Bariatric Surgery Is Associated with Alcohol-Related Liver Disease and Psychiatric Disorders Associated with AUD

Bariatric surgery can increase the risk of addictive disorders and nutritional deficiencies. The aim of this study was to evaluate the association between bariatric surgery and alcohol use disorder (AUD), alcohol-related liver disease (ALD), and psychiatric disorders associated with AUD. The impact of vitamin D deficiency in these associations was also investigated. A cross-sectional study was performed using the National Inpatient Sample database and its ICD-9 codes information. Diagnostic and comorbidity data from hospital discharges were obtained from patients with bariatric surgery and other abdominal surgeries between 2005 and 2015. The two groups were then compared for alcohol-related outcomes after propensity-score matching. The final study cohort included 537,757 patients with bariatric surgery and 537,757 with other abdominal surgeries. The bariatric surgery group had an increased risk of AUD [odds ratio (OR): 1.90; 95% CI: 1.85-1.95], ALD [OR: 1.29; 95% CI: 1.22-1.37], cirrhosis [OR, 1.39; 95% CI: 1.37-1.42], and psychiatric disorders associated with AUD [OR, 3.59; 95% CI: 3.37-3.84]. Vitamin D deficiency did not impact in the association between bariatric surgery and AUD, ALD, or psychiatric disorders associated with AUD. Bariatric surgery is associated with an increased prevalence of AUD, ALD, and psychiatric disorders associated with AUD. These associations appear to be independent from vitamin D deficiency. The online version contains supplementary material available at 10.1007/s11695-023-06490-w

Toll-like receptor 4 polymorphisms and bacterial infections in patients with cirrhosis and ascites

Altres ajuts: Cofinanced by Fondos FEDER (Fondo Europeo de Desarrollo Regional), "Una manera de hacer Europa", European Union, and CERCA Programme, Generalitat de Catalunya; Silvia Vidal was supported by Fondode Investigaciones Sanitarias (FIS) and is a participant in the Program for Stabilization of Investigators of the Direcció d'Estrategia i Coordinació del Departament de Salut, Generalitat de Catalunya.To assess the relationship between the presence of toll-like receptor 4 (TLR4) polymorphisms and bacterial infections in cirrhotic patients with ascites. We prospectively included consecutive patients with cirrhosis and ascites hospitalized during a 6-year period. Patients with human immunodeficiency virus (HIV) infection or any other immunodeficiency, patients with advanced hepatocellular carcinoma (beyond Milan's criteria) or any other condition determining poor short-term prognosis, and patients with a permanent urinary catheter were excluded. The presence of D299G and/or T399I TLR4 polymorphisms was determined by sequencing and related to the incidence and probability of bacterial infections, other complications of cirrhosis, hepatocellular carcinoma, and mortality during follow-up. A multivariate analysis to identify predictive variables of mortality in the whole series was performed. We included 258 patients: 28 (10.8%) were carriers of D299G and/or T399I TLR4 polymorphisms (polymorphism group) and 230 patients were not (wild-type group). The probability of developing any bacterial infection at one-year follow-up was 78% in the polymorphism group and 69% in the wild-type group (P = 0.54). The one-year probability of presenting infections caused by gram-negative bacilli (51% vs 44%, P = 0.68), infections caused by gram-positive cocci (49% vs 40%, P = 0.53), and spontaneous bacterial peritonitis (29% vs 34%, respectively, P = 0.99) did not differ between the two groups. The one-year probability of transplant-free survival was 55% in the polymorphism group and 66% in the wild-type group (P = 0.15). Multivariate analysis confirmed that age, Child-Pugh score, active alcohol intake, previous hepatic encephalopathy, hepatocellular carcinoma and serum creatinine were associated with a higher risk of death during follow-up. Genetic polymorphisms D299G and/or T399I of TLR4 do not seem to play a relevant role in the predisposition of cirrhotic patients with ascites to bacterial infections

Phase angle by electrical bioimpedance is a predictive factor of hospitalisation, falls and mortality in patients with cirrhosis

The phase angle is a versatile measurement to assess body composition, frailty and prognosis in patients with chronic diseases. In cirrhosis, patients often present alterations in body composition that are related to adverse outcomes. The phase angle could be useful to evaluate prognosis in these patients, but data are scarce. The aim was to analyse the prognostic value of the phase angle to predict clinically relevant events such as hospitalisation, falls, and mortality in patients with cirrhosis. Outpatients with cirrhosis were consecutively included and the phase angle was determined by electrical bioimpedance. Patients were prospectively followed to determine the incidence of hospitalisations, falls, and mortality. One hundred patients were included. Patients with phase angle ≤ 4.6° (n = 31) showed a higher probability of hospitalisation (35% vs 11%, p = 0.003), falls (41% vs 11%, p = 0.001) and mortality (26% vs 3%, p = 0.001) at 2-year follow-up than patients with PA > 4.6° (n = 69). In the multivariable analysis, the phase angle and MELD-Na were independent predictive factors of hospitalisation and mortality. Phase angle was the only predictive factor for falls. In conclusion, the phase angle showed to be a predictive marker for hospitalisation, falls, and mortality in outpatients with cirrhosis

Impact of ornithine phenylacetate (OCR-002) in lowering plasma ammonia after upper gastrointestinal bleeding in cirrhotic patients

Ornithine phenylacetate (OP) has been proven effective in lowering ammonia plasma levels in animals, and to be well tolerated in cirrhotic patients. A trial to assess OP efficacy in lowering plasma ammonia levels versus placebo in cirrhotic patients after an upper gastrointestinal bleeding was performed. The primary outcome was a decrease in venous plasma ammonia at 24 hours. A total of 38 consecutive cirrhotic patients were enrolled within 24 hours of an upper gastrointestinal bleed. Patients were randomized (1:1) to receive OP (10 g/day) or glucosaline for 5 days. The primary outcome was not achieved. A progressive decrease in ammonia was observed in both groups, being slightly greater in the OP group, with significant differences only at 120 hours. The subanalysis according to Child-Pugh score showed a statistically significant ammonia decrease in Child-Pugh C-treated patients at 36 hours, as well as in the time-normalized area under the curve (TN-AUC) 0-120 hours in the OP group [40.16 μmol/l (37.7-42.6); median (interquartile range) (IQR)] versus placebo group [65.5 μmol/l (54-126); p = 0.036]. A decrease in plasma glutamine levels was observed in the treated group compared with the placebo group, and was associated with the appearance of phenylacetylglutamine in urine. Adverse-event frequency was similar in both groups. No differences in hepatic encephalopathy incidence were observed. OP failed to significantly decrease plasma ammonia at the given doses (10 g/day). Higher doses of OP might be required in Child-Pugh A and B patients. OP appeared well tolerated

Phase angle by electrical bioimpedance is a predictive factor of hospitalisation, falls and mortality in patients with cirrhosis

The phase angle is a versatile measurement to assess body composition, frailty and prognosis in patients with chronic diseases. In cirrhosis, patients often present alterations in body composition that are related to adverse outcomes. The phase angle could be useful to evaluate prognosis in these patients, but data are scarce. The aim was to analyse the prognostic value of the phase angle to predict clinically relevant events such as hospitalisation, falls, and mortality in patients with cirrhosis. Outpatients with cirrhosis were consecutively included and the phase angle was determined by electrical bioimpedance. Patients were prospectively followed to determine the incidence of hospitalisations, falls, and mortality. One hundred patients were included. Patients with phase angle¿=¿4.6° (n¿=¿31) showed a higher probability of hospitalisation (35% vs 11%, p¿=¿0.003), falls (41% vs 11%, p¿=¿0.001) and mortality (26% vs 3%, p¿=¿0.001) at 2-year follow-up than patients with PA¿>¿4.6° (n¿=¿69). In the multivariable analysis, the phase angle and MELD-Na were independent predictive factors of hospitalisation and mortality. Phase angle was the only predictive factor for falls. In conclusion, the phase angle showed to be a predictive marker for hospitalisation, falls, and mortality in outpatients with cirrhosis.Postprint (published version

PREDICT identifies precipitating events associated with the clinical course of acutely decompensated cirrhosis

Background & Aims: Acute decompensation (AD) of cirrhosis may present without acute-on-chronic liver failure (ACLF) (ADNo ACLF), or with ACLF (AD-ACLF), defined by organ failure(s). Herein, we aimed to analyze and characterize the precipitants leading to both of these AD phenotypes. Methods: The multicenter, prospective, observational PREDICT study (NCT03056612) included 1,273 non-electively hospitalized patients with AD (No ACLF = 1,071; ACLF = 202). Medical history, clinical data and laboratory data were collected at enrolment and during 90-day follow-up, with particular attention given to the following characteristics of precipitants: induction of organ dysfunction or failure, systemic inflammation, chronology, intensity, and relationship to outcome. Results: Among various clinical events, 4 distinct events were precipitants consistently related to AD: proven bacterial infections, severe alcoholic hepatitis, gastrointestinal bleeding with shock and toxic encephalopathy. Among patients with precipitants in the AD-No ACLF cohort and the AD-ACLF cohort (38% and 71%, respectively), almost all (96% and 97%, respectively) showed proven bacterial infection and severe alcoholic hepatitis, either alone or in combination with other events. Survival was similar in patients with proven bacterial infections or severe alcoholic hepatitis in both AD phenotypes. The number of precipitants was associated with significantly increased 90day mortality and was paralleled by increasing levels of surrogates for systemic inflammation. Importantly, adequate first-line antibiotic treatment of proven bacterial infections was associated with a lower ACLF development rate and lower 90-day mortality. Conclusions: This study identified precipitants that are significantly associated with a distinct clinical course and prognosis in patients with AD. Specific preventive and therapeutic strategies targeting these events may improve outcomes in patients with decompensated cirrhosis. Lay summary: Acute decompensation (AD) of cirrhosis is characterized by a rapid deterioration in patient health. Herein, we aimed to analyze the precipitating events that cause AD in patients with cirrhosis. Proven bacterial infections and severe alcoholic hepatitis, either alone or in combination, accounted for almost all (96-97%) cases of AD and acute-on-chronic liver failure. Whilst the type of precipitant was not associated with mortality, the number of precipitant(s) was. This study identified precipitants that are significantly associated with a distinct clinical course and prognosis of patients with AD. Specific preventive and therapeutic strategies targeting these events may improve patient outcomes. (c) 2020 European Association for the Study of the Liver. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)

The PREDICT study uncovers three clinical courses of acutely decompensated cirrhosis that have distinct pathophysiology

Acute decompensation (AD) of cirrhosis is defined as the acute development of ascites, gastrointestinal hemorrhage, hepatic encephalopathy, infection or any combination thereof, requiring hospitalization. The presence of organ failure(s) in patients with AD defines acute-on-chronic liver failure (ACLF). The PREDICT study is a European, prospective, observational study, designed to characterize the clinical course of AD and to identify predictors of ACLF. A total of 1,071 patients with AD were enrolled. We collected detailed pre-specified information on the 3-month period prior to enrollment, and clinical and laboratory data at enrollment. Patients were then closely followed up for 3 months. Outcomes (liver transplantation and death) at 1 year were also recorded. Three groups of patients were identified. Pre-ACLF patients (n = 218) developed ACLF and had 3-month and 1-year mortality rates of 53.7% and 67.4%, respectively. Unstable decompensated cirrhosis (UDC) patients (n = 233) required ≥1 readmission but did not develop ACLF and had mortality rates of 21.0% and 35.6%, respectively. Stable decompensated cirrhosis (SDC) patients (n = 620) were not readmitted, did not develop ACLF and had a 1-year mortality rate of only 9.5%. The 3 groups differed significantly regarding the grade and course of systemic inflammation (high-grade at enrollment with aggravation during follow-up in pre-ACLF; low-grade at enrollment with subsequent steady-course in UDC; and low-grade at enrollment with subsequent improvement in SDC) and the prevalence of surrogates of severe portal hypertension throughout the study (high in UDC vs. low in pre-ACLF and SDC). Acute decompensation without ACLF is a heterogeneous condition with 3 different clinical courses and 2 major pathophysiological mechanisms: systemic inflammation and portal hypertension. Predicting the development of ACLF remains a major future challenge. ClinicalTrials.gov number: NCT03056612. Lay summary: Herein, we describe, for the first time, 3 different clinical courses of acute decompensation (AD) of cirrhosis after hospital admission. The first clinical course includes patients who develop acute-on-chronic liver failure (ACLF) and have a high short-term risk of death - termed pre-ACLF. The second clinical course (unstable decompensated cirrhosis) includes patients requiring frequent hospitalizations unrelated to ACLF and is associated with a lower mortality risk than pre-ACLF. Finally, the third clinical course (stable decompensated cirrhosis), includes two-thirds of all patients admitted to hospital with AD - patients in this group rarely require hospital admission and have a much lower 1-year mortality risk

Estadio compensado y descompensado de la cirrosis: implicaciones pronósticas y factores relacionados con la progresión de la enfermedad

En la historia natural de la cirrosis, se reconocen dos estadios bien diferenciados con pronósticos diferentes. En los pacientes con cirrosis compensada, el objetivo es retrasar la progresión de la enfermedad y evitar la descompensación. En el paciente con cirrosis descompensada el objetivo es prevenir la muerte. La circulación hiperdinámica juega un papel fundamental en el perfil hemodinámico sistémico y hepático, sobre todo en la respuesta a BBNS. El objetivo principal de esta tesis, es describir y comparar los perfiles hemodinámicos de los pacientes con cirrosis compensada con respecto a los pacientes con cirrosis descompensada, para identificar factores predictivos de descompensación (en los compensados), su capacidad predictiva en el tiempo; y evaluar si en los pacientes con cirrosis descompensada la respuesta hemodinámica a BBNS hepática y sistémica afecta la supervivencia. METODOS: Estudio observacional, retrospectivo con seguimiento prospectivo en el que se incluyeron pacientes derivados a la unidad de hemodinámica para el inicio de profilaxis primaria de hemorragia varicosa con BBNS. Se realizaron 2 estudios hemodinámicos, uno basal con respuesta aguda a BBNS (propranolol EV) y una segunda medición de 1-3 meses bajo tratamiento con BBNS. RESULTADOS: 403 pacientes fueron incluídos, de los cuales 213 eran compensados y 190 descompensados (todos con ascitis). Los pacientes descompensados tenían basalmente peor función hepática con respecto a los compensados (MELD 12.83±3.72 vs 9.39±2.10, P≤ 0.001), mayor presión portal (HVPG= 19.4 ± 5 mmHg vs 17.4 ± 4 mmHg, P≤ 0.001) y peor respuesta a BBNS (Descenso del GPVH = 14 ± 13% vs 10 ± 15%, P5 L/min ( 19% vs 5% , P< 0.001 by log-rank). CONCLUSION: En los pacientes compensados, la ausencia de respuesta hemodinámica y el Child-Pugh son factores predictivos independientes de descompensación. Factores predictivos como el MELD; albúmina y respuesta aguda a BBNS pierden capacidad predictiva a partir del 2º año. Los BBNS tienen más efecto sistémico en los pacientes descompensados con mayor descenso de GC/PAM y menor efecto sobre el GPVH. Sugiriéndose que los efectos beneficiosos de los BBNS en pacientes descompensados va más allá de la presión portal. Una titulación más dirigida a través de métodos cardiovasculares que permitan estimar el GC podría optimizar su empleo en estos pacientes.In the natural history of cirrhosis, two well differentiated stages with different prognoses are recognized. In patients with compensated cirrhosis, the goal is to delay the progression of the disease and prevent decompensation. In the patient with decompensated cirrhosis the goal is to prevent death. Hyperdynamic circulation plays a fundamental role in the systemic and hepatic hemodynamic profile, especially in the response to NSBB. The main objective of this thesis is to describe and compare the hemodynamic profiles of patients with compensated cirrhosis with respect to patients with decompensated cirrhosis, to identify predictors of decompensation (in those compensated), their predictive capacity over time; and to evaluate if in patients with decompensated cirrhosis the hemodynamic response to hepatic and systemic BBNS affects survival. METHODS: Observational, retrospective study with prospective follow-up in which patients referred to the hemodynamic unit were included for the start of primary prophylaxis of varicose hemorrhage with NSBB. Two hemodynamic studies were performed, one baseline with acute response to propranolol EV and a 2º measurement 1-3 months under treatment with NSBB. RESULTS: 403 patients were included, of which 213 were compensated and 190 decompensated (all with ascites). Decompensated patients had baseline worse liver function with respect to those compensated (MELD 12.83 ± 3.72 vs 9.39 ± 2.10, P≤ 0.001), higher portal pressure (HVPG = 19.4 ± 5 ​​mmHg vs 17.4 ± 4 mmHg, P≤ 0.001) and worse hemodynamic response to NSBB (GPVH decrease = 14 ± 13% vs 10 ± 15%, P 5 L / min (19% vs. 5%, P <0.001 by log-rank) CONCLUSION: In compensated patients, the absence of response hemodynamics and the Child-Pu gh are independent predictors of decompensation. Predictive factors such as MELD; albumin and acute response to NSBB lose predictive capacity as of the 2nd year. The NSBB have more systemic effect in decompensated patients with greater decrease in CO / MAP and less effect on HVPG. Suggesting that the beneficial effects of NSBB in decompensated patients goes beyond portal pressure. A more directed titration through cardiovascular methods that allow estimating the CG could optimize its use in these patients

Estadio compensado y descompensado de la cirrosis : implicaciones pronósticas y factores relacionados con la progresión de la enfermedad /

En la historia natural de la cirrosis, se reconocen dos estadios bien diferenciados con pronósticos diferentes. En los pacientes con cirrosis compensada, el objetivo es retrasar la progresión de la enfermedad y evitar la descompensación. En el paciente con cirrosis descompensada el objetivo es prevenir la muerte. La circulación hiperdinámica juega un papel fundamental en el perfil hemodinámico sistémico y hepático, sobre todo en la respuesta a BBNS. El objetivo principal de esta tesis, es describir y comparar los perfiles hemodinámicos de los pacientes con cirrosis compensada con respecto a los pacientes con cirrosis descompensada, para identificar factores predictivos de descompensación (en los compensados), su capacidad predictiva en el tiempo; y evaluar si en los pacientes con cirrosis descompensada la respuesta hemodinámica a BBNS hepática y sistémica afecta la supervivencia. METODOS: Estudio observacional, retrospectivo con seguimiento prospectivo en el que se incluyeron pacientes derivados a la unidad de hemodinámica para el inicio de profilaxis primaria de hemorragia varicosa con BBNS. Se realizaron 2 estudios hemodinámicos, uno basal con respuesta aguda a BBNS (propranolol EV) y una segunda medición de 1-3 meses bajo tratamiento con BBNS. RESULTADOS: 403 pacientes fueron incluídos, de los cuales 213 eran compensados y 190 descompensados (todos con ascitis). Los pacientes descompensados tenían basalmente peor función hepática con respecto a los compensados (MELD 12.83±3.72 vs 9.39±2.10, P≤ 0.001), mayor presión portal (HVPG= 19.4 ± 5 mmHg vs 17.4 ± 4 mmHg, P≤ 0.001) y peor respuesta a BBNS (Descenso del GPVH = 14 ± 13% vs 10 ± 15%, P 0.005). Durante un seguimiento medio de 36 meses (IQR, 16-66), el riesgo de hemorragia varicosa fue similar en ambos grupos (14 % vs 16%, P=0.82 by Gray test). En el grupo de pacientes compensados, al comparar los que permanecieron compensados vs los que se descompensaron, pudimos observar que los que presentaron descompensación tenían peor función hepática (CHild Pug y MELD score), peor respuesta hemodinámica a BBNS (menor descenso del GPVH) y mayor respuesta sistémica con PAM menor. Los principales factores predictivos independientes de descompensación en el seguimiento de 2 años fueron: ausencia de respuesta hemodinámica (HR= 2,05; IC 95%(1,4-2,9) P 0.001), Child Pugh HR:1,001 IC 95 (1,000-1,001)P 0.001. En el grupo de pacientes descompensados, aquellos que murieron en el seguimiento al comparar con los que sobrevivieron, eran mayor, con peor función hepática basal (Child-Pugh score (7.7±1.5 vs 7.2±1.6, P= 0.03) y más hipertensión portal con un GPVH (20.6±4 vs 18.9±4, P= 0.03). Sin embargo a los 1-3 meses de tratamiento con NNBS, los pacientes descompensados que murieron en el seguimiento, presentaron un descenso significativamente mayor de Gasto cardíaco y Presión arterial media con respecto a los que sobrevivieron. EL GC a los 1-3 meses de tratamiento con BBNS así como el Child-Pugh y el GPVH fueron identificados como factores predictivos independientes de mortalidad en los descompensados. LA probabilidad de muerte fue significativamente mayor en aquellos pacientes descompensados con GC 5 L/min ( 19% vs 5% , P 0.001 by log-rank). CONCLUSION: En los pacientes compensados, la ausencia de respuesta hemodinámica y el Child-Pugh son factores predictivos independientes de descompensación. Factores predictivos como el MELD; albúmina y respuesta aguda a BBNS pierden capacidad predictiva a partir del 2º año. Los BBNS tienen más efecto sistémico en los pacientes descompensados con mayor descenso de GC/PAM y menor efecto sobre el GPVH. Sugiriéndose que los efectos beneficiosos de los BBNS en pacientes descompensados va más allá de la presión portal. Una titulación más dirigida a través de métodos cardiovasculares que permitan estimar el GC podría optimizar su empleo en estos pacientes.In the natural history of cirrhosis, two well differentiated stages with different prognoses are recognized. In patients with compensated cirrhosis, the goal is to delay the progression of the disease and prevent decompensation. In the patient with decompensated cirrhosis the goal is to prevent death. Hyperdynamic circulation plays a fundamental role in the systemic and hepatic hemodynamic profile, especially in the response to NSBB. The main objective of this thesis is to describe and compare the hemodynamic profiles of patients with compensated cirrhosis with respect to patients with decompensated cirrhosis, to identify predictors of decompensation (in those compensated), their predictive capacity over time; and to evaluate if in patients with decompensated cirrhosis the hemodynamic response to hepatic and systemic BBNS affects survival. METHODS: Observational, retrospective study with prospective follow-up in which patients referred to the hemodynamic unit were included for the start of primary prophylaxis of varicose hemorrhage with NSBB. Two hemodynamic studies were performed, one baseline with acute response to propranolol EV and a 2º measurement 1-3 months under treatment with NSBB. RESULTS: 403 patients were included, of which 213 were compensated and 190 decompensated (all with ascites). Decompensated patients had baseline worse liver function with respect to those compensated (MELD 12.83 ± 3.72 vs 9.39 ± 2.10, P≤ 0.001), higher portal pressure (HVPG = 19.4 ± 5 ​​mmHg vs 17.4 ± 4 mmHg, P≤ 0.001) and worse hemodynamic response to NSBB (GPVH decrease = 14 ± 13% vs 10 ± 15%, P 0.005). During a mean follow-up of 36 months (IQR, 16-66), the risk of varicose hemorrhage was similar in both groups (14% vs 16%, P = 0.82 by Gray test). In the group of compensated patients, when comparing those who remained compensated vs those who decompensated, we observed that those who presented decompensation had worse liver function (Child Pug and MELD score), worse hemodynamic response to BBNS (lower decrease in GPVH) and greater systemic response with lower MAP. The main independent predictors of decompensation at the 2-year follow-up were: absence of hemodynamic response (HR = 2.05, 95% CI (1.4-2.9) P 0.001), Child Pugh (HR: 1.001 IC 95% (1,000-1,001) P 0.001). In the decompensated group, those who died in the follow-up compared with those who survived were older, with worse liver function (Child-Pugh score (7.7 ± 1.5 vs 7.2 ± 1.6, P = 0.03) and worse portal hypertension with a higher HVPG (20.6 ± 4 vs 18.9 ± 4, P = 0.03) However, after 1-3 months of treatment with NSBB, in the decompensated patients, those who died during FU had a significantly greater decrease in cardiac output (CO) and median arterial pressure (MAP) with respect to those who survived, the CO at 1-3 months of treatment with NSBB as well as Child-Pugh and HVPG were identified as independent predictive factors of mortality in the decompensated patients. Decompensated patients with CO 5 L / min (19% vs. 5%, P 0.001 by log-rank) CONCLUSION: In compensated patients, the absence of response hemodynamics and the Child-Pu gh are independent predictors of decompensation. Predictive factors such as MELD; albumin and acute response to NSBB lose predictive capacity as of the 2nd year. The NSBB have more systemic effect in decompensated patients with greater decrease in CO / MAP and less effect on HVPG. Suggesting that the beneficial effects of NSBB in decompensated patients goes beyond portal pressure. A more directed titration through cardiovascular methods that allow estimating the CG could optimize its use in these patients

Impact of the COVID-19 pandemic on the incidence and type of infections in hospitalized patients with cirrhosis : a retrospective study

Infections are a major cause of morbidity and mortality in cirrhosis, especially those caused by multi-drug resistant bacteria. During the COVID-19 pandemic, the incidence and type of infection in these patients may have been influenced by the restrictive measures implemented. We aimed to compare the infections in patients with cirrhosis hospitalized before the COVID-19 pandemic versus those hospitalized during the pandemic. We retrospectively compared infections in patients with cirrhosis hospitalized in the hepatology unit during the pre-pandemic period (3/2019-2/2020) with infections in patients hospitalized during the pandemic (3/2020-2/2021). Baseline characteristics, type of infections, type of bacteria, antimicrobial resistance and mortality were evaluated. There were 251 hospitalizations in 170 patients during the pre-pandemic period and 169 hospitalizations in 114 patients during the pandemic period. One or more infections were identified in 40.6% of hospitalizations during the pre-pandemic period and 43.8% of hospitalizations during the pandemic, P = 0.52. We found 131 infections in the pre-pandemic period and 75 infections during the pandemic. The percentage of nosocomial infections decreased in the pandemic period (25.3% vs. 37.4% in the pre-pandemic period, P = 0.06). We found a non-significant trend to a higher incidence of infections by multi-drug resistant organisms (MDRO) in the pandemic period than in the pre-pandemic period (6.5% vs. 4%). The incidence of infections was similar in both periods. However, during the pandemic, we observed a trend to a lower incidence of nosocomial infections with a higher incidence of MDRO infections