Version May 2024
Note: Avoid use in patients with swallowing difficulties, esophageal motility disorders, or the inability to stand or sit upright for ≥30 minutes. In patients treated for osteoporosis, correct hypocalcemia and vitamin D deficiency (eg, to a 25-hydroxyvitamin D level ≥20 ng/mL [≥50 nmol/L]) prior to initiating therapy and ensure adequate calcium and vitamin D intake during therapy (Ref).
Osteoporosis, fracture risk reduction:
Note: Prior to use, evaluate and treat any potential causes of secondary osteoporosis (eg, severe vitamin D deficiency) (Ref).
Males and postmenopausal females:
Patients with high fracture risk, including those with a history of fragility fracture, or males ≥50 years of age and postmenopausal females with a T-score of −2.5 or lower or a T-score between −1 and −2.5 at high fracture risk according to a risk assessment (Ref):
Treatment:
Immediate-release tablet: Oral: 5 mg once daily or 35 mg once weekly or 150 mg once monthly.
Delayed-release tablet: Oral: 35 mg once weekly.
Patients without high fracture risk, including those with a T-score between −1 and −2.5 and who are not at high fracture risk according to a risk assessment, but who desire pharmacologic therapy to prevent bone loss or fracture (Ref):
Prevention: Immediate-release tablet: Oral: 5 mg once daily or 35 mg once weekly or 150 mg once monthly.
Duration of therapy: The optimal duration of therapy has not been established. Consider discontinuing after 5 years if bone mineral density (BMD) is stable, there have been no previous fragility fractures, and short-term fracture risk is low. If fracture risk remains high (eg, fragility fracture before or during therapy), consider extending therapy for up to 10 years or switching to alternative therapy. If discontinued, the decision to resume therapy is based on multiple factors, including decline in BMD and risk factors for fracture (Ref).
Glucocorticoid induced:
Note: For use in males ≥50 years of age and postmenopausal females with low BMD (T-scores between −1 and −2.5 in either group) and expected to receive systemic glucocorticoid therapy for at least 3 months at a prednisone dose of ≥7.5 mg/day (or its equivalent) or in any patient whose baseline risk of fracture is high and is receiving a glucocorticoid at any dose or duration (Ref). In younger males and premenopausal females, patient selection must be individualized (Ref). Avoid use in females who are pregnant, who plan on becoming pregnant, or who are not using effective birth control (Ref).
Treatment and prevention: Oral: Immediate-release tablet: 5 mg once daily.
Duration of therapy: The optimal duration of treatment has not been established; duration should be individualized based on continuation of glucocorticoid therapy and fracture risk (Ref).
Paget disease of bone, treatment (alternative agent): Note: For symptomatic patients with active disease and select patients with asymptomatic disease at risk of future complications; or prior to planned surgery at an active pagetic site (Ref).
Initial: Oral: Immediate-release tablet: 30 mg once daily for 2 months.
Re-treatment: A second course (ie, 30 mg once daily for 2 months) may be considered following a posttreatment observation of ≥2 months if relapse occurs, or if treatment fails to normalize serum alkaline phosphatase. The Endocrine Society guidelines suggest retreatment may be required between 1 and 5 years (Ref).
Prostate cancer, bone loss associated with androgen deprivation therapy (alternative agent) (off-label use):
Note: For use in males without bone metastases treated long term with androgen deprivation therapy who are at elevated risk of osteoporotic fractures (eg, T-score of −2.5 or lower, prior fragility fracture, or T-score between −1 and −2.5 at high fracture risk according to a risk assessment tool) (Ref).
Oral: 35 mg once weekly (Ref).
Missed doses:
Once-weekly (immediate-release and delayed-release tablets): If a once-weekly dose is missed, administer the next morning after remembered. Then return to the original scheduled day of the week on the once-weekly schedule (original scheduled day of the week); however, do not administer 2 doses on the same day.
Monthly (150 mg once monthly immediate-release tablet): If 150 mg once-monthly dose is missed, administer the next morning after remembered if the next month's scheduled dose is >7 days away. If the next month's scheduled dose is within 7 days, wait until the next month's scheduled dose. For either scenario, then return to the original scheduled day of the month on the once-monthly schedule; however, do not administer >150 mg within 7 days.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Altered kidney function:
CrCl ≥30 mL/minute: Oral: No dosage adjustment necessary (Ref).
CrCl 15 to 30 mL/minute: Oral: Use generally not recommended (Ref). Based on limited data, use may be considered (in conjunction with patient’s nephrology team) for the treatment of osteoporosis in carefully selected patients with a history of fragility fracture and in whom the presence of CKD-MBD has been evaluated by a specialist and determined to be absent (Ref). If necessary, some experts recommend risedronate 35 mg every other week for not more than 3 years. Monitor serum creatinine at least annually and calcium, phosphorus, 25-hydroxyvitamin D, and parathyroid hormone concentrations regularly (eg, at least every 4 months) (Ref).
CrCl <15 mL/minute: Avoid use (Ref).
Hemodialysis, intermittent (thrice weekly): Not likely to be significantly dialyzed (large Vd) (Ref): Avoid use (Ref).
Peritoneal dialysis: Not likely to be significantly dialyzed (large Vd) (Ref): Avoid use (Ref).
CRRT: Avoid use (Ref).
PIRRT (eg, sustained, low-efficiency diafiltration): Avoid use (Ref).
There are no dosage adjustments provided in the manufacturer's labeling (has not been studied). However, dosage adjustment unlikely because risedronate is not metabolized by the liver.
Refer to adult dosing.
Atypical femur fractures (AFFs) have been reported with bisphosphonate use. The fractures include subtrochanteric femur (bone just below the hip joint) and diaphyseal femur (long segment of the thigh bone). The benefits of therapy (when used for osteoporosis) generally outweigh the absolute risk of AFF within the first 5 years of treatment, especially in patients with high fracture risk (Ref). The risk decreases after bisphosphonate discontinuation (Ref). AFF is estimated to occur in ~0.2 % of bisphosphonate users after ≥5 years of therapy (Ref).
Mechanism: Time-related. Long-term suppression of bone turnover may be primarily responsible; however, microdamage accumulation and alterations of collagen cross-linking have also been postulated (Ref).
Onset: Delayed; most fractures have occurred in patients receiving bisphosphonates for at least 3 to 5 years (Ref). Patients may experience prodromal pain weeks or months before the fracture occurs (Ref).
Risk factors:
• Long-term treatment (>3 to 5 years) (Ref)
• Asian race (in North America) (Ref)
• Femoral bowing (Ref)
• Glucocorticoid use (>1 year) (Ref)
Esophagitis, dysphagia, esophageal ulcer, erosive esophagitis, esophageal stenosis (rare) and esophageal perforation (rare) have been reported either with risedronate or with other oral bisphosphonates (Ref). Oropharyngeal ulcer has also been noted (Ref). Experiencing a GI event increases the likelihood of decreased compliance at 1 year (Ref) or discontinuation (Ref).
Mechanism: GI mucosal irritation is secondary to the local effect of risedronate on the gastric mucosa (as opposed to a systemic effect) (Ref).
Onset: Varied; dependent upon the type of mucosal injury but case reports with alendronate have noted onset within 2 days to 12 months after initiation (Ref).
Risk factors:
• Incorrect administration technique (ie, <180 mL water, lying down after administration) (Ref)
• Older adults (Ref)
• Concurrent nonsteroidal anti-inflammatory drug or antithrombotic use (Ref)
• Prior GI issues (Ref)
While transient decreases in serum calcium are expected with the use of risedronate (and all bisphosphonates) due to their mechanism of action, cases of symptomatic hypocalcemia have been reported (Ref). This has been seen in Paget disease and post-thyroidectomy settings and is reversible with discontinuation of risedronate, regardless of cause.
Mechanism: By decreasing osteoclast activity, calcium is not released into the bloodstream, causing a transient decrease in blood calcium. In patients with normally functioning parathyroid glands, calcium homeostasis is regained shortly after starting the bisphosphonate (Ref).
Onset: Intermediate; case reports have noted occurrence of symptomatic hypocalcemia within 10 days of initiation (Ref).
Risk factors:
• Baseline hypocalcemia (Ref)
• Impaired kidney function (Ref)
• Impaired parathyroid function (Ref)
• IV bisphosphonate (Ref)
• Vitamin D deficiency (Ref)
• Thyroidectomy (Ref)
Osteonecrosis of the jaw (ONJ) was first described in dental literature (Ref) with the use of IV bisphosphonates. However, there is conflicting evidence of whether this risk is seen with oral bisphosphonates, such as risedronate, or is simply an increased risk in those who are treated with agents for osteoporosis (Ref). ONJ is most commonly reversible and not life-threatening; however, the possibility of ONJ increases the risk of nonadherence (Ref).
Mechanism: Dose- and time-related; exact mechanism is unknown but several hypothesized mechanisms exist, such as oversuppression of bone turnover (Ref), mucosal toxicity (Ref), cytokine-mediated inflammation (Ref), and infection (Ref).
Onset: Varied; can be spontaneous or after insult, such as tooth extraction and/or dental implant procedures (Ref).
Risk factors:
• Alcohol use disorder (Ref)
• Anemia (Ref)
• Cancer and anticancer therapy (Ref)
• Corticosteroid therapy (Ref)
• Dental extraction, dental implant procedures, and other oral surgical procedures (Ref)
• Diabetes (Ref)
• Extended duration (>3 years) (Ref)
• High-dose, IV bisphosphonate (Ref)
• Immunological disorders (Ref)
• Oral surgery or trauma (Ref)
• Poor oral hygiene (Ref)
• Poorly fitting dental appliance (Ref)
• Radiotherapy to head and neck (Ref)
• Tobacco smoking (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Incidences may vary with product, dose, and indication.
>10%:
Cardiovascular: Hypertension (11%)
Dermatologic: Skin rash (8% to 12%)
Gastrointestinal: Abdominal pain (2% to 12%), diarrhea (5% to 20%), nausea (4% to 13%)
Genitourinary: Urinary tract infection (11%)
Infection: Infection (31%)
Nervous system: Headache (3% to 18%)
Neuromuscular & skeletal: Arthralgia (7% to 33%), back pain (6% to 28%)
1% to 10%:
Cardiovascular: Cardiac arrhythmia (2%), chest pain (7%), peripheral edema (8%)
Endocrine & metabolic: Hypocalcemia (≤5%), increased parathyroid hormone (8% to 9%; >1.5 x ULN: ≤2%)
Gastrointestinal: Constipation (3% to 7%), duodenitis (≤1%), dyspepsia (4% to 8%), gastritis (1% to 3%), gastroesophageal reflux disease (1% to 2%), glossitis (≤1%), upper abdominal pain (2% to 3%), vomiting (2% to 5%)
Genitourinary: Benign prostatic hyperplasia (5%), nephrolithiasis (3%)
Hypersensitivity: Acute phase reaction-like symptoms (≤8%; includes fever, influenza-like illness)
Infection: Influenza (6% to 7%)
Nervous system: Depression (7%), dizziness (3% to 7%)
Neuromuscular & skeletal: Arthropathy (7%), limb pain (2% to 4%), muscle spasm (1% to 2%), musculoskeletal pain (2%), myalgia (1% to 7%)
Ophthalmic: Cataract (7%)
Respiratory: Bronchitis (4%), flu-like symptoms (10%), pharyngitis (6%), rhinitis (6%), upper respiratory tract infection (3% to 4%)
<1%:
Hepatic: Abnormal hepatic function tests
Ophthalmic: Iritis, uveitis
Frequency not defined: Endocrine & metabolic: Hypophosphatemia (<3% decrease from baseline)
Postmarketing:
Dermatologic: Bullous skin disease, Stevens-Johnson syndrome, toxic epidermal necrolysis
Gastrointestinal: Esophageal ulcer, esophagitis, gastric ulcer
Hypersensitivity: Angioedema, hypersensitivity reaction
Neuromuscular & skeletal: Femur fracture (low-energy fractures, including atypical subtrochanteric and diaphyseal) (Park-Wyllie 2011), ostealgia, osteonecrosis of the jaw (rare: <1%) (Lewiecki 2011)
Respiratory: Exacerbation of asthma
Hypersensitivity to risedronate or any component of the formulation; hypocalcemia; inability to stand or sit upright for at least 30 minutes; abnormalities of the esophagus (eg, stricture, achalasia) which delay esophageal emptying
Concerns related to adverse effects:
• Bone/joint/muscle pain: Infrequently, severe (and occasionally debilitating) bone, joint, and/or muscle pain have been reported during bisphosphonate treatment. The onset of pain ranged from a single day to several months. Consider discontinuing therapy in patients who experience severe symptoms; symptoms usually resolve upon discontinuation. Some patients experienced recurrence when rechallenged with the same drug or another bisphosphonate; avoid use in patients with a history of these symptoms in association with bisphosphonate therapy.
Disease-related concerns:
• Bariatric surgery: Altered absorption and ulceration risk: Avoid oral bisphosphates after bariatric surgery; inadequate oral absorption and potential anastomotic ulceration may occur. If therapy is indicated, IV administered bisphosphonates are recommended.
• Glucocorticoid-induced osteoporosis: Evaluate sex steroid hormonal status prior to treatment initiation; consider appropriate hormone replacement if necessary.
• Renal impairment: Use with caution in patients with renal impairment (generally not recommended in patients with a CrCl <30 mL/minute).
Special populations:
• Pediatric: Not approved for use in pediatric patients with osteogenesis imperfecta due to lack of efficacy in reducing the risk of fracture.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral, as sodium:
Actonel: 35 mg
Actonel: 150 mg [contains fd&c blue #2 (indigo carm) aluminum lake]
Generic: 5 mg, 30 mg, 35 mg, 150 mg
Tablet Delayed Release, Oral, as sodium:
Atelvia: 35 mg [contains edetate (edta) disodium]
Generic: 35 mg
Yes
Tablet, EC (Atelvia Oral)
35 mg (per each): $79.97
Tablet, EC (Risedronate Sodium Oral)
35 mg (per each): $52.31 - $61.95
Tablets (Actonel Oral)
35 mg (per each): $102.30
150 mg (per each): $443.20
Tablets (Risedronate Sodium Oral)
5 mg (per each): $8.86
30 mg (per each): $61.95
35 mg (per each): $61.95
150 mg (per each): $233.39 - $318.58
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral, as sodium:
Actonel: 35 mg
Actonel: 150 mg [contains fd&c blue #2 (indigo carm) aluminum lake]
Generic: 5 mg, 30 mg, 35 mg, 150 mg
Tablet Delayed Release, Oral, as sodium:
Actonel DR: 35 mg [contains edetate (edta) disodium]
Generic: 35 mg
Oral: Note: Avoid administration of oral calcium supplements, antacids, magnesium supplements/laxatives, and iron preparations for ≥30 minutes after risedronate administration.
Immediate-release tablet: Administer on an empty stomach with a full glass (6 to 8 oz) of plain water (not mineral water) ≥30 minutes before any food, drink, or other medications orally to avoid interference with absorption. Patient must remain sitting upright or standing for ≥30 minutes after taking (to reduce esophageal irritation). Tablet should be swallowed whole; do not crush or chew.
Delayed-release tablet: Administer with ≥4 oz of plain water (not mineral water) immediately after breakfast. Patient must remain sitting upright or standing for ≥30 minutes after taking (to reduce esophageal irritation). Tablet should be swallowed whole; do not cut, split, crush, or chew.
Bariatric surgery: Some institutions may have specific protocols that conflict with these recommendations; refer to institutional protocols as appropriate. Immediate-release formulation is available. If safety and efficacy can be effectively monitored, no change in formulation or administration is required after bariatric surgery; however, bisphosphonate therapy is known to cause local irritation to gastric mucosa, and strong consideration should be given to converting to IV bisphosphonate (ibandronate, zoledronic acid).
An FDA-approved patient medication guide, which is available with the product information and as follows, must be dispensed with this medication:
Actonel: https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/020835s052lbl.pdf
Atelvia: https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/022560s011lbl.pdf#page=24
Osteoporosis, fracture risk reduction:
Actonel: Treatment and prevention of osteoporosis in postmenopausal females; treatment of osteoporosis in males; treatment and prevention of glucocorticoid-induced osteoporosis (daily dosage of ≥7.5 mg prednisone or equivalent).
Atelvia, Actonel DR [Canadian product]: Treatment of osteoporosis in postmenopausal females.
Paget disease: Actonel: Treatment of Paget disease of the bone.
Prostate cancer, bone loss associated with androgen deprivation therapy
Actonel may be confused with Actos
Risedronate may be confused with alendronate
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Aminoglycosides: May enhance the hypocalcemic effect of Bisphosphonate Derivatives. Aminoglycosides may enhance the nephrotoxic effect of Bisphosphonate Derivatives. Risk C: Monitor therapy
Angiogenesis Inhibitors (Systemic): May enhance the adverse/toxic effect of Bisphosphonate Derivatives. Specifically, the risk for osteonecrosis of the jaw may be increased. Risk C: Monitor therapy
Deferasirox: Bisphosphonate Derivatives may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Risk C: Monitor therapy
Histamine H2 Receptor Antagonists: May increase the serum concentration of Risedronate. This applies specifically to delayed-release risedronate. Risk X: Avoid combination
Inhibitors of the Proton Pump (PPIs and PCABs): May diminish the therapeutic effect of Risedronate. Inhibitors of the Proton Pump (PPIs and PCABs) may increase the serum concentration of Risedronate. This applies specifically to use of delayed-release risedronate. Management: Coadministration of PPIs or PCABs with delayed-release risedronate formulations is not recommended. Limit PPI/PCAB dose and duration during coadministration with risedronate as possible. Patients over age 70 are at higher risk of adverse effects. Risk D: Consider therapy modification
Nonsteroidal Anti-Inflammatory Agents: May enhance the adverse/toxic effect of Bisphosphonate Derivatives. Both an increased risk of gastrointestinal ulceration and an increased risk of nephrotoxicity are of concern. Risk C: Monitor therapy
Polyvalent Cation Containing Products: May decrease the serum concentration of Bisphosphonate Derivatives. Management: Avoid administration of oral medications containing polyvalent cations within: 2 hours before or after tiludronate/clodronate/etidronate; 60 minutes after oral ibandronate; or 30 minutes after alendronate/risedronate. Risk D: Consider therapy modification
Food reduces absorption (similar to other bisphosphonates); mean oral bioavailability is decreased when given with food. Management: Administer immediate release tablet with at least 6 oz of plain water (not mineral water) ≥30 minutes before the first food or drink of the day other than water. Administer delayed release tablet with at least 4 ounces of plain water immediately after breakfast.
Underlying causes of osteoporosis should be evaluated and treated prior to considering bisphosphonate therapy in premenopausal women; effective contraception is recommended when bisphosphonate therapy is required (Pepe 2020). Bisphosphonates are incorporated into the bone matrix and gradually released over time. Because exposure prior to pregnancy may theoretically increase the risk of fetal harm, most sources recommend discontinuing bisphosphonate therapy in females of reproductive potential as early as possible prior to a planned pregnancy. Use in premenopausal females should be reserved for special circumstances when rapid bone loss is occurring; a bisphosphonate with the shortest half-life should then be used (Bhalla 2010; Pereira 2012; Stathopoulos 2011). When bisphosphonate therapy is needed in a premenopausal woman, risedronate may be preferred based on its shorter half-life compared to other agents. Treatment should be discontinued 6 to 12 months prior to a planned conception (Machairiotis 2019).
Oral bisphosphonates can be considered for the prevention of glucocorticoid-induced osteoporosis in premenopausal females with moderate to high risk of fracture who do not plan to become pregnant during the treatment period and who are using effective birth control (or are not sexually active); intravenous therapy should be reserved for high risk patients only (Buckley [ACR 2017]).
It is not known if bisphosphonates cross the placenta, but fetal exposure is expected (Djokanovic 2008; Stathopoulos 2011).
Information related to the use of risedronate in pregnancy is available from small retrospective studies (Levy 2009; Sokal 2019).
Bisphosphonates are incorporated into the bone matrix and gradually released over time. The amount available in the systemic circulation varies by drug, dose, and duration of therapy. Theoretically, there may be a risk of fetal harm when pregnancy follows the completion of therapy (hypocalcemia, low birth weight, and decreased gestation have been observed in some case reports); however, available data have not shown that exposure to bisphosphonates during pregnancy significantly increases the risk of adverse fetal events (Djokanovic 2008; Green 2014; Levy 2009; Machairiotis 2019; Sokal 2019; Stathopoulos 2011). Exposed infants should be monitored for hypocalcemia after birth (Djokanovic 2008; Stathopoulos 2011).
It is not known if risedronate is present in breast milk.
According to the manufacturer, the decision to breastfeed during therapy should consider the risk of infant exposure, the benefits of breastfeeding to the infant, and the benefits of treatment to the mother.
Ensure adequate calcium and vitamin D intake; if dietary intake is inadequate, dietary supplementation is recommended. Patients should consume:
Calcium: 1,000 mg/day (males: 50 to 70 years of age) or 1,200 mg/day (females ≥51 years of age and males ≥71 years of age) (IOM 2011; NOF [Cosman 2014]).
Vitamin D: 800 to 1,000 units daily (age ≥50 years) (NOF [Cosman 2014]). Recommended Dietary Allowance (RDA): 600 units daily (age ≤70 years) or 800 units daily (age ≥71 years) (IOM 2011).
Osteoporosis: Serial bone mineral density (BMD) should be evaluated at baseline and every 1 to 3 years on treatment (usually at ~2 years following initiation of therapy, then more or less frequently depending on patient-specific factors and stability of BMD) (AACE/ACE [Camacho 2020]; ES [Eastell 2019]; NOF [Cosman 2014]); evaluate BMD every 2 to 4 years during a drug holiday (ES [Eastell 2019]); in patients with combined risedronate and glucocorticoid treatment, evaluate BMD at initiation of glucocorticoid therapy and after 6 to 12 months, then every 2 to 3 years if patient continues to have significant osteoporosis risk factors (ACR [Buckley 2017]); annual measurements of height and weight, assessment of chronic back pain; serum calcium (prior to and during therapy) and 25(OH)D; consider measuring biochemical markers of bone turnover (eg, fasting serum CTX or urinary NTX) at baseline, 3 months, and 6 months, to assess treatment response, adherence to therapy, and/or possible malabsorption (ES [Eastell 2019]).
Paget disease: Serum total alkaline phosphatase at 6 to 12 weeks for initial response to treatment (when bone turnover will have shown a substantial decline) and potentially at 6 months (maximal suppression of high bone turnover); following treatment completion, monitor at ~6- to 12-month intervals (ES [Singer 2014]); monitoring more specific biochemical markers of bone turnover (eg, serum P1NP, NTX, serum beta-CTx) is generally only warranted in patients with Paget disease who have abnormal liver or biliary tract function or when early assessment of response to treatment is needed (eg, spinal compression, very active disease) (ES [Singer 2014]); serum calcium (prior to and during therapy) and 25(OH)D; pain (posttreatment pain may not strictly correlate with increased biochemical markers [Ralston 2019]).
Femur fracture in patients presenting with thigh or groin pain (during or after treatment; if fracture identified, also evaluate contralateral limb).
A bisphosphonate which inhibits bone resorption via actions on osteoclasts or on osteoclast precursors; decreases the rate of bone resorption, leading to an indirect increase in bone mineral density. In Paget's disease, characterized by disordered resorption and formation of bone, inhibition of resorption leads to an indirect decrease in bone formation; but the newly-formed bone has a more normal architecture.
Onset of action: May require weeks
Absorption: Rapid
Distribution: Vd: 13.8 L/kg
Protein binding: ~24%
Metabolism: None
Bioavailability: Poor, ~0.54% to 0.75%
Half-life elimination: Initial: 1.5 hours; Terminal: 480 to 561 hours
Time to peak, serum: 1 to 3 hours
Excretion: Urine (up to 85%); feces (as unabsorbed drug)
Altered kidney function: Clearance decreased ~70% with CrCl 30 mL/minute.
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