Osteoporosis, corticoid-induced M81.4

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 24.09.2022

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Definition
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Steroid-induced secondary skeletal disease, characterized by a reduction in bone mass and deterioration of the microarchitecture of the bone tissue with correspondingly reduced strength and increased tendency to fracture.

Etiopathogenesis
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Bone formation appears to be suppressed by corticosteroids. Inhibition of proliferation and bone matrix synthesis of osteoblasts and promotion of bone resorption by osteoclasts. Direct steroid-induced decrease in IGF I and II (insulin-like growth factor) and TGF-ß. In addition, growth hormone and testosterone inhibition. Glucocorticoids inhibit active absorption of calcium ions in the intestine and promote calcium excretion by the kidney. Parathyroid hormone is activated.

Risk factors: previous vertebral fractures, postmenopausal women without hormone replacement therapy, hypogonadism or early menopause (< 45 LJ), age < 65 years, existing or planned corticosteroid use lasting more than 6 months, BMI < 20 kg m², alcohol abuse, rheumatoid arthritis, hyperparathyroidism.

Manifestation
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The greatest loss of bone mass occurs in the first 6 months of steroid treatment. Patients with e.g. long-standing rheumatoid arthritis usually already have reduced bone density, which is often further reduced by steroid therapy.

Localization
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Lumbar spine, femoral neck, calcaneus, radius.

Laboratory
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Blood count and exclusion of myeloproliferative diseases. Exclusion of hyperparathyroidism and osteomalacia by determination of calcium, phosphate, AP and albumin in blood serum. Exclusion of hyperthyroidism by determination of thyroid gland parameters. Exclusion of hypogonadism by determination of testosterone. In women additionally determination of FSH, LH, estrogen.

Histology
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The bone architecture is better preserved than in postmenopausal osteoporosis. General thinning of the trabecula.

Diagnosis
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Bone sonography, laboratory, medication history, osteodensitometry (if steroidal internal therapy above 7.5 mg/day or for longer than six months is planned); if necessary, chest X-ray, lumbar X-ray.

Differential diagnosis
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Postmenopausal osteoporosis.

General therapy
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Reduction of cigarette and alcohol consumption. Stopping or avoiding sedatives or benzodiazepines. Reduction of the risk of stumbling or falling. Reduction of steroid to the minimum necessary dosage. Attempt inhalation or rectal steroid administration. Hormone replacement therapy in all postmenopausal women.

Internal therapy
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Hormone replacement therapy, if necessary with the involvement of a gynecologist.

Often helpful are bisphosphonates, e.g. alendronate tbl. (Fosamax) 10 mg/day p.o. or risedronate tbl. (Actonel) 5 mg/day peroral.

Supportive Fluoride (Ossin Tbl.) 50 mg/day p.o., Calcium 1000 mg/day (e.g. Calzium Sandoz forte) in combination with Vitamin D3 500 IU/day orally (e.g. Merck Vigantoletten 500). Supportive calcitonin 50-100 IU s.c. (e.g. Calcitonin Stada ampoules).

Progression/forecast
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Conditionally reversible.

Literature
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  1. Angeli A et al (2002) Interactions between glucocorticoids and cytokines in the bone microenvironment. Ann N Y Acad Sci 966: 97-107
  2. Canalis E (2003) Mechanisms of glucocorticoid-induced osteoporosis. Curr Opin Rheumatol 15: 454-457
  3. Dawson-Hughes B (2001) Bone loss accompanying medical therapies. N Engl J Med 345: 989-991
  4. Niedermeier A et al (2001) Glucocorticoid-induced osteoporosis. A underestimated sequela of long-term treatment of autoimmune diseases. dermatologist 52: 477-483
  5. Solomon DH (2002) Management of glucocorticoid-induced osteoporosis in patients with rheumatoid arthritis: rates and predictors of care in an academic rheumatology practice. Arthritis Rheum 46: 3136-3142
  6. Watts NB et al (2003) Bisphosphonate treatment of osteoporosis. Clin Geriatr Med 19: 395-414

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Last updated on: 24.09.2022