About The AuthorDr 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 providingliterature to patient & conducting symposiums, the institute is also engaged in creatingpatients “Self Help Group” at every district level. The institute also conducts a certificatecourse for healthcare professionals & provide fellowship to experts in the field ofarthritis.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. kandoiC-202/203 Navare ArcadeShiv Mandir Road, Opposite Dena BankShiv mandir Road, Opposite Dena bankShivaji Chawk, Ambarnath(E) Dist: Thane Pin:421501State: Maharashtra Ph: (0251)2602404 Country: IndiaMembership Application forms of the IACR for patients & healthcare professionalscan be obtained from.Institute of Arthritis Care & PreventionC/o Ashirwad HospitalAlmas mension, SVP Road, New Colony,Ambarnath(W) Pin:421501 Dist: ThaneState: Maharashtra Country: IndiaPh: (0251) 2681457 Fax: (0251)2680020Mobile ;9822031683Email: email@example.comPreface:Studies have shown that people who are well informed & participate actively intheir 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 nothave 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 & selfmanagement 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 thebook.AcknowledgementI am thankful to Dr (Mrs) Sangita Kandoi for her immense help in proofreading & for herinvaluable suggestions. The help rendered by Nisha Jaiswal is probably unrivalled.Thanks also to vidya, praveen, rizwana and parvati for their continous supportthroughout the making of the book. The author is grateful to his family for the constantinspiration they offered. The author alone is responsible for the shortcoming in this pieceof 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 inconnective tissues such as cartilage (of joints or of the ears), the walls of bursa andligaments.Etiology: Exact etiology not known Hereditary predisposition postulated Any rapid change in uric acid can precipitate acute gouty attack. 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.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 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 neutrophilsRelease of crystals Release of lysomal enzymes Acute inflammationPathophysiology 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 ofcrystalline or amorphous urates surrounded by an intense inflammatory reaction ofmacrophages, 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 (plasterers hand). 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.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.
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. Differential diagnosis: Acute gouty arthritis: Infectious Arthritis Rheumatoid Arthritis Acute pseudogout Acute seronegative inflammatory arthritis Chronic tophaceous gout: Nodular Rheumatoid Arthritis Osteoarthritis 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 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
Treatment: Treatment protocolAcute attack colchichin, oral or intravenous Frequent attacks chronic gout NSAIDS especially indomethacin or naproxen intraarticular Steroids To reduce serum uric acid levels Allopurinol UricosuricsAcute 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. Its 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 developsor until a total dose of 8 mg has been given. Relief of clinical signs & symptoms isusually reached within 2 days.Alternatively it may be given as an IV initial dose of 2 mg followed by two separatedoses of 1 mg at 6 hours interval, with total dose not exceeding 4 mg with the first 24hours.Precautions: The dose should be halved in the elderly & in patients with renal & hepaticdysfunctions. The risk of renal, hepatic & CNS injury is more with parenteral route.Drugs like cimitidine or erythromycin are known to have harmful drug interaction withcolchicin. It iscontraindicated,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 attackInterval period 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 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 & lentilsProphylactic drug therapy:It includes:1. Colchicin2. Allopurinol3. 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 exacerbationof acute gaut due to sudden and rapid changes in uric acid levels a lower dose of 100mg/day is started which isgradually increased by 100 mg/week till the desired levels are reached.
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 - dihydroxyadenineContraindication: Children, acute gout.Precaution: Should not be used along with iron therapy To maintain adequate fluid intake Renal or hepatic impairementADR: These includeBone marrow supression HepatitisStevens Johnson syndrome UrticariaAcute renal failure VasculitisFever 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.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. 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.
Clinical typesAsymptomatic Acute Subacute Chronic PseudogoutPseudorheumatoid Pseudoosteoarthritis Pseudoneuropathic Arthritis ArthropathyAcute attacks may be precipitated by trauma, surgery of joint or even a long walk. Rapiddecline 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 kneewith h/o remissions or exacerbation: Usually there are no significant systemicmenifestations. Pseudorheumatoid arthritis: It resembles rheumatoid disease, involvingknees. Wrists, elbows and metacarpophalangeal joints. It is the least commonmenifestation of pseudogout.Pseudo- osteoarthritis: Bilateral symmetrical, acute, isolated inflammatory episodes ofarthritis 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 jointmonisci or articular hyaline cartilage.Definitive Diagnosis: It is based on demonstration of rod shaped or rhomboid crystalswith weak positive birefringence in synovial fluid.Clinical sequalae: 1. Induction or enhancement of peculiar form of osteoarthritis. 2. Induction of severe resorptive disease mimicking charcots 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 ProphylacticNSAID (intercritical interval)Local aspiration law dose colchicinIntraarticular steroid injectionCrystals and particles seen in synovial fluid:Monosodium urate crystalsCPPD, calcium hydroxyapetiteCalcium oxalate crystalsInjectable steroid crystalsLipid dropletsForeign organic matter (e.g. plant thorn)Metal debris from prosthetic jointCholesterol crystalCalcium HA deposition diseaseHA which is the primary mineral of bone & teeth, sometimes get deposited in areas oftissue damage mimicking other crystal deposition disease.Conditions associated with HA deposition disease:AgingOsteoarthritisHaemorragic shoulder effusions in the elderly (Millwaukees shoulder)Destructive arthropathyTendinitis. bursitisDisease associated: Hyperparathyroidism Renal failure I long-term dialysis Connective tissue disease Heterotropic calcification following stroke, spinal cord injuryHeriditary: Bursitis, arthritis Tumoral calcinosisClinical menifestations- More common in elderly- It may be associated with acute and/or chronic damage to the joint capsule, tendon,bursa, articular surface
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 arthopathyLaboratory findings:X-rays: It may/ may not show calcification with or without destructionSynovial 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 electronmicroscopyTreatment: It is similar to CPPD diseaseCaox deposition diseasePrimary oxalosis is a rare heriditary metabolic disorder with poor prognosis. Secondaryoxalate deposition may occur in end stage renal disease, those on long-term hemodialysisor peritoneal dialysis.Clinical features: There are similar to other crystal depositionDeposits have been documented in fingers, wrists, elbows, knees, ankles & feet.Diagnosis: Diagnosis is based on demonstration of bipyramidal crystals having strongpositive birefrigence on polarized microscope.Treatment: It is similar to other deposition disease.