Rheumatology Board Review E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 266

Veröffentlichungsjahr: 2014

Beschreibung

The field encompassed by rheumatology has evolved rapidly over the last decade to include multiple immune-modulating and biologic medications, new classification criteria, significant updates on bone metabolism, and completely new paradigms of treatment based on groundbreaking studies published within the last 5 years. Although much has been adopted as standard of care based on new data, most textbooks do not reflect these practice changes.

Rheumatology Board Review highlights the latest advances in the field and new standards of care, including references to current citations in the medical literature. It provides international standards and guidelines and is designed to convey a maximum amount of information quickly and efficiently, with many helpful schematics, radiographs, and tables.

Rheumatology Board Review offers chapter coverage of:

• Non-inflammatory joint and soft tissue disorders
• Selected topics in rheumatoid arthritis
• Selected topics in systemic lupus erythematosus
• Antiphospholipid antibody syndrome
• IgG4-related disease
• Myopathies
• Selected topics in pediatric rheumatology
• HIV and rheumatic diseases
• Miscellaneous arthropathies
• Osteoporosis
• Review of musculoskeletal radiology
• Study design, measurement, and basic statistical analysis
• Update on vasculitis

Rheumatology Board Review is a must-have reference for rheumatology fellows and professionals seeking a concise yet thorough review of state-of-the-art rheumatology.

Leseprobe

Table of Contents

Title page

Copyright page

List of Contributors

Preface

CHAPTER 1: Non-Inflammatory Joint and Soft Tissue Disorders

Introduction

Carpal Tunnel Syndrome

Osteoarthritis (OA)

Secondary Osteoarthritis

Inflammatory/Erosive Hand Osteoarthritis

Diffuse Idiopathic Skeletal Hyperostosis (DISH)

Gout

CHAPTER 2: Selected Topics in Rheumatoid Arthritis

Introduction

2010 ACR/EULAR RA Classification Criteria

Anti-Citrullinated Antibodies

Rheumatoid Arthritis and Cardiovascular Disease

Treatment Advances in Rheumatoid Arthritis

Appropriate Immunizations and Screening in RA Patients

CHAPTER 3: Selected Topics in Systemic Lupus Erythematosus: B Cells in Lupus and Lupus Nephritis

Introduction

B Cell Roles in SLE

Therapies Targeting B Cells

Existing Therapies for SLE

Additional Therapies Targeting B Cells in SLE under Investigation

Lupus Nephritis

CHAPTER 4: Antiphospholipid Antibody Syndrome

Introduction

Epidemiology

Classification Criteria

The Clinical Spectrum of APS

aPL Antibodies Laboratory Testing

Treatment

CHAPTER 5: IgG4-Related Disease

Introduction

Histology

Epidemiology

Etiology

Clinical Manifestations

Differential Diagnosis

Specific Organ Involvement in IgG4-RD

Diagnostic Studies

Treatment

Prognosis

CHAPTER 6: Myopathies

Introduction

Common Causes of Myopathy

Idiopathic Inflammatory Myopathies/Autoimmune-Mediated (AIM)

Other Considerations in Myopathies

CHAPTER 7: Selected Topics in Pediatric Rheumatology

Introduction

Juvenile Idiopathic Arthritis (JIA)

Pediatric Systemic lupus Erythematosus (pSLE)

Juvenile Dermatomyositis

Childhood Vasculitis

Outcome Measures in Pediatric Rheumatology

Further Reading

Juvenile Idiopathic Arthritis

CHAPTER 8: HIV and Rheumatic Diseases

Introduction

General Principles

The Spectrum of Rheumatic Disease in HIV

Approach to Evaluating Joint Pain in HIV

HIV-Associated Syndromes that Mimic/Overlap Rheumatic Syndromes

Further Reading

CHAPTER 9: Miscellaneous Arthropathies

Introduction

Arthritis from Malignancy and Hematologic Disorders

Endocrinopathies

Infectious Arthritis

CHAPTER 10: Osteoporosis

Introduction

Diagnosis

Therapeutic Options

Further reading

CHAPTER 11: Review of Musculoskeletal Radiology

Introduction

Radiographic Features of RA

Radiographic Features of Psoriatic Arthritis

Radiographic Features of Ankylosing Spondylitis

Radiographic Findings in Crystalline Arthropathies

Radiographic Features of Diffuse Idiopathic Skeletal Hyperostosis (DISH)

Radiographic Features of Sarcoidosis

Radiographic Features of Septic and Neuropathic Arthropathy

Radiographic Features of Paget's Disease of the Bone

Radiographic Features of Avascular Necrosis (AVN)

Radiographic Features of Osteoarthritis

CHAPTER 12: Study Design, Measurement, and Basic Statistical Analysis

Introduction

Epidemiologic Study Designs

Common Descriptors of Data

Disease Frequency and Risk Factors

Measurement Error

Basic Statistical Tests

Further reading

CHAPTER 13: Update on Vasculitis

Introduction

ANCA-Associated Vasculitides

ANCA-Positive Vasculitis Mimics

Index

List of Tables

Table 1.1

Table 1.2

Table 1.3

Table 2.1

Table 2.2

Table 3.1

Table 6.1

Table 6.2

Table 6.3

Table 6.4

Table 7.1

Table 7.2

Table 7.3

Table 10.1

Table 10.2

Table 10.3

Table 11.1

Table 11.2

Table 12.1

Table 12.2

Table 12.3

Table 12.4

List of Illustrations

Figure 1.1

Figure 5.1

Figure 5.2

Figure 5.3

Figure 11.1

Figure 11.2

Figure 11.3

Figure 11.4

Figure 11.5 (a,b)

Figure 11.6

Figure 11.7

Figure 11.8

Figure 11.9

Figure 11.10

Figure 11.11

Figure 11.12

Figure 11.13

Figure 11.14

Figure 11.15

Figure 11.16 (a,b)

Figure 11.17

Figures 11.18 (a,b)

Figure 11.19

Figure 11.20

Figure 11.21

Figure 11.22

Figure 11.23

Figure 11.24

Figure 11.25

Figure 11.26

Figure 11.27

Figure 11.28

Figure 11.29

Figure 11.30

Figure 11.31

Figure 11.32

Figure 12.1

Figure 12.2

Figure 12.3

Figure 12.4

Figure 12.5

Figure 13.1

Guide

Cover

Table of Contents

Start Reading

Preface

CHAPTER 1

Index

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Rheumatology Board Review

Editor

Karen Law, MD

Assistant Professor of Medicine

Division of Rheumatology

Emory University School of Medicine

Atlanta, GA, USA

Associate Editor

Aliza Lipson, MD

Assistant Professor of Medicine

Division of Rheumatology

Emory University School of Medicine

Atlanta, GA, USA

Publisher Cities

Publisher Imprint (e.g., Wiley-Interscience; John Wiley & Sons, Inc.; A John Wiley & Sons, Inc. company)

Copyright page

Copyright © 2014 by John Wiley & Sons, Inc. All rights reserved

Published by John Wiley & Sons, Inc., Hoboken, New Jersey

Published simultaneously in Canada

No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, scanning, or otherwise, except as permitted under Section 107 or 108 of the 1976 United States Copyright Act, without either the prior written permission of the Publisher, or authorization through payment of the appropriate per-copy fee to the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, [phone], fax [phone], or on the web at www.copyright.com. Requests to the Publisher for permission should be addressed to the Permissions Department, John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, [phone], fax [phone], or online at http://www.wiley.com/go/permissions.

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Library of Congress Cataloging-in-Publication Data

Rheumatology board review / editor, Karen Law ; associate editor, Aliza Lipson.

p. ; cm.

Includes bibliographical references and index.

ISBN 978-1-118-12791-9 (pbk. : alk. paper) – ISBN 978-1-118-47584-3 (ePub) – ISBN 978-1-118-47594-2 (ePdf) – ISBN 978-1-118-47596-6 (eMobi) – ISBN 978-1-118-47597-3

I. Law, Karen, editor of compilation. II. Lipson, Aliza, editor of compilation.

[DNLM: 1. Rheumatic Diseases–Outlines. 2. Rheumatology–Outlines. WE 18.2]

RC927

616.7'230076–dc23

2013026486

Cover image: Top image – iStock file #22909211 © zhongguo. Middle image – iStock file #2291786 © Dominik Pabis. Bottom image – iStock file #16004426 © GeorgHanf.

Cover design by Matt Kuhns

Printed in the United States of America

10 9 8 7 6 5 4 3 2 1

List of Contributors

Sheila Angeles-Han, MD, MSc

Assistant Professor of Pediatrics and Ophthalmology

Division of Pediatric Rheumatology

Emory University School of Medicine

Children's Healthcare of Atlanta

Atlanta, GA, USA

Schartess Culpepper-Pace, MD

Rheumatology and Internal Medicine

Chen Medical Centers

Miami, FL, USA

Cristina Drenkard, MD, PhD

Assistant Professor of Medicine

Division of Rheumatology

Emory University School of Medicine

Atlanta, GA, USA

Robin Geletka, MD

Rheumatology Medical Science Liaison

Actelion Pharmaceuticals Ltd

San Francisco, CA, USA

Arezou Khosroshahi, MD

Assistant Professor of Medicine

Division of Rheumatology

Emory University School of Medicine

Atlanta, GA, USA

Karen Law, MD

Assistant Professor of Medicine

Division of Rheumatology

Emory University School of Medicine

Atlanta, GA, USA

S. Sam Lim, MD, MPH

Associate Professor of Medicine

Clinical Director, Division of Rheumatology

Emory University School of Medicine

Atlanta, GA, USA

Aliza Lipson, MD

Assistant Professor of Medicine

Division of Rheumatology

Emory University School of Medicine

Atlanta, GA, USA

Courtney McCracken, PhD

Department of Pediatrics

Emory University School of Medicine

Atlanta, GA, USA

Laura Paxton, MD

Clinical Instructor of Medicine

Division of Rheumatology

Atlanta Veterans Affairs Medical Center;

Emory University School of Medicine

Atlanta, GA, USA

John Payan, MD, MPA

Section Chief of Musculoskeletal Imaging

Atlanta Veterans Affairs Medical Center;

Assistant Professor of Radiology

Emory University School of Medicine

Atlanta, GA, USA

Sampath Prahalad, MD, MS

Marcus Professor of Pediatric Rheumatology

Chief, Division of Pediatric Rheumatology

Associate Professor of Pediatrics and Human Genetics

Emory University School of Medicine

Children's Healthcare of Atlanta

Atlanta, GA, USA

Gnanesh Patel, MD

Fellow in Rheumatology

Emory University School of Medicine

Atlanta, GA, USA

Kelly A. Rouster-Stevens, MD, MS

Assistant Professor of Pediatrics

Division of Pediatric Rheumatology

Emory University School of Medicine

Children's Healthcare of Atlanta

Atlanta, GA, USA

Iñaki Sanz, MD

Mason I. Lowance Professor of Medicine and Pediatrics

Chief, Division of Rheumatology

Director, Lowance Center for Human Immunology

Emory University School of Medicine

Atlanta, GA, USA

Athan Tiliakos, DO

Assistant Professor of Medicine

Division of Rheumatology

Emory University School of Medicine

Atlanta, GA, USA

Larry Vogler, MD

Associate Professor of Pediatrics

Division of Pediatric Rheumatology

Emory University School of Medicine

Children's Healthcare of Atlanta

Atlanta, GA, USA

Preface

Rheumatology Board Review is offered as an up-to-date, concise review of the rheumatic diseases, with an emphasis on recent advances in the field, including immune-modulating and biologic medications, new classification criteria, pediatric topics, and new paradigms of treatment. Each chapter employs an outline format designed to efficiently convey a maximum amount of material, accented by simple figures, radiographs, and tables to enhance understanding.

This book is dedicated to health professionals at all levels of training who share an interest in our ever-evolving, fascinating field of rheumatology. We hope this book contributes to a deeper understanding of topics in the rheumatic diseases and a lifelong interest in rheumatology.

Karen Law

Aliza Lipson

CHAPTER 1Non-Inflammatory Joint and Soft Tissue Disorders

Laura Paxton1,3, Schartess Culpepper-Pace2, Karen Law3

1Atlanta Veterans Affairs Medical Center, Atlanta, GA, USA

2Rheumatology and Internal Medicine, Chen Medical Centers, Miami, FL, USA

3Emory University School of Medicine, Atlanta, GA, USA

Introduction

Rheumatologists often manage non-inflammatory arthritides and associated soft tissue disorders, including osteoarthritis, carpal tunnel syndrome, and gout. The diagnosis of these conditions as well as recent innovations in treatment will be reviewed here.

Carpal Tunnel Syndrome

Epidemiology

One of the most common and frequently diagnosed entrapment neuropathies

Accounts for up to 90% of entrapment neuropathies

Prevalence in the US population up to 5% of the general population

Estimated lifetime risk of 10%

Females affected more frequently than men

Peak age range 40–60 years

Risk factors include prolonged wrist flexion or extension, repeated use of flexor muscles, and exposure to vibration

Systemic medical conditions i.e. diabetes, hypothyroidism, obesity, pregnancy, vitamin toxicity or deficiency can predispose

Many cases remain idiopathic

Pathology

Median nerve entrapment is caused by chronic pressure at the level of the carpal tunnel

Compression of the median nerve is secondary to surrounding structures:

carpal bones

,

flexor tendons

, and the fibrous

transverse carpal ligament

leading to median nerve dysfunction

Carpal tunnel anatomy (

Figure 1.1

)

Superiorly: transverse carpal ligament

Posteriorly: carpal bones

Nine flexor tendons: (four) flexor digitorum profundus, (four) flexor digitorum superficialis, flexor pollicis

Median nerve

Repetitive compressive injury to the median nerve leads to demyelination

Blood flow may also be interrupted, altering the blood–nerve barrier

Figure 1.1

Components of the carpal tunnel (Color plate 1.1).

Clinical Presentation

Symptoms may include tingling and numbness, in the distribution of the median nerve (

first three fingers and radial aspect of the fourth finger

); pain involving the entire hand, decreased grip strength, and reduced dexterity

Symptoms occasionally worse at night (awakenings with

paresthetica nocturna

: sensation of tingling, burning or numb hand possibly secondary to flexion of wrist at night)

Patients with carpal tunnel syndrome (CTS) occasionally report subjective swelling of the hands and/or wrists

Atrophy of the thenar eminence occurs in later stages (this finding is associated with poor response to surgical decompression)

Diagnosis

Combination of the clinical history, examination, provocative tests, electrodiagnostic studies

Phalen's test

is positive when flexion at the wrist for 60 seconds causes pain and/or paresthesias in median nerve distribution

Sensitivity ranges from 67–83%

Specificity ranges from 40–98%

Tinel's test

is positive when tapping over the volar surface of the wrist (course of median nerve) causes pain and/or paresthesias in the distribution of the median nerve

Sensitivity ranges from 48–73%

Specificity reported as high as 100%

Electrodiagnostic studies lack standardized diagnostic criteria currently, making them inadequate as a universally recognized gold standard

Nerve conduction studies provide objective information regarding the median nerve across the carpal tunnel

Findings include prolonged motor and sensory latencies of median nerve

Reduction in median nerve compound motor or sensory action potential amplitude

Reductions in sensory and motor conduction velocities

Rules out other polyneuropathies included in the differential diagnosis

Ultrasonography may reveal flattening of the median nerve within the tunnel and bowing of the flexor retinaculum

Cross-sectional area of the median nerve is the most predictive of CTS; it has also been used in the classification of the severity of CTS

Magnetic resonance imaging assists in the determination of the severity of nerve compression; it is also helpful in observing anatomical structures that may be contributing to symptoms, i.e. ganglion cysts, bony deformities

Swelling of the median nerve and increased signal intensity on T2- weighted images assist in diagnosing CTS

Treatment

Mild to moderate symptoms

Oral anti-inflammatories

Oral corticosteroids may be effective in reducing edema and tenosynovitis associated with CTS

Carpal bone mobilization and hand splints are often first-line treatment options

Corticosteroid injection

along the proximal wrist crease just ulnar to the palmaris longus tendon

provides clinical improvement, however benefit beyond 1 month was not shown in a systematic review

Ultrasound therapy

Moderate to severe symptoms

Acupuncture therapy has been reported to improve median nerve function

Carpal tunnel release (CTR)

Surgical procedure to increase space in the carpal tunnel and reduce pressure on the median nerve, via division of the transverse carpal ligament

Good to excellent long-term outcomes following CTR in up to 90% of reported cases

Surgical treatment has been reported to demonstrate better long-term response when compared to splinting

Differential Diagnosis

Cervical radiculopathy

Proximal median neuropathy

Thoracic outlet syndrome

Central nervous system (CNS) disorders

Osteoarthritis (OA)

Epidemiology

Most common arthritis

A leading cause of chronic pain and disability in older adults

Commonly Involved Joints

Hand – most commonly involved in OA – distal interphalangeals (DIPs), proximal interphalangeals (PIPs), first carpometacarpal (CMC)

Feet – first metatarsophalangeal (MTP), subtalar joint

Knee

Hip

Spine

Rarely affects elbow, wrist, ankle – look for history of trauma, congenital abnormality, systemic or crystalline disease

Definition

OA can be defined pathologically, radiographically, or clinically

Radiographic OA has long been considered the reference standard for epidemiology

Not all subjects with radiographic OA are symptomatic and not all with symptoms have radiographic OA

Risk Factors

Age – the strongest risk factor, most commonly age >40 years

Females

Obesity – the strongest

modifiable

risk factor

Previous injury

Family history (genetic predisposition)

Joint malalignment (mechanical factors)

Pathogenesis

Caused by an interplay of multiple factors – joint integrity, genetics, local inflammation, mechanical forces, cellular and biochemical processes

Abnormal remodeling of joint tissues is driven by a host of inflammatory mediators within the joint

OA pathogenesis is now thought of as an

active response to injury

rather than a degenerative process

Degradation of matrix and articular cartilage

Chondrocytes become “activated” and increase production of matrix proteins and matrix-degrading enzymes during inadequate repair response

Aggrecanases, collagenases, serine and cysteine proteinases, matrix metalloproteinase (MMP)-3, MMP-13, ADAMTS-5 are all reported to play a role

Thickening of the subchondral bone

Bone remodeling may be initiated at sites of local bone damage resulting from excessive repetitive loading

Formation of osteophytes

At joint margins and entheseal sites – new bone is added by endochondral ossification, leading to osteophyte formation

Variable degrees of inflammation of the synovium

Synovial infiltrates have been identified in many OA patients, though lower in grade than in rheumatoid arthritis (RA)

Prevalence of synovitis increases with advancing age

Interleukin (IL)-1 beta

and

tumor necrosis factor (TNF) alpha

suppress matrix synthesis and promote cartilage catabolism,

IL-17

induces chemokine production by synovial fibroblasts and chondrocytes

Degeneration of ligaments, menisci in the knee, and hypertrophy of the joint capsule, as any meniscal or ligamentous injury predisposes to the development of OA

Symptoms

Hand

Pain on usage

Mild morning or inactivity stiffness, usually lasting <30 minutes

Characteristic sites – DIPs, PIPs, base of the thumb

Knee and hip

Usage-related pain

Often worse toward the end of the day

Pain relieved, usually incompletely, with rest

Mild morning or inactivity stiffness (gelling)

Advanced OA – may have rest or night pain

OA symptoms are often episodic or variable in severity and slow to change

Physical Examination

Hand

Heberden's (DIPs) and Bouchard's (PIPs) nodes

Squared appearance to the first CMC is classic

Feet

First MTP involvement may result in hallux valgus or hallux rigidus

Knees

Tenderness to palpation of joint

Crepitus

Joint effusion

Synovial fluid in OA typically exhibits

Normal viscosity

Mild pleocytosis (WBC <2000/mm

3

)

Osteophytes – may have palpable bony enlargements at periphery of joint

Restricted movement and range of motion

Hip

Hip pain worsened with internal or external rotation

Anterior and inguinal pain generally indicative of true hip joint involvement

Check both hips, as ∼20% have bilateral OA

Full exam should also include evaluation for referred pain sources

Trochanteric bursitis

Lumbosacral spine

Knee pathology

Osteoarthritis Treatment

Management is primarily symptomatic, as no treatments have been shown to slow or reverse joint damage. Patient education regarding the natural history of the disease is critical. Non-pharmacologic treatments must be balanced with judicious use of pharmacologic treatments.

Non-Pharmacologic Treatments

Instruction on joint protection techniques

Thermal modalities – paraffin wax treatments, heat packs, and heating pads

Strong recommendation for

weight loss

in patients with hip or knee OA

Exercise – cardiovascular and/or resistance land-based exercise, aquatic exercise, and manual therapy (physical/occupational therapy) in combination with supervised exercise have all been helpful

Participation in self-management programs and psychosocial interventions (diet, exercise instruction) can offer significant benefit

Tai chi programs have been reported to be beneficial in small studies

Assistive devices, orthotics, and splinting as needed:

Splints for trapeziometacarpal joint OA

Medially wedged insoles for lateral compartment knee OA

Laterally wedged subtalar strapped insoles for medial compartment knee OA

Medially directed patellar taping for knee OA

Pharmacologic Therapy

Acetaminophen

Topical capsaicin – efficacy is controversial, but some advocate for its use as adjunctive treatment

Topical non-steroidal anti-inflammatory drugs (NSAIDs), e.g. topical diclofenac, is a safe option especially if age >75 years

Oral NSAIDs, including non-selective and selective (cyclo-oxygenase (COX)-2 inhibitors) (

Table 1.1

)

Monitor for gastrointestinal (GI) and cardiac adverse effects (GI bleeding, abdominal pain, MI, worsening CHF)

Avoid in chronic kidney disease

COX-2 selective inhibitors are associated with increased cardiovascular risk and should be avoided in patients with cardiovascular risk factors

Tramadol can also play a role in pain relief, especially in patients for whom NSAIDs or acetaminophen are contraindicated

Intra-articular injection of long-acting corticosteroid can be effective for painful flares of OA, especially in trapeziometacarpal joint OA and knee OA

Clinical scenario

Recommended regimen

History of GI bleed, but none within the past year

Non-selective NSAID or COX-2 inhibitor + proton-pump inhibitor

History of GI bleed within the past year

COX-2 inhibitor + proton-pump inhibitor

Patient taking low-dose aspirin for cardioprotection

Non-selective NSAID other than ibuprofen

*

+ proton-pump inhibitor

*The FDA warns against ibuprofen and low-dose aspirin used in combination, due to a pharmacodynamic interaction causing a decreased cardiprotective effect

Table 1.1 Use of NSAIDs in high-risk populations.

Intra-Articular Viscosupplementation

Multiple brands available (

Table 1.2

)

Currently only FDA-approved for knee osteoarthritis

Few head-to-head comparisons and generally small studies

Mechanism

Hyaluronic acid (HA) is a constitutive component of the matrix cartilage

Plays a key role in maintenance of joint homeostasis

Biologically active component secreted by chondrocytes that protects cartilage from degradation by interacting with MMPs and pain mediators

In OA, concentration and molecular weight of HA is reduced

Exact mechanism not understood

Proposed mechanism

Biomechanical – improves synovial fluid viscoelasticity, increases joint lubrication, coats articular cartilage surface

Analgesic – reduces pain eliciting nerve activity, reduces prostaglandin- or bradykinin-induced pain

Anti-inflammatory – reduces levels of inflammatory mediators, decreases leukocyte chemotaxis

Antioxidant

Chondroprotective – stimulation of endogenous HA and extra matrix component synthesis, protects against chondrocyte apoptosis, inhibits cartilage degradation

Side effects

Generally well tolerated, most side effects related to injection site reactions

Rare

pseudosepsis reactions

, especially with high molecular weight HA

Patients present with acute joint swelling, pain, and warmth

Care must be taken to distinguish this syndrome from true septic joint

Clinical use

Used in knee OA patients who fail non-pharmacologic treatments, acetaminophen, NSAIDs, and intra-articular steroids

Studies have shown improvement in pain scores with viscosupplementation, however:

Appropriate patient selection is not well defined

Many studies do not control for concomitant pharmacologic therapy

Double-blind, placebo-controlled trials report a large placebo effect

Campbell et al. in 2007 reviewed six systematic reviews on viscosupplementation

Three reviews showed viscosupplementation more effective than placebo

Three reviews suggested no benefit

Rutjes et al. in 2012 systematic review and meta-analysis concluded that viscosupplementation is associated with a small and clinically irrelevant benefit and an increased risk for serious adverse events

Viscosupplementation is not recommended for OA of the hip due to lack of data

Product

Dosing

Molecular weight (in M Daltons)

Hyalgan (sodium hyaluronate)

Once weekly for 3–5 weeks

0.5–0.73

Supartz (sodium hyaluronate)

Once weekly for 3–5 weeks

0.6–1.1

Orthovisc (high molecular weight hyaluronan)

Once weekly for 3–4 weeks

1.0–2.9

Euflexxa (1% sodium hyaluronate)

Once weekly for 3 weeks

2.4–3.6

Synvisc (hylan G-F 20)

Once weekly for 3 weeks

6

Synvisc-One (hylan G-F 20)

Once

6

Table 1.2 Comparison of viscosupplementation products.

Glucosamine and Chondroitin Sulfate

Both are labeled as supplements in the United States and are therefore do not need to be approved by the FDA before they are marketed; therefore variations in dosage among the marketed supplements exist, making comparisons difficult

The GAIT trial for knee OA demonstrated that response to glucosamine and chondroitin alone or in combination were not different from placebo

A small subgroup analysis of patients with moderate-to-severe knee OA did show statistically significant improvement with combination therapy

2-year follow up did not demonstrate clinically significant differences between the treatment groups

Other studies have shown efficacy with these agents but were criticized for flaws, including failure to adhere to intention to treat, small numbers of patients, potential bias related to sponsorship of the study, and inadequate masking of the study agent

As a result, recommendations from leading organizations differ:

American College of Rheumatology (ACR) 2012 statement recommends against the use of glucosamine and chondroitin

European League against Rheumatism (EULAR) recommendations include glucosamine and chondroitin as viable treatment option for knee OA

OARSI (Osteoarthritis Research Society International) recommends a trial for 6 months, followed by reassessment and discontinuation if ineffective at that time

Surgery for Osteoarthritis

Joint replacement for the knee and hip should be considered in patients with radiographic evidence of OA along with chronic pain and disability that is refractory to treatment with non-pharmacologic and pharmacologic interventions

Surgical intervention should be performed before the development of significant deformities, contractures, functional loss, or muscle atrophy for optimal result

Knee surgical options include arthroscopy, osteotomy, and total knee arthroplasty. The type of surgical procedure is dependent on the location and stage of OA, comorbidities, age and physical activity level, and the degree of patient symptoms.

Arthroscopic lavage and debridement

Role in knee OA is controversial

Lack of evidence to show significant benefit

Unloading osteotomy

Can be used in young and active patients with unicompartmental OA

Aim to unload damaged compartment and transfer weight by slightly overcorrecting into a valgus or varus axis

Must have appropriate patient selection for satisfactory outcome

Typically good results in the first few years, however, satisfaction decreases thereafter

Arthroplasty

Unicompartmental knee arthroplasty

Indicated when OA involves only one compartment of the knee

Appropriate for younger patients with less severe disease

More rapid recovery

Provides preservation of bone stock, more normal knee kinematics, greater physiologic function

Poorer long-term survival of prosthetic than total knee arthroplasty

Total knee arthroplasty (TKA)

Indicated in advanced OA with more than one compartment involved

Durability of prosthetic components is approximately 15–20 years, therefore it is typically avoided in patients <60 years old

Main complications – femoropatellar problems, loosening of components, infections, residual stiffness

Hip surgical options are less varied than knee surgical options. Hip resurfacing is an option for young, more active patients who have an interest in a bone-conserving replacement procedure. Total hip arthroplasty (THA) has excellent long-term results in the treatment of late, symptomatic OA. Complications for THA are similar to those for TKA.

Secondary Osteoarthritis

Secondary osteoarthritis is caused by previous injury or disease of the target joint, due to conditions that adversely alter the articular cartilage or subchondral bone. Conditions that predispose to the development of secondary OA include trauma, infections, prior surgery, mineral deposition, and autoimmune disorders. Several of these conditions will be discussed further in this section.

Etiologies

Metabolic

Crystal-associated arthritis

(gout, pseudogout)

Both monosodium urate (MSU) and calcium-containing crystals (calcium pyrophosphate dihydrate [CPPD], basic calcium phosphate crystals) may contribute to inflammation in OA tissues through direct interactions with components of the innate immune system and the amplification of other inflammatory signals

Calcium-containing crystals are frequently found in tissues from patients with end-stage OA

Ochronosis

(hereditary alkaptonuria)

A rare hereditary autosomal recessive disease characterized by a defect in the gene coding for homogentisate 1,2–dioxygenase leading to accumulation of homogentisic acid

Black pigment produced by oxidation and polymerization of homogentisic acid deposits in connective tissues and binds irreversibly to them, causing ochronosis

Clinical manifestations

Arthropathy causing degeneration of major joints and intervertebral discs

Can also affect skin and sclera

Patients tend to be asymptomatic until approximately 30 years of age, when sequelae of ochronosis becomes apparent

Ochronotic arthritis may begin in the late 30s with low back pain and stiffness; knee symptoms resemble typical osteoarthritis

Symptoms simulate degenerative joint disease – articular space narrowing, bone sclerosis, effusion

Cartilage tends to be more easily damaged, promoting rapid progression to end–stage disease

Radiographic findings

Spine

Plain film and computed tomography (CT) scans of the spine show multilevel narrowing of intervertebral spaces, calcification, and vacuum phenomenon of intervertebral discs

Peripheral joints

Primarily affects weight-bearing joints (frequently knees, but also can involve hips, shoulders)

Joint space narrowing and subchondral sclerosis with cyst formation are apparent with minimal osteophytes

Treatment is primarily symptomatic for early-stage disease, with many patients progressing to total joint replacement as end-stage joint disease develops

Hemochromatosis

A relatively prevalent genetic disease characterized by tissue iron overload

Most frequent mutation is the

homozygous C282Y gene mutation

Patients can develop life-threatening organ damage – liver cirrhosis, carcinoma, diabetes, and heart failure

Other complications include arthropathy and osteoporosis;

pseudogout

is also commonly seen in patients with hemochromatosis

Diagnosis

Clinical symptoms

Chronic weakness

Arthralgias/arthritis

Chondrocalcinosis

Bronze skin pigmentation

Unexplained liver disease or hepatomegaly

Type 1 diabetes

Early onset osteopenia/osteoporosis

Cardiac symptoms (rhythm disturbances, cardiac failure)

Laboratory abnormalities

Plasma transferrin saturation and ferritin are increased

Must rule out increased ferritin from non-hemochromatosis causes – alcohol, inflammation, cell necrosis, dysmetabolic iron overload syndrome

Joint manifestations

Arthritis is common

If present, symptoms often precede diagnosis by up to 9 years

Two thirds of patients report joint symptoms as a major cause of impaired quality of life

One third of hemochromatosis cases are revealed through the workup of isolated articular pain

Symptoms can begin before 30 years of age in men but usually after menopause in women

Joint location

Classic joints involved – second and third metacarpophalangeals (MCPs)

Bony enlargement over second and third MCPs is common

Other common joint involvement – wrists, PIPs, hips, knees, ankles

Less frequent locations – shoulders, elbows, spine

Can have either a monoarthritis or polyarthritis and pain crises

Synovial fluid and laboratory studies may show either a degenerative or inflammatory profile

Radiological manifestations:

Most often seen in second and third MCPs

Hook-shaped osteophytes of the MCPs is very characteristic with associated joint space narrowing

Wrist and distal radioulnar joints are frequently affected

Can sometimes lead to erosive arthritis which can mimic RA

Chondrocalcinosis may also be seen, indicating concomitant CPPD

Treatment:

Iron removal by phlebotomy is often not helpful for joint symptoms

No evidence based treatment to date

NSAIDs and intra-articular glucocorticosteroids can be effective

Treatment for pseudogout, if present, can also alleviate symptoms

Wilson's disease