Other names: 2,3-dinor 11B-Prostaglandin F2a, U
2,3-dinor-11β-PGF2α is a urinary metabolite of prostaglandin D2 (PGD2)—a lipid mediator produced from arachidonic acid via the cyclooxygenase (COX) pathway. Mast cells are a major source of PGD2. After PGD2 is released in tissues, it is rapidly converted into more stable downstream metabolites, including 11β-PGF2α and 2,3-dinor-11β-PGF2α, which are excreted in urine. Measuring these metabolites provides a noninvasive index of in-vivo PGD2 production and, by extension, mast-cell activation.
Also known as:
2,3-dinor-11β-PGF2α (urine)
Dinor-11β-PGF2α, U
PGD2 metabolite (urine)
u-PGD2-M (terminology varies by lab)
PGD2 is a potent bioactive mediator that can cause bronchoconstriction, vasodilation, increased vascular permeability, flushing, and nasal congestion. Elevated urinary PGD2 metabolites are therefore used as supportive evidence in conditions featuring mast-cell activation, such as:
Mast Cell Activation Syndrome (MCAS) and systemic mastocytosis
Aspirin-exacerbated respiratory disease (AERD) / NSAID-exacerbated respiratory disease
Allergic reactions and anaphylaxis (often transient spikes)
Chronic spontaneous urticaria, atopic asthma, allergic rhinitis
Some cutaneous mastocytosis flares and food/venom allergies during reactions
Important: This marker is supportive, not diagnostic on its own. It is typically interpreted alongside clinical symptoms and companion markers (e.g., serum tryptase, urinary N-methylhistamine, urinary leukotriene E4 [uLTE4]).
Specimen: Urine (often a spot sample normalized to creatinine; some centers may request a 24-hour collection).
Method: Usually LC-MS/MS for specificity and sensitivity.
Reporting units: Commonly pg/mg creatinine or ng/mmol creatinine (varies by laboratory).
Stability/handling: Keep cool; follow lab instructions carefully—improper handling can affect results.
There is no universal cut-off. Reference intervals and decision thresholds vary by lab, assay, and whether the sample is a spot vs. 24-hour collection. Always compare your value with the lab’s own reference range on the report.
Suggests increased PGD2 pathway activity, commonly due to mast-cell activation. Consider the clinical context:
Symptoms consistent with mast-cell mediator release (flushing, wheeze/bronchospasm, nasal congestion/rhinorrhea, abdominal cramping/diarrhea, hypotension during reactions).
Co-elevations in urinary N-methylhistamine, uLTE4, or a rise in serum tryptase during episodes (Δ tryptase ≥20% + 2 ng/mL over baseline supports mast-cell involvement).
Recent allergen exposure, anaphylaxis, or NSAID challenge in AERD can produce transient spikes.
Non-disease contributors / confounders (can raise or alter levels):
Medications:
COX inhibitors (NSAIDs, high-dose aspirin) generally suppress prostaglandin synthesis; however, in AERD, reactions to aspirin/NSAIDs are complex and can be accompanied by transient mediator surges during provocation.
Corticosteroids and mast-cell stabilizers (e.g., cromolyn) may lower levels over time.
Active infections, acute inflammation, or vigorous allergic exposure shortly before sampling.
Collection timing relative to symptom flares (levels can be episodic).
What to do next (clinically, with your clinician):
Correlate with symptom diary and consider paired sampling: one sample during/just after a flare and one baseline when asymptomatic.
Review companion markers (tryptase, uLTE4, N-methylhistamine).
Evaluate medication effects (NSAIDs, steroids, biologics like omalizumab, dupilumab; leukotriene modifiers).
If mast-cell disease is suspected, consider referral to allergy/immunology or hematology (for systemic mastocytosis evaluation when indicated).
A normal value does not exclude mast-cell activation—mediator release can be intermittent and time-sensitive to flares. If suspicion remains high, clinicians often:
Repeat testing during symptoms,
Check other mediators, and
Assess tryptase dynamics (baseline vs. event-related rise).
Usually of limited standalone significance. Very low levels may reflect COX inhibition (e.g., steady NSAID use) or effective anti-inflammatory / anti-mast-cell therapy.
Because no single mediator fits all patients or all timepoints, clinicians often combine:
Serum tryptase (baseline and during events),
Urinary leukotriene E4 (uLTE4) for cysteinyl-leukotriene pathway activity,
Urinary N-methylhistamine (histamine turnover),
Prostaglandin metabolites like 2,3-dinor-11β-PGF2α and 11β-PGF2α (PGD2 pathway).
This multi-analyte approach improves sensitivity for detecting mast-cell involvement.
Timing: Collect as close to symptom onset as practical (often within 4–6 hours) for flare assessment.
Diet & supplements: Typically minimal effect, but always follow lab prep instructions.
Meds: NSAIDs/aspirin, COX-2 inhibitors, corticosteroids, mast-cell stabilizers, and certain biologics can shift levels (direction depends on drug and clinical context). Share a full med list with your clinician.
Renal function & hydration: Creatinine-normalized reporting helps, but extreme hydration or renal impairment can still affect interpretation.
Support diagnosis of mast-cell–mediated conditions in the right clinical setting.
Document objective mediator release in patients with unexplained flushing, anaphylactoid episodes, or bronchospasm.
Monitor response to therapy (e.g., after starting leukotriene modifiers, cromolyn, antihistamines, or biologics) when measured consistently with the same lab/method.
Ask whether your lab prefers a first-morning spot urine (with creatinine) or a 24-hour collection.
If evaluating flares, plan to collect during symptoms and consider a baseline sample on a stable day.
Verify units and reference range on your specific report; keep copies for comparison over time.
If you’re on medications that may affect prostaglandins, do not stop them without medical guidance—interpretation can account for them.
Is this the same as 8-iso-PGF2α (F2-isoprostanes)?
No. F2-isoprostanes are markers of oxidative stress formed non-enzymatically. 2,3-dinor-11β-PGF2α reflects enzymatic PGD2 pathway activity, often tied to mast-cell activation.
Do I need both 11β-PGF2α and 2,3-dinor-11β-PGF2α?
Many labs measure one or both. Patterns can be informative, but either can serve as a surrogate for PGD2 production. Use the same lab and method for trend monitoring.
What’s a “good” level?
“Good/abnormal” depends on the lab-specific reference interval and your clinical picture. Elevated values are only actionable when correlated with symptoms and other markers.
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I have been using Healthmatters.io since 2021. I travel all over the world and use different doctors and health facilities. This site has allowed me to consolidate all my various test results over 14 years in one place. And every doctor that I show this to has been impressed. Because with any health professional I talk to, I can pull up historical results in seconds. It is invaluable. Even going back to the same doctor, they usually do not have the historical results from their facility in a graph format. That has been very helpful.
Karin
Advanced Plan Member since 2020
What fantastic service and great, easy-to-follow layouts! I love your website; it makes it so helpful to see patterns in my health data. It's truly a pleasure to use. I only wish the NHS was as organized and quick as Healthmatters.io. You've set a new standard for health tracking!
Paul
Healthmatters Pro Member since 2024
As a PRO member and medical practitioner, Healthmatters.io has been an invaluable tool for tracking my clients' data. The layout is intuitive, making it easy to monitor trends and spot patterns over time. The ability to customize reports and charts helps me present information clearly to my clients, improving communication and outcomes. It's streamlined my workflow, saving me time and providing insights at a glance. Highly recommended for any practitioner looking for a comprehensive and user-friendly solution to track patient labs!
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