Sir,
We thank Yusuf and Watson1 for their insightful comments regarding our recent publication.2 Indeed, ocular inflammation is not always evident in Purtscher and Purtscher-like retinopathies (PuR). The hypothesis of a common pathological molecular pathway between PuR and thrombotic microangiopathy (TMA) deserves further exploration.
Both PuR and TMA share a mechanism of microvascular occlusion, which has been suggested for PuR by many authors in the past years3, 4 and include arteriolar precapillary occlusion and microvascular infarct of the retinal nerve fiber layer. Both include complement activation5 and capillary endothelial damage.3 However, there is no current evidence of a common pathway in some pathological mechanisms of PuR, such as microembolization,3 fat emboli6 or a rheological event7 that results in vascular endothelial dysregulation (as recently suggested as an alternative etiology).
These issues must be addressed in further studies to identify and characterize the etiology and mechanisms of PuR. Afterwards, new molecular targets can be explored for the treatment of Purtscher and Purtscher-like retinopathies.
The authors declare no conflict of interest.
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