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.

Glucocorticoid-induced osteoporosis

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

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

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

Treatment

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.

Avascular Necrosis (osteonecrosis)

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

The most affected sites Hips Knees Shoulders

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

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

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

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

Prevention Lipid-lowering agent Anticoagulant

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

Glucocorticoid-induced myopathy

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

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

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