About The Author

Dr Manoj R. kandoi is the founder president of “Institute of Arthritis Care & Prevention”

an NGO involved in the field of patient education regarding arthritis. Besides providing

literature to patient & conducting symposiums, the institute is also engaged in creating

patients “Self Help Group” at every district level. The institute also conducts a certificate

course for healthcare professionals & provide fellowship to experts in the field of

arthritis.

The author has many publications to his credit in various journals. He has also written a

book “ The Basics Of Arthritis” for healthcare professionals.

The author can be contacted at:

Dr manoj R. kandoi

C-202/203 Navare Arcade

Shiv Mandir Road, Opposite Dena Bank

Shiv mandir Road, Opposite Dena bank

Shivaji Chawk, Ambarnath(E) Dist: Thane Pin:421501

State: Maharashtra Ph: (0251)2602404 Country: India

Membership Application forms of the IACR for patients & healthcare professionals

can be obtained from.

Institute of Arthritis Care & Prevention

C/o Ashirwad Hospital

Almas mension, SVP Road, New Colony,

Ambarnath(W) Pin:421501 Dist: Thane

State: Maharashtra Country: India

Ph: (0251) 2681457 Fax: (0251)2680020

Mobile ;9822031683

Email: drkandoi@yahoo.co.in

Preface:

Studies have shown that people who are well informed & participate actively in

their own care experience less pain & make fewer visits to the doctor than do other

people with arthritis. Unfortunately in India & many third world countries we do not

have patient education & arthritis self management programs as well as support groups.

This is an attempt to give a brief account of various arthritis, their prevention & self

management methods which can serve as useful guide to the patients of arthritis.

It would be gratifying if the sufferers of the disease knew most of what is given in the

book.

Acknowledgement\

I am thankful to Dr (Mrs) Sangita Kandoi for her immense help in proofreading & for her

invaluable suggestions. The help rendered by Nisha Jaiswal is probably unrivalled.

Thanks also to vidya, praveen, rizwana and parvati for their continous support

throughout the making of the book. The author is grateful to his family for the constant

inspiration they offered. The author alone is responsible for the shortcoming in this piece

of work. He welcomes suggestions for improvement from the readers.

Gouty Arthritis: Introduction:

Gout is characterized by an altered purine metabolism with deposition of uric acid salts in

connective tissues such as cartilage (of joints or of the ears), the walls of bursa and

ligaments.

Etiology:

Exact etiology not known

Hereditary predisposition postulated

Any rapid change in uric acid can precipitate acute gouty attack.

Types:

1. Primary gout: This can be due to overproduction or underexcretion.

a. Underexcretors: Decreased excretion of uric acid by the kidneys

b. Overproducers: Increased production of uric acid

2. Secondary gout: This is acquired from underlying conditions such as

polycythemia, multiple

myeloma or sickle cell or other haemoglobinopathies.

Pathology: Normal Physiology

Increased uric Acid Rapidly decreased Uric Acid

-Sustained alcohol consumption -High dose aspirin use

-High purine intake -Use of uricosurics or allopurinol

-Diuretic use -Sudden stoppage of alcohol consumption

-Low dose aspirin intake

-Excessive cell turnover

(e.g. myelopoliferative diseases, cancers)

-Hypertension

-Intrinsic renal disease

-Cyclosporine use.

Denovo biosynthesis Nuclei acids

Nucleotides

Diet Nucleosides Salvage pathways

Bases

Urate Tophi

Urine Intestine

The total body urate pool is the net result between urate production & excertion.

Pathophysiology of acute gout attack:

Hyperuricemia

? factors

Precipiation of urate crystals in joints

Phagocytosis by neutrophis Activation of hageman factor

Damage to lysosomes Kinin production complement activation

Lysis of neutrophils

Release of crystals Release of lysomal enzymes Acute inflammation

Pathophysiology of chronic gout:

Underexcretors Overproducers

Serum urate levels

Sodium Biurate formation

Deposition in periarticular connective tissue and

damaged articular cartilage and non articular cartilage.

Disorganisation of joint Gouty tophi at

due to deposition in joint - Cartilage of ear

cartilage and ligaments -Olecrenon bursa etc.

Tophus: The pathognomic tissue lesion of gout is the tophus. The tophus is a mass of

crystalline or amorphous urates surrounded by an intense inflammatory reaction of

macrophages, lymphocytes and fibroblasts as large foreign body type giant cells.

Clinical menifestation:

A. More commonly in in males above 40 years of age & in postmenopausal females.

B. Arthritis: Acute onset pain, erythema, edema & stiffness of joints involving

mainly peripheral joints (such as toes, tarsus, ankle & hands) called PODAGRA.

First metatarsophalangeal joints is often the first joint to be affected because of

repeated exposures to microtrauma & a lower temperature compared to body

temperature.

C. Bursitis: Most commonly olecranon bursa is affected & it becomes distended with

fluid, there may be palpable deposits ot uric acid salts.

D. Nodules at ligamentum patella & ear cartilage due to gouty tophi deposition.

E. Renal invlovement: Three types of lesions may be seen.

1. Urate Nephropathy: It results from the deposition of crystals in the medullary

interstitium, the pyramids & papillae.

2. Acute Obstructive Renal Failure: It results from intratubular deposition of free

uric acid crystals. There cases are more common in secondary gout due to

chemotherapy or in myeloproliferative disorder.

3. Uric acid stone formation is common in patients excreting more than 1100 mg

of uric acid per day.

F) Palms of hands may show white streaks along the creases (plasterer's hand).

X-ray features:

Soft tissue swelling around the joint.

'C' shaped punched out lesions in subchondral region with sclerotic base.

Irregular soft tissue densities due to tophaceous deposits.

Role of laboratory studies in DID of crystalline arthropathies:

The joint aspiration must be done & synovial fluid sent for following analysis:

1. Cell count & Differential: A WBC count < 50,000 cells/mm is more suggestive of

crystalline arthropathy. WBC count more than that does not rule out gout.

2. Crystal Analysis under polarized microscopy: This is a definitive diagnostic tests

for determining appropriate crystal (monosodium urate in acute gouty arthritis &

calcium pyrophosphate in acute pseudogout).

3. Gram stain, routine culture & sensitivity.

Fever and crystal induced arthropathies:

Fever with temperature > 39 C accompanied with leukocytosis is common gout & pseudogout. In

40% of these cases serum uric acid levels are normal making differential diagnosis of crystal-induced

arthritis from septic arthritis difficult.

Differential diagnosis:

Acute gouty arthritis:

Infectious Arthritis

Rheumatoid Arthritis

Acute pseudogout

Acute seronegative inflammatory arthritis

Chronic tophaceous gout:

Nodular Rheumatoid Arthritis

Osteoarthritis

Course:

Recurrent attacks occur with normal joint between the acute attacks which last for few

days. In cases of chronic gout the affected joints are severely disorganized.

Treatment:

Goals:

Relieve the signs & symptoms of acute attack

Reduce uric acid levels

Reduce & if possible, eliminate the factors that produce gout

Serum uric acid as a diagnostic marker for gout:

1. Large number of general population have hyperuricemia, yet 19 out of 20 patients remain

asymptomatic throughout life

2. In about 40% of case of acute gout attacks, serum uric acid levels are normal.

3. Certain general medical conditions associated with asymptomatic hyperuricemia include

hypertension, obesity, heavy alcohol use, atherosclerosis, ischaemic heart disease & impaired

glucose tolerance.

DID of punched-out erosions in extremity bones:

1. Gout

2. Rheumatoid arthritis

3. Osteoauthritis

4. Sarcoid

5. Multiple myeloma

6. Hand-schullar -christian disease

7. Hyper parathyroidism

8. Leprosy

Treatment:

Treatment protocol

Acute attack colchichin, oral or intravenous Frequent attacks chronic gout

NSAIDS especially indomethacin

or naproxen intraarticular Steroids

To reduce serum

uric acid levels

Allopurinol Uricosurics

Acute Attack:

A. Patient is placed on absolute bed rest.

B. Immobilization of affected limb is done. Local cold or heat therapy may be used.

C. Adequate fluid intake, diet inclusive of glycine & rich in carbohydrate is advised.

D. Alcohol must be avoided.

Drug therapy:

Drugs commonly used in acute gout attacks are:

1. Colchicine: Oral or intravcl10us

2. NSAIDS ( Indomethacin, Naproxen are most commonly used)

3. Intra-articular corticosteroids.

a. Colchicine:

Mode of action:

I. It inhibits the phagocytosis of urate crystals by neutrophils.

II. It interferes with transport of phagocytosed materials to the

lysosomes.

III. It's interference with chemotactive response is believed to reduce

joint inflammation.

Dosage and administration: It is generally administered as 1 mg orally as an initial dose,

followed by 0.5 mg every 2 hours until gastrointestinal discomfort or diarrhea develops

or until a total dose of 8 mg has been given. Relief of clinical signs & symptoms is

usually reached within 2 days.

Alternatively it may be given as an IV initial dose of 2 mg followed by two separate

doses of 1 mg at 6 hours interval, with total dose not exceeding 4 mg with the first 24

hours.

Precautions: The dose should be halved in the elderly & in patients with renal & hepatic

dysfunctions. The risk of renal, hepatic & CNS injury is more with parenteral route.

Drugs like cimitidine or erythromycin are known to have harmful drug interaction with

colchicin. It is

contraindicated,ln pregnancy & lactation.

Role of NSAIDS in acute attack:

a. Indomethacin 50 mg orally 4-6 hourly until attack subsides, then tapered off over

7 -10 days

b. Phenylbutazone 200 mg tds after food

c. Corticotrophin gel: 60-100 units in daily for 2-3 days may terminate severe attack

Interval period

Indications for prophylactic therapy / interval therapy:

Recurrent Attacks

Tophaceous gout

Presence of renal disease

Family history of renal or heart disease

Young patient with high uric acid levels (> = 9 mg/lr)

Diet in chronic gout:

It should be low in purines & fats

No sweet bread, kidney, liver, meat extracts, peas, beans & lentils

Prophylactic drug therapy:

It includes:

1. Colchicin

2. Allopurinol

3. Uricosuric agents

I. Colchicin: It is a safe and effective drugs which prevents acute attacks. Since it

does not have uricosuric effect and does not affect tophceaus deposition, it should

be combined with uricosuric drugs or allopurinol. The suggested doss is 0.5

mg/day or twice daily.

II. Allopurinol: It is an inhibitor of the enzyme anthine oxidase; there by preventing

the final step in the production of uric acid. By reducing serum urate and

maintaining it at that level, the size of urate deposits can be reduced and

progression of renal lesion is halted.

Dosage and administration: It is started at 300 mg/day. In order to avoid exacerbation

of acute gaut due to sudden and rapid changes in uric acid levels a lower dose of 100

mg/day is started which is

gradually increased by 100 mg/week till the desired levels are reached.

Hyperuricemia (< 9 mg/dl.) Hyperuricemia > 9 mg/dl.

- Periodic examination - Prophylactic drug therapy

- Dietary restriction of purine rich food - Other preventive measures

- Gradual weight reduction

- Avoidance of drugs like thiazides

or cytotoxicdrugs

- Prophylactic drug therapy not indicated.

Indications:

1. Patients with gout and

a. Evidence of urate overproduction (24 hour urinary uric acid> 800 mg)

b. Nephrolithiasis

c. Renal insufliciency (creatinine clearance < 80 ml/min)

d. Tophaceous deposits.

e. Age over 60 years or

f. Inability to take uricosuric agents because of inaffectiveness or intolerance. .

2. Patient with nephrolithiasis of any type plus urinary uric acid excertion greater

than 600 mg

/ day

3. Patient with or at risk for acute uric acid nephropathy

4. Patient with renal calculi composed of 2,8 - dihydroxyadenine

Contraindication: Children, acute gout.

Precaution:

Should not be used along with iron therapy

To maintain adequate fluid intake

Renal or hepatic impairement

ADR: These include

Bone marrow supression Hepatitis

Stevens Johnson syndrome Urticaria

Acute renal failure Vasculitis

Fever

III. Uricosuric agents: These act by increasing renal excretion of uric acid and are

effective in the treatment of uncomplicated cases of gout. Due to high risk of

urolithiasis with these medication, these are contraindicated in renal diseases.

Dosage: Probenecid is effective at the dose of 1-2 gm/day Sulfinpyrazone is initially

started as 50- 100 mg twice daily with a gradual increase to 200 mg twice daily.

Precautions:

a. Adequate fluid intake must be maintained.

b. Sodium bicarbonate 1 gm three times a day to maintain alkaline urine levels is

recommended.

c. Probenecid prolongs the half-life of penicillin, heparin, salicylates and

indomethacin.

d. Intermittent treatment or the cessation of drug therapy may lead to recurrence of

acute attacks within 6 months and formation of tophi within 3 years. Urate-

lowering drug therapy therefore Should be continue lifelong.

Medications with uricosuric Activity:

-ACTH -Probencid

-Ascorbic acid -Phenylbutazone

-Calcitonin -Salicylates (>2g/d)

-Citrate -Sulfinpyrazone

-Estrogen -Radiographic contrast agent

-Glucocorticoids -Glycopyrrolate

Orthopaedic measures:

1. Immobilization and splintage for prevention of joint destruction.

2. Large tophi that interfere with joint and tendon motion may be removed.

Arthritis due to deposition of calcium crystals

CPPD Deposition Disease (calcium pyrophosphate dihydrate)

Pathogenesis: The deposition of CPDD crystals in articular cartilage, synovium &

periarticular ligaments & tendons is most common in elderly more than 65 years of age.

Conditions associated with CPDD disease

Aging

Disease – associated:

Primary hyperparathyroidism

Hemochromatosis

Hypophosphasia

Hypomagnesemia

Chronic tophacecus gaut

Postmeniscectomy

Epiphysical dysplasias ,

Hereditary: e.g. French, Swedish, English, Japanese etc.

Clinical menifestations:

The deposition is polyarticular in atleast 2-3rd

of patients. The knee joint is the joint most

frequently affected. Unlike osteoarthritis metacorpophalangeal, wrist, elbow, shoulder &

ankle joint may also be involved. Rarely tempnomandibular joint & ligament flavum of

the spinal canal are involved. In 50% of cases fever may be present making it difficult to

differentiate from pygenic arthritis.

Principles of surgery in gouty lesion:

1. Avoidance of local anaesthesia, which might interfere with local blood supply

2. Colchicin therapy few days prior to surgery and for a similar period postoperatively

3. Incisions parallel with course of blood vessels.

4. Sharp dissection

5. Loose suturing to allow escape of liquified deposits

6. Pressure dressing

7. Avoidance of prolonged splintage which may cause stiffness.

Clinical types

Asymptomatic Acute Subacute Chronic

Pseudogout

Pseudorheumatoid Pseudoosteoarthritis Pseudoneuropathic

Arthritis Arthropathy

Acute attacks may be precipitated by trauma, surgery of joint or even a long walk. Rapid

decline in serum calcium levels specially in severe medical illness or after surgery

(especially parathyroidectomy) can lead to pseudogout.

Isolated pseudogout: An acute inflammatory episode involving a large joint such as knee

with h/o remissions or exacerbation: Usually there are no significant systemic

menifestations. Pseudorheumatoid arthritis: It resembles rheumatoid disease, involving

knees. Wrists, elbows and metacarpophalangeal joints. It is the least common

menifestation of pseudogout.

Pseudo- osteoarthritis: Bilateral symmetrical, acute, isolated inflammatory episodes of

arthritis super imposed on osteoarthritic changes involving knees, wrists, shoulders,

elbows and ankles may be seen.

Asymptomatic: Incidental findings in largely asymptomatic joint.

Severe generalized febrile disorder: It is associated with high fever, elevated WBC count,

elevated ESR and polyarticular joint involvement.

X-rays: It may show punctate and/or linear radiolense deposits in fibrocartilaginous joint

monisci or articular hyaline cartilage.

Definitive Diagnosis: It is based on demonstration of rod shaped or rhomboid crystals

with weak positive birefringence in synovial fluid.

Clinical sequalae:

1. Induction or enhancement of peculiar form of osteoarthritis.

2. Induction of severe resorptive disease mimicking charcot's arthritis.

3. Production of symmetric proliferative synovitis, clinically similar to RA &

frequently seen in familial forms with early onset.

4. Intervertebral disk & ligament calcification with restriction of spinal mobility,

mimicking ankylosing spondylitis

5. Spinal stenosis

Treatment

Symptomatic presentation Prophylactic

NSAID (intercritical interval)

Local aspiration law dose colchicin

Intraarticular steroid injection

Calcium HA deposition disease HA which is the primary mineral of bone & teeth, sometimes get deposited in areas of

tissue damage mimicking other crystal deposition disease.

Conditions associated with HA deposition disease:

Aging

Osteoarthritis

Haemorragic shoulder effusions in the elderly (Millwaukees shoulder)

Destructive arthropathy

Tendinitis. bursitis

Disease associated:

Hyperparathyroidism

Renal failure I long-term dialysis

Connective tissue disease

Heterotropic calcification following stroke, spinal cord injury

Heriditary:

Bursitis, arthritis

Tumoral calcinosis

Clinical menifestations

- More common in elderly

- It may be associated with acute and/or chronic damage to the joint capsule, tendon,

bursa, articular surface

Crystals and particles seen in synovial fluid:

Monosodium urate crystals

CPPD, calcium hydroxyapetite

Calcium oxalate crystals

Injectable steroid crystals

Lipid droplets

Foreign organic matter (e.g. plant thorn)

Metal debris from prosthetic joint

Cholesterol crystal

with sometimes both periarticular and articular deposits coexisting

- Commonest joints involved are knees, shoulders, hips & fingers

- Clinically types: -Asymptomatic radiographic abnormalities

-Acute synovitis

-Tendinitis

-Chronic destructive arthopathy

Laboratory findings:

X-rays: It may/ may not show calcification with or without destruction

Synovial fluid: - Predominantly mononuclear, cell count is usually < 2000 cells /

uL but not more

Than 50,000 cells/uL

- Individual crystals are very small, nonbifrigent & can only be

seen by

electronmicroscopy

Treatment: It is similar to CPPD disease

Caox deposition disease

Primary oxalosis is a rare heriditary metabolic disorder with poor prognosis. Secondary

oxalate deposition may occur in end stage renal disease, those on long-term hemodialysis

or peritoneal dialysis.

Clinical features: There are similar to other crystal deposition

Deposits have been documented in fingers, wrists, elbows, knees, ankles & feet.

Diagnosis: Diagnosis is based on demonstration of bipyramidal crystals having strong

positive birefrigence on polarized microscope.

Treatment: It is similar to other deposition disease.