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Active ingredient: Etidronate - Brands, Medical Use, Clinical Data

Brands, Medical Use, Clinical Data

Drug Category

  • Antihypocalcemic Agents
  • Antineoplastic Agents
  • Bisphosphonates
  • Osteoporosis Prophylactic

Dosage Forms

  • Solution for injection (50mg/mL)
  • Tablet (200, 400 mg)

Brands / Synonyms

Acetodiphosphonic acid; Acide etidronique [INN-French]; Acido etidronico [INN-Spanish]; Acidum etidronicum [INN-Latin]; Cintichem Technetium 99m Hedspa; Dequest 2010; Dequest 2015; Dequest Z 010; Didronel; Didronel IV; EHDP; Etidronate Disodium; Etidronic acid; Etidronic acid [USAN:BAN:INN]; Etidronsaeure; Ferrofos 510; HEDP; Hydroxyethanediphosphonic acid; MPI Stannous Diphosphonate; Osteoscan; Oxyethylidenediphosphonic acid; Turpinal SL


For the treatment of symptomatic Paget's disease of bone and in the prevention and treatment of heterotopic ossification following total hip replacement or due to spinal cord injury.


Etidronate is a first generation (non-nitrogenous) bisphosphonate in the same family as clodronate and tiludronate. Etidronate affects calcium metabolism and inhibits bone resorption and soft tissue calcification. Of the etidronate that is resorbed (from oral preparation) or infused (for intravenous drugs), about 50% is excreted unchanged by the kidney. The remainder has a very high affinity for bone tissue, and is rapidly absorbed onto the bone surface. Etidronate has been shown to prevent or delay skeletal-related events and decrease bone pain as well as normalize calcium levels in the presence of hypercalcemia.

Mechanism of Action

Bisphosphonates, when attached to bone tissue, are absorbed by osteoclasts, the bone cells that breaks down bone tissue. Although the mechanism of action of non-nitrogenous bisphosphonates has not been fully elucidated, available data suggest that they bind strongly to hydroxyapatite crystals in the bone matrix, preferentially at the sites of increased bone turnover and inhibit the formation and dissolution of the crystals. Other actions may include direct inhibition of mature osteoclast function, promotion of osteoclast apoptosis, and interference with osteoblast-mediated osteoclast activation. Etidronate does not interfere with bone mineralization. In malignancy-related hypercalcemia, etidronate decreases serum calcium by inhibiting tumour-induced bone resorption and reducing calcium flow from the resorbing bone into the blood. Etidronate also reduces morbidity of osteolytic bone metastases by inhibiting tumour-induced bone resorption. Etidronate may promote osteoclast apoptosis by competing with adenosine triphosphate (ATP) in the cellular energy metabolism. The osteoclast initiates apoptosis and dies, leading to an overall decrease in the breakdown of bone.


The amount of drug absorbed after an oral dose is approximately 3%.


Clinical experience with acute etidronate overdosage is extremely limited. Decreases in serum calcium following substantial overdosage may be expected in some patients. Signs and symptoms of hypocalcemia also may occur in some of these patients. Some patients may develop vomiting. In one event, an 18-year-old female who ingested an estimated single dose of 4800 to 6000 mg (67 to 100 mg/kg) of etidronate was reported to be mildly hypocalcemic (7 .5 2 mg/ dl) and experienced paresthesia of the fingers.

Biotrnasformation / Drug Metabolism

Not metabolized.


Didronel tablets are contraindicated in patients with known hypersensitivity to etidronate disodium or in patients with clinically overt osteomalacia.

Drug Interactions

There have been isolated reports of patients experiencing increases in their prothrombin times when etidronate was added to warfarin therapy. The majority of these reports concerned variable elevations in prothrombin times without clinically significant sequelae. Although the relevance of these reports and any mechanism of coagulation alterations is unclear, patients on warfarin should have their prothrombin time monitored.

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