LETTERS

tion was, in fact, an epidemiologic study with no control group at all.

Thrombocytopenia, proteinuria, and hair loss are not common during pregnancy. Previous studies have shown that hypocomplementemia (C3) does not occur in pre- eclampsia (Buyon JP, Cronstein BN, Moms M, Tanner M, Weissmann G: Serum complement values [C3 and C4] to differentiate between systemic lupus activity and pre- eclampsia. Am J Med 81 : 194-200, 1986). It is not at all clear to us why thrombocytopenia, hypocomplementemia, and proteinuria were attributed to the anticardiolipin syndrome or to preeclampsia rather than to flares of SLE, since all of the patients studied fulfilled criteria for SLE. We would consider evidence of the anticardiolipin syndrome in SLE patients to be a marker of SLE disease activity rather than a sepamte entity. Prior to our knowledge of anticardiolipin antibodies, it was well known that some patients manifested active SLE by thrombophlebitis o r thrombosis.

Table 4 in the article by Lockshin certainly depicts active SLE during pregnancy in 21 patients, and clearly shows that 10 of 80 women studied (12.5%) experienced a worsening of their SLE disease activity. Since there was no control group, it is impossible to conclude whether these findings demonstrate an increase in disease activity over what would be expected. While we acknowledge that a flare of disease activity can be precipitated by the discontinuation of antimalarial therapy, how can the ahthor be sure that the rash did not get worse because of the pregnancy?

Dr. Lockshin concludes that exacerbation of disease activity occurred in not more than 1 of 3 or 4 pregnancies. We believe the risk of a flare of disease activity in 25% of the population at risk is not to be taken lightly. We do not recommend treating SLE patients with corticosteroids just because they are pregnant. We wish to emphasize that even if only 25% of pregnant SLE patients have a flare of disease activity, this is a sufficiently large number to cause concern. The title of the paper, “Pregnancy Does not Cause SLE to Worsen,” is misleading because the questions posed cannot be adequately answered with the data as presented and interpreted.

Ann L. Parke, MBBS, FRCP(C) Margaret Peterson, PhD Naomi F. Rothfield, MD University of Connecticut Health Center Farmington, C T

To the Editor: I appreciate the concerns of Dr. Parke and col-

leagues, but 1 am surprised by their comments, since my article clearly stated that the choices I made about attribu- tion of thrombocytopenia, proteinuria, and hypocomple- mentemia are subject to alternate interpretations. In fact, I analyzed the diagnosis of “flare” 4 separate ways to provide minimum and maximum ranges for determination of the diagnosis.

I do not, however, concede that the assertions of the correspondents are valid. The concept of using the patient as

her own control is subject to considerable bias. In a popu- lation of systemic lupus erythematosus (SLE) patients, the first years of illness tend to be different from the later years; patients have gone through learning curves. have experi- enced drug toxicities, etc., which will interfere with the diagnosis of “flare.” Dr. Parke et al could have quoted our 1984 study ( I ) , which, though small, was a matched-control prospective study that showed no difference between preg- nant patients and their matched controls. They quote a single study that attempted to distinguish “flare” from preeclamp- sia by the use of serum complement assays, but they do not refer to a large body of literature demonstrating hypocom- plementemia in non-SLE toxemic women (2,3), nor to an equally large body of literature clearly demonstrating throm- bocytopenia in women with apparently normal pregnancies (4) as well as toxemic pregnancies (2). They also do not discuss the diagnosis of toxemia, in which proteinuria is invariably present.

Thus, the assertion that hypocomplementemia, thrombocytopenia, and proteinuria must be attributed to active SLE strikes me as inappropriate. I, of course. cannot statc that rash occurring after discontinuation of hydroxy- chloroquine could not also have been due to active SLE; I said so in the article. I concede that my choice of title was deliberately flamboyant to attract readers.

The questions that the correspondents indirectly address have no answer: What is the proper definition of “flare”? (not a trivial question [S]). and how often does “flare” occur in a population of patients observed over long periods of time? To cite a risk of “flare” of up to 25% per 9 months as an issue of concern is meaningless if the risk turns out to be higher in a nonpregnant control group. While I did not offer a new control group, neither do the correspondents, and virtually no literature exists on “flare” rates per I 0 0 patient-years.

My point was not to advocate casualness in the management of a pregnant SLE patient, but to state that, based on low overall risks, prophylactic corticosteroid treat- ment is unnecessary. Dr. Parke and colleagues appear to disagree. I look forward to seeing their data.

Michael D. Lockshin, MD, FACP NIAMS. NIH Bethesda, MD

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Lockshin MD. Reinitz E, Druzin ML, Murrman M, Estes D: Lupus pregnancy: case-control study demonstrating absence of lupus exacerbation during or after pregnancy. Am J Med 77: 893-898, 1984 Lockshin MD. Harpel PC, Druzin ML, Becker CG. Klein RF, Watson KM. Elkon K B , Reinitz E: Lupus pregnancy. 11. Un- usual pattern of hypocomplementemia and thrombocytopenia in the pregnant patient. Arthritis Rheum 28:58-66, 1985 Lockshin MD, Qamar T. Redecha P, Harpel PC: Hypocomple- mentemia with low CIS-CI inhibitor complex in systemic lupus erythematosus. Arthritis Rheum 29: 147-1472, 1986 Burrows RF. Kelton JG: Incidentally detected thrombocytopenia in healthy mothers and their infants. N Engl J Med 319:142-145, 1988 Liang MH. Socher SA. Roberts WN, Esdaile JM: Measurement of systemic lupus erythematosus activity in clinical research. Arthritis Rheum 31:817-825. 1988