Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Generic: 70 mg/75 mL (75 mL)
Fosamax: 70 mg
Generic: 5 mg, 10 mg, 35 mg, 40 mg [DSC], 70 mg
Tablet Effervescent, Oral:
Binosto: 70 mg
Mechanism of Action
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 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.
28 L (exclusive of bone)
Urine; feces (as unabsorbed drug)
Exceeds 10 years
Use in Specific Populations
Special Populations: Renal Function Impairment
Elimination may be reduced.
Use: Labeled Indications
Binosto: Treatment of osteoporosis in postmenopausal females and to increase bone mass in males with osteoporosis
Fosamax: Treatment and prevention of osteoporosis in postmenopausal females; treatment to increase bone mass in males with osteoporosis; treatment of glucocorticoid-induced osteoporosis in males and females with low bone mineral density who are receiving a prednisone dosage of ≥7.5 mg/day (or equivalent)
Paget disease: Fosamax: Treatment of Paget disease of the bone in patients (males and females) who are symptomatic, at risk for future complications, or with alkaline phosphatase ≥2 times the upper limit of normal
Use: Off Label
Androgen deprivation therapy-associated osteoporosis, preventiona
Data from a randomized, double-blind, placebo-controlled, crossover study support the use of once-weekly alendronate (in conjunction with calcium and vitamin D supplementation) for the prevention of bone loss associated with androgen deprivation therapy (ADT) in nonmetastatic prostate cancer
Osteoporosis, glucocorticoid-induced preventionayes
Data from a randomized, placebo-controlled clinical study support the use of alendronate in the prevention of glucocorticoid-induced osteoporosis Saag 1998.
Based on the 2017 American College of Rheumatology (ACR) guideline for the prevention and treatment of glucocorticoid-induced osteoporosis, bisphosphonates (including alendronate) are effective and recommended for prevention of glucocorticoid-induced osteoporosis in women (either not of childbearing potential or who do not plan to become pregnant) and men with moderate to high fracture risk and who are initiating long-term glucocorticoid treatment.
Hypersensitivity to alendronate or any component of the formulation; hypocalcemia; abnormalities of the esophagus (eg, stricture, achalasia) which delay esophageal emptying; inability to stand or sit upright for at least 30 minutes; increased risk of aspiration (effervescent tablets; oral solution)
Canadian labeling: Additional contraindications (not in the US labeling): Renal insufficiency with CrCl <35 mL/minute
Documentation of allergenic cross-reactivity for bisphosphonates is limited. However, because of similarities in chemical structure and/or pharmacologic actions, the possibility of cross-sensitivity cannot be ruled out with certainty.
Dosage and Administration
Note: In order for alendronate to be sufficiently absorbed, it needs to be administered in the morning ≥30 minutes before the first food, beverage (except plain water), or other medications. Patients with swallowing difficulties, esophageal motility disorders, or the inability to stand or sit upright for ≥30 minutes should not receive oral bisphosphate therapy. Patients should receive supplemental calcium and vitamin D if dietary intake is inadequate. Calcium and other supplements/medications containing polyvalent cations (eg, aluminum, iron, magnesium, zinc) can cause bisphosphonates to be insufficiently absorbed; accordingly, wait ≥30 to 60 minutes after taking alendronate to take calcium or other medications and supplements that interfere with the absorption of alendronate (Gertz 1999; Rosen 2019).
Androgen deprivation therapy-associated osteoporosis, prevention (alternative agent) (off-label use): Note: For use in men with prostate cancer without bone metastases treated long term with androgen deprivation therapy who are at elevated risk of osteoporotic fractures. Due to uncertain efficacy relative to preferred agents, some experts recommend against the use of alendronate for this indication unless preferred agents are unavailable or inappropriate (Smith 2019).
Oral: 70 mg once weekly (Bruder 2006; Greenspan 2007; Klotz 2013).
Osteoporosis, prevention of fractures (males and postmenopausal females): Note: Prior to use, evaluate and treat any potential causes of secondary osteoporosis (eg, hypogonadism in males) (ES [Watts 2012]).
High fracture risk patients include those with a history of fragility fracture, as well as males ≥50 years of age and postmenopausal females with a T-score ≤−2.5, or a T-score between −1 and −2.5 at high fracture risk according to an assessment (Finkelstein 2019; NOF [Cosman 2014]):
Treatment: Oral: 70 mg once weekly or 10 mg once daily.
Patients with T-scores between −1 and −2.5 and not at high fracture risk according to an assessment but who desire pharmacologic therapy for prevention of bone loss and/or fracture (Lewiecki 2019):
Prevention: Oral: 35 mg once weekly or 5 mg once daily.
Duration of therapy: The optimal duration of therapy has not been established. If fracture risk remains high (eg, fragility fracture before or during therapy) after the initial 5 years, consider extending therapy for up to 10 years or switching to alternative therapy (AACE/ACE [Camacho 2016]; Adler 2016; ES [Eastell 2019]; Watts 2010). Alternatively, if bone mineral density (BMD) is stable, there have been no previous fragility fractures, and short-term fracture risk is low, consider discontinuation (ie, drug holiday) after the initial 5 years. The optimal length of a drug holiday has not been established, although it is usually for a period of up to 5 years for oral bisphosphonates (ES [Eastell 2019]). The decision to resume therapy following a drug holiday is based on multiple factors, including decline in BMD, duration of discontinuation, and risk factors for fracture (ES [Eastell 2019]; Rosen 2019).
Osteoporosis, glucocorticoid-induced: Note: Recommended 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. In younger males and premenopausal females, patient selection must be individualized (Rosen 2019). Avoid use in females who are pregnant, who plan on becoming pregnant, or who are not using effective birth control (ACR [Buckley 2017]).
Prevention (off-label use) or treatment: Oral: 70 mg once weekly (Stoch 2009; Yeap 2008) or 10 mg once daily (de Nijs 2006; Tee 2012).
Paget disease, treatment (alternative agent): Note: For symptomatic patients with active disease and select patients with asymptomatic disease (eg, abnormal biochemical marker, prior to planned surgery at an active pagetic site) (Charles 2019; ES [Singer 2014]).
Initial: Oral: 40 mg once daily for 6 months (ES [Singer 2014]; manufacturer's labeling).
Re-treatment: A second course (ie, 40 mg orally once daily for 6 months) may be considered following a 6-month posttreatment evaluation period in patients whose serum alkaline phosphatase normalized during initial treatment but then subsequently rose above normal after discontinuation or if serum alkaline phosphatase failed to normalize during the initial course (Charles 2019; manufacturer's labeling).
Missed doses (once weekly): 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; however, do not administer 2 doses on the same day.
Refer to adult dosing.
Note: Patients should receive supplemental calcium and vitamin D if dietary intake is inadequate.
Osteogenesis imperfecta: Limited data available, dosing regimens and efficacy results variable (Akcay 2008; Pizones 2005; Seikaly 2005; Ward 2011): Children ≥2 years and Adolescents:
≤30 kg: Oral: 5 mg once daily
30 to <40 kg: 5 or 10 mg once daily
≥40 kg: Oral: 10 mg once daily
Dosing based on several prospective and retrospective trials; most smaller studies reported increased bone mineral density (BMD), decreased frequency of fractures, alleviation of chronic pain, and in some patients increased mobility (Akcay 2008; Pizones 2005; Seikaly2005; Unal 2005; Vyskocil 2005). The largest trial, a multicenter, randomized, placebo-controlled trial (n=109 in treatment group, n=83 completed 2-year follow-up) reported significant increases in lumbar spine BMD; however, other efficacy markers including long-bone fracture rate and pediatric disability score were no different than placebo (Ward 2011).
Osteopenia associated with cystic fibrosis (CF): Limited data available: Children ≥5 years and Adolescents: Oral:
≤25 kg: 5 mg once daily
>25 kg: 10 mg once daily
Dosing based on a randomized, placebo-controlled trial of CF patients (n=128, treatment group: n=65) with low apparent BMD age and inadequate response to calcium and calcifediol treatment; results showed a significant increase in BMD (16.3% vs 3.1% from baseline); evaluation of effect on fracture rate not possible due to sample size and duration (trial duration: 2 years); alendronate appeared to be well-tolerated with no notable difference in adverse effects reported (Bianchi 2013)
Osteopenia, nonambulatory patients (eg, cerebral palsy, muscular dystrophy): Limited data available, efficacy results variable: Note: Due to added complexity of administration requirements (eg, remaining in an upright position for an extended time) weekly dosing is preferred in these patients.
Fixed dosing (Apkon 2008; Houston 2014; Sholas 2005): Children ≥6 years and Adolescents: Oral: Usual reported dose: 35 mg once weekly. Dosing based on experience in 42 patients (age range: 6 to 16 years) from two case series and a retrospective trial. In the retrospective cohort study (n=29 mean age: 12 years), treatment showed a non-statistically significant trend in Z-score stabilization (Houston 2014). A case series of 10 patients (age range: 6 to 16 years) reported fewer fractures after treatment started compared to the prior year; alendronate was reported as being well tolerated; one patient discontinued therapy for hematemesis (also receiving high-dose ibuprofen therapy) (Sholas 2005).
Weight-directed dosing: Children ≥3 years and Adolescents: Oral: 1 mg/kg/dose once weekly (Paksu 2012); if using a solid dosage form, consider dose rounding to the nearest 10 mg (up or down as appropriate) (Lethaby 2007). Dosing based on a prospective trial of 26 patients (age range: 3 to 17 years); results showed after one year of treatment, increased BMD and decreased alkaline phosphatase.
Osteopenia/Osteoporosis, rheumatology patients (eg, JIA, SLE, dermatomyositis): Limited data available: Children ≥4 years and Adolescents:
≤20 kg: Oral: 5 mg once daily
>20 kg to 30 kg: Oral: 5 or 10 mg once daily
>30 kg: Oral: 10 mg once daily
Dosing based on a prospective trial (multicenter and single center) (Bianchi 2000; Cimaz 2002; Unal 2006); results from trials showed bone mineral density (BMD) was significantly increased (to normal values in some patients) after alendronate therapy; in some cases, bone turnover markers were reduced without a reduction of inflammatory activity (underlying rheumatologic disease process)
Tablet, effervescent (Binosto): Dissolve effervescent tablet in 120 mL of room temperature plain water (not mineral water or flavored water); wait ≥5 minutes after effervescence stops, then stir for 10 seconds and administer.
Oral: Administer first thing in the morning and ≥30 minutes before the first food, beverage (except plain water), or other medication(s) of the day. Do not take with mineral water or with other beverages. Patients should be instructed to stay upright (not to lie down) for ≥30 minutes and until after first food of the day (to reduce esophageal irritation).
Oral solution: Administer oral solution, followed with ≥2 oz of plain water.
Tablet (Fosamax): Must be taken with 6 to 8 oz of plain water. The tablet should be swallowed whole; do not chew or suck.
Tablet, effervescent (Binosto): Dissolve one tablet in 4 oz of room temperature plain water only; once effervescence stops, wait ≥5 minutes and stir the solution for ~10 seconds and then drink.
Ensure adequate calcium and vitamin D intake; if dietary intake is inadequate, dietary supplementation is recommended. Males and females should consume:
Calcium: 1,000 mg/day (men: 50 to 70 years) or 1,200 mg/day (females ≥51 years and males ≥71 years) (IOM 2011; NOF [Cosman 2014]).
Vitamin D: 800 to 1,000 int. units/day (males and females ≥50 years) (NOF [Cosman 2014]). Recommended Dietary Allowance (RDA): 600 int. units daily (males and females ≤70 years) or 800 int. units/day (males and females ≥71 years) (IOM 2011).
Oral solution: Store at 25°C (77°F), excursions permitted to 15°C to 30°C (59°F to 86°F). Do not freeze.
Tablet (Fosamax): Store at room temperature of 15°C to 30°C (59°F to 86°F). Keep in well-closed container.
Tablet, effervescent (Binosto): Store at 20°C to 25°C (68°F to 77°F), excursions permitted to 15°C to 30°C (59°F to 86°F). Protect from moisture. Store in original blister package until use.
Aminoglycosides: May enhance the hypocalcemic effect of Bisphosphonate Derivatives. 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. Monitor therapy
Aspirin: May enhance the adverse/toxic effect of Alendronate. Specifically, the incidence of upper gastrointestinal adverse events may be increased 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. Monitor therapy
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. Monitor therapy
Parathyroid Hormone: Alendronate may diminish the therapeutic effect of Parathyroid Hormone. More specifically, Alendronate may interfere with normalization of blood calcium concentrations. Avoid combination
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. Consider therapy modification
Proton Pump Inhibitors: May diminish the therapeutic effect of Bisphosphonate Derivatives. Monitor therapy
Bisphosphonates may interfere with diagnostic imaging agents such as technetium-99m-diphosphonate in bone scans.
Note: Incidence of adverse effects (mostly GI) increases significantly in patients treated for Paget disease at 40 mg/day.
>10%: Endocrine & metabolic: Decreased serum calcium (18%; transient, mild)
1% to 10%:
Central nervous system: Headache (3%)
Endocrine & metabolic: Decreased serum phosphate (10%; transient, mild)
Gastrointestinal: Abdominal pain (2% to 7%), acid regurgitation (1% to 5%), flatulence (≤4%), gastroesophageal reflux disease (3%), constipation (≤3%), diarrhea (≤3%), dyspepsia (1% to 3%), nausea (1% to 3%), esophageal ulcer (2%), dysphagia (1%), melena (1%), abdominal distension (≤1%), gastric ulcer (≤1%; may be severe with complications), gastritis (≤1%)
Neuromuscular & skeletal: Musculoskeletal pain (≤6%; includes bone pain, joint pain, and muscle pain), muscle cramps (≤1%)
<1%, postmarketing, and/or case reports: Alopecia, conjunctivitis, dizziness, duodenal ulcer (may be severe with complications), dysgeusia, episcleritis, erythema, erosive esophagitis, esophageal perforation, esophageal stenosis, esophageal ulcer, esophagitis, exacerbation of asthma, femur fracture (low-energy fractures, including subtrochanteric and diaphyseal), fever, hypersensitivity reaction (includes angioedema and urticaria), hypocalcemia (symptomatic), joint swelling, malaise, oropharyngeal ulcer; osteonecrosis of the jaw, peripheral edema, pruritus, scleritis, skin rash (occasionally with photosensitivity), Stevens-Johnson syndrome, toxic epidermal necrolysis, uveitis, vertigo, weakness
Concerns related to adverse effects:
- Bone fractures: Atypical femur fractures (AFF) have been reported in patients receiving bisphosphonates. The fractures include subtrochanteric femur (bone just below the hip joint) and diaphyseal femur (long segment of the thigh bone). Some patients experience prodromal pain weeks or months before the fracture occurs. It is unclear if bisphosphonate therapy is the cause for these fractures; AFFs have also been reported in patients not taking bisphosphonates, and in patients receiving glucocorticoids. Patients receiving long-term (>3 to 5 years) bisphosphonate therapy may be at an increased risk (Adler 2016; NOF [Cosman 2014]); however, benefits of therapy (when used for osteoporosis) generally outweigh absolute risk of AFF within the first 5 years of treatment, especially in patients with high fracture risk (Adler 2016; ES [Eastell 2019]). Patients presenting with thigh or groin pain with a history of receiving bisphosphonates should be evaluated for femur fracture. Consider interrupting bisphosphonate therapy in patients who develop a femoral shaft fracture; assess for fracture in the contralateral limb.
- Bone/joint/muscle pain: 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.
- GI mucosa irritation: May cause irritation to upper GI mucosa. Esophagitis, dysphagia, esophageal ulcers, esophageal erosions, and esophageal stricture (rare) have been reported with oral bisphosphonates; risk increases in patients unable to comply with dosing instructions. Use with caution in patients with dysphagia, esophageal disease, gastritis, duodenitis, or ulcers (may worsen underlying condition). Discontinue use if new or worsening symptoms develop.
- Hypocalcemia: Hypocalcemia has been reported with the use of bisphosphonates. Prior to therapy initiation, hypocalcemia must be corrected; ensure adequate calcium and vitamin D intake.
- Ocular effects: Conjunctivitis, uveitis, episcleritis, and scleritis have been reported with alendronate; patients presenting with signs of ocular inflammation may require further ophthalmologic evaluation.
- Osteonecrosis of the jaw: Osteonecrosis of the jaw (ONJ), also referred to as medication-related osteonecrosis of the jaw (MRONJ), has been reported in patients receiving bisphosphonates. Known risk factors for MRONJ include invasive dental procedures (eg, tooth extraction, dental implants, boney surgery), cancer diagnosis, concomitant therapy (eg, chemotherapy, corticosteroids, angiogenesis inhibitors), poor oral hygiene, ill-fitting dentures, and comorbid disorders (anemia, coagulopathy, infection, preexisting dental or periodontal disease). Risk may increase with increased duration of bisphosphonate use. According to a position paper by the American Association of Maxillofacial Surgeons (AAOMS), MRONJ has been associated with bisphosphonate and other antiresorptive agents (denosumab), and antiangiogenic agents (eg, bevacizumab, sunitinib) used for the treatment of osteoporosis or malignancy; risk of MRONJ is significantly higher in cancer patients receiving antiresorptive therapy compared to patients receiving osteoporosis treatment (regardless of medication used or dosing schedule). MRONJ risk is also increased with intravenous antiresorptive use compared to the minimal risk associated with oral bisphosphonate use, although risk appears to increase with oral bisphosphonates when duration of therapy exceeds 4 years (AAOMS [Ruggiero 2014]). The manufacturer's labeling states that in patients requiring invasive dental procedures, discontinuing bisphosphonates may reduce the risk of ONJ and clinical judgment should guide the decision. However, the AAOMS suggests there is currently no evidence that interrupting oral bisphosphonate therapy alters the risk of ONJ following tooth extraction, and that in patients receiving oral bisphosphonates for <4 years who have no clinical risk factors, no alternations or delay in any procedure common to oral/maxillofacial surgeons, periodontists, and other dental providers is necessary (special considerations apply to patients receiving dental implants). Conversely, in patients receiving oral bisphosphonates for >4 years or in patients receiving oral bisphosphonates for <4 years who have also taken corticosteroids or antiangiogenic medications concomitantly, the AAOMS recommends considering a 2-month, drug-free period prior to invasive dental procedures (recommendation based on a theoretical benefit). Patients developing ONJ during therapy should receive care by an oral surgeon (AAOMS [Ruggiero 2014]). According to the manufacturer, discontinuation of the bisphosphonate therapy should be considered (based on risk/benefit evaluation) in patients who develop ONJ.
- 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.
- Renal impairment: Use with caution in patients with renal impairment (not recommended for use in patients with CrCl <35 mL/minute).
Concurrent drug therapy issues:
- Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information.
Dosage form specific issues:
- Effervescent tablet: Each effervescent tablet contains 650 mg of sodium (NaCl 1,650 mg). Use with caution in patients following a sodium-restricted diet.
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 2016]; ES [Eastell 2019]; NOF [Cosman 2014]); evaluate BMD every 2 to 4 years during a drug holiday (ES [Eastell 2019]); in patients with combined alendronate 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 and 25(OH)D; may consider monitoring 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]); pain (posttreatment pain may not strictly correlate with increased biochemical markers [Ralston 2019]); serum calcium and 25(OH)D
It is not known if bisphosphonates cross the placenta, but based on their lower molecular weight, fetal exposure is expected (Djokanovic 2008; Stathopoulos 2011).
Information related to the use of alendronate in pregnancy is available from case reports and small retrospective studies (Gerin 2016; Green 2014; Levy 2009; Ornoy 2006; Sokal 2019; Stathopoulos 2011).
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; Sokal 2019; Stathopoulos 2011). Exposed infants should be monitored for hypocalcemia after birth (Djokanovic 2008; Stathopoulos 2011).
Until additional data are available, 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).
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]).
What is this drug used for?
- It is used to prevent or treat soft, brittle bones (osteoporosis).
- It is used to treat Pagets disease.
- It may be given to you for other reasons. Talk with the doctor.
Frequently reported side effects of this drug
- Abdominal pain
Other side effects of this drug: Talk with your doctor right away if you have any of these signs of:
- Low calcium like muscle cramps or spasms, numbness and tingling, or seizures
- Black, tarry, or bloody stools
- Chest pain
- Coughing up blood
- Trouble swallowing
- Pain when swallowing
- Sore throat
- Vomiting blood
- Severe bone pain
- Severe joint pain
- Severe muscle pain
- Groin, hip, or thigh pain
- Mouth sores
- Jaw pain or swelling
- Signs of a significant reaction like wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat.
Note: This is not a comprehensive list of all side effects. Talk to your doctor if you have questions.
Consumer Information Use and Disclaimer: This information should not be used to decide whether or not to take this medicine or any other medicine. Only the healthcare provider has the knowledge and training to decide which medicines are right for a specific patient. This information does not endorse any medicine as safe, effective, or approved for treating any patient or health condition. This is only a brief summary of general information about this medicine. It does NOT include all information about the possible uses, directions, warnings, precautions, interactions, adverse effects, or risks that may apply to this medicine. This information is not specific medical advice and does not replace information you receive from the healthcare provider. You must talk with the healthcare provider for complete information about the risks and benefits of using this medicine.