2. Case 1
A 55-year-old woman, 6 months after renal transplantation and on corticosteroid treatment, presents with severe back pain after sudden bending. The pain refers into the flanks and anterior abdomen. Movement aggravate the pain. On physical examination, the patient experienced pain upon palpation and percussion of some spinous processes.

4. Glucocorticoid-induced osteoporosis

5. INTRODUCTION
GC increase the risk of fracture, particularly vertebral fractures
The incidence of fracture is higher with advanced age, larger dose, and longer duration of GC
The increased risk of fracture has been reported with doses of prednisone as low as 2.5 to 7.5 mg daily
Both high daily and high cumulative GC doses
>10% of patients who receive long-term GC are diagnosed with a fracture

6. INTRODUCTION 30–40% have radiographic evidence of vertebral fractures
The highest rate of bone loss occurs within the first 3–6 months
A slower decline continues with persistent use
Potentially reversible

9. Clinical fracture risk assessment
Details of GC use (dose, duration, pattern of use)
Malnutrition
Significant weight loss or low body weight
Hypogonadism
Secondary hyperparathyroidism
Thyroid disease
Family history of hip fracture
Alcohol use
Smoking
Other comorbidities
Physical examination

15. Treatment

18. Case 2 A 20-year-old woman was with MS since 10 years ago.
Treatment with Interferon
Intravenous Methylprednisolone (1g/day for 5 days) for three attacks
In a few days after her last steroid pulse she complained mild left groin pain. The pain was aggravated by Weightbearing and motion.
Physical findings: limitations of range of motion.

20. Avascular Necrosis (osteonecrosis)

21. Definition
Cellular death of bone components secondary to interruption of blood supply
Incidence: 21-37%
Mechanism:
Alterations in circulating lipids >>>> microemboli
Bone marrow adipocyte size and number >>> blocking venous outflow
Prolonged high doses

22. The most affected sites
Hips
Knees
Shoulders

23. Examination Limp Antalgic gait Restricted ROM Tenderness around bone
Joint deformity
Muscle wasting

24. Imaging: X ray Initially normal up to 3 months Sclerosis Flattening
Crescent sign
Collapse of cortex OA

26. Imaging: MRI 90% sensitive
Reduced subchondral intensity on T1 representing boundary between necrotic and reactive bone
Low signal on T1 and high signal on T2 – reactive zone (diagnostic)
Changes detected early

28. Radionuclide scan
Donut sign – central reduced uptake with surrounding rim of increased uptake
More sensitive than plain films in early AVN
Less sensitive than MRI
Necrotic zone surrounded by reactive new bone formation

30. Prevention
Lipid-lowering agent
Anticoagulant

31. Management principles
Early stages (I & II):
Bisphosphonates prevent collapse
Unloading osteotomies
Medullary decompression + bone grafting
Intermediate stage (III & IV):
Realignment osteototmies, decompression
Arthrodesis
Late stage (V & VI):
Analgesia, activity modification
Arthroplasties

32. Glucocorticoid-induced myopathy

33. The most common drug-induced myopathy
Dose? Rare in <10 mg/day
Duration?
Glucocorticoid preparation? Fluorinated corticosteroids
Gradual onset
Proximal muscle
Atrophy 
Myalgias ?
Lower extremity
Face, hand, and sphincter muscles are relatively spared
Other features of Cushing's syndrome

34. Diagnosis?
CK normal
Improved strength within three to four weeks after sufficient dose reduction
Course?

35. THANK YOU