ds4dh/ct-dosing-errors huggingface dataset:
Clinical trial NCT00826267
Conditions: Breast Neoplasms
Sponsor: Boehringer Ingelheim
Start date: 2009-01-01; Completion date: 2011-08-01
Enrollment: 29 participants; Allocation: RANDOMIZED; Intervention model: PARALLEL

Brief summary:
An open-label, randomized three-arm Phase II trial to explore the efficacy of BIBW 2992 as a single agent versus lapatinib versus trastuzumab in patients with HER2-positive treatment-naïve Stage IIIa locally advanced breast cancer. Additional information will be obtained on the safety profile and pharmacokinetics of BIBW 2992.

Detailed description:

Arms: arm 1: BIBW 2992 high dose once daily (allowed dose reduction to medium or low once daily in case of AE) arm 2: Lapatinib tablets 1500 mg daily. arm 3: Trastuzumab 4mg/kg i.v. week 1, followed by 2mg/kg i.v. weekly.
Interventions: intervention 1: lapatinib intervention 2: BIBW 2992 intervention 3: trastuzumab
Intervention descriptions: intervention 1: lapatinib tablets 1500 mg daily intervention 2: BIBW 2992 high dose once daily (allowed dose reduction to medium or low once daily in case of AE) intervention 3: trastuzumab 4mg/kg i.v. week 1, followed by 2mg/kg i.v. weekly

Protocol documents:
Clinical trial NCT00858273
Conditions: Diabetes Mellitus, Type 1
Keywords: Glutathione
Sponsor: Nemours Children's Clinic
Start date: 2008-03-01; Completion date: 2011-08-01
Enrollment: 41 participants; Allocation: RANDOMIZED; Intervention model: PARALLEL

Brief summary:
Glutathione is normally present at high levels in the blood and plays an important role in the body's defense against oxidative stress, that is, against the damage caused to the body by several reactive oxygen species produced by the metabolism of most nutrients, including glucose. Glutathione is a small peptide made from 3 amino acids, glutamate, cysteine, and glycine.

This study is looking at how blood sugar levels may affect the way glutathione is made and used by the body. Since glutathione is continuously synthesized and broken down, the amount of glutathione present in the blood depends on the balance between its rate of synthesis and its rate of use.

In earlier studies, we found that in poorly controlled diabetic teenagers, glutathione was low, not because it was not produced fast enough, but because it was used at an excessive rate. In this study, we want to find out whether improving blood sugar control will increase glutathione levels, and, if so, how long this will take. We also hope to find out if oral supplementation with a mixture of several antioxidant vitamins and minerals will increase glutathione levels more than taking a placebo.

Detailed description:
Forty adolescents with T1D will undergo a measurement of blood glutathione concentration and markers of oxidative stress (plasma protein-bound 3-nitrotyrosine, and urinary 8OH-2-dG, and F2-isoprostane excretion, markers of oxidative damage to protein, DNA and lipids, respectively) while at near normoglycemia, on two separate occasions:

* first, when in poor glucose control (HbA1c\>7.5%); and
* secondly, after 3 to 9 months months of improved blood glucose control, along with the administration of either a placebo, or a mixture of antioxidant minerals and vitamins based on a randomization scheme.

Between the two metabolic study days, patients will receive the same intensified diabetes regimen consisting of education and counseling, home blood glucose monitoring, multiple daily insulin injections (MDI), diet plan, and frequent phone contact with a certified diabetes educator.

Arms: arm 1: Vitamin C 250 mg; beta-carotene 6 mg; vitamin E 30 mg; selenium 100 mcg; zinc 20 mg arm 2: None
Interventions: intervention 1: Antioxidant supplement intervention 2: Diabetes treatment intervention 3: Regular Insulin
Intervention descriptions: intervention 1: 1 capsule daily with dinner intervention 2: Intensification of diabetes treatment regimen, including education and counseling, home blood glucose monitoring, multiple daily insulin injections (MDI), diet plan, and frequent phone contact with a certified diabetes educator intervention 3: Regular Insulin, IV, to maintain blood glucose in normoglycemic range (70-140) during metabolic study

Protocol documents:
Clinical trial NCT00868140
Conditions: Polycystic Ovary Syndrome
Sponsor: Virginia Commonwealth University
Start date: 2009-02-01; Completion date: 2011-08-01
Enrollment: 51 participants; Allocation: RANDOMIZED; Intervention model: PARALLEL

Brief summary:
Our hypothesis is that hyperinsulinemia increases the renal clearance of D-chiro-inositol (DCI) in women with polycystic ovary syndrome (PCOS) and that this leads to a reduction in circulating insulin-stimulated D-chiro-inositol-containing inositol phosphoglycan (DCI-IPG) release. To assess the effects of a chronic reduction in circulating insulin on DCI metabolism, we propose to reduce circulating insulin in obese women with PCOS by improving insulin sensitivity with the drug pioglitazone. Pioglitazone is a thiazolidinedione that improves peripheral insulin sensitivity, presumably by activation of the peroxisome proliferator-activated receptor gamma (PPARγ) receptor. Administration of pioglitazone to women with PCOS has been shown to improve insulin sensitivity, reduce insulin secretion, and decrease both fasting and post-prandial serum insulin concentrations.

Detailed description:
This protocol focuses on the hypothesis that a deficiency in a putative inositolphosphoglycan (IPG) mediator of insulin action, namely a D-chiro-inositol-containing IPG (DCI-IPG), contributes to the insulin resistance of some women with PCOS. Our interest in this area stems directly from our previous studies, which demonstrated that administration of the precursor, D-chiro-inositol (DCI), to both obese and lean women with PCOS improved glucose intolerance while reducing circulating insulin, and simultaneously improved ovulatory function and decreased serum androgens. These findings were recently confirmed in a large-scale study by an independent group. The findings of these three studies suggested that administration of DCI improved insulin sensitivity in PCOS, which then resulted in an improved hormonal and metabolic milieu.

Arms: arm 1: Pioglitazone in pill form at 45mg twice per day for 6 months arm 2: Placebo control to arm 1 in pill form identical to treatment form also twice per day for 6 months
Interventions: intervention 1: pioglitazone intervention 2: Placebo
Intervention descriptions: intervention 1: pioglitazone 45 mg intervention 2: placebo daily

Protocol documents:
Clinical trial NCT00871377
Conditions: Epilepsy
Keywords: epilepsy cardiac risk factors memory cognition n-3 fatty acids fish oil EPA DHA seizures
Sponsor: National Center for Complementary and Integrative Health (NCCIH)
Start date: 2008-05-01; Completion date: 2011-08-01
Enrollment: 24 participants; Allocation: RANDOMIZED; Intervention model: CROSSOVER

Brief summary:
The purpose of this study is to determine if Omega-3 fatty acids reduce seizures and modify cardiac risk factors in people with epilepsy.

Detailed description:
Epilepsy is a common and disabling condition, characterized by recurrent seizures. Sudden unexpected death (SUDEP) is a major cause of mortality in people with epilepsy. SUDEP accounts for up to 20% of all cause mortality, and is most common in younger people, especially in their 20's to 40's year olds. In those with drug resistant epilepsy, SUDEP is five times more common than in well-controlled epilepsy. Likely causes of death include cardiac arrhythmias due to impaired autonomic regulation and reduced heart rate variability. Similarly, patients with recent myocardial infarction and congestive heart failure are at higher risk for sudden death, and manifest markedly reduced heart rate variability. Clinical studies of heart disease indicate that n-3 fatty acids, prevent cardiac arrhythmias, reduce mortality after myocardial infarction, and reduce the risk of sudden cardiac death. The mechanism by which EPA and DHA exert their anti-arrhythmia effect is due to inactivation of high frequency sodium and L-type calcium channels in the heart. In addition, n-3 fatty acids improve HRV in cardiac patients, and this reduction in HRV is postulated to be a marker of the anti-arrhythmic effect of n-3 fatty acids. Preliminary data from our group indicates that n-3 fatty acids improve HRV in people with epilepsy, especially those with low HRV (SDNN \< 50). The commonality between n-3 fatty acids and improvement in HRV in patients with heart disease and epilepsy serves as a basis for our hypothesis that n-3 fatty acids may reduce the risk of SUDEP in epilepsy. The purpose of this proposal is to determine if n-3 fatty acids reduce seizures and modify cardiac risk in people with epilepsy who are at risk of SUDEP.

Arms: arm 1: Corn Oil Placebo (n-6 fatty acids) arm 2: 2160 mg of EPA + DHA arm 3: 1060 mg of EPA + DHA
Interventions: intervention 1: Placebo intervention 2: High Dose Fish Oil intervention 3: Low Dose Fish Oil
Intervention descriptions: intervention 1: corn oil (n-6 fatty acids) intervention 2: n-3 fatty acids, 1060 mg EPA + DHA intervention 3: n-3 fatty acids, 2160 mg EPA + DHA

Protocol documents:
Clinical trial NCT00875979
Conditions: Metastatic Breast Cancer
Keywords: MBC Breast Cancer HER2+ HER2+ breast cancer HER2 positive breast cancer herceptin Trastuzumab emtansine
Sponsor: Hoffmann-La Roche
Start date: 2009-05-01; Completion date: 2011-08-01
Enrollment: 67 participants; Allocation: NON_RANDOMIZED; Intervention model: SINGLE_GROUP

Brief summary:
This was a multi-institutional, multinational, open-label, single-arm Phase Ib/II study designed to evaluate the safety, tolerability, pharmacokinetics, and efficacy of trastuzumab emtansine (trastuzumab-MCC-DM1) administered by intravenous (IV) infusion in combination with pertuzumab in patients with human epidermal growth factor receptor-2 (HER2)-positive locally advanced or metastatic breast cancer who had previously received trastuzumab.

Detailed description:
There were 2 phases in the study, a Dose Escalation phase (Phase 1b) and a Dose Expansion phase (Phase 2a). In the Dose Escalation phase, 3 patients were enrolled at the first dose level (3.0 mg/kg trastuzumab emtansine) and and 6 patients were enrolled at the second dose level (3.6 mg/kg trastuzumab emtansine). An additional 58 patients were enrolled at the 3.6 mg/kg trastuzumab emtansine dose level in the Dose Expansion phase (Phase 2a) of the study.

Arms: arm 1: Patients received trastuzumab emtansine 3.0 mg/kg intravenously (IV) on Day 1 of every 3 week cycle until progressive disease, intolerable toxicity, initiation of another anti-cancer therapy, or patient discontinuation. Patients also received a loading dose of 840 mg of pertuzumab IV on Day 1 of Cycle 1 followed by pertuzumab 420 mg IV on Day 1 of every subsequent 3 week cycle. arm 2: Patients received trastuzumab emtansine 3.6 mg/kg intravenously (IV) on Day 1 of every 3 week cycle until progressive disease, intolerable toxicity, initiation of another anti-cancer therapy, or patient discontinuation. Patients also received a loading dose of 840 mg of pertuzumab IV on Day 1 of Cycle 1 followed by pertuzumab 420 mg IV on Day 1 of every subsequent 3 week cycle.
Interventions: intervention 1: Trastuzumab emtansine [Kadcyla] 3.0 mg/kg intervention 2: Trastuzumab emtansine [Kadcyla] 3.6 mg/kg intervention 3: Pertuzumab 420 mg
Intervention descriptions: intervention 1: Trastuzumab emtansine was provided as a single-use lyophilized formulation. intervention 2: Trastuzumab emtansine was provided as a single-use lyophilized formulation. intervention 3: Pertuzumab was provided as a single-use formulation.

Protocol documents:
Clinical trial NCT00878553
Conditions: Sleep Disorder Primary Insomnia
Keywords: insomnia middle of the night sleep maintenance
Sponsor: Somnus Therapeutics, Inc.
Start date: 2010-05-01; Completion date: 2011-08-01
Enrollment: 67 participants; Allocation: RANDOMIZED; Intervention model: CROSSOVER

Brief summary:
SKP-1041 is a new formulation of a marketed sleeping agent called zaleplon. Zaleplon is currently available as Sonata as well as several generic formulations. Sonata and its generics induce sleep soon after ingestion. SKP-1041, however, is a formulation that is designed to become active 2-3 hours after ingestion. It is intended for use in people who have no trouble falling to sleep but who often awaken in the middle of the night. This trial will determine the best dose to prevent those awakenings.

Detailed description:
Patients will participate in the study for approximately 44 to 56 days, including a 14- to 21-day Screening Period, 4 Treatment Periods each followed by washout periods, and a final Follow-up Visit. Patients will receive their randomly assigned study medication and spend 2 nights in a sleep laboratory, subsequently returning home for a 4- to 7-day washout period between each treatment period. The fourth and final treatment period will include a third night at the site during which all patients will continue to receive the same study medication as on the first 2 nights of this treatment period. Blood will be drawn from all patients for pharmacokinetic analyses at specific time intervals. Patients will undergo final safety assessments 2 to 5 days after the last dose of study medication.

Arms: arm 1: Two placebo tablets administered orally at bedtime for two consecutive nights to each patient per crossover randomized sequence arm 2: One 10 mg SKP-1041 controlled release zaleplon tablet plus one placebo tablet administered orally at bedtime for two consecutive nights to each patient per crossover randomized sequence arm 3: One 15 mg SKP-1041 controlled release zaleplon tablet plus one placebo tablet administered orally at bedtime for two consecutive nights to each patient per crossover randomized sequence arm 4: Two 10 mg SKP-1041 controlled release zaleplon tablets administered orally at bedtime for two consecutive nights to each patient per crossover randomized sequence
Interventions: intervention 1: placebo intervention 2: SKP-1041 (experimental formulation of zaleplon)
Intervention descriptions: intervention 1: tablet at bedtime intervention 2: tablet at bedtime

Protocol documents:
Clinical trial NCT00903331
Conditions: Idiopathic Pulmonary Fibrosis
Keywords: idiopathic pulmonary fibrosis MUSIC
Sponsor: Actelion
Start date: 2009-05-01; Completion date: 2011-08-01
Enrollment: 178 participants; Allocation: RANDOMIZED; Intervention model: PARALLEL

Brief summary:
The AC-055B201/MUSIC study is a Phase II study, comparing one dose of ACT-064922 (macitentan) 10 mg with placebo in patients with idiopathic pulmonary fibrosis (IPF). The main study objective is to demonstrate that macitentan positively affects the forced vital capacity (FVC) in comparison with placebo in patients with idiopathic pulmonary fibrosis (IPF).

The secondary objectives are to evaluate the effect of macitentan on the time to disease worsening or death in patients with IPF, and to evaluate the benefit/risk profile of macitentan in the treatment of patients with IPF.

Detailed description:
The study included two treatment periods: Period 1 (fixed duration) from randomization up to the primary endpoint evaluation (Month 12 or earlier in case of premature discontinuation of study drug) and Period 2 (variable duration) from the primary endpoint evaluation visit up to the end of study (EOS). EOS occurred when the last patient randomized and not prematurely discontinued completed Period 1.

Arms: arm 1: ACT-064922 tablet (macitentan), 10 mg, once daily arm 2: Matching placebo, once daily
Interventions: intervention 1: ACT-064992 (macitentan) intervention 2: Placebo
Intervention descriptions: intervention 1: ACT-064992 (macitentan) tablet, 10 mg, once daily intervention 2: matching placebo, once daily

Protocol documents:
Clinical trial NCT00903630
Conditions: Fallopian Tube Cancer Ovarian Cancer Peritoneal Cavity Cancer
Keywords: recurrent ovarian epithelial cancer fallopian tube cancer peritoneal cavity cancer
Sponsor: Masonic Cancer Center, University of Minnesota
Start date: 2009-04-01; Completion date: 2011-08-01
Enrollment: 15 participants; Allocation: NON_RANDOMIZED; Intervention model: SINGLE_GROUP

Brief summary:
RATIONALE: Lenalidomide may stop the growth of cancer by blocking blood flow to the tumor. Drugs used in chemotherapy, such as doxorubicin hydrochloride liposome, work in different ways to stop the growth of tumor cells, either by killing the cells or by stopping them from dividing. Giving lenalidomide together with doxorubicin hydrochloride liposome may kill more tumor cells.

PURPOSE: This phase I/II trial is studying the side effects and best dose of lenalidomide when given together with doxorubicin hydrochloride liposome in treating patients with recurrent ovarian epithelial cancer, fallopian tube cancer, or primary peritoneal cancer.

Detailed description:
OBJECTIVES:

Phase I - Primary

* To determine the maximum tolerated dose of lenalidomide when combined with fixed dose pegylated liposomal doxorubicin hydrochloride in women with recurrent ovarian epithelial, fallopian tube, or primary peritoneal cancer.

Phase II - Define the best overall response induced by lenalidomide in recurrent ovarian cancer patients

Secondary

* To obtain preliminary information on toxicity, response, and time to progression (duration of response) of these patients.
* Progression free survival

Phase I OUTLINE: This is a dose-escalation study of lenalidomide. Patients receive oral lenalidomide once daily on days 1-28 and pegylated liposomal doxorubicin hydrochloride intravenously (IV) on day 1. Treatment repeats every 28 days for up to 6 courses in the absence of disease progression or unacceptable toxicity.

Phase II OUTLINE: The phase II component will include patients with measurable disease per Response Evaluation Criteria In Solid Tumors (RECIST) criteria treated at lenalidomide 10 mg days 1-28 days of a 28 day cycle (Maximum Tolerated Dose from phase I) with liposomal doxorubicin 40 mg/m\^2 to determine efficacy and safety of the combination therapy. (Effective with April 2010 revision)

After completion of study therapy, patients are followed periodically.

Arms: arm 1: liposomal doxorubicin: 40mg/m2 IV Day 1 every 28 days plus lenalidomide: 10 mg daily on Days 1-28 every 28 days arm 2: liposomal doxorubicin: 40mg/m2 IV Day 1 every 28 days plus lenalidomide: 15 mg daily on Days 1-28 every 28 days arm 3: liposomal doxorubicin: 40mg/m2 IV Day 1 every 28 days plus lenalidomide: maximum tolerated dose from Phase I portion of the study (10mg) daily on Days 1-28 every 28 days
Interventions: intervention 1: Lenalidomide intervention 2: liposomal doxorubicin
Intervention descriptions: intervention 1: administered by mouth at the assigned dose daily for each 28 day cycle intervention 2: administered at a fixed dose of 40 mg/m\^2 intravenously (IV) on day 1 of each 28 day cycle

Protocol documents:
Clinical trial NCT00910520
Conditions: Overactive Bladder
Sponsor: Allergan
Start date: 2009-09-01; Completion date: 2011-08-01
Enrollment: 548 participants; Allocation: RANDOMIZED; Intervention model: PARALLEL

Brief summary:
The purpose of this study is to assess the safety and effectiveness of botulinum toxin type A (onabotulinumtoxinA) in treating patients with idiopathic overactive bladder with urinary incontinence.

Detailed description:

Arms: arm 1: OnabotulinumtoxinA (botulinum toxin Type A) 100 U injected into the detrusor at Day 1, followed by a repeat injection of onabotulinumtoxinA 100 U after a minimum of 12 weeks (if applicable). arm 2: Placebo (normal saline) injected into the detrusor at Day 1, followed by an injection of onabotulinumtoxinA (botulinum toxin Type A) 100 U after a minimum of 12 weeks (if applicable).
Interventions: intervention 1: onabotulinumtoxinA intervention 2: normal saline
Intervention descriptions: intervention 1: OnabotulinumtoxinA (botulinum toxin Type A) 100 U injected into the detrusor at Day 1, followed by a repeat injection of onabotulinumtoxinA 100 U after a minimum of 12 weeks (if applicable). Or, if placebo is administered at Day 1, onabotulinumtoxinA 100 U injected after a minimum of 12 weeks (if applicable). intervention 2: Normal saline (placebo) injected into the detrusor at Day 1.

Protocol documents:
Clinical trial NCT00942708
Conditions: Pulmonary Arterial Hypertension
Keywords: Pulmonary Arterial Hypertension Pulmonary Hypertension
Sponsor: University of Texas Southwestern Medical Center
Start date: 2009-09-01; Completion date: 2011-08-01
Enrollment: 6 participants; Allocation: NA; Intervention model: SINGLE_GROUP

Brief summary:
This study will evaluate the safety, tolerability and efficacy of open-label fluoxetine for three months among patients with pulmonary arterial hypertension.

Detailed description:
Idiopathic pulmonary arterial hypertension (PAH) is a life-threatening disorder of uncertain cause that leads to progressive right heart failure and death. Average survival has improved from about 2.8 years in the early 1990s to approximately 5-7 years with current treatments, but most patients will still die of their disease. Two classes of oral medications are approved for use in PAH: endothelin-1 antagonists, and phosphodiesterase-5 inhibitors. Both improve walk distance and symptoms in PAH, but most patients still have continued dyspnea, fatigue and significant elevations in pulmonary pressures. Those who remain severely impaired are generally started on a continuous intravenous prostacyclin. For those who are less ill but still symptomatic, few options are available.

Primary endpoint: the primary endpoint will be change in pulmonary vascular resistance (PVR) measured by right heart catheterization after three months of therapy.

Secondary endpoints

* Six minute walk distance
* QIDS-SR depression scale

Safety and tolerability endpoints will include a tabulation of adverse events to include but not limited to:

* Death
* Hospitalization
* Symptomatic hypotension
* Gastrointestinal side effects
* Depression

Arms: arm 1: Fluoxetine will be added starting at 20 mg and titrated as tolerated to 80 mg daily.
Interventions: intervention 1: Fluoxetine
Intervention descriptions: intervention 1: Total dose How to take:

Week 1-2 20 mg daily Week 3-4 40 mg daily Week 5-6 40 mg BID Week 7-12 40mg BID

Protocol documents: