Related Experiment Video
Updated: May 1, 2026

09:44
Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
Published on: November 27, 2019
10.7K
Fulminant hepatic failure with virtually undetectable serum alkaline phosphatase
Clinical Laboratory
|April 5, 2014
Summary
Fulminant hepatic failure as an initial symptom of Wilson's disease is rare but serious. Low alkaline phosphatase levels can be a key diagnostic clue for this condition.
Area of Science:
- Hepatology
- Genetic metabolic disorders
- Clinical diagnostics
Background:
- Wilson's disease is a rare autosomal recessive genetic disorder of copper metabolism.
- Fulminant hepatic failure (FHF) is an uncommon but severe presentation of Wilson's disease.
- High morbidity and mortality are associated with Wilson's disease presenting as FHF.
Observation:
- A young patient presented with FHF as the initial manifestation of Wilson's disease.
- Serum alkaline phosphatase levels were virtually undetectable in the patient.
- This unusual laboratory finding served as an early indicator for the diagnosis.
Findings:
- The case highlights the diagnostic utility of extremely low serum alkaline phosphatase in suspecting Wilson's disease.
- Liver transplantation was successfully performed, representing the definitive treatment for Wilsonian FHF.
- Discussion of laboratory clues aids in identifying this rare presentation.
Implications:
- Clinicians must maintain a high index of suspicion for Wilson's disease in cases of unexplained FHF.
- Early diagnosis and intervention are critical to prevent catastrophic outcomes.
- Understanding subtle laboratory findings can significantly improve patient management in Wilson's disease.
Related Concept Videos
Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test
271
In clinical practice, the direct measurement of hepatic blood flow to evaluate liver function presents significant challenges due to the intricate and specialized nature of the necessary techniques. Consequently, healthcare professionals often rely on empirical estimates derived from thorough patient examinations and liver function tests to gauge liver health. Among the tools at their disposal, the Child–Pugh and MELD scoring systems stand out for their ability to categorize and assess...
271
Hepatic Encephalopathy
53
DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic...
53
Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow
382
Chronic liver disease significantly impacts drug metabolism due to alterations in hepatic blood flow and enzyme accessibility. This disruption affects the body's pharmacokinetics—the movement and processing of drugs within the system. Key enzymes crucial for metabolizing medications become less accessible, changing how drugs are processed and utilized. Furthermore, liver disease influences the synthesis of plasma proteins, such as albumin and globulins, which play critical roles in drug...
382
Cirrhosis II: Pathophysiology
42
Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to...
42
Acute Pancreatitis II: Pathophysiology
46
The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
46
Chronic Pancreatitis II: Pathophysiology
30
Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
30

