I-123-MIBG (diagnostic)¹²³I-MIBG
Norepinephrine-analog imaging of neuroendocrine and catecholamine tumors
Quick Answer
I-123-MIBG is a norepinephrine analog taken up by the norepinephrine transporter (uptake-1) and stored in catecholamine vesicles, imaging pheochromocytoma, paraganglioma, neuroblastoma, and other neuroendocrine tumors. It is the diagnostic partner of therapeutic I-131-MIBG — a positive scan confirms avidity and gates MIBG therapy. The thyroid is blocked with stable iodine, and interfering drugs are held.
Mechanism
MIBG (metaiodobenzylguanidine) is a guanethidine/norepinephrine analog that enters adrenergic cells via the uptake-1 (norepinephrine) transporter and is stored in neurosecretory vesicles. Uptake therefore marks tissues with active catecholamine handling — the adrenal medulla and sympathetic/neural-crest tumors. Because uptake is transporter-mediated, drugs that block uptake-1 or deplete vesicles reduce it (false negatives).
Biodistribution
Physiologic uptake in salivary glands, liver, myocardium, spleen, bowel, and bladder; the normal adrenal medullae show faint or no uptake. Free iodide (inadequate labeling or in-vivo deiodination) localizes to thyroid and stomach — the reason for thyroid blockade.
Clinical Indications
- Pheochromocytoma / paraganglioma — localization and staging (though Ga-68-DOTATATE is now more sensitive for metastatic/head-and-neck/SDHx disease).
- Neuroblastoma — staging and response, with semiquantitative Curie and SIOPEN skeletal scores.
- Theranostic gate — documented MIBG avidity selects patients for I-131-MIBG therapy.
- Cardiac sympathetic innervation (H/M ratio) — a distinct application (see that page).
Protocol Notes
- Thyroid blockade (SSKI/Lugol or perchlorate) starting before and continuing after injection.
- Hold interfering drugs per protocol (see below).
- Typical adult activity ~10 mCi; LEHR collimator, 159 keV window.
- Planar + SPECT (SPECT/CT) at 24 h, sometimes with 48-h imaging; I-123 gives better image quality/dosimetry than diagnostic I-131-MIBG.
Interfering Drugs (Hold)
Labetalol, tricyclic antidepressants, sympathomimetics (decongestants), reserpine, cocaine, and certain calcium-channel blockers/antipsychotics reduce MIBG uptake and cause false negatives — reconcile the medication list before the study.
Interpretation Highlights
- Report avid disease sites; in neuroblastoma, apply Curie/SIOPEN semiquantitative scoring (post-induction score is prognostic).
- SPECT/CT improves localization and lesion detection.
- Confirm MIBG avidity before offering I-131-MIBG therapy.
I-123 vs I-131-MIBG
| I-123-MIBG (diagnostic) | I-131-MIBG | |
|---|---|---|
| Emission | γ 159 keV (imaging-ideal) | β⁻ (therapy) + γ 364 keV |
| Image quality | Superior | Poorer (high-energy γ) |
| Role | Diagnosis, avidity gate | Therapy (and post-therapy imaging) |
Reporting Checklist
- Describe avid disease sites and, for neuroblastoma, the Curie/SIOPEN score.
- State thyroid blockade and any held interfering drugs.
- Confirm suitability for I-131-MIBG therapy when relevant.
- Note physiologic myocardial/salivary/bowel and any free-iodide (thyroid/stomach) activity.
Common Pitfalls
- Medication interference causing false negatives (the commonest avoidable error).
- Inadequate thyroid blockade → thyroid/stomach free-iodide activity.
- Physiologic myocardial, brown-fat, and bowel uptake misinterpreted.
- Assuming MIBG suffices — SDHx/metastatic/head-and-neck disease is better imaged with DOTATATE.
Board Pearls
I-123-MIBG is a norepinephrine analog (uptake-1/NET-mediated) imaging pheo/para and neuroblastoma, and it is the diagnostic partner of therapeutic I-131-MIBG — a positive scan confirms avidity and gates MIBG therapy. Block the thyroid and hold interfering drugs (labetalol, tricyclics, sympathomimetics, reserpine).
In neuroblastoma, apply the Curie/SIOPEN semiquantitative scores — a falling post-induction score is prognostic — and use SPECT/CT for localization.
Ga-68-DOTATATE now outperforms MIBG for metastatic, head-and-neck, and SDHx paraganglioma (pseudohypoxia tumors are often MIBG-poor/FDG-avid), so genotype/scenario should drive tracer choice. Distinguish diagnostic I-123 (imaging-ideal γ) from therapeutic I-131-MIBG.
Related Pages
- Disease: pheochromocytoma/paraganglioma, neuroblastoma, neuroendocrine tumors.
- Therapy: I-131-MIBG; contrast tracer: DOTATATE PET agents.
- Pitfalls: Pearls, pitfalls & normal variants.
Figure / Diagram Suggestions
- An uptake-1 mechanism cartoon (NET transport → vesicular storage).
- A Curie/SIOPEN skeletal-scoring schematic (neuroblastoma).
- An interfering-drug checklist graphic.
Self-Check
Q1. By what transporter does MIBG enter cells, and what class of drugs causes false negatives?
Answer: The norepinephrine transporter (uptake-1); blockers include labetalol, tricyclics, sympathomimetics, and reserpine — hold them before imaging.
Q2. Why is I-123 preferred over I-131 for diagnostic MIBG imaging?
Answer: I-123's 159-keV γ gives superior image quality and lower dose than I-131's β⁻ + high-energy 364-keV γ (which is used for therapy).
Q3. A metastatic SDHB-related paraganglioma is MIBG-negative. What tracer is more appropriate and why?
Answer: Ga-68-DOTATATE — SDHx pseudohypoxia tumors are often MIBG-poor and SSTR-avid/FDG-avid, so DOTATATE is more sensitive for metastatic/HN/SDHx disease.
Q4. How is diagnostic I-123-MIBG used as a theranostic gate?
Answer: Documented MIBG avidity selects patients for I-131-MIBG therapy — non-avid disease will not respond.
Evidence & sources
https://nuc.med/mibg-i123/ Report an issue