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The antiphospholipid antibody dilemma

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Conclusions

In evaluating the literature, we have to be aware of some important drawbacks of most studies: 1) the relation between aPLab and thrombosis has not yet been proven in prospective studies, 2) almost all studies try to establish relationships between findings withactual blood samples andhistories of thrombosis, and 3) because aPLab occur relatively frequent in SLE patients, most studies include many patients with this disease for which the presence of a variety of circulating abnormal substances is almost characteristic. Effects of for instance immune complexes thus have to be separated from those of aPLab. Also the question whether aPLab are a primary phenomenon or develop secondary upon cellular damage caused by other factors is still unanswered.

Future studies will have to 1) focuss on differences between findings in samples taken at the time of thrombosis and samples taken before and after such episodes, 2) focuss on patients with aPLab and thrombosis, but no signs of systemic autoimmune disease (“primary aPLab syndrome”) (60,61) and 3) use purified aPLab instead of plasma or serum, in order to draw firm conclusions. Furthermore, 4) conformational aspects of the phospholipids used as the antigen of aPLab should be taken into account, and 5) instead of studying isolated parts of the hemostatic process, more complex systems should be used in which all components involved in the development of thrombosis, including blood flow, are present.

Although many relevant findings have emerged over the past decade, a pathogenetic role of aPLab in thrombosis is still far from proven.

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Supported in part by grants (87/CR/19 and 88/CR/028) from the Nederlandse Vereniging voor Reumabestrijding.

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Derksen, R.H.W.M., Hasselaar, P., Oosting, J.D. et al. The antiphospholipid antibody dilemma. Clin Rheumatol 9 (Suppl 1), 39–44 (1990). https://doi.org/10.1007/BF02205550

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