Related Experiment Video

Updated: Jul 5, 2026

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
05:26

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction

Published on: May 28, 2019

Biochemical diagnosis of placental infarction/damage: acutely rising alkaline phosphatase

L Ranganath1, W Taylor, L John

  • 1Department of Clinical Biochemistry and Metabolic Medicine, Royal Liverpool University Hospital, Liverpool, UK. lrang@liv.ac.uk

Annals of Clinical Biochemistry
|May 17, 2008
PubMed

There are currently no simple tests in clinical use to detect acute placental damage. A case is described to demonstrate that a routinely used measurement such as alkaline phosphatase (ALP) can be employed to detect acute damage to the placenta. Seventeen serial blood samples, three pre-delivery, were collected from a 22-year-old primigravida who delivered a stillborn baby. Retrospectively, blood samples were analysed for total and heat-stable ALP as well as human chorionic gonadotropin (hCG) and alpha-fetoprotein (AFP) as a measure of placental function when an unusual pattern of change in ALP was noticed. Histological examination of the placenta revealed new and old placental infarcts. Total and heat-stable ALPs as well as AFP peaked by more than eight-, 19- and two-fold, respectively over 16 h. Plasma hCG fell sharply even before delivery of placenta by five-fold over 16 h before further falling slowly to baseline. The fall in hCG is also consistent with the placental damage being acute and critical. As far as we are aware this is the first description of changes in circulating proteins reflecting placental damage.

More Related Videos

A Plate-based Cytotoxicity Assay for the Assessment of Rat Placental Natural Killer Cell Cytolytic Function10:44

A Plate-based Cytotoxicity Assay for the Assessment of Rat Placental Natural Killer Cell Cytolytic Function

Published on: June 2, 2019

Related Concept Videos

Blood Studies for Cardiovascular System I: Cardiac Biomarkers01:20

Blood Studies for Cardiovascular System I: Cardiac Biomarkers

Cardiac biomarkers are enzymes, proteins, and hormones released into the blood when cardiac cells are injured. They are powerful tools for triaging.
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
Acute Coronary Syndrome III: Diagnostic Studies01:30

Acute Coronary Syndrome III: Diagnostic Studies

Diagnosing acute coronary syndrome or ACS begins with a thorough patient history. Notable symptoms include central, crushing chest pain radiating to the left arm, neck, jaw, or back, along with shortness of breath, sweating (diaphoresis), nausea, vomiting, dizziness, and palpitations.It is crucial to note any history of cardiac illnesses and assess risk factors, including age, gender, smoking, hypertension, diabetes, hyperlipidemia, and a sedentary lifestyle.During physical examination, vital...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

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...
Acute Coronary Syndrome I: Introduction01:30

Acute Coronary Syndrome I: Introduction

Acute Coronary Syndrome (ACS) encompasses a spectrum of heart conditions caused by sudden obstruction of coronary arteries, typically resulting from the rupture of an atherosclerotic plaque and subsequent thrombus (blood clot) formation. This obstruction can lead to partial or complete blockage of blood flow, causing varying degrees of myocardial ischemia or infarction.ACS includes the following clinical entities:Unstable Angina (UA)Non-ST-Elevation Myocardial Infarction (NSTEMI)ST-Elevation...
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...