Sir,

The article by Chhablani et al1 has several shortcomings that prevent the validation and extrapolation of their results and that can be specifically summarized as follows:

  1. 1

    Several critical data are missing from the article (Table 1).

    Table 1 Missing data from the article by Chhablani et al1
    Full size table
  2. 2

    The patients belonged to two different etiological groups with definitely different prognoses, namely, patients in the monotherapy group were older than 50 years, where common systemic vascular conditions should be considered; by contrast, patients in the combination group had <50 years of age and to which other mechanisms (hyperviscosity/inflammation) should be specifically accounted for.

  3. 3

    Initially, a comparison had to be carried out between the two groups to establish whether or not they are comparable. Accordingly, this comparison should have been conducted only if there were no significant differences between all variables of the two groups. It sounds that patients in the monotherapy group had a less-progressed disease (eg, thinner macula and better visual acuity) than those in the combination group.

  4. 4

    Evaluation of the outcomes has to be guided by anatomical measure data with visual changes as a secondary guide. Although improving vision was progressive and ascending, decreasing central subfield thickness (CST) was significant to 515.2 and 623 μm in the monotherapy and combination groups, respectively. Notably, these values are much more than the cutoff (315.2 μm) for the upper level of normal foveal thickness (270.2±22.5)2 plus 2 SDs. We believe that despite remarkable improvements in vision, the persistence of high values of the CST indicates insufficient macular deturgescence, as well as that the disease process is still active and progressive. Presumably, ischemic damages appeared during the period of time when the patients went without treatment because therapy was initiated within 9 months (mean 2.7 and 1.37 months in the monotherapy and combination groups, respectively) of central retinal vein occlusion (CRVO) onset.3 These lesions were exacerbated during the follow-up when the treatment applied was insufficient. The standard injection scheme during the first year of intravitreal bevacizumab (IVB; Avastin, Genentech Inc., South San Francisco, CA, USA) therapy for macular edema due to CRVO was definitely set by the level I evidence of the Swedish trials.4

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