ds4dh/ct-dosing-errors huggingface dataset:
Clinical trial NCT02365233
Conditions: Type II Diabetes Nonalcoholic Fatty Liver
Keywords: Type II Diabetes Nonalcoholic fatty liver
Sponsor: The University of Texas Medical Branch, Galveston
Start date: 2013-05-01; Completion date: 2016-12-31
Enrollment: 5 participants; Allocation: RANDOMIZED; Intervention model: PARALLEL

Brief summary:
The primary objective of this trial is to measure changes in hepatic lipid content using three common alternative therapeutic strategies to improve glycemic control in patients with type 2 diabetes who are not controlled with metformin alone.

Detailed description:
In patients with type 2 diabetes whose glycemic control is not accomplished with Metformin alone, there are several options for additional hypoglycemic agent. As per recent National guidelines at least three "second line" agents can be added to metformin: thiazolidinediones, Lantus insulin, and DPP4 inhibitors. All three approaches have been proven to help accomplishing goals of therapy for glycemic control (HbA1c\<7%) in clinical trials. Whether one approach is superior to the other in improving associated non-glycemic metabolic abnormalities and risk for future morbidity and mortality in patients with type 2 diabetes remains a matter of intense debate. Among these abnormalities, excessive triglyceride content in the liver (fatty liver or liver steatosis) is a major predictor of risk for non-alcoholic steato-hepatitis (NASH) and liver cirrhosis. Fatty liver is highly prevalent in patients with type 2 diabetes. There are no clinical studies done to determine if any of these three therapeutic options is superior at reducing the liver triglyceride content in patients with type 2 diabetes and fatty Liver. Therefore, in this study we propose to measure and compare the effects on liver triglyceride content when either pioglitazone, lantus insulin, or DPP4 inhibitors are added to metformin in patients with poorly controlled type 2 diabetes (HbA1c\>7.6%) and fatty liver (presence of "bright" liver in abdominal ultrasound). The primary objective of this trial is to measure changes in hepatic lipid content using three common alternative therapeutic strategies to improve glycemic control in patients with type 2 diabetes who are not controlled with metformin alone.

Arms: arm 1: (Pioglitazone, 15 mg/day) arm 2: 0.35 U per kg body weight once daily arm 3: Sitagliptin, 100 mg/day or Saxagliptin, 5 mg/day
Interventions: intervention 1: DPP4 inhibitor intervention 2: Pioglitazone intervention 3: Lantus insulin
Intervention descriptions: intervention 1: Comparison between three common alternative therapeutic strategies to improve glycemic control in patients with type 2 diabetes who are not controlled with metformin alone. intervention 2: Comparison between three common alternative therapeutic strategies to improve glycemic control in patients with type 2 diabetes who are not controlled with metformin alone. intervention 3: Comparison between three common alternative therapeutic strategies to improve glycemic control in patients with type 2 diabetes who are not controlled with metformin alone.

Protocol documents:
Clinical trial NCT02561702
Conditions: Charcot Marie Tooth Disease
Sponsor: University of Rochester
Start date: 2015-09-01; Completion date: 2016-12-31
Enrollment: 4 participants; Allocation: RANDOMIZED; Intervention model: CROSSOVER

Brief summary:
Charcot Marie Tooth Disease is a family of inherited peripheral neuropathies, with over 70 causative genes identified to date.1-4 Muscle cramps are frequent in CMT, affecting up to 85% of patients with some subtypes of CMT. These cramps impact quality of life and have been identified as an important therapeutic target for clinical trials in CMT.1-4 There is no FDA approved treatment for muscle cramps.5 Mexiletine is a sodium channel blocker approved for treatment of arrhythmias. As a sodium channel blocker, mexiletine offers the promise of effective therapy for muscle cramps.

Detailed description:
This study will provide data on the short term efficacy of oral mexiletine in helping to prevent muscle cramps in adults with CMT. The study will also assess the short-term safety and tolerability of low dose mexiletine in adults with CMT.

Arms: arm 1: Participants will receive 150 mg of mexiletine by mouth 3 times daily for 5-7 days followed by 7 day washout period and 5-7 days of placebo (240 mg of lactose powder) taken by mouth 3 times daily arm 2: Participants will receive placebo (240 mg of lactose powder) taken by mouth 3 times daily for 5-7 days followed by 7 day washout period and 5-7 days of 150 mg of mexiletine by mouth 3 times daily
Interventions: intervention 1: Placebo intervention 2: Mexiletine
Intervention descriptions: intervention 1: 240 mg lactose powder in a size 3 capsule taken by mouth 3 times daily for 5-7 days intervention 2: 150 mg Mexiletine taken by mouth in capsule form 3 times daily for 5-7 days

Protocol documents:
Clinical trial NCT02742649
Conditions: Open-Angle Glaucoma Ocular Hypertension
Sponsor: ForSight Vision5, Inc.
Start date: 2016-04-30; Completion date: 2016-12-31
Enrollment: 55 participants; Allocation: RANDOMIZED; Intervention model: PARALLEL

Brief summary:
The purpose of this study is to determine if a combination of two drugs (bimatoprost and timolol) delivered to the surface of the eye over 10 weeks is better at lowering intraocular pressure (IOP) than either of the drugs delivered alone.

Detailed description:

Arms: arm 1: Washout plus Placebo Ocular Insert in each eye for 24 to 48 days, followed by one segment of bimatoprost and one segment of timolol maleate combined onto a single ocular insert in each eye for 70 days. Following a second washout period, 0.5% timolol drops twice daily in each eye from Day 99 to 112. arm 2: Washout plus Placebo Ocular Insert in each eye for 24 to 48 days, followed by one segment of bimatoprost and one placebo segment (no drug product) combined onto a single ocular insert in each eye for 70 days. Following a second washout period, 0.5% timolol drops twice daily in each eye from Day 99 to 112. arm 3: Washout plus Placebo Ocular Insert in each eye for 24 to 48 days, followed by one segment of timolol and one placebo segment (no drug product) combined onto a single ocular insert in each eye for 70 days. Following a second washout period, 0.5% timolol drops twice daily in each eye from Day 99 to 112.
Interventions: intervention 1: Fixed Combination intervention 2: Bimatoprost intervention 3: Timolol intervention 4: Placebo Segment intervention 5: Timolol 0.5%
Intervention descriptions: intervention 1: Continuous elution from the ocular insert. intervention 2: Continuous elution from the ocular insert. This is an active control arm. intervention 3: Continuous elution from the ocular insert. This is an active control arm. intervention 4: One segment of placebo (no drug product) intervention 5: 0.5% timolol drops twice daily.

Protocol documents:
Clinical trial NCT02777073
Conditions: Type 1 Diabetes
Keywords: Diabetic ketoacidosis Insulin Type 1 Diabetes glucose (sugar) control
Sponsor: University at Buffalo
Start date: 2016-03-01; Completion date: 2016-12-31
Enrollment: 43 participants; Allocation: RANDOMIZED; Intervention model: PARALLEL

Brief summary:
1. To compare levels of ketone bodies (beta-hydroxybutyrate and acetoacetate) in plasma and urine following a single dose treatment of either liraglutide 1.8mg, dapagliflozin 10mg or placebo in insulinopenic state.
2. To compare plasma levels of free fatty acid, glucagon, hs-CRP, Ll-6 and IL-1 before and after administration of liraglutide/placebo.

Detailed description:
Diabetic ketoacidosis is an important cause of mortality and morbidity in type 1 patients. The decreased ratio of insulin to glucagon in insulin deficient subjects promotes ketogenesis. In patients with type 1 diabetes, the suppressive effect of hyperglycemia and the paracrine inhibitory effect of insulin and GABA from the β cell on α cell are absent. Thus, plasma glucagon concentrations are elevated and in combination with insulin deficiency, lead to lipolysis, increased plasma FFA concentrations and an increased fatty acid supply to the liver. Thus, both fatty acid oxidation and ketogenesis are enhanced.

Our recent work has shown that liraglutide, a GLP 1 agonist, improves glycemic control and reduces glycemic excursions in patients with type 1 diabetes within a few days of the initiation of treatment.

With this background, the investigators hypothesize that suppression of glucagon with liraglutide in patients with type 1 diabetes may protect them from lipolysis, increased bio-availability of FFAs, ketogenesis and ketoacidosis.

It is essential to investigate this area further as there are no prior studies that have investigated the acute effects of liraglutide on FFAs or ketogenesis. This study will be the first randomized controlled prospective study investigating the effect of liraglutide on ketogenesis. Also, it would be important to measure the mediators of inflammation at the same time to investigate whether there is a concomitant changes of inflammatory factors in parallel with the lipolysis and ketogenesis.

After the screening visit, subjects who meet the inclusion and exclusion criteria will be randomized to receive a single dose of either liraglutide, dapagliflozin or placebo and will be monitored for a total of 8 hours.

Arms: arm 1: single dose of Victoza ( liraglutide) 1.8 mg arm 2: Single dose of placebo arm 3: Single dose of Dapagliflozin 10 mg oral tablet
Interventions: intervention 1: Victoza intervention 2: Placebo intervention 3: Dapagliflozin 10mg Tab
Intervention descriptions: intervention 1: Single dose of Liraglutide intervention 2: Single dose of generic placebo intervention 3: single dose of 10 mg dapagliflozin

Protocol documents:
Clinical trial NCT03061513
Conditions: Parkinson Disease
Keywords: Parkinson Disease ubiquinol CoQ10 magnetic resonance spectroscopy lactate glutathione
Sponsor: Weill Medical College of Cornell University
Start date: 2012-02-28; Completion date: 2016-12-31
Enrollment: 11 participants; Allocation: RANDOMIZED; Intervention model: PARALLEL

Brief summary:
The purpose of this study is to find out whether ubiquinol is well tolerated, can affect the symptoms of Parkinson's Disease and change the energy levels in the brain. Subjects will be randomized to taking ubiquinol or placebo and will have a neurological evaluation, magnetic resonance spectroscopy (MRS) and blood test for biological markers taken during the study.

Detailed description:
Multiple lines of evidence have implicated abnormal energy metabolism and deficient mitochondrial function in Parkinson's disease, presenting a unique target for therapy. A pilot study of ubiquinol in PD was therefore undertaken to determine its effects upon physiologic measures of mitochondrial metabolic function. The incorporation of a neuroimaging biomarker is particularly important, since changes would demonstrate our ability to achieve Central Nervous System (CNS) access from this an formulation, accompanied by a meaningful neurophysiologic effect. Hydrogen Proton Magnetic Resonance Spectroscopy Imaging (1H MRSI) is a technique that provides insight into the metabolism of several endogenous brain compounds, most notably N-acetyl-L-aspartate (NAA), choline-containing compounds (Cho), and creatine and phosphocreatine (Cr). A number of studies of mitochondrial function have now firmly established the utility of 1H MRSI in probing potential mitochondrial energy metabolism dysfunction, in primary mitochondrial disorders, but also in PD. This pilot study is therefore designed to test whether oral ubiquinol affects cerebral indices of mitochondrial dysfunction, as measured by 1H MRSI in patients with Parkinson's disease, and to gather preliminary information on the safety and tolerability of ubiquinol in individuals with PD.

Arms: arm 1: 600mg ubiquinol daily for 24 weeks arm 2: Placebo daily for 24 weeks
Interventions: intervention 1: Ubiquinol intervention 2: Placebo
Intervention descriptions: intervention 1: Ubiquinol caplets 600mg/day intervention 2: placebo

Protocol documents:
Clinical trial NCT03238924
Conditions: PTSD
Keywords: posttraumatic stress disorder oxytocin Prolonged Exposure
Sponsor: Medical University of South Carolina
Start date: 2015-01-01; Completion date: 2016-12-31
Enrollment: 17 participants; Allocation: RANDOMIZED; Intervention model: PARALLEL

Brief summary:
Posttraumatic stress disorder (PTSD) is a chronic, debilitating anxiety disorder that may develop after direct or indirect exposure to traumatic events. Prolonged Exposure (PE) is a cognitive-behavioral psychotherapy modality with a wealth of empirical support demonstrating its efficacy to treat PTSD in a variety of populations. The neuropeptide oxytocin is a promising new pharmacotherapeutic agent with prominent anxiolytic effects . Despite a strong biological and theoretical rationale for investigating the potential effectiveness of augmenting PE with intranasal oxytocin, no studies to date have done so. The current study aims to address this important gap in the literature by examining changes in PTSD symptoms following PE treatment combined with a) 40 IU of intranasal oxytocin or b) placebo.

Detailed description:

Arms: arm 1: 40 IU intranasal oxytocin spray arm 2: Placebo is matching saline nasal spray
Interventions: intervention 1: Oxytocin intervention 2: Placebos
Intervention descriptions: intervention 1: 40 IU oxytocin nasal spray, self-administered intervention 2: Saline nasal spray, self-administered

Protocol documents:
Clinical trial NCT01465997
Conditions: Epilepsy Monotherapy
Keywords: Lacosamide
Sponsor: UCB BIOSCIENCES GmbH
Start date: 2012-05-01; Completion date: 2017-01-01
Enrollment: 551 participants; Allocation: NON_RANDOMIZED; Intervention model: PARALLEL

Brief summary:
Compare safety of Lacosamide (LCM) to Carbamazepine Controlled-Release (CBZ-CR) as monotherapy in newly or recently newly diagnosed subjects with primary safety variables including spontaneous reports of Adverse Events (AEs), withdrawal of subjects due to AEs, reporting of Serious AEs (SAEs).

Detailed description:

Arms: arm 1: 50 and 100 mg tablets of Lacosamide given as 100 mg/day, 200 mg/day, 300 mg/day, 400 mg/day, 500 mg/day or 600 mg/day throughout the Treatment Period (Maximum 3.5 Years) arm 2: 200 mg tablets of Carbamazepine-CR given as 200 mg/day, 400 mg/day, 600 mg/day, 800 mg/day, 1000 mg/day or 1200 mg/day throughout the Treatment Period (Maximum of 3.5 Years)
Interventions: intervention 1: Lacosamide intervention 2: Carbamazepine-Controlled Release (CBZ-CR)
Intervention descriptions: intervention 1: 50 and 100 mg tablets of Lacosamide given as 100 mg/day, 200 mg/day, 300 mg/day, 400 mg/day, 500 mg/day or 600 mg/day throughout the Treatment Period (Maximum 3.5 Years) intervention 2: 200 mg tablets of Carbamazepine-CR given as 200 mg/day, 400 mg/day, 600 mg/day, 800 mg/day, 1000 mg/day or 1200 mg/day throughout the Treatment Period (Maximum 3.5 Years)

Protocol documents:
Clinical trial NCT02120417
Conditions: Breast Cancer
Keywords: Breast Cancer
Sponsor: Incyte Corporation
Start date: 2014-05-01; Completion date: 2017-01-01
Enrollment: 149 participants; Allocation: RANDOMIZED; Intervention model: PARALLEL

Brief summary:
This was a randomized, double-blind, placebo-controlled phase 2 clinical trial comparing the overall survival of women with advanced or metastatic HER2-negative breast cancer who received treatment with capecitabine in combination with ruxolitinib versus those who received treatment with capecitabine alone.

Detailed description:

Arms: arm 1: None arm 2: None
Interventions: intervention 1: Ruxolitinib intervention 2: Capecitabine intervention 3: Placebo
Intervention descriptions: intervention 1: 5 mg tablets to be administered by mouth

Ruxolitinib 15 mg BID (starting dose) intervention 2: Capecitabine 2000 mg/m\^2 daily given as 1000 mg/m\^2 twice a day (BID) (starting dose) Day 1-14 of each 21 day cycle intervention 3: 5 mg matching placebo tablets to be administered by mouth

Protocol documents:
Clinical trial NCT00179010
Conditions: Ischemia
Keywords: Adenosine AMP Microdialysis Blood Flow
Sponsor: Vanderbilt University Medical Center
Start date: 2003-10-01; Completion date: 2017-01-01
Enrollment: 13 participants; Allocation: RANDOMIZED; Intervention model: CROSSOVER

Brief summary:
Adenosine and AMP are substances normally present in the body. Adenosine is also given for the treatment of some heart rhythm problems and may be used to reduce heart damage during heart attacks. The problem in using adenosine is that it is taken up by cells and, therefore, very little of the adenosine we give by vein or in the artery actually reaches the tissue. We propose to use AMP as a way to improve delivery of adenosine. AMP is inactive by itself, but is converted to adenosine in tissue. We hope that by giving AMP we will increase levels of adenosine in tissue. To see if this is true, we will give either adenosine or AMP into the forearm artery while we measure how much adenosine reaches the forearm tissue.

Detailed description:

Arms: arm 1: Intrarterial infusion of adenosine then same subject switch to AMP one month apart. arm 2: Intrarterial infusion of AMP then same subject switch to Adenosine one month apart.
Interventions: intervention 1: Adenosine intervention 2: Adenosine Mono Phosphate (AMP)
Intervention descriptions: intervention 1: Adenosine intrarterial (intrabrachial) infusion at 3 diferent doses for 15 minutes each intervention 2: Intraterial infusion of AMP at 3 different doses for 15 minutes each (at equimolar doses as adenosine)

Protocol documents:
Clinical trial NCT00897676
Conditions: Congenital Hyperinsulinism
Keywords: Hyperinsulinism Hypoglycemia KATP channel
Sponsor: Diva De Leon
Start date: 2009-05-01; Completion date: 2017-01-01
Enrollment: 17 participants; Allocation: RANDOMIZED; Intervention model: CROSSOVER

Brief summary:
The purpose of this study is to examine the effects of exendin-(9-39) on fasting blood glucose and protein induced hypoglycemia on subjects with Congenital Hyperinsulinism. Funding Source - FDA Office of Orphan Products Development (OODP).

Detailed description:
This is a placebo controlled study with randomized crossover design to evaluate the effect of the glucagon-like peptide-1 (GLP-1) receptor antagonist, exendin-(9-39), on fasting blood glucose levels, protein-induced hypoglycemia, and fasting tolerance of subjects with congenital hyperinsulinism due to mutations in the ATP- sensitive potassium channel (KATP) channel.

Arms: arm 1: An infusion of vehicle (0.9%NaCl) will run for 60 minutes(time -60 to 0) before starting the study infusion of vehicle or exendin-(9-39). At time 0, vehicle (0.9%NaCl) will be started and will continue for 6 hours. The following day, at time 0, exendin-(9-39) at a dose ranging from 100-500pmol/kg/min will be started and continue for 6 hours. During both infusions, blood glucose, insulin, c-peptide, GLP-1, and glucagon will be measured every 30 minutes. arm 2: An infusion of vehicle (0.9%NaCl) will run for 60 minutes(time -60 to 0) before starting the study infusion of vehicle or exendin-(9-39). . At time 0, exendin-(9-39) at a dose ranging from 100-500pmol/kg/min will be started and continue for 6 hours. The following day, at time 0, vehicle (0.9%NaCl) will be started and will continue for 6 hours. During both infusions, blood glucose, insulin, c-peptide, GLP-1, and glucagon will be measured every 30 minutes.

.
Interventions: intervention 1: Exendin-(9-39) intervention 2: placebo
Intervention descriptions: intervention 1: 100-500pmol/kg/min intervention 2: placebo (0.9% NaCl)

Protocol documents:
Clinical trial NCT00997334
Conditions: Non-small Cell Lung Cancer
Keywords: erlotinib EGFR mutation NSCLC
Sponsor: David M. Jackman, MD
Start date: 2010-02-01; Completion date: 2017-01-01
Enrollment: 60 participants; Allocation: NA; Intervention model: SINGLE_GROUP

Brief summary:
Erlotinib is a drug which targets non small cell lung cancer with a genetic change (mutation) in the epidermal growth factor receptor (EGFR). This drug has been used in other cancer research studies and information from those studies suggests that Erlotinib can control the growth of these cancer cells.

Detailed description:
PRIMARY OBJECTIVE

-To prospectively assess the frequency of different genetic mechanisms of secondary resistance in patients' tumors during treatment with erlotinib (e.g., T790M mutations, MET amplification).

* Correlate these genetic changes with patient demographic data and clinical outcomes (time to progression, survival, sites of recurrence/progression).
* Search for novel mechanisms of acquired resistance to erlotinib.
* Identify whether these genetic changes are present at low levels in initial pretreatment tumor specimens.

SECONDARY OBJECTIVE(S)

1. To measure the steady-state plasma concentrations of erlotinib during the course of patients' treatment.

   * Determine if the development and/or resolution of skin toxicity is related to plasma erlotinib concentrations.
   * Determine if the development of disease progression while on erlotinib is correlated with declines in plasma erlotinib concentrations.
   * Assess the plasma levels in patients whose smoking status has been biochemically verified to determine if smoking is associated with lower erlotinib plasma concentration.
2. To analyze from both free plasma DNA and DNA from circulating tumor cells of erlotinib-treated patients for the original sensitizing EGFR mutations and genetic changes associated with secondary resistance.
3. To measure clinical outcomes in patients with known sensitizing mutations in their tumor EGFR when treated with first-line erlotinib.

   * Response rate
   * Time to progression
   * Median overall survival

Arms: arm 1: Erlotinib was given at a dose of 150mg orally once per day for 28 days (+/- 3 days); Patients are treated until disease progression or until unaccepted drug toxicity.
Interventions: intervention 1: Erlotinib
Intervention descriptions: intervention 1: None

Protocol documents: