Historia natural de la cirrosis hepática compensada diagnosticada por elastografía hepática transitoria en pacientes coinfectados por el virus de la inmunodeficiencia humana y el virus de la hepatitis C

Pacientes y métodos Estudio multicéntrico prospectivo de cohortes llevado a cabo en 7 hospitales andaluces. A partir de Febrero de 2006 todos los pacientes infectados por el VIH con infección crónica activa por el VHC que fueron diagnosticados de cirrosis hepática en base a la presencia de una RH ≥ 14 KPa y que no habían presentado previamente o de forma simultánea al diagnóstico de la cirrosis una descompensación de la misma fueron incluidos en este estudio. Los pacientes fueron seguidos prospectivamente hasta la muerte, el trasplante hepático o la fecha de censura del estudio (31 Enero 2015). Se analizaron las asociaciones entre distintas covariables, incluyendo la RH inicial, y el tiempo hasta la descompensación de la cirrosis o la muerte mediante el test de log-rank. Posteriormente, se construyeron modelos multivariantes de Cox para identificar los factores asociados de forma independiente con la descompensación o la muerte. Además, se comparó la capacidad predictiva de la RH con la de otros índices pronósticos clásicos como el estadio de Child-Turcotte-Pugh (CTP) o el índice MELD mediante el cálculo del área bajo la curva dependiente del operador (AUROC) y el índice de la mejoría de la discriminación (IDI) de los distintos modelos. Resultados Cuatrocientos cuarenta y seis pacientes fueron incluidos en nuestro estudio. Después de una mediana (rango intercuartílico) de seguimiento de 49 (25-68) meses, 80 (17.9%; intervalo de confianza [IC] al 95%: 14.2-21.6) pacientes presentaron una primera descompensación de la cirrosis. Los valores basales de RH se asociaron con la probabilidad de aparición de una descompensación de la cirrosis en el seguimiento. Así, la probabilidad de descompensación a 3 años fue del 5% en los pacientes con una RH inicial < 21 KPa, del 13% en los pacientes con una RH inicial de 21-39,9 KPa y del 28% en los pacientes con una RH ≥ 40 KPa (p< 0.0001). Tras el análisis multivariante, las variables que se asociaron de forma independiente con la aparición de una descompensación de la cirrosis en el seguimiento fueron la edad (hazard ratio [HR] 1.06, IC 95%: 1.02-1.10; p=0.001), la coinfección por el virus de la hepatitis B (HR 6.93, IC 95%: 2.17-18.76; p=0.001), la consecución de respuesta viral sostenida (RVS) durante el seguimiento (HR 0.34, IC 95%: 0.13-9.87; p=0.024), el diagnóstico de SIDA previo (HR 1.67, IC 95%: 1.05-2.66; p=0.028), el estadio CTP B (vs A) (HR 4.18; IC 95% 2.38-7.32; p<0.0001) y la RH al inicio de seguimiento (grupo de comparación: RH < 21 KPa) (RH 21-39,9 KPa: HR 2.48, IC 95%: 1.31-4.66, p=0.005; RH ≥ 40 KPa: HR 3.68, IC 95%: 1.88-7.19, p< 0.0001). Las comparaciones de la capacidad predictiva de la RH con la de los índices CTP y MELD mostraron una mayor capacidad predictiva de la RH que la del índice MELD (IDI 3.3%; p=0.01), siendo similar a la del índice CTP (IDI 0.13%; p=0.9). Sin embargo, la combinación de la RH con el estadio CTP en una nueva variable pronostica mejoró la predicción de eventos, siendo el AUROC del modelo que incluía esta nueva variable superior a la de un modelo basado sólo en el índice CTP (AUROC [IC 95%] 0.612 [0.544-0.681] vs AUROC 0.575 [0.501-0.648]; p=0.06). Sesenta y un (13.6%, IC 95%: 10.3-16.9) pacientes fallecieron durante el seguimiento. En 37 (8.3%, IC 95%: 5.7-10.9) pacientes la muerte ocurrió como consecuencia de la enfermedad hepática. Además, 3 pacientes fueron sometidos a trasplante hepático, por lo que 40 pacientes fallecieron de causa hepática y/o sufrieron un trasplante hepático. Las variables asociadas de forma independiente con este evento tras el análisis multivariante fueron una cifra de plaquetas al inicio del seguimiento inferior a 50.000/mm3 (HR 2.97, IC 95%: 1.33-6.62; p=0.008), una RH ≥ 21 KPa (HR 2.17, IC 95%: 0.98-4.78, p=0.054) y, como factor protector, la consecución de RVS durante el seguimiento (HR 0.14, IC 95%: 0.02-1.05; p=0.057). La RH no mostró una asociación independiente con la mortalidad de cualquier causa, siendo las variables asociadas con la misma en el análisis multivariante la edad (HR 1.04, IC 95%: 1.01-1.08; p=0.035), un recuento de plaquetas inferior a 50.000/mm3 (HR 2.15, IC 95% 1.05-4.38; p=0.034), el índice MELD (HR 5.24, IC 95%: 2.74-10.03; p< 0.0001) y, como factor protector, la consecución de RVS (HR 0.25, IC 95%: 0.07-0.81; p=0.020). Quince (3.4%, IC 95%: 1.7-5) pacientes presentaron un primer evento hemorrágico relacionado con la hipertensión portal durante el seguimiento. En todos los casos la RH al inicio del seguimiento era igual o mayor a 21 KPa, por lo que el valor predictivo negativo del punto de corte de 21 KPa para la predicción de eventos hemorrágicos durante el seguimiento fue del 100%. En el momento del episodio hemorrágico todos los pacientes mostraron un valor de RH igual o superior a 21 KPa. Conclusiones La RH es un predictor independiente de la aparición de descompensaciones de la cirrosis y de la muerte de causa hepática en los pacientes coinfectados por el VIH/VHC con cirrosis compensada y proporciona información pronostica adicional a la 13 que aportan los índices CTP y MELD. La combinación de la RH y el estadio CTP en un nuevo índice pronóstico mejora la capacidad predictiva del índice CTP por sí solo. Además, un valor de RH menor de 21 KPa identifica a un grupo de pacientes con un riesgo mínimo de aparición de eventos hemorrágicos a medio plazo, lo que permite evitar la realización de endoscopias de cribado de varices esofágicas en estos pacientes mientras la RH se mantenga por debajo de dicho dintel. Nuestras observaciones proporcionan nuevas evidencias que apoyan la inclusión de la determinación periódica de la RH dentro del manejo clínico rutinario de estos pacientes.Patients and Methods Multicenter prospective cohort study conducted in 7 hospitals from Andalusia. From February 2006, all consecutive HIV-infected patients with active chronic HCV infection diagnosed of cirrhosis on the basis of a LS ≥14 kPa were included in the study, provided that they did not have a previous or simultaneous liver decompensation (LD) at the date of the diagnosis of cirrhosis. Patients were prospectively followed-up until death, liver transplant or the censoring date (31 January 2015). The associations between variables, including baseline LS, and the time to LD or death was analysed by means of the log-rank test. Multivariate Cox regression models were built to identify independent predictors of LD and death. Besides, the ability of LS to predict outcomes was compared to that of other classical prognostic scores, as the Child-Turcotte-Pugh (CTP) or the MELD score, by means of the comparisons of the area under the receiver operating characteristic curve (AUROC) and the integrated discrimination improvement (IDI) between models. Results: Four hundred and forty-six patient were included in the study. After a median (Q1-Q3) follow-up of 49 (25-68) months, 80 (17.9%; 95% confidence interval [CI]: 14.2-21.6) patients developed a first LD. Baseline LS values were associated with the probability of the emergence of a LD during follow-up. Thus, the probability of LD at 3 years was 5% in patients with baseline LS < 21 kPa, 13% in those harbouring a LS between 21 and 39,9 kPa and 28% in patients with baseline LS ≥ 40 kPa (p< 0.0001). After multivariate analyses, the variables that showed an independent association with the emergence of LD were age (hazard ratio [HR] 1.06, 95% CI: 1.02-1.10; p=0.001), hepatitis B virus coinfection (HR 6.93, 95% CI: 2.17-18.76; p=0.001), the consecution of sustained virological response (SVR) during follow-up (HR 0.34, 95% CI: 0.13-9.87; p=0.024), clinical AIDS (HR 1.67, 95% CI: 1.05-2.66; p=0.028), CTP stage B (vs A) (HR 4.18; 95% CI: 2.38-7.32; p<0.0001) and baseline LS (comparison group: LS < 21 kPa) (LS 21-39,9 kPa: HR 2.48, 95% CI: 1.31-4.66, p=0.005; LS ≥ 40 kPa: HR 3.68, 95% CI: 1.88-7.19, p< 0.0001). Comparisons of the ability of LS to predict a LD with that of CTP or MELD scores yielded a better performance of LS than MELD (IDI 3.3%; p=0.01) and a similar performance of LS and CTP (IDI 0.13%; p=0.9). By contrast, the combination of LS and CTP stage in a new predictive variable improved the ability to predict outcomes, being the AUROC of the model including this new variable higher than that of the model only based on the CTP stage (AUROC [95% CI] 0.612 [0.544-0.681] vs AUROC 0.575 [0.501-0.648]; p=0.06). Sixty-one (13.6%, 95% CI: 10.3-16.9) patients died during follow-up. In 37 (8.3%, 95% CI: 5.7-10.9) patients, death was liver-related. Besides, 3 patients underwent a liver transplant. Thus, 40 patients developed a liver-related death or a liver transplant. The variables independently associated with this outcome were a platelet count < 50.000/mm3 (HR 2.97, 95% CI: 1.33-6.62; p=0.008), a baseline LS ≥ 21 kPa (HR 2.17, 95% CI: 0.98-4.78, p=0.054) and the consecution of SVR during follow-up (HR 0.14, 95% CI: 0.02-1.05; p=0.057). LS was not independently associated with overall mortality. Independent predictors of overall death were age (HR 1.04, 95% CI: 1.01-1.08; p=0.035), a platelet count < 50.000/mm3 (HR 2.15, 95% CI: 1.05-4.38; p=0.034), MELD score (HR 5.24, 95% CI: 2.74-10.03; p< 0.0001) and the consecution of SVR (HR 0.25, 95% CI: 0.07-0.81; p=0.020). Fifteen (3.4%, 95% CI: 1.7-5) patients developed a first bleeding episode related to portal hypertension during follow-up. In all cases, baseline LS was ≥ 21 kPa. Thus, the NPV of a LS < 21 kPa to predict a bleeding episode during follow-up was 100%. At the moment of the bleeding episode, LS was also above this threshold. Conclusions: LS is an independent predictor of LD and liver-mortality in HIV/HCV-coinfected patients with compensated cirrhosis and provides additional prognostic information to that provided by CTP or MELD scores. The combination of LS and CTP stage in a new predictive index improves the ability of CTP to predict outcome. Besides, a LS < 21 kPa identifies HIV/HCV-coinfected patients with compensated cirrhosis with a very low risk of presenting a variceal bleeding episode, allowing to spare upper endoscopy aimed to screen for esophagueal varices in these patients, provided that LS maintains below this level. Our observations provide new evidence that support the inclusion of periodic LS determinations in the routine clinical care of these patients

Prediction of liver stiffness by serum indexes in HCV-infected patients with or without HIV coinfection

Identification of advanced fibrosis/cirrhosis in hepatitis C virus (HCV)-infected patients should be a mainstay before starting treatment; however, the limited access of many centres to transient elastography (TE) is often a barrier for early assessments. We aimed to investigate the diagnostic accuracy of serum indexes for predicting liver stiffness.Retrospective analysis of HCV patients (with or without HIV coinfection) routinely assessed in 7 centres in Spain. The diagnostic accuracy of aspartate aminotransferase-to-platelet ratio index (APRI), fibrosis-4 (FIB-4), and their combinations was evaluated using a recent TE examination as a reference test (liver stiffness¿=¿9.5¿kPa and¿=12.5¿kPa for advanced fibrosis and cirrhosis, respectively). In addition to area under the receiving operating characteristic curves, sensitivity, specificity, and negative predictive value (NPV) and positive predictive value were estimated.The analysis included 1391 patients: 346 (25%) HIV-positive, 732 (53%) people who inject drugs, and 178 (13%) incarcerated. Advanced fibrosis and cirrhosis were found in 557 (40%) and 351 (25%) patients, respectively. APRI¿ 2 and FIB-4 > 3.25 (n¿=¿134; 10%) had a positive predictive value of 89% for advanced fibrosis. Globally, this approach would avoid the need for TE in 53% of patients. HIV coinfection did not influence diagnostic accuracy.Inexpensive and simple serum indexes confidently allowed identifying the absence of cirrhosis and the presence of advanced fibrosis in 53% of a heterogeneous series of real-world HCV patients with or without HIV infection

Impact of COVID19 pandemic on the incidence of health-care associated Clostridioides difficile infection

Objective: To investigate the impact of COVID19 pandemic on the incidence of health-care associated Clostridioides difficile infection (HA-CDI). Methods: Retrospective study conducted in the Hospital Universitario de Valme (HUV) and the Hospital General Universitario de Alicante (HGUA) in Spain between January 2019 and February 2021. The study period was divided into non-COVID19 period (2019 and months from 2020 to 2021 with 30 hospi talized COVID19 patients) and COVID19 period (months from 2020 to 2021 with >30 COVID19 patients). HA-CDI incidence rates (IR) were calculated as the number of new CDI cases per 10.000 occupied bed days (OBD) and antimicrobial consumption by means of the defined daily dose (DDD) per 1000 OBD. Results: During the COVID19 period, HA-CDI IR in the HUV was 2.6 per 10.000 OBD, which was lower than what was observed during the non-COVID19 period (4.1 per 10.000 OBD; p ¼ 0.1). In the HGUA, HA CDI IR during COVID19 period was 3.9 per 10.000 OBD, which was not significantly different to the IR observed during the non-COVID19 period (3.7 per 10.000 OBD; p ¼ 0.8). There was a slight increase in the total antibiotic consumption during COVID19 period in both hospitals, with significant increases of certain high-risk antibiotics as cephalosporins. Conclsusions: HA-CDI incidence has not increased during the COVID19 pandemic in two tertiary centers in Spain, in spite of a slightly higher antibiotic consumption during the COVID19 period in both hospitals. These findings suggest that, in the presence of strict infection control measures, hospital antibiotic consumption might have a lower impact than expected on HA-CDI

Hepatocellular carcinoma recurrence after direct-acting antiviral therapy: An individual patient data meta-analysis

Abstract Objective The benefit of direct-acting antivirals (DAAs) against HCV following successful treatment of hepatocellular carcinoma (HCC) remains controversial. This meta-analysis of individual patient data assessed HCC recurrence risk following DAA administration. Design We pooled the data of 977 consecutive patients from 21 studies of HCV-related cirrhosis and HCC, who achieved complete radiological response after surgical/locoregional treatments and received DAAs (DAA group). Recurrence or death risk was expressed as HCC recurrence or death per 100 person-years (100PY). Propensity score-matched patients from the ITA.LI.CA. cohort (n=328) served as DAA-unexposed controls (no-DAA group). Risk factors for HCC recurrence were identified using random-effects Poisson. Results Recurrence rate and death risk per 100PY in DAA-treated patients were 20 (95% CI 13.9 to 29.8, I2=74.6%) and 5.7 (2.5 to 15.3, I2=54.3), respectively. Predictive factors for recurrence were alpha-fetoprotein logarithm (relative risk (RR)=1.11, 95% CI 1.03 to 1.19; p=0.01, per 1 log of ng/mL), HCC recurrence history pre-DAA initiation (RR=1.11, 95% CI 1.07 to 1.16; p<0.001), performance status (2 vs 0, RR=4.35, 95% CI 1.54 to 11.11; 2 vs 1, RR=3.7, 95% CI 1.3 to 11.11; p=0.01) and tumour burden pre-HCC treatment (multifocal vs solitary nodule, RR=1.75, 95% CI 1.25 to 2.43; p<0.001). No significant difference was observed in RR between the DAA-exposed and DAA-unexposed groups in propensity score-matched patients (RR=0.64, 95% CI 0.37 to 1.1; p=0.1). Conclusion Effects of DAA exposure on HCC recurrence risk remain inconclusive. Active clinical and radiological follow-up of patients with HCC after HCV eradication with DAA is justified

Reassessment of genotype 1 hepatitis c virus subtype misclassification by LiPA 2.0: implications for direct-acting antiviral treatment

The accuracy of LiPA 2.0 for hepatitis C virus 1 (HCV-1) subtype classification was analyzed. LiPA 2.0 genotype results from 101 HCV-1-infected patients were compared to genotype findings determined by direct core sequencing. Eleven (11%) samples were misclassified. Given the influence of the HCV-1-subtype in the anti-HCV therapy response, an alternative classification method is warranted.Fil: Guelfo, Javier R.. Hospital Universitario de Valme. Unidad de Enfermedades Infecciosas y Microbiología; EspañaFil: Macias, Juan. Hospital Universitario de Valme. Unidad de Enfermedades Infecciosas y Microbiología; EspañaFil: Neukam, Karin. Hospital Universitario de Valme. Unidad de Enfermedades Infecciosas y Microbiología; EspañaFil: Di Lello, Federico Alejandro. Hospital Universitario de Valme. Unidad de Enfermedades Infecciosas y Microbiología; España. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Mira José Antonio. Hospital Universitario de Valme. Unidad de Enfermedades Infecciosas y Microbiología; EspañaFil: Merchante, Nicolás. Hospital Universitario de Valme. Unidad de Enfermedades Infecciosas y Microbiología; EspañaFil: Mancebo, María. Hospital Universitario de Valme. Unidad de Enfermedades Infecciosas y Microbiología; EspañaFil: Nuñez Torres, Rocío. Hospital Universitario de Valme. Unidad de Enfermedades Infecciosas y Microbiología; EspañaFil: Pineda, Juan A.. Hospital Universitario de Valme. Unidad de Enfermedades Infecciosas y Microbiología; EspañaFil: Real. Luis M.. Hospital Universitario de Valme. Unidad de Enfermedades Infecciosas y Microbiología; Españ

Treatment with tocilizumab or corticosteroids for COVID-19 patients with hyperinflammatory state: a multicentre cohort study (SAM-COVID-19)

Objectives: The objective of this study was to estimate the association between tocilizumab or corticosteroids and the risk of intubation or death in patients with coronavirus disease 19 (COVID-19) with a hyperinflammatory state according to clinical and laboratory parameters. Methods: A cohort study was performed in 60 Spanish hospitals including 778 patients with COVID-19 and clinical and laboratory data indicative of a hyperinflammatory state. Treatment was mainly with tocilizumab, an intermediate-high dose of corticosteroids (IHDC), a pulse dose of corticosteroids (PDC), combination therapy, or no treatment. Primary outcome was intubation or death; follow-up was 21 days. Propensity score-adjusted estimations using Cox regression (logistic regression if needed) were calculated. Propensity scores were used as confounders, matching variables and for the inverse probability of treatment weights (IPTWs). Results: In all, 88, 117, 78 and 151 patients treated with tocilizumab, IHDC, PDC, and combination therapy, respectively, were compared with 344 untreated patients. The primary endpoint occurred in 10 (11.4%), 27 (23.1%), 12 (15.4%), 40 (25.6%) and 69 (21.1%), respectively. The IPTW-based hazard ratios (odds ratio for combination therapy) for the primary endpoint were 0.32 (95%CI 0.22-0.47; p < 0.001) for tocilizumab, 0.82 (0.71-1.30; p 0.82) for IHDC, 0.61 (0.43-0.86; p 0.006) for PDC, and 1.17 (0.86-1.58; p 0.30) for combination therapy. Other applications of the propensity score provided similar results, but were not significant for PDC. Tocilizumab was also associated with lower hazard of death alone in IPTW analysis (0.07; 0.02-0.17; p < 0.001). Conclusions: Tocilizumab might be useful in COVID-19 patients with a hyperinflammatory state and should be prioritized for randomized trials in this situatio

Genetic markers of lipid metabolism genes associated with low susceptibility to HCV infection

GEHEP 012 study group.Due to the relation between lipids and Hepatitis C virus (HCV) life-cycle, we aimed to explore the existence of single nucleotide polymorphisms (SNPs) associated with low susceptibility to HCV-infection within lipid metabolism genes. This was a case-control study in three phases: (I) allelic frequencies of 9 SNPs within 6 genes were compared in 404 HCV-infected patients and 801 population controls; (II) results were validated in 602 HCV-infected individuals and 1352 controls; (III) results were confirmed in 30 HCV-exposed uninfected (EU) individuals. In phase I, only the LDLRAP1-rs4075184-A allele was differentially distributed in patients and controls (358 of 808 alleles [44.3%] and 807 of 1602 alleles [50.3%], respectively) (p = 0.004). In phase II, the A allele frequency was 547 of 1204 alleles (45.4%) in patients and 1326 of 2704 alleles (49.0%) in controls (p = 0.037). This frequency in EU was 36 of 60 alleles (60%), which was higher than that observed in patients from phase I (p = 0.018) and phase II (p = 0.027). The LDLRAP1-mRNA expression was lower in AA carriers than in non-AA carriers (median [Q1-Q3]: 0.85 [0.17–1.75] relative-units [ru] versus 1.71 [1.00–2.73] ru; p = 0.041). Our results suggest that LDLRAP1-rs4075184-A allele is associated with lower susceptibility to HCV-infection and with reduced expression of LDLRAP1-mRNA.This work was supported by grants from the Consejería de Salud de la Junta de Andalucía (PI-0001/2017), the Grupo de Estudio de Hepatitis Víricas from the Sociedad Española de Enfermedades Infecciosas y Microbiología Clínica (GEHEP-SEIMC) (GEHEP-012), the Plan Nacional de I + D + I cofinanced by ISCIII-Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER) (www.red.es/redes/inicio) (RD16/0025/0040, RD12/0017/0012), the Acción Estratégica en Salud, integrated in the Spanish National R + D + I Plan and financed by ISCIII-Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER- “Una manera de Hacer Europa”) (PI13/02434 and PI16/01861), the Ministerio de Economía Industria y Competitividad (SAF2016–8015-R), Fundación Bancaria “La Caixa” and Grifols SA (GR@ACE project). LMR and JM are the recipients of grants from the Servicio Andaluz de Salud de la Junta de Andalucía (C-0009-2015 and B-0037, respectively). JAP has received a research extension grant from the Programa de Intensificación de la Actividad de Investigación del Servicio Nacional de Salud Carlos III (I3SNS).Peer reviewe

Early Use of Sarilumab in Patients Hospitalized with COVID-19 Pneumonia and Features of Systemic Inflammation: the SARICOR Randomized Clinical Trial

The objective of this study was to investigate the efficacy and safety of early treatment with sarilumab, added to standard of care (SOC), in hospitalized adults with COVID-19. Methods included phase II, open-label, randomized, controlled clinical trial of hospitalized patients with COVID-19 pneumonia and interleukin (IL)-6 levels ≥ 40 pg/mL and/or d-dimer > 1,500 ng/mL. Participants were randomized (1:1:1) to receive SOC (control group), SOC plus a single subcutaneous dose of sarilumab 200 mg (sarilumab-200 group), or SOC plus a single subcutaneous dose of sarilumab 400 mg (sarilumab-400 group). The primary outcome variable was the development of acute respiratory distress syndrome (ARDS) requiring high-flow nasal oxygenation (HFNO), non-invasive mechanical ventilation (NIMV) or invasive mechanical ventilation (IMV) at day 28. One-hundred and 15 participants (control group, n = 39; sarilumab-200, n = 37; sarilumab-400, n = 39) were included. At randomization, 104 (90%) patients had supplemental oxygen and 103 (90%) received corticosteroids. Eleven (28%) patients in the control group, 10 (27%) in sarilumab-200, and five (13%) in sarilumab-400 developed the primary outcome (hazard ratio [95% CI] of sarilumab-400 vs control group: 0.41 [0.14, 1.18]; P = 0.09). Seven (6%) patients died: three in the control group and four in sarilumab-200. There were no deaths in sarilumab-400 (P = 0.079, log-rank test for comparisons with the control group). In patients recently hospitalized with COVID-19 pneumonia and features of systemic inflammation, early IL-6 blockade with a single dose of sarilumab 400 mg was safe and associated with a trend for better outcomes. (This study has been registered at ClinicalTrials.gov under identifier NCT04357860.

Similar recovery of liver function after response to all‐oral HCV therapy in patients with cirrhosis with and without HIV coinfection

Among patients with cirrhosis, recovery of liver function after SVR to all‐oral direct‐acting antivirals (DAA ) in HIV /HCV coinfection could be different to that in HCV monoinfection. Because of this, we compared the changes in several markers of liver function between HCV ‐monoinfected and HIV /HCV ‐coinfected patients with cirrhosis who achieved SVR 12 to DAA combinations. In this retrospective cohort study, cirrhotics included in the HEPAVIR ‐DAA and GEHEP ‐MONO cohorts were selected if they had SVR 12 to all‐oral DAA s. Patients treated with atazanavir were excluded. Liver function improvement was defined as Child‐Pugh‐Turcotte (CPT ) decrease ≥1 and/or MELD decrease ≥2 between baseline and SVR 12. Liver function worsening was defined as a CPT increase ≥1 and/or MELD increase ≥2 and/or decompensations between baseline and SVR 12. We included 490 patients, 270 (55%) of them with HIV coinfection. Liver function improved in 50 (56%) HCV ‐infected individuals and in 82 (57%) HIV /HCV ‐coinfected patients (P = 0.835). Liver function worsened in 33 (15%) HCV ‐monoinfected patients and in 33 (13%) HIV /HCV ‐coinfected patients (P = 0.370). Factors independently related with liver function improvement were male gender [adjusted OR (AOR ) 2.1 (95% confidence interval, 95% CI : 1.03‐4.2), P = 0.040], bilirubin < 1.2 mg/dL (AOR 1.8 [95% CI : 1.004‐3.3], P = 0.49), and INR < 1.3 (AOR 2.4 [95% CI : 1.2‐5.0], P = 0.019) at baseline. After multivariate analysis, albumin < 3.5 g/dL was associated with liver function worsening (AOR 6.1 [95% CI : 3‐12.5], P < 0.001). Liver function worsening and improvement rates after responding to DAA are similar among HCV ‐monoinfected and HIV /HCV ‐coinfected cirrhotics. Gender, INR , bilirubin, and albumin levels were associated with liver function changes after response to DAA s.This study was partly supported by projects “PI15/01607” and “PI16/01443,” funded by Instituto de Salud Carlos III, integrated in the national I+D+i 2013‐2016, and cofunded by European Union (ERDF/ESF, “Investing in your future”) and by a grant from the Grupo para el Estudio de las Hepatitis Víricas (GEHEP) (grant GEHEP 001 2017). J.M. is the recipient of a grant from the Servicio Andaluz de Salud de la Junta de Andalucía (grant number B‐0037). J.A.P. is recipient of an intensification grant from the Instituto de Salud Carlos III (grant number Programa‐I3SNS). This work has been partially funded by the Spanish AIDS Research Network RD16/0025/0010 and RD16/0025/0034—ISCIII—FEDER.Peer reviewe