Kelsey Rife, Alessandra Lyman, and Kristina Pascuzzi are Clinical Pharmacy Specialists; Corinna Falck-Ytter is the Section Chief of Primary Care, Christopher J. Burant is a Statistician in the Geriatric Research, Education, and Clinical Center; and Yngve Falck-Ytter is the Section Chief of Gastroenterology and Hepatology; all at the VA Northeast Ohio Healthcare System in Cleveland. Sheena LeClerc-Kamieniecki is a Clinical Pharmacy Specialist at the Chillicothe Veterans Affairs Medical Center in Ohio. Corinna Falck-Ytter is an Associate Professor of Medicine, Christopher Burant is an Associate Professor of Nursing, and Yngve Falck-Ytter is a Professor of Medicine, all at Case Western Reserve University in Cleveland, Ohio.
Correspondence: Kelsey Rife (kelsey.rife@ va.gov)
Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.
Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the US Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.
This retrospective cohort study was performed at the Department of Veterans Affairs (VA) Northeast Ohio Healthcare System (VANEOHS) in Cleveland. This study received approval from the VANEOHS Institutional Review Board. Retrospective patient data were collected from the Veterans Health Administration (VHA) Computerized Patient Record System (CPRS) electronic health record. Collectively, the VHA has treated > 100,000 patients with DAAs, making it the largest provider of HCV treatment in the US. VANEOHS has treated nearly 2,000 patients with DAAs, rendering it one of the largest single-institution cohorts to be able to examine the effects of HCV treatment on subpopulations, such as patients with T2DM.
Patients were identified using ICD-9/10 codes for T2DM and medication dispense history of hepatitis C DAAs. Patients were included if they had a diagnosis of T2DM, were initiated on a hepatitis C DAA between February 1, 2014 to September 26, 2016. To be eligible, patients were required to have both a baseline HbA1c within 6 months prior to starting HCV treatment as well as a HbA1c within 4 months posttreatment. The HCV treatment included were new short-course DAAs, including sofosbuvir, simeprevir, ombitasvir/paritaprevir/ritonavir ± dasabuvir, ledipasvir/sofosbuvir, elbasvir/grazoprevir, and sofosbuvir/velpatasvir. Patients were excluded if they were not on any antihyperglycemic medications at the start of HCV treatment or did not complete a full HCV treatment course.
Pertinent demographic data collected at baseline included patient age, gender, HCV genotype, and presence of advanced fibrotic liver disease (defined as a Metavir fibrosis stage 4 on liver biopsy, transient elastography > 12.5 kPa, or radiologic evidence of cirrhosis). HCV treatment initiation and completion dates were collected along with treatment response at 12 weeks posttreatment. Patients were considered to have achieved SVR12 if their hepatitis C viral load remained undetectable at posttreatment day 77 or thereafter. Treatment relapse was defined as a patient who achieved an undetectable HCV RNA by the end of treatment but subsequently had detectable HCV RNA following treatment cessation.
Baseline HbA1c was defined as the HbA1c drawn closest to the date of HCV treatment initiation, at least 6 months prior to treatment. Immediate posttreatment HbA1c was defined as HbA1c drawn up to 4 months posttreatment, and sustained HbA1c was captured up to 18 months posttreatment. Antihyperglycemic medication regimens and doses were collected at baseline, the end of treatment, and 3 months posttreatment via medication dispense history as well as provider notes documented in CPRS. Changes in antihyperglycemic medications were defined as net de-escalation, escalation, or no change. De-escalation of antihyperglycemic medication was defined as an overall decrease in dose, decrease in number of medications, or discontinuation of insulin (eg, if same overall number of medications but insulin was changed to an oral antihyperglycemic would have been considered a de-escalation). No change was defined as no overall change in insulin dose, or number of medications (eg, including patients who may have changed from one oral antihyperglycemic to another while overall number of medications did not change). Escalation was defined as an increase in dose, increase in number of medications, or initiation of insulin.
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