Assessment of Bone Microarchitecture in Patients with Systemic Mastocytosis and its Association with Clinical and Biochemical Parameters of the Disease

Patients with systemic mastocytosis (SM) are at high risk of bone deterioration. However, the evaluation of bone microarchitecture in this disease remains unclear. We aimed to assess bone microarchitecture in patients with SM. This was a cross-sectional study of 21 adult patients with SM conducted in a quaternary referral hospital in Sao Paulo, Brazil. A healthy, age-, weight-, and sex-matched cohort of 63 participants was used to provide reference values for bone microarchitecture, assessed by high resolution peripheral quantitative computed tomography (HR-pQCT). Total volumetric bone mineral density (vBMD), cortical vBMD, and cortical thickness at the radius were significantly lower in the control group compared with the SM group (all P < 0.001). Patients with aggressive SM had significantly lower trabecular number (Tb.N) (P = 0.035) and estimated failure load (F.load) (P = 0.032) at the tibia compared with those with indolent SM. Handgrip strength was significantly higher in patients who had more Tb.N at the radius (rho, 0.46; P = 0.036) and tibia (rho, 0.49; P = 0.002), and lower who had more trabecular separation at the radius (rho, -0.46; P = 0.035) and tibia (rho, -0.52; P = 0.016). Strong and positive associations between F.load (rho, 0.75; P < 0.001) and stiffness (rho, 0.70; P < 0.001) at the radius, and between F.load at the tibia (rho, 0.45; P = 0.038) were observed with handgrip strength. In this cross-sectional study, aggressive SM was more susceptible to bone deterioration compared with indolent SM. In addition, the findings demonstrated that handgrip strength was associated with bone microarchitecture and bone strength.

Palavras-chave

Bone metabolism, HR-pQCT, Handgrip, Secondary osteoporosis, Tryptase

URI

https://observatorio.fm.usp.br/handle/OPI/58780

Referências

Alvarenga JC, 2022, OSTEOPOROSIS INT, V33, P1309, DOI 10.1007/s00198-021-06288-5
Alvarenga JC, 2017, OSTEOPOROSIS INT, V28, P1335, DOI 10.1007/s00198-016-3876-0
Biosse-Duplan M, 2009, AM J PATHOL, V174, P1426, DOI 10.2353/ajpath.2009.080871
Broesby-Olsen S, 2016, AM J HEMATOL, V91, P1069, DOI 10.1002/ajh.24490
Degboé Y, 2019, OSTEOPOROSIS INT, V30, P1235, DOI 10.1007/s00198-019-04918-7
Degboé Y, 2017, BONE, V105, P219, DOI 10.1016/j.bone.2017.09.005
Dobigny C, 1997, J CELL PHYSIOL, V173, P10, DOI 10.1002/(SICI)1097-4652(199710)173:1<10::AID-JCP2>3.0.CO;2-M
Figueiredo CP, 2022, INT J RHEUM DIS, V25, P1038, DOI 10.1111/1756-185X.14376
Fitzpatrick LA, 2003, P NATL ACAD SCI USA, V100, P6027, DOI 10.1073/pnas.0934373100
Fuller H, 2015, REV BRAS REUMATOL, V55, P352, DOI [10.1016/j.rbre.2014.07.010, 10.1016/j.rbr.2014.07.010]
Gehlen M, 2021, CALCIFIED TISSUE INT, V109, P685, DOI 10.1007/s00223-021-00887-4
GENANT HK, 1993, J BONE MINER RES, V8, P1137, DOI 10.1002/jbmr.5650080915
Greiner G, 2018, CLIN CHEM, V64, P547, DOI 10.1373/clinchem.2017.277897
Guillaume N, 2013, AM J MED, V126, DOI 10.1016/j.amjmed.2012.07.018
Hans D, 2011, J CLIN DENSITOM, V14, P302, DOI 10.1016/j.jocd.2011.05.005
Orsolini G, 2018, IMMUNOL ALLERGY CLIN, V38, P443, DOI 10.1016/j.iac.2018.04.013
Pardanani A, 2021, AM J HEMATOL, V96, P508, DOI 10.1002/ajh.26118
Rossini M, 2014, IMMUNOL ALLERGY CLIN, V34, P383, DOI 10.1016/j.iac.2014.01.011
Rossini M, 2011, BONE, V49, P880, DOI 10.1016/j.bone.2011.07.004
Seitz S, 2013, OSTEOPOROSIS INT, V24, P2325, DOI 10.1007/s00198-013-2305-x
Siebenhaar F, 2018, ALLERGY, V73, P1489, DOI 10.1111/all.13425
Theoharides TC, 2015, NEW ENGL J MED, V373, P163, DOI 10.1056/NEJMra1409760
Ulivieri FM, 2022, J CLIN MED, V11, DOI 10.3390/jcm11092284
Ulivieri FM, 2020, CALCIFIED TISSUE INT, V107, P551, DOI 10.1007/s00223-020-00749-5
Valent P, 2017, BLOOD, V129, P1420, DOI 10.1182/blood-2016-09-731893
van der Veer E, 2012, ALLERGY, V67, P431, DOI 10.1111/j.1398-9995.2011.02780.x

Coleções

Artigos e Materiais de Revistas Científicas - FM/MCM

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