Cost-Effectiveness of Surveillance Strategies After Treatment for High-Grade Anal Dysplasia in High-Risk Patients
†Division of Infectious Diseases, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA Sexually transmitted diseases
(Impact Factor: 2.84).
04/2013; 40(4):298-303. DOI: 10.1097/OLQ.0b013e31827f4fe9
Anal cancer is one of the most common cancers affecting human immunodeficiency virus (HIV)-infected male patients. Currently, there is no consensus on posttreatment surveillance of HIV-infected men who have sex with men (MSM) who have been treated for high-grade intraepithelial neoplasia (HGAIN), the likely precursor to anal cancer.
The aim of this study was to assess the cost-effectiveness of a range of strategies for anal cancer surveillance in HIV-infected MSM previously treated for HGAIN.
We developed a Markov model to project quality-adjusted life expectancy, lifetime costs, and the incremental cost-effectiveness ratios of 5 strategies using high-resolution anoscopy (HRA) and/or anal cytology testing after treatment.
Performing HRA alone at 6- and 12-month visits was associated with a cost-effectiveness ratio of $4446 per quality-adjusted life year gained. In comparison, combined HRA and anal cytology at both visits provided greater health benefit at a cost of $17,373 per quality-adjusted life year gained. Our results were robust over a number of scenarios and assumptions including patients' level of immunosuppression. Results were most sensitive to test characteristics and cost, as well as progression rates of normal to HGAIN and HGAIN to cancer.
Our results suggest that combined HRA and anal cytology at 6 and 12 months may be a cost-effective surveillance strategy after treatment of HGAIN in HIV-infected MSM.
Available from: Christopher Mathews
- "Interpretation of these findings may be model dependent. Multi-state Markov models have been used to understand the natural history of cervical neoplasia – as well as to model the cost-effectiveness of screening programs for anal cancer and its precursors –. A recent analysis of cervical cytology and human papilloma virus (HPV) DNA samples in a cohort of HIV-infected and high risk HIV-negative women used a 3-state cytology-based Markov model ( no SIL,  SIL, and  the absorbing state of treatment for SIL or invasive cervical cancer) to determine factors associated with transitions between cervical cytopathologic states . "
[Show abstract] [Hide abstract]
ABSTRACT: Objectives(1) To model the natural history of anal neoplasia in HIV-infected patients using a 3-state Markov model of anal cancer pathogenesis, adjusting for cytology misclassification; and (2) to estimate the effects of selected time-varying covariates on transition probabilities.DesignA retrospective cytology-based inception screening cohort of HIV-infected adults was analyzed using a 3-state Markov model of clinical pathogenesis of anal neoplasia.MethodsLongitudinally ascertained cytology categories were adjusted for misclassification using estimates of cytology accuracy derived from the study cohort. Time-varying covariate effects were estimated as hazard ratios.Results(1) There was a moderate to high probability of regression of the high grade squamous intraepithelial lesion (HSIL) state (27–62%) at 2 years after initial cytology screening; (2) the probability of developing invasive anal cancer (IAC) during the first 2 years after a baseline HSIL cytology is low (1.9–2.8%); (3) infrared coagulation (IRC) ablation of HSIL lesions is associated with a 2.2–4.2 fold increased probability of regression to <HSIL; and (4) antiretroviral therapy, suppressed HIV plasma viral load, and CD4 ≥350/mm3 are each associated with reduced probability of progression from <HSIL to HSIL.ConclusionsThe finding of moderate to high rates of regression of the HSIL state accompanied by low rates of progression to IAC should inform both screening and precursor treatment guideline development. There appears to be a consistent and robust beneficial effect of antiretroviral therapy, suppressed viral load, and higher CD4 on the transition from the <HSIL state to the HSIL state.
PLoS ONE 08/2014; 9(8):e104116. DOI:10.1371/journal.pone.0104116 · 3.23 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: Invasive anal cancer has become an important cause of non AIDS-related cancer among HIV-infected individuals. Human papillomavirus is the main etiological agent. This review explains the pathophysiologic role of human papillomavirus in the development of invasive anal cancer, summarizes recent epidemiological trends of invasive anal cancer, and reviews the evidence to address common clinical questions posed when screening for anal cancer in HIV-infected patients. The effect of highly active antiretroviral therapy on human papillomavirus oncogenesis is still unclear, but given the increased clinical burden of invasive anal cancer among HIV-infected patients, many clinics have implemented screening programs for anal cancer and its precursors. Despite the availability of several modalities for treatment of precursors of anal cancer, evidence that current treatment modalities favorably alter the natural history of human papillomavirus oncogenesis in the anal and perianal regions is still inconclusive. However, there is sufficient evidence to state that the accuracy of anal cancer screening procedures (cytology and high-resolution anoscopy directed biopsy) is comparable to the accuracy of those used in screening for cervical cancer precursors. Studies that systematically assess the efficacy of these anal cancer screening programs in reducing the incidence of and morbidity and mortality from invasive anal cancer among HIV-infected patients are needed.
AIDS reviews 05/2013; 15(2):122-133. · 3.79 Impact Factor
Medicina Clínica 11/2013; 142(4). DOI:10.1016/j.medcli.2013.09.012 · 1.42 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.