Deborah R Erickson

American Urological Association, Linthicum, Maryland, United States

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Publications (48)141.77 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The purpose of this amendment is to provide an updated clinical framework for the diagnosis and treatment of interstitial cystitis/bladder pain syndrome based upon data received since the publication of original guideline in 2011. A systematic literature review using the MEDLINE(®) database (search dates 1/1/83-7/22/09) was conducted to identify peer-reviewed publications relevant to the diagnosis and treatment of IC/BPS. This initial review yielded an evidence base of 86 treatment articles after application of inclusion/exclusion criteria. The AUA update literature review process, in which an additional systematic review is conducted periodically to maintain guideline currency with newly published relevant literature, was conducted in July 2013. This review identified an additional 31 articles, which were added to the evidence base of this Guideline. Newly incorporated literature describing the treatment of IC/BPS was integrated into the Guideline with additional treatment information provided as Clinical Principles and Expert Opinions when insufficient evidence existed. The diagnostic portion of the Guideline remains unchanged from the original publication and is still based on Expert Opinions and Clinical Principles. The management of IC/BPS continues to evolve as can be seen by an expanding literature on the topic. This document constitutes a clinical strategy and is not intended to be interpreted rigidly. The most effective approach for a particular patient is best determined by the individual clinician and patient. As the science relevant to IC/BPS evolves and improves, the strategies presented will require amendment to remain consistent with the highest standards of care. Copyright © 2015 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.
    The Journal of Urology 01/2015; 193(5). DOI:10.1016/j.juro.2015.01.086 · 3.75 Impact Factor
  • John B Forrest, Christopher K Payne, Deborah R Erickson
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    ABSTRACT: Cyclosporine A is a fifth-tier treatment option in the American Urological Association guidelines for interstitial cystitis/bladder pain syndrome. It was more effective than pentosanpolysulfate in a Finnish trial, but experience elsewhere is limited. Some centers use cyclosporine A off label for carefully selected patients but the number of patients in each center is small. We performed a retrospective review combining data from 3 tertiary centers that focus on interstitial cystitis/bladder pain syndrome. Charts were reviewed for patients with interstitial cystitis/bladder pain syndrome who received cyclosporine A. Response was defined as markedly improved on the 7-point global response assessment (2 centers) or as at least a 50% decrease in Interstitial Cystitis Symptom Index score (1 center). The study included 14 men and 30 women. Mean patient age was 55.5 years (range 27 to 75) and mean followup was 20.8 months (range 3 to 81). A total of 34 patients had Hunner lesions. Of these patients 29 (85%) responded but 6 eventually stopped cyclosporine A for adverse events, resulting in a success rate of 68% (23 of 34) for patients with Hunner lesions. In contrast, only 3 of 10 patients without Hunner lesions responded (30%). For all responders, the response occurred within 4 months. Cyclosporine A had a high success rate for patients with Hunner lesions in whom more conservative options, including endoscopic treatment, had failed. The success rate was low for patients without Hunner lesions. A 3 to 4-month trial is sufficient time to assess response. Adverse events were common and led to discontinuation of cyclosporine A for some patients. Close monitoring is needed, especially for blood pressure and renal function.
    The Journal of urology 08/2012; 188(4):1186-91. DOI:10.1016/j.juro.2012.06.023 · 3.75 Impact Factor
  • Renee B Quillin, Deborah R Erickson
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    ABSTRACT: Management of interstitial cystitis/bladder pain syndrome (IC/BPS) is individualized for each patient. All patients benefit from education and self-care advice. Patients with Hunner lesions usually respond well to fulguration or triamcinolone injection, which can be repeated when the symptoms and lesions recur. For patients without Hunner lesions, numerous treatment options are available. The tiers of the American Urological Association Guidelines present these options in an orderly progression, balancing the benefits, risks, and burdens. Along with specific IC/BPS treatments, it is also important to have resources for stress reduction, pain management, and treatment of comorbid conditions.
    Urologic Clinics of North America 08/2012; 39(3):389-96. DOI:10.1016/j.ucl.2012.05.007 · 1.35 Impact Factor
  • Renee B Quillin, Deborah R Erickson
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    ABSTRACT: The American Urological Association recently developed guidelines to assist clinicians who evaluate and treat interstitial cystitis/bladder pain syndrome. Knowledge in this area continues to advance, and some of the guideline statements differ from what clinicians may have been previously taught. This review includes the 27 guideline statements, which address both evaluation and treatment. This review lists the guideline statements and, when applicable, comments on their practical implementation and the most recent research. Practical information includes the following: key questions that help in the differential diagnosis, when to perform cystoscopy and urodynamics, how to recognize and treat Hunner lesions, useful practical resources for patients and clinicians, information on elimination diet and stress management, initial selection of oral and intravesical medications, and description of advanced treatment options (limited to dedicated, experienced clinicians).
    Current Urology Reports 07/2012; 13(5):394-401. DOI:10.1007/s11934-012-0263-z · 1.51 Impact Factor
  • Deborah R Erickson
    The Journal of urology 04/2012; 187(6):1958-9. DOI:10.1016/j.juro.2012.02.2520 · 3.75 Impact Factor
  • William B Rogers, Deborah R Erickson
    The Journal of urology 03/2012; 187(3):783-4. DOI:10.1016/j.juro.2011.12.025 · 3.75 Impact Factor
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    ABSTRACT: We determined whether gene expression profiles in urine sediment could provide noninvasive markers for interstitial cystitis/bladder pain syndrome with and/or without Hunner lesions. Fresh catheterized urine was collected and centrifuged from 5 controls, and 5 Hunner lesion-free and 5 Hunner lesion bearing patients. RNA was extracted from pelleted material and quantified by gene expression microarray using the GeneChip® Human Gene ST Array. Three biologically likely hypotheses were tested, including 1) all 3 groups are distinct from each other, 2) controls are distinct from the 2 types combined of patients with interstitial cystitis/bladder pain syndrome and 3) patients with Hunner lesion-interstitial cystitis/bladder pain syndrome are distinct from controls and patients with nonHunner-lesion interstitial cystitis/bladder pain syndrome combined. For statistical parity an unlikely fourth hypothesis was included, that is patients with nonHunner-lesion interstitial cystitis/bladder pain syndrome are distinct from controls and patients with Hunner lesion-interstitial cystitis/bladder pain syndrome combined. Analysis supported selective up-regulation of genes in the Hunner lesion interstitial cystitis/bladder pain syndrome group (hypothesis 3), which were primarily associated with inflammation. The inflammatory profile was statistically similar to that reported in a prior Hunner lesion interstitial cystitis/bladder pain syndrome bladder biopsy study. Gene expression analysis of urine sediment was feasible in this pilot study. Expression profiles failed to discriminate nonHunner-lesion interstitial cystitis/bladder pain syndrome from controls and they are unlikely to be a noninvasive marker for nonHunner-lesion interstitial cystitis/bladder pain syndrome. In contrast, patients with Hunner lesion had increased proinflammatory gene expression in urine sediment, similar to that in a prior microarray study of bladder biopsies. If these preliminary results are validated in future research, they may lead to a noninvasive biomarker for Hunner lesion-interstitial cystitis/bladder pain syndrome.
    The Journal of urology 12/2011; 187(2):725-32. DOI:10.1016/j.juro.2011.09.142 · 3.75 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To provide a clinical framework for the diagnosis and treatment of interstitial cystitis/bladder pain syndrome. A systematic review of the literature using the MEDLINE® database (search dates 1/1/83-7/22/09) was conducted to identify peer reviewed publications relevant to the diagnosis and treatment of interstitial cystitis/bladder pain syndrome. Insufficient evidence-based data were retrieved regarding diagnosis and, therefore, this portion of the Guideline is based on Clinical Principles and Expert Opinion statements. The review yielded an evidence base of 86 treatment articles after application of inclusion/exclusion criteria. These publications were used to create the majority of the treatment portion of the Guideline. When sufficient evidence existed, the body of evidence for a particular treatment was assigned a strength rating of A (high), B (moderate) or C (low). Additional treatment information is provided as Clinical Principles and Expert Opinion when insufficient evidence existed. See text and algorithm for definitions, and detailed diagnostic management, and treatment frameworks. The evidence-based guideline statements are provided for diagnosis and overall management of interstitial cystitis/bladder pain syndrome as well as for various treatments. The panel identified first through sixth line treatments as well as developed guideline statements on treatments that should not be offered. Interstitial cystitis/bladder pain syndrome is best identified and managed through use of a logical algorithm such as is presented in this Guideline. In the algorithm the panel identifies an overall management strategy for the interstitial cystitis/bladder pain syndrome patient. Diagnosis and treatment methodologies can be expected to change as the evidence base grows in the future.
    The Journal of urology 06/2011; 185(6):2162-70. DOI:10.1016/j.juro.2011.03.064 · 3.75 Impact Factor
  • Deborah R Erickson, Bernard Boulanger
    The Journal of urology 02/2011; 185(4):1177-8. DOI:10.1016/j.juro.2011.01.042 · 3.75 Impact Factor
  • Deborah R Erickson
    The Journal of urology 10/2010; 184(6):2237-8. DOI:10.1016/j.juro.2010.09.044 · 3.75 Impact Factor
  • Deborah R Erickson
    The Journal of urology 09/2009; 182(4):1251-2. DOI:10.1016/j.juro.2009.07.074 · 3.75 Impact Factor
  • Deborah R Erickson
    The Journal of urology 02/2009; 181(3):945-6. DOI:10.1016/j.juro.2008.12.028 · 3.75 Impact Factor
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    ABSTRACT: We evaluated gene expression profiles after inducing differentiation in cultured interstitial cystitis and control urothelial cells. Bladder biopsies were taken from patients with interstitial cystitis and controls, that is women undergoing surgery for stress incontinence. Primary cultures were grown in keratinocyte growth medium with supplements. To induce differentiation in some plates the medium was changed to Dulbecco's modified Eagle's minimal essential medium-F12 (Media Tech, Herndon, Virginia) with supplements. RNA was analyzed with Affymetrix(R) chips. Three patients with nonulcerative interstitial cystitis were compared with 3 controls. After inducing differentiation 302 genes with a described function were altered at least 3-fold in interstitial cystitis and control cells (p <0.01). Functions of the 162 up-regulated genes included cell adhesion (eg claudins, occludin and cingulin), urothelial differentiation, the retinoic acid pathway and keratinocyte differentiation (eg skin cornified envelope components). The 140 down-regulated transcripts included genes associated with basal urothelium (eg p63, integrins beta4, alpha5 and alpha6, basonuclin 1 and extracellular matrix components), vimentin, metallothioneins, and members of the Wnt and Notch pathways. When comparing interstitial cystitis control cells after differentiation, only 7 genes with a described function were altered at least 3-fold (p <0.01). PI3, SERPINB4, CYP2C8, EFEMP2 and SEPP1 were decreased, and AKR1C2 and MKNK1 were increased in interstitial cystitis cases. Differentiation associated changes occurred in interstitial cystitis and control cells. Comparing interstitial cystitis vs control cases revealed few differences. This study may have included patients with interstitial cystitis and minimal urothelial deficiency, and/or we may have selected cells that were most robust in culture. Also, the abnormal urothelium in interstitial cystitis cases may be due to post-translational changes and/or to the bladder environment.
    The Journal of urology 10/2008; 180(6):2681-7. DOI:10.1016/j.juro.2008.08.007 · 3.75 Impact Factor
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    ABSTRACT: We tested for associations between urine markers, bladder biopsy features and bladder ulcers in interstitial cystitis/painful bladder syndrome. Subjects were 72 patients with interstitial cystitis/painful bladder syndrome undergoing bladder distention and biopsy. Urine was collected before the procedure. Urine marker levels were correlated with biopsy and cystoscopic findings. Patients with no previous interstitial cystitis/painful bladder syndrome treatments (47) were analyzed separately from previously treated patients (25). For untreated patients urine interleukin-6 and cyclic guanosine monophosphate were associated with urothelial epidermal growth factor receptor staining (for interleukin-6 r = 0.29; 95% CI 0.07, 0.51; p = 0.01 and for cyclic guanosine monophosphate r = 0.34; 95% CI 0.13, 0.55; p = 0.002). Urine interleukin-8 was negatively associated with urothelial heparin-binding epidermal growth factor-like growth factor staining (r = -0.34; 95% CI -0.55, -0.12; p = 0.002) and positively associated with lamina propria mast cell count (r = 0.29; 95% CI 0.06, 0.52; p = 0.01). The latter association also was seen in treated patients (r = 0.46; 95% CI 0.20, 0.73; p <0.001). None of the urine markers was significantly different for ulcer vs nonulcer groups. All of the patients with ulcer had extensive inflammation on bladder biopsy including severe mononuclear cell infiltration, moderate or strong interleukin-6 staining in the urothelium and lamina propria, and leukocyte common antigen staining in more than 10% of the lamina propria. However, these features also were seen in 24% to 76% of the patients without ulcer. Overall urine markers did not associate robustly with biopsy findings. The strongest association was a positive association between urine interleukin-8 levels and bladder mast cell count. Patients with ulcer consistently had bladder inflammation but the cystoscopic finding of ulcers was not a sensitive indicator of inflammation on bladder biopsy.
    The Journal of urology 05/2008; 179(5):1850-6. DOI:10.1016/j.juro.2008.01.047 · 3.75 Impact Factor
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    ABSTRACT: We evaluated changes in urine markers and symptom scores after bladder distention in patients with interstitial cystitis. Study subjects were 33 new patients who had undergone no prior interstitial cystitis treatment. Urine specimens were taken before and 1 month after bladder distention. University of Wisconsin symptom scores were done the same day as the urine specimen collection. Urine marker levels and symptom scores before and after distention were compared. Changes in markers were tested for associations with changes in symptom scores and other markers. Markers and specific symptoms before distention were tested for their association with post-distention symptom improvement. After distention the median total University of Wisconsin score decreased significantly (28.5 before, 20 after, p <0.001). A total of 12 patients (36%) had at least 30% improvement in University of Wisconsin score, and 8 patients (24%) had at least 50% improvement. No pre-distention markers or symptoms predicted which patients would have a good response. There were 2 urine markers that improved significantly after distention: anti-proliferative factor activity (median -96% before, -17% after, p <0.001) and heparin-binding epidermal growth factor-like growth factor levels (median 0.34 ng/mg creatinine before, 4.1 after, p <0.001). None of the changes in urine markers associated with changes in symptom scores. The median symptom score for newly diagnosed patients with interstitial cystitis decreased after distention, but only a minority of patients had at least 30% symptom improvement. Bladder distention altered urine anti-proliferative factor activity and heparin-binding epidermal growth factor-like growth factor levels toward normal, but the mechanism of symptom relief after distention is still unknown.
    The Journal of Urology 03/2007; 177(2):556-60. DOI:10.1016/j.juro.2006.09.029 · 3.75 Impact Factor
  • Deborah R Erickson, Kathleen J Propert
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    ABSTRACT: Painful bladder syndrome (PBS) and interstitial cystitis (IC) often affect women of child-bearing age. This article includes information of interest to PBS/IC patients who are pregnant or contemplating pregnancy, and to the clinicians who care for them. One topic is how pregnancy affects PBS/IC symptoms, although little is known at this time. The article also describes the pregnancy risks associated with the most commonly used PBS/IC treatments. Finally, the current knowledge regarding genetic factors in IC is discussed.
    Urologic Clinics of North America 03/2007; 34(1):61-9. DOI:10.1016/j.ucl.2006.10.006 · 1.35 Impact Factor
  • Deborah R. Erickson
    Urologic Clinics of North America 02/2007; 34(1):XIII-XIII. DOI:10.1016/j.ucl.2006.10.012 · 1.35 Impact Factor
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    ABSTRACT: In human subjects only a small percent of oral PPS is found in urine. Commercially available PPS is a heterogeneous mixture with varying molecular weights. Our hypothesis was that only the low molecular weight fraction reaches the urine. Urine was obtained from patients with IC who were chronically receiving PPS. The amount and molecular size of PPS in the urine were determined by enzyme-linked immunosorbent assay and molecular sieve chromatography. PPS was purified from Elmiron capsules and fractionated into LMW and HMW fractions. Urine recovery of PPS was measured in rabbits after oral or intravenous administration of unfractionated, LMW or HMW PPS. The median urine PPS level in 34 patients with IC was 1.2 microg/ml (range 0.5 to 27.7). All PPS recovered from IC urine was LMW. After intravenous administration in rabbits the median recovery in urine was 47.2% (range 19.7% to 73.2%) for unfractionated PPS, 74.6% (range 31.4% to 96.3%) for LMW and 3.3% (range 2.5% to 5.0%) for HMW. After oral administration in rabbits the median recovery in urine was 7.4% (range 2.1% to 46.0%) for LMW and 0.10% (range 0.0% to 0.3%) for HMW. In patients with IC who are on oral PPS the PPS recovered in the urine is all of LMW. In rabbits the HMW fraction of PPS is recovered in small amounts from urine after intravenous administration and not at all after oral administration.
    The Journal of Urology 03/2006; 175(3 Pt 1):1143-7. DOI:10.1016/S0022-5347(05)00319-8 · 3.75 Impact Factor
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    ABSTRACT: To attach galactosyl residues to pentosan polysulfate (PPS) and heparin so that these drugs will bind to the endogenous lectins in the bladder. The increased binding may improve their efficacy for treating interstitial cystitis. The anionic polysaccharides, PPS, and heparin were modified by attachment of lactose. The covalent modification was by chemical linking of lactose derivatives or by beta-lactosyl transfer reaction from p-nitrophenyl beta-lactoside using the transglycosylation activity of Trichoderma reesei cellulase enzymes. The unmodified and modified PPS and heparin, as well as various mucin glycoproteins, were radiolabeled or biotinylated and examined for their ability to bind to rabbit and human bladder. Both biotinylated and radiolabeled PPS and heparin bound very weakly or not at all to human and rabbit bladders. In contrast, the PPS and heparin modified by attachment of lactose, as well as the asialo mucin glycoproteins, bound strongly to human and rabbit bladders. This binding is apparently mediated by the interaction of the endogenous bladder galactins and the non-reducing galactose terminals in the lactose attached to the anionic polysaccharides or the asialoglycoproteins. Lactose-pentosan sulfate and lactose-heparin bind more avidly to the bladder epithelium than the unmodified molecules. Thus, they may be more effective for interstitial cystitis than the parent drugs. Other possible applications of this approach include modification of intravesical chemotherapeutic agents for bladder cancer, or intravesically placed antibiotics, to improve their adherence and retention in the bladder.
    Urology 02/2006; 67(1):209-13. DOI:10.1016/j.urology.2005.07.048 · 2.13 Impact Factor
  • Shou Ling Leong, Deborah R Erickson, Richard C Pees
    The Journal of family practice 06/2005; 54(5):428-36. · 0.74 Impact Factor

Publication Stats

1k Citations
141.77 Total Impact Points

Institutions

  • 2015
    • American Urological Association
      Linthicum, Maryland, United States
  • 2004–2012
    • University of Kentucky
      • Department of Surgery
      Lexington, Kentucky, United States
  • 2001–2005
    • University of Maryland, Baltimore
      • Division of Infectious Diseases
      Baltimore, Maryland, United States
  • 1996–2003
    • Penn State Hershey Medical Center and Penn State College of Medicine
      • • Department of Surgery
      • • Biochemistry and Molecular Biology
      Hershey, Pennsylvania, United States
  • 1995–2000
    • Pennsylvania State University
      • • Department of Surgery
      • • Department of Pathology
      • • Department of Biochemistry and Molecular Biology
      University Park, Maryland, United States