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CompletedNCT03401060DenosuMastUpdated Mar 31, 2026

Interest of Denosumab Treatment in Osteoporosis Associated to Systemic Mastocytosis

A Phase 3 interventional study of Denosumab and Placebo in Osteoporosis and Systemic Mastocytosis, sponsored by Assistance Publique - Hôpitaux de Paris. Completed at 11 sites in France. Open to participants aged 18 Years and older. Per ClinicalTrials.gov, last updated 2026-03-31.

Sponsored by Assistance Publique - Hôpitaux de Paris · Phase 3, Interventional, and Treatment

Phase
Phase 3
Study type
Interventional
Enrollment
24
Allocation
Randomized
Ages
18 Years and older
Sex
All
01

Study summary

The study is looking at the efficacy of subcutaneously administrated denosumab 60 mg every 6 months versus placebo after 3 years, by analyze of lumbar spine bone mineral density (BMD) in systemic mastocytosis.

Investigators hypothesize that use of denosumab subcutaneously in patients with osteoporosis related to systemic mastocytosis is effective and safe to improve bone mineral density and prevent new bone events, based on targeted specific RANKL secretion by mast cells and short half-life of denosumab.

Read the detailed description

Systemic mastocytosis (SM) represents a heterogenous group of disease characterized by abnormal proliferation of mast cells caused by activating mutations in c-Kit receptor; a tyrosine kinase family receptor present in mast cell that control cell proliferation. Prevalence of SM is estimated to 1/20 000 person. According to the World Health Organization (WHO) criteria (Johnson et al, 2009), SM can be separated into two different groups : indolent SM and aggressive SM.

Aggressive SM are defined by a poor prognostic disease either because of an important mast cell tumor mass as sarcoma mastocytosis or mast cell leukemia, or due to an association with an other myeloid hemopathy as myelodysplasic/myeloproliferative syndrome.

Indolent SM are the most common cases with a very good prognostic similar to general population. Symptoms related to mast cell proliferation in indolent SM are very various (Theoharides et al., 2015) and could be divided into 2 entities : those related to mast cell proliferation in tissue as the urticaria pigmentosa and those related to the mast cell degranulation.

There are many clinical relevant mediators released by mast cells after activation that could have putative effects on different systems as cardiovascular, cutaneous, neurologic, digestive, systemic, respiratory and musculoskeletal (Frenzel et al., 2013). Tryptase, histamine, prostaglandin, interleukine-6 and Tumor Necrosis Factor (TNF)-α are the most common and ubiquitous mediators released by mast cells but there are also some specific mediator targeting an organ as RANKL ; expression of RANKL by mast cells directly control regulation of osteoclast activity and is involved in osteoporosis associated to SM (Rabenhorst et al., 2013).

In systemic mastocytoses, bone lesions are found in about half of patients. A third have osteoporosis defined as a lumbar spine or hip bone T score of -2,5 Standard Deviation (SD) or less. In most cases, osteoporosis was complicated at least by one vertebral fracture with pain and functional disorders (Barete et al, 2010). The median time to fragility fracture after mastocytoses diagnosis is up to 5 years, even in very young population usually considering as low risk of fracture in non mastocytoses associated osteoporosis (Van de Veer et al., 2014)

By default, these patients are generally treated with bisphosphonate per os or intravenously with some efficiency on bone mineral density gain and bone turnover marker decrease (Rossini et al, 2014). However, no study with bisphosphonate in SM has showed durable prevention of new bone events and there are no randomized studies that proved their efficacy in systemic mastocytosis. Moreover, these drugs are not well tolerated in SM wether per os due to worsening of digestive symptoms by mast cells activation, or intravenously with an important number of acute phase characterized by some systemic symptoms as fever ; really experiences with intravenous biphosphonate but very increased in SM. Additional, the use of a bisphosphonate ask the question of the residual long-term effect of this drug that may be several years or even decades with a significant risk of atypical fracture secondary to a adynamic bone remodeling (Edwards et al. , 2013) and the long-term presence of crystals of bisphosphonate in the skeleton, particularly worrying in women of childbearing age. In postmenopausal osteoporosis, importance of residual long-term effect is weighted with advanced median age of patient. The fact that mostly patients with a systemic mastocytosis are young people led to restrict the use of bisphosphonate due to those effects.

Among different treatment available in post menopausal osteoporosis, the use of an anti-RANKL antibody, denosumab, in SM associated osteoporosis could be interesting. First, denosumab has already shown significant efficacy in the treatment of postmenopausal osteoporosis in women (Cummings et al , 2009). Second, this treatment is proposed every 6 months by a subcutaneous injection with very few side effects and half-life drug is shorter than biphosphonate with probably low residual long-time effect. Third, as mast cells expressed mainly RANKL with a direct role on bone turnover in SM. The use of a specific drug seems to be obvious and attractive.

02

Conditions studied

  • Osteoporosis
  • Systemic Mastocytosis

Keywords

  • Systemic mastocytosis
  • Osteoporosis
  • Bone mineral density (BMD)
  • Denosumab
  • RANKL
03

Who can participate

Ages eligible
18 Years and older
Sexes eligible
All
Accepts healthy volunteers
No

Inclusion criteria

  • Male or female >/= 18 years of age at time of informed consent
  • Willingness and ability to sign informed consent, comply with scheduled visits, treatment plan, laboratory tests and other study procedures.
  • Patient with Indolent systemic or cutaneous mastocytosis according to WHO criteria (Appendix 4) with any specific treatment including corticosteroid, chemotherapy and immunomodulating drugs.
  • Patient with:

    • osteoporosis defined as bone mineral density T score ≤ -2.5 at the lumbar spine, OR
    • osteopenia defined as BMD T-score >-2,5 and ≤ -1 at the lumbar spine and low energy fracture (defined as fractures that are associated with decreased bone mineral density. Are excluded fractures of skull, face, mandible, metacarpals, fingers, or toes, pathologic fracture, and fracture that are associated with severe trauma).

(in case of osteoarthritis at the lumbar spine, the T score at left femoral neck or total left hip can be used to define osteoporosis or osteopenia)

Exclusion criteria

Exclusion Criteria:

  • Patient with aggressive mastocytosis or/and Associated Hematologic Non-Mastocytosis Disease (AHNMD)
  • Patient with conditions that influence bone metabolism (primitive hyperparathyroidism, hyperaldosteronism, hypercorticism, etc …)
  • Patient treated with intravenous bisphosphonate within 1 year prior to enrolment or with any other antiosteoporotic treatment within 3 months before enrolment. (per os bisphosphonate, strontium ranelate) Calcium and vitamin supplementation will be accepted
  • Patient previously treated with denosumab
  • Patient with hypocalcemia and/or hypo25-hydroxyvitamin D level non substituted prior enrolment
  • Woman without contraceptive treatment if of childbearing age.
  • Pregnant or breastfeeding woman
  • Patient with contraindication to denosumab
  • Patient with medical, psychiatric or other conditions that may interfere with patient safety
  • Patient with dental problem that need any dental surgery within 6 months after enrolment.
  • Patient with clearance of creatinine less than 30 mL/min/1,73m2 (MDRD) or patient receiving dialysis
04

Study design

Phase
Phase 3
Primary purpose
Treatment
Allocation
Randomized
Intervention model
Parallel assignment
Masking
Double (Participant, Investigator)
Enrollment
24 participants (actual)

Study arms

  • Experimental
    Experimental medication 1

    Denosumab 60 mg subcutaneously injection with prefilled syringe

    Drug: Denosumab

  • Placebo comparator
    Experimental medication 2

    NaCl 0.9%, 20ml phial, solution for injection

    Drug: Placebo

Interventions

  • DrugDenosumab

    Each subcutaneous injection will occur every 6 months during 3 years for a total of 7 injections

    Also known as: XGeva®

  • DrugPlacebo

    Each subcutaneous injection will occur every 6 months during 3 years for a total of 7 injections

05

What researchers measure

Primary outcomes

  1. Analysis of the lumbar spine bone mineral density (BMD)

    Dual energy x-ray absorptiometry at lumbar spine (L2-L4)

    Time frame: 3 years

Secondary outcomes

  1. Occurrence of a low energy vertebral fracture and non vertebral fracture

    Lateral and front lumbar x-ray

    Time frame: Baseline, 1 year, 2 years and 3 years

  2. BMD at the total left hip

    Dual energy x-ray absorptiometry at lumbar spine (L2-L4)

    Time frame: Baseline, 3 years

  3. BMD at lumbar spine and the total left hip

    Dual energy x-ray absorptiometry at left femoral neck and total left hip

    Time frame: Baseline, 1 year, 2 years

  4. Biological assays with bone turnover marker of resorption and tryptase levels to assess mastocytosis activity

    Withdrawal of 45 ml of blood

    Time frame: Baseline, then every 6 months in 3 years

  5. Number of serious adverse events to evaluate drug tolerance

    * Biological assessment: complete blood count, creatinemia, electrolytes, aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, c-reactive protein (CRP), phosphocalcic analyses with calcemia, phosphoremia, parathormone, vitamin D (25-OH-D), β-Human Chorionic Gonadotropin (HCG) (if needed) * Clinical assessment: blood pressure, pulse, weight, height, PS, temperature

    Time frame: Every 6 months in 3 years

  6. Number of non-serious adverse events to evaluate drug tolerance

    * Biological assessment: complete blood count, creatinemia, electrolytes, aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, c-reactive protein (CRP), phosphocalcic analyses with calcemia, phosphoremia, parathormone, vitamin D (25-OH-D), β-Human Chorionic Gonadotropin (HCG) (if needed) * Clinical assessment: blood pressure, pulse, weight, height, PS, temperature

    Time frame: Every 6 months in 3 years

  7. Annual variation of BMD in placebo group and number of low energy fracture compared to historical postmenopausal data

    Dual energy x-ray absorptiometry at lumbar spine (L2-L4), left femoral neck and total left hip

    Time frame: Baseline, 1 year, 2 years, 3 years

06

Study locations

11 sites
  • Jean Minjoz Hospital, Dermatology department
    Besançon, 25030, France
  • Caen Hospital, Clinical haematology department
    Caen, 14033, France
  • Estaing Hospital, Cellular therapy and clinical haematology department
    Clermont-Ferrand, 63100, France
  • Lille CHRU Hospital, Internal medicine and clinical immunology department
    Lille, 59037, France
  • La Timone Hospital, Dermatology and cutaneous oncology department
    Marseille, 13385, France
  • Lapeyronie Hospital, Rheumatology and Immunology department
    Montpellier, 34295, France
  • La Pitié-Salpêtrière Hospital, Internal medicine and clinical immunology department
    Paris, 75013, France
  • Cochin Hospital, Rheumatology department
    Paris, 75014, France
  • Necker Hospital, Adult haematology department
    Paris, 75015, France
  • Strasbourg Hospital, Rheumatology department
    Strasbourg, 67098, France
  • Toulouse Hospital, Dermatology department
    Toulouse, 31060, France
07

References and documents

Publications

  • Johnson MR, Verstovsek S, Jorgensen JL, Manshouri T, Luthra R, Jones DM, Bueso-Ramos CE, Medeiros LJ, Huh YO. Utility of the World Heath Organization classification criteria for the diagnosis of systemic mastocytosis in bone marrow. Mod Pathol. 2009 Jan;22(1):50-7. doi: 10.1038/modpathol.2008.141. Epub 2008 Sep 19. PubMed 19116630 ↗
  • Theoharides TC, Valent P, Akin C. Mast Cells, Mastocytosis, and Related Disorders. N Engl J Med. 2015 Jul 9;373(2):163-72. doi: 10.1056/NEJMra1409760. No abstract available. PubMed 26154789 ↗
  • Frenzel L, Hermine O. Mast cells and inflammation. Joint Bone Spine. 2013 Mar;80(2):141-5. doi: 10.1016/j.jbspin.2012.08.013. Epub 2012 Oct 30. PubMed 23116710 ↗
  • Rabenhorst A, Christopeit B, Leja S, Gerbaulet A, Kleiner S, Forster A, Raap U, Wickenhauser C, Hartmann K. Serum levels of bone cytokines are increased in indolent systemic mastocytosis associated with osteopenia or osteoporosis. J Allergy Clin Immunol. 2013 Nov;132(5):1234-1237.e7. doi: 10.1016/j.jaci.2013.06.019. Epub 2013 Jul 31. No abstract available. PubMed 23910691 ↗
  • Barete S, Assous N, de Gennes C, Grandpeix C, Feger F, Palmerini F, Dubreuil P, Arock M, Roux C, Launay JM, Fraitag S, Canioni D, Billemont B, Suarez F, Lanternier F, Lortholary O, Hermine O, Frances C. Systemic mastocytosis and bone involvement in a cohort of 75 patients. Ann Rheum Dis. 2010 Oct;69(10):1838-41. doi: 10.1136/ard.2009.124511. Epub 2010 Jun 22. PubMed 20570833 ↗
  • van der Veer E, Arends S, van der Hoek S, Versluijs JB, de Monchy JGR, Oude Elberink JNG, van Doormaal JJ. Predictors of new fragility fractures after diagnosis of indolent systemic mastocytosis. J Allergy Clin Immunol. 2014 Dec;134(6):1413-1421. doi: 10.1016/j.jaci.2014.05.003. Epub 2014 Jun 27. PubMed 24985401 ↗
  • Rossini M, Zanotti R, Viapiana O, Tripi G, Idolazzi L, Biondan M, Orsolini G, Bonadonna P, Adami S, Gatti D. Zoledronic acid in osteoporosis secondary to mastocytosis. Am J Med. 2014 Nov;127(11):1127.e1-1127.e4. doi: 10.1016/j.amjmed.2014.06.015. Epub 2014 Jun 20. PubMed 24954632 ↗
  • Edwards BJ, Bunta AD, Lane J, Odvina C, Rao DS, Raisch DW, McKoy JM, Omar I, Belknap SM, Garg V, Hahr AJ, Samaras AT, Fisher MJ, West DP, Langman CB, Stern PH. Bisphosphonates and nonhealing femoral fractures: analysis of the FDA Adverse Event Reporting System (FAERS) and international safety efforts: a systematic review from the Research on Adverse Drug Events And Reports (RADAR) project. J Bone Joint Surg Am. 2013 Feb 20;95(4):297-307. doi: 10.2106/JBJS.K.01181. PubMed 23426763 ↗
  • Cummings SR, San Martin J, McClung MR, Siris ES, Eastell R, Reid IR, Delmas P, Zoog HB, Austin M, Wang A, Kutilek S, Adami S, Zanchetta J, Libanati C, Siddhanti S, Christiansen C; FREEDOM Trial. Denosumab for prevention of fractures in postmenopausal women with osteoporosis. N Engl J Med. 2009 Aug 20;361(8):756-65. doi: 10.1056/NEJMoa0809493. Epub 2009 Aug 11. PubMed 19671655 ↗

Individual participant data

Plan to share: No

08

Registry details

Key details

Study ID
NCT03401060
Lead sponsor
Assistance Publique - Hôpitaux de Paris
Collaborators
CEREMAST, URC-CIC Paris Descartes Necker Cochin
Responsible party
Sponsor
First posted
Jan 17, 2018
Start date
Mar 5, 2018
Primary completion
Mar 11, 2024
Completion
Mar 11, 2024
Last update
Mar 31, 2026

Study contacts

Olivier Hermine, MD
study director · Assistance Publique - Hôpitaux de Paris
Laurent FRENZEL, MD
principal investigator · Assistance Publique - Hôpitaux de Paris

Oversight

Data monitoring committee
No
FDA-regulated drug
No
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

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