Table of Contents
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General:
Preface
List of Contributors
Introduction of Diagnostic Approach for Systemic Lupus Erythematosus
Abstract
1. INTRODUCTION
2. CLASSIFICATION OF LUPUS ARTHROPATHY
2.1. Frequency of Arthritis Subtypes
2.2. Arthritis Subtypes
2.2.1. Non-erosive Arthritis
2.2.2. Erosive Arthritis
2.3. Osteonecrosis, Avascular Osteonecrosis (AVN)
2.4. Osteoporosis
2.5. Insufficient Fractures
3. APPROACHES TO DIAGNOSIS OF SLE
3.1. Approach to Hand X-rays
3.1.1. Posteroanterior View, Posterior-anterior View (PA View)
3.1.2. Oblique View
3.1.3. Ball-catcher’s View, Norgaard’s View
3.1.4. Lateral View
Conclusion
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References
Alignment of Musculoskeletal System in Systemic Lupus Erythematosus
Abstract
1. INTRODUCTION
2. NON-EROSIVE ARTHROPATHY, JACCOUD’S ARTHROPATHY
3. CHRONIC FIXED DEFORMITIES
4. MECHANISM OF DEFORMITIES OF JOINTS
5. HANDS
5.1. Deformities of Metacarpophalangeal Joints
5.1.1. Ulnar Deviation of Metacarpophalangeal Joints
5.1.2. Flexion Deformities of MCP Joints
5.2. Deformities of DIP and PIP Joints
5.2.1. Boutonniere Deformities
5.2.2. Swan-neck Deformities
5.3. Dislocation
5.4. Flexion Contracture of Digits
5.5. Osteoarthritis of Hands in SLE
5.6. Thumbs
5.6.1. Swan-neck Deformities
5.6.2. Z-thumbs, Boutonniere Deformities
6. WRISTS
6.1. Radial Deviation of Wrists
6.2. Carpal Collapse
7. SHOULDERS
8. HIPS
8.1. Osteonecrosis of Hips
9. KNEES
10. FEET
10.1. Hallux Valgus
10.2. Hammer Toes, Mallet-toes, and Claw-toes
10.2.1. Hammer Toes
10.2.2. Crossover Toe Deformities
10.2.3. Mallet-toes
10.2.4. Claw-toes and Curly Toes
10.3. Tailor’s Bunion, Digitus Quintus Varus
10.4. Flat Feet and Pedes Spinatus
10.5. Widening of Forefeet
11. SPINE
11.1. Lumbar Spine
11.2. Cervical Spine
12. FRACTURES
12.1. Hands
12.2. Feet (Fig. 63)
12.3. Spine (Figs. 64-65)
12.4. Pelvis
12.4.1. Fractures of Pubic Bones (Figs. 66-67)
12.4.2. Fractures of Ischiopubic Ramus (Fig. 68)
Conclusion
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Bone Lesions of Systemic Lupus Erythematosus
Abstract
1. INTRODUCTION
2. BONE MINERALIZATION
2.1. Periarticular (Juxta-articular) Osteoporosis
2.1.1. Hands
2.1.1.1. DIP Joints (Figs. 7-14)
2.1.1.2. IP Joints (Figs. 15-16)
2.1.1.3. PIP joints (Figs. 17-24)
2.1.1.4. MCP Joints (Figs. 25-34)
2.1.1.5. CMC (Carpometacarpal) Joints (Figs. 35-44)
2.1.2. Wrists (Fig. 45)
2.1.2.1. RC (Radiocarpal) Joints (Fig. 46)
2.1.3. Elbows (Figs. 47-51)
2.1.4. Shoulders (Fig. 52)
2.1.5. Knees (Fig. 53)
2.1.6. Ankles (Fig. 54)
2.1.7. Feet (Fig. 55)
2.1.7.1. IP and PIP joints (Fig. 56)
2.1.7.1. MTP joints (Figs. 57-58)
2.2. Generalized Osteopenia, Generalized Osteoporosis
3. OSTEOSCLEROSIS
3.1. Hands
3.1.1. Acro-osteosclerosis
3.1.2. Osteosclerosis of Tufts
3.1.3. DIP Joints (Figs. 64-65)
3.1.4. IP joints (Fig. 66)
3.1.5. PIP Joints (Fig. 67)
3.1.6. MCP Joints (Fig. 68)
3.2. Hips
3.3. Knees (Figs. 69-70)
3.4. Feet
3.4.1. MTP Joints (Fig. 71)
3.5. Sacroiliac Joints (Fig. 72)
3.6. Vertebral End Plates (Fig. 73)
4. BONE SHAPE
4.1. Erosions
4.1.1. Erosions in Rhupus
4.1.1.1. Erosions in Jaccouds Arthropathy and Non-deforming and Non-erosive Lupus Arthritis
4.1.1.2. Ultrasonography
4.1.2. MRI
4.1.3. Hands
4.1.3.1. Resorption and Erosive changes of Tufts
4.1.3.2. DIP Joints (Fig. 78)
4.1.3.3. PIP Joints (Figs. 79-85)
4.1.3.4. MCP Joints (Fig. 86)
4.1.3.4.1. First MCP joints (Fig. 87)
4.1.3.4.2. Second MCP Joints (Figs. 88-90)
4.1.3.4.3. Third MCP Joints (Figs. 91-94)
4.1.3.5. CMC Joints (Figs. 95-96)
4.1.4. Wrists (Figs. 97-103)
4.1.5. Feet
4.1.5.1. MTP Joints (Figs. 104-107)
4.1.5.2. TMT joints (Fig. 108)
4.1.5.3. Calcaneuses (Fig. 109)
4.2. Cystic Changes
4.2.1. Hands
4.2.1.1. DIP joints (Figs. 110-111)
4.2.1.2. IP Joints (Fig. 112)
4.2.1.3. PIP joints (Figs. 113-114)
4.2.1.4. CMC joints (Figs. 115-116)
4.4.2. Hips (Fig. 117)
4.4.3. Feet
4.4.3.1. MTP Joints (Fig. 118)
4.3. New Bone Formation: Osteophytes and Syndesmophytes
4.3.1. Osteophytes
4.3.1.1. Hands
4.3.1.1.1. DIP Joints (Figs. 119-123)
4.3.1.1.2. IP Joints (Figs. 124-125)
4.3.1.1.3. PIP Joints (Figs. 126-129)
4.4.1.1.4. MCP Joints (Fig. 130)
4.4.1.2. Elbows (Fig. 131)
4.4.1.3. Knees (Fig. 132)
4.4.1.4. Ankles (Fig. 133)
5. AVASCULAR NECROSIS OF BONES
Conclusion
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Cartilaginous and Capsular Changes in Systemic Lupus Erythematosus
Abstract
1. INTRODUCTION
2. SYNOVITIS
2.1. Jaccoud’s Arthropathy
2.2. DIP Joints (Figs. 1-3)
2.3. IP Joints (Figs. 4-5)
2.4. PIP Joints
2.4.1. Second PIP Joints (Figs. 6-8)
2.4.2. Third PIP Joints (Figs. 9-17)
2.4.3. Fourth PIP Joints (Figs. 18-22)
2.4.4. Fifth PIP Joints (Figs. 23-24)
2.5. MCP Joints
2.5.1. First MCP joints (Figs. 25-27)
2.5.2. Second MCP Joints (Figs. 28-32)
2.5.3. Third MCP Joints (Figs. 33-45)
2.5.4. Fourth MCP Joints (Figs. 46-49)
2.5.5. Fifth MCP Joints (Figs. 50-51)
2.6. Wrists (Fig. 52)
2.6.1. First Digit Line of Wrist (Figs. 53-55)
2.6.2. Second Digit Line of the Wrist (Figs. 56-60)
2.6.3. Third Digit Line of the Wrist (Figs. 61-62)
2.6.3.1. Radiocarpal Joints, RC Joints (Figs. 63-67)
2.6.3.2. Midcarpal Joints, MC Joints (Figs. 68-69)
2.6.3.3. Common Carpometacarpal and Carpometacarpal Joints, CCMC and CMC Joints (Figs. 70-71)
2.6.3.4. Carpal Joints (RC, MC, and CMC Joints) (Figs. 72-75)
2.6.4. Fourth Digit Line of the Wrist (Figs. 76-78)
2.6.5. Ulna Line of the Wrist (Figs. 79-85)
2.7. Elbows (Figs. 86-88)
2.8. Knees (Figs. 89-90)
2.9. Ankles (Fig. 91)
2.10. Feet (Figs. 92-96)
2.11. Sacroiliac Joints
3. JOINT EFFUSIONS
3.1. Hands
3.1.1. MCP Joints (Figs. 97-99)
3.2. Wrists (Figs. 100-102)
3.3. Elbows (Fig. 103)
3.4. Knees (Figs. 104-117)
4. JOINT SPACES
4.1. Rhupus
4.2. Joint Space Narrowing
4.2.1. Hands
4.2.1.1. DIP Joints (Figs. 118-121)
4.2.1.1. PIP Joints (Figs. 122-129)
4.2.1.3. MCP Joints (Figs. 130-131)
4.2.2. Elbows (Fig. 132)
4.2.3. Knees (Figs. 133-134)
4.2.4. Sacroiliac Joints
4.3. Joint Space Widening (JSW)
4.4. Pseudo Joint Space Narrowing (Fig. 135)
5. CALCIFICATIONS
5.1. Calcifications of Joint Capsules
5.1.1. DIP Joints (Figs. 136-138)
5.1.2. IP Joints (Figs. 139-140)
5.1.3. PIP Joints (Figs. 141-142)
5.1.4. MCP Joints (Figs. 143-144)
5.1.5. Carpal Joints (Fig. 145)
Conclusion
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References
Distribution, Pattern of Joint Involvement in Systemic Lupus Erythematosus
Abstract
1. INTRODUCTION
1.1. Gallium Scintigraphy (Figs. 2-8)
1.2. Bone Scintigraphy (Figs. 9-11)
2. DISTRIBUTION OF ARTHRITIS
2.1. General Distribution
2.1.1. Distribution of Arthritis by Subtypes
2.1.1.1. Distribution of Non-deforming Non-erosive (NDNE) Arthropathy
2.1.1.2. Jaccoud’s Arthropathy
2.1.2. Distribution of Bone Cysts
2.1.3. Distribution of Osteonecrosis
2.1.4. Distribution of Osteonecrosis in Antiphospholipid Antibody Syndrome (APS)
2.1.5. Distribution of Bone Infarcts
2.1.6. Distribution of Insufficient Fractures
2.1.7. Distribution of Myositis
2.1.8. Distribution of Infection
2.2. Distribution in Regions
2.2.1. Hands
2.2.2. Lower Limbs
2.2.2.1. Knees
2.2.2.2. Lupus Feet
2.2.3. Sacroiliac Joints
2.2.4. Tenosynovitis (Distribution of Tenosynovitis in the Hands) (Figs. 18-19)
2.2.5. Axial Skeleton
2.3. Distribution in Joints
2.4. Distribution of Timeline
2.4.1. Early Phase
2.4.2. Active Phase
2.4.3. Terminal Phase
Conclusion
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Extra-Articular Soft Tissue and Muscular Involvement in Systemic Lupus Erythematosus
Abstract
1. INTRODUCTION
2. PERIPHERAL SOFT TISSUE SWELLING
2.1. Hand (Figs. 1-15)
2.2. Wrists (Figs. 16 and 17)
2.3. Knees (Figs. 18-21)
2.4. Ankles (Figs. 22 and 23)
3. CALCIFICATIONS
3.1. Soft Tissue Calcifications
3.2. Calcification Around Joints
3.3. Arterial Calcifications
4. BURSAE
4.1. Knees (Figs. 27-33)
4.2. Ankles
4.2.1. Lateral Premalleolar Bursitis (Figs. 34-43)
5. TENDONS
5.1. Involvement of Tendons
5.2. Tendon Sheaths, Tenosynovitis
5.2.1. Hands and Wrists
5.2.1.1. Extensor Tendon Sheaths (Fig. 46)
5.2.1.1.1. Compartment 1
5.2.1.1.2. Compartment 2
5.2.1.1.3. Compartment 3
5.2.1.1.4. Compartment 4
5.2.1.1.5. Compartment 5
5.2.1.1.6. Compartment 6
5.2.1.2. Flexor Tendon Sheaths (Fig. 59)
5.2.2. Digits
5.2.2.1. Volar Plates (Fig. 60)
5.2.2.2. First Digits (Figs. 61-63)
5.2.2.3. Second Digits (Figs. 64-65)
5.2.2.3.1. MCP Joints (Figs. 66-67)
5.2.2.3.2. PIP Joints (Fig. 68)
5.2.2.3.3. DIP Joints (Fig. 69)
5.2.2.4. Third Digits
5.2.2.4.1. MCP Joints (Figs. 70-74)
5.2.2.4.2. PIP Joints (Figs. 75 and 76)
5.2.2.5. Fourth and Fifth Digits
5.2.2.5.1. MCP Joints (Fig. 77)
5.2.3. Wrists (Figs. 78-80)
5.2.4. Knees (Figs. 81-83)
5.3. Peritenon Extensor Tendon Inflammation (PTI)
7. ENTHESITIS / ENTHESEAL INVOLVEMENTS
7.1. DIP Joints (Figs. 92-97)
7.2. PIP Joints (Figs. 98-100)
7.3. MCP Joints (Figs. 101 and 102)
7.4. Knees (Fig. 103)
8. Lupus Myopathy (Fig. 104)
Conclusion
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Skin Manifestations in Patients with Systemic Lupus Erythematosus
Abstract
1. INTRODUCTION
2. ACUTE CUTANEOUS LUPUS ERYTHEMATOSUS (ACLE)
2.1. Lupus Malar Rash
2.1.1. Typical Malar Rash (Figs. 1-3)
2.1.2. Mild Malar Rash (Figs. 4-5)
2.1.3. Atypical Malar Rash (Figs. 6-8)
2.2. Maculopapular Lupus Rashes, Widespread Erythematous Maculopapular Lesions
2.2.1. Hands
2.2.1.1. Dorsal Side Of Hands (Figs. 9-17)
2.2.1.2. Palmar Side of Hands (Figs. 18-20)
2.2.1.3. Wrists (Fig. 21)
2.2.2. Forearms (Figs. 22-23)
2.2.3. Elbows (Figs. 24-25)
2.2.4. Upper Arms (Figs. 26-27)
2.2.5. Faces (Figs. 28-32)
2.2.6. Necks and Jaws (Figs. 33-36)
2.2.7. Backs (Figs. 37-39)
2.2.8. Abdomens (Fig. 40)
2.2.9. Thighs (Fig. 41)
2.2.10. Knees (Figs. 42-43)
2.2.11. Lower Limbs (Figs. 44-46)
2.2.12. Feet (Figs. 47-52)
2.3. Palmar Erythema (Fig. 53)
2.4. Bullous LE Skin Rashes, Bullous Lesions (BSLE), Bullous Lupus Erythematosus (Figs. 54-58)
2.5. Toxic epidermal necrolysis (TEN) (Fig. 59)
2.6. Photosensitivity
2.7. Periungual Erythema (Figs. 60-65)
2.8. Periungual Telangiectasias (Figs. 66-68)
3. SUBACUTE CUTANEOUS LUPUS ERYTHEMATOSUS (SCLE)
3.1. Annulare SCALE, large polycyclic lesions or small cyclic lesions (Fig. 69)
3.2. Mixed form with both annular and psoriasiform lesions (Figs. 70-78)
3.3. Papulosquamous Psoriasiform Lesions
3.3.1. Hands (Figs. 79-84)
3.3.2. Wrists (Fig. 85)
3.3.3. Elbows (Fig. 86)
3.3.4. Upper Arms (Figs. 87-88)
3.3.5. Feet (Fig. 89)
4. CHRONIC CUTANEOUS LUPUS
4.1. Classic Discoid Rashes, Discoid Lupus Erythematosus (DLE)
4.1.1. Ears (Fig. 90)
4.1.2. Hands (Figs. 91-93)
4.1.3. Elbows (Fig. 94)
4.1.4. Knees (Figs. 95-96)
4.1.5. Backs (Figs. 97-98)
4.1.6. Abdomens (Fig. 99)
4.2. Chilblain Lupus Erythematosus, Chilblain Lupus
4.2.1. Hands (Figs. 100-105)
4.2.2. Feet (Figs. 106-108)
4.3. Hypertrophic or Verrucous Lupus
4.3.1. Hands (Figs. 109-112)
4.3.2. Elbows (Fig. 113)
4.3.3. Knees (Figs. 114-115)
4.3.4. Feet (Figs. 116-117)
4.4. Lupus Erythematosus Profundus (Figs. 118-122)
4.5. Mucosal Lupus
4.5.1. Oral Ulcers (Figs. 123-126)
4.5.2. Cheilitis (Figs. 127-128)
4.5.3. Angular Cheilitis (Fig. 129)
4.6. Nodular Cutaneous Lupus Mucinosis; NCLM (Fig. 130)
5. OTHER MANIFESTATIONS OF SKIN
5.1. Urticarial Vasculitis in SLE (Figs. 131-132)
5.2. Livedo Reticularis (Fig. 133)
5.3. Raynaud’s Phenomenon (Figs. 134-142)
5.4. Acrocyanosis (Fig. 143)
5.5. Erythromelalgia (Figs. 144-146)
5.6. Gangrene of Extremities (Figs. 147-149)
5.7. Subcutaneous Hematoma (Fig. 150)
5.8. Internal Bleeding (Fig. 151)
5.9. Subcutaneous Nodules
5.10. Necrotizing Fasciitis (Fig. 152)
5.11. Subcutaneous Edema (Figs. 153-154)
5.12. Soft Tissue Calcifications (Figs. 155-158)
5.13. Nonscarring Alopecia, Hair Loss/alopecia (Figs. 159-160)
6. NON-SPECIFIC SKIN LESIONS
7. INFECTIONS
7.1. Herpes Zoster (Figs. 161-165)
Conclusion
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References
Respiratory Involvement in Systemic Lupus Erythematosus
Abstract
1. INTRODUCTION
2. PLURA
2.1. Pleural Effusions
2.1.1. Imaging Findings
2.1.1.1. Conventional Chest Radiography (Figs. 1-4)
2.1.1.2. Chest CT (Fig. 5)
2.2. Pleuritis (Fig. 6)
3. PARENCHYMA
3.1. Interstitial Pneumonia, Interstitial Lung Disease (ILD)
3.1.1. Lupus Pneumonitis
3.1.1.1. Imaging Findings
3.1.1.1.1. Chest Radiography (Fig. 7)
3.1.1.1.2. Chest CT (Fig. 8)
3.1.2. Chronic Lupus Pneumonitis
3.1.2.1. Imaging Findings
3.1.2.1.1. Chest Radiography (Fig. 9)
3.1.2.1.2. Chest CT (Fig. 10)
3.2. Diffuse Alveolar Hemorrhage (DAH)
3.2.1. Imaging Findings
3.2.1.1. Chest Radiography (Figs. 11-12)
3.2.2. Chest CT Scans (Figs. 13-15)
3.2.2.1. MRI
4. BRONCHI
4.1. Bronchiectasis
5. DIAPHRAGM
5.1. Diaphragmatic Dysfunction
5.1.1. Imaging Findings
5.1.1.1. Chest Radiography (Figs. 16-17)
6. PULMONARY INFECTIONS
6.1. Bronchopulmonary Infections
6.1.1. Pneumonia
6.1.1.1. Chest Radiography (Figs. 18-20)
6.1.1.2. Chest CT (Fig. 21)
6.1.1.3. Gram Stain (Fig. 22)
6.1.2. Pneumocystis Pneumonia (PCP)
6.1.2.1. Partial Interstitial Shadows (Figs. 23-24)
6.1.2.2. Mild Interstitial Opacities in All Lung Fields (Figs. 25-27)
6.1.2.3. Patchy Interstitial Opacities in All Lung Fields (Figs. 28-29)
6.1.3. Aspergillus Pneumonia, Pulmonary Aspergillosis (Figs. 30-34)
6.1.4. Cryptococcal Pneumonia (Figs. 35-37)
6.1.5. Legionella Pneumonia (Figs. 38-41)
6.1.6. Pulmonary Tuberculosis
6.1.6.1. Mild Pulmonary Tuberculosis (Figs. 42-45)
6.1.6.2. Intermediate Pulmonary Tuberculosis (Figs. 46-51)
6.1.6.3. Severe Pulmonary Tuberculosis (Figs. 52-55)
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Neuropsychiatric Systemic Lupus Erythematosus (NP-SLE)
Abstract
1. INTRODUCTION
2. CENTRAL NERVOUS SYSTEM
2.1. Cerebral Atrophy (Figs. 1-2)
2.2. Diffuse Cerebral Edema with Leukoencephalopathy (Figs. 3-6)
2.3. White-matter Lesions in Central Nervous System (CNS) (Fig. 7)
2.4. CNS Ischemia
2.4.1. Medial Longitudinal Fasciculus Syndrome (Fig. 8)
2.4.1.1. Small Infarcts (Fig. 9)
2.4.1.1.1. Single Photon Emission Computed Tomography (SPECT) (Figs. 10-11)
2.5. Occlusion of Dural Venous Sinuses and Deep Cerebral Veins (Fig. 12)
2.6. Intracranial Hemorrhage (ICH) (Figs. 13-16)
2.7. Posterior Reversible Encephalopathy Syndrome (PRES) (Fig. 17)
2.8. Lupus Meningitis (Fig. 18)
3. Peripheral Neuropathy in SLE
Conclusion
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Cardiovascular and Renal Diseases in Systemic Lupus Erythematosus
Abstract
1. INTRODUCTION
2. PERICARDITIS (Figs. 1-2)
3. MYOCARDITIS
3.1. Libman-Sacks Endocarditis
3.2. Valvulopathy (Figs. 3-4)
4. CORONARY VESSELS
4.1. Left Anterior Descending (LAD) (Fig. 5)
4.2. Right Coronary Artery (RCA) (Fig. 6)
4.3. Left Circumflex Artery (LCx) (Fig. 7)
5. AORTA AND ITS BRANCHES (Fig. 8)
6. PULMONARY ARTERIAL HYPERTENSION (PAH)
6.1. Radiography (Fig. 9)
6.2. Electrocardiogram (ECG) (Figs. 10-11)
6.3. Echocardiography (Figs. 12-13)
6.4. Pulmonary Embolism (PE) (Fig. 14)
7. RENAL SYSTEM
Conclusion
ACKNOWLEDGEMENTS
References
Gastrointestinal System in Systemic Lupus Erythematosus
Abstract
1. INTRODUCTION
2. SEROSITIS (Fig. 1)
3. GASTRITIS (Fig. 2)
4. LUPUS ENTERITIS (Fig. 3)
5. CHOLECYSTITIS (Fig. 4)
6. SPLEEN (Figs. 5-6)
7. SALIVARY GLANDS (Fig. 7)
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Frontiers in Arthritis
(Volume 4)
Systemic Lupus Erythematosus:
A Systematic Approach to Arthritis of Rheumatic Diseases
Edited by
Syuichi Koarada
Department of Medical Technology and Sciences
International University of Health and Welfare
Okawa
Japan
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Preface
Syuichi KoaradaSystemic lupus erythematosus (SLE) is a chronic multisystem inflammatory connective tissue disease with immunologic abnormalities producing autoantibody, including anti-ds (double strand)-DNA antibodies. In SLE, joint symptoms are the most common and one of the first signs.
The objective of our monograph is to integrate information on musculoskeletal and systemic pathophysiology in SLE. Although SLE is one of the rheumatic diseases, lesions extend not only to joints but to the whole body, causing inflammation in diverse organs, such as the skin, lungs, nervous system, serous membranes, kidneys and virtually all organs of the body. Therefore, patients with SLE have various presentations of disorders of organs. It is necessary to understand the findings of various organs throughout the body for proper diagnosis and treatment of patients with SLE.
Early diagnosis and treatment are required for rheumatic diseases, but early diagnosis is often difficult due to the enormous and diverse findings. Therefore, we are widely advocating a methodology called the ABCDEFGHI method as a comprehensive diagnostic approach based on the clinical, imaging, and immunological characteristics of rheumatic diseases.
The ABCDEFGHI method consists of A (Alignment): malalignment and deformation, B (Bone): bone changes, C (Capsular lesions): cartilage and intra-articular lesions, D (Distribution): four-dimensional altered distribution: 1 intra-articular, 2 intra region, 3 intra-body, 4 timeline, E (Extra-bone): extra-articular soft tissue, F (Further information): further additional medical information, G (Goal): general analysis and diagnosis, I (Integration): integrated and comprehensive diagnosis from the above data and information, H (Heal and Heath): treatment and prognosis, and I (Immunological analyzes): immunological interpretations (cytokines and immune cell phenotypes).
It is a method of making a comprehensive diagnosis by individually performing interpretations based on various symptoms, images, laboratory findings, and immunological analysis. This diagnostic procedure is being approved by medical students and evaluated from various fields.
The cases and images of patients with SLE discussed in this book are only a small part of the cases we have experienced. In the future, we would like to consider adding more cases to make the contents more complete. If there are any inadequacies in this book, we would like to receive suggestions from valuable readers. We would also be happy to receive suggestive cases and images from readers so that we can compose even better content.
I dedicate this book to my parents and my beloved Miwako and Sakura.
Syuichi Koarada Department of Medical Technology and Sciences
International University of Health and Welfare
Okawa, Japan
List of Contributors
Maruyama Akihito, Division of Rheumatology, Faculty of MedicineSaga UniversitySagaJapanHirose Hijiri, Department of Medical Technology and SciencesInternational University of Health and WelfareOkawaJapanMouri Honoka, Department of Medical Technology and SciencesInternational University of Health and WelfareOkawaJapanHirano Jun, Department of Medical Technology and SciencesInternational University of Health and WelfareOkawaJapanTakedomi Kouki, Department of Medical Technology and SciencesInternational University of Health and WelfareOkawaJapanTakayama Makiko, Department of Medical Technology and SciencesInternational University of Health and WelfareOkawaJapanSakai Mariko, Division of Rheumatology, Faculty of MedicineSaga UniversitySagaJapanAkahoshi Mitsuteru, Division of Rheumatology, Faculty of MedicineSaga UniversitySagaJapanSoejima Sachiko, Division of RheumatologyTakagi HospitalOkawaJapanTashiro Satoko, Division of Rheumatology, Faculty of MedicineSaga UniversitySagaJapanKoarada Syuichi, Department of Medical Technology and SciencesInternational University of Health and WelfareOkawaJapanDivision of RheumatologyTakagi HospitalOkawaJapanDivision of Rheumatology, Faculty of MedicineSaga UniversitySagaJapanMaesaki Tetsuhiro, Division of RheumatologyTakagi HospitalOkawaJapanTada Yoshifumi, Division of Rheumatology, Faculty of MedicineSaga UniversitySagaJapanNakao Yoshinobu, Division of Rheumatology, Faculty of MedicineSaga UniversitySagaJapanMiyajima Yuiko, Department of Medical Technology and SciencesInternational University of Health and WelfareOkawaJapanOno Yukihide, Division of RheumatologyTakagi HospitalOkawaJapanTakeyama Yukiko, Division of Rheumatology, Faculty of MedicineSaga UniversitySagaJapanShirahama Yuri, Division of Rheumatology, Faculty of MedicineSaga UniversitySagaJapanMaeda Yuumi, Department of Medical Technology and SciencesInternational University of Health and WelfareOkawaJapan
Introduction of Diagnostic Approach for Systemic Lupus Erythematosus
Syuichi Koarada1,2,3,*,Yoshifumi Tada 3
1 Department of Medical Technology and Sciences, International University of Health and Welfare, Okawa, Japan
2 Division of Rheumatology, Takagi Hospital, Okawa, Japan
3 Division of Rheumatology, Faculty of Medicine, Saga University, Saga, Japan
Abstract
Musculoskeletal symptoms occur in up to 90% of systemic lupus erythematosus (SLE) patients. Lesions extend not only to joints but to the whole body, causing inflammation in diverse organs such as the skin, kidneys, lungs, nervous system, serous membranes and virtually across all organs of the body. The ABCDEFGHI method consists of A (Alignment): malalignment and deformation; B (Bone): bone changes; C (Capsular lesions): cartilage and intra-articular lesions; D (Distribution): four dimensional distributions: 1 intra-articular, 2 Intra region, 3 intra-body, 4 timeline; E (Extra-bone): extra-articular soft tissue; F (Further information): further additional medical information; G (Goal): general analysis and integrated, a comprehensive diagnosis from the information; H (Heal and Heath): treatment and prognosis; and I (Immunological analyzes): immunological interpretation (cytokines and phenotypes of immune cells). This chapter outlines a methodology for diagnosing the musculoskeletal and systemic manifestations of SLE.
Keywords: Musculoskeletal symptoms, Systemic lupus erythematosus (SLE), Systemic manifestations.
*Corresponding author Syuichi Korada: Department of Medical Technology and Sciences, International University of Health and Welfare, Okawa, Japan; Email:
[email protected]1. INTRODUCTION
Systemic lupus erythematosus (SLE) is a complex and clinically heterogeneous autoimmune disease. Musculoskeletal symptoms occur in up to 90% of SLE patients [1, 2]. Musculoskeletal disorders cause disabling symptoms in 70% of patients [3].
Despite being one of the most common symptoms, medical and basic researchers do not always pay the utmost attention to musculoskeletal symptoms. Joint symptoms may be neglected in SLE because systemic, cutaneous, and organ lesions are more prominent.
Both directly and indirectly, musculoskeletal symptoms affect patient quality of life (QOL), causing immobility and frailty. Ultimately, the musculoskeletal symptoms have a significant effect on the prognosis of the musculoskeletal system due to osteoporosis, compression fractures, necrosis of the femoral heads, and are irreversible.
Suppose patients with SLE are not diagnosed early. In that case, treatment may be delayed, the lesions and disorders will persist, and delayed diagnosis is often the cause of impaired patient quality of life.
Patients with rheumatoid arthritis always have joint radiography performed at the first visit and on regular examinations thereafter. On the other hand, in SLE patients, even if they have joint symptoms/deformities, radiography of the joints may not always be taken. It is the patient's desire to relieve the pain without using glucocorticoids in the treatment with more attention to lupus arthritis and musculoskeletal symptoms. SLE is a systemic disease, but it is important to recognize that SLE is also a joint disease.
Musculoskeletal involvement is one of the most common manifestations of SLE and is present in 69-95% of lupus patients [4-9]. Moreover, joint symptoms are frequently one of the earliest manifestations. Many patients with SLE can develop non-erosive arthritis. Joint lesions range from mild to severe, but clinically and historically, joint symptoms of SLE, including joint pain or arthritis, have usually been considered transient, mild, or moderate [10].
Arthritis in SLE is very important symptomatology, as 58% of patients have active musculoskeletal lesions even at relapse in one cohort study [10]. Historically, in 1872, Kaposi identified SLE arthritis and reported that joint lesions were a precursor to the more severe symptoms of lupus.
However, most researchers did not adequately study arthritis in SLE as a milder symptom compared to systemic symptoms. Even now, in daily practice, joint symptoms in SLE may be milder. Furthermore, it has been reported that arthralgia is one of the most influential symptoms on the quality of daily life from the perspective of the patient [11, 12]. Because it has been shown that joint involvement deeply impacts on quality of life in SLE patients [11]. Recently, many studies have shown that joint deformities also occur in SLE patients,causing erosive arthritis, the so-called rhupus syndrome, in up to 15% and Jaccoud’s arthropathy [10, 13-16]. Musculoskeletal ultrasonography and magnetic resonance imaging (MRI) have become useful tools in assessing patients with arthritis.
Surprisingly, these new imaging techniques have shown articular involvement of SLE in an unexpected higher prevalence [12]. The evaluation of various forms of lupus arthropathy with clinical and laboratory functions and images, including conventional radiography, musculoskeletal ultrasound, MRI, and other modalities, is described. In addition, images of musculoskeletal lesions are used to determine overlap with other diseases, rheumatoid arthritis (RA), spondyloarthritis, vasculitis syndrome, fractures, septic arthritis, and osteomyelitis. To diagnose lupus arthropathy, it is necessary to perform and interpret typical conventional and other diagnostic imaging.
The cause of the disease is still unknown. Genetic, hormonal, and environmental factors are thought to play important roles in the pathophysiology of SLE. Multiple genes show genetic susceptibility to SLE. Environmental factors such as ultraviolet (UV) light, viral infections, female gender, and exposure to estrogen-containing drugs induce SLE.
This book will serve as a useful reference in clinical and radiological diagnosis.
2. CLASSIFICATION OF LUPUS ARTHROPATHY
Arthropathy of SLE is clinically extremely diverse. There are two indicating categories: 1) non-erosive or erosive, and 2) non-deformable or deformable. However, it is clinically useful to divide into three categories: non-specific arthritis, non-erosive arthropathy (Jaccoud’s arthritis), and erosive arthritis (rhupus) [17]. Moreover, lupus arthropathy is clinically highly diverse and can be divided into at least six clinical forms.
Musculoskeletal abnormalities in SLE patients have tremendous clinical variability and include myositis, fasciitis, symmetric arthritis, non-erosive degenerative arthritis, spontaneous tendon rupture, soft tissue calcification, osteomyelitis, septic arthritis, terminal phalangeal sclerosis, erosion, and osteonecrosis (Table 1).
Table 1Musculoskeletal Manifestations of Systemic Lupus Erythematosus.MyositisNon-specific polyarthritisDeforming non-erosive arthropathy (Jaccoud’s arthropathy)Deforming erosive arthritis (Rhupus)Subchondral cystsTenosynovitisTendon weakening and ruptureOsteonecrosisSoft tissue calcificationOsteomyelitis and septic arthritisAcrosclerosisTuft resorptionInsufficiency fracture
2.1. Frequency of Arthritis Subtypes
Most patients with SLE have non-erosive and non-deforming arthritis. Patients with non-erosive arthritis are the most common (up to 35% of patients with SLE) [18
