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The Patient With Acute Monoarticular Arthritis
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A 64-year-old man presented to the emergency department with a 3-day history of swelling of the left knee. He has had hypertension for the past 8 years, and has been taking telmisartan 40 mg once daily and hydrochlorothiazide 12.5 mg once daily.
His physical exam reveals him to be afebrile with a blood pressure of 136/88 mg Hg bilaterally. The left knee is swollen, warm, and tender with impaired range of motion.
Sedimentation rate are 57 mm/h and complete blood count, renal function and uric acid levels are normal. Arthrocentesis reveals the leukocyte count is 22,000/µL with 90% neutrophils. Numerous rhomboid-shaped positively birefringent crystals within the neutrophils and extracellularly are seen with polarized light microscopy. Gram stain is negative for bacteria.
Radiographs of the left knee demonstrate soft tissue swelling with joint space narrowing and linear calcifications with the cartilage, parallel to the subchondral bone surface.
Key Supporting Information
Formation and deposition of calcium pyrophosphate (CPP) crystals in and around joints can result in an acute inflammatory arthritis (pseudo-gout). However, this metabolic arthropathy in articular cartilage and fibrocartilage may present in many ways including asymptomatic chondrocalcinosis, chronic inflammatory arthritis and degenerative cartilage disease.
Patients affected with this disorder are usually older than 60 years and is slightly more common in women. When it occurs before 40 years old, it is usually associated with underlying metabolic disease, or inherited disorder. Almost any joint may be involved by calcium pyrophosphate dihydrate (CPPD), although the knees, wrists and hips are most often affected. In addition to acute pseudo-gout, patients also can present with pseudo-neuropathic joints and pseudo-rheumatoid arthritis RA.
Calcium pyrophosphate deposition can be associated with various metabolic disturbances including, hypercalemia, hypomagnesemia, hypothyroidism, hemochromatosis, familial hypocalciuric hypercalcemia, amyloidosis, Wilson’s disease and hypophosphatasia.
Although the exact mechanism for the development of CPPD crystal formation remains unknown, increased adenosine triphosphate breakdown, changes in the cartilage matrix, and abnormal pyrophosphate handling by joint cells, due to aging, genetic factors or both, can result in increased intra-articular inorganic pyrophosphate. Chondrocytes also may generate increase quantities of pyrophosphate due to increased activity of nucleoside triphosphate pyrophosphohydrolase, forming crystals when combined with extracellular calcium. The crystals, subsequently formed, may be deposited within cartilage causing chondrocalcinosis, or stimulate joint-space inflammation by being released directly into the joints. Most often, hyaline cartilage is affected, resulting in fine linear densities parallel to the subchondral bone surface However, fibrocartilage, ligaments and joint capsules also can be involved, resulting in diffuse punctate and linear densities.
Image: Codario RA
Although rare, hereditary forms of CPPD are generally inherited as an autosomal dominant disorder, in the COL and ANKH genes, the latter of which has been shown to be involved in cellular transport of inorganic phosphate.
Osteoprotegerin, which is encoded by the TNFRSF11B gene, plays a critical role in the regulation of osteoclast development. A mutation in this gene can result in an osteoprotegerin with an increased capacity to inhibit bone resorption and osteoclastogenesis. Upregulation of TNFRSF11B is also involved in the pathophysiological causation of osteoarthritis (OA).
Acute monoarthritis, most commonly involves the knee, while the ankle, wrist and shoulder can be involved. The CPP deposits are usually linear, parallel and below the surface of the cartilage (Figure), and include features of osteoarthritis, such as cyst and osteophyte formation, joint space narrowing and bony sclerosis. Unlike OA, pseudo-gout predominantly involves the patellofemoral articular surfaces, the talocalcaneal joint of the midfoot, or the radiocarpal wrist joint.
Acute Attacks of Pseudo-Gout
Acute attacks of pseudo-gout, are usually monoarticular, reach a peak in 12 hours to 36 hours, can be precipitated by surgery, trauma or medical illness, and usually resolve in 1 week to 2 weeks. In contrast to gout, pseudo-gout is less likely to be polyarticular or involve the metatarsophalangeal joint.
Chronic pyrophosphate arthropathy is characterized by chronic pain, morning stiffness usually lasting less than 30 minutes and decreased range of motion of shoulders, elbows, hips, ankles and metacarpophalangeal joints. Occasionally patients with chronic arthropathy can experience fatigue, synovial proliferation and flexion deformities, leading to progressive joint destruction with a symmetric pattern that can be similar to RA.
Acute pseudo-gout can be diagnosed by examination of the synovial fluid with a polarizing microscope and demonstrating positively birefringent, rhomboid-shaped crystals and neutrophils. Typically the sedimentation rate and/or the C-reactive protein levels are elevated, while hypercalcemia may occasionally be present.
Learning Objectives:
Upon successful completion of this educational activity, participants should be better able to assess ankylosing spondylitis.
Overview
Author(s)/Faculty: Ronald A. Codario, MD, FACP, FNLA, RPVI, CCMEP
Source: Healio Rheumatology Education Lab
Type: Monograph
Articles/Items: 7
Release Date: 2/15/2016
Expiration Date: 2/15/2017
Credit Type: CME
Number of Credits: 1
Cost: Free
Provider: Vindico Medical Education
CME Information
Provider Statement: This continuing medical education activity is provided by Vindico Medical Information.
Support Statement: No commercial support for this activity.
Target Audience: This activity is designed for this activity is rheumatologists and other health care professionals involved in the treatment of patients with rheumatological disorders.