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Purpose of the study To examine the cause of treatment failures in Type 1 retinopathy of prematurity (ROP). Patients and methods The medical charts of all infants with disease persistence after laser treatment at Uppsala University Hospital, Sweden, during a 10-year period (2009-2019) were reviewed. RetCam photography and angiography were used to document the retinal appearance before and after retreatment. Results Ten infants (18 eyes), of whom nine were referred from other hospitals, had persistence of Type 1 ROP in zone I or zone II despite previous laser treatment. Their mean gestational age was 24 weeks and their mean birth weight was 618 g. Seven eyes were diagnosed as stage 3 plus, eight eyes as stage 4A and three eyes as stage 4B. In eight infants (14 eyes), inadequate laser coagulation was suspected to be the cause for persistence of type 1 disease. Two infants (four eyes) were appreciated to have persistence of plus disease because of presence of zone I disease. For persistence of Type 1 ROP, five infants (seven eyes) were treated with vitrectomy, two infants (three eyes) with laser photocoagulation and anti-vascular endothelial growth factor (VEGF), two infants (four eyes) with anti-VEGF alone and finally two infants (four eyes) with laser photocoagulation alone. The anatomical outcome was good in 14 eyes and poor in four eyes (three infants). Conclusions Inadequate laser coagulation is an important cause of treatment failure of ROP Type 1. Another cause is laser coagulation in zone I. To minimize remaining visual disability, some kind of centralization of the ROP treatment is suggested.

Dense accumulation of mononuclear cells (lymphocytesmacrophages) in the dermal-epidermal interface and a T cell-mediated cytotoxic reaction against basal keratinocytes are hallmarks of lichen planus lesions. In this study, we focused on the chemotactic signals responsible for the selective recruitment of these cells. Using in situ hybridization and immunohistochemistry, the expression and localization of the lymphocyte-and/or monocyte/macrophage-attractant CC chemokines macrophage chemoattractant protein-1 (MCP-1), regulated on activation, normal T cell expressed, and secreted (RANTES), macrophage inflammatory protein-1alpha and -1alpha (MIP-1alpha/beta), I-309 and the CXC chemokines monokine induced by interferon-gamma (MIG), interferon-gamma-inducible protein-10 (IP-10), interleukin-8 (IL-8), epithelial-derived neutrophil attractant-78, and growth-related oncogene-alpha were investigated. Strong mRNA expression of MIG, IP-10, and MCP-1 and moderate mRNA expression of RANTES and MIP-1alpha were detected exclusively within foci characterized by strong infiltration with CD3+ lymphocytes (CD4+ cellsCD8+ cells) and CD68+ macrophages. All other chemokines investigated were minimally expressed or absent. With more than 11% of total cells strongly expressing MIG transcripts, this selectively lymphotactic chemokine was by far the dominant chemokine and thus may significantly contribute to the inflammatory reaction in lichen planus lesions. According to the mRNA expression profiles, MIG, IP-10, and MCP-1 were expressed by both basal keratinocytes above and mononuclear cells within the inflammatory foci. Our findings indicate that a set of chemokines composed of IP-10, MCP-1, RANTES, MIP-1alpha, and especially MIG contributes to the cytokine network and preferential trafficking of mononuclear cells to the interface region of lichen planus lesions.

Dense focal accumulation of neutrophils in the upper epidermis is a hallmark of psoriasis. Because the signals for neutrophil diapedesis and migration in vivo are not fully understood, psoriatic lesions with pronounced migration of neutrophils may serve as an important model for studying neutrophil chemotaxis. In this study, we present evidence for differential expression of the neutrophil chemotactic cytokines growth-related oncogene alpha, interleukin-8, and ENA-78 (epithelial cell derived and neutrophil-activating properties, 78 amino acids) in psoriatic lesions. In situ hybridization and immunohistochemistry of serial sections were employed to identify and microanatomically localize the cells producing these chemokines. High levels of focal interleukin-8 message were found to be expressed in the upper epidermis by keratinocytes and, most importantly, neutrophils themselves. Growth-related oncogene alpha transcripts were detected in clusters of keratinocytes of the upper epidermis at the same sites where interleukin-8 mRNA was abundant. In contrast to interleukin-8, growth-related oncogene alpha was also detected in the papillary dermis produced by vessel-associated cells. Sites of interleukin-8 and growth-related oncogene alpha mRNA expression were associated with infiltration of neutrophils. Interestingly, mRNA expression of the highly homologous chemokine ENA-78 was quiescent. In conclusion, our data indicate that growth-related oncogene alpha is an important chemoattractant for neutrophil diapedesis in vivo, whereas further migration of neutrophils and formation of micropustules appears to be influenced by the cooperative action of both growth-related oncogene alpha and interleukin-8.