Avascular Necrosis in a Corticosteroid-treated Rheumatic Disease Population.
- Author:
Hyun Ah KIM
1
;
Yeong Wook SONG
Author Information
1. Department of Internal Medicine, Seoul National University, College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Avascular necrosis;
Corticosteroid
- MeSH:
Alcoholism;
Dermatomyositis;
Diagnosis;
Drug Therapy;
Follow-Up Studies;
Hip;
Humans;
Humerus;
Incidence;
Lupus Coagulation Inhibitor;
Lupus Erythematosus, Systemic;
Medical Records;
Mixed Connective Tissue Disease;
Necrosis*;
Osteonecrosis;
Partial Thromboplastin Time;
Polymyositis;
Raynaud Disease;
Research Personnel;
Retrospective Studies;
Rheumatic Diseases*;
Risk Factors;
Talus;
Vasculitis
- From:The Journal of the Korean Rheumatism Association
1996;3(2):110-117
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVES: Avascular necrosis of bone has been frequently documented in association with systemic lupus erythematosus and it has been suggested by many investigators that systemic factors may be implicated in its pathogenesis. In order to define the incidence, clinical feature and related risk factors of avascular necrosis in corticosteroid- treated rheumatic disease patients, we conducted this retrospective study. METHODS: Medical records of 278 patients with diagnoses of systemic lupus erythematosus (SLE), polymyositis/dermatomyositis, overlap syndrome comprising either of SLE, polymyositis, or dermatomyositis, and mixed connective tissue disease were reviewed with regards to the following: 1) duration of disease, risk factors of avascular necrosis, such as the presence of Raynaud phenomenon, small vessel vasculitis, alcoholism. 2) history of steroid treatment, including duration, initial dose, cumulative dose and mean daily dose during follow-up, cumulative dose and mean daily dose during the first year of disease, history of steroid pulse therapy, and history of cytotoxic drug therapy. 3) laboratory findings including false positive VDRL, lupus anticoagulant, anti-phospholipid antibody, and activated partial thromboplastin time. 4) Development of avascular necrosis, duration of disease, activity of disease at the time of diagnosis of avascular necrosis, and the site. RESULTS: Nineteen patients developed avascular necrosis leading to the incidence rate of 18.5/1,000 patient-year. Sites of involvement were hip in 16 cases(84.2%), talus in 2 cases(10.5% ), and phalanx, scaphoid, and humerus in 1 case(5.3% ), respectively. Fifty-eight percent of patients had involvement in more than one site. Presence of Raynaud phenomenon, small vessel vasculitis, history of cytotoxic therapy, history of steroid pulse therapy, cumulative dose and mean daily dose of steroid during follow-up and 1st year of diagnosis were not significantly different between the 2 groups. CONCLUSIONS: The incidence of avascular necrosis in our patient population was similar to that reported in SLE patients previously, but other risk factor including steroid dosage could not be identified.
