[18F]Fluoride PET Indicates Reduced Bone Formation in Severe Glucocorticoid-induced Osteoporosis

SummaryA 61-year-old female patient presenting with mixed connective tissue disease (Sharp syndrome), underwent a long-term high dose glucocorticoid treatment because of multiple organ manifestations. Under steroid therapy she developed severe osteoporosis resulting in multiple fractures. A dynamic [18F]fluoride PET study in this patient revealed reduced fluoride influx in non-fractured vertebrae. This finding corresponds to pathogenetic concepts which propose an inhibition of bone formation as major cause of glucocorticoid-induced osteoporosis. In the light of the presented case it seems to be promising to evaluate the diagnostic benefit of [18F]fluoride PET in osteoporosis.

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Steroid osteoporosis within the framework of the Itsenko-Cushing drug syndrome: demonstration of a clinical case

Clinical Medicine and Pharmacology ◽

10.12737/2409-3750-2021-7-2-12-16 ◽

2021 ◽

Vol 7 (2) ◽

pp. 12-16

Author(s):

A. Fleyshman ◽

Elena Belyaeva

Keyword(s):

Young Patient ◽

Clinical Case ◽

Underlying Disease ◽

Late Diagnosis ◽

High Dose ◽

Still’S Disease ◽

Multiple Fractures ◽

Medical Supervision ◽

And Control

A case of severe systemic osteoporosis complicated by multiple fractures of the ribs and vertebrae in a young patient with late diagnosis of Still's disease as a result of independent long-term uncontrolled use of corticosteroids is presented. Lack of medical supervision, taking a high dose (35 mg / day) of prednisolone without recommendation and control of treatment led to untimely recognition and treatment of the underlying disease and the development of irreversible disabling transformations of the skeleton.

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New onset of multiple organ dysfunction after receiving long-term high-dose piperacillin for outpatient treatment of osteomyelitis

Pediatric Critical Care Medicine ◽

10.1097/00130478-200204000-00019 ◽

2002 ◽

Vol 3 (2) ◽

pp. 187-189

Author(s):

Lucian K. DeNicola ◽

Bryan Blackwelder ◽

Nagma Khan

Keyword(s):

Organ Dysfunction ◽

Outpatient Treatment ◽

Multiple Organ ◽

High Dose ◽

Multiple Organ Dysfunction ◽

New Onset

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Effects of long-term diabetes and/or high-dose 17β-estradiol on bone formation, bone mineral density, and strenght in ovariectomized rats

Bone ◽

10.1016/s8756-3282(97)00029-x ◽

1997 ◽

Vol 20 (5) ◽

pp. 421-428 ◽

Cited By ~ 19

Author(s):

J. Verhaeghe ◽

G. Oloumi ◽

E. van Herck ◽

R. van Bree ◽

J. Dequeker ◽

...

Keyword(s):

Bone Mineral Density ◽

Bone Formation ◽

Bone Mineral ◽

Ovariectomized Rats ◽

High Dose ◽

Mineral Density ◽

17Β Estradiol

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Growth Failure in Children with Systemic Juvenile Idiopathic Arthritis and Prolonged Inflammation despite Treatment with Biologicals: Late Normalization of Height by Combined Hormonal Therapies

Hormone Research in Paediatrics ◽

10.1159/000489778 ◽

2018 ◽

Vol 90 (5) ◽

pp. 337-343 ◽

Cited By ~ 1

Author(s):

Francis de Zegher ◽

Nele Reynaert ◽

Lien De Somer ◽

Carine Wouters ◽

Mathieu Roelants

Keyword(s):

Juvenile Idiopathic Arthritis ◽

Pubertal Development ◽

Systemic Juvenile Idiopathic Arthritis ◽

Growth Failure ◽

High Dose ◽

Combination Strategy ◽

Glucocorticoid Treatment ◽

Height Gain ◽

Adult Stature

Background: Biologicals targeting the interleukin (IL)-1β or IL-6 pathway are becoming prime choices for the treatment of children with systemic juvenile idiopathic arthritis (sJIA). Up to 1 in 3 sJIA children receiving such treatment continues to have inflammatory activity and to require supra-physiological glucocorticoid doses which may reduce growth velocity for years and may lead to an extremely short stature for age, if not for life. Currently, there is no long-term proposal to normalize the adult height of these children with sJIA. Methods and Results: We present long-term (up to 10 years), proof-of-concept evidence that the adult stature and adipose body composition of short sJIA children can be normalized with a hormonal combination strategy: (i) pubertal onset is postponed with a gonadotropin-releasing hormone analog (triptorelin) until a minimum height is reached, or until prepubertal growth is exhausted, and (ii) height gain is promoted with growth hormone (≈50 μg/kg/day), once inflammation is under control and high glucocorticoid doses are no longer needed. The latter treatment takes advantage of the window of relative glucocorticoid deficiency, which is known to open after prolonged glucocorticoid administration, and to be uniquely favorable to height gain. Conclusion: A long-term combination of biological and hormonal treatments for short sJIA children can be guided by a simple concept that involves (i) postponement of pubertal development and (ii) growth-promoting therapy after the episodes of major inflammation and high-dose glucocorticoid treatment. Limited long-term experience in short sJIA children suggests that this strategy leads consistently – albeit late – to a normal adult stature.

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Microprobe analysis of inclusion bodies related to two benzofuran derivatives

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100127785 ◽

1987 ◽

Vol 45 ◽

pp. 672-673

Author(s):

T. L. Benning ◽

P. Ingram ◽

J. D. Shelburne

Keyword(s):

Inclusion Bodies ◽

Uranyl Acetate ◽

Multiple Organ ◽

High Dose ◽

En Bloc ◽

Tissue Samples ◽

Transmission Electron ◽

Organ Systems ◽

Dense Inclusion ◽

Melanin Complex

Two benzofuran derivatives, chlorpromazine and amiodarone, are known to produce inclusion bodies in human tissues. Prolonged high dose chlorpromazine therapy causes hyperpigmentation of the skin with electron-dense inclusion bodies present in dermal histiocytes and endothelial cells ultrastructurally. The nature of the deposits is not known although a drug-melanin complex has been hypothesized. Amiodarone may also cause cutaneous hyperpigmentation and lamellar lysosomal inclusion bodies have been demonstrated within the cells of multiple organ systems. These lamellar bodies are believed to be the product of an amiodarone-induced phospholipid storage disorder. We performed transmission electron microscopy (TEM) and energy dispersive x-ray microanalysis (EDXA) on tissue samples from patients treated with these drugs, attempting to detect the sulfur atom of chlorpromazine and the iodine atom of amiodarone within their respective inclusion bodies.A skin biopsy from a patient with hyperpigmentation due to prolonged chlorpromazine therapy was fixed in 4% glutaraldehyde and processed without osmium tetroxide or en bloc uranyl acetate for Epon embedding.

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