Arthritis and associated systemic diseases

1. REACTIVE ARTHRITIS and
Systemic diseases associated
with Arthritis
Moderator; Dr Shobhit Shakya
Assistant professor
RMLIMS
Presenter; Dr Sachin Giri
DNB Gen Medicine

2. Contents;
1. Definition
2. Etiology
3. Pathophysiology
4. Clinical features
5. Diagnosis
6. Treatment
7. Other systemic diseases

3. Definition
• ReA is acute nonpurulent arthritis complicating an infection elsewhere in
the body
• Antecedent Infections 1-4 Weeks before onset of symptoms
• Triad of Arthritis
Urethritis Conjunctivitis
• Also knows as Reiter syndrome
• It is autoimmune
• Additional mucocutaneous lesions

4. Etiology
• Post enteric infections
1 Salmonella
2 Shigella
3 Yersinia
4 Campylobacter
• Venereal
Chlamidia
• Others
viral, or parasitic infections, intravesicular bacillus Calmette-
Guérin (BCG) treatment for bladder cancer

5. Etiology continue…
• Clostridium difficile,
• Campylobacter coli,
• Certain toxigenic Escherichia coli,
• Ureaplasma urealyticum and Mycoplasma genitalium as potential
triggers of ReA.
• Chlamydia pneumoniae is also a trigger of ReA, but far less commonly
so than C. trachomatis. There have been numerous isolated reports of
acute arthritis preceded by many others organism

6. HLA B27 +ve ReA Triggered by infection
• High prevalence
Caused by Shigella, Yersinia, or Chlamydia
• Low prevalence
Caused By Salmonella
• No or very low prevalence
Caused By Campylobacter
• The attack rate of postenteric ReA ranges from 1 to 30%
• The attack rate of postchlamydial ReA is about 4–8%.

7. Pathophysiology
• ReA is usually triggered by a GU or GI infection. Chlamydia respiratory
infection may also trigger ReA. The frequency of ReA after enteric
infection averages 1-30%.
• ReA is associated with HLA antigen B-27 (HLA-B27), a major
histocompatibility complex (MHC) class I molecule involved in T-cell
antigen presentation. Results for HLA-B27 are positive in 65-96% of
patients (average, 75%) with ReA.
• ReA arthritis is affected by the levels of certain killer cell
immunoglobulin-like receptors (KIRs), which correspond with specific
HLA-C ligand genotypes.

8. Pathophysiology continue…
• In individuals with high levels of activating and low levels of inhibitory
KIR signals, pathogens can more easily trigger natural killer cell and T
cell innate and adaptive immune responses, resulting in the
overproduction of cytokines that contribute to the pathogenesis of
ReA.
• The mechanism by which the interaction of the inciting organism with
the host leads to the development of ReA is possible that microbial
antigens cross-react with self-proteins, stimulating and perpetuating
an autoimmune response mediated by type 2 T helper (Th2) cells.
• Chronicity and joint damage have been associated with a Th2
cytokine profile that leads to decreased bacterial clearance.

9. Pathophysiology continue…
• ReA can occur in patients with HIV infection or AIDS—most likely
because both conditions can be sexually acquired.
• The course of ReA in these patients tends to be severe, with a
generalized rash resembling psoriasis, profound arthritis, and frank
AIDS.
• HLA-B27 frequency is the same as that associated with non–AIDS-
related ReA in a similar demographic group.

10. Clinical features
• Acute onset of ReA, with malaise, fatigue, and fever
• Asymmetrical, predominantly lower-extremity, oligoarthritis as the major
presenting symptom, sometimes with early myalgias
• Initial nongonococcal urethritis, with frequency, dysuria, urgency, and
urethral discharge

11. Continue…
• In addition to conjunctivitis, ophthalmologic symptoms that include
erythema, burning, tearing, photophobia, pain, and decreased vision
(rare)
• Mild recurrent abdominal complaints after a precipitating episode of
diarrhea
• In HIV-positive patients, severe psoriasiform dermatitis, commonly
involving the flexures, scalp, palms, and soles

12. Physical findings in ReA may include the following:
• Musculoskeletal system - Asymmetric oligoarthritis affecting the
weight-bearing joints, predominantly of the lower extremities;
sausage-shaped finger (dactylitis); enthesopathy; sacroiliitis
• Skin and nails - Keratoderma blennorrhagicum; erythema nodosum
(uncommon); onychodystrophy
• Eyes - Conjunctivitis; anterior uveitis; keratitis; scleritis; episcleritis;
cataracts; hypotony; glaucoma; corneal ulceration; disc or retinal
edema; retinal vasculitis; optic neuritis; dacryoadenitis………

13. Continue…..
• GU tract - Meatal edema and erythema and clear mucoid discharge;
prostatitis; vulvovaginitis; circinate balanitis (balanitis circinata); cervicitis;
cystitis; salpingo-oophoritis; pyelonephritis; bartholinitis
• GI tract - Diarrhea; abdominal pain; lesions resembling inflammatory
bowel disease on ileocolonoscopy
• Other systems - Cardiac (aortitis, aortic regurgitation, transient conduction
abnormalities, myocarditis, pericarditis); renal (proteinuria,
microhematuria, amyloid deposits, immunoglobulin A [IgA] nephropathy)

14. Diagnosis
The following laboratory studies may be helpful:
• White blood cell (WBC) and red blood cell (RBC) counts
• Erythrocyte sedimentation rate (ESR)
• C-reactive protein (CRP) and other acute-phase reactants
• IgA antibodies to specific bacterial antigens
• Serology and cultures (blood, urine, stool, cervix, urethra),
particularly for Chlamydia

15. Continue…
• Human leukocyte antigen (HLA)–B27
• Tuberculin skin test
• HIV
• Urine analysis
• PCR assay for Neisseria gonorrhoeae and C. trachomatis

16. Imaging modalities that may be considered include the following:
• Imaging modalities that may be considered include the following:
• Plain radiography (reveals findings in only 40-70% of cases)
• Whole-body scintigraphy
• Positron emission tomography
• Magnetic resonance imaging (MRI), especially of the sacroiliac joints
• Computed tomography (CT)
• Ultrasonography or echocardiography

17. Management
• High-dose NSAIDs, although acute symptoms are rarely completely
ameliorated, and some patients fail to respond at all.
• sulfasalazine, up to 3 g/d in divided doses, may be beneficial to
patients with persistent ReA.
• Patients with persistent disease may respond to azathioprine, 1–2
mg/ kg per day, or to methotrexate, up to 20 mg per week;
• Trials of anti-TNF-α in ReA have been reported, anecdotal evidence
supports the use of these agents in severe chronic cases, although
lack of response has also been observed.

18. Continue..
• Tendinitis and other enthesitic lesions may benefit from intralesional
glucocorticoids.
• Uveitis may require aggressive treatment to prevent serious sequelae.
• Skin lesions ordinarily require only symptomatic topical treatment.
• In patients with HIV infection and ReA, many of whom have severe
skin lesions, the skin lesions in particular respond to antiretroviral
therapy.
• Cardiac complications are managed conventionally;
• management of neurologic complications is symptomatic.

19. Continue…
• 6-month course of rifampin 300 mg daily plus azithromycin 500 mg
daily for 5 days, then twice weekly,
• 6 months of rifampin 300 mg daily plus doxycycline 100 mg twice
daily.

20. Prophylaxis
• Appropriate antibiotic treatment of acute chlamydial urethritis or
enteric infection may prevent the emergence of ReA, but is not
universally successful
• Comprehensive management includes counseling of patients in the
avoidance of sexually transmitted disease and exposure to
enteropathogens, as well as appropriate use of physical therapy,
vocational counseling, and continued surveillance for long-term
complications such as AS. Patients with a history of ReA are at
increased risk for recurrent attacks following repeated exposures

21. Other systemic diseases

22. SLE
• Joint pain is one of the most common reasons for the initial clinical
presentation of patients with SLE.
• Arthralgia, myalgia, and frank arthritis
• may involve the small joints of the hands, wrists, and knees (usually
symmetrical, polyarticular).
• may be asymmetrical, with pain that is disproportionate to swelling.
• SLE arthropathy is rarely erosive or deforming. Characteristic hand
deformities are swan neck deformities that result from recurrent synovitis
and inflammation of the joint capsule, tendons, and ligaments. These
deformities are usually reducible and nonerosive.
• Another important consideration is the increased prevalence of avascular
necrosis (AVN) in the SLE population

23. Psoriatic Arthritis
• Arthritis of the DIP joints 5%
• Asymmetrical oligoarticular arthritis 30%
• Symmetrical polyarthritis 40%
• Arthritis mutilans small percentage
• Spondylitis with or without sacroiliitis 5%

24. IBD
• Peripheral arthritis develops in 15–20% of IBD patients.
• More common in CD.
• Worsens with exacerbations of bowel activity.
• It is asymmetric, polyarticular, and migratory
• Most often affects large joints of the upper and lower extremities.
• Treatment is directed at reducing bowel inflammation.
• In severe UC, colectomy frequently cures the arthritis.

25. Rheumatic Fever
• The most common form of joint involvement in ARF is arthritis,
• Tender joints, and involvement of more than one joint (polyarthritis).
• Polyarthritis is typically migratory, moving from one joint to another
over a period of hours.
• ARF almost always affects the large joints—most commonly the
knees, ankles, hips, and elbows—and is asymmetric.
• Aseptic monoarthritis may be a presenting feature of ARF.

26. Rheumatoid Arthritis
• RA typically result from inflammation of the joints, tendons, and bursae.
• Patients often complain of early morning joint stiffness lasting more than
1 hr that eases with physical activity.
• The earliest involved joints are typically the small joints of the hands and
feet.
• The initial pattern of joint involvement may be monoarticular,
oligoarticular (≤4 joints), or polyarticular (>5 joints).
• usually in a symmetric distribution.

27. Continue
• Once the disease process of RA is established.
• The wrists, metacarpophalangeal (MCP), and proximal interphalangeal
(PIP) joints stand out as the most frequently involved joints.
• Distal interphalangeal (DIP) joint involvement may occur in RA, but it
usually is a manifestation of coexistent osteoarthritis.
• Flexor tendon tenosynovitis is a frequent hallmark of RA and leads to
decreased range of motion, reduced grip strength, and “trigger” fingers.

28. Continue…
• Progressive destruction of the joints and soft tissues may lead to chronic,
irreversible deformities.
• Ulnar deviation results from subluxation of the MCP joints, with
subluxation, or partial dislocation, of the proximal phalanx to the volar side
of the hand.
• Hyperextension of the PIP joint with flexion of the DIP joint (“swan-neck
deformity”),
• Flexion of the PIP joint with hyperextension of the DIP joint (“boutonnière
deformity”).
• subluxation of the first MCP joint with hyperextension of the first
interphalangeal (IP) joint (“Z-line deformity”)

29. Thank you