Herein we describe the case of a man who was diagnosed as having
relapsing polychondritis (RP) when he was 18 years of age and was treated over the course of 2 years with numerous
immunosuppressive agents, including
tumor necrosis factor alpha (
TNFalpha) inhibitors. His respiratory symptoms were refractory to treatment. Serum and urine samples were obtained periodically for measurement of erythrocyte sedimentation rate (ESR),
C-reactive protein (CRP) levels, anti-
type II collagen (anti-CII)
antibodies, and urinary
type II collagen neoepitope (uTIINE) levels. The uTIINE assay is specific for
collagenase cleavage products CII present in urine. ESRs and CRP levels varied widely but were rarely normal. Anti-CII antibody titers were high initially and decreased slowly and steadily for a year following the start of immunosuppressive medication, remaining low throughout the remainder of the patient's monitored disease course. The uTIINE levels were elevated prior to the initiation of
TNFalpha inhibitors. Upon initiation of
etanercept, they decreased abruptly to normal and stayed nearly normal. The uTIINE levels rose abruptly again upon discontinuation of
TNFalpha inhibitor treatment. The dramatic decline in CII degradation, coincident with the administration of the
TNFalpha inhibitors, suggested that this treatment dramatically reduced the chondritis. Serum levels of Th1
cytokines (
interferon-gamma,
interleukin-12 [
IL-12], and IL-2) paralleled changes in uTIINE levels, while those of Th2
cytokines (IL-4, IL-5, IL-6, and IL-10) showed little or no association with disease state or uTIINE levels. These results indicate that RP might be a Th1-mediated disease process. Moreover, the uTIINE assay appears to provide an objective measure of the severity of chondritis that could assist clinical decisions regarding adjustments of
steroid and other immunosuppressive therapy. This outcome measure merits investigation in a broader spectrum of RP patients.