Adjuvant Brachytherapy with Ruthenium-106 to Reduce the Risk of Recurrence of Conjunctival Melanoma after Excision.

Introduction: Local recurrence of conjunctival melanoma (CM) is common after excision. Local radiotherapy is an effective adjuvant treatment option, and brachytherapy with ruthenium-106 (106Ru) is one such option. Thus, herein, we aimed to describe our experience with and the clinical results of post-excision adjuvant 106Ru plaque brachytherapy in patients with CM. Methods: Nineteen patients (8 men and 11 women) received adjuvant brachytherapy with a 106Ru plaque after tumor excision. The mean adjuvant dose administered was 109 Gy (range, 80-134 Gy), and a depth of only 2.2 mm was targeted because the tumor had been excised. A full ophthalmological examination including visual acuity testing, slit-lamp examination, and indirect ophthalmoscopy was performed before therapy and at every postoperative follow-up. The mean follow-up period was 62 months (range, 2-144 months). Results: Three patients developed a recurrence in a nontreated area, at either the conjunctiva bulbi or the conjunctiva tarsi. None of the patients developed a recurrence in the treated area. The local control rate was 84% (16/19). Conclusion: 106Ru plaque brachytherapy is an effective adjuvant treatment to minimize the risk of local recurrence after excision of a CM. Patients have to be followed up regularly and carefully for the early detection of recurrence.

Treatment of radiation-induced maculopathy with fluocinolone acetonide.

PURPOSE: Chronic macular oedema is a well-known presentation of radiation-induced maculopathy (RM) following external beam photon therapy, plaque radiotherapy and proton beam radiotherapy for choroidal tumours. Current therapies vary in respect of efficacy and clinical benefit. The potential of fluocinolone acetonide (FAc) slow-release implants is unknown. We hypothesised that local continuous delivery of low-dose corticosteroids might improve symptoms of RM. METHODS: Five-two male and three female-patients from 37 to 68 years presented with RM following 106Ru-plaque brachytherapy or stereotactic radiation therapy (STx) with photons using a hypofractionated schedule of 5 × 10 Gy. All were treated with triamcinolone injections in first line and proofed to be refractory to steroids. In addition, two patients had received Ozurdex® implants as a second-line treatment, though without any clinical benefit. FAc slow-release implants were injected, and patients were followed up to monitor clinical improvement. RESULTS: All patients responded to therapy by means of a decrease in macular oedema. In four of five (80%) patients, visual acuity improved, and one patient showed stable visual acuity. No toxic effects or complications were observed. CONCLUSION: Slow-release implants of FAc are a promising therapeutic potent steroid treatment option to benefit anatomical structures of the fovea and visual function. Slow-release implants with FAc reduce the frequency of intravitreal injections and the therapeutic burden.

Antimony-trioxide- and arsenic-trioxide-induced apoptosis in myelogenic and lymphatic cell lines, recruitment of caspases, and loss of mitochondrial membrane potential are enhanced by modulators of the cellular glutathione redox system.

During the last years remission rates of more than 72% for arsenic(III)-oxide (As(2)O(3)) treatment in relapsed or refractory acute promyelocytic leukemia have been published. As(2)O(3) is under clinical investigation for therapy of leukemia and solid tumors. Due to the chemical affinity of arsenic and antimony, we analyzed the potency of antimony(III)-oxide (Sb(2)O(3)) to exert As(2)O(3)-like effects. Based on the same molar concentrations, lower efficacy in apoptosis induction and caspase-independent decrease of mitochondrial membrane potential was observed for Sb(2)O(3). No difference in sensitivity to As(2)O(3) or Sb(2)O(3) was detected in CEM cells when compared to their multiple drug resistant derivatives. Apoptosis was induced by combining sub-apoptotic concentrations of Sb(2)O(3) or As(2)O(3) with sub-apoptotic concentrations of DL: -buthionine-[S,R]-sulfoximine (BSO). Other modulators of the cellular redox system showed this effect to a lower extent and enhancement was not consistent for the different cell lines tested. Caspase inhibitors protected cell lines from Sb(2)O(3)- and As(2)O(3)-induced apoptosis. When BSO was added, the inhibitors lost their protective ability. The ability of modulators of the cellular redox system in clinically applicable concentrations to enhance the apoptotic effects of the two oxides in a synergistic way may be helpful to reduce their toxicity by optimizing their dose.

Ocular syphilis--indicator of previously unknown HIV-infection.

OBJECTIVES: To detect the prevalence of HIV-co-infection in patients with ocular syphilis and to compare ocular syphilis in HIV-positive and -negative patients. METHODS: 24 consecutive patients treated for ocular syphilis at our hospital between 1998 and 2006 were evaluated retrospectively. Patients' characteristics, laboratory results (including syphilis serology, HIV status, CSF examination), major ophthalmologic finding, treatment and course were assessed. Data of HIV-positive and -negative patients were compared. RESULTS: Of the 24 patients with ocular syphilis, 11 were co-infected with HIV. Notably, the HIV-infection had previously been unknown in 7 of the 11 HIV-positive patients. 6 of these were in an early disease stage (CDC category A). Clinical and laboratory findings did not differ between HIV-positive and -negative patients except for the C-reactive protein (CRP), which was significantly higher in HIV-infected patients. CONCLUSIONS: Ocular syphilis led to new diagnosis of HIV-infection in an unexpectedly high number of patients, which emphasises that patients with ocular syphilis must be screened for HIV-co-infection. According to our study the expected benefit is high because most of the patients newly diagnosed with HIV had high CD4(+) cell counts. These patients can be monitored and treated before the development of AIDS.