In addition to telangiectatic vessels, our patients had right‐angle venules, greyish‐white opacification of the macula, and inner retinal crystalline deposits, all of which are typical for IPT. Because of these findings, the likelihood of the vascular findings being congenital is unlikely. Congenital macrovessels2
have been reported with increased vascularity in the foveal region; however, macrovessels are usually solitary, unilateral, and are not associated with retinal opacification or inner retinal crystalline deposits. During embryological development, a superficial layer of capillaries forms in association with astrocytes around the future site of the foveal depression.3
These vessels are excluded from the central foveal region during development.4
Later, a deeper layer of capillaries forms, apparently secondary to vascular endothelial growth factor release by Muller cells.3,5
After the vessels form, the astrocytes retreat from around the fovea.4
For vessels to invade the central fovea later in life, some stimuli for their growth must be present. There are two principle cell types in the central fovea: photoreceptors and Muller cells. As Muller cells are responsible for directing the deeper layer of capillaries during embryology and our patients had a deep proliferation of capillaries into a region that is ordinarily occupied only by photoreceptors and Muller cells, there seems a possibility that the abnormal vessel growth was directed by Muller cells.
Abnormalities involving Muller cells have been implicated in macular structural abnormalities seen in IPT,6
including foveal cavitation, which occurred in one eye of the current cases. We6
suggested that such cavitation is probably attributed to the alteration at the site of a specialized Muller cell found in the inner portion of the fovea centralis—namely, the Muller cell cone.7
Recent reports have also demonstrated a gap at the level of the boundary of photoreceptor inner and outer segments as a characteristic OCT finding in IPT.8,9
Interestingly, experimental disruption of Muller cell metabolism induces photoreceptor dysmorphogenesis.10
Although speculative, Muller cell abnormalities may secondarily affect photoreceptors in eyes with IPT, leading to the deep capillary proliferation.