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Occurs mainly in young women Rash over areas exposed to sunlight Joint symptoms in 90% of patients Multiple system involvement Anemia, leukopenia, thrombocytopenia Glomerulonephritis, central nervous system disease, and complications of antiphospholipid antibodies are major sources of disease morbidity Serologic findings: antinuclear antibodies (100%), anti-native DNA antibodies (approximately twothirds), and low serum complement levels (particularly during disease flares)
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Still s disease is considered a form of juvenile chronic arthritis in which high spiking fevers are much more prominent, especially at the outset, than arthritis This syndrome also occurs in adults Most adults are in their 20s
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SLE is an inflammatory autoimmune disorder characterized by autoantibodies to nuclear antigens It can affect multiple organ systems Many of its clinical manifestations are secondary to the trapping of antigen-antibody complexes in
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capillaries of visceral structures or to autoantibody-mediated destruction of host cells (eg, thrombocytopenia) The clinical course is marked by spontaneous remission and relapses The severity may vary from a mild episodic disorder to a rapidly fulminant, life-threatening illness The prevalence of SLE is influenced by many factors, including gender, race, and genetic inheritance About 85% of patients are women Sex hormones appear to play some role; most cases develop after menarche and before menopause Among older individuals, the gender distribution is more equal Race is also a factor, as SLE occurs in 1:1000 white women but in 1:250 black women Familial occurrence of SLE has been repeatedly documented, and the disorder is concordant in 25 70% of identical twins If a mother has SLE, her daughters risks of developing the disease are 1:40 and her sons risks are 1:250 Aggregation of serologic abnormalities (positive antinuclear antibody) is seen in asymptomatic family members, and the prevalence of other rheumatic diseases is increased among close relatives of patients The importance of specific genes in SLE is emphasized by the high frequency of certain HLA haplotypes, especially DR2 and DR3, and null complement alleles Genes that regulate programmed cell death (apoptosis) also appear to be important in the pathogenesis of SLE Before making a diagnosis of SLE, it is imperative to ascertain that the condition has not been induced by a drug (Table 20 8) Procainamide, hydralazine, and isoniazid are the best-studied drugs While antinuclear antibody tests
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Table 20 9 Criteria for the classification of SLE (A patient is classified as having SLE if any 4 or more of 11 criteria are met)
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1 2 3 4 5 6 7 Malar rash Discoid rash Photosensitivity Oral ulcers Arthritis Serositis Renal disease a > 05 g/d proteinuria, or b 3+ dipstick proteinuria, or c Cellular casts Neurologic disease a Seizures, or b Psychosis (without other cause) Hematologic disorders a Hemolytic anemia, or b Leukopenia (< 4000/mcL), or c Lymphopenia (< 1500/mcL), or d Thrombocytopenia (< 100,000/mcL) Immunologic abnormalities a Positive LE cell preparation, or b Antibody to native DNA, or c Antibody to Sm, or d False-positive serologic test for syphilis Positive ANA
8 9
SLE, systemic lupus erythematosus; ANA, antinuclear antibody Modified and reproduced, with permission, from Tan EM et al The 1982 revised criteria for the classification of systemic lupus erythematosus Arthritis Rheum 1982 Nov;25(11):1271 7
Table 20 8 Drugs associated with lupus erythematosus
Definite association Chlorpromazine Hydralazine Isoniazid Possible association -Blockers Captopril Carbamazepine Cimetidine Ethosuximide Levodopa Lithium Methimazole Unlikely association Allopurinol Chlorthalidone Gold salts Griseofulvin Methysergide Oral contraceptives Modified and reproduced, with permission, from Hess EV et al Drugrelated lupus Bull Rheum Dis 1991;40(4):1 8 Penicillin Phenylbutazone Reserpine Streptomycin Tetracyclines Nitrofurantoin Penicillamine Phenytoin Propylthiouracil Sulfasalazine Sulfonamides Trimethadione Methyldopa Procainamide Quinidine
and other serologic findings become positive in many persons receiving these agents, clinical manifestations occur in only a few Four features of drug-induced lupus separate it from SLE: (1) the sex ratio is nearly equal; (2) nephritis and central nervous system features are not ordinarily present; (3) hypocomplementemia and antibodies to native DNA are absent; and (4) the clinical features and most laboratory abnormalities usually revert toward normal when the offending drug is withdrawn The diagnosis of SLE should be suspected in patients having a multisystem disease with serologic positivity (eg, antinuclear antibody, false-positive serologic test for syphilis) Differential diagnosis includes rheumatoid arthritis, systemic vasculitis, scleroderma, inflammatory myopathies, viral hepatitis, sarcoidosis, acute drug reactions, and drug-induced lupus The diagnosis of SLE can be made with reasonable probability if 4 of the 11 criteria set forth in Table 20 9 are met These criteria, developed as guidelines for the inclusion of patients in research studies, do not supplant clinical judgment in the diagnosis of SLE
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