A rheumatology expert provides a quick overview of three main kinds of arthritis, along with recommendations for diagnosis and treatment.
In the primary-care setting, determining what type of treatment to prescribe when a patient complains of musculoskeletal pain (not related to trauma) is difficult unless one knows the essentials of the three major types of arthritis—osteoarthritis, rheumatoid arthritis, and psoriatic arthritis. Providers must be familiar with the clinical and laboratory features that differentiate each type (Table 1) and how they are managed.
Osteoarthritis (OA) is the most common arthropathy seen in adults. This noninflammatory condition is the result of degenerative changes and progressive loss of cartilage, with resultant hypertrophic changes in surrounding bone. The most common characteristic is joint pain with tenderness, limitation of movement, crepitus, and evening stiffness. The pain worsens with activity and improves with rest. Stiffness is experienced more in the evening and after sitting for extended periods due to the gelling phenomenon. The etiology is unknown, but trauma and repetitive stress on the joints (as seen most commonly in athletes) can lead to earlier disease. Exacerbating factors include changes in the weather. Notably, as joint cartilage starts to lose water content, the number of chondrocytes decreases and bone becomes more fragile, making it prone to fissuring, pitting, and ulceration.
Who is affected
This disease can strike at any age but is more common in older people and more often seen in women than in men. Besides age and gender, other predisposing risk factors include obesity, family history, neuromuscular dysfunction, and metabolic disorders.
When obtaining the patient history, it is imperative to learn the precise nature of the pain. What score does the patient give to his pain on the visual analog pain scale? Where is the pain? Is it only in the joints? When is it worse? What other symptoms accompany it? Is there stiffness? If so, when and for how long? Is there swelling? Does it interfere with mobility?
Key physical findings are joint instability, bony enlargement(especially in distal interphalangeal joints [Heberden’s nodes]), restricted movement, and asymmetry. Distribution of primary OA typically involves a variable number of joints in characteristic locations. Exceptions may occur, but they should trigger consideration of secondary causes of OA.
No specific laboratory tests are available for OA, but in the future, there may be testing for cartilage-degradation products in serum and joint fluid. Radiographic findings may include joint-space narrowing, marginal osteophytes, subchondral cysts, bony sclerosis, and malalignment. Secondary OA can be due to neuromuscular diseases, such as in diabetes, or due to metabolic disorders, such as pseudogout, so the patient comorbidities should be carefully evaluated in the differential.
Stopping the pain
OA therapy is directed at pain relief, and the goal is to maintain function. Patient and family education are paramount to understanding the nature of this disease so it is not confused with other types of arthritis that may be treated differently. Exercise, especially aquatic, is recommended and physical/occupational therapy may be offered. Yoga and tai chi help to stretch the muscles to prevent atrophy; this is especially helpful in those older than 60 years.
Pharmacologic therapy may start with OTC pain relievers. Nonsteroidal anti-inflammatory drugs (NSAIDs) should be used with caution and may be combined with a proton-pump inhibitor to prevent GI problems. Injection of corticosteroids or viscosupplementation may be indicated for some patients. Topical creams and ice may also be helpful.
For a particularly painful joint not helped with these measures, the lidocaine patch (Lidoderm) can be prescribed, but this is an off-label use. The patch is FDA-approved for postherpetic neuralgia, and insurance companies could require a letter of medical necessity to provide coverage. Glucosamine and chondroitin have been touted to help with pain relief, but the most recent study data do not show that it is effective in OA. A systematic literature review demonstrated that antioxidants are also ineffective in treating arthritis. “Medical foods” currently being marketed are directed at dietary management of OA, but the evidence for efficacy remains limited.
OA can easily be managed in the primary-care setting until the damage becomes so advanced that joint replacement is necessary. Surgery may then be the only option for some patients who have intractable pain or loss of function or mobility.
Rheumatoid arthritis (RA) is a chronic, inflammatory, systemic autoimmune disease that causes functional disability and reduced quality of life because of pain and joint destruction.
Who is at risk
The disease causes significant morbidity, with peak incidence in young adults. Smokers are at increased risk for the disease. RA is three times more common in women than men and its incidence rises with age. There is no entirely satisfactory treatment. Mortality is similar to that of stage III Hodgkin’s disease. If RA is diagnosed early, therapy can be initiated sooner to slow its progression.
Radiographic changes develop in 70% of patients within three years of RA onset.If not treated, a patient can become disabled within 10 years of diagnosis. Worldwide, RA is estimated to affect 0.8% of the adult population, with onset beginning between ages 30 and 50 years. RA is responsible for an estimated 250,000 hospitalizations and 9 million clinician visits each year in the United States.
The primary sites affected by RA are the joints (generally small ones, such as those in the hands), but the disease can affect other parts of the body (e.g., the lungs). When RA is active and untreated, constitutional symptoms (including fatigue) are common. In 1987, the American College of Rheumatology revised the criteria for the classification of RA (Table 2).
The etiology of RA is not fully understood. Researchers have postulated that there is a persistent immunologic response to some unknown antigen. Many infectious agents have been suggested, both viral and bacterial, but conclusive evidence is lacking. The pathogenesis involves complex interactions between antigen-presenting cells, T cells, B cells, and pro-inflammatory cytokines that initiate and perpetuate the inflammatory process and tissue damage. Because of the complications of the disease and newer therapies, it is highly recommended that RA patients be referred to a rheumatologist for appropriate therapy and necessary sequential follow-up.
Making the diagnosis
RA is a clinical diagnosis based on history and clinical findings. Laboratory findings may help direct therapy, but it is the number of swollen and tender joints that is the cornerstone for determining the severity of the disease (Figures 1 and 2). Onset can be slow or overnight, with development of symmetrical arthritis. The disease is usually seen first in the smaller joints, generally the metacarpophalangeal joints and the wrists. As the disease progresses, it can spread to other joints.
Joint deformity is common. Shortening of tendons and ligaments may appear later in the disease course. Morning stiffness may last more than one hour. RA is an effective masquerader, so other diseases, such as hepatitis, must be ruled out.
When patients are assessed with laboratory findings, it is important to know that rheumatoid factor (RF) is present in only 75%-85% of patients, and some patients may be seronegative. The higher the RF, the more aggressive the disease.
Several new enzyme-linked immunosorbent assays for cyclic citrullinated peptide antibodies are more specific for RA and can identify its presence up to 10 years before development of symptoms. Acute phase reactants, such as C-reactive protein, and erythrocyte sedimentation rate are used to gauge the amount of inflammation.
This should be correlated with the clinical examination. The complete blood count is used to assess anemia, which is frequently seen with RA. Anemia of chronic disease is often normochromic and normocytic. Thrombocytosis may be seen with uncontrolled inflammation.
Radiographs of both hands and wrists are used to stage the disease and its prognosis. Early stages may show only soft-tissue swelling or joint effusion. Osteopenia and erosions may develop several months to two years after diagnosis. MRI and ultrasonography can pick up erosions earlier than x-rays. Neither is widely used, primarily because of cost.
Only in the past 10 years has there been a breakthrough in prescribed therapies for RA. The goals are to minimize joint pain and damage, control systemic involvement, prevent disease progression, and avoid adverse side effects of the newer pharmacologic agents. Comorbidities often accompany this disease, making it more difficult to treat. Even if RA is the only disease the patient has, treatment of other issues involving sleep, depression, and pain is frequently necessary. Multiple therapies may be used to include both medications and alternative approaches, such as physical and occupational therapies.
Depending on the severity of the disease and its stage, some therapies could begin in the primary-care office. Pain treatment could be initiated in the same manner as that for OA (i.e., with NSAIDs: OTC drugs, such as acetaminophen or ibuprofen; moving on to prescription NSAIDs with a proton-pump inhibitor). Low doses of prednisone may be used for the inflammatory component.
If these agents prove inadequate, the disease-modifying antirheumatic drug methotrexate could be started at a very low dose along with folic-acid supplementation. A rheumatologist may prescribe biologic response modifiers (BRMs). Several BRMs are designed to work on various cells within the immune system. These include interleukin-1-receptor antagonist, selective co-stimulatory modulator, tumor necrosis factor antagonist, and B-cell monoclonal antibody therapies, which are either injected or infused.
Clinicians should use a team approach to treat patients with RA. Despite advances in biologic therapies, a significant number of patients respond inadequately to treatment. Education of the patient and family is crucial, since this is a lifelong disease with no cure. The Arthritis Foundation Web site (www.arthritis.org) is a useful resource for this and any of the arthritis diseases.
Psoriatic arthritis is an inflammatory arthropathy that usually occurs in cases of established cutaneous psoriasis with or without nail changes. Most patients have mild-to-moderate symptoms that are manageable, but some exhibit progressive, erosive, or disabling arthritis.
What to look for
The skin is generally affected first with psoriasis, so the patient may initially go to the dermatologist to seek treatment. Years later, when the disease starts to afflict the joints, it becomes psoriatic arthritis. At this point, the patient should be referred to the rheumatologist for appropriate therapy.
Musculoskeletal characteristics include asymmetrical arthritis, dactylitis/sausage digits, tenosynovitis, enthesitis, heel pain, sacroiliitis, and spondylitis (Table 3). Skin and nail manifestations include psoriasis (Figure 3), erythroderma, nail pitting (Figure 4), and onycholysis. Occasionally, conjunctivitis or iritis may be seen.
Disease onset is usually slow but steadily progressive. X-rays are helpful in showing soft-tissue swelling, erosions, and periostitis. Distal interphalangeal joints may show a “pencil-in-cup” deformity that is specific for psoriatic arthritis. Lab tests are generally nonspecific.
It is best to direct therapy at reducing joint pain and swelling. New biologic agents can be used to treat the skin plaques, with improvements seen in as little as two to six weeks.
Ms. Davis is assistant professor of rheumatology and internal medicine at the University of North Texas Health Science Center in Fort Worth.
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