Hypercalcemia After Cosmetic Oil Injections: Unraveling Etiology, Pathogenesis, and Severity

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Hypercalcemia After Cosmetic Oil Injections: Unraveling Etiology, Pathogenesis, and Severity. / Eldrup, Ebbe; Theilade, Simone; Lorenzen, Mette; Andreassen, Christine H.; Poulsen, Katrine H.; Nielsen, John E.; Hansen, Ditte; El Fassi, Daniel; Berg, Jais O.; Bagi, Per; Jørgensen, Anne; Blomberg Jensen, Martin.

I: Journal of Bone and Mineral Research, Bind 36, Nr. 2, 2021, s. 322-333.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Eldrup, E, Theilade, S, Lorenzen, M, Andreassen, CH, Poulsen, KH, Nielsen, JE, Hansen, D, El Fassi, D, Berg, JO, Bagi, P, Jørgensen, A & Blomberg Jensen, M 2021, 'Hypercalcemia After Cosmetic Oil Injections: Unraveling Etiology, Pathogenesis, and Severity', Journal of Bone and Mineral Research, bind 36, nr. 2, s. 322-333. https://doi.org/10.1002/jbmr.4179

APA

Eldrup, E., Theilade, S., Lorenzen, M., Andreassen, C. H., Poulsen, K. H., Nielsen, J. E., Hansen, D., El Fassi, D., Berg, J. O., Bagi, P., Jørgensen, A., & Blomberg Jensen, M. (2021). Hypercalcemia After Cosmetic Oil Injections: Unraveling Etiology, Pathogenesis, and Severity. Journal of Bone and Mineral Research, 36(2), 322-333. https://doi.org/10.1002/jbmr.4179

Vancouver

Eldrup E, Theilade S, Lorenzen M, Andreassen CH, Poulsen KH, Nielsen JE o.a. Hypercalcemia After Cosmetic Oil Injections: Unraveling Etiology, Pathogenesis, and Severity. Journal of Bone and Mineral Research. 2021;36(2):322-333. https://doi.org/10.1002/jbmr.4179

Author

Eldrup, Ebbe ; Theilade, Simone ; Lorenzen, Mette ; Andreassen, Christine H. ; Poulsen, Katrine H. ; Nielsen, John E. ; Hansen, Ditte ; El Fassi, Daniel ; Berg, Jais O. ; Bagi, Per ; Jørgensen, Anne ; Blomberg Jensen, Martin. / Hypercalcemia After Cosmetic Oil Injections: Unraveling Etiology, Pathogenesis, and Severity. I: Journal of Bone and Mineral Research. 2021 ; Bind 36, Nr. 2. s. 322-333.

Bibtex

@article{e55afb6c37fd4e1ea9ab6692e240c237,
title = "Hypercalcemia After Cosmetic Oil Injections: Unraveling Etiology, Pathogenesis, and Severity",
abstract = "Intramuscular injections of paraffin oil can cause foreign body granuloma formation and hypercalcemia. Macrophages with the ability to produce high levels of 1,25(OH)2D3 may induce the mineral disturbance, but no major series of patients have been published to date. Here, medical history, physical evaluation, biochemical, and urinary analysis for calcium homeostasis were obtained from 88 males, who 6 years previously had injected paraffin or synthol oil into skeletal muscle. Moreover, granuloma tissue from three men was cultured for 48 hours ex vivo to determine 1,25(OH)2D3 production supported by qPCR and immunohistochemistry of vitamin D metabolism and immune cell populations after treatment with 14 different drugs. The 88 men were stratified into men with hypercalcemia (34%), whereas normocalcemic men were separated into men with either normal (42%) or suppressed parathyroid hormone (PTH) (24%). All men had high calcium excretion, and nephrolithiasis was found in 48% of hypercalcemic men, 22% of normocalcemic men with normal PTH, and 47% of normocalcemic men with suppressed PTH. Risk factors for developing hypercalcemia were oil volume injected, injection of heated oil, high serum interleukin‐2 receptor levels, and high urine calcium. High 1,25(OH)2D3/25OHD ratio, calcium excretion, and low PTH was associated with nephrolithiasis. The vitamin D activating enzyme CYP27B1 was markedly expressed in granuloma tissue, and 1,25(OH)2D3 was released in concentrations corresponding to 40% to 50% of the production by human kidney specimens. Dexamethasone, ketoconazole, and ciclosporin significantly suppressed granulomatous production of 1,25(OH)2D3. In conclusion, this study shows that injection of large oil volumes alters calcium homeostasis and increases the risk of nephrolithiasis. Hypercalciuria is an early sign of disease, and high granulomatous 1,25(OH)2D3 production is part of the cause. Prospective clinical trials are needed to determine if ciclosporin, ketoconazole, or other drugs can be used as prednisolone‐sparing treatment. {\textcopyright} 2020 American Society for Bone and Mineral Research (ASBMR).",
keywords = "HYPERCALCEMIA, COSMETIC OILS, NEPHROLITHIASIS",
author = "Ebbe Eldrup and Simone Theilade and Mette Lorenzen and Andreassen, {Christine H.} and Poulsen, {Katrine H.} and Nielsen, {John E.} and Ditte Hansen and {El Fassi}, Daniel and Berg, {Jais O.} and Per Bagi and Anne J{\o}rgensen and {Blomberg Jensen}, Martin",
year = "2021",
doi = "10.1002/jbmr.4179",
language = "English",
volume = "36",
pages = "322--333",
journal = "Journal of Bone and Mineral Research",
issn = "0884-0431",
publisher = "Wiley-Blackwell",
number = "2",

}

RIS

TY - JOUR

T1 - Hypercalcemia After Cosmetic Oil Injections: Unraveling Etiology, Pathogenesis, and Severity

AU - Eldrup, Ebbe

AU - Theilade, Simone

AU - Lorenzen, Mette

AU - Andreassen, Christine H.

AU - Poulsen, Katrine H.

AU - Nielsen, John E.

AU - Hansen, Ditte

AU - El Fassi, Daniel

AU - Berg, Jais O.

AU - Bagi, Per

AU - Jørgensen, Anne

AU - Blomberg Jensen, Martin

PY - 2021

Y1 - 2021

N2 - Intramuscular injections of paraffin oil can cause foreign body granuloma formation and hypercalcemia. Macrophages with the ability to produce high levels of 1,25(OH)2D3 may induce the mineral disturbance, but no major series of patients have been published to date. Here, medical history, physical evaluation, biochemical, and urinary analysis for calcium homeostasis were obtained from 88 males, who 6 years previously had injected paraffin or synthol oil into skeletal muscle. Moreover, granuloma tissue from three men was cultured for 48 hours ex vivo to determine 1,25(OH)2D3 production supported by qPCR and immunohistochemistry of vitamin D metabolism and immune cell populations after treatment with 14 different drugs. The 88 men were stratified into men with hypercalcemia (34%), whereas normocalcemic men were separated into men with either normal (42%) or suppressed parathyroid hormone (PTH) (24%). All men had high calcium excretion, and nephrolithiasis was found in 48% of hypercalcemic men, 22% of normocalcemic men with normal PTH, and 47% of normocalcemic men with suppressed PTH. Risk factors for developing hypercalcemia were oil volume injected, injection of heated oil, high serum interleukin‐2 receptor levels, and high urine calcium. High 1,25(OH)2D3/25OHD ratio, calcium excretion, and low PTH was associated with nephrolithiasis. The vitamin D activating enzyme CYP27B1 was markedly expressed in granuloma tissue, and 1,25(OH)2D3 was released in concentrations corresponding to 40% to 50% of the production by human kidney specimens. Dexamethasone, ketoconazole, and ciclosporin significantly suppressed granulomatous production of 1,25(OH)2D3. In conclusion, this study shows that injection of large oil volumes alters calcium homeostasis and increases the risk of nephrolithiasis. Hypercalciuria is an early sign of disease, and high granulomatous 1,25(OH)2D3 production is part of the cause. Prospective clinical trials are needed to determine if ciclosporin, ketoconazole, or other drugs can be used as prednisolone‐sparing treatment. © 2020 American Society for Bone and Mineral Research (ASBMR).

AB - Intramuscular injections of paraffin oil can cause foreign body granuloma formation and hypercalcemia. Macrophages with the ability to produce high levels of 1,25(OH)2D3 may induce the mineral disturbance, but no major series of patients have been published to date. Here, medical history, physical evaluation, biochemical, and urinary analysis for calcium homeostasis were obtained from 88 males, who 6 years previously had injected paraffin or synthol oil into skeletal muscle. Moreover, granuloma tissue from three men was cultured for 48 hours ex vivo to determine 1,25(OH)2D3 production supported by qPCR and immunohistochemistry of vitamin D metabolism and immune cell populations after treatment with 14 different drugs. The 88 men were stratified into men with hypercalcemia (34%), whereas normocalcemic men were separated into men with either normal (42%) or suppressed parathyroid hormone (PTH) (24%). All men had high calcium excretion, and nephrolithiasis was found in 48% of hypercalcemic men, 22% of normocalcemic men with normal PTH, and 47% of normocalcemic men with suppressed PTH. Risk factors for developing hypercalcemia were oil volume injected, injection of heated oil, high serum interleukin‐2 receptor levels, and high urine calcium. High 1,25(OH)2D3/25OHD ratio, calcium excretion, and low PTH was associated with nephrolithiasis. The vitamin D activating enzyme CYP27B1 was markedly expressed in granuloma tissue, and 1,25(OH)2D3 was released in concentrations corresponding to 40% to 50% of the production by human kidney specimens. Dexamethasone, ketoconazole, and ciclosporin significantly suppressed granulomatous production of 1,25(OH)2D3. In conclusion, this study shows that injection of large oil volumes alters calcium homeostasis and increases the risk of nephrolithiasis. Hypercalciuria is an early sign of disease, and high granulomatous 1,25(OH)2D3 production is part of the cause. Prospective clinical trials are needed to determine if ciclosporin, ketoconazole, or other drugs can be used as prednisolone‐sparing treatment. © 2020 American Society for Bone and Mineral Research (ASBMR).

KW - HYPERCALCEMIA

KW - COSMETIC OILS

KW - NEPHROLITHIASIS

U2 - 10.1002/jbmr.4179

DO - 10.1002/jbmr.4179

M3 - Journal article

C2 - 32931047

VL - 36

SP - 322

EP - 333

JO - Journal of Bone and Mineral Research

JF - Journal of Bone and Mineral Research

SN - 0884-0431

IS - 2

ER -

ID: 250604058