Shoulder adhesive capsulitis and hypercholesterolemia: role of APO A1 lipoprotein polymorphism on etiology and severity
Purpose Relationship between shoulder adhesive capsulitis (AC) and hypercholesterolemia is known. The connecting link might be represented by the correlation between HDL and transforming growth factor beta (TGF-β): normally, HDLs stimulate TGF-β expression; the latter is employed in the development...
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| Veröffentlicht in: | Musculoskeletal surgery 2018-10, Vol.102 (Suppl 1), p.35-40 |
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| creator | Gumina, S. Candela, V. Castagna, A. Carnovale, M. Passaretti, D. Venditto, T. Giannicola, G. Villani, C. |
| description | Purpose
Relationship between shoulder adhesive capsulitis (AC) and hypercholesterolemia is known. The connecting link might be represented by the correlation between HDL and transforming growth factor beta (TGF-β): normally, HDLs stimulate TGF-β expression; the latter is employed in the development of fibrous tissue. We assess whether the presence of the Apo-A1-G75A-polymorphism, which is correlated to an enhanced HDL function, could be a risk factor for the genesis and severity of AC.
Methods
Peripheral blood samples of 27 patients [7M; 20F, mean age 54.81 (41–65)] with AC and hypercholesterolemia were submitted to polymerase chain reaction in order to evaluate the Apo-A1-G75A-polymorphism. Genome database was used as control. Two categories were obtained according to AC severity: type I (active forward flexion ≥ 100°) and type II ( 0.05), respectively. Patients with type I and II capsulitis were 11 [flexion 148.0° (range 100°–165°)] and 16 [flexion 82.5° (range 50°–95°)], respectively. The prevalence of Apo-A1-G75A in type I was 18.1% (2AG; 9GG) and in type II was 56.3% (8GA; 1AA; 7GG), respectively (RR 1.87, IC 1.005–3.482,
p
|
| doi_str_mv | 10.1007/s12306-018-0557-5 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_2126914518</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A715473565</galeid><sourcerecordid>A715473565</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3545-a01bfb7066404812c2918ef32576f860621d572d7ee74a17fb3eae33aa0998b13</originalsourceid><addsrcrecordid>eNp1kUtv1TAQhSMEoqXwA9ggS2zYpHj8TNhdVbykSkUC1paTTG5cOXGwk1b33-NwSysQyIsZ2d85mvEpipdAz4FS_TYB41SVFKqSSqlL-ag4ZZTLUgKIx_c9VSfFs5SuKVWikvXT4oRTLrjQ1Wlx-3UIq-8wEtsNmNwNktbOafVucYnYqSPDYcbYDsFjWjDmMjr7jmwNCT3ZfbkiOyDezWGOYUE3kTn4wxjiPLg0kjARXFzwYX_45ZbwBqNbDs-LJ731CV_c1bPi-4f33y4-lZdXHz9f7C7LlkshS0uh6RtNlRJUVMBaVkOFPWdSq75SVDHopGadRtTCgu4bjhY5t5bWddUAPyveHH3zdD_WvIIZXWrRezthWJNhwFQNQkKV0dd_oddhjVOebqM4V4wL-kDtrUfjpj4s0babqdlpkEJzqWSmzv9B5dPl72vDhL3L938I4ChoY0gpYm_m6EYbDwao2cI2x7BNDttsYZtN8-pu4LUZsbtX_E43A-wIpPw07TE-bPR_15_vKbMo</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2123362340</pqid></control><display><type>article</type><title>Shoulder adhesive capsulitis and hypercholesterolemia: role of APO A1 lipoprotein polymorphism on etiology and severity</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Gumina, S. ; Candela, V. ; Castagna, A. ; Carnovale, M. ; Passaretti, D. ; Venditto, T. ; Giannicola, G. ; Villani, C.</creator><creatorcontrib>Gumina, S. ; Candela, V. ; Castagna, A. ; Carnovale, M. ; Passaretti, D. ; Venditto, T. ; Giannicola, G. ; Villani, C.</creatorcontrib><description>Purpose
Relationship between shoulder adhesive capsulitis (AC) and hypercholesterolemia is known. The connecting link might be represented by the correlation between HDL and transforming growth factor beta (TGF-β): normally, HDLs stimulate TGF-β expression; the latter is employed in the development of fibrous tissue. We assess whether the presence of the Apo-A1-G75A-polymorphism, which is correlated to an enhanced HDL function, could be a risk factor for the genesis and severity of AC.
Methods
Peripheral blood samples of 27 patients [7M; 20F, mean age 54.81 (41–65)] with AC and hypercholesterolemia were submitted to polymerase chain reaction in order to evaluate the Apo-A1-G75A-polymorphism. Genome database was used as control. Two categories were obtained according to AC severity: type I (active forward flexion ≥ 100°) and type II (< 100°). Data were submitted to statistics.
Results
The prevalence of Apo-A1-G75A-polymorphism in the studied group and in the control group was 22.2% (10AG; 1AA; 16GG) and 19% (OR 1.22, IC 0.59–2.53,
p
> 0.05), respectively. Patients with type I and II capsulitis were 11 [flexion 148.0° (range 100°–165°)] and 16 [flexion 82.5° (range 50°–95°)], respectively. The prevalence of Apo-A1-G75A in type I was 18.1% (2AG; 9GG) and in type II was 56.3% (8GA; 1AA; 7GG), respectively (RR 1.87, IC 1.005–3.482,
p
< 0.05).
Conclusions
Apo-A1-G75A-polymorphism is not necessary for the genesis, but it is a risk factor for severity of AC.
Level of Evidence
III.</description><identifier>ISSN: 2035-5106</identifier><identifier>EISSN: 2035-5114</identifier><identifier>DOI: 10.1007/s12306-018-0557-5</identifier><identifier>PMID: 30343478</identifier><language>eng</language><publisher>Milan: Springer Milan</publisher><subject>Adult ; Aged ; Apolipoprotein A-I - genetics ; Bursitis - genetics ; Development and progression ; Etiology ; Female ; Genetic aspects ; Genomics ; Humans ; Hypercholesterolemia ; Hypercholesterolemia - genetics ; Lipoproteins ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Original Article ; Orthopedics ; Polymorphism ; Polymorphism, Genetic ; Prospective Studies ; Risk Factors ; Severity of Illness Index ; Shoulder ; Surgical Orthopedics ; Transforming growth factors</subject><ispartof>Musculoskeletal surgery, 2018-10, Vol.102 (Suppl 1), p.35-40</ispartof><rights>Istituto Ortopedico Rizzoli 2018</rights><rights>COPYRIGHT 2018 Springer</rights><rights>MUSCULOSKELETAL SURGERY is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3545-a01bfb7066404812c2918ef32576f860621d572d7ee74a17fb3eae33aa0998b13</citedby><cites>FETCH-LOGICAL-c3545-a01bfb7066404812c2918ef32576f860621d572d7ee74a17fb3eae33aa0998b13</cites><orcidid>0000-0002-6097-4136</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12306-018-0557-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12306-018-0557-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30343478$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gumina, S.</creatorcontrib><creatorcontrib>Candela, V.</creatorcontrib><creatorcontrib>Castagna, A.</creatorcontrib><creatorcontrib>Carnovale, M.</creatorcontrib><creatorcontrib>Passaretti, D.</creatorcontrib><creatorcontrib>Venditto, T.</creatorcontrib><creatorcontrib>Giannicola, G.</creatorcontrib><creatorcontrib>Villani, C.</creatorcontrib><title>Shoulder adhesive capsulitis and hypercholesterolemia: role of APO A1 lipoprotein polymorphism on etiology and severity</title><title>Musculoskeletal surgery</title><addtitle>Musculoskelet Surg</addtitle><addtitle>Musculoskelet Surg</addtitle><description>Purpose
Relationship between shoulder adhesive capsulitis (AC) and hypercholesterolemia is known. The connecting link might be represented by the correlation between HDL and transforming growth factor beta (TGF-β): normally, HDLs stimulate TGF-β expression; the latter is employed in the development of fibrous tissue. We assess whether the presence of the Apo-A1-G75A-polymorphism, which is correlated to an enhanced HDL function, could be a risk factor for the genesis and severity of AC.
Methods
Peripheral blood samples of 27 patients [7M; 20F, mean age 54.81 (41–65)] with AC and hypercholesterolemia were submitted to polymerase chain reaction in order to evaluate the Apo-A1-G75A-polymorphism. Genome database was used as control. Two categories were obtained according to AC severity: type I (active forward flexion ≥ 100°) and type II (< 100°). Data were submitted to statistics.
Results
The prevalence of Apo-A1-G75A-polymorphism in the studied group and in the control group was 22.2% (10AG; 1AA; 16GG) and 19% (OR 1.22, IC 0.59–2.53,
p
> 0.05), respectively. Patients with type I and II capsulitis were 11 [flexion 148.0° (range 100°–165°)] and 16 [flexion 82.5° (range 50°–95°)], respectively. The prevalence of Apo-A1-G75A in type I was 18.1% (2AG; 9GG) and in type II was 56.3% (8GA; 1AA; 7GG), respectively (RR 1.87, IC 1.005–3.482,
p
< 0.05).
Conclusions
Apo-A1-G75A-polymorphism is not necessary for the genesis, but it is a risk factor for severity of AC.
Level of Evidence
III.</description><subject>Adult</subject><subject>Aged</subject><subject>Apolipoprotein A-I - genetics</subject><subject>Bursitis - genetics</subject><subject>Development and progression</subject><subject>Etiology</subject><subject>Female</subject><subject>Genetic aspects</subject><subject>Genomics</subject><subject>Humans</subject><subject>Hypercholesterolemia</subject><subject>Hypercholesterolemia - genetics</subject><subject>Lipoproteins</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Original Article</subject><subject>Orthopedics</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Prospective Studies</subject><subject>Risk Factors</subject><subject>Severity of Illness Index</subject><subject>Shoulder</subject><subject>Surgical Orthopedics</subject><subject>Transforming growth factors</subject><issn>2035-5106</issn><issn>2035-5114</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kUtv1TAQhSMEoqXwA9ggS2zYpHj8TNhdVbykSkUC1paTTG5cOXGwk1b33-NwSysQyIsZ2d85mvEpipdAz4FS_TYB41SVFKqSSqlL-ag4ZZTLUgKIx_c9VSfFs5SuKVWikvXT4oRTLrjQ1Wlx-3UIq-8wEtsNmNwNktbOafVucYnYqSPDYcbYDsFjWjDmMjr7jmwNCT3ZfbkiOyDezWGOYUE3kTn4wxjiPLg0kjARXFzwYX_45ZbwBqNbDs-LJ731CV_c1bPi-4f33y4-lZdXHz9f7C7LlkshS0uh6RtNlRJUVMBaVkOFPWdSq75SVDHopGadRtTCgu4bjhY5t5bWddUAPyveHH3zdD_WvIIZXWrRezthWJNhwFQNQkKV0dd_oddhjVOebqM4V4wL-kDtrUfjpj4s0babqdlpkEJzqWSmzv9B5dPl72vDhL3L938I4ChoY0gpYm_m6EYbDwao2cI2x7BNDttsYZtN8-pu4LUZsbtX_E43A-wIpPw07TE-bPR_15_vKbMo</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Gumina, S.</creator><creator>Candela, V.</creator><creator>Castagna, A.</creator><creator>Carnovale, M.</creator><creator>Passaretti, D.</creator><creator>Venditto, T.</creator><creator>Giannicola, G.</creator><creator>Villani, C.</creator><general>Springer Milan</general><general>Springer</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6097-4136</orcidid></search><sort><creationdate>20181001</creationdate><title>Shoulder adhesive capsulitis and hypercholesterolemia: role of APO A1 lipoprotein polymorphism on etiology and severity</title><author>Gumina, S. ; Candela, V. ; Castagna, A. ; Carnovale, M. ; Passaretti, D. ; Venditto, T. ; Giannicola, G. ; Villani, C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3545-a01bfb7066404812c2918ef32576f860621d572d7ee74a17fb3eae33aa0998b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Apolipoprotein A-I - genetics</topic><topic>Bursitis - genetics</topic><topic>Development and progression</topic><topic>Etiology</topic><topic>Female</topic><topic>Genetic aspects</topic><topic>Genomics</topic><topic>Humans</topic><topic>Hypercholesterolemia</topic><topic>Hypercholesterolemia - genetics</topic><topic>Lipoproteins</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Original Article</topic><topic>Orthopedics</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Prospective Studies</topic><topic>Risk Factors</topic><topic>Severity of Illness Index</topic><topic>Shoulder</topic><topic>Surgical Orthopedics</topic><topic>Transforming growth factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gumina, S.</creatorcontrib><creatorcontrib>Candela, V.</creatorcontrib><creatorcontrib>Castagna, A.</creatorcontrib><creatorcontrib>Carnovale, M.</creatorcontrib><creatorcontrib>Passaretti, D.</creatorcontrib><creatorcontrib>Venditto, T.</creatorcontrib><creatorcontrib>Giannicola, G.</creatorcontrib><creatorcontrib>Villani, C.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Musculoskeletal surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gumina, S.</au><au>Candela, V.</au><au>Castagna, A.</au><au>Carnovale, M.</au><au>Passaretti, D.</au><au>Venditto, T.</au><au>Giannicola, G.</au><au>Villani, C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Shoulder adhesive capsulitis and hypercholesterolemia: role of APO A1 lipoprotein polymorphism on etiology and severity</atitle><jtitle>Musculoskeletal surgery</jtitle><stitle>Musculoskelet Surg</stitle><addtitle>Musculoskelet Surg</addtitle><date>2018-10-01</date><risdate>2018</risdate><volume>102</volume><issue>Suppl 1</issue><spage>35</spage><epage>40</epage><pages>35-40</pages><issn>2035-5106</issn><eissn>2035-5114</eissn><abstract>Purpose
Relationship between shoulder adhesive capsulitis (AC) and hypercholesterolemia is known. The connecting link might be represented by the correlation between HDL and transforming growth factor beta (TGF-β): normally, HDLs stimulate TGF-β expression; the latter is employed in the development of fibrous tissue. We assess whether the presence of the Apo-A1-G75A-polymorphism, which is correlated to an enhanced HDL function, could be a risk factor for the genesis and severity of AC.
Methods
Peripheral blood samples of 27 patients [7M; 20F, mean age 54.81 (41–65)] with AC and hypercholesterolemia were submitted to polymerase chain reaction in order to evaluate the Apo-A1-G75A-polymorphism. Genome database was used as control. Two categories were obtained according to AC severity: type I (active forward flexion ≥ 100°) and type II (< 100°). Data were submitted to statistics.
Results
The prevalence of Apo-A1-G75A-polymorphism in the studied group and in the control group was 22.2% (10AG; 1AA; 16GG) and 19% (OR 1.22, IC 0.59–2.53,
p
> 0.05), respectively. Patients with type I and II capsulitis were 11 [flexion 148.0° (range 100°–165°)] and 16 [flexion 82.5° (range 50°–95°)], respectively. The prevalence of Apo-A1-G75A in type I was 18.1% (2AG; 9GG) and in type II was 56.3% (8GA; 1AA; 7GG), respectively (RR 1.87, IC 1.005–3.482,
p
< 0.05).
Conclusions
Apo-A1-G75A-polymorphism is not necessary for the genesis, but it is a risk factor for severity of AC.
Level of Evidence
III.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>30343478</pmid><doi>10.1007/s12306-018-0557-5</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-6097-4136</orcidid></addata></record> |
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| ispartof | Musculoskeletal surgery, 2018-10, Vol.102 (Suppl 1), p.35-40 |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Adult Aged Apolipoprotein A-I - genetics Bursitis - genetics Development and progression Etiology Female Genetic aspects Genomics Humans Hypercholesterolemia Hypercholesterolemia - genetics Lipoproteins Male Medicine Medicine & Public Health Middle Aged Original Article Orthopedics Polymorphism Polymorphism, Genetic Prospective Studies Risk Factors Severity of Illness Index Shoulder Surgical Orthopedics Transforming growth factors |
| title | Shoulder adhesive capsulitis and hypercholesterolemia: role of APO A1 lipoprotein polymorphism on etiology and severity |
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