Risedronate Sodium (Risedronic acid)
Indications
Risedronate Sodium (Risedronic acid) is used for:
Paget's disease of bone, postmenopausal or corticosteroid-induced osteoporosis, increase bone mass in men with osteoporosis
Adult Dose
Oral
Paget's disease of bone
Adult: 30 mg once daily for 2 mth, may repeat if necessary after 2 mth interval.
Treatment and prophylaxis of postmenopausal or corticosteroid-induced osteoporosis
Adult: 5 mg daily. Alternatively, for postmenopausal osteoporosis, 35 mg once wkly, or 75 mg on 2 consecutive days of each mth, or 150 mg once mthly.
Increase bone mass in men with osteoporosis
Adult: 35 mg once wkly.
Child Dose
Renal Dose
Renal impairment:
CrCl (ml/min)
<30 Avoid use.
Administration
Contra Indications
Hypocalcaemia, abnormalities of the oesophagus which may delay emptying (e.g. stricture or achalasia), inability to stand or sit upright for at least 30 min. Severe renal impairment (CrCl <30 mL/min);. Lactation.
Precautions
Correct hypocalcaemia and evaluate sex steroid hormonal status prior to therapy. Mild to moderate renal impairment. Pregnancy. Patient Counselling Ensure adequate Ca and vit D intake. Monitoring Parameters Monitor serum Ca; biochemical markers of bone turnover; bone mineral density (osteoporosis); alkaline phosphatase (Paget's disease).
Pregnancy-Lactation
Interactions
Co-admin with calcium, antacids or oral medications containing divalent cations may affect the absorption of risedronate. May have additive calcium lowering effects when used with aminoglycosides.
Adverse Effects
Side effects of Risedronate Sodium (Risedronic acid) :
Arthralgia, back pain, GI disturbances (e.g. abdominal pain, dyspepsia), hypersensitivity reactions (e.g. angioedema, rash, bullous skin reactions), Stevens-Johnson syndrome, toxic epidermal necrolysis, leukocytoclastic vasculitis, alopecia, hepatic disorders, eye disorders (e.g. iritis, uveitis), osteonecrosis of the jaw, atypical femur fractures; bone, joint or muscle pain.
Mechanism of Action
Risedronic acid inhibits bone resorption by inhibiting osteoclasts. It also prevents formation and dissolution of hydroxyapatite crystals, and therefore may interfere with bone mineralisation.