Causes of Systemic Juvenile Rheumatoid Arthritis
Systemic Juvenile Rheumatoid Arthritis Causes: Book Excerpts
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As with all medical conditions,
there may be many causal factors.
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Causes of Systemic Juvenile Rheumatoid Arthritis: Online Medical Books
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Arthritis – Single Joint:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
- Septic arthritis
–Rapid diagnosis critical: Untreated septic arthritis causes irreversible joint and bone destruction
–Usually presents hyperacutely with very tender, swollen, warm, red joint with severely restricted range of motion
–Usual pathogens: Haemophilus influenzae type b, Staphylococcus aureus, group B strep in neonates, and Neisseria gonorrhoeae in adolescents; fungal and mycobacterial arthritis are seen rarely, may have chronic course
-
Lyme arthritis
–Second most common manifestation of Lyme disease (after erythema migrans)
–Monoarthritis of a knee occurs in about two-thirds of children with Lyme disease
-
Reactive arthritis
–Probably the most common etiology of childhood rheumatic diseases
–Transient sterile arthritis following a bacterial GI infection
–Usually full resolution, but a few children have a chronic course
-
Trauma, overuse, fracture
–Often acute onset with significant pain
-
Malignancy such as leukemia, neuroblastoma and osteogenic sarcoma
-
Pauciarticular juvenile rheumatoid arthritis (JRA)
-
Spondyloarthropathies (SpA)
-
Congenital hip dysplasia
-
Slipped capital femoral epiphysis (SCFE)
–Most common adolescent hip disorder
–Separation of the femoral growth plate
–More common in obese males
-
Spontaneous osteonecrosis of the joint
–Mostly in hip (Legg-Calvé-Perthes disease), shoulder, and knee
–More common in males
-
Internal structural abnormality
–Discoid meniscus, osteochondritis dissecans, synovial chondromatosis
-
Hemarthrosis due to trauma, bleeding disorder such as hemophilia, or benign tumors such as hemangiomas and pigmented villonodular synovitis
-
Periodic fever syndromes such as familial Mediterranean fever
» READ BOOK EXCERPT ONLINE »
Source: In A Page: Pediatric Signs and Symptoms, 2007
Juvenile rheumatoid arthritis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
The cause of JRA remains puzzling. Research continues to test several theories, such as those linking the disease to genetic factors or to an abnormal immune response. Viral or bacterial (particularly streptococcal) infection, trauma, and emotional stress may be precipitating factors, but their relationship to JRA remains unclear.
Considered the major chronic rheumatic disorder of childhood, JRA affects an estimated 150,000 to 250,000 children in the United States; overall incidence is twice as high in females, with variation among the types of JRA.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Rheumatoid arthritis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
RA occurs worldwide, striking three times more females than males. Although it can occur at any age, it begins most often between ages 25 and 55. This disease affects more than 7 million people in the United States alone.
What causes the chronic inflammation characteristic of RA isn’t known, but various theories point to infectious, genetic, and endocrine factors. Currently, it’s believed that a genetically susceptible individual develops abnormal or altered immunoglobulin (Ig) G antibodies when exposed to an antigen. This altered IgG antibody isn’t recognized as “self,” and the individual forms an antibody against it — an antibody known as RF. By aggregating into complexes, RF generates inflammation. Eventually, cartilage damage by inflammation triggers additional immune responses, including activation of complement. This in turn attracts polymorphonuclear leukocytes and stimulates release of inflammatory mediators, which enhance joint destruction.
Much more is known about the pathogenesis of RA than about its causes. If unarrested, the inflammatory process within the joints occurs in four stages. First, synovitis develops from congestion and edema of the synovial membrane and joint capsule. Formation of pannus — thickened layers of granulation tissue — marks the second stage’s onset. Pannus covers and invades cartilage and eventually destroys the joint capsule and bone. Progression to the third stage is characterized by fibrous ankylosis — fibrous invasion of the pannus and scar formation that occludes the joint space. Bone atrophy and malalignment cause visible deformities and disrupt the articulation of opposing bones, causing muscle atrophy and imbalance and, possibly, partial dislocations or subluxations. In the fourth stage, fibrous tissue calcifies, resulting in bony ankylosis and total immobility.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Septic arthritis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
In most cases of septic arthritis, bacteria spread from a primary site of infection — usually in adjacent bone or soft tissue — through the bloodstream to the joint. Common infecting organisms in children are group B Streptococcus and Haemophilus influenzae. Adults are usually infected by Staphylococcus, Streptococcus (pneumonia), and group B Streptococcus, whereas chronic septic arthritis is caused by Mycobacterium tuberculosis and Candida albicans.
Various factors can predispose a person to septic arthritis. Any concurrent bacterial infection (of the genitourinary or the upper respiratory tract, for example) or serious chronic illness (such as malignancy, renal failure, rheumatoid arthritis, systemic lupus erythematosus, diabetes, or cirrhosis) heightens susceptibility. Consequently, elderly people and those who abuse I.V. drugs run a higher risk of developing septic arthritis. Of course, diseases that depress the immune system and immunosuppressive therapy increase susceptibility. Other predisposing factors include recent articular trauma, joint arthroscopy or other surgery, intra-articular injections, and local joint abnormalities.
Septic arthritis may be seen at any age in children, but it occurs most often in children younger than age 3. It’s uncommon from age 3 until adolescence, at which time the incidence increases again.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Polyarticular Arthritis:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Osteoarthritis
❑ Rheumatoid arthritis
❑ Lyme arthritis
❑ Systemic lupus erythematosus
❑ Psoriatic arthritis
❑ Polyarticular gout
❑ Viral arthritis
❑ Scleroderma
❑ Reiter syndrome
❑ Inflammatory bowel disease
❑ Gonococcal arthritis
❑ Ankylosing spondylitis
❑ Systemic vasculitis
❑ Sarcoidosis
❑ Pseudogout (CPPD)
❑ Acute rheumatic fever
❑ Still disease
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Acute Monoarticular Arthritis:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Injury
❑ Gout
❑ Osteoarthritis
❑ Lyme disease
❑ Gonococcal arthritis
❑ Seronegative spondyloarthropathy
❑ Septic arthritis
❑ Pseudogout
❑ Septic bursitis
❑ Avascular necrosis
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Juvenile rheumatoid arthritis:
Causes
(Handbook of Diseases)
JRA is thought to be an autoimmune disorder. Research has linked causation to genetic and immune factors. Viral or bacterial (particularly streptococcal) infection, trauma, and emotional stress have been identified as precipitating factors.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Rheumatoid arthritis:
Causes
(Handbook of Diseases)
What causes the chronic inflammation characteristic of RA isn’t known. One theory states that abnormal immune activation (occurring in a genetically susceptible individual) leads to inflammation, complement activation, and cell proliferation within joints and tendon sheaths. Although no single environmental factor has been found to be a consistent and reproducible cause of this response, infection (viral or bacterial), hormonal factors, and lifestyle factors may all influence disease onset.
Some RA patients develop an immunoglobulin (Ig) M antibody against their body’s own IgG, which is called RF. Increased production of this antibody may also play a role in genetic inflammation.
Pathogenesis
Much more is known about the pathogenesis of RA than about its causes. If unarrested, the inflammatory process within the joints occurs in four stages.
In the first stage, synovitis develops from congestion and edema of the synovial membrane and joint capsule. Infiltration by lymphocytes, macro-phages, and neutrophils perpetuates the local inflammatory response. These cells, as well as fibroblast-like synovial cells, produce enzymes that help to degrade bone and cartilage.
Formation of pannus — thickened layers of granulation tissue — marks the onset of the second stage. Pannus covers and invades cartilage and eventually destroys the joint capsule and bone.
Progression to the third stage is characterized by fibrous ankylosis — fibrous invasion of the pannus and scar formation that occludes the joint space. Bone atrophy and malalignment cause visible deformities and disrupt the articulation of opposing bones, causing muscle atrophy and imbalance and, possibly, partial dislocations or subluxations.
In the fourth stage, fibrous tissue calcifies, resulting in bony ankylosis and total immobility.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Septic arthritis:
Causes
(Handbook of Diseases)
In most cases of septic arthritis, bacteria spread from a primary site of infection, usually in adjacent bone or soft tissue, through the bloodstream to the joint.
Common infecting organisms include four strains of gram-positive cocci — Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and Streptococcus viridans — and two strains of gram-negative cocci — Neisseria gonorrhoeae and Haemophilus influenzae. Various gram-negative bacilli — Escherichia coli, Salmonella, and Pseudomonas, for example — also cause infection.
Anaerobic organisms such as gram-positive cocci usually infect adults and children older than age 2. H. influenzae most often infects children younger than age 2.
Risk factors
Various factors can predispose a person to septic arthritis. Any concurrent bacterial infection (of the genitourinary or the upper respiratory tract, for example) or serious chronic illness (such as cancer, renal failure, rheumatoid arthritis, systemic lupus erythematosus, diabetes, or cirrhosis) heightens susceptibility. Consequently, alcoholics and elderly people run a higher risk of developing septic arthritis.
Of course, susceptibility increases with diseases that depress the autoimmune system or with prior immunosuppressant therapy. I.V. drug abuse (by heroin addicts, for example) can also cause septic arthritis.
Other predisposing factors include recent articular trauma, joint surgery, intra-articular injections, and local joint abnormalities.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Septic Arthritis:
Septic Arthritis - pathophysiology
(The 5-Minute Pediatric Consult)
- Entry of bacteria into joint space:
- Hematogenous spread
- Direct inoculation (penetrating trauma)
- Extension from bone infection (mainly in children <1 year old when vessels cross from metaphysis to epiphysis)
- Influx of inflammatory cells within the joint capsule
- Rapid destruction of cartilaginous structures within the joint by bacterial and lysosomal enzymes:
- If untreated, may progress to necrosis of the intra-articular epiphysis
Septic Arthritis - etiology
- Bacteria:
- Staphylococcus aureus most common etiology outside of perinatal period (Methicillin-sensitive and Methicillin-resistant)
- Streptococci
- Kingella kingae
- Haemophilus influenzae
- Salmonella
- N. gonorrhoeae
- Neisseria meningitidis
- Borrielia burgdorfderi (Lyme)
- Aseptic arthritis:
- Rubella
- Parvovirus
- Hepatitis B or C
- Mumps
- Herpesviruses (Epstein-Barr virus, cytomegalovirus, herpes simplex virus, varicella zoster virus)
- Epstein-Barr virus
- Varicella
- Candida albicans (neonatal)
>
» READ BOOK EXCERPT ONLINE »
Source: The 5-Minute Pediatric Consult, 2008
Osteomyelitis and Septic Arthritis:
Etiology
(Pediatric Infectious Disease)
Children are colonized with a variety of bacteria; a culture of the nasopharynx
of an asymptomatic child could yield any number of bacteria, including
Staphylococcus aureus and Streptococcus pneumoniae. Usually, these organisms reside on body surfaces with no ill effects. However,
by a process not always well defined, these colonizing bacteria enter the
bloodstream.
Once the bacteria enter the bloodstream, numerous things can occur (Fig. 2.1).
Bacteremia can be transient and resolve without sequelae; this is often the
case with viridans streptococci. Bacteremia, by its very presence in the
systemic circulation, can cause overwhelming sepsis, as is often the case with
Neisseria meningitidis. Bacteria can also be deposited in secondary sites, such as the cerebrospinal
fluid or bone.
The bones are a frequent site of secondary infection because the blood supply
takes a hairpin turn at the metaphyses of long bones, increasing the chance of
the bacteria being deposited. This secondary seeding of bones from the blood is
the major mechanism of pediatric osteomyelitis. This is in contrast to adults,
who usually acquire osteomyelitis from direct inoculation following trauma or
surgical procedures.
Pyogenic arthritis develops in a fashion similar to osteomyelitis, whereby
blood-borne organisms are deposited in the synovium of the joint space. Similar
to the long bones of children, the joint space is highly vascularized and is an
area where bacteremic organisms are readily deposited. Bacterial arthritis can
also spread from a contiguous osteomyelitis; blood vessels can deposit
infection from the metaphysis into the joint space. The organisms of septic
arthritis are similar to those of osteomyelitis.
S. aureus is the most common organisms, followed by S. pneumoniae, Kingella kingae, and group A streptococcus.
» READ BOOK EXCERPT ONLINE »
Source: Pediatric Infectious Disease, 2004
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