Hemoglobin A1c Has Suboptimal Performance to Diagnose and Monitor Diabetes Mellitus in Patients with Cirrhosis.

BACKGROUND: Glycated hemoglobin A1c (HbA1c) is routinely used to diagnose and monitor type 2 diabetes mellitus (T2DM) in cirrhotic patients. Remarkably, HbA1c may be falsely low in such patients. AIMS: We assessed the diagnostic and monitoring yield of HbA1c in cirrhotic patients with T2DM (DM-Cirr) and without T2DM (NoDM-Cirr). METHODS: We conducted a composite study allocating 21 NoDM-Cirr into a cross-sectional module and 16 DM-Cirr plus 13 controls with T2DM only (DM-NoCirr) into a prospective cohort. Oral glucose tolerance test (OGTT) was performed in NoDM-Cirr. DM-Cirr and DM-NoCirr were matched by sex, age, BMI, and T2DM treatment and studied with continuous glucose monitoring (CGM). Percent deviations from target, low/high blood glucose indexes (LBGI/HBGI) were calculated from CGM, as well as the average daily risk range (ADRR) as a marker of glucose variability. RESULTS: Overall, HbA1c and OGTT diagnostic yield agreed in 12 patients (57%, ρ = 0.45, p < 0.03). CGM captured 3463 glucose determinations in DM-Cirr and 4273 in DM-NoCirr (p = 0.42). Regression analysis showed an inferior association between HbA1c and CGM in DM-Cirr (R2 = 0.52), when compared to DM-NoCirr (R2 = 0.94), and fructosamine did not improve association for DM-Cirr (R2 = 0.31). Interestingly, cirrhosis and Child-Turcotte-Pugh class accounted for HbA1c variance (p < 0.05). Patients in DM-Cirr were less frequently within target glucose (70-180 mg/dL), but at higher risk for hyperglycemia (HBGI > 9) when compared to DM-NoCirr, and they also showed higher glucose variability (ADRR 13.9 ± 2.5 vs. 8.9 ± 1.8, respectively, p = 0.03). CONCLUSION: HbA1c inaccurately represents chronic glycemia in patients with cirrhosis, likely in relation to increased glucose variability.

Myocardial Infarct Size by CMR in Clinical Cardioprotection Studies: Insights From Randomized Controlled Trials.

OBJECTIVES: The aim of this study was to review randomized controlled trials (RCTs) using cardiac magnetic resonance (CMR) to assess myocardial infarct (MI) size in reperfused patients with ST-segment elevation myocardial infarction (STEMI). BACKGROUND: There is limited guidance on the use of CMR in clinical cardioprotection RCTs in patients with STEMI treated by primary percutaneous coronary intervention. METHODS: All RCTs in which CMR was used to quantify MI size in patients with STEMI treated with primary percutaneous coronary intervention were identified and reviewed. RESULTS: Sixty-two RCTs (10,570 patients, January 2006 to November 2016) were included. One-third did not report CMR vendor or scanner strength, the contrast agent and dose used, and the MI size quantification technique. Gadopentetate dimeglumine was most commonly used, followed by gadoterate meglumine and gadobutrol at 0.20 mmol/kg each, with late gadolinium enhancement acquired at 10 min; in most RCTs, MI size was quantified manually, followed by the 5 standard deviation threshold; dropout rates were 9% for acute CMR only and 16% for paired acute and follow-up scans. Weighted mean acute and chronic MI sizes (≤12 h, initial TIMI [Thrombolysis in Myocardial Infarction] flow grade 0 to 3) from the control arms were 21 ± 14% and 15 ± 11% of the left ventricle, respectively, and could be used for future sample-size calculations. Pre-selecting patients most likely to benefit from the cardioprotective therapy (≤6 h, initial TIMI flow grade 0 or 1) reduced sample size by one-third. Other suggested recommendations for standardizing CMR in future RCTs included gadobutrol at 0.15 mmol/kg with late gadolinium enhancement at 15 min, manual or 6-SD threshold for MI quantification, performing acute CMR at 3 to 5 days and follow-up CMR at 6 months, and adequate reporting of the acquisition and analysis of CMR. CONCLUSIONS: There is significant heterogeneity in RCT design using CMR in patients with STEMI. The authors provide recommendations for standardizing the assessment of MI size using CMR in future clinical cardioprotection RCTs.

Increase of drug use and genotype 3 in HCV-infected patients from Central West and Northeast Mexico.

BACKGROUND: The evolving pattern of HCV genotypes (GTs) and risk factors (RFs) in HCV-infected patients in Mexico is poorly understood. This study aimed to access the temporal trend of HCV GTs and RFs in HCV patients from two care centers. MATERIAL AND METHODS: Chronic HCV patients [177 and 153 patients from the Northeast (NE) and Central West (CW) regions, respectively] were selected. Baseline features were demographics, date of birth (DOB), blood transfusion before 1992 (BTb1992), RFs, sexual promiscuity (SP), dental procedure (DP), injection drug use (IDU), viral load (VL), GTs, cirrhosis status and antiviral therapy (AT). Data were analyzed by Chi-square test for trends, unpaired T-test, and logistic regression. RESULTS: HCV GT distribution was: GT1, 67%; GT2, 16%; GT3, 12% and GT4, 1%. RFs were BTb1992, 56%; surgeries, 56%; tattooing, 18% and IDU, 16%. GT1a mostly prevailed in CW than NE patients. GT1b, surgeries, BTb1992 and cirrhosis were more prevalent in older patients (p < 0.05); GT3, male gender IDU, SP, and tattooing showed an upward trend as younger were the patients in both regions (p < 0.05), contrariwise to the prevalence of GT1b. BTb1992 and surgeries were seen in elder women; BTb1992 was an independent RF for GT1. Age ≥ 50 years old, GT1 and exposure to AT (p < 0.05) were associated with cirrhosis. CONCLUSION: GT1a prevalence in CW Mexico remained stable, whereas GT3 increased and GT1b decreased in younger patients in both regions, along with associated RFs. Further regional molecular epidemiology and RF analyses are required in order to avoid the dissemination of new cases of HCV infection.

Interferon-based therapy delays but metabolic comorbidity accelerates progression of chronic hepatitis C.

BACKGROUND: We compared mortality and complications of chronic hepatitis C between treated and untreated Mexican patients after long-term follow-up. We used a time-to-event analysis and identified the prognostic factors. MATERIAL AND METHODS: Seventy-four patients with chronic hepatitis C were studied. They were ≥ 18 years of age and had a molecular diagnosis of chronic hepatitis C and ≥ 6 months of follow-up. Patients with neoplasia or those infected with human immunodeficiency virus or hepatitis B Virus were excluded. Kaplan-Meier analysis, log-rank test, annualized incidence per 100 person-years, and stepwise discriminant analysis were used to analyse mortality and complications. RESULTS: The end-point of annualized incidence was lowest in sustained virological responders, intermediate in non-responders, and highest in untreated patients. The absence of treatment impacted adversely on cirrhosis development and the occurrence of portal hypertension and hepatic decompensation/hepatocellular carcinoma (logrank, p < 0.05). Diabetes impacted adversely on liver-related death/liver transplantation among untreated patients. Stepwise discriminant analysis showed that diabetes, high blood pressure, and no retreatment predicted cirrhosis development (eigenvalue ≥ 0.8; p < 0.05). A MELD score ≥ 18 and age ≥ 50 years predicted hepatic decompensation/hepatocellular carcinoma (eigenvalue < 0.8; p < 0.05). APRI ≥ 1.5 predicted mortality/liver transplantation and liver-related death/liver transplantation (eigenvalue < 0.8; p < 0.05). CONCLUSIONS: This is the first long-term study of chronic hepatitis C among Mexican patients. Treated patients showed less progression of liver disease. Treated patients showed less progression of liver disease; and older patients, those with metabolic comorbidities, with MELD score ≥ 18 and APRI ≥ 1.5 exhibited adverse effects.