Immobilization Hypercalcemia in Acute Spinal Cord Injury Treated With Etidronate

Merli, Geno J.; McElwain, Guy E.; Adler, Alan G.; Martin, John H.; Roberts, Jay D.; Schnall, Barry; Ditunno, John F.

doi:10.1001/archinte.1984.00350180234034

Cited by 26 publications

(4 citation statements)

References 10 publications

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“…The rapid total bone mass loss in the first 4 months in our study is consistent with metabolic changes known to occur in 4-6 months after spinal cord injury and is attributed to an increased rate of bone resorption. These metabolic alterations include increased alkaline phosphatase as well as urinary calcium, hydroxyproline, zinc, and constituents of bone matrix (4,7,10, 17,24,28,30,31,36). Some studies have indicated that these acute metabolic alterations appear to normalize at 4 months.…”

Section: Fig 4 Amentioning

confidence: 99%

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Osteoporosis after spinal cord injury

Garland

Stewart

Adkins³

et al. 1992

Journal Orthopaedic Research

352

218

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Dual-photon absorptiometry characterized bone loss in males aged less than 40 years after complete traumatic paraplegic and quadriplegic spinal cord injury. Total bone mass of various regions and bone mineral density (BMD) of the knee were measured in 55 subjects. Three different populations were partitioned into four groups: 10 controls (healthy, age matched); 25 acutely injured (114 days after injury), with 12 reexamined 16 months after injury; and 20 chronic (greater than 5 years after injury). Significant differences (p less than 0.0001) in bone mass mineral between groups at the arms, pelvis, legs, distal femur, and proximal tibia were found, with no differences for the head or trunk. Post hoc analyses indicated no differences between the acutely injured at 16 months and the chronically injured. Paraplegic and quadriplegic subjects were significantly different only at the arms and trunk, but were highly similar at the pelvis and below. In the acutely injured, a slight but statistically insignificant rebound was noted above the pelvis. Regression techniques demonstrated early, rapid, linear (p less than 0.0001) decline of bone below the pelvis. Bone mineral loss occurs throughout the entire skeleton, except the skull. Most bone loss occurs rapidly and below the pelvis. Homeostasis is reached by 16 months at two thirds of original bone mass, near fracture threshold.

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Section: Fig 4 Amentioning

confidence: 99%

“…Because the pathophysiologic state of spinal cord injury is clearly one of decreased BMD, a new BMD baseline must be selected as a target, presumably above the fracture threshold. Early treatment may be best directed at blocking osteoclastic activity (19,20,24,25).…”

Section: Fig 4 Amentioning

confidence: 99%

Osteoporosis after spinal cord injury

Garland

Stewart

Adkins³

et al. 1992

Journal Orthopaedic Research

352

218

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“…9 In some subjects with tetraplegia, during the early phase after SCI the calcium balance can become negative and can lead to a serious hypercalcemia. 28 An increase in bone mineral density resulting from intensive training programs could not feasibly be achieved, but some in¯uence on bone mineral density could be shown by passive weight bearing, 26,29 walking with orthoses 30 or electrically induced ergometry training for lower extremities. 31 The aim of the present study was to evaluate the trabecular and cortical BMD development for upper and lower extremities in subjects with paraand tetraplegia and to obtain more detailed information about the factors in¯uencing this development over the time after SCI.…”

Section: Introductionmentioning

confidence: 99%

Bone mineral density in upper and lower extremities during 12 months after spinal cord injury measured by peripheral quantitative computed tomography

et al. 2000

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Objective: To evaluate the loss of trabecular and cortical bone mineral density in radius, ulna and tibia of spinal cord injured persons with dierent levels of neurologic lesion after 6, 12 and 24 months of spinal cord injury (SCI). Design: Prospective study in a Paraplegic Centre of the University Hospital Balgrist, Zurich. Subjects and methods: Twenty-nine patients (27 males, two females) were examined by the highly precise peripheral quantitative computed tomography (pQCT) soon after injury and subsequently at 6, 12 and in some cases 24 months after SCI. Using analysis of the bone mineral density (BMD), various degrees of trabecular and cortical bone loss were recognised. A rehabilitation program was started as soon as possible (1 ± 4 weeks) after SCI. The in¯uence of the level of neurological lesion was determined by analysis of variance (ANOVA). Spasticity was assessed by the Ashworth Scale. Results: The trabecular bone mineral density of radius and ulna was signi®cantly reduced in subjects with tetraplegia 6 months (radius 19% less, P50.01; ulna 6% less, P40.05) and 12 months after SCI (radius 28% less, P50.01; ulna 15% less, P50.05). The cortical bone density was signi®cantly reduced 12 months after SCI (radius 3% less, P50.05; ulna 4% less, P50.05). No changes in BMD of trabecular or cortical bone of radius and ulna were detected in subjects with paraplegia. The trabecular BMD of tibia was signi®cantly reduced 6 months (5% less, P50.05) and 12 months after SCI (15% less, P50.05) in all subjects with SCI. The cortical bone density of the tibia only was decreased after a year following SCI (7% less, P50.05). No signi®cant dierence between both groups, subjects with paraplegia and subjects with tetraplegia was found for tibia cortical or trabecular BMD. There was no signi®cant in¯uence for the physical activity level or the degree of spasticity on bone mineral density in all subjects with SCI. Conclusions: Twelve months after SCI a signi®cant decrease of BMD was found in trabecular bone in radius and in tibia of subjects with tetraplegia. In subjects paraplegia, a decrease only in tibia BMD occurred. Intensity of physical activity did not signi®cantly in¯uence the loss of BMD in all subjects with para-and tetraplegia. However, in some subjects regular intensive loading exercise activity in early rehabilitation (tilt table, standing) can possibly attenuate the decrease of BMD of tibia. No in¯uence was found for the degree of spasticity on the bone loss in all subjects with SCI. Spinal Cord (2000) 38, 26 ± 32

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“…On the other side, based on the proven ability of etidronate to inhibit bone resorption, it was hypothesized that it was also effective in high turnover bone diseases such as Paget's disease of bone (PDB), which was confirmed by a clinical study on humans in which etidronate proved to be effective in reducing some biochemical indexes of bone turnover including serum ALP and urinary hydroxyproline [30]. Subsequent studies confirmed this specific antiresorptive activity; therefore, etidronate was approved for the treatment of PDB, as well as for the prevention and treatment of heterotopic ossification after hip arthroplasty or spinal cord injury, and for malignant hypercalcemia [31][32][33][34][35][36].…”

Section: Bisphosphonates As Therapeutic Moleculesmentioning

confidence: 91%

The Rationale for Using Neridronate in Musculoskeletal Disorders: From Metabolic Bone Diseases to Musculoskeletal Pain

Iolascon

Moretti

2022

IJMS

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Neridronate or ((6-amino-1-hydroxy-1-phosphonohexyl) phosphonic acid) is an amino-bisphosphonate (BP) synthetized in Italy in 1986. Bisphosphonates are molecules with a P-C-P bond in their structure that allows strong and selectively binding to hydroxyapatite (HAP) as well as osteoclasts inhibition through different mechanisms of action. Neridronate was initially used to treat Paget disease of the bone, demonstrating effectiveness in reducing bone turnover markers as well as pain. The interesting molecular properties of neridronate foster its wide use in several other conditions, such as osteogenesis imperfecta, and osteoporosis. Thanks to the unique safety and efficacy profile, neridronate has been used in secondary osteoporosis due to genetic, rheumatic, and oncological diseases, including in pediatric patients. In the last decade, this drug has also been studied in chronic musculoskeletal pain conditions, such as algodystrophy, demonstrating effectiveness in improving extraskeletal outcomes. This review highlights historical and clinical insights about the use of neridronate for metabolic bone disorders and musculoskeletal pain conditions.

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Immobilization Hypercalcemia in Acute Spinal Cord Injury Treated With Etidronate

Cited by 26 publications

References 10 publications

Osteoporosis after spinal cord injury

Osteoporosis after spinal cord injury

Bone mineral density in upper and lower extremities during 12 months after spinal cord injury measured by peripheral quantitative computed tomography

The Rationale for Using Neridronate in Musculoskeletal Disorders: From Metabolic Bone Diseases to Musculoskeletal Pain

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