Sickle Cell DiseasePhase 2NCT01932554
Abciximab (ReoPro) as a Therapeutic Intervention for Sickle Cell Vaso-Occlusive Pain Crisis
A Phase 2 study testing Abciximab, Intravenous hydration and Ibuprofen in people with Sickle Cell Disease and Hb-SS Disease With Vasoocclusive Pain, run by St. Louis University at 1 site in United States.
Trial summary
The purpose of this study is to determine whether giving abciximab (ReoPro) to children with sickle cell disease who are hospitalized for acute pain crisis will improve their pain and shorten the time spent in the hospital, when compared with standard supportive care. Read more about this study
- Who is it for?
- Ages 5 to 25 years
- Conditions the study is for
- Sickle Cell Disease, Hb-SS Disease With Vasoocclusive Pain, Hemoglobin SS Disease With Vasoocclusive Crisis
- What is being tested?
- Abciximab, Intravenous hydration and Ibuprofen
- Type of treatment
- Injection or infusion
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 0 participants
- Where
- 1 siteUnited States
- Study dates
- Nov 2013to Mar 2015
- Phase
- Phase 2
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 5 to 25 years
- All sexes
- No healthy volunteers
- Child, Adult
Who may be able to join
- Diagnosis of sickle cell disease (Hb SS, HbSC, HbS-β0-thalassemia)
- Age 5.00 to 24.99 years
- Pain consistent with vaso-occlusive crisis that meets the criteria for hospitalization and parenteral narcotics: moderate-severe pain unresponsive to oral medications (NSAIDS + narcotics) that has no alternative etiology (e.g., trauma)
- Platelet count >100,000
- INR <1.2, PTT < 40 seconds
- Negative urine pregnancy test for females of child-bearing potential, including any female ≥10 years of age
- Informed consent by patient (≥18 years of age) or parent (if patient <18 years of age); assent from patients 12-18 years of age
- Ability to start drug/placebo infusion within 16 hours of admission
Who cannot join
- History of stroke (either ischemic or hemorrhagic)
- Currently receiving anticoagulation medication (heparin within 1 week, Coumadin within 3 weeks) or medication with irreversible anti-platelet effect (e.g., aspirin, ticlopidine) within 14 days
- Red cell transfusion within 60 days
- Major surgery within 30 days
- Treatment with hydroxyurea within 30 days (due to evidence that hydroxyurea can reverse platelet activation in patients with SCD)
- Tmax ≥ 102.0o F without concomitant signs of infection, or ≥ 100.4o F with any finding suggestive of bacterial infection, including acute chest syndrome (fever, respiratory symptoms, and new infiltrate on chest X-ray)
Show all 14Show fewer
- Active internal bleeding
- Known allergy to abciximab or murine proteins
- Recent (within 6 weeks) gastrointestinal or genitourinary bleeding of clinical significance
- Bleeding diathesis
- History of vasculitis
- Intracranial neoplasm, arteriovenous malformation or aneurysm
- Severe uncontrolled hypertension
- Patients who previously participated in the study must be excluded due to the increased risk of severe thrombocytopenia.
Trial locations and contacts
1 site in 1 country.
United States1 site
Cardinal Glennon Children's Medical Center
St Louis, Missouri, 63104
About this study
The purpose of this study is to determine whether giving abciximab (ReoPro) to children with sickle cell disease who are hospitalized for acute pain crisis will improve their pain and shorten the time spent in the hospital, when compared with standard supportive care.
Read the detailed description
Sickle cell disease (SCD) is one of the more common genetic diseases worldwide, affecting approximately 1 in 500 African-Americans and 1 in 1000 Hispanic-Americans. A single amino acid substitution decreases the solubility of deoxygenated hemoglobin, leading to polymer formation and subsequent distortion of erythrocyte shape from the normal biconcave disc into a relatively rigid crescent or sickle shape. Initially reversible, the polymer formation and shape distortion eventually becomes permanent. Clinical manifestations of sickle cell disease relate both to increased clearance of these misshapen erythrocytes (causing a chronic hemolytic anemia) as well as occlusion of small (and sometimes large) blood vessels.
Vaso-occlusive phenomena are responsible for much of the acute morbidity of sickle cell disease, including episodes of pain resulting from bone infarcts, splenic infarction with a secondary increased risk of infection, and a relatively high incidence of ischemic stroke (~10% in the first 2 decades of life). In addition, chronic and cumulative ischemic episodes contribute to long-term morbidity (including avascular necrosis of bone, retinopathy, renal insufficiency, and pulmonary hypertension) and a significantly shortened life span. Vaso-occlusive pain crises often require hospitalization for the administration of parenteral narcotics; the average duration of hospitalization is 4-5 days, and a significant proportion of patients experience multiple crises per year. In most episodes, pain continues to intensify over the first 2-3 days before beginning to abate, suggesting that there is ongoing extension of tissue damage for some time following initiation of the episode; also, many patients will develop additional foci of pain even during the course of hospitalization.
While direct mechanical blockage of small vessels by sickled erythrocytes is undoubtedly an important factor in vaso-occlusion, there are other secondary phenomena that are likely to contribute to these episodes, including increased erythrocyte adhesion to the endothelium of post-capillary venules. SCD patients also exhibit chronic pro-coagulation changes in soluble clotting factors, as well as increased platelet number and activation. The relative contribution of these various changes to the pathophysiology of vaso-occlusive crises is unclear. One published study showed that the antiplatelet drug ticlopidine decreased frequency, duration, and severity of pain crises in SCD patients, suggesting that the increase in platelet activation does indeed contribute to vaso-occlusion.
Current therapy for vaso-occlusive pain crises is mostly supportive (maintaining adequate hydration and oxygenation and administering pain medication). With the possible exception of exchange transfusion-a procedure with significant potential morbidity-there is no therapy that directly targets the vaso-occlusion.
Abciximab (ReoPro) is the Fab fragment of the chimeric human-mouse monoclonal antibody 7E3. It avidly binds to both glycoprotein IIb/IIIa and to integrin αvβ3, and so would potentially inhibit both erythrocyte binding to vascular endothelial as well as platelet adhesion, thus targeting two separate mechanisms that are felt to be components of the vaso-occlusive phenomenon in SCD.
The relatively prolonged course of most pain crises-which typically involves increasing intensity of pain and often development of new areas of pain over the first few days-suggests that treatment during the early phases of a crisis might be effective in ameliorating the course of the episode, resulting not only in decreased acute morbidity but possibly also in less long-term tissue damage. The study hypothesis is that administration of abciximab early in the course of a vaso-occlusive sickle cell pain crisis will reduce the median length of hospitalization without an accompanying increase in bleeding or other serious complications.
Participants will be randomized in a double blind fashion to receive either abciximab (ReoPro) or placebo intravenously over 12 hours. Randomization will be stratified by sickle cell genotype: Sickle Cell Anemia (SS) vs. Sickle-Hemoglobin C Disease (SC). All patients will receive standard supportive care, including hydration, supplemental oxygen as needed to maintain oxygen saturation >92%, scheduled use of NSAIDS, and narcotics titrated to effect.
- Conditions
- Sickle Cell Disease, Hb-SS Disease With Vasoocclusive Pain, Hemoglobin SS Disease With Vasoocclusive Crisis, Other Sickle Cell Disease With Vaso-Occlusive Pain, Hemoglobin SS Disease With Crisis
- Being tested
- Abciximab, Placebo, Intravenous hydration, Ibuprofen, Parenteral narcotic
- Keywords
- Sickle Cell Pain Crisis, Abciximab, Integrins, Cell Adhesion Molecules
- Medical subject headings
- Anemia, Sickle Cell, Vaso-Occlusive Crises
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
AbciximabDrug
Also called ReoPro
Abciximab will be administered as initial bolus of dose of 0.25 mg/kg, delivered via syringe pump over 15 minutes, followed by a continuous infusion of 0.125 microgram/kg/min (max of 10 micrograms/min) infused over the next 12 hours. Infusion to start within 16 hours of admission. All patients will receive standard supportive care measures.
PlaceboDrug
Inactive placebo will be administered as initial bolus followed by a continuous infusion over the next 12 hours, in syringes and volumes identical with the drug administered in the experimental arm. Infusion to begin within 16 hours of admission. All patients will also receive standard supportive care measures.
Intravenous hydrationOther
intravenous hydration to provide total fluid intake of 1.25-1.5 times maintenance fluid requirements
IbuprofenDrug
Also called Advil, Motrin
Scheduled ibuprofen,~10 mg/kg every 6-8 hours
Parenteral narcoticDrug
Also called morphine, hydromorphone, Dilaudid, fentanyl
Parenteral morphine administered by bolus or patient-controlled analgesia to maintain pain control. Hydromorphone or fentanyl will be used in patients who do not tolerate morphine.
Incentive spirometryOther
Patients will perform incentive spirometry every 2 hours while awake
Supplemental oxygenOther
Supplemental oxygen by nasal cannula or mask will be provided if needed to maintain oxygen saturation of 92% or greater.
| Study group | Role | What they receive |
|---|---|---|
| Abciximab | Experimental | Abciximab will be administered as initial bolus of dose of 0.25 mg/kg, delivered via syringe pump over 15 minutes, followed by a continuous infusion of 0.125 microgram/kg/min (max of 10 micrograms/min) infused over the next 12 hours. Infusion to start within 16 hours of admission.
Patients will receive standard supportive care, including intravenous hydration, supplemental oxygen, incentive spirometry, ibuprofen, and parenteral narcotic pain medications (morphine, hydromorphone or fentanyl) Receives: Drug: Abciximab; Other: Intravenous hydration; Drug: Ibuprofen; Drug: Parenteral narcotic; Other: Incentive spirometry; Other: Supplemental oxygen |
| Placebo | Placebo comparator | Inactive placebo will be administered as initial bolus followed by a continuous infusion over the next 12 hours, in syringes and volumes identical with the drug administered in the experimental arm. Infusion to begin within 16 hours of admission.
Patients will receive standard supportive care, including intravenous hydration, supplemental oxygen, incentive spirometry, ibuprofen, and parenteral narcotic pain medications (morphine, hydromorphone or fentanyl) Receives: Drug: Placebo; Other: Intravenous hydration; Drug: Ibuprofen; Drug: Parenteral narcotic; Other: Incentive spirometry; Other: Supplemental oxygen |
What is being measured
The primary outcome is the main question the study is designed to answer.
Duration of hospitalization
Total duration from admission to the inpatient service until discharge order is written, measured in days.
Measured: Duration of hospital stay, expected average of 5 days
Secondary outcomes (4)
Total narcotic dose
Total dose of parenteral narcotic administered during hospitalization, expressed as morphine equivalent per kg, will be calculated.
Measured: Duration of hospital stay, expected average of 5 days
Bleeding complications
All major or minor bleeding manifestations during hospitalization or in the immediate post-discharge period, including site and severity, will be tracked
Measured: From randomization until 10 days following initial discharge from hospital
Complications (other than bleeding) attributed to study drug
All complications potentially related to abciximab therapy, other than bleeding, will be tracked.
Measured: From randomization until 3 months following initial discharge from hospital
Readmission rate
All readmissions for any cause occurring within 3 months of discharge will be tracked.
Measured: From discharge date until 3 months following initial discharge from hospital
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted30 Aug 2013 (estimated)
- Study startNov 2013
- Primary completionMar 2015 (estimated)
- Study completionMar 2015
Why it stopped: Insufficient recruitment
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (13)Papers the sponsor has linked to this study.
- Other trials for Sickle Cell DiseaseStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 2
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Triple blind
- Who is masked
- Participant, Care provider, Investigator
- Enrolment
- 0 participants (actual)
Sponsor and investigators
- Lead sponsor
- St. Louis University
- Sponsor type
- University, hospital or other
- Collaborators
- Janssen Services, LLC
- Responsible party
- Principal investigator, William Ferguson M.D., St. Louis University
- Investigators
- William S Ferguson, MD, Principal investigator, St. Louis University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01932554
- Sponsor's protocol ID
- SLU 23331
- Status last verified
- Mar 2015
- First submitted
- 19 Aug 2013
- Last updated
- 26 Mar 2015
- Results posted
- No
- Data monitoring committee
- Yes
Publications
Dean J, Schechter AN. Sickle-cell anemia: molecular and cellular bases of therapeutic approaches (first of three parts). N Engl J Med. 1978 Oct 5;299(14):752-63. doi: 10.1056/NEJM197810052991405. No abstract available.
PubMed 357967Dean J, Schechter AN. Sickle-cell anemia: molecular and cellular bases of therapeutic approaches (second of three parts). N Engl J Med. 1978 Oct 12;299(15):804-11. doi: 10.1056/NEJM197810122991504. No abstract available.
PubMed 692564Bunn HF. Pathogenesis and treatment of sickle cell disease. N Engl J Med. 1997 Sep 11;337(11):762-9. doi: 10.1056/NEJM199709113371107. No abstract available.
PubMed 9287233Lane PA. Sickle cell disease. Pediatr Clin North Am. 1996 Jun;43(3):639-64. doi: 10.1016/s0031-3955(05)70426-0.
PubMed 8649903Platt OS, Brambilla DJ, Rosse WF, Milner PF, Castro O, Steinberg MH, Klug PP. Mortality in sickle cell disease. Life expectancy and risk factors for early death. N Engl J Med. 1994 Jun 9;330(23):1639-44. doi: 10.1056/NEJM199406093302303.
PubMed 7993409Platt OS, Thorington BD, Brambilla DJ, Milner PF, Rosse WF, Vichinsky E, Kinney TR. Pain in sickle cell disease. Rates and risk factors. N Engl J Med. 1991 Jul 4;325(1):11-6. doi: 10.1056/NEJM199107043250103.
PubMed 1710777Steinberg MH. Management of sickle cell disease. N Engl J Med. 1999 Apr 1;340(13):1021-30. doi: 10.1056/NEJM199904013401307. No abstract available.
PubMed 10099145Rees DC, Olujohungbe AD, Parker NE, Stephens AD, Telfer P, Wright J; British Committee for Standards in Haematology General Haematology Task Force by the Sickle Cell Working Party. Guidelines for the management of the acute painful crisis in sickle cell disease. Br J Haematol. 2003 Mar;120(5):744-52. doi: 10.1046/j.1365-2141.2003.04193.x. No abstract available.
PubMed 12614204Hebbel RP. Perspectives series: cell adhesion in vascular biology. Adhesive interactions of sickle erythrocytes with endothelium. J Clin Invest. 1997 Jun 1;99(11):2561-4. doi: 10.1172/JCI119442. No abstract available.
PubMed 9169483Kaul DK, Tsai HM, Liu XD, Nakada MT, Nagel RL, Coller BS. Monoclonal antibodies to alphaVbeta3 (7E3 and LM609) inhibit sickle red blood cell-endothelium interactions induced by platelet-activating factor. Blood. 2000 Jan 15;95(2):368-74.
PubMed 10627437Finnegan EM, Barabino GA, Liu XD, Chang HY, Jonczyk A, Kaul DK. Small-molecule cyclic alpha V beta 3 antagonists inhibit sickle red cell adhesion to vascular endothelium and vasoocclusion. Am J Physiol Heart Circ Physiol. 2007 Aug;293(2):H1038-45. doi: 10.1152/ajpheart.01054.2006. Epub 2007 May 4.
PubMed 17483236Ataga KI, Orringer EP. Hypercoagulability in sickle cell disease: a curious paradox. Am J Med. 2003 Dec 15;115(9):721-8. doi: 10.1016/j.amjmed.2003.07.011.
PubMed 14693325Ataga KI, Key NS. Hypercoagulability in sickle cell disease: new approaches to an old problem. Hematology Am Soc Hematol Educ Program. 2007:91-6. doi: 10.1182/asheducation-2007.1.91.
PubMed 18024615
Study at a glance
From the registry record, last updated by the sponsor on 26 Mar 2015. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Abciximab (ReoPro) as a Therapeutic Intervention for Sickle Cell Vaso-Occlusive Pain Crisis
- ClinicalTrials.gov ID
- NCT01932554
- Acronym / sponsor ID
- SLU 23331
- Conditions
- Sickle Cell Disease, Hb-SS Disease With Vasoocclusive Pain, Hemoglobin SS Disease With Vasoocclusive Crisis, Other Sickle Cell Disease With Vaso-Occlusive Pain, Hemoglobin SS Disease With Crisis
- Keywords
- Sickle Cell Pain Crisis, Abciximab, Integrins, Cell Adhesion Molecules
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- WithdrawnReason stopped: Insufficient recruitment
- Enrolment
- 0 participants (actual)
- Lead sponsor
- St. Louis UniversityUniversity, hospital or other
- Collaborators
- Janssen Services, LLC
- Study start
- Nov 2013
- Primary completion
- Mar 2015 (estimated)
- Study completion
- Mar 2015 (actual)
- First posted
- 30 Aug 2013 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The purpose of this study is to determine whether giving abciximab (ReoPro) to children with sickle cell disease who are hospitalized for acute pain crisis will improve their pain and shorten the time spent in the hospital, when compared with standard supportive care.
Detailed description
Sickle cell disease (SCD) is one of the more common genetic diseases worldwide, affecting approximately 1 in 500 African-Americans and 1 in 1000 Hispanic-Americans. A single amino acid substitution decreases the solubility of deoxygenated hemoglobin, leading to polymer formation and subsequent distortion of erythrocyte shape from the normal biconcave disc into a relatively rigid crescent or sickle shape. Initially reversible, the polymer formation and shape distortion eventually becomes permanent. Clinical manifestations of sickle cell disease relate both to increased clearance of these misshapen erythrocytes (causing a chronic hemolytic anemia) as well as occlusion of small (and sometimes large) blood vessels.
Vaso-occlusive phenomena are responsible for much of the acute morbidity of sickle cell disease, including episodes of pain resulting from bone infarcts, splenic infarction with a secondary increased risk of infection, and a relatively high incidence of ischemic stroke (~10% in the first 2 decades of life). In addition, chronic and cumulative ischemic episodes contribute to long-term morbidity (including avascular necrosis of bone, retinopathy, renal insufficiency, and pulmonary hypertension) and a significantly shortened life span. Vaso-occlusive pain crises often require hospitalization for the administration of parenteral narcotics; the average duration of hospitalization is 4-5 days, and a significant proportion of patients experience multiple crises per year. In most episodes, pain continues to intensify over the first 2-3 days before beginning to abate, suggesting that there is ongoing extension of tissue damage for some time following initiation of the episode; also, many patients will develop additional foci of pain even during the course of hospitalization.
While direct mechanical blockage of small vessels by sickled erythrocytes is undoubtedly an important factor in vaso-occlusion, there are other secondary phenomena that are likely to contribute to these episodes, including increased erythrocyte adhesion to the endothelium of post-capillary venules. SCD patients also exhibit chronic pro-coagulation changes in soluble clotting factors, as well as increased platelet number and activation. The relative contribution of these various changes to the pathophysiology of vaso-occlusive crises is unclear. One published study showed that the antiplatelet drug ticlopidine decreased frequency, duration, and severity of pain crises in SCD patients, suggesting that the increase in platelet activation does indeed contribute to vaso-occlusion.
Current therapy for vaso-occlusive pain crises is mostly supportive (maintaining adequate hydration and oxygenation and administering pain medication). With the possible exception of exchange transfusion-a procedure with significant potential morbidity-there is no therapy that directly targets the vaso-occlusion.
Abciximab (ReoPro) is the Fab fragment of the chimeric human-mouse monoclonal antibody 7E3. It avidly binds to both glycoprotein IIb/IIIa and to integrin αvβ3, and so would potentially inhibit both erythrocyte binding to vascular endothelial as well as platelet adhesion, thus targeting two separate mechanisms that are felt to be components of the vaso-occlusive phenomenon in SCD.
The relatively prolonged course of most pain crises-which typically involves increasing intensity of pain and often development of new areas of pain over the first few days-suggests that treatment during the early phases of a crisis might be effective in ameliorating the course of the episode, resulting not only in decreased acute morbidity but possibly also in less long-term tissue damage. The study hypothesis is that administration of abciximab early in the course of a vaso-occlusive sickle cell pain crisis will reduce the median length of hospitalization without an accompanying increase in bleeding or other serious complications.
Participants will be randomized in a double blind fashion to receive either abciximab (ReoPro) or placebo intravenously over 12 hours. Randomization will be stratified by sickle cell genotype: Sickle Cell Anemia (SS) vs. Sickle-Hemoglobin C Disease (SC). All patients will receive standard supportive care, including hydration, supplemental oxygen as needed to maintain oxygen saturation >92%, scheduled use of NSAIDS, and narcotics titrated to effect.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Triple blind (participant, care provider, investigator)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Abciximab | Experimental | Drug: Abciximab, Other: Intravenous hydration, Drug: Ibuprofen, Drug: Parenteral narcotic, Other: Incentive spirometry, Other: Supplemental oxygenAbciximab will be administered as initial bolus of dose of 0.25 mg/kg, delivered via syringe pump over 15 minutes, followed by a continuous infusion of 0.125 microgram/kg/min (max of 10 micrograms/min) infused over the next 12 hours. Infusion to start within 16 hours of admission. Patients will receive standard supportive care, including intravenous hydration, supplemental oxygen, incentive spirometry, ibuprofen, and parenteral narcotic pain medications (morphine, hydromorphone or fentanyl) |
| Placebo | Placebo comparator | Drug: Placebo, Other: Intravenous hydration, Drug: Ibuprofen, Drug: Parenteral narcotic, Other: Incentive spirometry, Other: Supplemental oxygenInactive placebo will be administered as initial bolus followed by a continuous infusion over the next 12 hours, in syringes and volumes identical with the drug administered in the experimental arm. Infusion to begin within 16 hours of admission. Patients will receive standard supportive care, including intravenous hydration, supplemental oxygen, incentive spirometry, ibuprofen, and parenteral narcotic pain medications (morphine, hydromorphone or fentanyl) |
Who may qualify
- Ages
- 5 to 25 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult
Key inclusion criteria (8 listed)
- Diagnosis of sickle cell disease (Hb SS, HbSC, HbS-β0-thalassemia)
- Age 5.00 to 24.99 years
- Pain consistent with vaso-occlusive crisis that meets the criteria for hospitalization and parenteral narcotics: moderate-severe pain unresponsive to oral medications (NSAIDS + narcotics) that has no alternative etiology (e.g., trauma)
- Platelet count >100,000
- INR <1.2, PTT < 40 seconds
Key exclusion criteria (14 listed)
- History of stroke (either ischemic or hemorrhagic)
- Currently receiving anticoagulation medication (heparin within 1 week, Coumadin within 3 weeks) or medication with irreversible anti-platelet effect (e.g., aspirin, ticlopidine) within 14 days
- Red cell transfusion within 60 days
- Major surgery within 30 days
- Treatment with hydroxyurea within 30 days (due to evidence that hydroxyurea can reverse platelet activation in patients with SCD)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| AbciximabAlso: ReoProAbciximab will be administered as initial bolus of dose of 0.25 mg/kg, delivered via syringe pump over 15 minutes, followed by a continuous infusion of 0.125 microgram/kg/min (max of 10 micrograms/min) infused over the next 12 hours. Infusion to start within 16 hours of admission. All patients will receive standard supportive care measures. | Drug | Abciximab |
| PlaceboInactive placebo will be administered as initial bolus followed by a continuous infusion over the next 12 hours, in syringes and volumes identical with the drug administered in the experimental arm. Infusion to begin within 16 hours of admission. All patients will also receive standard supportive care measures. | Drug | Placebo |
| Intravenous hydrationintravenous hydration to provide total fluid intake of 1.25-1.5 times maintenance fluid requirements | Other | Abciximab, Placebo |
| IbuprofenAlso: Advil, MotrinScheduled ibuprofen,~10 mg/kg every 6-8 hours | Drug | Abciximab, Placebo |
| Parenteral narcoticAlso: morphine, hydromorphone, Dilaudid, fentanylParenteral morphine administered by bolus or patient-controlled analgesia to maintain pain control. Hydromorphone or fentanyl will be used in patients who do not tolerate morphine. | Drug | Abciximab, Placebo |
| Incentive spirometryPatients will perform incentive spirometry every 2 hours while awake | Other | Abciximab, Placebo |
| Supplemental oxygenSupplemental oxygen by nasal cannula or mask will be provided if needed to maintain oxygen saturation of 92% or greater. | Other | Abciximab, Placebo |
Primary outcome
Duration of hospitalization
Time frame: Duration of hospital stay, expected average of 5 days
Total duration from admission to the inpatient service until discharge order is written, measured in days.
4 secondary outcomes
Total narcotic dose
Time frame: Duration of hospital stay, expected average of 5 days
Bleeding complications
Time frame: From randomization until 10 days following initial discharge from hospital
Complications (other than bleeding) attributed to study drug
Time frame: From randomization until 3 months following initial discharge from hospital
Readmission rate
Time frame: From discharge date until 3 months following initial discharge from hospital
Results and safety
The study was withdrawn before enrolling participants, so there are no results.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 26 Mar 2015.
- Background: PubMed 357967Dean J, Schechter AN. Sickle-cell anemia: molecular and cellular bases of therapeutic approaches (first of three parts). N Engl J Med. 1978 Oct 5;299(14):752-63. doi: 10.1056/NEJM197810052991405. No abstract available.
- Background: PubMed 692564Dean J, Schechter AN. Sickle-cell anemia: molecular and cellular bases of therapeutic approaches (second of three parts). N Engl J Med. 1978 Oct 12;299(15):804-11. doi: 10.1056/NEJM197810122991504. No abstract available.
- Background: PubMed 9287233Bunn HF. Pathogenesis and treatment of sickle cell disease. N Engl J Med. 1997 Sep 11;337(11):762-9. doi: 10.1056/NEJM199709113371107. No abstract available.
- Background: PubMed 8649903Lane PA. Sickle cell disease. Pediatr Clin North Am. 1996 Jun;43(3):639-64. doi: 10.1016/s0031-3955(05)70426-0.
- Background: PubMed 7993409Platt OS, Brambilla DJ, Rosse WF, Milner PF, Castro O, Steinberg MH, Klug PP. Mortality in sickle cell disease. Life expectancy and risk factors for early death. N Engl J Med. 1994 Jun 9;330(23):1639-44. doi: 10.1056/NEJM199406093302303.
- Background: PubMed 1710777Platt OS, Thorington BD, Brambilla DJ, Milner PF, Rosse WF, Vichinsky E, Kinney TR. Pain in sickle cell disease. Rates and risk factors. N Engl J Med. 1991 Jul 4;325(1):11-6. doi: 10.1056/NEJM199107043250103.
- Background: PubMed 10099145Steinberg MH. Management of sickle cell disease. N Engl J Med. 1999 Apr 1;340(13):1021-30. doi: 10.1056/NEJM199904013401307. No abstract available.
- Background: PubMed 12614204Rees DC, Olujohungbe AD, Parker NE, Stephens AD, Telfer P, Wright J; British Committee for Standards in Haematology General Haematology Task Force by the Sickle Cell Working Party. Guidelines for the management of the acute painful crisis in sickle cell disease. Br J Haematol. 2003 Mar;120(5):744-52. doi: 10.1046/j.1365-2141.2003.04193.x. No abstract available.
- Background: PubMed 9169483Hebbel RP. Perspectives series: cell adhesion in vascular biology. Adhesive interactions of sickle erythrocytes with endothelium. J Clin Invest. 1997 Jun 1;99(11):2561-4. doi: 10.1172/JCI119442. No abstract available.
- Background: PubMed 10627437Kaul DK, Tsai HM, Liu XD, Nakada MT, Nagel RL, Coller BS. Monoclonal antibodies to alphaVbeta3 (7E3 and LM609) inhibit sickle red blood cell-endothelium interactions induced by platelet-activating factor. Blood. 2000 Jan 15;95(2):368-74.
- Background: PubMed 17483236Finnegan EM, Barabino GA, Liu XD, Chang HY, Jonczyk A, Kaul DK. Small-molecule cyclic alpha V beta 3 antagonists inhibit sickle red cell adhesion to vascular endothelium and vasoocclusion. Am J Physiol Heart Circ Physiol. 2007 Aug;293(2):H1038-45. doi: 10.1152/ajpheart.01054.2006. Epub 2007 May 4.
- Background: PubMed 14693325Ataga KI, Orringer EP. Hypercoagulability in sickle cell disease: a curious paradox. Am J Med. 2003 Dec 15;115(9):721-8. doi: 10.1016/j.amjmed.2003.07.011.
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Not yet recruitingPhase 1
Buprenorphine for the Management of Pain in Children With Sickle Cell Disease
Sickle Cell Disease (SCD), Sickle Cell Disease Vaso-occlusive Crisis
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
William S Ferguson, MD principal investigator
St. Louis University
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 2 study testing Abciximab, Intravenous hydration and Ibuprofen in people with Sickle Cell Disease and Hb-SS Disease With Vasoocclusive Pain, run by St. Louis University at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 8 inclusion and 14 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: withdrawn, as of the sponsor's last update on 26 Mar 2015. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 2 studies give the treatment to a larger group to see whether it has the intended effect and to keep checking safety.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study was withdrawn before enrolling participants, so there are no results.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Duration of hospitalization (time frame: Duration of hospital stay, expected average of 5 days). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT01932554, which also lists 13 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 26 Mar 2015.