What are three possible causes of low back pain (LBP) in young men?

What features in the history and physical examination are helpful in differentiating inflammatory LBP in ankylosing spondylitis (AS) from mechanical LBP?

What five diseases are classified as seronegative spondyloarthropathies?

What is the definition of sciatica and what are three possible causes of it?

In AS, inflammation occurs at the insertion of a ligament, tendon, or articular capsule into bone, a structure known as the enthesis. The cause of this localized inflammation remains unknown. Sites of enthesopathy in AS include the sacroiliac joints; ligamentous structures of the intervertebral discs, manubriosternal joints, and symphysis pubis; ligamentous attachments in the spinous processes, the iliac crests (whiskering), trochanters, patellae, clavicles, and calcanei (Achilles enthesitis or plantar fasciitis); and capsules and intracapsular ligaments of large synovial joints. Inflammation can also be seen in the synovium, the tissue lining the joints.

Ocular involvement presents as anterior uveitis (25% to 40% of patients); secondary glaucoma and cataracts can also occur. Cardiac involvement includes aortic insufficiency, aortitis, conduction abnormalities, diastolic dysfunction, and pericarditis. Pulmonary involvement includes upper lobe fibrosis and restrictive changes. Renal involvement includes IgA nephropathy, secondary amyloidosis, and chronic prostatitis. Peripheral joint involvement (particularly hips and shoulders) can occur in approximately 30% of patients. Significant spinal osteoporosis can occur. Neurologic involvement includes atlantoaxial subluxations and cauda equina syndrome.

The three clinical manifestations characteristic of AS are inflammatory arthritis of the spine, Achilles tendinitis, and plantar fasciitis. These three findings are extremely rare in patients with RA.

Typically, there is a family history of AS, particularly in male family members. In fact, it occurs more commonly in men than women (3:1). This disease is very highly associated with the presence of HLA-B27. Two percent of HLA-B27–positive persons develop AS. Among those HLA-B27–positive persons with an affected first-degree relative, the rate rises to 15% to 20%.

The treatment of AS includes nonsteroidal antiinflammatory drugs (NSAIDs), extension exercises for the back, and physical therapy. It is recommended that all three forms of therapy be used in affected patients. It is thought that extension exercises for the back may help patients maintain a more normal upright posture as the back fuses over time. Sulfasalazine or low-dose weekly methotrexate (MTX) therapy may be beneficial in patients having progressive disease with peripheral arthritis but does not alter the sacroiliitis. Oral corticosteroids are of no value. Local corticosteroid injections may be useful in the treatment of enthesopathies and recalcitrant peripheral synovitis. The tumor necrosis factor α (TNF-α) blocking drugs are very effective in AS, act on both spinal and peripheral joints, and may possibly delay or prevent spinal ankylosis (treatment results in improvement in magnetic resonance imaging (MRI) appearance of enthesitis and sacroiliitis). The use of anti-TNF agents should be considered in patients with active AS who have failed to respond to two or more NSAIDs for axial disease and one or more disease-modifying antirheumatic drug (DMARD) for peripheral arthritis.

What are three different forms of crystal-induced arthritis, and what are the crystals involved?

What are four different diseases that characteristically present with arthritis of a single joint?

What three joints are most commonly involved in acute attacks of gout?

What are some historical features often found in patients with gout?

What are three laboratory test findings that may be abnormal in the setting of gout?

The diagnosis of gout requires aspiration of synovial fluid or a tophus for crystal analysis by polarized microscopy. MSU crystals are needle-shaped and negatively birefringent. In contrast, CPPD crystals (pseudogout) are rhomboid-shaped and positively birefringent. In gout, synovial fluid is inflammatory (typically 20,000 to 100,000 leukocytes/mm³). The synovial fluid should be sent for Gram’s stain and culture as in rare cases, septic joint fluids can contain MSU crystals. Elevated serum uric acid levels are not diagnostic of gout as many individuals have asymptomatic hyperuricemia and never develop gout.

Uric acid is the end product of the degradation of purines. Humans lack the enzyme uricase, which oxidizes uric acid to the highly soluble compound allantoin. The lack of this enzyme subjects humans to the potential risk of developing hyperuricemia and gout. Although humans possess the uricase gene, it is inactive. Uric acid may have antioxidant and free radical scavenger properties.

The reversible secondary causes of hyperuricemia include alcohol consumption, diets containing purine-rich foods (meats and organ meats; seafood, particularly shellfish), medications that decrease the renal excretion of uric acid (cyclosporine, nicotinic acid, diuretics, ethambutol, low-dose aspirin, pyrazinamide), and obesity (weight loss can improve hyperuricemia). The current dietary recommendations are consumption of meat, seafood, and alcohol have to be in moderation; purine-rich vegetables are acceptable; and low-fat dairy products and wine may be protective from gout.

The four stages of gout are asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout (the asymptomatic interval between attacks), and chronic tophaceous gout. Many patients with asymptomatic hyperuricemia do not progress to gouty arthritis. There may not be sharp demarcations between the last three stages of gout because some patients have both chronic tophaceous gout as well as intermittent acute attacks.

The preferred treatment for an acute attack of gout is an oral NSAID, if not contraindicated. This should be given in high doses for a few days followed by a tapering, with discontinuation by 7 to 10 days. Oral colchicine can only be used in younger patients with normal renal and hepatic function. Its use is limited by the high incidence of acute gastrointestinal side effects. Intravenous colchicine should be avoided because of the potential for excess dosing in high-risk patients, likely resulting in death. Both orally and intraarticularly administered corticosteroids are effective in the management of acute attacks of gout in patients who are intolerant of or have contraindications to the aforementioned medications. Patients with chronic symptomatic hyperuricemia require lifelong therapy with a urate-lowering medication. Probenecid, a uricosuric, can be used if they are renal underexcretors of uric acid (<700 mg per 24 hours), have a creatinine clearance greater than 50 mL per minute, and are not taking more than 81 mg of aspirin per day. Allopurinol, a xanthine oxidase inhibitor, is indicated if they are overproducers (>700 mg per 24 hours), have uric acid or calcium stones, or tophaceous disease. Allopurinol is more commonly used as it works for both underexcretors and overproducers of uric acid, and is taken only once daily which increases compliance. New therapies under investigation include intravenous polyethylene glycol (PEG)-uricase and febuxostat (a nonpurine, selective inhibitor of xanthine oxidase).

What is the definition of nonarticular rheumatism and what are the four forms of the disorder?

Name four common types of tendinitis and bursitis, and the major structure involved in each type?

What are the criteria for diagnosis of fibromyalgia syndrome (FMS)?

What are five medical illnesses that may exhibit symptoms similar to those of FMS?

The sleep disorder seen in the context of FMS is characterized by early morning awakening and unrefreshing or nonrestorative sleep. Disruption of delta-wave sleep (non-REM stage IV sleep) occurs due to alpha-wave intrusion, and is termed the alpha-delta sleep pattern of FMS. Obstructive sleep apnea and restless leg syndrome should also be considered in patients presenting with FMS.

Patients with FMS have a normal physical examination except for tender points in precise locations. These tender points are typically located at the occiput, at the midportion of the trapezius, the origin of the supraspinatus, low anterior cervical region, second costochondral junction, lateral epicondyle, outer upper quadrant of the buttocks, greater trochanter region, and medial knee area. These areas are usually tender bilaterally in patients with FMS. Control points such as the midforearm and anterior midthigh are not normally painful in patients with FMS.

All laboratory test results in the setting of FMS are usually completely normal. To initially exclude disorders that may mimic FMS, a complete blood count, ESR, creatinine, liver function tests, thyroid-stimulating hormone, creatine phosphokinase (CPK), calcium, phosphorus, and urinalysis should be performed. Antinuclear antibody (ANA) testing should not be performed unless there is pretest probability of a connective tissue disease (CTD) since a substantial number of individuals with FMS (12% to 30%) can have a low titer, nonspecific positive ANA.

The appropriate therapy for FMS includes patient education, analgesics such as acetaminophen or tramadol, low-dose tricyclic antidepressants or cyclobenzaprine at bedtime to improve the sleep cycle, and low-impact aerobic exercises. Antiinflammatory medications are not generally helpful. Selective serotonin reuptake inhibitors (SSRIs) and pregabalin may have some efficacy in FMS. This is a very frustrating disorder for both the patient and physician. Many patients may be helped by this approach to therapy, the most important element of which is an exercise program.

Functional psychiatric disorders, such as the somatoform disorders, and organic psychiatric disorders, such as major depression and anxiety disorders, have been associated with FMS in approximately 30% of patients. The anxiety and mild depression that often present in FMS may be secondary to chronic pain and concerns regarding personal independence and debility.

What is the joint structure that is primarily involved in OA?

Why is pain at the base of the thumb and the gradual onset of pain in a knee with minimal swelling more characteristic of OA than of RA?

What are the risk factors for developing OA?

What are some of the characteristic findings encountered during physical examination in patients with OA?

Abnormal joint mechanical factors result in pits, clefts, and ulcerations in the gross articular cartilage surface in OA. Microscopically, osteoarthritic cartilage reveals initial chondrocyte proliferation followed by eventual chondrocyte death; decreased proteoglycan and collagen concentrations with resultant increased water content of the cartilage; increased amounts of matrix metalloproteinases (MMPs) and inflammatory mediators; and decreased amounts of tissue inhibitors of metalloproteinases (TIMPs). This results in cartilage loss with secondary thickening of the subchondral bone and formation of osteophytes.

Radiographic findings typically encountered in patients with OA include loss of joint space, cysts in subchondral bone, subchondral sclerosis or eburnation, and osteophytes (bony spurs) at the joint margins.