Sensitivity of indocyanine green angiography compared to fluorescein angiography and enhanced depth imaging optical coherence tomography during tapering and fine-tuning of therapy in primary stromal choroiditis: A case series

Abstract

Purpose: To investigate indocyanine green angiography (ICGA), fluorescein angiography (FA), and enhanced depth imaging optical coherence tomography measured choroidal thickness (EDI-OCT-CT) in the follow-up of inflammatory activity in stromal choroiditis [Vogt-Koyanagi-Harada disease (VKH) and birdshot retinochoroiditis (BRC)] under treatment in order to monitor tapering of therapy or readjustment of therapy in case of subclinical disease recurrence.

Methods: Patients with initial onset disease and/or treatment-naive stromal choroiditis (VKH & BRC) at entry, quiet under therapy, and having had a follow-up of at least four years monitored with dual FA and ICGA and EDI-OCT-CT measurements were analyzed retrospectively. ICGA and FA scores and EDI-OCT-CT values were correlated with therapy, and significant changes of each modality were correlated with disease evolution.

Results: Of the 31 VKH and 29 BRC patients seen from 1995 to 2017 in our center, four patients (2 VKH and 2 BRC patients) fulfilled the inclusion criteria. During tapering, two patients (both VKH) showed no significant ICGA, FA, and EDI-OCT-CT changes (mean follow-up time 5.6 years) and allowed for safe tapering. In the other two (BRC) patients (mean follow-up time 6.25 years), a total of seven significant subclinical changes were demonstrated by ICGA alone after therapy modifications due to side-effects or during attempted tapering of therapy, while FA and EDI-OCT-CT remained unchanged.

Conclusions: ICGA was the most sensitive monitoring modality of stromal choroiditis, able to identify subclinical recurrences following change of therapy and inversely treatment responses after readjusted therapy, events otherwise missed by FA and EDI-OCT. ICGA proved efficient for safe therapy tapering or for timely adjustment of therapy in stromal choroiditis when necessary.

Keywords: Birdshot retinochoroiditis; Indocyanine green angiography; Stromal choroiditis; Treatment; VKH; Vogt-Koyanagi-Harada disease.

Fig. 1

Evolution of fluorescein angiography (FA) and indocyanine green angiography (ICGA) findings in a birdshot retinochoroiditis (BRC) patient after modification of therapy. As shown in Table 2 (2nd column), there is no score change for FA, whereas the score change was 5 for ICGA, which is well illustrated on this figure. FA (2 left sets of 9 frames) before (top left) and after change of therapy (bottom left) have the same aspect. ICGA (2 sets of 9 right frames) shows a substantial decrease of hypofluorescent dark dots (HDDs) (bottom right set of 9 frames). When compared to the situation before therapeutic intervention (top right set of 9 frames).

Fig. 2

Fine-tuning of therapy in a birdshot retinochoroiditis (BRC) patient where treatment had to be adjusted because of side-effects of ongoing therapy. MYF: Myfortic^®, mycophenolic acid. REM: Remicade^®, infliximab, anti-TNF-α agent. CsA: cyclosporine. Prograf^® = tacrolimus. P: Prednisone. Pink shadowed area accounts for disease evolution and treatment combinations before disease was under control.

Fig. 3

Recurrence detected by indocyanine green angiography (ICGA) during tapering of therapy in a birdshot retinochoroiditis (BRC) patient. MYF: Myfortic^® = mycophenolic acid. CsA: Cyclosporine. Pink shadowed area accounts for disease evolution and treatment combinations before disease was under control.

Fig. 4

Indocyanine green angiography (ICGA) detection of disease recurrence during therapy tapering. A. Disease controlled under Myfortic^® (1440 daily). Scars are visible as therapy had been started ∼4 years after disease onset but no active hypofluorescent dark dots (HDDs) are present. B. Thirteen months after reduction of Myfortic dosage to 720 mg, massive reappearance of HDDs, that responded to the introduction to cyclosporine (CsA) with disappearance of HDDs (C).

Fig. 5

Safe tapering of therapy in a Vogt-Koyanagi-Harada disease (VKH) patient. CS: Corticosteroids, prednisone, ¼CS: Quarter dose of prednisone, CsA: Cyclosporine. MYF: Myfortic^® 0 mycophenolic acid. REM: Remicade^® REM = infliximab, anti-TNF-α agent. REM X 8 = Remicade every 8 weeks (5 mg/kg). Pink shadowed area shows that several treatment combinations were necessary until disease was under control. MYF: Myfortic, REM: Remicade, CsA: Ciclosporine, P: Prednisone, ttt: Treatment.

Fig. 6

Safe tapering of therapy in a Vogt-Koyanagi-Harada disease (VKH) patient. Maxinal treatment = methylprednisolone IV (1000 mg per day for 3 days) followed by oral prednisone (1 mg/kg) and azathioprine (2.5 mg/kg). P: Prednisone followed by the dosage in mg. I: Imurek^®, azathioprine, followed by the dosage in mg. MYF: Myfortic^® = mycophenolic acid, CsA: Cyclosporine. Pink shadowed area accounts for disease evolution and treatment combinations before disease was under control.