Acute liver failure linked to OxyShred pre-workout supplement: A case report and review of literature

HE liver plays a key role in the synthesis of proteins, metabolism of toxins and drugs, and in modulation of immunity. In critically ill patients, hypoxic, toxic, and inflammatory insults can affect hepatic excretory, synthetic, and/or purification functions, leading to systemic complications such as coagulopathy, increased risk of infection, hypoglycemia, and acute kidney injury. In severe cases, hepatic encephalopathyorbraindysfunction(acuteliverfailure)may occur. Because of the lack of specificity of standard laboratory investigations, identifying liver injury or dysfunction in critically ill patients remains a significant challenge. In addition, the great heterogeneity of criteria used to define the consequences of liver insults increases the difficulties for the clinician to properly interpret hepatic biochemical abnormalities. In this review, we choose to defineliver injuryas an elevation in serum concentrations of routinely measured hepatic enzymes, including aminotransferases (aspartate aminotransferase [AST]; alanine aminotransferase, [ALT]), alkaline phosphatase (ALP), or!-glutamyl transpeptidase. Hepatic dysfunctionrefers to derangement of pathways related to synthetic or clearance function, including international normalized ratio (INR) and bilirubin.Hepatotoxicity refers to hepatic injury and dysfunction caused by a drug or another noninfectious agent. 1 Acute liver failuredesignates

This case report describes a patient with major depressive disorder (MDD) who developed acute hepatocellular liver injury after being treated with sertraline, a selective serotonin reuptake inhibitor (SSRI). The diagnosis of MDD was made two years prior, and the patient had previously responded partially to escitalopram and cognitive-behavioral therapy (CBT). Upon switching to sertraline 50 mg daily, the patient presented with severe symptoms indicative of acute liver injury, including elevated liver enzymes, jaundice, and gastrointestinal distress. Following the discontinuation of sertraline, the patient's liver function tests gradually normalized over a 90-day period, confirming the diagnosis of sertraline-induced hepatotoxicity. This case underscores the importance of continuous monitoring for potential liver injury in patients treated with sertraline. The findings contribute to the existing body of evidence on the hepatotoxic risks associated with SSRIs and highlight the need for personalized treatment strategies to mitigate adverse effects and enhance patient safety. Further research is needed to explore the long-term safety and efficacy of sertraline, particularly in vulnerable populations.

Globally, people are struggling with obesity. Many effective, nonconventional methods of weight reduction, such as herbal and natural dietary supplements, are increasingly being sought. Fat burners are believed to raise metabolism, burn more calories and hasten fat loss. Despite patient perceptions that herbal remedies are free of adverse effects, some supplements are associated with severe hepatotoxicity. The present report describes a young healthy woman who presented with fulminant hepatic failure requiring emergent liver transplantation caused by a dietary supplement and fat burner containing usnic acid, green tea and guggul tree extracts. Thorough investigation, including histopathological examination, revealed no other cause of hepatotoxicity. The present case adds to the increasing number of reports of hepatotoxicity associated with dietary supplements containing usnic acid, and highlights that herbal extracts from green tea or guggul tree may not be free of adverse effects. Until these products are more closely regulated and their advertising better scrutinized, physicians and patients should become more familiar with herbal products that are commonly used as weight loss supplements and recognize those that are potentially harmful.

Acute liver failure is a rare and devastating clinical condition resulting from sudden loss of hepatic parenchyma and metabolic function. The Scottish Liver Transplant Unit (SLTU) offers specialist management and emergency liver transplantation to patients with acute liver failure from across Scotland. To describe temporal changes in number of admissions, aetiology of acute liver failure, severity of disease at presentation and outcomes over a 22-year period. Retrospective analysis of the SLTU database, including all patients admitted with acute liver injury or acute liver failure between November 1992 and March 2014. There has been no change in the number of patients presenting with acute liver injury or failure secondary to paracetamol overdose, but a reduction in the number of admissions with acute liver injury or failure secondary to non paracetamol causes. Over time, disease severity at presentation has not changed in the paracetamol cohort; those with a non paracetamol aetiology have latterly presented with milder hepatic encephalopathy. Spontaneous survival rates improved significantly over time for those patients with acute liver failure due to paracetamol and non paracetamol aetiologies. The most marked improvement in survival is observed in the sickest patients meeting Kings College Hospital poor prognostic criteria. The number of admissions to the SLTU with acute liver failure is decreasing, due to reduced numbers of non paracetamol cases. Outcomes in this condition are improving, due to improvements in intensive care management and use of liver transplantation, and the increase in survival is most marked in patients meeting Kings College Hospital poor prognostic criteria.

Correction

Rodenticide (Yellow Phosphorus Poison)-Induced Hepatotoxicity in India: Constraints During Management

Acute Liver Failure Caused by Use of Fat Burner: A Case Report

Without a specific biomarker the diagnosis of drug-induced liver injury (DILI) relies on exclusion of other causes of liver injury. This review examines the importance of testing for hepatitis C (HCV) and hepatitis E (HEV) in patients with suspected DILI. Several national DILI registries have reported HCV and HEV infection in patients initially diagnosed with DILI. Particularly in patients with suspected DILI who have acute hepatocellular liver injury, acute HCV and acute HEV infection should be considered even in the absence of traditional risk factors. For HCV infection, testing for HCV RNA and HCV antibody are recommended. For HEV, the high prevalence of HEV IgG antibody means that HEV IgM antibody testing is suggested to exclude this infection. There should be a high clinical suspicion for acute HCV and HEV infection in patients with acute hepatocellular liver injury suspected of being due to DILI.

Fat burner-induced acute liver injury: Case series of four patients.

Pathogenesis of Liver Injury in Acute Liver Failure

Introduction Acute liver injury and progression to acute liver failure can be life-threatening conditions that require prompt careful clinical assessment and therapeutic management. Areas covered The aim of this article is to review the safety and side effect profile of pharmacological therapies used in the treatment of acute liver injury with specific focus on hepatic toxicity. We performed an extensive literature search with the terms ‘acute liver injury,’ ‘acute liver failure,’ ‘therapy,’ ‘safety,’ ‘adverse reactions’ and ‘drug induced liver injury.’ A thorough discussion of the main drugs and devices used in patients with acute liver injury and acute liver failure, its safety profile and the management of complications associated to therapy of these conditions is presented. Expert opinion Several pharmacological approaches are used in acute liver injury and acute liver failure in an empirical basis. Whilst steroids are frequently tried in serious drug-induced liver injury there is concern on a potential harmful effect of these agents because of the higher mortality in patients receiving the drug; hence, statistical approaches such as propensity score matching might help resolve this clinical dilemma. Likewise, properly designed clinical trials using old and new drugs for subjects with serious drug-induced liver injury are clearly needed.

Herpes simplex virus (HSV) hepatitis by definition constitutes disseminated herpes simplex infection; it is rare, with only approximately 130 cases reported in the literature. Although HSV hepatitis typically occurs in immunocompromised hosts, pregnancy—especially the third trimester, has been identified as a risk factor for its development. This is likely because of the fact that humoral and cell-mediated immunity decrease throughout pregnancy and nadir in the third trimester with decreased T-cell counts and altered B/T lymphocyte ratios. Here, we report on a patient with HSV 2 hepatitis in a previously healthy 27-year-old woman in her 23rd week of pregnancy. She initially presented with nausea, vomiting, and abdominal pain and was found to have acute hepatocellular liver injury and a systemic inflammatory response syndrome. Broad-spectrum antibiotics and acyclovir were promptly initiated. Liver biopsy, serum DNA polymerase chain reaction (PCR) as well as a labial ulcer culture and PCR were all positive for HSV 2. The patient recovered completely; however, her fetus did not survive. Review of the literature emphasizes that presentation with disseminated HSV infection typically occurs in the third trimester of pregnancy. This report emphasizes that abdominal pain combined with fever and hepatic dysfunction in pregnancy should prompt immediate consideration of the diagnosis of HSV hepatitis. Furthermore, given the high mortality rate and effective treatment, empiric treatment with acyclovir should be considered early in all potential cases.

Acute liver failure is a life-threatening condition characterized by acute liver injury, encephalopathy, and coagulopathy in a patient with preexisting liver disease. Etiologies are broad, but given the poor prognosis rapid recognition is key to treatment. Those diagnosed with acute liver failure should be treated in the ICU at a transplant facility. Acute liver injury itself can result from a wide array of causes, though elevation of AST and ALT rarely exceed the low 1,000s. We present a case of a patient with an acute change in mental status, found down with LFTs exceeding the upper limit of detection concerning for acute liver failure. A 57 year-old male with a history of alcoholism, HTN, COPD, and a-1 antitrypsin deficiency was found down surrounded by liquor bottles. Per his family, he had reported epigastric pain and trouble breathing for two weeks with several episodes of brown, non-bloody vomitus. He was afebrile, tachycardic, hypotensive requiring pressors, and was intubated for airway protection. Labs showed no leukocytosis, no coagulopathy, an elevated Creatinine of 1.94mg/dL, AST >7,000U/L, ALT of 2,907U/L, Lactate of 7.5mmol/L, and CK of 9,333U/L. Urine Toxicology, Salicylate Level, and Acetaminophen Level were all unremarkable. Given the alteration of mental status with LFTs beyond the upper limit of detection, there was concern for acute liver failure. The patient was admitted to the ICU, the nearest liver transplant center was contacted, and the gastroenterology service was consulted. In the absence of a coagulopathy, hyperbilirubinemia, thrombocytopenia, and no evidence of cirrhosis on imaging, it was decided that the patient's acute liver injury was multifactorial and due to causes other than fulminant hepatic failure. With aggressive fluid resuscitation for rhabdomyolysis, the patient's LFTs returned to normal levels. Comprised of acute liver injury, coagulopathy, and encephalopathy in a patient with preexisting liver disease, acute liver failure is a life-threatening condition that requires rapid diagnosis and treatment. Acute liver injury itself presents with an elevation in LFTs attributable to a number of etiologies, however these values rarely exceed the low 1,000s. Our case is unique as the elevated lab tests were attributable to rhabdomyolysis and acute liver injury, not hepatic failure. While extremes like this are rare, acute liver failure must be recognized and ruled out to ensure the best patient outcome.2242 Figure 1. An axial CT scan image of the patient's abdomen demonstrating a liver without findings suggestive of cirrhosis (nodularity, heterogeneity)

Hepatocellular Necrosis Associated With Labetalol

Do Hepatotoxicity Registries Have a Role in Health Care?