physicians' forum bhopal - Presentation Transcript
Reiters arthritis
It is a clinical syndrome triggered by a specific etiological agent in a susceptible host following enteric or urogenital infections targeting predominantly HLA-B27 +ve person
It is a triad of Arthritis ,urethritis,and uveitis plus mucocutaneous lesions
History Described by Hans Reiter in 1916
Epidemiology
Prevalence world wide
Incidence 30-40 /one lack
More common in 18-40 yrs of age
But all age group can suffer
both sex equally affected slightly more common in males.
Very severe form seen in patient of AIDS.
Family clustering
Strongly associated with HLA B27
Association of HLA B 27 and Spondyloarthropathies(in whites) -8% General healthy population -50% Acute iritis -70% UnspA -40-50% Psoriatic spA -35-75% Enteropathic spA -70% Juvenile spondyloarthropathy 40-80% ReA -90% Ankylosing spondylitis HLA B 27 prevalence Disease
Pathology
Synovial histolgy is similar to inflammatory arthropathies.
Enthesitis is very common
Microscopic evidence of inflammation is seen colon and Ilium lesion
Skin lesions similar to Psoriatic lesions
Etiology and pathogenesis
Bacteria responsible for triggering disease are
Shigella
Sonnei
Boyedii
Flexneri
dysenterioe
Solmonella
Y. Enterocolitica
C.Trachomatis
Closridium difficle
Nesseria Gonorrhoea
Isolated reports of acute arthritis preceded by even viral and parasitic infection
Immune response inYersinia triggered arthritis
Initial, weak IgM-class antibody production
Later,strong and persisting IgG and IgA antibody production
IgA ab.increases in avidity with time
Ab. Are directd against several antigenic epitopes ofYersinia
Nonspecific immune complex are always found in serum
Specific Ic. Containing Yersinia and anti-Yersinia ab. May be found in se rum and synovial fluid
Peripheral T cells shows weak response to Yersinia
Tcells in synovial fluid shows vigrous but somewhat nonspecific response
In summery advance in molecular research have revealed that an imbalance in inflammation cytokines is central in there pathogenesis
Clinical Features
History
A vast majority of cases of reactive arthritis are oligosymptomatic, and conjunctivitis or urethritis are present weeks before the patient's first visit
A syndrome, with malaise, low-grade fever, and generalized myalgia or headache can be present
Symptoms of triggering infection would be mild in 9-10 % cases may go unnoticed
Manifestations of the urogenital system Circinate balanitis is characteristic. Circinate balanitis is defined by circinate or gyrate white plaques that grow centrifugally and eventually cover the entire surface of the glans penis. The penile shaft and scrotum can be involved. The lesions become rapidly keratotic in a circumcised penis. Circinate vulvitis is reported in women. Prostatitis, cystitis, and pyelonephritis are rare but possible urogenital manifestations of reactive arthritis. Bartholinitis can be present in women. Proctitis caused by Chlamydia species can occur in both sexes after anal intercourse.
Conjunctivitis Eye involvement is common. Conjunctivitis appears in approximately 50% of patients with reactive arthritis. Conjunctivitis is often bilateral, and it may be overlooked because of its transitory course. An intense red, velvetlike conjunctival injection characterizes the conjunctivitis. Edema and a purulent discharge are not rare in reactive arthritis–associated conjunctivitis.
Other ocular manifestations Iritis, iridocyclitis, and uveitis are seldom reported. Iritis is more common in late recurrent episodes, and it only occurs in 3-8% of patients in the first attack. At clinical examination, redness, pain, impaired vision, and exudation with hypopyon can suggest iritis. Recurrent episodes can lead to pupillary synechia and glaucoma. Keratitis rarely is reported.
Asymmetric Mono or oligoarthritis . Mostly knees,ankles and hips.
Shoulders elbow,wrist,and small joints of hands and feet can also get involved
Dactilitis is not uncommon
Pain in sacroiliac region in late stage.
Enthesopathy (ie, inflammation at the tendinous insertion into bone) is common in reactive arthritis and in other seronegative arthritides (eg, plantar fasciitis, digital periostitis, Achilles tendinitis).
Cutaneous and mucus membrane involvement
Erythema nodosum
Keratoderma blenorrhagicum indistinguisible from psoariasis both clinically and histopathologically.
Circinate balanitis ,cystitis and prostatitis
GIT
Abd. Pain diarrhoea, iliocolonoscopic picture like U.C. or Crohns both micro and macroscopically.
Investigations
ESR
CRP
CBC
LFT
RFT
RAFactor
Urine analysis
ECG
Joint fluid analysis
Cellcount
Crystals exlusion
Gram stain
Bact. Culture
Bacterialculture
Feces
Urine or urethralswab
Cervical sample
throat
Antibody determination at admission
HLA B27 After 2-4 weeks
Radiographs of affected joints
ophthalmologicalexamination
AIM of treatment
Rapid control of inflammation
Prevent tissue damage
Improve QOL
Try to achieve long term remission
Treatment
Antibodies if infections still persist
Rest
NSAIDs
Intra-articular corticosteroids
Systemic corticosteroids
Rarely DMARDs
Summery box
Biologic agents are highly effective-modifying medications.
currently licenced biologics target TNF α,interleukin-1,Tcell activation and Bcells.
Biologic agents improve the s/s and QOL with RA,Crohn’s disease psoriasis and many orphan conditions.
Needs vigilance for side effects.
Treatment should be commenced early for ultimate outcome.
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