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Prospective Study on Gynaecological Effects of Two Antioestrogens Tamoxifen and Toremifene in Postmenopausal Women
British Journal of Cancer (2001) 84(7), 897–902 © 2001 Cancer Research Campaign doi: 10.1054/ bjoc.2001.1703, available online at http://www.idealibrary.com on http://www.bjcancer.com Prospective study on gynaecological effects of two antioestrogens tamoxifen and toremifene in postmenopausal women MB Marttunen1, B Cacciatore1, P Hietanen2, S Pyrhönen2, A Tiitinen1, T Wahlström3 and O Ylikorkala1 1Departments of Obstetrics and Gynecology, Helsinki University Central Hospital, P.O. Box 140, FIN-00029 HYKS, Finland; 2Department of Oncology, Helsinki University Central Hospital, P.O. Box 180, FIN-00029 HYKS, Finland; 3Department of Pathology, Helsinki University Central Hospital, P.O. Box 140, FIN-00029 HYKS, Finland Summary To assess and compare the gynaecological consequences of the use of 2 antioestrogens we examined 167 postmenopausal breast cancer patients before and during the use of either tamoxifen (20 mg/day, n = 84) or toremifene (40 mg/day, n = 83) as an adjuvant treatment of stage II–III breast cancer. Detailed interview concerning menopausal symptoms, pelvic examination including transvaginal sonography (TVS) and collection of endometrial sample were performed at baseline and at 6, 12, 24 and 36 months of treatment. In a subgroup of 30 women (15 using tamoxifen and 15 toremifene) pulsatility index (PI) in an uterine artery was measured before and at 6 and 12 months of treatment. The mean (±SD) follow-up time was 2.3 ± 0.8 years. 35% of the patients complained of vasomotor symptoms before the start of the trial. This rate increased to 60.0% during the first year of the trial, being similar among patients using tamoxifen (57.1%) and toremifene (62.7%). -
Study Protocol and Statistical Analysis Plan
Propranolol and Gene Expression in HCT Protocol v3.0, January 15, 2016 RANDOMIZED CONTROLLED PILOT STUDY USING PROPRANOLOL TO DECREASE GENE EXPRESSION OF STRESS-MEDIATED BETA- ADRENERGIC PATHWAYS IN HEMATOPOIETIC STEM CELL TRANSPLANT RECIPIENTS Version 3.0 Principal Investigator: Jennifer M. Knight, MD Medical College of Wisconsin 8701 Watertown Plank Road Milwaukee, WI 53226 Telephone: 414-955-8908 Fax: 414-955-6285 Email: [email protected] Co-Investigator: J. Douglas Rizzo, MD, MS CIBMTR Froedtert and the Medical College of Wisconsin Clinical Cancer Center 9200 W. Wisconsin Avenue Suite C5500 Milwaukee, WI 53226 Telephone: 414-805-0700 Fax: 414-805-0714 Email: [email protected] Co-Investigator: Parameswaran Hari, MD, MS Froedtert and the Medical College of Wisconsin Clinical Cancer Center 9200 W. Wisconsin Avenue Suite C5500 Milwaukee, WI 53226 Telephone: 414-805-4600 Fax: 414-805-4606 Email: [email protected] Consultant Steve W. Cole, PhD and Statistician: UCLA-David Geffen School of Medicine 10833 LeConte Ave 11-934 Factor Bldg Los Angeles, CA 90095-1678 Telephone: 310-267-4243 Email: [email protected] 1 Propranolol and Gene Expression in HCT Protocol v3.0, January 15, 2016 Sponsor: Medical College of Wisconsin Funding Sponsor: This project has an offer of sponsorship from the National Cancer Institute, National Institutes of Health, under Contract No. HHSN261200800001E. 2 Propranolol and Gene Expression in HCT Protocol v3.0, January 15, 2016 PROTOCOL SYNOPSIS Randomized Controlled Pilot Study Using Propranolol to Decrease Gene Expression of Stress-Mediated Beta-Adrenergic Pathways in Hematopoietic Stem Cell Transplant Recipients Principal Investigator: Jennifer M. Knight, MD Study Design: This is a randomized controlled pilot study designed to evaluate whether the beta-adrenergic antagonist propranolol is effective in decreasing gene expression of stress-mediated beta-adrenergic pathways among a cohort of individuals receiving an autologous hematopoietic stem cell transplant (HCT) for multiple myeloma. -
Avoid the Stop and Go of BPH Start and Stay on RAPAFLO® for BPH Symptom Relief
Avoid the Stop and Go of BPH Start and Stay on RAPAFLO® for BPH Symptom Relief Using RAPAFLO® RAPAFLO® is available only by prescription and is approved to treat male urinary symptoms due to BPH, also called an enlarged prostate. RAPAFLO® should not be used to treat high blood pressure. Important Safety Information Who should not take RAPAFLO® (silodosin) capsules? Do not take RAPAFLO® if you: • have certain kidney problems. • have certain liver problems. Please see additional Important Safety Information throughout this brochure and accompanying full Prescribing Information in pocket. Have BPH symptoms? What they may mean Enlarged prostate— uncomfortable but not uncommon Your doctor has diagnosed you with having BPH, benign prostatic hyperplasia, also known as an enlarged prostate. As men age, having BPH is not unusual. In fact, BPH is the most common prostate problem for men over 50. It affects about 50% of men aged 51-60 and up to 90% of men over 80. The prostate is about But it can grow to the size of a walnut the size of a baseball. in younger men. BLADDER The prostate is located below the bladder and surrounds the urethra, the tube that carries urine from the bladder. BPH symptoms occur when the “smooth” muscle of the prostate squeezes the urethra. This, in turn, can affect your bladder URETHRA control. Unfortunately, there is little you can do PROSTATE to avoid BPH. 2 Is BPH linked to prostate cancer? No. While many men share this belief, BPH is not linked to prostate cancer, and men with BPH are not more likely to get prostate cancer. -
2021 Step Therapy Criteria
SelectHealth Advantage 2021 Step Therapy Criteria Step Therapy Group Drug Name Criteria ACNE ADAPAL/BEN P Previous trial on at least ONE: AZELEX Generic topical acne treatment TRETINOIN ACTONEL RISEDRON SOD Previous trial on: RISEDRONATE alendronate ADAPALENE ADAPALENE Previous use of non-micronized tretinoin TAZAROTENE ANTICONVULSANT APTIOM Previous trial on at least TWO of the following: SPRITAM carbamezapine, divalproex, epitol, ethosuximide, felbamate, lamotrigine, XCOPRI levetiracetam, oxcarbazepine, phenytoin, tiagabine, topiramate, valproic acid, zonisamide ANTIDEPRESSION APLENZIN Previous trial on at least TWO of the following: EMSAM bupropion, citalopram, escitalopram, fluoxetine, fluvoxamine, maprotiline, FETZIMA mirtazapine, paroxetine, sertraline, venlafaxine, desvenlafaxine PEXEVA TRINTELLIX VIIBRYD ANTIPSYCHOTIC ARISTADA Previous trial on at least ONE of the following: ASENAPINE aripiprazole, clozapine, fluoxetine-olanzapine, haloperidol, olanzapine, FANAPT quetiapine, risperidone, ziprasidone LATUDA PALIPERIDONE SECUADO VRAYLAR BELSOMRA BELSOMRA Previous trial on at least ONE of the following: zaleplon, zolpidem, eszopiclone BUDESONIDE BUDESONIDE TAB Previous trial of ONE of the following: Mesalamine, Pentasa CADUET AMLOD/ATORVA Previous trial on at least ONE of the following: atorvastatin, lovastatin, pravastatin, simvastatin AND Previous trial on: amlodipine Updated 8/25/2021 1 SelectHealth Advantage 2021 Step Therapy Criteria Step Therapy Group Drug Name Criteria CAPEX CAPEX Previous trial on: clobetasol shampoo OR ciclopirox -
Silodyx, INN-Silodosin
ANNEX I SUMMARY OF PRODUCT CHARACTERISTICS 1 1. NAME OF THE MEDICINAL PRODUCT Silodyx 4 mg hard capsules Silodyx 8 mg hard capsules 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Silodyx 4 mg hard capsules Each hard capsule contains 4 mg silodosin. Silodyx 8 mg hard capsules Each hard capsule contains 8 mg silodosin. For the full list of excipients, see section 6.1. 3. PHARMACEUTICAL FORM Hard capsule. Silodyx 4 mg hard capsules Yellow, opaque, hard gelatin capsule, size 3 (approximately 15.9 x 5.8 mm). Silodyx 8 mg hard capsules White, opaque, hard gelatin capsule, size 0 (approximately 21.7 x 7.6 mm). 4. CLINICAL PARTICULARS 4.1 Therapeutic indications Treatment of the signs and symptoms of benign prostatic hyperplasia (BPH) in adult men. 4.2 Posology and method of administration Posology The recommended dose is one capsule of Silodyx 8 mg daily. For special patient populations, one capsule of Silodyx 4 mg daily is recommended (see below). Elderly No dose adjustment is required in the elderly (see section 5.2). Renal impairment No dose adjustment is required for patients with mild renal impairment (CLCR ≥ 50 to ≤ 80 mL/min). A starting dose of 4 mg once daily is recommended in patients with moderate renal impairment (CLCR ≥ 30 to < 50 mL/min), which may be increased to 8 mg once daily after one week of treatment, depending on the individual patient’s response. The use in patients with severe renal impairment (CLCR < 30 mL/min) is not recommended (see sections 4.4 and 5.2). Hepatic impairment No dose adjustment is required for patients with mild to moderate hepatic impairment. -
Treatment Options for Motor and Non-Motor Symptoms of Parkinson’S Disease
biomolecules Review Treatment Options for Motor and Non-Motor Symptoms of Parkinson’s Disease Frank C. Church Department of Pathology and Laboratory Medicine, The University of North Carolina School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; [email protected] Abstract: Parkinson’s disease (PD) usually presents in older adults and typically has both motor and non-motor dysfunctions. PD is a progressive neurodegenerative disorder resulting from dopamin- ergic neuronal cell loss in the mid-brain substantia nigra pars compacta region. Outlined here is an integrative medicine and health strategy that highlights five treatment options for people with Parkinson’s (PwP): rehabilitate, therapy, restorative, maintenance, and surgery. Rehabilitating begins following the diagnosis and throughout any additional treatment processes, especially vis-à-vis consulting with physical, occupational, and/or speech pathology therapist(s). Therapy uses daily administration of either the dopamine precursor levodopa (with carbidopa) or a dopamine ago- nist, compounds that preserve residual dopamine, and other specific motor/non-motor-related compounds. Restorative uses strenuous aerobic exercise programs that can be neuroprotective. Maintenance uses complementary and alternative medicine substances that potentially support and protect the brain microenvironment. Finally, surgery, including deep brain stimulation, is pursued when PwP fail to respond positively to other treatment options. There is currently no cure for PD. In conclusion, the best strategy for treating PD is to hope to slow disorder progression and strive to achieve stability with neuroprotection. The ultimate goal of any management program is to improve the quality-of-life for a person with Parkinson’s disease. -
Ribociclib (LEE011)
Clinical Development Ribociclib (LEE011) Oncology Clinical Protocol CLEE011G2301 (EarLEE-1) / NCT03078751 An open label, multi-center protocol for U.S. patients enrolled in a study of ribociclib with endocrine therapy as an adjuvant treatment in patients with hormone receptor-positive, HER2- negative, high risk early breast cancer Authors Document type Amended Protocol Version EUDRACT number 2014-001795-53 Version number 02 (Clean) Development phase II Document status Final Release date 17-Apr-2018 Property of Novartis Confidential May not be used, divulged, published or otherwise disclosed without the consent of Novartis Template version 22-Jul-2016 Novartis Confidential Page 2 Amended Protocol Version 02 (Clean) Protocol No. CLEE011G2301 Table of contents Table of contents ................................................................................................................. 2 List of tables ........................................................................................................................ 5 List of abbreviations ............................................................................................................ 6 Glossary of terms ................................................................................................................. 9 Protocol summary .............................................................................................................. 10 Amendment 2 (17-Apr-2018) ............................................................................................ 14 -
Guideline for Preoperative Medication Management
Guideline: Preoperative Medication Management Guideline for Preoperative Medication Management Purpose of Guideline: To provide guidance to physicians, advanced practice providers (APPs), pharmacists, and nurses regarding medication management in the preoperative setting. Background: Appropriate perioperative medication management is essential to ensure positive surgical outcomes and prevent medication misadventures.1 Results from a prospective analysis of 1,025 patients admitted to a general surgical unit concluded that patients on at least one medication for a chronic disease are 2.7 times more likely to experience surgical complications compared with those not taking any medications. As the aging population requires more medication use and the availability of various nonprescription medications continues to increase, so does the risk of polypharmacy and the need for perioperative medication guidance.2 There are no well-designed trials to support evidence-based recommendations for perioperative medication management; however, general principles and best practice approaches are available. General considerations for perioperative medication management include a thorough medication history, understanding of the medication pharmacokinetics and potential for withdrawal symptoms, understanding the risks associated with the surgical procedure and the risks of medication discontinuation based on the intended indication. Clinical judgement must be exercised, especially if medication pharmacokinetics are not predictable or there are significant risks associated with inappropriate medication withdrawal (eg, tolerance) or continuation (eg, postsurgical infection).2 Clinical Assessment: Prior to instructing the patient on preoperative medication management, completion of a thorough medication history is recommended – including all information on prescription medications, over-the-counter medications, “as needed” medications, vitamins, supplements, and herbal medications. Allergies should also be verified and documented. -
Toremifene (Fareston)
Clinical Policy: Toremifene (Fareston) Reference Number: PA.CP.PMN.126 Effective Date: 10.17.18 Last Review Date: 04.17.19 Revision Log Description Toremifene (Fareston®) is an estrogen agonist/antagonist. FDA Approved Indication(s) Fareston is indicated for the treatment of metastatic breast cancer in postmenopausal women with estrogen-receptor positive or unknown tumors. Policy/Criteria Provider must submit documentation (such as office chart notes, lab results or other clinical information) supporting that member has met all approval criteria. It is the policy of health plans affiliated with PA Health & Wellness® that Fareston is medically necessary when the following criteria are met: I. Initial Approval Criteria A. Breast Cancer (must meet all): 1. Diagnosis of recurrent or metastatic breast cancer; 2. Prescribed by or in consultation with an oncologist; 3. Failure of a 1-month trial of tamoxifen at up to maximally indicated doses, unless contraindicated or clinically significant adverse effects are experienced; 4. Failure of a 1-month trial of an aromatase inhibitor (e.g., anastrozole, exemestane, letrozole) at up to maximally indicated doses, unless contraindicated or clinically significant adverse effects are experienced (see Appendix B); 5. Request meets one of the following (a or b): a. Dose does not exceed 60 mg per day (1 tablet/day); b. Dose is supported by practice guidelines or peer-reviewed literature for the relevant off-label use (prescriber must submit supporting evidence). Approval duration: 12 months B. Soft Tissue Sarcoma - Desmoid Tumors (off-label) (must meet all): 1. Diagnosis of desmoid tumor or aggressive fibromatosis; 2. Prescribed by or in consultation with an oncologist; 3. -
Effects of Toremifene, a Selective Estrogen Receptor Modulator, On
ISSN 2472-1972 Effects of Toremifene, a Selective Estrogen Receptor Modulator, on Spontaneous and Stimulated GH Secretion, IGF-I, and IGF-Binding Proteins in Healthy Elderly Subjects Ferdinand Roelfsema,1 Rebecca J. Yang,2 Paul Y. Takahashi,3 Dana Erickson,4 Cyril Y. Bowers,5 and Johannes D. Veldhuis2 1Department of Internal Medicine, Section of Endocrinology and Metabolism, Leiden University Medical Center, 2333 ZA Leiden, Netherlands; 2Endocrine Research Unit, Mayo School of Graduate Medical Education, Center for Translational Science Activities, Mayo Clinic, Rochester, Minnesota 55905; 3Department of Primary Care Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905; 4Department of Endocrinology, Mayo Clinic, Rochester, Minnesota 55905; and 5Department of Internal Medicine, Tulane University Health Sciences Center, New Orleans, Louisiana 70112 Context: Estrogens amplify spontaneous and stimulated growth hormone (GH) secretion, whereas they diminish GH-dependent insulin-like growth factor (IGF)-I in a dose-dependent manner. Selective es- trogen receptor modulators (SERMs), including tamoxifen and toremifene, are widely adjunctively used in breast and prostate cancer. Although some endocrine effects of tamoxifen are known, few data are available for toremifene. Objective: To explore sex-dependent effects of toremifene on spontaneous 10-hour overnight GH se- cretion, followed by GH-releasing hormone–ghrelin stimulation. Additionally, effects on IGF-I, its binding proteins, and sex hormone–binding globulin (SHBG) were quantified. Participants and Design: Twenty men and 20 women, within an allowableagerangeof50to80years, volunteered for this double-blind, placebo-controlled prospective crossover study. Ten-minute blood sampling was done for 10 hours overnight and then for 2 hours after combined GH-releasing hormone–ghrelin injection. Main Outcome Measures: Pulsatile GH and stimulated GH secretion, and fasting levels of IGF-I, IGF- binding protein (IGFBP)1, IGFBP3, and SHBG. -
Development and Validation of High Performance LCMS Methods For
na al A lyti tic ca u l e C c h a e Nair et al., Pharm Anal Chem 2016, 3:1 m m r i s a Pharmaceutical Analytical t DOI: 10.4172/2471-2698.1000118 h r y P ISSN: 2471-2698 Chemistry Research Article Open Access Development and Validation of High Performance LCMS Methods for Estimation of Silodosin and Silodosin β-D-Glucuronide in Human Plasma Sheeba Manoj Nair1*, Ravi Kumar P1, Malini Sharma1 and Denish Karia2 1Semler Research Center, Bangalore, Karnataka, India 2Department of Chemistry, Patel JDK Science College, Borsad, Gujarat, India Abstract The aim of present study is to development and validation of analytical methods for estimation of Silodosin and Silodosin β-D-Glucuronide in human plasma in API, method in LCMS. Silodosin is a prescription medication that acts as an alpha-adrenergic blockers used in the treatment for men with benign prostatic hyperplasia, presently commercially available and marketed as Rapaflo in USA and Rapilif, Silodal in other countries worldwide. Drug showed linearity in the concentration range of 0.502 ng/ml to 207.376 ng/ml for Silodosin and 4.121 ng/ml to 302.836 ng/ml for Silodosin β-D-Glucuronide with correlation coefficient consistently greater than 0.99 for Silodosin and Silodosin β-D-Glucuronide. Mass parameters, 496.2/261.0 and 672.2/479.3/261.2 were chosen for analysis by Solid phase extraction method. Different validation parameters to be considered are Accuracy, Precision, Repeatability, Intermediate Precision, Specificity, Detection Limit, Quantitation Limit, and Linearity Range. The results were found to be acceptable as per the guidelines of International Conference on Harmonization (ICH). -
INTERRELATIONSHIPS of the ESTROGEN-PRODUCING ENZYMES NETWORK in BREAST CANCER DISSERTATION Presented in Partial Fulfillment Of
INTERRELATIONSHIPS OF THE ESTROGEN-PRODUCING ENZYMES NETWORK IN BREAST CANCER DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Wendy L. Rich, M.S. ∗∗∗∗∗ The Ohio State University 2009 Dissertation Committee: Approved by Pui-Kai Li, Ph.D., Adviser Robert W. Brueggemeier, Ph.D. Karl A. Werbovetz, Ph.D. Adviser Graduate Program in Pharmacy Charles L. Shapiro M.D. ABSTRACT In the United States, breast cancer is the most common non-skin malignancy and the second leading cause of cancer-related death in women. However, earlier detection and new, more effective treatments may be responsible for the decrease in overall death rates. Approximately 60% of breast tumors are estrogen receptor (ER) positive and thus their cellular growth is hormone-dependent. Elevated levels of estrogens, even in post- menopausal women, have been implicated in the development and progression of hormone-dependent breast cancer. Hormone therapies seek to inhibit local estrogen action and biosynthesis, which can be produced by pathways utilizing the enzymes aromatase or steroid sulfatase (STS). Cyclooxygenase-2 (COX-2), typically involved in inflammation processes, is a major regulator of aromatase expression in breast cancer cells. STS, COX-2, and aromatase are critical for estrogen biosynthesis and have been shown to be over-expressed in breast cancer. While there continues to be extensive study and successful design of potent aromatase inhibitors, much remains unclear about the regulation of STS and the clinical applications for its selective inhibition. Further studies exploring the relationships of STS with COX-2 and aromatase enzymes will aid in the understanding of its role in cancer cell growth and in the development of future hormone- dependent breast cancer therapies.