institute of Hygiene and Medical Microbiology, Division of Clinical Microbiology, Medical University of Vienna, Vienna - Austria.

Background: Endocarditis, and prosthetic valve endocarditis in particular, is a serious disease with high morbidity and mortality. We investigate the effects of tigecycline, linezolid and vancomycin on biofilms of viridans group streptococci (VGS) isolated from patients with definite native or prosthetic valve endocarditis.

Methods and Results: Ten of 20 VGS blood stream isolates from patients with endocarditis formed biofilms in the microtiter plate biofilm model. The minimal inhibitory concentrations (MIC) for tigecycline, linezolid and vancomycin were determined using the microdilution broth method. Biofilms were grown for 24 hours and were incubated with tigecycline, linezolid and vancomycin at increasing concentrations from 1-128x MIC of the isolate being tested. Biofilm thickness was quantified by measuring the optical density (OD) after dyeing it with crystal violet. The incubation of the biofilms with tigecycline, linezolid or vancomycin resulted in a significant reduction of OD compared to the control biofilm without antibiotic (p<0.05).>

Conclusions: In the present study on viridans streptococci isolated from patients with endocarditis, tigecycline and linezolid reduced the density of the biofilms as effectively as vancomycin. However, linezolid and vancomycin were bactericidal at higher concentrations. Linezolid and vancomycin at very high doses may be useful in the treatment of biofilm-associated diseases caused by VGS infections.

PMID: 17918125 [PubMed - as supplied by publisher]