scholarly journals Fulminant hepatitis B

2003 ◽  
Vol 60 (3) ◽  
pp. 353-360
Author(s):  
Milomir Djokic ◽  
Vesna Begovic ◽  
Radmila Rajic-Dimitrijevic ◽  
Rada Aleksic ◽  
Svetlana Popovic ◽  
...  

Fulminant hepatitis, or fulminant hepatic failure, is defined as a clinical syndrome of severe liver function impairment, which causes hepatic coma and the decrease in synthesizing capacity of liver, and develops within eight weeks of the onset of hepatitis. Several independent factors influence the survival of patients: age, the cause of liver disease, the degree and the duration of encephalopathy in relation to the onset of the disease, and the prevention of complications. Over the years many intensive treatments have been practiced. Liver transplantation is expensive, and patients who survive transplantation require life-long immunosupression, clinical care and complications management. Without transplantation fulminant hepatitis and hepatic failure might be completely recovered spontaneously, and the patient could expect a normal life. Two cases of fulminant B hepatitis with intensive care treatment, and their survival despite unfavorable prognosis are presented in this paper. The menagement of patients with fulminant hepatitis required intensive monitoring and therapeutic measures, including corticosteroids. The prognosis for survival without transplantation in fulminant hepatitis is limited by the measures of medical treatment and new specific therapeutic modalities which must be developed through basic research.

1994 ◽  
Vol 28 (10) ◽  
pp. 1159-1161 ◽  
Author(s):  
Preston P. Purdum ◽  
Stacey L. Shelden ◽  
John W. Boyd ◽  
Mitchell L. Shiffman

OBJECTIVE: To report oxaprozin-induced fulminant hepatic failure. CASE SUMMARY: A 56-year-old woman was admitted with fulminant hepatic failure. Work-up for potential etiologies was negative except for the use of oxaprozin for the preceding two months. Results of premortem liver biopsy were consistent with drug-induced hepatic injury similar to that previously reported with diclofenac. DISCUSSION: Although the literature describes elevation in hepatic transaminase concentrations associated with oxaprozin, fulminant hepatic failure has not been described previously. CONCLUSIONS: Elevations in hepatic transaminase concentrations and now fulminant hepatic failure have been shown to occur with oxaprozin, as previously seen with other nonsteroidal antiinflammatory drugs (NSAIDs). Transaminitis is a known adverse effect of NSAID use, but is usually mild and reversible with discontinuation of drug. Transaminitis may be more likely to occur in the elderly, in patients receiving concurrent potentially hepatotoxic medications, and possibly with the newer long-acting NSAIDs. The existence of fulminant hepatitis, although rare, supports the need for monitoring liver function enzymes during NSAID therapy.


2001 ◽  
Vol 3 (10) ◽  
pp. 1-19 ◽  
Author(s):  
Mingfeng Liu ◽  
Camie W.Y. Chan ◽  
Ian McGilvray ◽  
Qin Ning ◽  
Gary A. Levy

Fulminant hepatic failure is defined by the sudden onset of severe liver injury accompanied by hepatic encephalopathy in an individual who previously had no evidence of liver disease. This disease causes multiple organ failure and is associated with a high mortality. The most frequently recognised cause of fulminant or subfulminant hepatic failure is viral hepatitis. Data are now emerging to support the hypothesis that, irrespective of the aetiology of fulminant hepatic failure, the host's immune response (including production of proinflammatory cytokines and mediators) contributes to microcirculatory disturbances that result in hypoxic injury and cell death (apoptosis). Impairment of the scavenger function of the reticuloendothelial cell system further contributes to reduced hepatic blood flow and ischaemic necrosis. An increased understanding of the molecular pathogenesis of fulminant hepatic failure now enables new molecular therapeutic modalities to be tested. Given the complexity of this multi-dimensional disorder, the challenge is to provide a rational basis for treatment. This might include enhancement or suppression of immune responsiveness by manipulation of endogenous cytokine synthesis or by cytokine administration and, at the same time, use of strategies to increase hepatic regeneration.


2019 ◽  
Vol 8 (12) ◽  
pp. 2222
Author(s):  
Martin A. Schaller-Paule ◽  
Christian Foerch ◽  
Sara Kluge ◽  
Peter Baumgarten ◽  
Jürgen Konczalla ◽  
...  

(1) Background: A lesion within the dentato-rubro-olivary pathway (DROP) in the posterior fossa can cause secondary neurodegeneration of the inferior olivary nucleus: so-called hypertrophic olivary degeneration (HOD). The clinical syndrome of HOD occurs slowly over months and may be overlooked in progressive neuro-oncological diseases. Posterior fossa tumors are often located near these strategic structures. The goal of this study was to analyze the systematics of HOD occurrence in neuro-oncological patients. (2) Methods: The neuroradiological database of the university healthcare center was scanned for HOD-related terms from 2010 to 2019. After excluding patients with other causes of HOD, 12 datasets from neuro-oncological patients were analyzed under predetermined criteria. (3) Results: Patients received multimodal tumor treatments including neurosurgery, radiotherapy, and chemotherapy. HOD occurred both unilaterally (left n = 4; right n = 5) and bilaterally (n = 3). Though the mass effect of posterior fossa tumors had already affected strategic structures of the DROP, none of the patients showed signs of HOD on MRI until therapeutic measures including neurosurgery affecting the DROP were applied. HOD was visible on MRI within a median of 6 months after the neurosurgical intervention. In 67%, the presumed underlying surgical lesion in the DROP lay in the contralateral dentate nucleus. (4) Conclusion: In a selected cohort of neuro-oncological patients, therapeutic lesions within the DROP were associated with HOD occurrence.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S I Im ◽  
H S Park

Abstract Background There was limited data about the association between the electrocardiographic characteristics and irreversible fulminant hepatitis (IFH) in patients with acute hepatic failure (AHF) in the long-term follow up. Purpose The aim of this study was to analysis the electrocardiographic characteristics for prediction of IFH in patients with AHF. Methods Our University echocardiography, electrocardiogram (ECG) and viral hepatitis database were reviewed from 2008 to 2017 to identify patients with AHF. Patients were followed for a mean 32.0±0.8 months and were analyzed to find out the predictors for IFH. Results Among 202 patients with AHF, 23 (11.4%) patients had IFH. In our study, there are 118 (58.7%) viral hepatitis patients (hepatitis A, 83 patients, 41.3%; hepatitis B, 19 patients, 9.5%; hepatitis C, 15 patients, 7.5%) and alcoholic hepatitis patients (83 patients, 41.3%). Based on the ROC curve, we set the corrected QT interval (QTc) cutoff value of 425 msec for prediction of IFH, which gave a sensitivity of 66.7% and a specificity of 66.0% (P=0.002). In univariate analysis, age, QTc, diabetes mellitus (DM), heavy alcoholics, labile INR, hemoglobin, albumin, total bilirubin, sodium, and c-reactive protein were significantly associated with IFH. In multivariate analysis, age, QTc, DM, heavy alcoholics, and total bilirubin were independent risk factors for IFH at the long-term follow-up. Conclusion Longer QTc (>425msec) in patients with AHF was associated with higher IFH, suggesting close clinical and electrocardiographic follow-up will be required. Acknowledgement/Funding None


2020 ◽  
Vol 8 ◽  
pp. 232470962092420 ◽  
Author(s):  
Rohan Sharma ◽  
Nidhi Kapoor ◽  
Kaustubh Suresh Chaudhari ◽  
Robert Hal Scofield

Background. Fulminant hepatitis is acute hepatic injury with severe decline in hepatic function manifested by encephalopathy, hypercoagulable state, jaundice, renal failure, hypoglycemia, or a constellation of these symptoms in patients without preexisting liver disease. Etiologies include viral infections, hepatotoxic drugs, autoimmune diseases, vaso-occlusive diseases, sepsis, and malignant infiltration. Case Report. A 56-year-old man presented with acute heart failure in the setting of cocaine use. The patient subsequently developed fulminant hepatic failure manifested by acute hypoglycemia, elevated liver enzyme, and worsening liver function, which resolved over 1 week with supportive care. The patient was on β-blocker, which was stopped during the admission. He was again admitted on several different occasion for cocaine-induced acute heart failure but did not develop hepatic failure as his β-blocker was discontinued. Discussion. Cocaine has been known to cause hepatotoxicity in humans. However, our patient developed fulminant hepatic failure in the setting of concomitant cocaine and β-blocker use likely secondary to unopposed α-adrenergic activity and ischemic hepatopathy. The patient did not develop hepatic failure on subsequent admissions with cocaine use after discontinuation of β-blockers.


2010 ◽  
Vol 437 ◽  
pp. 299-303
Author(s):  
Peter Rolfe

This paper reviews the ways in which micro and nano sensors have evolved within biology and medicine. The target measurands include an ever-increasing number of simple and complex molecules, physical quantities, and electrical and magnetic phenomena. Micro sensors based on electrochemical, acoustic, piezoelectric and optical principles are contributing to clinical care of patients who may benefit from the continuous monitoring of critical variables in intensive care or from the ability to perform convenient self-monitoring during normal daily life. Sensors constructed on the nano-scale are now emerging, especially for complex bio-molecules such as DNA. These are strengthening basic research, for example in the study of genetic factors in disease and for discovery of new drugs. Scanning probe technology and nano optics, including surface enhanced Raman spectroscopy, play important roles in these developments. Sensor science and technology has gained significant benefits through inspiration arising from biological sensory systems. This includes the sense of olfaction, which has led to the artificial nose, and the sense of vision that has been emulated in several versions of the artificial retina. The impact of micro and nano sensors on fundamental understanding in biomedicine and on clinical diagnosis and care are highlighted.


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