Ecstasy: An Important Cause of Acute Liver Failure

2006 ◽  
Vol 5 (3) ◽  
pp. 93-95
Author(s):  
Ajay Kiran Muddu ◽  
◽  
Mark Wright ◽  
Nick Sheron ◽  
◽  
...  

A twenty year old female was referred to hospital by her GP, after he received the results of blood tests taken earlier in the day. She had presented to him complaining of malaise, nausea and anorexia over a 3 day period. On the day of referral she had also become jaundiced with dark urine, but normal stool colour. There was no abdominal pain. She had no significant past medical history with no history of jaundice, liver disease or autoimmune conditions, and no apparent risk factors for blood-borne hepatitis infection. There was no relevant family history. She was taking no prescribed medication, had not taken any over the counter medication or herbal remedies. She denied excessive alcohol use or use of intravenous drugs in the past, although she was not specifically questioned on the use of other recreational drugs. She was a single mother and admitted to being under considerable stress recently. On examination she appeared well, apart from marked jaundice. There were no signs of hepatic encephalopathy or chronic liver disease. Abdominal examination revealed mild left upper quadrant tenderness, but no significant hepatomegaly. Liver function tests (LFTs) taken by her GP are shown in Table 1, revealing marked elevation of the Alanine Transaminase (ALT) (Table 1), with a relatively preserved albumin. Unfortunately her International Normalised Ratio (INR) had not been measured. An Ultrasound of the abdomen demonstrated a normal size liver with normal contour and texture with no other abnormality.

2016 ◽  
Vol 2016 ◽  
pp. 1-2
Author(s):  
Seth Shaffer ◽  
Mayur Brahmania ◽  
Hemant Shah

A 49-year-old Brazilian male presented to the emergency department with a five-day history of abdominal pain, dark stools, and syncope. Physical examination did not reveal any melena on digital rectal examination and there were no stigmata of chronic liver disease. Laboratory results showed hemoglobin of 47 g/L, MCV of 80 fL, and ferritin of 6 ng/mL. Liver enzymes and liver function tests were normal. Abdominal ultrasound showed a cirrhotic liver with splenomegaly and varices suggestive of portal hypertension. His past history was significant for cirrhosis based on a previous variceal bleed but a workup for chronic liver disease was negative and a liver biopsy did not show steatosis, fibrosis, or cirrhosis. A gastroscopy in this admission showed large esophageal varices without high-risk stigmata and no overt bleeding was seen. A colonoscopy was subsequently completed to the terminal ileum and was normal aside from a 5 mm sessile polyp in the descending colon.


2014 ◽  
Vol 306 (10) ◽  
pp. G819-G823 ◽  
Author(s):  
Stephanie Mathews ◽  
Mingjiang Xu ◽  
Hua Wang ◽  
Adeline Bertola ◽  
Bin Gao

Over the last four decades, chronic ethanol feeding studies in rodents using either ad libitum feeding or intragastric infusion models have significantly enhanced our understanding of the pathogenesis of alcoholic liver disease (ALD). Recently, we developed a chronic plus binge alcohol feeding model in mice that is similar to the drinking patterns of many alcoholic hepatitis patients: a history of chronic drinking and recent excessive alcohol consumption. Chronic+binge ethanol feeding synergistically induced steatosis, liver injury, and neutrophil infiltration in mice, which may be useful for the study of early alcoholic liver injury and inflammation. Using this chronic+binge model, researchers have begun to identify novel mechanisms that participate in the pathogenesis of alcoholic liver injury, thereby revealing novel therapeutic targets. In this review article, we briefly discuss several mouse models of ALD with a focus on the chronic+binge ethanol feeding model.


1977 ◽  
Author(s):  
Joel A. Spero ◽  
Jessica H. Lewis ◽  
Ute Hasiba

Abnormal liver function tests (LFTs) in patients with Hemophilia A and B who have been treated with commercial factor concentrates have been observed since 1973. One hundred and seventeen of these had had LFTs performed at least twice and at least six months apart. Of these, 13 were chronically HbsAg positive and the rest anti-Hbs positive. Forty percent of the anti-Hbs group had persistently abnormal LFTs for greater than 6 months, the majority for more than two years. Owing to the uncertain relationship of this “transaminitis” with true liver pathology, especially in the anti-body positive patients, seven closed liver biopsies were performed without incident under high coverage with factor VIII replacement. All patients were asymptomatic at the time of biopsy. One had a prior episode of illness probably related to subclinical hepatitis. An eighth patient underwent an open liver biopsy as part of a staging laparotomy for Hodgkins Disease. Six biopsies showed varying degrees of chronic persistent hepatitis (CPH). One was not evaluable owing to changes related to a retrospectively obtained history of ETOH intake. Finally, the individual with previous clinical liver disease had post-necrotic cirrhosis. Fluorescent studies with anti-Hbs and-anti-Hbc as well as electron microscopy were done on the seven closed biopsy specimens. The biopsy results suggest that the “transaminitis” found in transfused hemophiliacs represents histologic liver disease. In the majority of patients studied, CPH, a relatively benign entity, was present; and this does not justify withdrawal of concentrate therapy at this time.


Blood ◽  
1997 ◽  
Vol 90 (11) ◽  
pp. 4628-4633 ◽  
Author(s):  
Anna Locasciulli ◽  
Marina Testa ◽  
Patrizia Pontisso ◽  
Luisa Benvegnù ◽  
Donatella Fraschini ◽  
...  

Abstract The aim of this study was to ascertain prevalence and natural history of hepatitis C virus (HCV) infection in a large cohort of patients cured of childhood leukemia who had been followed prospectively for liver disease for at least 10 years since chemotherapy withdrawal: 114 consecutive patients entered the study. Liver function tests and ultrasonography were used to assess presence of liver disease. Patients were tested for antibody to HCV and for serum HCV-RNA at the end of chemotherapy and at the end of follow-up. At chemotherapy withdrawal, 56 patients (49%) were HCV-RNA positive, often without detectable anti-HCV, and in these cases, transaminase levels were more elevated during (P = .08) and after (P = .04) chemotherapy compared with HCV-RNA negative cases. Patients were then followed-up 13 to 27 years (mean, 17) after chemotherapy withdrawal. During this period, 38 initially anti-HCV negative patients seroconverted to anti-HCV and 17 initially anti-HCV positive cases lost reactivity. Forty patients were persistently HCV-RNA positive in serum, while 16 initially viremic patients became HCV-RNA negative during follow-up. At the end of the observation period, a persistent transaminase elevation was detected only in four HCV-RNA positive and anti-HCV positive cases, while no patient developed signs or symptoms of decompensated liver disease. Thus, hepatitis C was a frequent finding in long-term survivors after chemotherapy. It was associated with an atypical serologic profile and did not cause severe liver impairment over a period of 13 to 27 years.


Author(s):  
Е. V. Garanina

Introduction. Hyperammonaemia develops both in cirrhosis and earlier fibrotic stages during metabolic-associated fatty liver disease (MAFLD). Besides neurotropic, ammonia exerts the hepatotoxic and profibrotic effects. L-ornithine-L-aspartate (LOLA) has been proved effective in treatment for hyperammonaemia in cirrhosis patients.Aim. An impact study of the LOLA course therapy on inflammation, steatosis and liver fibrosis biomarkers in MAFLD.Materials and methods. A total of 90 patients were divided between two cohorts. The control cohort included patients with liver steatosis S0–S1, absent liver fibrosis, normal liver function tests, clean history of liver disease, while MAFLD cohort gathered liver steatosis S2–S3 and METAVIR fibrosis F1. Steatosis and fibrosis were assessed with a Fibroscan 502 unit with CAP measurement. All patients had ammonia estimated from whole blood. At high ammonia, LOLA was ordered at 9 g/day for 8 weeks, with control of blood ammonia, AST, ALT, GGT, CRP and ferritin, as well as fibrosis and steatosis post-therapy.Results. The study enrolled 45 patients of the MAFLD and 45 — of control cohort. Hyperammonaemia was revealed in 26 (58 %) MAFLD and 3 (7 %) control patients (p <0.001). MAFLD-hyperammonaemic patients also had the significantly higher male ratio, type 2 diabetes and severer hepatic steatosis rates vs. hyperammonaemia-negative MAFLD individuals. In 8 weeks of LOLA therapy, the ALT, AST, GGT, ferritin and CRP levels decreased significantly, and blood ammonia attained normal range (p <0.001). Elastometry liver stiffness decreased in 22 (85 %) patients, reaching F0 values in 6 cases (p <0.001). The steatosis grade reduced in 18 (69 %) individuals.Conclusion. LOLA normalises blood ammonia levels and reduces the severity of inflammation, steatosis and liver fibrosis. 


Blood ◽  
1997 ◽  
Vol 90 (11) ◽  
pp. 4628-4633 ◽  
Author(s):  
Anna Locasciulli ◽  
Marina Testa ◽  
Patrizia Pontisso ◽  
Luisa Benvegnù ◽  
Donatella Fraschini ◽  
...  

The aim of this study was to ascertain prevalence and natural history of hepatitis C virus (HCV) infection in a large cohort of patients cured of childhood leukemia who had been followed prospectively for liver disease for at least 10 years since chemotherapy withdrawal: 114 consecutive patients entered the study. Liver function tests and ultrasonography were used to assess presence of liver disease. Patients were tested for antibody to HCV and for serum HCV-RNA at the end of chemotherapy and at the end of follow-up. At chemotherapy withdrawal, 56 patients (49%) were HCV-RNA positive, often without detectable anti-HCV, and in these cases, transaminase levels were more elevated during (P = .08) and after (P = .04) chemotherapy compared with HCV-RNA negative cases. Patients were then followed-up 13 to 27 years (mean, 17) after chemotherapy withdrawal. During this period, 38 initially anti-HCV negative patients seroconverted to anti-HCV and 17 initially anti-HCV positive cases lost reactivity. Forty patients were persistently HCV-RNA positive in serum, while 16 initially viremic patients became HCV-RNA negative during follow-up. At the end of the observation period, a persistent transaminase elevation was detected only in four HCV-RNA positive and anti-HCV positive cases, while no patient developed signs or symptoms of decompensated liver disease. Thus, hepatitis C was a frequent finding in long-term survivors after chemotherapy. It was associated with an atypical serologic profile and did not cause severe liver impairment over a period of 13 to 27 years.


1987 ◽  
Vol 57 (02) ◽  
pp. 196-200 ◽  
Author(s):  
R M Bertina ◽  
I K van der Linden ◽  
L Engesser ◽  
H P Muller ◽  
E J P Brommer

SummaryHeparin cofactor II (HC II) levels were measured by electroimmunoassay in healthy volunteers, and patients with liver disease, DIC, proteinuria or a history of venous thrombosis. Analysis of the data in 107 healthy volunteers revealed that plasma HC II increases with age (at least between 20 and 50 years). HC II was found to be decreased in most patients with liver disease (mean value: 43%) and only in some patients with DIC. Elevated levels were found in patients with proteinuria (mean value 145%). In 277 patients with a history of unexplained venous thrombosis three patients were identified with a HC II below the lower limit of the normal range (60%). Family studies demonstrated hereditary HC II deficiency in two cases. Among the 9 heterozygotes for HC II deficiency only one patient had a well documented history of unexplained thrombosis. Therefore the question was raised whether heterozygotes for HC II deficiency can also be found among healthy volunteers. When defining a group of individuals suspected of HC II deficiency as those who have a 90% probability that their plasma HC II is below the 95% tolerance limits of the normal distribution in the relevant age group, 2 suspected HC II deficiencies were identified among the healthy volunteers. In one case the hereditary nature of the defect could be established.It is concluded that hereditary HC II deficiency is as prevalent among healthy volunteers as in patients with thrombotic disease. Further it is unlikely that heterozygosity for HC II deficiency in itself is a risk factor for the development of venous thrombosis.


1985 ◽  
Vol 54 (03) ◽  
pp. 617-618 ◽  
Author(s):  
J C Kirchheimer ◽  
K Huber ◽  
P Polterauer ◽  
B R Binder

SummaryPlasma urokinase antigen levels were studied in 78 patients suffering from liver diseases. Blood was drawn before any specific medication was initiated. Impairment of liver function was comparable in all patients. In both groups of cirrhotic liver disease (alcoholic and non-alcoholic), normal levels of plasma urokinase antigen were found as compared to age-matched control groups. In both groups of patients with hepatomas (with or without a history of liver cirrhosis), however, significantly increased plasma urokinase antigen levels could be determined. These data indicate that an increase in plasma urokinase antigen might rather relate to malignant growth in liver disease than to impaired liver function.


2014 ◽  
Vol 25 (2) ◽  
pp. 75-83
Author(s):  
Md Akmat Ali ◽  
Farida Yeasmin ◽  
MN Nag

Drug induced liver disease is a global problem. The aims of the study are to know the recreational drugs causing harmful effect on liver, epidemiology of addiction; pathophysiology and their consequences. The major findings published to date concerning different agents causing addiction and liver disease, their implications with regard to understanding disease mechanisms and their amplitude or spectrum are described. Addiction not only invites lot of sufferings to the family and the country, but also responsible for different types of liver disease including fatty liver, hepatitis and liver failure; responsible for mortality and morbidity. Among the addiction causing substances alcohol playing the main role for liver disease worldwide. Indirect effects of addiction on liver are hepatitis B, hepatitis C and their complication, mainly due to contamination of sharing needle. Majority of people in Bangladesh are life long abstainer. Excessive alcohol beverages and other substances like heroin, amphetamine are not harmless, rather they can cause serious liver diseases. There are some differences in prevalence of addiction and liver diseases among countries. Intravenous drug users are affected both directly and indirectly due to contaminated needle sharing . DOI: http://dx.doi.org/10.3329/medtoday.v25i2.17926 Medicine Today 2013 Vol.25(2): 75-83


2019 ◽  
Vol 98 (8) ◽  
pp. 326-327 ◽  

Introduction: The umbilical vein can become recanalised due to portal hypertension in patients with liver cirrhosis but the condition is rarely clinically significant. Although bleeding from this enlarged vein is a known complication, the finding of thrombophlebitis has not been previously described. Case report: We report the case of a 62-year-old male with a history of liver cirrhosis due to alcoholic liver disease presenting to hospital with epigastric pain. A CT scan of the patient’s abdomen revealed a thrombus with surrounding inflammatory changes in a recanalised umbilical vein. The patient was managed conservatively and was discharged home the following day. Conclusion: Thrombophlebitis of a recanalised umbilical vein is a rare cause of abdominal pain in patients with liver cirrhosis.


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