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Medication Update in the Treatment of Osteoporosis in Cerebral Palsy Teresa Bailey [email protected]

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Medication Update in the Treatment of Osteoporosis in Cerebral Palsy Teresa Bailey Teresabailey@Ferris.Edu Wednesday, 1:00 – 2:30, E6 Medication Update in the Treatment of Osteoporosis in Cerebral Palsy Teresa Bailey [email protected] Objective: Identify effective methods for the practical application of concepts related to improving the delivery of services for persons with developmental disabilities at the level of the state. Notes: Bone Mineral Density Definition Osteoporosis in Cerebral Palsy Adults – T-score » Compared to a Teresa Bailey, PharmD, BCPS, BCACP, FCCP young-normal mean Professor BMD Ferris State University Children College of Pharmacy – Z-score < -2.0 » Adjusted for age, gender, body size, history of fractures Incidence Risks for Osteoporosis Cerebral palsy is most prevalent Vitamin D and Calcium deficiency childhood condition associated with – Difficulty eating and drinking osteoporosis – Takes longer to eat and eat less Greater the severity of CP, greater – Less sunlight the risk of osteoporosis Limited weight-bearing exercise As CP population ages, incidence of Limited mobility osteoporosis increases Low body weight Risks for Osteoporosis Treatment Options Nettekoven, 2008 Anticonvulsant medications Minimize the risks – Phenobarbital, phenytoin, Adequate vitamin D and calcium carbamazepine, valproic acid Activity and weight bearing – Study showed 75% of patient taking these meds were deficient in Vitamin D Pharmacological treatment – More pronounced with combinations 1 Prevention Guidelines Ozel et al. 2016 Calcium Products http://ods.od.nih.gov/factsheets/Cal cium_pf.asp Calcium Products Calcium Administration Must be soluble and ionized for absorption Individual doses >500 mg will not be – Acidic pH increases solubility absorbed – Vitamin D also necessary – Use BID or TID schedule Insoluble salts should be taken with food Vitamin D 400-1,000 IU/day advised to – Calcium carbonate, phosphates, “shell” products ensure absorption 2 Counseling Points Take in divided doses to ensure absorption Take with fluids during or after meals to increase absorption Avoid concomitant use with tetracyclines, iron, quinolones Side Effects: constipation, GI irritation, flatulence Vitamin D Weight Bearing Exercise 800-1000 IU/day in healthy adults Some may require higher doses – 25-OH Vitamin D level » Normal = 30-75 ng/mL » Insufficient = 20-29 » Deficient = < 20 Treatment Guidelines Ozel et al. 2016 3 Treatment Options for Osteoporosis Bisphosphonates Bisphosphonates – Alendronate, risedronate, pamidronate Indications Estrogen/progestin – Treatment/prevention of osteoporosis, – Premarin, Prempro Paget’s Disease, glucocorticoid induced Selective estrogen receptor modulators osteoporosis – Raloxifene (Evista) Mechanism of Action Parathyroid hormone – Inhibits normal and abnormal bone – Teriparatide (Forteo) resorption – Selective inhibitor unlike etidronate RANKL antibody (inhibitor of bone formation) – Denosumab (Prolia) Bisphosphonates Bisphosphonates Warnings Side Effects Rare-osteonecrosis of the jaw with Gastrointestinal bisphosphonates – Flatulence, acid regurgitation, – Most associated with dental procedures esophageal ulcer, dysphasia, abdominal – Most in cancer patients after prolonged distention, gastritis use Miscellaneous – Intravenous administration greater risk – Headache, musculoskeletal pain, rash than oral Rare-may cause bone, muscle, joint pain 4 Bisphosphonates Bisphosphonates Interactions Dosage Decreased bioavailability Dosage for osteoporosis – Calcium/antacids – Alendronate: 10 mg/day or 70 mg/week – Food/coffee/OJ – Risedronate: 5 mg/day or 35 mg/week Increased GI side effects – Ibandronate: 2.5 mg/day or 150 mg once – Aspirin monthly orally – – NSAIDs Zoledronic acid: 5 mg intravenously × 1 annually – Pamidronate: 1 mg/kg IV x 3 days, every 3-4 months for 1 year – With water 2 hours before breakfast Bisphosphonates Counseling Points Dosage Renal impairment Sit upright for 30 min (once monthly – CrCl = 35-60 ml/min, no dose change requires 60 min) – CrCl < 35 ml/min, not recommended Drink 6-8 oz of water Do not eat, drink other beverages or take other medications for 30 min after taking – (once monthly requires 60 min) Women’s Health Initiative Women’s Health Initiative Study Study Objective: HRT alter risk of CHD Outcomes Methods Primary CHD events 29% increase – R, DB, PC, 20 US Centers, FU 4 years Stroke/TIA 41% increase – N=2763 women < 80 years old with CHD Deep vein thrombosis 50% increase – Treatment Breast cancer 26% increase » Prempro 0.625/2.5 daily Hip fracture 33% decrease » Placebo Any fracture 24% decrease Colorectal cancer 37% decrease 5 Evista-raloxifene Raloxifene Indication: prevention of Adverse reactions osteoporosis in postmenopausal – Hot flashes: 25% women – Leg cramps: 6% Mechanism: selective estrogen Contraindications receptor modulator – Pregnancy, nursing, pediatrics – Reduction of resorption of bone – History of venous thromboembolic – Decrease of overall bone turnover events; greatest risk of venous – Preclinical data suggests estrogen thromboembolic events occurs during antagonist in uterine and breast tissue first 4 months Teriparatide (Forteo) Teriparatide (Forteo) Recombinant human parathyroid Efficacy hormone – Reserved for treating women at high – Regulates bone metabolism risk of fracture, including those with – Intestinal calcium absorption very low BMD (T-score worse than −3.0) and a previous vertebral fracture – Renal tubular calcium and phosphate reabsorption – Decreases vertebral fractures by 65% and nonvertebral fractures by 54% Not studied in cerebral palsy Teriparatide (Forteo) Teriparatide (Forteo) Black box warning of osteosarcoma Dose: 20mcg SC QD in thigh or in animals abdomen – No occurrence in patients, but as a precaution do not use in patients at Side effects increased risk of osteosarcoma – Hypercalcemia » Children or adolescents (growing bones are – Leg cramps at increased risk for osteosarcomas) – Nausea » Paget’s disease » – Dizziness Prior radiation » Bone metastasis » Hypercalcemia » History of skeletal malignancy 6 Denosumab (Prolia) Denosumab in Cerebral Palsy Scheinberg et al. 2015 Antiresorptive RANKL antagonist – Decreases fracture incidence by increasing BMD in postmenopausal women – Faster and more profound inhibition of bone turnover compared to oral bisphosphonates – Increasing BMD at all sites – Inhibits osteoclast-mediated bone resorption different than bisphosphonates Bone Formation Turnover Prolia Marker Osteocalcin Side Effects Dermatologic reactions – Dermatitis, rashes, and eczema – Consider discontinuing if severe symptoms develop Severe bone, joint, muscle pain – Discontinue use if severe symptoms develop Prolia Dosing Calcitonin (salmon) - Miacalcin Indication Administer 60 mg – Postmenopausal osteoporosis every 6 months as a subcutaneous Mechanism of Action injection in the – Inhibition of bone resorption upper arm, upper – Not a first-line drug thigh, or abdomen – Useful for bone pain caused by vertebral compression fractures Efficacy – Nasal calcitonin reduced the incidence of new vertebral fractures by 36% 7 Calcitonin (salmon) - Miacalcin Calcitonin (salmon) - Miacalcin Dose Adverse effects – 200 IU daily in one nostril, alternation – Nasal (10%–12%): rhinitis, epistaxis, nostrils daily irritation, nasal sores, dryness, – 200 IU per actuation so 1 bottle will last tenderness approximately 2-3 weeks – Other (3%–5%): backache, arthralgia, headache Treatment Options for Treatment Options Osteoporosis in Cerebral Palsy Bisphosphonates Minimize the risks – Alendronate, risedronate, pamidronate Adequate vitamin D and calcium Estrogen/progestin Activity and weight bearing – Premarin, Prempro Medication options Selective estrogen receptor modulators – Evista, raloxifene Parathyroid hormone – Forteo, teriparatide RANKL antibody – Denusomab, Prolia 8 NIH Public Access Author Manuscript Phys Med Rehabil Clin N Am. Author manuscript; available in PMC 2010 March 11. NIH-PA Author Manuscript Published in final edited form as: Phys Med Rehabil Clin N Am. 2009 August ; 20(3): 493±508. doi:10.1016/j.pmr.2009.04.004. Bone Density in Cerebral Palsy Christine Murray Houlihan, MD* and Richard D. Stevenson, MD Department of Pediatrics, University of Virginia, 2270 Ivy Road, Charlottesville, VA 22903, USA Abstract Osteoporosis is a skeletal disorder characterized by compromised bone strength predisposing a person to an increased risk of fracture.1 Osteoporosis remains a major health problem worldwide, costing an estimated $13.8 billion in health care each year in the United States. Despite advances in treating osteoporosis in the elderly, no cure exists. Osteoporosis has its roots in childhood. Accrual of bone mass occurs throughout childhood and early adulthood, and peak bone mass is a key determinant of the lifetime risk of osteoporosis. Because the foundation for skeletal health is NIH-PA Author Manuscript established so early in life, osteoporosis prevention begins by optimizing gains in bone mineral throughout childhood and adolescence.2,3 Osteoporosis evaluation and prevention is relevant to children with cerebral palsy (CP). CP is the most prevalent childhood condition associated with osteoporosis. Bone density is significantly decreased, and children with CP often sustain painful fractures with minimal trauma that impair their function and quality of life. Preventing or improving osteoporosis and maximizing bone accrual during critical stages of growth will minimize the future lifelong risks of fractures in children with CP. This article addresses the anatomy
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