The Ugly Side of Colchicine

We report a rare case of a 32-year-old male who ingested 32.4 to 54 mg of colchicine and presented after 44 hours. He developed progressive multiple organ failure with shock, acute kidney failure, troponemia, pancytopenia, absolute neutropenia, disseminated intravascular coagulation, acute liver failure, rhabdomyolysis, and lactic acidosis. He also developed electrolyte abnormalities and refractory hypoglycemia. Initial treatment consisted of activated charcoal, fluids, and broad-spectrum antibiotics with supportive treatment of mechanical ventilation, hemodialysis, vasopressors, N-acetylcysteine, colony-stimulating factors, and blood products. Literature shows potential benefit of colchicine-specific Fab fragments for acute toxicity with limited studies and is not currently available in the United States. Further research for N-acetylcysteine protocol for acute liver failure in colchicine toxicity and potential use of colchicine-specific Fab fragments is needed. Our case demonstrates the importance of early use of activated charcoal for ingestion overdose with the incorporation of poison control into multidisciplinary team for coordinated patient care.

Download Full-text

Acute Liver Failure in the United States

Seminars in Liver Disease ◽

10.1055/s-2003-42641 ◽

2003 ◽

Vol 23 (3) ◽

pp. 217-226 ◽

Cited By ~ 244

Keyword(s):

United States ◽

Liver Failure ◽

Acute Liver Failure ◽

The United States

Download Full-text

Acute Liver Failure in the United States

Annals of Internal Medicine ◽

10.7326/0003-4819-139-12-200312160-00024 ◽

2003 ◽

Vol 139 (12) ◽

pp. 1045 ◽

Cited By ~ 3

Author(s):

William M. Lee ◽

Anne Larson ◽

Robert Fontana ◽

George Ostapowicz

Keyword(s):

United States ◽

Liver Failure ◽

Acute Liver Failure ◽

The United States

Download Full-text

Acute Liver Failure in the United States

Annals of Internal Medicine ◽

10.7326/0003-4819-137-12-200212170-00002 ◽

2002 ◽

Vol 137 (12) ◽

pp. I

Keyword(s):

United States ◽

Liver Failure ◽

Acute Liver Failure ◽

The United States

Download Full-text

Etiology and Outcome of Acute Liver Failure: Experience from a Liver Transplantation Centre in Montreal

Canadian Journal of Gastroenterology ◽

10.1155/2002/328415 ◽

2002 ◽

Vol 16 (10) ◽

pp. 672-676 ◽

Cited By ~ 20

Author(s):

Geneviève Tessier ◽

Edith Villeneuve ◽

Jean-Pierre Villeneuve

Keyword(s):

Liver Transplantation ◽

Liver Injury ◽

Liver Failure ◽

Acute Liver Failure ◽

Rapid Development ◽

Significant Proportion ◽

Rare Condition ◽

Unknown Origin ◽

The United States ◽

Drug Induced

BACKGROUND: Acute liver failure is a rare condition in which massive liver injury is associated with the rapid development of hepatic encephalopathy. Although viral hepatitis and drug-induced liver injury are the most common causes, no specific etiology is found in a substantial proportion of cases reported from Europe and the United States.AIM: To determine the etiology and outcome of patients with acute liver failure in the authors’ institution.PATIENTS AND METHODS: The charts of 81 consecutive patients admitted to Saint-Luc between 1991 and 1999 were reviewed.RESULTS: The etiology was viral in 27 cases (33.2%), toxic or drug-induced in 22 (27.2%), of unknown origin in 22 (27.2%) and due to various causes in 10 (12.3%) (autoimmune, vascular, cancer). Of the 81 patients, 16% survived without liver transplantation, and 84% died or underwent liver transplantation. Survival without liver transplantation differed according to the mode of presentation: the survival rate was 27% in patients with hyperacute liver failure, 7% in those with acute liver failure and 0% in those with subacute liver failure. Among the 38 patients who underwent liver transplantation, survival one year after transplantation was 71%. In the 30 patients who died without liver transplantation, the main causes of death were cerebral edema and sepsis.CONCLUSIONS: Acute liver failure is associated with a high mortality, and liver transplantation is the treatment of choice. In a significant proportion of cases, the etiology remains undetermined and is probably related to yet unidentified hepatotropic viruses.

Download Full-text

HMGB1 and Extracellular Histones Significantly Contribute to Systemic Inflammation and Multiple Organ Failure in Acute Liver Failure

Mediators of Inflammation ◽

10.1155/2017/5928078 ◽

2017 ◽

Vol 2017 ◽

pp. 1-6 ◽

Cited By ~ 23

Author(s):

Runkuan Yang ◽

Xiaoping Zou ◽

Jyrki Tenhunen ◽

Tor Inge Tønnessen

Keyword(s):

Liver Failure ◽

Acute Liver Failure ◽

Multiple Organ Failure ◽

Organ Failure ◽

Systemic Inflammation ◽

Cell Injury ◽

Inflammatory Responses ◽

Multiple Organ ◽

Hepatocyte Regeneration ◽

Extracellular Histones

Acute liver failure (ALF) is the culmination of severe liver cell injury from a variety of causes. ALF occurs when the extent of hepatocyte death exceeds the hepatic regenerative capacity. ALF has a high mortality that is associated with multiple organ failure (MOF) and sepsis; however, the underlying mechanisms are still not clear. Emerging evidence shows that ALF patients/animals have high concentrations of circulating HMGB1, which can contribute to multiple organ injuries and mediate gut bacterial translocation (BT). BT triggers/induces systemic inflammatory responses syndrome (SIRS), which can lead to MOF in ALF. Blockade of HMGB1 significantly decreases BT and improves hepatocyte regeneration in experimental acute fatal liver injury. Therefore, HMGB1 seems to be an important factor that links BT and systemic inflammation in ALF. ALF patients/animals also have high levels of circulating histones, which might be the major mediators of systemic inflammation in patients with ALF. Extracellular histones kill endothelial cells and elicit immunostimulatory effect to induce multiple organ injuries. Neutralization of histones can attenuate acute liver, lung, and brain injuries. In conclusion, HMGB1 and histones play a significant role in inducing systemic inflammation and MOF in ALF.

Download Full-text