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The ocular complications of rheumatoid arthritis include aqueous tear deficiency, scleritis, and central or paracentral corneal ulceration or perforation. The corneal ulcers are said to be non-inflammatory but ultrastructural changes have been found in the corneal stroma surrounding ulcers. Electron-dense deposits, thought possibly to indicate aggregated collagen, have been seen in the extracellular stromal matrix. On light microscopy, however, there are few inflammatory cells. Researchers in Germany have demonstrated increased gene expression for TNF-α and IL-6 in keratocytes around corneal ulcers or perforations in patients with rheumatoid arthritis.
They examined corneal samples from seven patients with rheumatoid arthritis and ulceration or perforation, using systematic non-radioactive in situ hybridisation with gene probes for TNF-α and IL-6 labelled with digoxigenin. Corneal samples from two patients with keratoconus were used as controls. High levels of IL-6 mRNA were demonstrated in keratocytes of all seven patients and of TNF-α mRNA in five of the seven. The two control samples gave negative results. TNF-α-positive keratocytes were seen mostly around the corneal epithelium whereas IL-6-positive keratocytes tended to be deeper in the stroma. The two patients with low TNF-α gene expression both had acute infections, one with herpes zoster and one with Staphylococcus species. The authors comment that neither of these patients had clear rheumatic symptoms confirmed.
TNF-α and IL-6 are both expressed in keratocytes around the corneal ulcers or perforations of patients with rheumatoid arthritis. It is suggested that these cytokines may modify metalloproteinase production, causing lysis of collagen. Inflammatory cytokine production may be a cause or a consequence of corneal ulceration or perforation in patients with rheumatoid arthritis.
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