Last reviewed by Dr. Dharmender Malik on 13 May 2026 · this article reflects the published primary literature and current clinical practice at FMRI Gurugram.
Introduction
Peptide receptor radionuclide therapy (PRRT) with Lu-177 DOTATATE — marketed as Lutathera — is a well-tolerated treatment for most patients with somatostatin-receptor-positive neuroendocrine tumours (NETs). In the NETTER-1 phase III trial, no patient withdrew from the Lu-177 DOTATATE arm because of treatment-related toxicity[1]. But "well-tolerated" is a population statement; an individual patient's experience depends on baseline organ function, prior treatments, and the specific tumour pattern.
This guide covers what to expect: the acute side effects during and after infusion, the bone marrow and kidney effects over the treatment course, the rare but recognised late effects (myelodysplastic syndrome and acute leukaemia), the differences with Ac-225 alpha PRRT, and the specific risks for patients with hormone-secreting tumours. Every figure is sourced to the original publication.
Why PRRT has the side effects it does
AI Overview · short answer
PRRT side effects come from three sources: (1) the amino-acid infusion that protects the kidneys, which causes most of the acute nausea and vomiting; (2) somatostatin receptor expression in normal tissues (kidney tubules, bone marrow precursors); and (3) the Lutetium-177 radiation itself, which produces transient cytopenia and rare late marrow effects[1][2].
Somatostatin receptors — particularly SSTR2 — are highly expressed on NET cells, which is what makes PRRT work. The same receptors are also expressed at lower levels on some normal tissues, including parts of the proximal renal tubule and bone marrow precursors[3]. This biology is the foundation of the side-effect profile.
A separate but related contributor is the amino-acid co-infusion (lysine plus arginine) that runs during and after each PRRT cycle. The amino acids saturate proximal tubular reabsorption, reducing kidney radiation dose by approximately 40 percent compared with no protection[4]. The trade-off is that amino-acid infusions reliably cause nausea — and this accounts for most of the acute symptoms patients experience on cycle day[5].
Acute side effects during and after infusion
AI Overview · what most patients experience
The most common acute side effects on PRRT cycle day are nausea (~59% of patients on NETTER-1), vomiting (~47%), and fatigue (~40%). Most of these are mild-to-moderate and most resolve within 24-48 hours. Severe (Grade 3/4) acute side effects are uncommon[1].
The NETTER-1 trial reported the following all-grade acute and short-term adverse events in the Lu-177 DOTATATE arm versus high-dose octreotide control[1]:
| Side effect | Lu-177 DOTATATE | Octreotide control |
|---|
| Nausea (any grade) | 59% | 12% |
| Vomiting (any grade) | 47% | 10% |
| Fatigue (any grade) | 40% | 27% |
| Abdominal pain (any grade) | 26% | 26% |
| Headache (any grade) | 16% | 5% |
The substantial difference in nausea and vomiting rates between the two arms reflects the amino-acid infusion, which the octreotide control patients did not receive. Most centres now use anti-emetic premedication (typically a 5-HT3 antagonist such as ondansetron, sometimes combined with a neurokinin-1 antagonist like aprepitant) to manage this[5]. Lysine-arginine-only amino-acid formulations produce less nausea than older compound amino-acid solutions and are now standard practice at most experienced centres[4].
Fatigue typically peaks in the days after each cycle and resolves over the following one to two weeks. It cumulates modestly across the four-cycle course but is rarely severe[1][2].
Bone marrow effects — cytopenia and the NETTER-1 grade rates
Lu-177 emits beta radiation with an effective tissue range of approximately 2.5 millimetres. Some of this radiation reaches active bone marrow, producing transient reductions in blood counts. The NETTER-1 trial reported the following Grade 3-4 hematologic events in the Lu-177 DOTATATE arm versus control[1]:
| Grade 3-4 event | Lu-177 DOTATATE | Octreotide control |
|---|
| Lymphopenia | 9% | 0% |
| Anaemia | 4% | 1% |
| Thrombocytopenia | 2% | 1% |
| Neutropenia | 1% | 0% |
In real-world experience reported by Brabander and colleagues — a cohort of 1,214 patients treated with Lu-177 DOTATATE at Erasmus MC — the rates of severe persistent cytopenia were broadly comparable to NETTER-1[6]. Most cytopenias recover between cycles and the four-cycle course completes on schedule. Bergsma and colleagues reported that severe (Grade 3-4) cytopenia lasting beyond three months occurred in approximately 11 percent of patients in a 274-patient cohort, more commonly in those with extensive prior chemotherapy or bone marrow involvement at baseline[7].
Standard management is dose-interval extension (delaying the next cycle by 2-4 weeks until recovery), occasional transfusion support, and rarely dose modification. Growth factor support is used selectively. Cycles are not routinely cancelled for transient cytopenia[8].
Kidney effects — short-term changes and long-term data
The kidneys are the dose-limiting organ for PRRT. Lu-177 DOTATATE is cleared by the kidneys, and the proximal renal tubules reabsorb a small fraction of the radioligand. The amino-acid co-infusion (lysine plus arginine, typically 50 g over 4 hours starting 30 minutes before each Lu-177 infusion) reduces kidney absorbed dose by approximately 40 percent[4].
In NETTER-1, no Grade 3-4 renal adverse events were reported in either arm[1]. The Brabander real-world cohort reported persistent clinically significant nephrotoxicity (defined as sustained reduction in creatinine clearance) in approximately 1.5 percent of 1,214 patients followed for a median of 49 months[6]. Bodei and colleagues, using detailed individual dosimetry, identified a kidney-dose threshold of approximately 28 Gy below which clinically significant nephrotoxicity is rare in patients without baseline risk factors[9].
Clinical note · renal protection
Baseline risk factors for PRRT nephrotoxicity include pre-existing chronic kidney disease, diabetes mellitus, hypertension, and prior nephrotoxic chemotherapy. Patients with these factors should be assessed with a measured glomerular filtration rate (Tc-99m DTPA or chromium-EDTA clearance) rather than relying on creatinine-based estimation, and may receive intensified amino-acid protection or modified dosing[10].
Standard monitoring during a four-cycle PRRT course includes serum creatinine and estimated GFR before each cycle and at follow-up. A measured GFR is typically repeated at the end of the course and at 12-month follow-up. Cycles are delayed for >25% drop in eGFR until recovery is documented[10].
Late effects — myelodysplastic syndrome and acute leukaemia
Long-term myeloid neoplasms — myelodysplastic syndrome (MDS) and acute leukaemia — are the most serious late effects of PRRT. They are uncommon but real, and their existence justifies the careful long-term haematological follow-up that accompanies the treatment.
The published rates, from the largest and longest-followed cohorts:
- Brabander et al. (Erasmus MC, n=1,214, median follow-up 49 months): MDS in 1.5%, acute leukaemia in 0.7%. Median time from start of PRRT to MDS development was 41 months[6].
- Sansovini et al. (Italian cohort, n=164): MDS in 1.8% during long-term follow-up[11].
- NETTER-1 final analysis (n=111 evaluable in Lu arm, median follow-up 76 months): 2 cases of MDS and 1 case of acute leukaemia, with no excess versus a control population[2].
Risk factors for MDS after PRRT include prior alkylating chemotherapy, prior external-beam radiotherapy to bone-marrow-containing areas, and persistent severe cytopenia during PRRT itself[12]. Patients with extensive prior cytotoxic exposure should have this risk discussed explicitly as part of informed consent, and may benefit from baseline bone marrow assessment before starting PRRT in selected cases[10].
Annual complete blood count monitoring is recommended for at least five years after completion of PRRT, and longer in patients with prior cytotoxic exposure[10].
How Ac-225 alpha PRRT differs in side effects
Ac-225 DOTATATE — alpha-emitter PRRT — is used as salvage therapy in patients who have progressed on Lu-177 DOTATATE. Alpha particles deposit far more energy per micrometre of tissue than beta particles, which produces meaningful differences in the side-effect profile.
The published evidence base for Ac-225 DOTATATE in NETs is smaller than for Lu-177 DOTATATE. Ballal and colleagues reported on 32 patients treated at AIIMS New Delhi: progression-free survival was prolonged in this heavily pre-treated cohort, with manageable acute toxicity. No Grade 4 nephrotoxicity was observed in short-term follow-up[13]. Kratochwil and colleagues — whose work has been more extensively published in Ac-225 PSMA than Ac-225 DOTATATE — have reported that hematologic and constitutional toxicity of Ac-225 is more pronounced than Lu-177, justifying its use as a second-line rather than first-line agent[14].
Governance · informed consent
Ac-225 DOTATATE is not yet a fully FDA-approved standard therapy for NETs. At FMRI we deliver it under the Helsinki Declaration framework with written informed consent that explicitly covers the more pronounced toxicity profile, the smaller evidence base, and the salvage-line role. Patient selection is restricted to those whose disease has progressed on Lu-177 DOTATATE with documented PSMA-positive or DOTATATE-positive uptake on follow-up imaging[15].
For a comparison of the broader alpha-versus-beta therapy framework, see our pillar guide: Alpha PRRT for NETs.
Hormone-secreting tumours and carcinoid crisis prevention
Patients whose NETs actively secrete bioactive amines or peptides — particularly carcinoid syndrome (serotonin), insulinoma (insulin), gastrinoma (gastrin), and VIPoma (vasoactive intestinal peptide) — face an additional risk during PRRT: sudden release of stored hormone from rapidly killed tumour cells. The clinical manifestation is a hormonal crisis, most commonly carcinoid crisis (severe flushing, hypotension or hypertension, bronchospasm, tachycardia, diarrhoea), which can be life-threatening if untreated[16].
The reported incidence of clinically significant carcinoid crisis during PRRT is approximately 1 percent of treated patients with active carcinoid syndrome, based on combined trial and real-world cohorts[16][1]. Prevention is standard practice at experienced centres and involves:
- Octreotide pre-medication. Patients with carcinoid syndrome typically receive an octreotide bolus 30-60 minutes before PRRT infusion, followed by continuous intravenous octreotide infusion through the procedure and for several hours afterward[16].
- Inpatient observation. First PRRT cycle in carcinoid-syndrome patients is typically performed with overnight monitored observation, with cardiac monitoring and intravenous access maintained throughout[16].
- Crisis kit at bedside. Additional octreotide, intravenous fluids, vasopressors, and antihistamines available for immediate use if a crisis develops[16].
For insulinoma patients, the risk is post-PRRT hypoglycaemia from sudden release of stored insulin; management involves continuous glucose monitoring and dextrose infusion as needed. For gastrinoma patients, sustained proton pump inhibitor coverage is maintained throughout the treatment course[17].
How PRRT side effects are managed at FMRI — and how to read this list
The management framework at FMRI is built on three principles: thorough pre-treatment counselling so that no side effect comes as a surprise; active monitoring at every visit (blood tests, kidney function, clinical review, weight, and symptoms); and prompt intervention for any side effect that occurs, including dose-interval extension or, in rare cases, dose modification. Hormone-secreting tumours follow the specific protocols above. Inpatient observation is standard for first cycles in higher-risk patients.
For patients reading this list and feeling concerned: the most useful framing is that nothing on this list is inevitable. Most patients complete the four-cycle course with mild-to-moderate transient nausea and fatigue, modest reductions in blood counts that recover between cycles, and no significant long-term effects. The serious side effects (severe persistent cytopenia, clinically significant nephrotoxicity, MDS) are uncommon — typically affecting 1-2% of patients — and are screened for, monitored, and managed actively when they occur[6].
The point of this guide is not to alarm but to inform: informed consent is meaningful only when the realistic picture is in front of you. If you are considering PRRT, the most useful next step is a consultation where the specific risks for your individual situation — your prior treatments, your baseline kidney and marrow function, your tumour type and behaviour — are discussed in detail.
Important
This article is general medical information for patient education and is not a substitute for individualised clinical advice. Decisions about PRRT and its management should be made with a qualified nuclear medicine team that knows your personal medical history, baseline organ function, and treatment context.
"In our PRRT practice at FMRI, the most common conversation with a new patient is not about whether PRRT will work — for the right indication it usually does — but about what side effects to expect and which ones to call us about immediately. The honest version of that conversation is what makes informed consent meaningful, not a formality."
Dr. Ishita B. Sen, MD · Director & Chief, Nuclear Medicine, FMRI
Personalised side-effect review · before you start PRRT
The realistic side-effect picture depends on your specific situation: prior chemotherapy, baseline kidney function, marrow reserve, and tumour type. FMRI's nuclear medicine team can walk you through what to expect from your PRRT course in detail before you start, so nothing on cycle day comes as a surprise.
Discuss your PRRT side-effect risk · WhatsApp +91 8800 988936
For patients & referring clinicians
Frequently asked questions
Q01
What are the most common side effects of PRRT?
The most common side effects, drawn from the NETTER-1 trial of 229 patients, are: nausea (59% of patients, mostly from the amino-acid co-infusion, mostly mild-to-moderate), vomiting (47%), fatigue (40%), and abdominal pain (26%) [1]. Mild reductions in blood counts (anaemia, thrombocytopenia, lymphopenia) are also common but usually transient and recover between cycles. Severe (Grade 3-4) acute side effects are uncommon — no patient in NETTER-1 discontinued treatment because of toxicity [1].
Q02
Is PRRT painful?
PRRT itself is not painful — it is delivered as an intravenous infusion through a peripheral cannula, no different from a routine chemotherapy infusion. Some patients experience mild abdominal discomfort during the amino-acid co-infusion, but this is not severe and typically resolves once the infusion completes [1]. There is no radiation sensation; the radiation is internal and does not produce skin reactions or local pain at the treatment site.
Q03
How long do PRRT side effects last?
Acute side effects (nausea, vomiting, fatigue) typically peak in the 24-48 hours after each cycle and resolve within one to two weeks. Modest reductions in blood counts reach their lowest point 4-6 weeks after each cycle and recover before the next cycle in most patients [1]. Fatigue may cumulate modestly across the four-cycle course and can take 6-12 weeks to fully resolve after the final cycle. The overwhelming majority of patients return to their usual activities within weeks of completing PRRT [6].
Q04
Can PRRT cause kidney damage?
Severe kidney damage from PRRT is uncommon. In the Brabander real-world cohort of 1,214 patients followed for a median of 49 months, persistent clinically significant nephrotoxicity occurred in approximately 1.5% [6]. NETTER-1 reported no Grade 3-4 renal events in the Lu-177 DOTATATE arm [1]. Risk is higher in patients with baseline chronic kidney disease, diabetes, hypertension, or prior nephrotoxic chemotherapy. The amino-acid co-infusion is the primary protective mechanism, reducing kidney absorbed dose by approximately 40% [4].
Q05
Can PRRT cause leukaemia?
Yes, rarely. Acute leukaemia after PRRT has been reported in approximately 0.7% of treated patients in the largest published real-world cohort (Brabander et al., n=1,214, median follow-up 49 months) [6]. Myelodysplastic syndrome — a related but distinct condition — has been reported in approximately 1.5% in the same cohort, with a median time from PRRT start to MDS development of 41 months [6]. Risk is higher with prior alkylating chemotherapy, prior external-beam radiotherapy, or persistent severe cytopenia during PRRT itself [12]. Annual complete blood count monitoring for at least 5 years after PRRT is standard [10].
Q06
What is carcinoid crisis and how is it prevented?
Carcinoid crisis is a sudden severe hormonal release that can occur when PRRT rapidly kills hormone-secreting NET cells. Symptoms include severe flushing, blood pressure swings, bronchospasm, tachycardia, and diarrhoea. The reported incidence in patients with active carcinoid syndrome is approximately 1% of treated patients [16]. Prevention is standard at experienced centres: octreotide bolus 30-60 minutes before PRRT infusion, continuous intravenous octreotide infusion through the procedure, inpatient overnight observation for the first cycle, and crisis-management kit available at bedside [16].
Q07
Does PRRT make my hair fall out?
No. PRRT does not cause hair loss. Hair loss is a side effect of cytotoxic chemotherapy, which damages rapidly dividing cells in hair follicles. PRRT works through targeted radiation delivered to somatostatin-receptor-expressing cells and does not affect hair follicles. Patients can expect their hair to remain unaffected throughout the four-cycle course [1].
Q08
Can I work during PRRT?
Most patients continue working during the four-cycle PRRT course, with brief time off around each cycle day. Each cycle requires one inpatient or extended outpatient day, with most patients returning to usual activities within 3-5 days. Fatigue is the most common reason patients reduce activity in the days after each cycle. Radiation safety precautions for the household (maintaining distance from young children and pregnant women for a few days) are simple and do not preclude working. Specific occupational guidance — for instance, healthcare workers or those with frequent close patient contact — is reviewed individually [10].
Q09
What is the risk of MDS after PRRT?
In the largest published real-world cohort (Brabander et al., n=1,214 patients followed for a median of 49 months), MDS occurred in approximately 1.5% of patients [6]. Sansovini et al. reported MDS in approximately 1.8% of a 164-patient cohort during long-term follow-up [11]. Risk is higher with prior alkylating chemotherapy, prior external-beam radiotherapy to bone-marrow-containing areas, and persistent severe cytopenia during PRRT. Annual complete blood count for at least 5 years after PRRT — and longer in higher-risk patients — is standard surveillance [10].
Q10
How is Alpha PRRT (Ac-225 DOTATATE) different in side effects?
Ac-225 alpha PRRT produces more pronounced hematologic and constitutional toxicity than Lu-177 beta PRRT because alpha particles deposit far more energy per micrometre of tissue [14]. The published evidence base for Ac-225 DOTATATE is smaller; Ballal et al. reported on 32 patients with manageable acute toxicity and no Grade 4 nephrotoxicity in short-term follow-up [13]. At FMRI, Ac-225 DOTATATE is used as salvage therapy after Lu-177 DOTATATE progression, delivered under the Helsinki Declaration framework with written informed consent that explicitly covers the toxicity differences [15].
Q11
When should I call my team during PRRT?
Contact your nuclear medicine team for: persistent fever or signs of infection; new or worsening shortness of breath; unusual bleeding or bruising; severe persistent nausea or vomiting beyond what was discussed; severe persistent fatigue beyond expectation; new pain or change in pain pattern; symptoms suggestive of hormonal crisis (severe flushing, blood pressure swings, breathing difficulty) if you have a hormone-secreting tumour; or any symptom that feels worrying or different. Earlier contact is always better than later. At FMRI, the nuclear medicine team is reachable through WhatsApp during the treatment course.
Q12
Can PRRT be repeated if I had side effects before?
Yes, in most cases. Repeat PRRT — "salvage Lutathera" — is an established option for patients whose disease progresses after an initial four-cycle course. Published response rates in the salvage setting are approximately 40-50% in patients whose tumours remain DOTATATE-positive on follow-up imaging [18]. Patients who experienced significant side effects during the first course are assessed carefully: baseline organ function (kidney, marrow) must support a second course, dose modifications may be considered, and the risk-benefit conversation is individualised. The decision is made in multidisciplinary review based on your specific situation [10].
Citations & references
All clinical numbers above are sourced from the primary literature listed below. Every reference links to the open journal page or the FDA archive — open in a new tab to verify.
[1] Strosberg J, El-Haddad G, Wolin E, et al. Phase 3 Trial of
177Lu-Dotatate for Midgut Neuroendocrine Tumors (NETTER-1).
N Engl J Med. 2017;376(2):125-135.
View source ↗[2] Strosberg JR, Caplin ME, Kunz PL, et al.
177Lu-Dotatate plus long-acting octreotide versus high-dose long-acting octreotide in patients with midgut neuroendocrine tumours (NETTER-1): final overall survival and long-term safety results.
Lancet Oncol. 2021;22(12):1752-1763.
View source ↗[3] Reubi JC, Schär JC, Waser B, et al. Affinity profiles for human somatostatin receptor subtypes SST1-SST5 of somatostatin radiotracers.
Eur J Nucl Med. 2000;27(3):273-282.
View source ↗[4] Rolleman EJ, Valkema R, de Jong M, et al. Safe and effective inhibition of renal uptake of radiolabelled octreotide by a combination of lysine and arginine.
Eur J Nucl Med Mol Imaging. 2003;30(1):9-15.
View source ↗[5] Hicks RJ, Kwekkeboom DJ, Krenning E, et al. ENETS Consensus Guidelines for the Standards of Care in Neuroendocrine Neoplasms: Peptide Receptor Radionuclide Therapy with Radiolabelled Somatostatin Analogues.
Neuroendocrinology. 2017;105(3):295-309.
View source ↗[6] Brabander T, van der Zwan WA, Teunissen JJM, et al. Long-Term Efficacy, Survival, and Safety of [
177Lu-DOTA
0,Tyr
3]octreotate in Patients with Gastroenteropancreatic and Bronchial Neuroendocrine Tumors.
Clin Cancer Res. 2017;23(16):4617-4624.
View source ↗[7] Bergsma H, van Lom K, Raaijmakers MHGP, et al. Persistent Hematologic Dysfunction After Peptide Receptor Radionuclide Therapy with
177Lu-DOTATATE: Incidence, Course, and Predicting Factors.
J Nucl Med. 2018;59(3):452-458.
View source ↗[8] Strosberg J, Wolin E, Chasen B, et al. Health-Related Quality of Life in Patients With Progressive Midgut Neuroendocrine Tumors Treated With
177Lu-Dotatate in the Phase III NETTER-1 Trial.
J Clin Oncol. 2018;36(25):2578-2584.
View source ↗[9] Bodei L, Cremonesi M, Ferrari M, et al. Long-term evaluation of renal toxicity after peptide receptor radionuclide therapy with
90Y-DOTATOC and
177Lu-DOTATATE: the role of associated risk factors.
Eur J Nucl Med Mol Imaging. 2008;35(10):1847-1856.
View source ↗[10] Bodei L, Mueller-Brand J, Baum RP, et al. The joint IAEA, EANM, and SNMMI practical guidance on peptide receptor radionuclide therapy (PRRNT) in neuroendocrine tumours.
Eur J Nucl Med Mol Imaging. 2013;40(5):800-816.
View source ↗[11] Sansovini M, Severi S, Ianniello A, et al. Long-term follow-up and role of FDG PET in advanced pancreatic neuroendocrine patients treated with
177Lu-D OTATATE.
Eur J Nucl Med Mol Imaging. 2017;44(3):490-499.
View source ↗[12] Goncalves I, Burbury K, Michael M, et al. Characteristics and outcomes of therapy-related myeloid neoplasms after peptide receptor radionuclide/chemoradionuclide therapy (PRRT/PRCRT) for metastatic neuroendocrine neoplasia: a single-institution series.
Eur J Nucl Med Mol Imaging. 2019;46(9):1902-1910.
View source ↗[13] Ballal S, Yadav MP, Bal C, et al. Broadening horizons with
225Ac-DOTATATE targeted alpha therapy for gastroenteropancreatic neuroendocrine tumour patients stable or refractory to
177Lu-DOTATATE PRRT: first clinical experience on the efficacy and safety.
Eur J Nucl Med Mol Imaging. 2020;47(4):934-946.
View source ↗[14] Kratochwil C, Bruchertseifer F, Giesel FL, et al.
225Ac-PSMA-617 for PSMA-Targeted α-Radiation Therapy of Metastatic Castration-Resistant Prostate Cancer.
J Nucl Med. 2016;57(12):1941-1944.
View source ↗[15] World Medical Association. Declaration of Helsinki — Ethical Principles for Medical Research Involving Human Subjects.
JAMA. 2013;310(20):2191-2194.
View source ↗[16] Strosberg JR, Halfdanarson TR, Bellizzi AM, et al. The North American Neuroendocrine Tumor Society Consensus Guidelines for Surveillance and Medical Management of Midgut Neuroendocrine Tumors.
Pancreas. 2017;46(6):707-714.
View source ↗[17] Pavel M, Öberg K, Falconi M, et al. Gastroenteropancreatic neuroendocrine neoplasms: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up.
Ann Oncol. 2020;31(7):844-860.
View source ↗[18] Severi S, Sansovini M, Ianniello A, et al. Feasibility and utility of re-treatment with
177Lu-DOTATATE in GEP-NENs relapsed after first-line PRRT.
Eur J Nucl Med Mol Imaging. 2015;42(13):1955-1963.
View source ↗[19] U.S. Food and Drug Administration. LUTATHERA (lutetium Lu 177 dotatate) prescribing information. Current label.
View source ↗[20] Singh S, Halperin D, Myrehaug S, et al.
177Lu-DOTATATE plus long-acting octreotide versus high-dose long-acting octreotide for the treatment of newly diagnosed, advanced grade 2-3, well-differentiated, gastroenteropancreatic neuroendocrine tumours (NETTER-2).
Lancet. 2024;403(10446):2807-2817.
View source ↗[21] Kwekkeboom DJ, de Herder WW, Kam BL, et al. Treatment with the radiolabeled somatostatin analog [
177Lu-DOTA
0,Tyr
3]octreotate: toxicity, efficacy, and survival.
J Clin Oncol. 2008;26(13):2124-2130.
View source ↗[22] Hope TA, Calais J, Zhang L, et al.
111In-Pentetreotide Scintigraphy Versus
68Ga-DOTATATE PET: Impact on Krenning Scores and Effect of Tumor Burden.
J Nucl Med. 2019;60(9):1266-1269.
View source ↗[23] Krenning EP, Kwekkeboom DJ, Bakker WH, et al. Somatostatin receptor scintigraphy with [
111In-DTPA-D-Phe
1]- and [
123I-Tyr
3]-octreotide: the Rotterdam experience with more than 1000 patients.
Eur J Nucl Med. 1993;20(8):716-731.
View source ↗[24] Bushnell DL Jr, O'Dorisio TM, O'Dorisio MS, et al.
90Y-edotreotide for metastatic carcinoid refractory to octreotide.
J Clin Oncol. 2010;28(10):1652-1659.
View source ↗[25] Sabet A, Ezziddin K, Pape UF, et al. Long-term hematotoxicity after peptide receptor radionuclide therapy with
177Lu-octreotate.
J Nucl Med. 2013;54(11):1857-1861.
View source ↗[26] Hicks RJ, Jackson P, Kong G, et al.
64Cu-SARTATE PET Imaging of Patients with Neuroendocrine Tumors Demonstrates High Tumor Uptake and Retention, Potentially Allowing Prospective Dosimetry for Peptide Receptor Radionuclide Therapy.
J Nucl Med. 2019;60(6):777-785.
View source ↗[27] Cremonesi M, Ferrari ME, Bodei L, et al. Correlation of dose with toxicity and tumour response to
90Y- and
177Lu-PRRT provides the basis for optimization through individualized treatment planning.
Eur J Nucl Med Mol Imaging. 2018;45(13):2426-2441.
View source ↗[28] Garske U, Sandström M, Johansson S, et al. Minor Changes in Effective Half-Life During Fractionated
177Lu-Octreotate Therapy.
Acta Oncol. 2012;51(1):86-96.
View source ↗[29] Strosberg J, Leeuwenkamp O, Siddiqui MK. Peptide receptor radiotherapy re-treatment in patients with progressive neuroendocrine tumors: A systematic review and meta-analysis.
Cancer Treat Rev. 2021;93:102141.
View source ↗[30] Hörsch D, Ezziddin S, Haug A, et al. Effectiveness and side-effects of peptide receptor radionuclide therapy for neuroendocrine neoplasms in Germany: A multi-institutional registry study with prospective follow-up.
Eur J Cancer. 2016;58:41-51.
View source ↗[31] Tafreshi NK, Doligalski ML, Tichacek CJ, et al. Development of Targeted Alpha Particle Therapy for Solid Tumors.
Molecules. 2019;24(23):4314.
View source ↗[32] Eychenne R, Chérel M, Haddad F, et al. Overview of the Most Promising Radionuclides for Targeted Alpha Therapy: The "Hopeful Eight".
Pharmaceutics. 2021;13(6):906.
View source ↗
About the Author
Dr. Ishita B. Sen
MBBS · MD (Nuclear Medicine) · DNB · Post-doctoral Fellowship, Memorial Sloan Kettering Cancer Center, New York
Director and Chief of Nuclear Medicine at Fortis Memorial Research Institute. Co-founder of Theranostic Physicians Private Limited (TPPL). Two decades of clinical practice in PSMA imaging and PSMA-directed radioligand therapy, with one of the largest Indian institutional experiences in Lu-PSMA.