Prevalence Of Hepatic Dysfunction Research Articles

Hepatic Dysfunction during Induction Chemotherapy in Children with Acute Lymphoblastic Leukemia and Lymphoblastic Lymphoma and Its Effects on Subsequent Therapy and Outcome

Abstract Introduction The overall survival rate for childhood acute lymphoblastic leukemia (ALL) and lymphoblastic lymphoma (LBL) has shown tremendous growth in the recent years. Hepatic dysfunction is one of the complications seen during therapy and can add to the underlying morbidity of the disease, delay in chemotherapy, modification of drugs, and rarely fulminant hepatic failure. Objective This article aims to find out the prevalence of hepatic dysfunction during induction chemotherapy for ALL and LBL. Materials and Methods This was a retrospective study, where the data of all children between 1 and 18 years of age with ALL and LBL treated at our center as per the UK-ALL 2003 protocol between December 2013 and December 2021 have been included from the medical records. Hepatic dysfunction was defined as grade 3 and 4 alanine transaminase (ALT) and aspartate transaminase (AST) levels as per Common Terminology Criteria for Adverse Events v5.0 and hyperbilirubinemia as ≥ 1.4 mg/dL as the chemotherapy modification begins at this cutoff. Data from children with hepatic dysfunction was compared with those without hepatic dysfunction using chi-squared test and Student's t-tests. Those variables with a p-value of < 0.2 were analyzed with multivariate regression analysis. Kaplan–Meier survival estimates were used to calculate the event-free survival (EFS). Results A total of 142 children were included in the study. Thirty-one (21.8%) children developed hepatic dysfunction, 14 (9.9%) of them with ALT/AST elevation and 27 (19%) with bilirubin elevation. Weight (mean 25 ± 13.5, p 0.01), body surface area (mean 0.87 ± 0.29, p 0.02), and National Cancer Institute high risk (p 0.005) were associated with hepatic dysfunction in univariate analysis but none of them were significant in multivariate regression analysis. Treatment modification was required in 14/31 children with hepatic dysfunction. Death in induction was more among children with hepatic dysfunction (p < 0.001). There was no significant impact on minimal residual disease outcomes. Five-year EFS (death or relapse) was 59.93 ± 9% in children with hepatic dysfunction as opposed to 72 ± 5.0% in those without hepatic dysfunction (95% confidence interval, p = 0.07). Conclusion One in five children with ALL and LBL on induction therapy developed hepatic dysfunction. Almost half of those with hepatic dysfunction required chemotherapy modifications.

Prevalence of hepatic dysfunction in paediatric patients with Fontan circulation

Prevalence of hepatic dysfunction in paediatric patients with Fontan circulation

Prevalence of hepatic dysfunction during induction chemotherapy for acute lymphoblastic leukaemia and lymphoblastic lymphoma in children and its effects on subsequent therapy

Prevalence of hepatic dysfunction during induction chemotherapy for acute lymphoblastic leukaemia and lymphoblastic lymphoma in children and its effects on subsequent therapy

Prevalence of hepatic dysfunction in children with dengue fever

Background:Dengue is one disease entity with different clinical presentations and often with unpredictable clinical evolution and outcome. The degree of liver dysfunction in children with dengue infection varies from mild injury with elevation of transaminases to severe injury with jaundice and liver cell failure. This study was undertaken to find the prevalence of hepatic dysfunction in children admitted with Dengue fever. Methods:All children with serologically (dengue NS1 antigen detection and/or dengue IgM Mac ELISA) confirmed dengue fever aged between 2 months and 12 years were included in the study. Children with other etiologies of hepatitis were excluded. Liver function tests including bilirubin, transaminases and prothrombin time (PT) were done. Prevalence and severity of hepatic dysfunction were statistically analysed and compared between different categories of dengue fever severity. Results:Hepatic dysfunction was present in 35 (67.30%) of the 52 children included in the study.About 85.71% of the children with dengue fever in the age group of 2 months to 1 year had hepatic dysfunction. In children with severe dengue, 83.3% had hepatic dysfunction.Raised liver enzymes in 32(61.53%), hepatomegaly in 21(40.48%), INR≥1.5 in 8(15.38%) and jaundice in 1(1.92%) children were the manifestations. None of the patients had acute hepatic failure or hepatic encephalopathy.Association of hepatomegaly with increasing disease severity was statistically significant (p = 0.0262). Hepatic dysfunction was present in 83.33% and 87.5% of children with abdominal pain and clinical fluid accumulation respectively. Of the 32 patients (61.53%) with elevated transaminases, 18 (51.42%) had elevated levels of AST alone, 40% had elevation of AST and ALT both. Conclusions: The prevalence of hepatic dysfunction among children with dengue fever is 67.30%, more commonly observed in severe forms of dengue. Spectrum of hepatic involvement ranges from raised liver enzymes without jaundice to clinically evident jaundice. Hepatic dysfunction is commonly observed in children with abdominal pain and clinical fluid accumulation.

Hepatic dysfunction after shock: Clinical parameters and biological pathways for therapeutic intervention

The prevalence of hepatic dysfunction was thought to be ≈ 1% in intensive care unit (ICU) patients, but is now being recognized to be > 10%. Mortality and length of ICU stay are directly affected by hepatic dysfunction, raising the need for a better understanding of this disorder in order to develop therapeutic options that go beyond the current practice of supportive care. The etiologies of hypoxic hepatitis are discussed, together with their differentiating physiological parameters. The liver's compensatory mechanisms are examined at the level of the microcirculation. The cytokine milieu and cells responsible are considered. Survival versus cell death by means of necrosis, apoptosis, or autophagy is determined by the interplay of intracellular pathways. Specific pathways discussed involve reactive oxygen species, Toll-like receptor 4, heme oxygenase, transcription factors such as nuclear factor-κB, mitogen-activated protein kinase and protein kinase B. From this basis, current and future therapeutic str...

P1164 CONTEMPORARY RATES, RISK FACTORS AND OUTCOMES OF HEPATIC DYSFUNCTION IN INFANTS ON PARENTERAL NUTRITION THERAPY.

Introduction: The efficacious use of Parenteral Nutrition (PN) therapy was initially reported three decades ago. However, shortly thereafter, hepatic dysfunction was recognized as a major clinical problem and frequent indication for termination of PN therapy. Major changes have since occurred in PN including change from 10% to 20% Intralipid emulsions, increased use of Trophamine as the aminoacid source in infants, and advances in tertiary care. The objective of this study was to re-evaluate the contemporary rates, risk factors and outcomes of PN-associated hepatic dysfunction (HD) in infants. Methods: Retrospective study of all infants (age <12-months) that received PN therapy during the 12-month period from September 2002 to August 2003 at a tertiary care Children’s Hospital. Infants on prolonged PN (>2-wks) were reviewed for birth wt, diagnosis, duration and mortality during PN therapy. Medical risk factors were categorized as low birth wt (<1500 g); sepsis (bacteremia, pneumonia, urosepsis); intestinal failure (NEC, gastrointestinal surgery, short gut syndrome); and cardio-respiratory failure (CRF: surgical congenital heart disease and severe pulmonary hypertension). PN-associated HD was defined as rise in conjugated bilirubin to >1.5 mg/dl during PN therapy. Prevalence and resolution of HD were determined. Logistic regression analysis was used to determine the effect of medical risk factors and duration of PN therapy on onset and resolution of HD. Significance wad determined as p <0.05. Results: 508 infants received PN therapy during the 12-m period; and 102 (birth wt 560–3800 g) received PN for a duration >2-wks. The prevalence of HD in subjects receiving prolonged PN therapy (>2-wks) was 37.5% (95% CI: 27.9, 47.4%). Duration of PN therapy for >4-wk was associated with a four-fold risk of HD compared to duration of 2 to 3-wk (OR 4.4; 95% CI: 1.75, 11). Duration of PN was the most significant risk factor for onset of HD (p = 0.0031), along with CRF (p = 0.0042). After controlling for duration on PN, HD was 5.6 times (95% CI: 1.7, 17.8) more likely to resolve in infants with CRF. CRF was the risk factor most associated with mortality while on PN therapy (p = 0.0002). Conclusion: HD is a common complication in ill infants on prolonged PN therapy; however, mortality while on PN therapy most commonly occurred in infants with CRF. Duration of PN therapy was the major risk factor associated with onset, resolution and persistence of HD in infants.

Occult herpes family viral infections are endemic in critically ill surgical patients.

Herpes family viruses have been recognized as pathogens for many years in immunosuppressed transplant or human immunodeficiency virus patients, but they have garnered little attention as potential pathogens in the nonimmunosuppressed critically ill. The objective of this study was to define the prevalence of and risk factors for development of herpes family virus infection in chronic critically ill surgical patients. Prospective epidemiologic study. A 38-bed surgical intensive care unit in a major university hospital. Nonimmunosuppressed intensive care unit patients in intensive care unit for >/=5 days. None; patients received no antiviral treatment during the study. Weekly cultures for cytomegalovirus (CMV) and herpes simplex virus, viral serologies, and T-cell counts were performed. The prevalence (95% confidence interval) of positive respiratory cultures for herpes simplex or CMV was 35% (22-49%); 15% (5-25%) cultured positive for CMV, 23% (11-35%) cultured positive for herpes simplex virus, and one patient's respiratory secretions culturing positive for both CMV and herpes simplex virus. The prevalence of CMV viremia was only 5.8% (1-10%). CMV+ patients had longer hospital admissions, intensive care unit admissions, and periods of ventilator dependence than CMV- patients, despite having comparable severity of illness scores. CMV+ patients also had significantly higher numbers of blood transfusions, prevalence of steroid exposure, and prevalence of hepatic dysfunction, and all were immunoglobulin G positive at the beginning of the study. In contrast, herpes simplex virus-positive patients had lengths of hospital admissions, lengths of intensive care unit admissions, and periods of ventilator dependence comparable with patients without viral infections (p >.05). There is a significant prevalence (22-49%) of occult active herpes family viruses in chronic critically ill surgical patients. The clinical significance of these viral infections is unknown, although CMV+ patients have significantly higher morbidity rates than CMV- patients. Several factors suggest pathogenicity, but further study is needed to define causality.

Nonhepatitis B-Associated Liver Disease in a Renal Transplant Population

The spectrum of liver disease in a population of 293 patients receiving 353 renal transplants (1971-1984) was reviewed. This study looked retrospectively at the histological features of liver disease in this population, and prospectively at the clinical and biochemical features of liver disease associated with renal transplantation. In all patients, infection with hepatitis B was excluded. Six deaths, primarily attributable to hepatic failure have occurred: one, acute herpes simplex infection; one, subacute massive hepatic necrosis of uncertain etiology; two, pretransplant liver disease; and two, posttransplantation cirrhosis of uncertain etiology. Review of the hepatic histology of 26 patients with known liver disease following transplantation revealed a wide range of pathologies with few specific correlations with their clinical status or biochemical tests of liver function. The prevalence of hepatic dysfunction following transplantation in our patient population was assessed by prospective biochemical screening of 111 transplant recipients over a 6-month interval. During this time period, 27 patients (24%) displayed biochemical evidence of hepatic dysfunction. Liver disease was known to have predated transplantation in only three of 27. Episodes of abnormal liver function occasionally occurred during an identifiable acute illness (six of 27), although the majority (21 of 27) had chronic hepatic dysfunction. Transplant recipients with abnormal liver function could not be differentiated from a cohort with normal liver function on the basis of age, sex, duration of graft function, or alcohol/drug intake. The possible etiologies of nonhepatitis B liver dysfunction following renal transplantation are discussed, and the high prevalence of biochemical evidence of hepatic dysfunction in this population free of hepatitis B infection is emphasized.

Liver Function and Illicit Opioid Use

To the Editor.— In a recent letter toThe Journal(234:1320, 1975), Dr Thornton has retrospectively reviewed the prevalence of laboratory evidence of hepatic dysfunction in 603 persons admitted to the Illinois Drug Abuse Program. From this review he concluded that when a larger population of narcotic addicts is studied, the prevalence of laboratory abnormalities in liver function is considerably lower (42%) than figures previously reported in the literature (60%-80%).1-3Although one would not dispute Dr Thornton's findings, the possibility does exist that such data might be explained on several bases other than sample size. The reported percentage of abnormal values found by Dr Thornton in individual tests of hepatic dysfunction (5% to 42%, depending on the specific examination) was not adjusted to give a value for the overall prevalence of hepatic dysfunction seen if an abnormality was noted in any one value. If this had been done, it