Kelley and Firestein's Textbook of Rheumatology, Tenth Edition과 Harrison'
s 20th edition에서 언급된 SLE의 disease activity에 관한 내용입니다.
질병 활성도를 예견하는 단일의 reliable indicator는 없으며 (모든 경우에 해당되는 것은 아니지만) complement 감소와 anti-dsDNA 역가가 질병 활성도와 관련이 있습니다(여러가지가 있지만 대표적인 2가지).
비교) 류마티스 관절염에서 CRP, ESR과 같은 acute phase reactants는 질병 활성도를 평가하는데 유용하며 DAS28, CDAI와 같은 질병 활성도 평가 수단의 구성 요소입니다. Hb 감소는 anemia of chronic inflammation를 반영하고, 혈청 알부민 또한 질병 활성도가 증가함에 따라서 감소합니다. 추가적으로 혈소판 수는 염증이 진행됨에 따라서 경하게 상승합니다(전형적으로는 40만~45만/microL).
※ 류마티스 관절염과 SLE에서 질병 활성도를 물어보는 문제가 출제
It is useful to follow tests that indicate the status of organ involvement known to be present during SLE flares. These might include urinalysis for hematuria and proteinuria, hemoglobin levels, platelet counts, and serum levels of creatinine or albumin. There is great interest in identification of additional markers of disease activity. Candidates include levels of anti-DNA and anti-C1q antibodies, several components of complement (C3 is most widely available), activated complement products (an assay is commercially available that measures binding to the C4d receptor on erythrocytes and B cells), IFN-inducible gene expression in peripheral blood cells, serum levels of BLyS (B lymphocyte stimulator, also called BAFF), and urinary levels of TNF-like weak inducer of apoptosis (TWEAK), neutrophil gelatinase-associated lipocalin (NGAL), or monocyte chemotactic protein 1 (MCP-1). None is uniformly agreed upon as a reliable indicator of flare or of response to therapeutic interventions.
The utility of serologic tests in assessing disease activity and predicting disease flares remains a topic of controversy. In the absence of a hereditary complement deficiency, hypocomplementemia is a reliable indicator that the disease is active, but normal complement levels do not rule out active disease. Titers of anti-dsDNA antibodies correlate with disease activity in some patients, but not in others. One recent study attempted to resolve the long-standing debate about the prognostic value of changes in lupus serology. In this study, patients with clinically quiescent lupus underwent monthly monitoring for levels of anti-dsDNA, C3a, C3, C4, and CH50 to identify patients with serologically active, clinically quiescent disease. These patients were then randomly assigned to treatment with corticosteroids or placebo to determine whether treatment of serologically active disease could prevent impending clinical flares. The results were equivocal. Some patients with serologically active disease flared, and some flares were apparently prevented. However, in most control subjects, serologic deterioration was not followed by a clinical flare, and most of the flares that occurred in the original patient population that had been monitored were not preceded by serologic deterioration. Thus there remains no substitute for knowledge of a particular patient's disease pattern or whether there is an association between clinical and serologic manifestations in that patient.
REF. Kelley and Firestein's Textbook of Rheumatology, Tenth Edition
Harrison's 20th edition
