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MyDeficiencies

Lanreotide

somatostatin and analogues

Also sold as Somatuline Depot, Somatuline Autogel.

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Lanreotide is a cyclic octapeptide with no meaningful hepatic CYP450 substrate role and no renal electrolyte-wasting mechanism of its own; less than 5% of a dose is excreted unchanged in urine and less than 0.5% unchanged in feces, with the remainder cleared largely through peptide catabolism and biliary routes. Like octreotide, it has no classical enzyme-induction or renal-wasting depletion machinery. Its nutrient-relevant pathway is the same broad anti-secretory mechanism common to somatostatin analogs: high-affinity binding at SSTR2 and SSTR5 suppresses growth hormone and IGF-1, insulin and glucagon, the nocturnal TSH surge, gallbladder motility, meal-stimulated pancreatic enzyme and bicarbonate secretion, and gastric acid output.

somatostatin and analogues · ATC H01CB03 · also sold as Somatuline Depot and Somatuline Autogel and lanreotide acetate · reviewed 2026-09-26. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Lanreotide in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe
severe. ≥2 independent Tier A sources with this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate
moderate. ≥1 Tier A source with this drug in the cohort showing a real deficit, but bounded by exposure window, subgroup, frequency, or a functional (not circulating) marker.
Yellow — Low
low/theoretical. Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction/protective findings.
Not graded — disclosed evidence gap
Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: evidence gap. No Tier B/C evidence to support even yellow, and no circulating claim to rebut as white. A disclosed absence of evidence, not a finding of safety.

What the research found

Fat-soluble vitamins and trace elements

Orange — Moderate

See study details

Chronic somatostatin-analog therapy, lanreotide included, can suppress pancreatic enzyme output enough to cause clinically apparent exocrine pancreatic insufficiency, and patients who develop it show measurable vitamin and trace-element deficiency, but this is bounded to that diagnosed subgroup, not a universal finding.

Full detail, limits and 2 references

What the grade means here: moderate. ≥1 Tier A source with this drug in the cohort showing a real deficit, but bounded by exposure window, subgroup, frequency, or a functional (not circulating) marker. Orange

Limits on what this shows

  • Null findings: Neither study reports a comparator arm without any SSA exposure; both describe within-treatment prevalence rather than a placebo-controlled deficit. Lamarca 2018 did not itself measure fat-soluble vitamin or trace-element levels, only fecal elastase-1 and clinical EPI criteria.
  • At-risk subgroups: Patients with new or worsening steatorrhea, loose stools, or unexplained weight loss on chronic therapy; the Lamarca cohort's median time to EPI (2.9 months) was much shorter than Saif's median time to diagnosis (12 months), suggesting under-recognition rather than a uniformly late-onset process.

Regulatory status

FDA label (Section 5.6 / DailyMed): somatostatin analogs "reversibly inhibit secretion of pancreatic enzymes and bile acids, which may result in malabsorption of dietary fats and subsequent symptoms of steatorrhea, loose stools, abdominal bloating, and weight loss." The label does not name vitamin A, E, K, or any trace element specifically, and carries no monitoring mandate for them.

Population evidence

Lamarca et al, 2018, Expert Rev Gastroenterol Hepatol, PMID 29923433, prospective observational, n=50 GEP-NET patients on long-acting SSA (60% octreotide, 40%/20 patients lanreotide): 24% (12/50) developed SSA-induced exocrine pancreatic insufficiency (EPI) at a median of 2.9 months, confirmed by fecal elastase-1; 92% of those with EPI required pancreatic enzyme replacement therapy. Saif et al, 2020, Cancer Med J, PMID 32405630, retrospective chart review, n=110 GEP-NET patients on SSA (104 octreotide, 6 lanreotide/Somatuline Depot, not separately stratified): EPI confirmed in 19 patients by quantitative fecal fat testing; "deficiency of vitamins and trace elements was found in 11 of 19 patients who received supplementation," with a median time to EPI onset of 12 months.

Mechanism

Named, Tier A for lanreotide specifically at the upstream step: reduced meal-stimulated pancreatic enzyme and bicarbonate secretion (FDA label Section 12.2) impairs fat digestion, producing steatorrhea and, in a meaningful minority of patients, measurable fat-soluble vitamin and trace-element deficiency. The downstream vitamin/trace-element deficiency data (Saif 2020) come from a cohort in which lanreotide was a small, unstratified minority (6/110), so the deficit is confirmed for the SSA class with lanreotide present, not isolated to lanreotide.

Counter-evidence held on record

No contradicting Tier A evidence was found for the EPI-diagnosed subgroup specifically; the boundary here is one of subgroup and diagnostic under-recognition (Saif 2020 explicitly frames EPI as "under-recognized"), not of a null comparator study. Framing caution: this entry describes a deficit conditional on developing EPI, not a universal lanreotide effect. Lanreotide's own representation in both source cohorts is a minority (40% and 5.5% respectively), so this grade should be read as SSA-class evidence with lanreotide present, bounded accordingly, rather than a lanreotide-isolated finding.

  • Lamarca A, McCallum L, Nuttall C, Barriuso J, Backen A, Frizziero M, Leon R, Mansoor W, McNamara MG, Hubner RA, Valle JW. Somatostatin analogue-induced pancreatic exocrine insufficiency in patients with neuroendocrine tumors: results of a prospective observational study. Expert Rev Gastroenterol Hepatol. 2018;12(7):723-731. PMID 29923433. — Prospective, n=50 (60% octreotide, 40%/20 patients lanreotide). EPI in 24% (12/50), median onset 2.9 months; 92% of EPI patients required PERT.
  • Saif MW, Romano A, Smith MH, Patel RJ, Relias V. Chronic Use of Long-Acting Somatostatin Analogues (SSAs) and Exocrine Pancreatic Insufficiency (EPI) in Patients with Gastroenteropancreatic Neuroendocrine Tumors (GEP-NETs): An Under-recognized Adverse Effect. Cancer Med J. 2020;3(2). PMID 32405630. — Retrospective chart review, n=110 (104 octreotide, 6 lanreotide/Somatuline Depot, not stratified by outcome). EPI confirmed in 19 patients; vitamin/trace-element deficiency in 11 of 19.Lanreotide is a small (5.5%), unstratified minority of this cohort; findings are SSA-class evidence with lanreotide present, not lanreotide-isolated.

Vitamin B12

Yellow — Low

See study details

Lanreotide shares the pancreatic-protease-suppressing mechanism that depresses vitamin B12 in octreotide-treated patients, but no lanreotide-specific study or regulatory statement documents an actual B12 deficit, a meaningful asymmetry with the rest of its own drug class.

Full detail, limits and 1 references

What the grade means here: low/theoretical. Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction/protective findings. Yellow

Limits on what this shows

  • Null findings: None found either way for lanreotide specifically; this is a true data gap rather than a tested-and-refuted claim.
  • At-risk subgroups: Not established by direct evidence. By analogy to the octreotide finding, long-duration continuous high-dose depot therapy would be the plausible highest-risk subgroup if the mechanism holds for lanreotide as well.

Regulatory status

Neither the FDA label (2024 revision) nor the DailyMed label for Somatuline Depot mentions vitamin B12, cobalamin, or the Schilling test anywhere in the document; this was confirmed by two independent full-text searches during this review. This is a direct contrast with octreotide's FDA label, which explicitly states depressed B12 and abnormal Schilling tests have been observed and recommends monitoring.

Population evidence

None found. A PubMed search for "lanreotide AND vitamin AND B12" returned zero results on the date of this review.

Mechanism

Tier C, class extrapolation. Lanreotide, like octreotide, "inhibits meal-stimulated pancreatic secretions" and "reduces duodenal bicarbonate and amylase concentrations" (FDA label Section 12.2), the same class of anti-secretory action documented to depress B12 in a dedicated octreotide cohort (Plöckinger et al, 1990, J Clin Endocrinol Metab, PMID 2229321, independently verified for this review: n=10 acromegaly patients on long-term octreotide, serum B12 fell from 380±32 to 172±21 pmol/L, P=0.023, abnormal in 4/10). Lanreotide's somewhat broader receptor affinity profile (SSTR2 and SSTR5, versus octreotide's predominant SSTR2 binding) does not obviously rule this mechanism in or out; no lanreotide-specific test exists to say which way it falls.

Counter-evidence held on record

The absence of any B12 statement in lanreotide's own label, despite the FDA having reviewed and required this exact statement for octreotide, is itself a form of counter-evidence that the two drugs may not behave identically here. Do not present this as an established lanreotide deficiency by extension from octreotide. It is a plausible, unconfirmed, class-level hypothesis only, and the two drugs' regulatory histories on this specific point currently diverge.

  • Plöckinger U, Dienemann D, Quabbe HJ. Gastrointestinal side-effects of octreotide during long-term treatment of acromegaly. J Clin Endocrinol Metab. 1990;71(6):1658-1662. PMID 2229321. — Prospective, n=10, octreotide only (not lanreotide). Serum B12 declined significantly (P=0.023), abnormal in 4/10. Cited only as the class-member evidence underpinning the Vitamin B12 entry's Tier C extrapolation; independently re-verified for this review rather than taken on the companion octreotide dossier's word.Octreotide-only cohort; does not itself contain lanreotide data.

Vitamin D

Yellow — Low

See study details

The fat-malabsorption mechanism that would make vitamin D plausible is real and label-documented, but the one study most often cited for this class did not report which specific somatostatin analog its patients received, so it cannot be confirmed as lanreotide-specific evidence.

Full detail, limits and 2 references

What the grade means here: low/theoretical. Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction/protective findings. Yellow

Limits on what this shows

  • Null findings: Motylewska 2016 is itself the null finding for the SSA class as a whole, whichever analogs it covered: no drug-attributable vitamin D deficit was found.
  • At-risk subgroups: Not established by lanreotide-specific evidence. Laing et al, 2019, Neuroendocrinology, PMID 31550712, a narrative review (not drug-stratified, Tier C), notes deficiency of fat-soluble vitamins is described "particularly" among NET patients treated with somatostatin analogs generally, without isolating lanreotide.

Regulatory status

Not addressed by name in the FDA label beyond the general steatorrhea/fat-malabsorption warning (Section 5.6, see Fat-soluble vitamins entry above).

Population evidence

Motylewska et al, 2016, Nutr Cancer, PMID 27028957, controlled comparison, n=36 NET patients (subgrouped by somatostatin-analog, SSA, therapy or not) versus 16 controls: serum 25(OH)D did not differ significantly between NET patients and controls, and SSA therapy did not aggravate vitamin D deficiency within the NET group; both groups' average 25(OH)D met deficiency criteria regardless of SSA use. The abstract and reconstructed full record identify the treatment variable only as "somatostatin analog (SSA)," without naming octreotide, lanreotide, or a per-drug breakdown; full text was not accessible during this review (closed access, no PMC or open-access copy located), so which analog(s) were actually used could not be confirmed.

Mechanism

Named (Tier A, label): pancreatic enzyme and bile-acid suppression causing dietary fat malabsorption/steatorrhea, a plausible route to fat-soluble vitamin loss, equally applicable to lanreotide's anti-secretory profile. The downstream claim that this measurably lowers vitamin D status is Tier C for lanreotide specifically, since the one direct test available cannot be confirmed to have included lanreotide.

Counter-evidence held on record

Motylewska 2016 is a direct, class-level null result, whichever analogs its cohort used, and argues against assuming SSA therapy uniformly worsens vitamin D status. Do not present vitamin D as an established lanreotide deficiency: the most relevant available study found no drug-attributable effect, and its cohort's specific drug composition could not be verified during this review.

  • Laing E, Kiss NK, Michael M, Krishnasamy M. Nutritional Complications and the Management of Patients with Gastroenteropancreatic Neuroendocrine Tumors. Neuroendocrinology. 2020;110(5):430-442. PMID 31550712. — Narrative review, not drug-stratified. Describes fat-soluble vitamin and niacin deficiency in NET patients generally, "particularly" those on somatostatin analogs.Tier C: class-level review, no per-drug breakdown; not used to support a lanreotide-specific claim above yellow.
  • Motylewska E, Gawrońska J, Niedziela A, Melen-Mucha G, Ławnicka H, Komorowski J, Świętosławski J, Stępień H. Somatostatin Analogs and Tumor Localization Do Not Influence Vitamin D Concentration in Patients with Neuroendocrine Tumors. Nutr Cancer. 2016;68(3):428-434. PMID 27028957. — Controlled comparison, n=36 NET patients (SSA-treated and untreated subgroups) vs 16 controls. No SSA effect on 25(OH)D.Full text closed-access; the specific analog(s) used (octreotide, lanreotide, or both) could not be confirmed from the abstract or metadata during this review.

Niacin

Yellow — Low

See study details

Patients treated with lanreotide for carcinoid syndrome carry a real, well-documented risk of biochemical niacin deficiency, but this is driven by the tumor's own serotonin overproduction diverting dietary tryptophan away from niacin synthesis, not by lanreotide itself, and lanreotide's serotonin-suppressing action plausibly works in the opposite, protective direction.

Full detail, limits and 1 references

What the grade means here: low/theoretical. Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction/protective findings. Yellow

Limits on what this shows

  • Null findings: None located specifically testing whether SSA treatment changes niacin status in carcinoid-syndrome patients; this remains an untested direction in either sense.
  • At-risk subgroups: Patients with active, hormonally functioning carcinoid syndrome (the population for whom lanreotide is indicated), particularly with high urinary 5-HIAA or poor dietary protein intake; this is a pre-existing, indication-linked risk present before lanreotide is started, per Hard Rule 6 (confounding by indication).

Regulatory status

Not addressed in the FDA label; niacin/tryptophan status is not a labeled lanreotide effect.

Population evidence

Shah et al, 2005, Am J Gastroenterol, PMID 16181385, cross-sectional biochemical assessment, n=92 (36 carcinoid-syndrome patients, 32 carcinoid patients without syndrome, 24 non-carcinoid controls): biochemical niacin deficiency (whole-blood niacin number <130) in 27.8% (10/36) of carcinoid-syndrome patients versus 12.5% (4/32) of carcinoid patients without syndrome and 0% (0/24) of controls, P<0.05. Somatostatin-analog treatment status was not reported as an analyzed variable in this study.

Mechanism

Named, but disease-driven rather than drug-driven: functioning carcinoid tumors divert dietary tryptophan toward serotonin synthesis, reducing substrate available for endogenous niacin (NAD/NADP) synthesis. Lanreotide's own pharmacology (suppression of serotonin secretion, part of its therapeutic mechanism in carcinoid syndrome) would, if anything, be expected to reduce this diversion rather than worsen it; no study was located that directly measured niacin status before and after lanreotide treatment to confirm this predicted protective direction.

Counter-evidence held on record

The Shah 2005 cohort shows the deficiency tracks with carcinoid syndrome status (functioning tumor), not with any specific drug exposure; no comparator arm isolates SSA-treated from SSA-naive carcinoid-syndrome patients. Framing caution: this is a disease-driven finding relevant to lanreotide's own patient population, not a lanreotide-caused deficiency. It must never be marketed as "lanreotide depletes niacin"; if anything, the drug's intended antisecretory effect on the tumor plausibly reduces this risk over time, though that direction is unconfirmed.

  • Shah GM, Shah RG, Veillette H, Kirkland JB, Pasieka JL, Warner RRP. Biochemical assessment of niacin deficiency among carcinoid cancer patients. Am J Gastroenterol. 2005;100(10):2307-2314. PMID 16181385. — Cross-sectional, n=92 (36 carcinoid syndrome, 32 carcinoid without syndrome, 24 controls). Niacin deficiency 27.8% vs 12.5% vs 0%, P<0.05. No SSA-treatment variable analyzed.Disease/indication-driven finding, not a lanreotide-cohort drug-effect study; filed as context per Hard Rule 6, not as a drug-caused deficiency.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden

Yellow — Low

See study details

A human surgical-tissue study found mitochondrial ultrastructural damage in pituitary somatotropinoma cells from patients treated preoperatively with lanreotide, but this occurred as part of lanreotide-induced tumor-cell apoptosis, the drug's own anticancer mechanism, not as evidence of systemic mitochondrial toxicity in healthy tissue.

Full detail, limits and 1 references

What the grade means here: low/theoretical. Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction/protective findings. Yellow

Limits on what this shows

  • Null findings: None identified within this single study; comparator (non-lanreotide-treated) tissue showed markedly lower apoptosis grade, consistent with a drug effect on tumor tissue specifically.
  • At-risk subgroups: Not applicable in the deficiency sense — this finding is specific to somatotropinoma tumor tissue removed surgically, not to systemic or healthy-tissue exposure, and has not been examined in any non-tumor human tissue.

Regulatory status

Not addressed in the FDA label.

Population evidence

Waśko et al, 2003, Neuro Endocrinol Lett, PMID 14647007, n=35 patients with somatotropinoma-type pituitary tumors treated preoperatively with lanreotide before transsphenoidal adenomectomy; surgical specimens examined by light and electron microscopy and chromosomal-ladder assay. Apoptotic cells showed chromatin condensation and fragmentation, vacuolization, damage of the inner mitochondrial structure, and oligonucleosomal DNA fragmentation; the grade of apoptosis in lanreotide-treated macroadenomas ranged from 4.0% to 17.1% (mean 8.7±2.6%), versus no more than 3.5% in patients not preceded by lanreotide treatment.

Mechanism

Named as the drug's intended pharmacologic action: the study's own conclusion is that lanreotide-induced apoptosis "may be involved in the anticancer activity of somatostatin analogue" in tumor tissue. Mitochondrial ultrastructural damage was reported as one morphological feature of this induced apoptosis, not as an independent toxicity endpoint.

Counter-evidence held on record

None found; this is a single Tier A (lanreotide-specific, human) but tissue-restricted study and should not be over-weighted or generalized beyond pituitary tumor tissue. Per Hard Rule 2, this must not be filed as a systemic mitochondrial-burden or nutrient-deficiency claim: it describes the drug's own intended antitumor mechanism in target adenoma tissue removed at surgery, not an adverse effect on the patient's healthy mitochondria. It is graded yellow, not higher, specifically to prevent this tissue-specific, mechanism-of-action finding from being read as a general toxicity claim.

  • Waśko R, Jankowska AK, Kotwicka M, Liebert W, Sowiński J, Warchoł JB. Effects of treatment with somatostatin analogues on the occurrence of apoptosis in somatotropinomas. Neuro Endocrinol Lett. 2003;24(5):334-338. PMID 14647007. — Human, n=35, lanreotide administered preoperatively, surgical tissue examined. Mitochondrial ultrastructural damage as part of induced tumor-cell apoptosis. Independently verified via abstract reconstruction during this review, not cited from the companion octreotide dossier.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress

Yellow — Low

See study details

In a rat ovarian ischemia-reperfusion injury model that tested lanreotide directly (not merely a class relative), lanreotide reduced tissue oxidative and nitrosative stress markers rather than increasing them.

Full detail, limits and 1 references

What the grade means here: low/theoretical. Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction/protective findings. Yellow

Limits on what this shows

  • Null findings: None identified within this study; both lanreotide arms (pre-torsion and post-detorsion dosing) showed the same protective direction.
  • At-risk subgroups: Not applicable — this is a protective-direction finding in an acute surgical-injury disease model, not a risk finding, and has not been tested in chronic, non-injury dosing conditions typical of acromegaly or GEP-NET maintenance therapy.

Regulatory status

Not addressed in the FDA label.

Population evidence

Kalyoncu et al, 2020, J Obstet Gynaecol Res, PMID 32748523, animal study, 56 rats in seven groups including sham, surgical control, multiple octreotide-dosing arms, and single-dose lanreotide given before torsion or after detorsion: histopathological damage scores and tissue oxidative/nitrosative stress markers were significantly lower in both octreotide- and lanreotide-treated groups than in surgical controls, with lanreotide administered and analyzed as its own treatment arm, independently verified for this review.

Mechanism

Not fully characterized molecularly in this study; the direction (reduced oxidative/nitrosative markers in the lanreotide arms specifically) suggests a real pharmacologic antioxidant-adjacent effect of somatostatin-receptor agonism in acute ischemia-reperfusion injury, distinct from any nutrient-cofactor mechanism.

Counter-evidence held on record

None found contradicting the protective direction for lanreotide in this model. Reverse-direction finding: the opposite of a depletion claim. This is Tier B, single-study, animal, acute-injury-model evidence and must never be read as grounds for a consumer "lanreotide protects against oxidative stress" claim in routine chronic use, nor as grounds for withholding antioxidant nutrients. It exists here only to correct any circulating claim that lanreotide causes oxidative damage.

  • Kalyoncu S, Yılmaz B, Demir M, Tuncer M, Bozdağ Z, İnce O, Bozdayi MA, Ulusal H, Tayşi S. Octreotide and lanreotide decreased ovarian ischemia-reperfusion injury by improving oxidative and nitrosative stress in rats. J Obstet Gynaecol Res. 2020;46(10):2050-2058. PMID 32748523. — Animal, n=56 rats in 7 groups, lanreotide administered and analyzed as its own treatment arm (not merely alongside octreotide). Reduced oxidative/nitrosative stress markers vs surgical control. Independently verified via abstract reconstruction during this review.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Iron

Yellow — Low

See study details

Lanreotide transiently reduces gastric acidity, a mechanistic pathway toward impaired non-heme iron absorption, but a lanreotide-specific study shows the drug's therapeutic use for gastrointestinal angiodysplasia bleeding measurably raised hemoglobin and reduced iron-infusion needs, the opposite direction from depletion.

Full detail, limits and 1 references

What the grade means here: low/theoretical. Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction/protective findings. Yellow

Limits on what this shows

  • Null findings: None found testing iron absorption/status directly and specifically in lanreotide-treated patients outside the bleeding-disorder context.
  • At-risk subgroups: Unclear for the theoretical absorption-interference pathway; by contrast, the population studied for the therapeutic benefit is specifically patients with recurrent GI angiodysplasia bleeding, where iron status is expected to improve, not worsen, with treatment.

Regulatory status

FDA label (Section 12.2): lanreotide "produces transient, mild... reduced gastric acidity" as part of its pharmacodynamic profile; no iron-specific warning appears anywhere in the label.

Population evidence

No study directly measuring non-heme iron absorption in lanreotide-treated patients was located. Countervailing Tier A evidence: Frago et al, 2018, Scand J Gastroenterol, PMID 30621520, prospective, n=27 patients with recurrent GI angiodysplasia/obscure GI bleeding treated long-term with lanreotide (median 27.1 months): hemoglobin values improved significantly (P=.007), and blood/iron infusions and endoscopy frequency decreased significantly (P<.05) by the second year of treatment.

Mechanism

Named for the theoretical absorption-interference pathway (Mechanism A: gastric acid suppression reduces reduction/solubilization of non-heme dietary iron), Tier A for the gastric-acidity fact itself, Tier C for the downstream iron-absorption inference (drawn from general GI physiology, not lanreotide-specific data). Separately, the Frago 2018 hemoglobin improvement reflects lanreotide's intended hemostatic/antisecretory effect on bleeding angiodysplastic lesions, a distinct and better-evidenced mechanism working in the opposite direction.

Counter-evidence held on record

Frago 2018 is direct, Tier A, lanreotide-specific counter-evidence in the protective direction; this is a stronger and more direct counter-example than exists for most somatostatin-analog class members. Two opposite-direction pathways exist for this drug (theoretical acid-mediated absorption impairment versus a real, quantified hemostatic benefit in a specific bleeding-disorder population); neither is a general dietary iron effect, and the label carries no iron-specific warning in either direction.

  • Frago S, Alcedo J, Peña-Galo EM, Lázaro M, Ollero L, De la Llama N. Long-term results with lanreotide in patients with recurrent gastrointestinal angiodysplasias bleeding or obscure gastrointestinal bleeding. Benefits in efficacy and procedures consumption. Scand J Gastroenterol. 2018;53(12):1496-1502. PMID 30621520. — Prospective, n=27, lanreotide in cohort, median 27.1 months treatment. Hemoglobin improved (P=.007); blood/iron infusions decreased significantly (P<.05) by year 2.

Copper

Not graded — disclosed evidence gap

See study details

No mechanism, no drug-specific or class-level data, and no circulating consumer claim were found linking lanreotide to copper status.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: The mechanism screen identified no plausible pathway: lanreotide does not chelate copper, does not induce or inhibit any copper-dependent enzyme system named in its label, and is not renally wasting. A drug-specific literature search was attempted across multiple phrasings ("lanreotide copper," "lanreotide trace element," "lanreotide ceruloplasmin") and multiple hosts (PubMed search-listing pages, OpenAlex, Europe PMC) on separate occasions during this review; results returned were consistently off-target (radiotracer/nanoparticle chemistry papers unrelated to endogenous copper status, or unrelated somatostatin-receptor imaging studies), and several attempted follow-up queries were blocked by session-wide HTTP 429 rate-limiting shared across a concurrent multi-medication batch rather than returning confirmed zero-result searches every time.

Circulating-claim check

No claim about lanreotide and copper was found in three independent consumer/professional drug-reference checks (Drugs.com professional monograph, Drugs.com consumer side-effects page, RxList, Memorial Sloan Kettering patient education page), none of which name copper, zinc, or any trace element in connection with lanreotide.

Disclosure

This is a combination of a likely genuine evidence gap and a partially tooling-limited search. A future revision should re-run the literature search once host rate-limits have cleared, using additional phrasings.

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk

Yellow — Low

See study details

Lanreotide's suppression of the migrating motor complex and pancreatobiliary secretions is mechanistically identical to the pathway documented for octreotide altering small-bowel bacterial counts, but no lanreotide-specific microbiome or bacterial-overgrowth study was located despite a thorough search.

Full detail, limits and 1 references

What the grade means here: low/theoretical. Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction/protective findings. Yellow

Limits on what this shows

  • Null findings: None found either way for lanreotide specifically; a true data gap.
  • At-risk subgroups: By analogy to the octreotide precedent: continuous, higher-dose depot regimens plausibly carry more motility suppression than intermittent low-dose use, though this has not been tested for lanreotide.

Regulatory status

FDA label documents "loose stools" and steatorrhea as recognized GI effects of the anti-secretory mechanism (Section 5.6), consistent with, though not diagnostic of, altered small-bowel flora; no explicit "bacterial overgrowth/dysbiosis" language appears in the label.

Population evidence

None found specific to lanreotide. A PubMed search for "lanreotide AND (microbiome OR microbiota OR dysbiosis OR bacterial overgrowth)" returned zero results on the date of this review. The class-level precedent is Soudah et al, 1991, N Engl J Med, PMID 1944424 (independently verified for this review: n=5 scleroderma patients with bacterial overgrowth plus 6 healthy controls, octreotide only, not lanreotide), where low-dose octreotide increased migrating motor complex frequency, reduced breath hydrogen excretion, and improved symptoms.

Mechanism

Named, Tier C class extrapolation. Continuous dosing of a broad-spectrum somatostatin analog suppresses the interdigestive migrating motor complex and reduces pancreatobiliary secretions (both antibacterial and motility-promoting); lanreotide's FDA label documents the same core anti-secretory and GI-motility-relevant pharmacology (Section 12.2) as octreotide's, though the two drugs' distinct SSTR2/5 versus SSTR2-predominant binding profiles have not been directly compared for this specific effect.

Counter-evidence held on record

The Soudah 1991 precedent is itself a counter-example to a simple depletion framing even at the class level: low-dose octreotide treated, rather than caused, bacterial overgrowth in that specific scleroderma context. Whether this generalizes to lanreotide is untested. Direction is unconfirmed for lanreotide specifically and, in the one class-level study available, ran protective rather than harmful. Do not present this as a demonstrated "lanreotide harms the gut microbiome" claim.

  • Soudah HC, Hasler WL, Owyang C. Effect of octreotide on intestinal motility and bacterial overgrowth in scleroderma. N Engl J Med. 1991;325(21):1461-1467. PMID 1944424. — n=5 scleroderma patients with bacterial overgrowth plus 6 controls, octreotide only (not lanreotide). Increased migrating motor complex frequency, reduced breath hydrogen, improved symptoms. Independently re-verified for this review rather than taken on the companion octreotide dossier's word.Octreotide-only cohort; used solely as Tier C class-level precedent for the Gut microbiome risk entry.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

Oxygen delivery/utilization

Not graded — disclosed evidence gap

See study details

No mechanism was found by which lanreotide directly affects hemoglobin synthesis, erythropoietin, red-cell mass, or arterial oxygenation.

Full detail, limits and 1 references

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: The mechanism screen found no pathway for a direct lanreotide effect on oxygen-carrying capacity. The only oxygen-adjacent literature located is the same GI-angiodysplasia-bleeding literature discussed under Iron above (Frago et al, 2018, PMID 30621520), where hemoglobin improved as a downstream consequence of reduced bleeding from vascular lesions, not from any direct effect on erythropoiesis or oxygen transport. This is the drug's own intended clinical effect on a bleeding outcome, not a nutrient- or oxygen-delivery-style mechanism, so it is not filed as a graded finding here; it is cross-referenced under Iron, where the same source appears as primary evidence (see Overlap map). Attempts to search specifically for growth-hormone/IGF-1 suppression effects on erythropoietin or hematocrit (a theoretically distinct pathway, since GH/IGF-1 have their own erythropoietic effects and lanreotide suppresses both) were repeatedly blocked by PubMed bot-verification challenges during this review and could not be completed.

Circulating-claim check

No claim about lanreotide and oxygen delivery, hemoglobin, or anemia was found in the four consumer/professional references checked (Drugs.com x2, RxList, MSKCC).

Disclosure

The growth-hormone/erythropoietin angle in particular remains genuinely untested in this review due to tooling access, not confirmed absence of literature, and should be revisited in a future revision.

  • Frago S, Alcedo J, Peña-Galo EM, Lázaro M, Ollero L, De la Llama N. Long-term results with lanreotide in patients with recurrent gastrointestinal angiodysplasias bleeding or obscure gastrointestinal bleeding. Benefits in efficacy and procedures consumption. Scand J Gastroenterol. 2018;53(12):1496-1502. PMID 30621520. — Prospective, n=27, lanreotide in cohort, median 27.1 months treatment. Hemoglobin improved (P=.007); blood/iron infusions decreased significantly (P<.05) by year 2.

ATP production

Not graded — disclosed evidence gap

See study details

No study measuring lanreotide's effect on ATP synthesis, oxidative phosphorylation, or cellular energy output specifically was located, and the one relevant mitochondrial-structure study did not report any energy-production endpoint.

Full detail, limits and 1 references

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: The Waśko et al 2003 study cited under Mitochondrial burden (PMID 14647007) documented mitochondrial ultrastructural damage as a morphological feature of tumor-cell apoptosis but reported no ATPase activity, ATP concentration, or other functional energy-metabolism readout, unlike the equivalent octreotide literature (which includes a rat pancreatitis model measuring Na⁺-K⁺-ATPase and Ca²⁺-Mg²⁺-ATPase activity). No lanreotide-specific or class-level equivalent was located despite searches across multiple phrasings and hosts (PubMed, OpenAlex), some of which were degraded by rate-limiting during this review.

Circulating-claim check

No "low energy" or ATP-related claim attributed to lanreotide was found in the four consumer/professional references checked.

Disclosure

This category is kept separate from Mitochondrial burden per Hard Rule 7 even though both ultimately trace back to the same underlying gap in the literature (structural mitochondrial data exists in tumor tissue only; no ATP/energy-metabolism functional data exists at any tier for lanreotide). A future revision should re-search once rate-limiting has cleared, and should specifically look for any lanreotide analogue of the octreotide ATPase-activity literature.

  • Waśko R, Jankowska AK, Kotwicka M, Liebert W, Sowiński J, Warchoł JB. Effects of treatment with somatostatin analogues on the occurrence of apoptosis in somatotropinomas. Neuro Endocrinol Lett. 2003;24(5):334-338. PMID 14647007. — Human, n=35, lanreotide administered preoperatively, surgical tissue examined. Mitochondrial ultrastructural damage as part of induced tumor-cell apoptosis. Independently verified via abstract reconstruction during this review, not cited from the companion octreotide dossier.
All references used above
  1. FDA prescribing information, Somatuline Depot (lanreotide acetate) injection, NDA 022074, Supplement 32, 2024 revision. — Regulatory label. Clinical pharmacology, pharmacokinetics, warnings and precautions (cholelithiasis, glucose metabolism, thyroid, cardiac, steatorrhea), specific populations, drug interactions. Confirmed by full-text search to contain no mention of vitamin B12, cobalamin, Schilling test, iron, calcium, magnesium, potassium, zinc, copper, or electrolyte.
  2. DailyMed, Somatuline Depot (lanreotide acetate) injection, solution, label, Ipsen Biopharmaceuticals, Inc. — Regulatory label. Mechanism of action, pharmacodynamics, pharmacokinetics, warnings.
  3. WHO Collaborating Centre for Drug Statistics Methodology. ATC/DDD Index, H01CB03 (lanreotide). — ATC code and defined-daily-dose reference.
  4. Waśko R, Jankowska AK, Kotwicka M, Liebert W, Sowiński J, Warchoł JB. Effects of treatment with somatostatin analogues on the occurrence of apoptosis in somatotropinomas. Neuro Endocrinol Lett. 2003;24(5):334-338. PMID 14647007. — Human, n=35, lanreotide administered preoperatively, surgical tissue examined. Mitochondrial ultrastructural damage as part of induced tumor-cell apoptosis. Independently verified via abstract reconstruction during this review, not cited from the companion octreotide dossier.
  5. Kalyoncu S, Yılmaz B, Demir M, Tuncer M, Bozdağ Z, İnce O, Bozdayi MA, Ulusal H, Tayşi S. Octreotide and lanreotide decreased ovarian ischemia-reperfusion injury by improving oxidative and nitrosative stress in rats. J Obstet Gynaecol Res. 2020;46(10):2050-2058. PMID 32748523. — Animal, n=56 rats in 7 groups, lanreotide administered and analyzed as its own treatment arm (not merely alongside octreotide). Reduced oxidative/nitrosative stress markers vs surgical control. Independently verified via abstract reconstruction during this review.
  6. Frago S, Alcedo J, Peña-Galo EM, Lázaro M, Ollero L, De la Llama N. Long-term results with lanreotide in patients with recurrent gastrointestinal angiodysplasias bleeding or obscure gastrointestinal bleeding. Benefits in efficacy and procedures consumption. Scand J Gastroenterol. 2018;53(12):1496-1502. PMID 30621520. — Prospective, n=27, lanreotide in cohort, median 27.1 months treatment. Hemoglobin improved (P=.007); blood/iron infusions decreased significantly (P<.05) by year 2.
  7. Lamarca A, McCallum L, Nuttall C, Barriuso J, Backen A, Frizziero M, Leon R, Mansoor W, McNamara MG, Hubner RA, Valle JW. Somatostatin analogue-induced pancreatic exocrine insufficiency in patients with neuroendocrine tumors: results of a prospective observational study. Expert Rev Gastroenterol Hepatol. 2018;12(7):723-731. PMID 29923433. — Prospective, n=50 (60% octreotide, 40%/20 patients lanreotide). EPI in 24% (12/50), median onset 2.9 months; 92% of EPI patients required PERT.
  8. Saif MW, Romano A, Smith MH, Patel RJ, Relias V. Chronic Use of Long-Acting Somatostatin Analogues (SSAs) and Exocrine Pancreatic Insufficiency (EPI) in Patients with Gastroenteropancreatic Neuroendocrine Tumors (GEP-NETs): An Under-recognized Adverse Effect. Cancer Med J. 2020;3(2). PMID 32405630. — Retrospective chart review, n=110 (104 octreotide, 6 lanreotide/Somatuline Depot, not stratified by outcome). EPI confirmed in 19 patients; vitamin/trace-element deficiency in 11 of 19.Lanreotide is a small (5.5%), unstratified minority of this cohort; findings are SSA-class evidence with lanreotide present, not lanreotide-isolated.
  9. Laing E, Kiss NK, Michael M, Krishnasamy M. Nutritional Complications and the Management of Patients with Gastroenteropancreatic Neuroendocrine Tumors. Neuroendocrinology. 2020;110(5):430-442. PMID 31550712. — Narrative review, not drug-stratified. Describes fat-soluble vitamin and niacin deficiency in NET patients generally, "particularly" those on somatostatin analogs.Tier C: class-level review, no per-drug breakdown; not used to support a lanreotide-specific claim above yellow.
  10. Motylewska E, Gawrońska J, Niedziela A, Melen-Mucha G, Ławnicka H, Komorowski J, Świętosławski J, Stępień H. Somatostatin Analogs and Tumor Localization Do Not Influence Vitamin D Concentration in Patients with Neuroendocrine Tumors. Nutr Cancer. 2016;68(3):428-434. PMID 27028957. — Controlled comparison, n=36 NET patients (SSA-treated and untreated subgroups) vs 16 controls. No SSA effect on 25(OH)D.Full text closed-access; the specific analog(s) used (octreotide, lanreotide, or both) could not be confirmed from the abstract or metadata during this review.
  11. Shah GM, Shah RG, Veillette H, Kirkland JB, Pasieka JL, Warner RRP. Biochemical assessment of niacin deficiency among carcinoid cancer patients. Am J Gastroenterol. 2005;100(10):2307-2314. PMID 16181385. — Cross-sectional, n=92 (36 carcinoid syndrome, 32 carcinoid without syndrome, 24 controls). Niacin deficiency 27.8% vs 12.5% vs 0%, P<0.05. No SSA-treatment variable analyzed.Disease/indication-driven finding, not a lanreotide-cohort drug-effect study; filed as context per Hard Rule 6, not as a drug-caused deficiency.
  12. Plöckinger U, Dienemann D, Quabbe HJ. Gastrointestinal side-effects of octreotide during long-term treatment of acromegaly. J Clin Endocrinol Metab. 1990;71(6):1658-1662. PMID 2229321. — Prospective, n=10, octreotide only (not lanreotide). Serum B12 declined significantly (P=0.023), abnormal in 4/10. Cited only as the class-member evidence underpinning the Vitamin B12 entry's Tier C extrapolation; independently re-verified for this review rather than taken on the companion octreotide dossier's word.Octreotide-only cohort; does not itself contain lanreotide data.
  13. Soudah HC, Hasler WL, Owyang C. Effect of octreotide on intestinal motility and bacterial overgrowth in scleroderma. N Engl J Med. 1991;325(21):1461-1467. PMID 1944424. — n=5 scleroderma patients with bacterial overgrowth plus 6 controls, octreotide only (not lanreotide). Increased migrating motor complex frequency, reduced breath hydrogen, improved symptoms. Independently re-verified for this review rather than taken on the companion octreotide dossier's word.Octreotide-only cohort; used solely as Tier C class-level precedent for the Gut microbiome risk entry.
  14. Drugs.com. Somatuline Depot (lanreotide) professional prescribing information monograph. — Tier D consumer/professional drug reference mirroring the FDA label; used to cross-check circulating claims. Confirmed no mention of sodium, hyponatremia, electrolyte, B12, vitamin, iron, or calcium.
  15. Drugs.com. Lanreotide side effects (consumer reference). — Tier D consumer reference. Lists "Blood sodium decreased" as an uncommon (0.1%-1%) adverse event; this could not be corroborated against the FDA label, DailyMed, or Drugs.com's own professional monograph during this review and is disclosed, not graded, in Fails verification.
  16. RxList. Somatuline Depot (lanreotide) drug reference. — Tier D consumer/professional drug reference, cross-check for circulating nutrient claims; named only insulin/glucagon among hormone-adjacent substances, no vitamin/mineral claim found.
  17. Memorial Sloan Kettering Cancer Center. Lanreotide patient education page. — Tier D consumer reference, cross-check for circulating nutrient claims; no vitamin, mineral, or electrolyte named.
  18. Baldini L, Dell'Unto E, Di Pangrazio R, Laviano A, Rinzivillo M, Lamberti G, Andrini E, Panzuto F, Campana D. Niacin deficiency in carcinoid syndrome: Definitions, biomarkers, and a pragmatic framework for clinical assessment. Nutrition. 2026. PMID 42735610. — Recent review identified by title/authorship during this review as directly on-topic for the Niacin entry.Full abstract could not be retrieved: repeated HTTP 429 rate-limiting during this review. Not used as evidence beyond confirming the topic exists in the current literature; should be retrieved in a future revision.