This document provides an overview of arthritis pain management strategies without compromising patient safety. It discusses the disease states and diagnostic criteria for osteoarthritis and rheumatoid arthritis. It then reviews the goals and treatment options for managing the pain and symptoms of osteoarthritis and rheumatoid arthritis, including both non-pharmacologic and pharmacologic approaches. It also discusses the efficacy and gastrointestinal safety profile of the drug celecoxib for treating arthritis pain.
Was recently asked to discuss whether there is evidence to support the use of B vitamins in managing different aches and pains. Here's my talk delivered last 16 Sept 2016 at the 12th Post Graduate Course of the East Avenue Medical Center Department of Internal Medicine.
Evidence based management of osteoarthritis in primary care - Dr Jonathan Quickepcsciences
Dr Jonathan Quicke is an NIHR Academic Clinical Lecturer in Physiotherapy (Keele University). Dr Quicke presented at the 2017 Musculoskeletal Education Day, where he discussed how we can ensure that best practice can be implemented within general practice for patients suffering with osteoarthritis
Was recently asked to discuss whether there is evidence to support the use of B vitamins in managing different aches and pains. Here's my talk delivered last 16 Sept 2016 at the 12th Post Graduate Course of the East Avenue Medical Center Department of Internal Medicine.
Evidence based management of osteoarthritis in primary care - Dr Jonathan Quickepcsciences
Dr Jonathan Quicke is an NIHR Academic Clinical Lecturer in Physiotherapy (Keele University). Dr Quicke presented at the 2017 Musculoskeletal Education Day, where he discussed how we can ensure that best practice can be implemented within general practice for patients suffering with osteoarthritis
Dr Jennifer Walsh's presentation from Osteoporosis 2016: Management of osteoporosis in the young adult.
Find out more at: https://nos.org.uk/conference
Diabetes mellitus and erectile dysfunction by Dr. Mohand Yaghi PgDip (urol) C...Mohand Yaghi
A lecture about the effect of diabetes mellitus on the erectile function. Dr. Mohand Yaghi was an invited speaker in Al-Jahra scientific day, Kuwait 2015.
Artigo (4) importante para a preparação para o curso de dor lombar crônica. "Características sensoriais da dor lombar crônica inespecífica: uma investigação de subgrupos."
Dr Jennifer Walsh's presentation from Osteoporosis 2016: Management of osteoporosis in the young adult.
Find out more at: https://nos.org.uk/conference
Diabetes mellitus and erectile dysfunction by Dr. Mohand Yaghi PgDip (urol) C...Mohand Yaghi
A lecture about the effect of diabetes mellitus on the erectile function. Dr. Mohand Yaghi was an invited speaker in Al-Jahra scientific day, Kuwait 2015.
Artigo (4) importante para a preparação para o curso de dor lombar crônica. "Características sensoriais da dor lombar crônica inespecífica: uma investigação de subgrupos."
Knee osteoarthritis (OA), also known as degenerative joint disease, is typically the result of wear and tear and progressive loss of articular cartilage. It is most common in the elderly. Knee osteoarthritis can be divided into two types, primary and secondary. Primary osteoarthritis is articular degeneration without any apparent underlying reason. Secondary osteoarthritis is the consequence of either an abnormal concentration of force across the joint as with post-traumatic causes or abnormal articular cartilage, such as rheumatoid arthritis (RA).
Osteoarthritis is typically a progressive disease that may eventually lead to disability. The intensity of the clinical symptoms may vary for each individual. However, they typically become more severe, more frequent, and more debilitating over time. The rate of progression also varies for each individual. Common clinical symptoms include knee pain that is gradual in onset and worse with activity, knee stiffness and swelling, pain after prolonged sitting or resting, and pain that worsens over time. Treatment for knee osteoarthritis begins with conservative methods and progresses to surgical treatment options when conservative treatment fails. While medications can help slow the progression of RA and other inflammatory conditions, no proven disease-modifying agents for the treatment of knee osteoarthritis currently exist.
Pearls about NSAIDs and their usage in the managaement of chronic pain, considering safety profile of both selective cox-2 or non selective cox-2 inhibitors
A comprehensive talk about rheumatic autoimmune diseases for patients and family or people interested in understanding SLE, Systremic sclerosis, dermatomyositis, rheumatoid arthritis. Some slides in Bahasa Indonesia.
A systematic approach as to how general physician assessing a patient with musculoskeletal pain with confident; with rheumatoid arthritis as a model. prepared with help of Dr. Perdana Aditya SpPD.KR from UNIBRAW Malang
A brief review about the role of vitamin D in health and disease. Most of the content in these slides were taken from another author with some editing to custom it for the purpose of general physician workshop scientific material. Some figures were our own data in our hospital
This is a brief introduction regarding selected rheumatic autoimmune disease for laymen. Some of these figures in the slides were cited from textbook and another authors elesewhere, and some of them were photos of patient taken with their permission
Penyakit Autoimun penting dikenali masyarakat awam karena gejalanya yang tersamar antar sesama autoimun, bahkan dengan penyakit lain yang bukan autoimun.
Sebuah edukasi pasien tentang lupus, meliputi berbagai aspek yang patut diketahui, agar pasien dan keluarganya tidak larut dalam fase denial dan bargaining yang berkepanjangan
Komordibitas pada pasien dengan gout di poliklinik reumatologi (edit)Rachmat Gunadi Wachjudi
Bagaimana komorbiditas pasien Gout di Indonesia ? Ini merupakan penelitian di satu rumah sakit di Bandung mengenai komorbiditas para penderita pirai alias gout
Beberapa kondisi klini yang harus membuat para praktisi klinis mulai mencurigai adanya penyakit autoimmune. Dijelaskan dengan beberapa contoh autoimmune dseases
Pengenalan artritis reumatoid berdasarkan gejala dan tanda klinis
Bisa dipakai sebagai rujukan bagi dokter umum yangh ingin mempelajari manifestasi klinis AR yang tidak klasik seperti di buku teks
an overview of Lupus for journalist
Lupus has a wide spectrum of manifestation. Some mild but in most cases it has a high impact of life and quality of life
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Evaluation of antidepressant activity of clitoris ternatea in animals
Arthritis pain management gunadi Bandung
1. A Current Arthritis Pain Management
Without Compromising the Patient's
Safety
Rachmat Gunadi Wachjudi
Perhimpunan Reumatologi Indonesia
Cabang Bandung
4. Factors Implicated in the Development of OA
Obesity Aging
Anatomic
abnormalities Genetic and
metabolic
Microfractures diseases
and bony Abnormal stresses Abnormal cartilage
remodeling Inflammation
Loss of joint
stability Immune
Compromised cartilage system
Trauma activity
Biophysical changes Biochemical changes
• Collagen network fracture • Inhibitors reduced
• Proteoglycan unraveling • Proteolytic enzymes increased
Cartilage breakdown
Mandelbaum B et al. Orthopedics. 2005;28(2 suppl):s207-s214.
Adapted with permission from 2002 Medtronic Sofamor Danek, Basic Bone Biology.
5. EULAR Diagnostic Criteria for Knee OA (2010)
■ Based on review of studies from 1950-2008 and expert consensus
■ Focuses on clinical diagnosis: presence of three symptoms and
three signs correctly diagnoses 99% of cases
Symptoms
1 Persistent knee pain √
2 Limited morning stiffness √
3 Reduced function √
Signs
4 Joint crepitus √
5 Restricted movement √
6 Bony enlargement √
EULAR=European League Against Rheumatism.
Zhang W et al. Ann Rheum Dis. 2010;69(3):483-489.
6. ACR Diagnostic Criteria for Knee OA (1986)
■ Clarified and standardized definition of osteoarthritis
Joint symptoms and signs associated with defective integrity of
articular cartilage and changes in underlying joints at bone margin
■ Focuses on clinical examination of knee pain plus:
Presence of 3 of the following
1 Age >50 years √
2 Morning stiffness <30 minutes √
3 Joint crepitus on active motion √
4 Bony tenderness √
5 Bony enlargement √
6 No palpable warmth of synovium √
■ Sensitivity, 95%; specificity, 69%
ACR=American College of Rheumatology.
Altman RD et al. Arthritis Rheum. 1986;29(8):1039-1049.
7. Goals of OA Management:
OARSI Recommendations
Maintain and
improve joint
mobility
Reduce Reduce
joint pain and physical
stiffness disability
Knee and Hip OA:
Goals of
Treatment
Improve Educate
HRQoL patients
Limit
progression of
joint damage
HRQoL=health-related quality of life; OARSI=Osteoarthritis Research Society International.
Zhang W et al. Osteoarthritis Cartilage. 2008;16(2):137-162.
8. Integrated Approach to Treating Patients With OA
Nonpharmacologic Pharmacologic
■ Patient education ■ APAP
■ Phone contact (promote self-care) ■ Oral NSAIDs
■ Referral to physical therapist ■ Topical NSAIDs and capsaicin
■ Aerobic, strengthening, and/or water- ■ Corticosteroid injections
based exercise ■ Hyaluronate injections
■ Weight reduction ■ Glucosamine, chondroitin sulphate,
■ Walking aids, knee braces and/or diacerein
■ Proper footwear, insoles ■ Weak opioids and narcotic analgesics
■ Thermal modalities for refractory pain*
■ TENS
■ Acupuncture
Surgical
■ Total joint replacement ■ Lavage/debridement in knee OA†
■ Unicompartmental knee replacement ■ Joint fusion after failure of joint
■ Osteotomy and other joint preserving replacement
surgical procedures
* Pain resistant to ordinary treatment. † Controversial.
TENS=transcutaneous electrical nerve stimulation.
Zhang W et al. Osteoarthritis Cartilage. 2008;16(2):137-162.
9. US Prevalence of
Rheumatoid Arthritis (RA)
■ May affect between 1.3 and 1.5 million
adults1,2
Incidence lowest in individuals aged ≤34 years
Incidence increases progressively with age
Occurs more commonly in women than in men
* Costs in 2005 US dollars.
1. Myasoedova E et al. Arthritis Rheum. 2010;62(6):1576-1582.
2. Helmick CG et al. Arthritis Rheum. 2008;58(1):15-25.
3. Birnbaum H et al. Curr Med Res Opin. 2010;26(1):77-90.
10. Hand RA
Photos from Towheed TE, Anastassiades TP. Can Fam Phys. 1994;40:1303-1309. Used with permission.
11. 2010 ACR / EULAR Diagnostic Criteria for RA
Criterion Score
1 large joint 0
2-10 large joints 1
A Joint Involvement* 1-3 small joints (± large-joint involvement) 2
4-10 small joints (± large-joint involvement) 3
>10 joints (at least 1 small joint) 5
Negative RF and negative ACPA 0
B Serology† Low-positive RF or low-positive ACPA 2
High-positive RF or high-positive ACPA 3
Acute-Phase Normal CRP and normal VHS 0
C
Reactants‡ Abnormal ESR or CRP Total score ≥6/10
Total score ≥6/10 1
needed to classify
needed to classify
Duration of Less than 6 weeks definite RA
definite RA 0
D
Symptoms§ 6 or more weeks 1
* Any swollen or tender joint on examination. Excluded are distal interphalangeal joints, first carpometacarpal joints, and first
metatarsophalangeal joints. Large joints = shoulders, elbows, hips, knees, and ankles. Small joints = metacarpophalangeal joints, proximal
interphalangeal joints, 2nd through 5th metatarsophalangeal joints, thumb interphalangeal joints, and wrists. The >10 category can include large
and small joints, and other joints not listed elsewhere (eg, temporomandibular, acromioclavicular, or sternoclavicular). † Negative: IU values
≤ULN for lab and assay. Low-positive: IU > ULN but ≤3x ULN. High-positive: IU >3x ULN. When only RF-positive or RF-negative is known,
positive scored as low-positive. ‡ Normal/abnormal determined by local lab standards. § Patient self-report of duration of signs/symptoms of
synovitis in joints clinically involved at time of assessment, regardless of treatment status.
ACPA=anti-citrullinated protein/peptide antibodies; CRP=C-reactive protein; VHS =erythrocyte sedimentation rate; RF=rheumatoid factor.
Aletaha D et al. Arthritis Rheum. 2010;62(9):2569-2581.
12. Goals of RA Management
Early and Sustained
Suppression of Disease Activity
Prevent or
Reduce pain control joint
damage
Prevent Maximize
functional patient
decline quality of life
ACR Subcommittee on Rheumatoid Arthritis Guidelines. Arthritis Rheum. 2002;46(2):328-346.
13. Treatment Options for Patients With RA1-3
NSAIDs Symptomatic treatment to reduce joint swelling and pain
Reduce/prevent joint damage, preserve joint integrity and function
Methotrexate, leflunomide, hydroxychloroquine, minocycline,
DMARDs sulfasalazine
(biologic and Etanercept, infliximab, adalimumab (TNF inhibitors)
nonbiologic) Rituximab (anti-CD20)
Abatacept (cytotoxic T-lymphocyte antigen 4 immunoglobulin)
Tocilizumab (anti-interleukin 6 receptor)
Short-term use during flare-ups (oral or intramuscular)
Glucocorticoids
Local treatment for individual active joints (intra-articular)
Carpal tunnel release, synovectomy, resection of metatarsal heads,
Surgery total joint arthroplasty, joint fusion
Supportive Patient education, cognitive-behavioral interventions
Strategies Rehabilitation interventions
DMARDs=disease-modifying antirheumatic drugs; TNF=tumor necrosis factor.
1. ACR Subcommittee on Rheumatoid Arthritis Guidelines. Arthritis Rheum. 2002;46(2):328-346.
2. Saag KG et al. Arthritis Rheum. 2008;59(6):762-784.
3. Smolen JS et al. Lancet. 2007;370(9602):1861-1874.
14. Distinguishing OA From RA1
Characteristic OA RA
Prevalence in US adults 27 million2 1.3–1.5 million3,4
Pathophysiologic process Degenerative Autoimmune
Hips, knees, spine,
Commonly affected joints Hands, feet
fingers
Typically symmetrical
No Yes
involvement
Morning stiffness Transient Persistent
Joint swelling Hard tissue Soft tissue
Hand involvement Distal joints Proximal joints
Extraarticular involvement No Yes
Elevated autoimmune markers No Yes
1. Goldman L, Ausiello D. Cecil Textbook of Medicine. 23rd ed. Philadelphia, PA: Saunders Elsevier; 2007.
2. Lawrence RC et al. Arthritis Rheum. 2008;58(1):26-35.
3. Helmick CG et al. Arthritis Rheum. 2008;58(1):15-25.
4. Myasoedova E et al. Arthritis Rheum. 2010;62(6):1576-1582.
16. CELECOXIB vs. diclofenac:
6-week Knee OA Trial
McKenna et al. 2001: Patient’s Assessment of Pain
Patient’s Assessment of Pain (VAS): Mean change at
week 6 *p=0.001 vs. placebo
Mean Change (mm)
Less Pain
placebo celecoxib diclofenac
(n=200) 100 mg BID 50 mg TID
(n=199) (n=199)
VAS=visual analogue scale.
McKenna F et al. Scand J Rheumatol 2001;30:11–18.
17. CELECOXIB vs. diclofenac:
6-week Knee OA Trial
McKenna et al. 2001: American Pain Society – Pain
Measure
American Pain Society (APS) Pain Measure:
Worst Pain in the Past 24 Hours
Baseline Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Day 7
0.0
-0.5
p=0.05, active treatment vs.
Mean Change in Score
placebo (days 1-7).
-1.0
Less Pain
-1.5
-2.0
-2.5
-3.0
placebo (n=200)
-3.5
celecoxib 100 mg BID (n=199)
-4.0 diclofenac 50 mg TID (n=199)
McKenna F et al. Scand J Rheumatol. 2001;30:11-18.
19. Adult RA: Celecoxib Significantly Reduced the
Number of Tender/Painful and Swollen Joints
Tender/Painful Joints Swollen Joints
0
Reduction in Mean Number of
Affected Joints at 12 Weeks
-5
-5.5
-6.9*
-7.6 -7.5*
-10 -9.5 -9.1*
t ne m v o p m
e r I
-11.6*
-11.7*
-15
Placebo (n=231)
Celecoxib 100 mg BID (n=240)
Celecoxib 200 mg BID (n=235)
-20 Naproxen 500 mg BID (n=225)
* P<.05 vs placebo.
Simon LS et al. JAMA. 1999;282(20):1921-1928.
20. Adult RA: Celecoxib and Naproxen Improved
Physical Function
0.4
HAQ-FDI Score at 12 Weeks
LS Mean Improvement in
0.29*
0.3
0.22*
0.2 0.17
0.1
0.1
0
Placebo Celecoxib Celecoxib Naproxen
(n=231) 100 mg BID 200 mg BID 500 mg BID
(n=240) (n=235) (n=225)
* Statistically significant vs placebo.
HAQ-FDI=Health Assessment Questionnaire Functional Disability Index.
Zhao SZ et al. Arthritis Care Res. 2000;13(2):112-121.
22. Ankylosing Spondylitis: Celecoxib and Naproxen Reduced
Pain, Disease Activity, and Functional Impairment (12 Weeks)
Pain Intensity Disease Activity BASFI
10
Baseline to Week 12 (100 mm VAS)
LS Mean (± SE) Change From
0
-10
-20 †
-30
t ne m v o p m
e r I
* Placebo
Celecoxib 200 mg QD
-40
Celecoxib 400 mg QD
Naproxen 500 mg BID
-50
P<.001 for all active treatments vs placebo.
* P<.05 vs celecoxib 200 mg QD.
† P<.01 vs celecoxib 200 mg QD.
BASFI=Bath Ankylosing Spondylitis Functional Index.
Barkhuizen A et al. J Rheumatol. 2006;33(9):1805-1812.
24. Guidelines for Prevention of
NSAID-Related Ulcer Complications
(ACG Practice Guidelines 2009)
za FL et al. Am J Gastroenterol 2009;104:728-738
25. Celecoxib vs Omeprazole aNd
Diclofenac in patients with
Osteoarthritis and Rheumatoid
arthritis (CONDOR)
Chan FKL et al. Lancet 2010. DOI:10.1016/S0140-6736(10)60673-3
n FKL et al. Lancet 2010. DOI:10.1016/S0140-6736(10)60673-3
27. Chan FKL et al. Lancet 2010. DOI:10.1016/S0140-6736(10)60673-3
28. RESULT OF CONDOR STUDY 2010
Patient with celecoxib has lower risk on gastrointestinal events than
those with diclofenac SR + omeprazole
4 3.8
Proportion of patients %
3.5
(81 events,
3
95% CI, 2.9-
2.5
4.3)
2
1.5
0.9
1
0.5 (20 events, 95%
CI, 0.5-1.3)
0
celecoxib 200 mg BID (n=2238)
diclofenac SR 75 mg BID + omeprazole 20 mg OD (n=2246)
P<0.0001
Chan FKL et al. Lancet 2010; DOI:10.1016/S0140-6736(10)60673-3
29. Conclusion CONDOR Study
Risk of clinical outcomes throughout the upper
& lower GI tract was lower in patients treated
with a COX-2-selective NSAID than in those
receiving a non-selective NSAID plus a PPI.
Celecoxib, when used alone, carries less risk
of clinically significant events through the entire
GI tract when compared with diclofenac +
omeprazole
Chan FKL et al. Lancet 2010. DOI:10.1016/S0140-6736(10)60673-3
31. Boxed Warning for All Prescription NSAIDs
Cardiovascular Risk
Cardiovascular Risk
NSAIDs may cause an increased risk of serious cardiovascular thrombotic
NSAIDs may cause an increased risk of serious cardiovascular thrombotic
events, myocardial infarction, and stroke, which can be fatal. This risk may
events, myocardial infarction, and stroke, which can be fatal. This risk may
increase with duration of use. Patients with cardiovascular disease or risk
increase with duration of use. Patients with cardiovascular disease or risk
factors for cardiovascular disease may be at greater risk.
factors for cardiovascular disease may be at greater risk.
[Product] is contraindicated for the treatment of perioperative pain in the
[Product] is contraindicated for the treatment of perioperative pain in the
setting of coronary artery bypass graft (CABG) surgery.
setting of coronary artery bypass graft (CABG) surgery.
Gastrointestinal Risk
Gastrointestinal Risk
NSAIDs, including [product], cause an increased risk of serious
NSAIDs, including [product], cause an increased risk of serious
gastrointestinal adverse events including bleeding, ulceration, and
gastrointestinal adverse events including bleeding, ulceration, and
perforation of the stomach or intestines, which can be fatal. These events
perforation of the stomach or intestines, which can be fatal. These events
can occur at any time during use and without warning symptoms. Elderly
can occur at any time during use and without warning symptoms. Elderly
patients are at greater risk for serious gastrointestinal (GI) events.
patients are at greater risk for serious gastrointestinal (GI) events.
32. APTC Composite End Point (Adjudicated):
Celecoxib vs ns-NSAIDs
Meta-analysis of 25 RCTs
2.0
P =.59 (NS)
Relative Risk (CI) of Serious
1.5
CV Adverse Events
1.0 0.90
1.0 (95% CI: 0.60-1.33)
49 events
54 events
0.5
0
ns-NSAIDs Celecoxib 200-800 mg daily
(n=13,990) (n=19,773)
White et al. Am J Cardiol. 2007. 09/25/09
34. CELECOXIB vs. diclofenac
Dahlberg et al. 2009: CV / renal & hepatic AEs
Incidence of patients with treatment-related
CV, renal, and hepatic AEs
6 5.2
5 4.1
% Patients
4
3
1.7
2 1.1
1
0
CV / renal AE Hepatic AE
celecoxib 200 mg OD diclofenac 50 mg BID
One-year, randomized, multicentre, double-blind, parallel-group study to assess the AE-related discontinuation rate with
celecoxib and diclofenac in elderly patients with OA.
No p-values reported for related/not-related-to-treatment incidence. Significantly fewer patients in the celecoxib group than
the diclofenac group experienced cardiovascular/renal AEs (70/458 vs. 95/458, p=0.039) or hepatic AEs (10/458 vs. 39/458,
p<0.0001).
Dahlberg LE et al. Scand J Rheumatol 2009;38:133-143.
35. SUMMARY
■ Arthritis Pain is major health problem in elderly patients
■ Selective COX-2 inhibitors relief pain by selectively inhibit
COX-2 enzyme which is mainly responsible for
inflammation and pain process
■ Celecoxib is scientifically proven to alleviate arthritis pain
(OA, RA, and AS)
■ Celecoxib, when used alone, carries less risk of clinically
significant events through the entire GI tract when
compared with diclofenac + omeprazole
■ Celecoxib is the only coxib approved by US FDA
■ Celecoxib has a well-tolerated safety profille
35
Please see Full Prescribing Information available at this presentation.
36.
37. THANK YOU
37
Please see Full Prescribing Information available at this presentation.