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Transcript
The Musculoskeletal system
HIV and other infections
Johan van Rensburg
HIV AND THE MUSCULOSKELETAL SYSTEM
Important concepts in HIV and the
musculoskeletal system
 Concerning the HIV infection
 HIV modifies the presentation, clinical picture and outcome of auto-immune
diseases
 HIV infection may mimic many auto-immune diseases
 Auto-antibodies may be present in both HIV (low titers) and auto-immune
diseases
 Considering immune suppression
 HIV-virus more responsible for manifestations in early disease
 Opportunistic infections and malignancies more prominent in late disease
 Concerning the drugs
 The drugs used to modify auto-immune disease may modify the outcome of
HIV infection
 HAART may present with musculoskeletal adverse events
 Drug interactions must always be considered
 Associated conditions
 Same principles of diagnosis and management apply as in patient without HIV
(after consideration of the above)
Musculoskeletal manifestations
in HIV
More prevalent in late stages
Wide spectrum of disease
Prevalence uncertain
Quality of life influenced by pain, loss of
function and systemic complications
Risk factors for HIV
Sexual history
IDU
Hemophiliacs
Examples of HIV and MS System
Keep the normal course of HIV infection in mind
Remember
 Components of the MS-system
 Soft tissue
 Muscles
•
Miopathy (virus and drugs), miositis (inflammatory or infective)
 Ligaments and enthesis
•
involved in reactive athritis and other sero-negative spondyloarthropathies
 Blood vessels
•
Vasculitis, drug reactions and coagulopathies
 Fat and other connective tissue
•
Involved in infection, drug reactions and crystal induced inflammation
 Joints
 Synovial joints
•
•
•
Infective: virus, septic arthritis, TB
Reactive
Auto-immune
 Fibrous joints
•
Reactive athritis and other sero-negative spondyloarthropathies
 Bone
 Infections
 Malignancies
Muscles
 Any stage of HIV
 Presents with
 Bilateral proximal muscle
weakness
 Elevated CK levels
 Pathogenesis uncertain
 Diagnosis
 Electromyography
 MRI
 Muscle biopsy
 (Nerve conduction
studies)
 Treatment limited
 HAART
 Corticosteroids
 Advanced HIV
 Presents with
 Insidious muscle pain &
swelling
 With or without systemic
symptoms
 Requires prior muscle injury
 Imaging
 CT
 MRI
 Sonar
 Treatment
 Anti-microbials
 Supportive
 Surgery
Long term use
Dose-related mitochondrial toxicity
Prevalence 17%
Clinical picture
Similar presentation to polymyositis
Keep lactic acidosis in mind
Management
Discontinuation
Joints
Early disease
Acute HIV syndrome
Most patients seek medical attention
Fever, fatigue, maculopapular rash
50-70% myalgias, arthralgias, paresthesias
Painful Articular Syndrome
10% of HIV patients
 Resembles rheumatoid arthritis
 Characterized
 Swan neck deformities
 Ulnar deviation of the hand & digits
 Radiographic results
 Non erosive
 Differentiation from RA
 Atypical onset
 RF usually negative (may be low positive
with HIV)
 Anti-CCP negative in HIV
 Treatment




HAART
Symptomatic
Corticosteroids
Chloroquin
 Acute asymmetric oligoarthritis (Occurs late)
Resembles reactive arthritis
Presents
Acute severe pain
Large joints
6 weeks to 6 months
Negative HLA B27 and RF
Treatment
HAART
Symptomatic
Corticosteroids
Opportunistic infections and
other auto-immune diseases
 Prevalence controversial 5-10%
 Pathogenesis
 HLA B27 positivity (more susceptible)
 Clinical picture
 “Incomplete” Reiter’s syndrome
 Assymetrical arthritis and enthesopathies
 Extra-articular manifestations
 Treatment
 HAART
 Symptomatic
 Corticosteroids
 Salazopyrin
 Prevalence 3%
10-40 X more frequent
in HIV infected patients
 Clinical picture
resembles psoriasis in
the general population
but may be more
severe
 Associated with
 PCP
 Bronchus Ca
 Clinical picture
 Severe pain in lower extremity
 Clubbing
 Arthralgias/periarticular soft tissue inflammation
 Non-pitting oedema
 Special investigations
 Radiography
 Periosteal reaction
 Scintigraphy
 Inflammation of distal ends of long bones
 Treatment
 Underlying cause
 AVN and HAART
 Possible link
 HIV related risk factors




Corticosteroid
Megestrol
Hyperlipidemia
Pancreatitis
 Non HIV related risk factors
 Alcoholism
 Hypercoagulability
 Smoking
 Common sites




Femoral head
Humeral head
Lunate (Kienbock disease)
Scaphoid (Preiser disease)
 Septic Arthritis
 Tuberculosis
Osteomyelitis
 Bacillary
Angiomatosis
 Toxoplasmosis
Other conditions affecting the
musculoskeletal system in HIV
 Non-Hodgkin Lymphoma
 Rhabdomyolysis
 Myesthenia Gravis
 Nemaline (Rod) myopathy
 Fibromyalgia
Important concepts in HIV and the
musculoskeletal system
 Concerning the HIV infection
 HIV modifies the presentation, clinical picture and outcome of auto-immune
diseases
 HIV infection may mimic many auto-immune diseases
 Auto-antibodies may be present in both HIV (low titers) and auto-immune
diseases
 Considering immune suppression
 HIV-virus more responsible for manifestations in early disease
 Opportunistic infections and malignancies more prominent in late disease
 Concerning the drugs
 The drugs used to modify auto-immune disease may modify the outcome of
HIV infection
 HAART may present with musculoskeletal adverse events
 Drug interactions must always be considered
 Associated conditions
 Same principles of diagnosis and management apply as in patient without HIV
(after consideration of the above)
Principles for management
 Musculoskeletal syndromes in HIV may be unrelated to
HIV infection
 Treat the underlying cause if possible
 Rule out or correctly diagnosis infections
 Probability of opportunistic infection depends on stage of HIV
 Consider HIV related medications in differential
diagnosis
 High threshold when using immunosuppressive drugs
Acute monoarthritis
Pitfalls Septic Joint
Acute Monoarthritis is a rheumatologic
emergency
Infection may destroy a joint in 48 hours
Septic Arthritis
Viral
Bacterial
Gram positive
Gram negative
Neiseria (GC, MC)
Anaerobic
Mycobacteria
Fungal
Septic Arthritis (Risk factors)
Immunosuppression (drugs, HIV)
Intravenous Drug Abuse
Abnormal joint (increased risk for septic arthritis)
• OA
• RA
• Prosthesis
Remote infectious source
Patient with monoarticular complaint
Periarticular
syndrome
Tendinitis,
bursitis, strain,
sprain,
osteomyelitis, soft
tissue rheumatism
Severe
symptoms
CBC, ESR,
physical exam
Ultrasound-guided
aspiration or
CT/MRI
Complete history and
Physical examination
Careful exam
reveals
poliarticular
arthritis
True monoarticular
arthritis
Acute Fracture,
changes avulsion
Significant trauma or Yes
Radiograph
focal bone pain?
No
Effusion or
inflammation?
Yes
Arthrocentesis
Chronic
changes OA,
CPPD
Arthrocentesis
Synovial fluid
WBC > 5000
Synovial fluid
WBC < 1000
Synovial fluid
bloody
Acute inflammatory
arthritis
Non-inflammatory
arthritis
(OA, internal
derangement)
Occult fracture,
tumor, internal
derangement
MRI
Arthroscopy
Internal
derangement
Acute inflammatory arthritis
(synovial fluid WBC > 5000/cm3)
+
Gram stain
_
+
Gout, CPPD
r/o superinfection
Infection
Young: GC > staph >strep
Old: staph > strep > GC
Immunocompromised:
Staph, gram-negative,
other unusual organisms
Crystal
exam
CBC, ESR, RF,
ANA, Ricketsae
CPPD, reactive arthritis,
systemic rheumatic disease
Anti-inflammatory medication;
Follow-up in 24-48 hours;
Re-aspirate joint if worsens
Systemic
toxicity?
+
+
Empiric antibiotics
x24 hours, awaiting
cultures
Back
TUBERCULOSIS
Pott’s disease
Involvement of bone and discs with
collapse of vertebrae
TUBERCULOSIS
Monoarthritis and Tendosynovitis
Destructive joint disease
Monitor for extra-articular TB