Safety and efficacy of cyclooxygenase-2 inhibition for treatment of primary hypertrophic osteoarthropathy: A single-arm intervention trial.

COX, Cyclooxygenase COX-2 inhibitor HPGD, hydroxyprostaglandin dehydrogenase PGE2, prostaglandin E2 PHO, Primary hypertrophic osteoarthropathy Primary hypertrophic osteoarthropathy Prostaglandin SLCO2A1, solute carrier organic anion transporter family, member 2A1 Treatment

Journal

Journal of orthopaedic translation
ISSN: 2214-031X
Titre abrégé: J Orthop Translat
Pays: Singapore
ID NLM: 101625127

Informations de publication

Date de publication:
Jul 2019
Historique:
received: 28 06 2018
revised: 27 09 2018
accepted: 02 10 2018
entrez: 12 9 2019
pubmed: 12 9 2019
medline: 12 9 2019
Statut: epublish

Résumé

Primary hypertrophic osteoarthropathy (PHO) is a rare disease involving joint, bone and skin. Two underlying genes responsible for this disease-hydroxyprostaglandin dehydrogenase ( We recruited patients presenting to Peking Union Medical Hospital between January 2009 and December 2016 who were diagnosed with PHO. Participants were given the COX-2 inhibitor etoricoxib (60 mg once daily) and followed up for 9 months. Gene analysis was performed at baseline. The following data were collected at baseline and during treatment: visual analogue score (VAS), volume of the distal middle finger (VDMF), knee joint circumference (KJC), serum and urinary levels of prostaglandin E2 (PGE2) and PGE metabolite (PGE-M) and serum levels of inflammatory markers. A total of 27 patients were recruited, including seven patients with PHO type I (PHOAR1) carrying We found COX-2 inhibitor to be safe and effective for the treatment of PHO in our cohort. The underlying genes responsible for PHO suggest COX inhibitor as potential therapy, and our study demonstrates the efficacy and safety of this treatment.

Sections du résumé

BACKGROUND BACKGROUND
Primary hypertrophic osteoarthropathy (PHO) is a rare disease involving joint, bone and skin. Two underlying genes responsible for this disease-hydroxyprostaglandin dehydrogenase (
METHODS METHODS
We recruited patients presenting to Peking Union Medical Hospital between January 2009 and December 2016 who were diagnosed with PHO. Participants were given the COX-2 inhibitor etoricoxib (60 mg once daily) and followed up for 9 months. Gene analysis was performed at baseline. The following data were collected at baseline and during treatment: visual analogue score (VAS), volume of the distal middle finger (VDMF), knee joint circumference (KJC), serum and urinary levels of prostaglandin E2 (PGE2) and PGE metabolite (PGE-M) and serum levels of inflammatory markers.
RESULTS RESULTS
A total of 27 patients were recruited, including seven patients with PHO type I (PHOAR1) carrying
CONCLUSIONS CONCLUSIONS
We found COX-2 inhibitor to be safe and effective for the treatment of PHO in our cohort.
THE TRANSLATIONAL POTENTIAL OF THIS ARTICLE UNASSIGNED
The underlying genes responsible for PHO suggest COX inhibitor as potential therapy, and our study demonstrates the efficacy and safety of this treatment.

Identifiants

pubmed: 31508314
doi: 10.1016/j.jot.2018.10.001
pii: S2214-031X(18)30101-3
pmc: PMC6718875
doi:

Types de publication

Journal Article

Langues

eng

Pagination

109-118

Subventions

Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States

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Auteurs

Lu Yuan (L)

Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Shuaifuyuan No. 1, Dongcheng District, Beijing 100730, China.

Ruo-Xi Liao (RX)

Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Shuaifuyuan No. 1, Dongcheng District, Beijing 100730, China.

Yuan-Yuan Lin (YY)

Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Shuaifuyuan No. 1, Dongcheng District, Beijing 100730, China.

Yan Jiang (Y)

Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Shuaifuyuan No. 1, Dongcheng District, Beijing 100730, China.

Ou Wang (O)

Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Shuaifuyuan No. 1, Dongcheng District, Beijing 100730, China.

Mei Li (M)

Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Shuaifuyuan No. 1, Dongcheng District, Beijing 100730, China.

Xiao-Ping Xing (XP)

Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Shuaifuyuan No. 1, Dongcheng District, Beijing 100730, China.

Qian-Qian Pang (QQ)

Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Shuaifuyuan No. 1, Dongcheng District, Beijing 100730, China.

Evelyn Hsieh (E)

Section of Rheumatology, Department of Internal Medicine, Yale School of Medicine, P.O. Box 208031, New Haven, CT 06520, USA.

Wei-Bo Xia (WB)

Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Shuaifuyuan No. 1, Dongcheng District, Beijing 100730, China.

Classifications MeSH