Exercise recommendations are tricky for arthritis. Research is changing quickly on this topic. Mention that fibromyalgia is also increasingly diagnosed (refer to fact sheets).
(RF) is the autoantibody (antibody directed against an organism's own tissues) that is most relevant in rheumatoid arthritis. It is defined as an antibody against the Fc portion of IgG. RF and IgG join to form immune complexes that contribute to the disease process Raised rheumatoid factor levels of 25-50 IU/mL, 50.1-100 IU/mL and more than 100 IU/mL were compared with normal levels (less than 25 IU/mL).
slow acting anti-rheumatic drugs (SAARDs),,,, A period during which symptoms of disease are reduced (partial remission) or disappear (complete remission). With regard to cancer, remission means there is no sign of it on scans or when the doctor examines you. Doctors use the word 'remission' instead of cure when talking about cancer because they cannot be sure that there are no cancer cells at all in the body. So the cancer could come back in the future, although there is no sign of it at the time.
Chemotaxis is the phenomenon whereby somatic cells, bacteria, and other single-cell or multicellular organisms direct their movements according to certain chemicals in their environment. This is important for bacteria to find food (for example, glucose) by swimming towards the highest concentration of food molecules, or to flee from poisons (for example, phenol). In multicellular organisms, chemotaxis is critical to early development (e.g. movement of sperm towards the egg during fertilization) and subsequent phases of development (e.g. migration of neurons orlymphocytes) as well as in normal function. In addition, it has been recognized that mechanisms that allow chemotaxis in animals can be subverted during cancer metastasis.
RHEUMATOID ARTHRITIS (VK)
What is Arthritis?
There are 127 different kinds of
degeneration of joint cartilage.
Minor degree of inflammation.
Rheumatoid arthritis: Severe
inflammation that involves many
joints and moves beyond
Gout: Very painful form of
arthritis characterized by the
formation of uric acid crystals
and severe inflammation.
Rheumatoid arthritisChronic progressive, autoimmune disease in
which there is joint inflammation, synovial
proliferation, and destruction (crippling) of
articular cartilages with waxing and waning
IgM activates complements and release infl. Mediators
Release of Lysosomal enzymes
Damage to cartilage, bone errosion
edema & pain
Early diagnosis is the first step to easy control
1.Morning stiffness >1hour
2.Symetrical joint swelling for 6 weeks.
3.Swelling in 3 or more joint areas lasting for
6 weeks or more.
The treatment approach:
1. Aims to reduce & possibly prevent damage to the joints & other
2. Relief of pain –primary aim.
3. Rx of pathology-
Arrest of disease process
- Modification of disease process
o Traditional physical therapy includes-heat & cold therapy
o Motion exercises, Aerobic exercise with muscle strength.
o DISEASE MODIFYING ANTIRHEUMATIC DRUGS
o Adjuvant: GLUCOCORTICOIDS
NSAIDs• Used in first; they afford symptomatic relief of
pain, swelling, morning stiffness, immobility.
• Donot arrest disease process.
Diclofenac sodium (75-100mg BD)
(500mg single dose)
DISEASE MODIFYING ANTIRHEUMATIC
• Suppress the rheumatoid process i.e.
arrest the basic process of joint
• Bring about remission.
• Also called as SAARDs
2. Agents used in mild disease or in combination with MTX.
3.Traditional DMARDs -(limited used currently)
Gold salts (Aurothiomalate sodium)…..X
4. Biological agents
Methoterxate, Azathioprine, Cyclosporine are IMMUNOSUPPRESANT
Leflunomide IMMUNO MODULATOR
• An anti metabolite (inhibit dihydrofolate reductase)
inhibits folic acid synthesis.
• 1st line DMARD at present
• RA-Primary MOA is anti-inflammatory rather than
antimetabolites -Inhibit cytokine production, cell
mediated immune reaction, chemotaxis.
• Dose-7.5-10 mg oral weekly.
• Onset of symptom relief is relatively rapid –
preferred for initial treatment
• PK- Oral BV of Mtx is variable, may effected by food
- Excretions is dec. in renal disease pt.
• S/E-GIT distress (parenteral therapy effective to reduce
30mg/wk. i.v, less expensive.)
-Pneumonia (dec. By use of FA)
-Dose dependent progressive liver damage
• Antirheumatic-found to induce remission in 50% patients.
• MOA-inhibit inflammatory cells: monocytes interleukins,
• RA- long periods
• Dose-200mg bd
• Combined with MTX.
• S/ERetinal damage
Graying of hairs
Irritable bowel syndrome
• Combination of sulphapyridine and 5 aminosalicylic
• Inhibits generation of superoxides and cytokines by
the inflammatory cells.
• Efficacy is equal to chloroquine.
• 1-3g/day (3divided dose)
• Few adverse effect / good alternative for Mtx
• Group III broad spectrum antibiotic inhibit
• Used in com. With MTX.
Gold salts (Aurothiomalate sodium)
• Introduced in 1929.
• Gold is most effective agent for arresting
rheumatic process and preventing
involvement of additional joints.
• It reduce chemotaxis, phagocytosis,
macrophages and lysosomal activity and
inhibit cell mediated immunity
• Benefit - 4-6wks
• Starting dose10mg im/wk gradually inc. to
50mg/im/wk up to 1g.then maintain
50mg /im/ for few months.
• PK:-Gold is heavily bound to plasma and
tissue proteins, specially in kidney, stay in
the body for years
• Toxicity:– Vasodilatation, postural hypotension
– Dermtitis, pruritic rash,
– Hepatitis, peripheral neuritis, pulmonary
– Eosinophilia , bone marrow suppression
• Copper chelating agent
• Gold compound like action but less
• Toxicity is similar like gold
• Toxicity: Rash, Proteinurea, Kidney damage,
bone marrow depression
• Dose: Start with 125-250mg OD, then 250mg
• Purine antimetabolite
• Potent suppressant of cell mediated
• Affect differentiation and function of T-cells
and natural killer cells
• Remission in RA is less but some cases
not responding to gold may respond to it.
• Given along with corticosteroid
• Dose: 2.5-5mg/kg/day
Infliximab• Chimeric IgG1-kappa monoclonal antibody
• Anti TNF antibodies
• Binds to soluble, bound both the forms of TNF
and thus causes dose dependent neutralization
of TNF alpha.
• Useful in patients resistant to DMARDs and
• Given IV, half life 8-12 days.
• A/E: N,V,H and coughing.
other use-Crohn’s disease.
• Dimer consisting of TNF receptor joined to Fc
domain of human IgG…..binds to TNFα & β.
• Given by SC route thrice a wk.
• Effective in juvenile RA where Infliximab is found
• Antihelminthic in a dose of 150 mg.
• A/E- Agranulocytosis
• Recently introduced immunomodulator
• It inhibits proliferation of activated lymphocytes in
patients with active RA.
• Arthritic symptoms are suppressed and radiological
progression is retarded
• It is rapidly converted in the body to active
metabolite, which inhibits dihydroorotate
dehydrogenase and pyrimidine synthesis in actively
• It is alternative for MTX or Sulfasalazine
• Dose: Loading dose of 100mg daily for
3days followed by 20mg OD (t1/2 2 wks)
• S/E: Elevation of liver enzymes, renal
impairment and teratogenic effect
• Adverse effects:- D, H, N, rashes, loss of
hair, thrombocytopenia, chest infection
• C/I:children, pregnant and lactating
• Potent immunosuppressants and
• Inducted at any stage in RA.
• They do not arrest the rheumatoid process nor
• Long term use of corticosteroid carries serious
disadvantages.. Low dose 5-10mg
• High dose employed over short periods in cases
with severe systemic manifestations.