<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT02972138</url>
  </required_header>
  <id_info>
    <org_study_id>Vit.D-Bisph-SCD</org_study_id>
    <nct_id>NCT02972138</nct_id>
  </id_info>
  <brief_title>Vitamin D and Bisphosphonates in the Treatment of Sickle Cell Disease</brief_title>
  <official_title>Vitamin D Supplementation and Anti-resorptive Therapy (Bisphosphonates) Treatment of Young Adult Patients With Sickle Cell Disease</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Società Italiana Talassemie ed Emoglobinopatie</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Società Italiana Talassemie ed Emoglobinopatie</source>
  <oversight_info>
    <has_dmc>No</has_dmc>
  </oversight_info>
  <brief_summary>
    <textblock>
      Sickle cell disease (SCD) is a worldwide distributed hereditary red cell disorder, which&#xD;
      affects approximately 75,000 individuals in the United States and almost 20,000- 25,000&#xD;
      subjects in Europe, this latter mainly related to the immigration fluxes from endemic areas&#xD;
      such as Sub-Saharian Africa to European countries. Studies of global burden disease have&#xD;
      pointed out the invalidating impact of SCD on patient quality of life. This requires the&#xD;
      development of new therapeutic options to treat sickle cell related acute and chronic&#xD;
      complications. SCD is caused by a point mutation in the β-globin gene resulting in the&#xD;
      synthesis of pathological hemoglobin S (HbS). HbS displays peculiar biochemical&#xD;
      characteristics, polymerizing when deoxygenated with associated reduction in cell ion and&#xD;
      water content (cell dehydration), increased red cell density and further acceleration of HbS&#xD;
      polymerization. Pathophysiological studies have shown that dense, dehydrated red cells play a&#xD;
      central role in acute and chronic clinical manifestations of SCD, in which intravascular&#xD;
      sickling in capillaries and small vessels leads to vaso-occlusion and impaired blood flow&#xD;
      with ischemic/reperfusion injury. In microcirculation, vaso-occlusive events (VOC) result&#xD;
      from a complex and still partially known scenario, involving the interactions between&#xD;
      different cell types, including dense red cells, reticulocytes, abnormally activated&#xD;
      endothelial cells, leukocytes, platelets and plasma factors. Target organs, such as bone or&#xD;
      lung, are involved in both acute and chronic clinical manifestations of SCD, related to their&#xD;
      peculiar anatomic organization mainly characterized by sluggish circulation and relative&#xD;
      local hypoxia. VOCs combined with marrow hyperplasia and inflammation has been suggested to&#xD;
      contribute to the development of sickle bone disease (SBD). Recently, it has been proposed a&#xD;
      possible role of vitamin D deficiency in SBD, which appears to be subordinated to the primary&#xD;
      defect in bone homeostasis. In a humanized mouse model for SCD, we recently reported that SBD&#xD;
      is due to imbalance between osteoblast/osteoclast activity induced by recurrent VOCs. In&#xD;
      addition, we show that zoledronic acid prevents bone impairment related to SCD, reducing&#xD;
      osteoclast activity and improving osteoblast performance.&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      This is a retrospective study aimed to evaluate sickle bone disease (SBD) in a population of&#xD;
      young adult patients with sickle cell disease treated with vitamin D supplementation and&#xD;
      anti-resorptive therapy (bisphosphonates). We plan to analyze data from 1 January 2010 to 31&#xD;
      December 2015.&#xD;
&#xD;
      In addition to the standard hematological analysis, the following parameters and radiologic&#xD;
      exams will be evaluated:&#xD;
&#xD;
        -  Serum levels of Ca2+, P, Vitamin D, parathormone , creatinine, blood urea nitrogen , Na,&#xD;
           K, Cl&#xD;
&#xD;
        -  Bone turnover markers: C-terminal telopeptide (CTX), N-terminal propeptide of type I&#xD;
           procollagen (PINP)&#xD;
&#xD;
        -  Bone densitometry (DXA) at lumbar spine and proximal femur&#xD;
&#xD;
        -  Standard X-Ray at dorsal-lumbar spine in LL projection for morphometric analysis&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Completed</overall_status>
  <start_date>January 2010</start_date>
  <completion_date type="Actual">September 2017</completion_date>
  <primary_completion_date type="Actual">December 2015</primary_completion_date>
  <study_type>Observational</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <observational_model>Cohort</observational_model>
    <time_perspective>Retrospective</time_perspective>
  </study_design_info>
  <primary_outcome>
    <measure>Incidence of vertebral fracture</measure>
    <time_frame>5 years follow up</time_frame>
  </primary_outcome>
  <secondary_outcome>
    <measure>severity of vertebral fracture</measure>
    <time_frame>5 years follow up</time_frame>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Incidence of non-vertebral fracture</measure>
    <time_frame>5 years follow up</time_frame>
  </secondary_outcome>
  <enrollment type="Actual">80</enrollment>
  <condition>Sickle Cells Disease</condition>
  <eligibility>
    <study_pop>
      <textblock>
        Patients with sickle cell disease older than 18 years of age and younger than 50 years of&#xD;
        age&#xD;
      </textblock>
    </study_pop>
    <sampling_method>Non-Probability Sample</sampling_method>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  Young adult patients with sickle cell disease (older than 18 years of age) and younger&#xD;
             than 50 years of age&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  Women with positive pregnant test, patients with history of heart, renal and liver&#xD;
             failure, patients taking drugs influencing bone metabolisms within the two years&#xD;
             before the beginning of the study (i.e.: glucocorticoids, hormonal replacement)&#xD;
&#xD;
          -  Patients in meonopause, patients with traumatic vertebral fracture&#xD;
&#xD;
          -  Patients with hypo/hyperthyroidism&#xD;
&#xD;
          -  Patients with hyperparathyroidism&#xD;
&#xD;
          -  Patients with osteomalacia, patients with history of Paget disease&#xD;
&#xD;
          -  Patients with Cushing syndrome&#xD;
&#xD;
          -  Patients with malabsorption diseases (i.e.: caeliac disease)&#xD;
&#xD;
          -  Patients with history of cancer&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>50 Years</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Luca G Dalle Carbonare, MD</last_name>
    <role>Principal Investigator</role>
    <affiliation>Università degli studi di Verona</affiliation>
  </overall_official>
  <location>
    <facility>
      <name>Ospedali Galliera - S.S.D. Microcitemia, anemie congenite e dismetabolismo del ferro</name>
      <address>
        <city>Genova</city>
        <zip>16128</zip>
        <country>Italy</country>
      </address>
    </facility>
  </location>
  <location>
    <facility>
      <name>Ospedali Galliera - S.S.D. Ortogeriatria per intensità di cure</name>
      <address>
        <city>Genova</city>
        <zip>16128</zip>
        <country>Italy</country>
      </address>
    </facility>
  </location>
  <location>
    <facility>
      <name>Università degli Studi di Verona</name>
      <address>
        <city>Verona</city>
        <zip>37129</zip>
        <country>Italy</country>
      </address>
    </facility>
  </location>
  <location_countries>
    <country>Italy</country>
  </location_countries>
  <reference>
    <citation>Modell B, Darlison M. Global epidemiology of haemoglobin disorders and derived service indicators. Bull World Health Organ. 2008 Jun;86(6):480-7. doi: 10.2471/blt.06.036673.</citation>
    <PMID>18568278</PMID>
  </reference>
  <reference>
    <citation>Weatherall DJ, Clegg JB. Inherited haemoglobin disorders: an increasing global health problem. Bull World Health Organ. 2001;79(8):704-12. Epub 2001 Oct 24.</citation>
    <PMID>11545326</PMID>
  </reference>
  <reference>
    <citation>De Franceschi L, Cappellini MD, Olivieri O. Thrombosis and sickle cell disease. Semin Thromb Hemost. 2011 Apr;37(3):226-36. doi: 10.1055/s-0031-1273087. Epub 2011 Mar 31.</citation>
    <PMID>21455857</PMID>
  </reference>
  <reference>
    <citation>Eaton WA, Hofrichter J. Sickle cell hemoglobin polymerization. Adv Protein Chem. 1990;40:63-279. doi: 10.1016/s0065-3233(08)60287-9. No abstract available.</citation>
    <PMID>2195851</PMID>
  </reference>
  <reference>
    <citation>De Franceschi L, Corrocher R. Established and experimental treatments for sickle cell disease. Haematologica. 2004 Mar;89(3):348-56.</citation>
    <PMID>15020275</PMID>
  </reference>
  <reference>
    <citation>Ballas SK, Smith ED. Red blood cell changes during the evolution of the sickle cell painful crisis. Blood. 1992 Apr 15;79(8):2154-63.</citation>
    <PMID>1562742</PMID>
  </reference>
  <reference>
    <citation>Vinchi F, De Franceschi L, Ghigo A, Townes T, Cimino J, Silengo L, Hirsch E, Altruda F, Tolosano E. Hemopexin therapy improves cardiovascular function by preventing heme-induced endothelial toxicity in mouse models of hemolytic diseases. Circulation. 2013 Mar 26;127(12):1317-29. doi: 10.1161/CIRCULATIONAHA.112.130179. Epub 2013 Feb 27.</citation>
    <PMID>23446829</PMID>
  </reference>
  <reference>
    <citation>Hebbel RP, Vercellotti G, Nath KA. A systems biology consideration of the vasculopathy of sickle cell anemia: the need for multi-modality chemo-prophylaxsis. Cardiovasc Hematol Disord Drug Targets. 2009 Dec;9(4):271-92. doi: 10.2174/1871529x10909040271.</citation>
    <PMID>19751187</PMID>
  </reference>
  <reference>
    <citation>Hebbel RP. Adhesion of sickle red cells to endothelium: myths and future directions. Transfus Clin Biol. 2008 Feb-Mar;15(1-2):14-8. doi: 10.1016/j.tracli.2008.03.011. Epub 2008 May 23.</citation>
    <PMID>18501652</PMID>
  </reference>
  <reference>
    <citation>Platt OS. The acute chest syndrome of sickle cell disease. N Engl J Med. 2000 Jun 22;342(25):1904-7. doi: 10.1056/NEJM200006223422510. No abstract available. Erratum In: N Engl J Med 2000 Aug 24;343(8):591.</citation>
    <PMID>10861328</PMID>
  </reference>
  <reference>
    <citation>Lal A, Fung EB, Pakbaz Z, Hackney-Stephens E, Vichinsky EP. Bone mineral density in children with sickle cell anemia. Pediatr Blood Cancer. 2006 Dec;47(7):901-6. doi: 10.1002/pbc.20681.</citation>
    <PMID>16317761</PMID>
  </reference>
  <reference>
    <citation>Dalle Carbonare L, Innamorati G, Valenti MT. Transcription factor Runx2 and its application to bone tissue engineering. Stem Cell Rev Rep. 2012 Sep;8(3):891-7. doi: 10.1007/s12015-011-9337-4.</citation>
    <PMID>22139789</PMID>
  </reference>
  <reference>
    <citation>Bruzzaniti A, Baron R. Molecular regulation of osteoclast activity. Rev Endocr Metab Disord. 2006 Jun;7(1-2):123-39. doi: 10.1007/s11154-006-9009-x.</citation>
    <PMID>16951988</PMID>
  </reference>
  <reference>
    <citation>Dalle Carbonare L, Zanatta M, Gasparetto A, Valenti MT. Safety and tolerability of zoledronic acid and other bisphosphonates in osteoporosis management. Drug Healthc Patient Saf. 2010;2:121-37. doi: 10.2147/DHPS.S6285. Epub 2010 Aug 19.</citation>
    <PMID>21701624</PMID>
  </reference>
  <reference>
    <citation>Dalle Carbonare L, Arlot ME, Chavassieux PM, Roux JP, Portero NR, Meunier PJ. Comparison of trabecular bone microarchitecture and remodeling in glucocorticoid-induced and postmenopausal osteoporosis. J Bone Miner Res. 2001 Jan;16(1):97-103. doi: 10.1359/jbmr.2001.16.1.97.</citation>
    <PMID>11149495</PMID>
  </reference>
  <reference>
    <citation>Nouraie M, Cheng K, Niu X, Moore-King E, Fadojutimi-Akinsi MF, Minniti CP, Sable C, Rana S, Dham N, Campbell A, Ensing G, Kato GJ, Gladwin MT, Castro OL, Gordeuk VR. Predictors of osteoclast activity in patients with sickle cell disease. Haematologica. 2011 Aug;96(8):1092-8. doi: 10.3324/haematol.2011.042499. Epub 2011 May 5.</citation>
    <PMID>21546502</PMID>
  </reference>
  <reference>
    <citation>Neves FS, Oliveira LS, Torres MG, Toralles MB, da Silva MC, Campos MI, Campos PS, Crusoe-Rebello I. Evaluation of panoramic radiomorphometric indices related to low bone density in sickle cell disease. Osteoporos Int. 2012 Jul;23(7):2037-42. doi: 10.1007/s00198-011-1810-z. Epub 2011 Oct 18.</citation>
    <PMID>22006042</PMID>
  </reference>
  <reference>
    <citation>Nur E, Mairuhu W, Biemond BJ, van Zanten AP, Schnog JJ, Brandjes DP, Otten HM; CURAMA study group. Urinary markers of bone resorption, pyridinoline and deoxypyridinoline, are increased in sickle cell patients with further increments during painful crisis. Am J Hematol. 2010 Nov;85(11):902-4. doi: 10.1002/ajh.21856.</citation>
    <PMID>20882525</PMID>
  </reference>
  <reference>
    <citation>Miller RG, Segal JB, Ashar BH, Leung S, Ahmed S, Siddique S, Rice T, Lanzkron S. High prevalence and correlates of low bone mineral density in young adults with sickle cell disease. Am J Hematol. 2006 Apr;81(4):236-41. doi: 10.1002/ajh.20541.</citation>
    <PMID>16550513</PMID>
  </reference>
  <verification_date>December 2015</verification_date>
  <study_first_submitted>October 28, 2016</study_first_submitted>
  <study_first_submitted_qc>November 21, 2016</study_first_submitted_qc>
  <study_first_posted type="Estimate">November 23, 2016</study_first_posted>
  <last_update_submitted>October 5, 2017</last_update_submitted>
  <last_update_submitted_qc>October 5, 2017</last_update_submitted_qc>
  <last_update_posted type="Actual">October 6, 2017</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor</responsible_party_type>
  </responsible_party>
  <keyword>Sickle-cells Disease</keyword>
  <keyword>bisphosphonates</keyword>
  <keyword>Vitamine D</keyword>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Anemia, Sickle Cell</mesh_term>
  </condition_browse>
  <patient_data>
    <sharing_ipd>Undecided</sharing_ipd>
  </patient_data>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT02972138
org study id: Vit.D-Bisph-SCD
nct id: NCT02972138
lead sponsor: 
has dmc: No
Sickle cell disease (SCD) is a worldwide distributed hereditary red cell disorder, which
      affects approximately 75,000 individuals in the United States and almost 20,000- 25,000
      subjects in Europe, this latter mainly related to the immigration fluxes from endemic areas
      such as Sub-Saharian Africa to European countries. Studies of global burden disease have
      pointed out the invalidating impact of SCD on patient quality of life. This requires the
      development of new therapeutic options to treat sickle cell related acute and chronic
      complications. SCD is caused by a point mutation in the β-globin gene resulting in the
      synthesis of pathological hemoglobin S (HbS). HbS displays peculiar biochemical
      characteristics, polymerizing when deoxygenated with associated reduction in cell ion and
      water content (cell dehydration), increased red cell density and further acceleration of HbS
      polymerization. Pathophysiological studies have shown that dense, dehydrated red cells play a
      central role in acute and chronic clinical manifestations of SCD, in which intravascular
      sickling in capillaries and small vessels leads to vaso-occlusion and impaired blood flow
      with ischemic/reperfusion injury. In microcirculation, vaso-occlusive events (VOC) result
      from a complex and still partially known scenario, involving the interactions between
      different cell types, including dense red cells, reticulocytes, abnormally activated
      endothelial cells, leukocytes, platelets and plasma factors. Target organs, such as bone or
      lung, are involved in both acute and chronic clinical manifestations of SCD, related to their
      peculiar anatomic organization mainly characterized by sluggish circulation and relative
      local hypoxia. VOCs combined with marrow hyperplasia and inflammation has been suggested to
      contribute to the development of sickle bone disease (SBD). Recently, it has been proposed a
      possible role of vitamin D deficiency in SBD, which appears to be subordinated to the primary
      defect in bone homeostasis. In a humanized mouse model for SCD, we recently reported that SBD
      is due to imbalance between osteoblast/osteoclast activity induced by recurrent VOCs. In
      addition, we show that zoledronic acid prevents bone impairment related to SCD, reducing
      osteoclast activity and improving osteoblast performance.
This is a retrospective study aimed to evaluate sickle bone disease (SBD) in a population of
      young adult patients with sickle cell disease treated with vitamin D supplementation and
      anti-resorptive therapy (bisphosphonates). We plan to analyze data from 1 January 2010 to 31
      December 2015.

      In addition to the standard hematological analysis, the following parameters and radiologic
      exams will be evaluated:

        -  Serum levels of Ca2+, P, Vitamin D, parathormone , creatinine, blood urea nitrogen , Na,
           K, Cl

        -  Bone turnover markers: C-terminal telopeptide (CTX), N-terminal propeptide of type I
           procollagen (PINP)

        -  Bone densitometry (DXA) at lumbar spine and proximal femur

        -  Standard X-Ray at dorsal-lumbar spine in LL projection for morphometric analysis
observational model: Cohort
time perspective: Retrospective
measure: Incidence of vertebral fracture
time frame: 5 years follow up
measure: severity of vertebral fracture
time frame: 5 years follow up
measure: Incidence of non-vertebral fracture
time frame: 5 years follow up
study pop: 
sampling method: Non-Probability Sample
criteria: 
gender: All
minimum age: 18 Years
maximum age: 50 Years
healthy volunteers: No
last name: Luca G Dalle Carbonare, MD
role: Principal Investigator
affiliation: Università degli studi di Verona
facility: 
facility: 
facility: 
country: Italy
citation: Modell B, Darlison M. Global epidemiology of haemoglobin disorders and derived service indicators. Bull World Health Organ. 2008 Jun;86(6):480-7. doi: 10.2471/blt.06.036673.
PMID: 18568278
citation: Weatherall DJ, Clegg JB. Inherited haemoglobin disorders: an increasing global health problem. Bull World Health Organ. 2001;79(8):704-12. Epub 2001 Oct 24.
PMID: 11545326
citation: De Franceschi L, Cappellini MD, Olivieri O. Thrombosis and sickle cell disease. Semin Thromb Hemost. 2011 Apr;37(3):226-36. doi: 10.1055/s-0031-1273087. Epub 2011 Mar 31.
PMID: 21455857
citation: Eaton WA, Hofrichter J. Sickle cell hemoglobin polymerization. Adv Protein Chem. 1990;40:63-279. doi: 10.1016/s0065-3233(08)60287-9. No abstract available.
PMID: 2195851
citation: De Franceschi L, Corrocher R. Established and experimental treatments for sickle cell disease. Haematologica. 2004 Mar;89(3):348-56.
PMID: 15020275
citation: Ballas SK, Smith ED. Red blood cell changes during the evolution of the sickle cell painful crisis. Blood. 1992 Apr 15;79(8):2154-63.
PMID: 1562742
citation: Vinchi F, De Franceschi L, Ghigo A, Townes T, Cimino J, Silengo L, Hirsch E, Altruda F, Tolosano E. Hemopexin therapy improves cardiovascular function by preventing heme-induced endothelial toxicity in mouse models of hemolytic diseases. Circulation. 2013 Mar 26;127(12):1317-29. doi: 10.1161/CIRCULATIONAHA.112.130179. Epub 2013 Feb 27.
PMID: 23446829
citation: Hebbel RP, Vercellotti G, Nath KA. A systems biology consideration of the vasculopathy of sickle cell anemia: the need for multi-modality chemo-prophylaxsis. Cardiovasc Hematol Disord Drug Targets. 2009 Dec;9(4):271-92. doi: 10.2174/1871529x10909040271.
PMID: 19751187
citation: Hebbel RP. Adhesion of sickle red cells to endothelium: myths and future directions. Transfus Clin Biol. 2008 Feb-Mar;15(1-2):14-8. doi: 10.1016/j.tracli.2008.03.011. Epub 2008 May 23.
PMID: 18501652
citation: Platt OS. The acute chest syndrome of sickle cell disease. N Engl J Med. 2000 Jun 22;342(25):1904-7. doi: 10.1056/NEJM200006223422510. No abstract available. Erratum In: N Engl J Med 2000 Aug 24;343(8):591.
PMID: 10861328
citation: Lal A, Fung EB, Pakbaz Z, Hackney-Stephens E, Vichinsky EP. Bone mineral density in children with sickle cell anemia. Pediatr Blood Cancer. 2006 Dec;47(7):901-6. doi: 10.1002/pbc.20681.
PMID: 16317761
citation: Dalle Carbonare L, Innamorati G, Valenti MT. Transcription factor Runx2 and its application to bone tissue engineering. Stem Cell Rev Rep. 2012 Sep;8(3):891-7. doi: 10.1007/s12015-011-9337-4.
PMID: 22139789
citation: Bruzzaniti A, Baron R. Molecular regulation of osteoclast activity. Rev Endocr Metab Disord. 2006 Jun;7(1-2):123-39. doi: 10.1007/s11154-006-9009-x.
PMID: 16951988
citation: Dalle Carbonare L, Zanatta M, Gasparetto A, Valenti MT. Safety and tolerability of zoledronic acid and other bisphosphonates in osteoporosis management. Drug Healthc Patient Saf. 2010;2:121-37. doi: 10.2147/DHPS.S6285. Epub 2010 Aug 19.
PMID: 21701624
citation: Dalle Carbonare L, Arlot ME, Chavassieux PM, Roux JP, Portero NR, Meunier PJ. Comparison of trabecular bone microarchitecture and remodeling in glucocorticoid-induced and postmenopausal osteoporosis. J Bone Miner Res. 2001 Jan;16(1):97-103. doi: 10.1359/jbmr.2001.16.1.97.
PMID: 11149495
citation: Nouraie M, Cheng K, Niu X, Moore-King E, Fadojutimi-Akinsi MF, Minniti CP, Sable C, Rana S, Dham N, Campbell A, Ensing G, Kato GJ, Gladwin MT, Castro OL, Gordeuk VR. Predictors of osteoclast activity in patients with sickle cell disease. Haematologica. 2011 Aug;96(8):1092-8. doi: 10.3324/haematol.2011.042499. Epub 2011 May 5.
PMID: 21546502
citation: Neves FS, Oliveira LS, Torres MG, Toralles MB, da Silva MC, Campos MI, Campos PS, Crusoe-Rebello I. Evaluation of panoramic radiomorphometric indices related to low bone density in sickle cell disease. Osteoporos Int. 2012 Jul;23(7):2037-42. doi: 10.1007/s00198-011-1810-z. Epub 2011 Oct 18.
PMID: 22006042
citation: Nur E, Mairuhu W, Biemond BJ, van Zanten AP, Schnog JJ, Brandjes DP, Otten HM; CURAMA study group. Urinary markers of bone resorption, pyridinoline and deoxypyridinoline, are increased in sickle cell patients with further increments during painful crisis. Am J Hematol. 2010 Nov;85(11):902-4. doi: 10.1002/ajh.21856.
PMID: 20882525
citation: Miller RG, Segal JB, Ashar BH, Leung S, Ahmed S, Siddique S, Rice T, Lanzkron S. High prevalence and correlates of low bone mineral density in young adults with sickle cell disease. Am J Hematol. 2006 Apr;81(4):236-41. doi: 10.1002/ajh.20541.
PMID: 16550513
responsible party type: Sponsor
mesh term: Anemia, Sickle Cell
sharing ipd: Undecided