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To quantify the presence of inflammatory/fibrogenic cytokines and procollagens type I (PICP) and III (PIIIP) in active and non-active tarsal and limbal forms of vernal keratoconjunctivitis (VKC), tear and blood samples were collected from 27 VKC patients (20 active and 7 non-active) and 15 normal subjects. Upper tarsal conjunctival biopses were obtained from 8 controls and 8 tarsal VKC patients. From biopses of 4 tarsal VKC, fibroblasts were cultured in F12 medium with 10% FCS. TGF-beta 1, IL-1 alpha, IL-1 beta, IL-6 and TNF-alpha, PICP and PIIIP were measured in: (1) tears, (2) homogenized conjunctival tissues, (3) serum, (4) supernatants of tissue cultures at 24 hr, and fibroblast primary passage cultures. Results showed: (1) in tears, TGF-beta 1 and TNF were identified in several active VKC patients without significant differences between the tarsal and the limbal forms. IL-1 beta (27 +/- 51 pg ml-1, P = 0.03) and IL-6 (28 +/- 43 pg ml-1, P = 0.006) were significantly increased in tarsal VKC compared to controls. Both control and non-active VKC tear samples had undetectable levels of all of the above cytokines. PICP and PIIIP were significantly increased in tarsal VKC compared to both limbal VKC and controls. Non-active VKC levels were similar to controls. (2) In homogenized VKC tissues, TGF-beta 1 and IL-6 were both significantly increased compared to controls (P0.01) while no increases were observed in IL-1 and TNF-alpha. (3) In serum, IL-1 alpha, IL-1 beta and TNF-alpha were higher in VKC patients compared to controls. (4) In vitro fibroblasts from VKC patients showed an increased production of TGF-beta 1, IL-1 alpha, IL-1 beta, IL-6, TNF-alpha, PICP, and PIIIP over time. Increased levels of TGF-beta 1, IL-1 and IL-6 in VKC tissues and tears indicate a local production of these cytokines in active VKC. Collagen hyperproduction occurs only in active tarsal VKC and may be related to high levels of TGF-beta 1, IL-1 and IL-6. Increased serum levels of IL-1 and TNF-alpha suggests that systemic immunological changes occur in VKC. Cell culture can be used as a model to further study the pathogenesis of VKC and its characteristic local fibroblast activation.

The efficacy, tolerability and safety of low doses (5-7 mg/kg/day) of oral ciclosporin (CS) for treatment of endogenous uveitis resistant to conventional therapy were studied in an open, noncontrolled, multicenter long-term trial. CS was shown to be effective for patients with posterior or intermediate noninfectious uveitis; it limited the progression of the disease, decreased the number and severity of inflammatory relapses, and improved visual acuity while reducing signs of intraocular inflammation. Moreover, in corticodependent patients, a steroid-sparing effect was also obtained. At low doses and by means of the careful monitoring of safety parameters, the side effects (especially renal function impairment) were well controlled. Efficacy was maintained during long-term treatment.

Normal rabbit lenses exposed in vitro to heterologous antibody (Ab)--antigen (Ag) interactions lose control of the intracellular 86Rb; this membrane damage, which seems to be related to the quantitative ratio Ab/Ag, is relatively complement independent and is followed by a subsequent leakage of lenticular proteins. A possible implication of these findings in the development of complicated cataracts in uveitis (as 'permeability cataracts') and in the self-maintenance of recurrent uveal inflammation is shortly discussed.

Normal rabbit lenses exposed in vitro to heterologous antilens and antiuveoretina antibodies lose control of the intracellular 86Rb and this effect is followed by a late leakage of lenticular proteins; both phenomena take place only in the presence of complement. This antibody-induced complement-dependent membrane damage might be involved in the pathogenesis of complicated cataracts in uveitis and in the self-maintenance of recurrent uveal inflammations.