Acute Liver Failure Due to Echovirus 9 Associated With Persistent B-Cell Depletion From Rituximab.
Ontology highlight
ABSTRACT:
SUBMITTER: Bajema KL
PROVIDER: S-EPMC5604094 | biostudies-literature | 2017
REPOSITORIES: biostudies-literature
Publications
Acute Liver Failure Due to Echovirus 9 Associated With Persistent B-Cell Depletion From Rituximab.
Bajema Kristina L KL Simonson Paul D PD Greninger Alex L AL Çoruh Basak B Pottinger Paul S PS Bhattacharya Renuka R Liou Iris W IW Jalikis Florencia G FG Fligner Corinne L CL Rakita Robert M RM
Open forum infectious diseases 20170814 3
We describe a case of fatal acute liver failure due to echovirus 9 in the setting of persistent B-cell depletion and hypogammaglobulinemia 3 years after rituximab therapy. Metagenomic next-generation sequencing further specified the etiologic agent. Early recognition may provide an opportunity for interventions including intravenous immunoglobulin and liver transplantation. ...[more]
Similar Datasets
Project description:We describe a case of acute liver failure caused by echovirus 25 (E25) in a previously healthy 2-year-old boy. Initial serological studies were consistent with hepatitis A virus (HAV), with prozone phenomenon. The similarity of E25 to HAV may obscure accurate diagnosis in some cases of hepatitis.
| S-EPMC4290943 | biostudies-literature
Project description:Background and aimThe effect of elevated ammonia on organ failures (OF), apart from hepatic encephalopathy, in patients with acute decompensation (AD) of cirrhosis and acute-on-chronic liver failure (ACLF) is unclear. We aimed to assess the effect of persistent or incident hyperammonemia on OF and outcomes in patients with AD and ACLF.MethodsA total of 229 patients with ACLF and 83 with AD were included. Arterial ammonia was measured on day 1 and day 3 of admission. Persistent or incident hyperammonemia was defined as a level of ≥79.5 μmol/L on day 3. The changes in ammonia levels during the first 3 days were analyzed with respect to the complications and outcomes.ResultsAt admission, the median level of arterial ammonia was higher in ACLF compared to AD patients (103 vs 86 μmol/L, P < 0.001). Persistent or incident hyperammonemia was noted in 206 (66.0%) patients and was more frequent in ACLF compared to AD patients (70.7 vs 53.0%, P = 0.013). Patients with persistent or incident hyperammonemia, compared to those without it, developed a higher proportion of new-onset OF during hospitalization involving liver (P = 0.018), kidney (P = 0.001), brain (P = 0.005), coagulation (P = 0.036), circulation (P = 0.002), and respiratory (P = 0.003) issues and had higher 28-day mortality (log-rank test, P < 0.001). After adjustment for chronic liver failure consortium ACLF score, persistent or incident hyperammonemia (hazard ratio, 3.174) was independently associated with 28-day mortality. The presence of infection was an independent predictor of persistent or incident hyperammonemia.ConclusionPersistent or incident hyperammonemia during first 3 days of hospitalization in patients with AD or ACLF is associated with increased risk of OF and death.
| S-EPMC7578315 | biostudies-literature
Project description:Influenza vaccination is generally recommended for non-Hodgkin's lymphoma (NHL) patients, but no data are available about the activity of this vaccine after treatment with rituximab-containing regimens. We evaluated the humoral response to the trivalent seasonal influenza vaccine in a group of NHL patients in complete remission for ?6 mo (median, 29 mo) after treatment with rituximab-containing regimens (n = 31) compared with age-matched healthy subjects (n = 34). B cell populations and incidence of influenza-like illness were also evaluated. For each viral strain, the response was significantly lower in patients compared with controls and was particularly poor in patients treated with fludarabine-based regimens. In the patient group, the response to vaccination did not fulfill the immunogenic criteria based on the European Committee for Medicinal Products for Human Use requirements. Among the patients, CD27(+) memory B cells were significantly reduced, and their reduction correlated with serum IgM levels and vaccine response. Episodes of influenza-like illness were recorded only in patients. These results showed that NHL patients treated with rituximab-containing regimens have persisting perturbations of B cell compartments and Ig synthesis and may be at particular risk for infection, even in long-standing complete remission.
| S-EPMC3530046 | biostudies-literature
Project description:Acute liver failure in infancy accompanied by lactic acidemia was previously shown to result from mtDNA depletion. We report on 13 unrelated infants who presented with acute liver failure and lactic acidemia with normal mtDNA content. Four died during the acute episodes, and the survivors never had a recurrence. The longest follow-up period was 14 years. Using homozygosity mapping, we identified mutations in the TRMU gene, which encodes a mitochondria-specific tRNA-modifying enzyme, tRNA 5-methylaminomethyl-2-thiouridylate methyltransferase. Accordingly, the 2-thiouridylation levels of the mitochondrial tRNAs were markedly reduced. Given that sulfur is a TRMU substrate and its availability is limited during the neonatal period, we propose that there is a window of time whereby patients with TRMU mutations are at increased risk of developing liver failure.
| S-EPMC2771591 | biostudies-literature
Project description:Although elevated liver enzymes are common in hospitalized children with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, pediatric acute liver failure is an uncommon manifestation of COVID-19 disease. We describe the case of a 3-year-old previously healthy female who developed acute liver failure secondary to type 2 autoimmune hepatitis preceded by mild infection with SARS-CoV-2. Testing for viral hepatitis was negative, and the patient did not meet diagnostic criteria for multisystem inflammatory disease in children (MIS-C). A liver biopsy showed acute submassive hepatocyte necrosis with brisk CD3+ T lymphocyte infiltration and no evidence of fibrosis or chronic liver disease. Treatment with high-dose methylprednisolone resulted in rapid normalization of alanine aminotransferase (ALT), aspartate aminotransferase (AST), international normalized ratio (INR), and ammonia levels, and liver transplantation was avoided. This case highlights a possible association between SARS-CoV-2 infection and subsequent development of autoimmune liver disease presenting with acute liver failure.
| S-EPMC9052356 | biostudies-literature
Project description:Background/aimsStress hyperglycemia is common in critical illness but it has not been clearly studied in patients with acute pancreatitis (AP). This study aimed to investigate the specific blood glucose (BG) level that defines stress hyperglycemia and to determine the impact of stress hyperglycemia on clinical outcomes in AP patients.MethodsAP patients admitted ≤ 48 h after abdominal pain onset were retrospectively analyzed. Patients were stratified by pre-existing diabetes and stress hyperglycemia was defined using stratified BG levels for non-diabetes and diabetes with clinical outcomes compared.ResultsThere were 967 non-diabetic and 114 diabetic (10.5%) patients met the inclusion criteria and the clinical outcomes between these two groups were not significantly different. In non-diabetes, the cut-off BG level of ≥ 180 mg/dl was selected to define stress hyperglycemia with an 8.8-fold higher odds ratio for persistent organ failure (POF) (95% CI 5.4-14.3; P < 0.001). For diabetes, ≥ 300 mg/dl was selected with a 7.5-fold higher odds ratio for POF (95% CI 1.7-34.3; P = 0.009). In multivariable logistic regression, stress hyperglycemia was independently associated with POF, acute necrotic collection, major infection and mortality. The combination of BG and systemic inflammatory response syndrome (SIRS) score in predicting POF was better than SIRS or Glasgow score alone.ConclusionsThis study identifies a cut-off BG level of ≥ 180 mg/dl and ≥ 300 mg/dl was optimal to define stress hyperglycemia for non-diabetic and diabetic AP patients, respectively. There was a significant relationship between stress hyperglycemia and adverse clinical outcomes.
| S-EPMC9142444 | biostudies-literature
Project description:ObjectivesAcute liver failure (ALF) is an orphan disease often complicated by acute kidney injury (AKI). We assessed the impact of transient versus persistent AKI on survival in patients with ALF.DesignInternational multicenter retrospective cohort.SettingU.S. ALF Study Group prospective registry.PatientsPatients with greater than or equal to 18 years and ALF in the registry from 1998 to 2016 were included. Patients with less than 3 days of follow-up, without kidney function evaluation on day 3, or with cirrhosis were excluded.InterventionsAKI was defined by Kidney Disease Improving Global Outcomes guidelines on day 1. Kidney recovery was defined on day 3 as transient AKI, by a return to no-AKI within 48 hours or persistent AKI if no such recovery or renal replacement therapy (RRT) was observed. Primary outcome was transplant-free survival (TFS) at 21 days.Measurements and main resultsAmong 1,071 patients with ALF, 339 (31.7%) were males, and median (interquartile range) age was 39 years (29-51 yr). Acetaminophen-related ALF was found in 497 patients (46.4%). On day 1, 485 of 1,071 patients (45.3%) had grade 3-4 hepatic encephalopathy (HE), 500 of 1,070 (46.7%) required invasive mechanical ventilation (IMV), 197 of 1,070 (18.4%) were on vasopressors, and 221 of 1,071 (20.6%) received RRT. On day 1, 673 of 1,071 patients (62.8%) had AKI. On day 3, 72 of 1,071 patients (6.7%) had transient AKI, 601 of 1,071 (56.1%) had persistent AKI, 71 of 1,071 (6.6%) had late onset AKI, and 327 of 1,071 (30.5%) remained without AKI. Following adjustment for confounders (age, sex, race, etiology, HE grade, use of IMV and vasopressors, international normalized ratio, and year), although persistent acute kidney injury (adjusted odds ratio [aOR] [95% CI] 0.62 [0.44-0.88]) or late onset AKI (aOR [95% CI] 0.48 [0.26-0.89]) was associated with lower TFS, transient AKI was not (aOR [95% CI] 1.89 [0.99-3.64]).ConclusionsIn a multicenter cohort of patients with ALF, persistent but not transient AKI was independently associated with lower short-term TFS.
| S-EPMC10681629 | biostudies-literature
Project description:Acute liver failure is a rare and severe consequence of abrupt hepatocyte injury, and can evolve over days or weeks to a lethal outcome. A variety of insults to liver cells result in a consistent pattern of rapid-onset elevation of aminotransferases, altered mentation, and disturbed coagulation. The absence of existing liver disease distinguishes acute liver failure from decompensated cirrhosis or acute-on-chronic liver failure. Causes of acute liver failure include paracetamol toxicity, hepatic ischaemia, viral and autoimmune hepatitis, and drug-induced liver injury from prescription drugs, and herbal and dietary supplements. Diagnosis requires careful review of medications taken, and serological testing for possible viral exposure. Because of its rarity, acute liver failure has not been studied in large, randomised trials, and most treatment recommendations represent expert opinion. Improvements in management have resulted in lower mortality, although liver transplantation, used in nearly 30% of patients with acute liver failure, still provides a life-saving alternative to medical management.
| S-EPMC10836844 | biostudies-literature
Project description:BackgroundOrgan failure determines outcome in acute pancreatitis (AP). It is controversial if infected pancreatic necrosis (IPN) is also an independent determinant of mortality. We hypothesized that the predictors of mortality in AP might have changed with advances in management and consequent decline in mortality over the past decades. Our objective was to study the predictors of mortality in patients with AP.MethodsConsecutive patients with a first episode of AP hospitalized from January 2015 to December 2016 were included in an observational study. Patients with IPN were treated with a conservative first approach followed by intervention. Necrosectomy, if required, was delayed beyond 4 weeks and done primarily employing minimally invasive techniques. The primary outcome measure was independent predictors of in-hospital mortality.ResultsOf 209 patients with AP, 81 (39%) had persistent organ failure (OF) and 108 (52%) developed IPN. Overall, 46/209 (22%) patients died. Independent predictors of mortality were OF (odds ratio [OR]19; 95% CI: 6.1-58.8), and IPN due to infection with multidrug resistant (MDR) organisms (OR: 8.4; 95% CI:3.1-22.5). Infected pancreatic necrosis by itself was not found to be a significant predictor of mortality (OR 2; 95% CI: 0.4-9.5).ConclusionPersistent OF and complicated IPN due to MDR infection were independent predictors of mortality in patients with AP. Renewed efforts to prevent MDR infection with antibiotic stewardship and strategies for early control of sepsis are urgently required.
| S-EPMC6172262 | biostudies-literature
Project description:BackgroundAcute liver failure (ALF) is a life-threatening complication that is relatively uncommon. ALF causes severe hepatocyte damage and necrosis, which can lead to liver dysfunction and even multi-organ failure. A growing body of evidence suggests that immune cell infiltration and some abnormally expressed genes are associated with ALF development. However, in ALF, they have yet to be thoroughly investigated.MethodsThe Gene Expression Omnibus (GEO) database was used to obtain microarray datasets such as GSE74000, GSE120652, GSE38941, and GSE14668, which were then examined via GEO2R to determine differentially expressed genes (DEGs) associated with ALF. Metascape was employed to annotate the underlined genes using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. The mechanism of IGF1 in 2 different kinds of ALF including acetaminophen-induced ALF and hepatitis B virus (HBV)-induced ALF was studied using gene set enrichment analysis (GSEA). Next, immune cell infiltration was investigated and differentiated in ALF using CIBERSORT.ResultsSix genes (HAO2, IGF1, PLA2G7, SC5D, GNE, SLC1A1) were found to be abnormally expressed in the 2 distinct types of ALF i.e., acetaminophen-induced ALF and HBV-induced ALF. IGF1 was identified as a hub gene in ALF and was found to be associated with several developmental cascades including immune responses, inflammatory responses, and intracellular calcium homeostasis. Additionally, the number of CD4 naive T cells, CD8 T cells, and follicular helper T cells was increased in acetaminophen-induced ALF, whereas the number of activated NK cells, resting NK cells, and plasma cells was increased in HBV-induced ALF.ConclusionsThe present study determined a potential molecular target, namely IGF1, in acetaminophen-induced ALF and HBV-induced ALF, which may provide novel insights into the pathophysiology and management of ALF. Concurrently, the putative immunological pathways have been found.
| S-EPMC9372688 | biostudies-literature