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Luca Cimino

Publications and source records attributed to Luca Cimino.

12 recordsLinked to original sources

Interleukin-10 promoter polymorphisms in giant cell arteritis.

OBJECTIVE: To investigate potential associations between interleukin-10 (IL-10) promoter polymorphisms and susceptibility to, and clinical features of, giant cell arteritis (GCA). METHODS: A total of 140 patients with biopsy-proven GCA who were residents of Reggio Emilia, Italy, and 200 population-based controls from the same geographic area were genotyped for promoter polymorphisms of the IL-10 gene, by molecular methods. The patients were subgrouped according to the presence or absence of polymyalgia rheumatica (PMR) and ischemic complications (any or all of the following: vision loss, jaw claudication, cerebrovascular accidents, or aortic arch syndrome). RESULTS: The distribution of the C/A 592 genotype differed significantly between the GCA patients and the controls (P(corr) = 0.003). Carriers of the A592 allele (A/A or C/A) were significantly more frequent among the GCA patients than among the controls (P(corr) = 0.004, odds ratio [OR] 2.0 [95% confidence interval (95% CI) 1.3-3.1]). Homozygosity for the A592 allele was significantly more frequent among the GCA patients than among the controls (P(corr) = 0.002, OR 3.4 [95% CI 1.6-7.2]). The distribution of the A/G 1082 genotype was similar in GCA patients and controls. In the haplotype analysis, the frequency of the ATA haplotype was significantly higher in GCA patients than in the controls (P = 0.0001), whereas the frequencies of the ACC and GTA haplotypes were significantly lower (P = 0.0001 for both comparisons). No significant associations were found for comparisons of GCA patients with and those without PMR or GCA patients with and those without ischemic complications. CONCLUSION: Our findings show that the -592 C/A promoter polymorphism of the IL-10 gene is associated with susceptibility to GCA.

Aged↗

Risk factors for visual loss in an Italian population-based cohort of patients with giant cell arteritis.

OBJECTIVE: To evaluate the frequency of visual manifestations at presentation in an Italian population-based cohort of patients with biopsy-proven giant cell arteritis (GCA), and to investigate predictors for the development of permanent visual loss. METHODS: We identified 136 Reggio Emilia (Italy) residents with biopsy-proven GCA diagnosed between 1986 and 2002. Medical records of these 136 patients were reviewed, and demographic, clinical, and laboratory data were collected.Multivariate analysis with multiple logistic regression models was performed to identify the best predictors of visual loss. RESULTS: Visual manifestations developed in 41 patients (30.1%). Partial or total visual loss was observed in 26 patients (19.1%). Anterior ischemic optic neuropathy was seen in 24 patients, and 2 patients had central retinal artery occlusion. Unilateral vision loss occurred in 19 patients, and bilateral visual loss in 7. In 25 patients, visual loss developed before glucocorticoid therapy for GCA was started. The age at disease onset was significantly higher in patients with permanent visual loss compared with those without it. The frequency of systemic signs/symptoms and erythrocyte sedimentation rate (ESR) and C-reactive protein values at diagnosis were significantly lower in patients with permanent visual loss. By multivariate logistic regression, the only statistically significant predictor for the development of permanent visual loss was the absence of high levels of ESR at diagnosis (tertile 2: Odds ratio [OR] 0.08; tertile 3: OR 0.11). Other predictors included in the model were the absence of systemic manifestations (OR 0.24), an older age at disease diagnosis (quintile 5: OR 5.60), and the presence of an elevated platelet count at diagnosis (OR 4.99), however they were only of borderline statistical significance. CONCLUSION: The proportion of Italian patients with GCA that developed visual loss was similar to that reported from other countries. The patients with low inflammatory response had a higher risk of visual loss.

Age of Onset↗

Bronchial reactivity in healthy individuals undergoing long-term topical treatment with beta-blockers.

OBJECTIVE: To assess the impact of long-term treatment with topical timolol on bronchial reactivity in healthy individuals. METHODS: Twenty-one otherwise healthy individuals with high-pressure primary open-angle glaucoma were enrolled in a randomized controlled clinical trial. Eleven patients underwent 3 years of topical 0.5% timolol treatment followed by a 1-year washout period; 10 patients underwent primary argon laser trabeculoplasty. Functional variables and bronchial reactivity (forced expiratory volume in 1 second and metacholine challenge test results) were assessed in both groups at enrollment and after 3 and 4 years of follow-up. RESULTS: After 3 years, a measurable response to metacholine challenge was recorded in 6 of 11 otherwise symptom-free individuals treated with 0.5% timolol twice daily. A detectable response to metacholine challenge was still present in half of these individuals (3 of 6) when further washed out for 1 year from the topical beta-blocker. No significant variation in bronchial reactivity was measured in the laser-treated group during 4 years of follow-up. CONCLUSIONS: Healthy individuals who undergo long-term topical application of a nonselective beta-blocker (0.5% timolol) can develop a subclinical increase in bronchial reactivity. This phenomenon may not be completely reversible on withdrawal of the beta-blocker.

Administration, Topical↗

Ocular vasculitis: a multidisciplinary approach.

PURPOSE OF REVIEW: The ophthalmologist has direct visual access to inflamed vessels when examining the retina, and "vasculitis" in ophthalmology has so far mainly referred to retinal vasculitis. In the past few years the means to explore vasculitis in the ocular sphere have improved. Indocyanine green angiography now enables the analysis of choroidal inflammatory vasculopathy as well as vasculitis of the sclera (scleritis) and episclera (episcleritis) in addition to retinal vasculitis. Because vasculitis detected by the ophthalmologist can be the presenting sign of a systemic disease and has to be approached in a multidisciplinary fashion, the emerging term "ocular vasculitis," instead of retinal vasculitis, should be used in the future. The term covers vasculitis affecting all structures of the eye and the periocular tissues as detailed in this article. The ocular findings have to be integrated within the established and accepted classification of systemic vasculitis, which is divided into primary vasculitides, where the vessel itself is the target of the inflammatory reaction, and secondary vasculitides, caused by other inflammatory processes. This review will deal with recently published articles on ocular vasculitis, including its clinical aspects, its link with systemic diseases, and its investigation and management. The discussion will be conducted within the framework of the new classification put forward here. RECENT FINDINGS: Novel imaging techniques such as indocyanine green angiography have made it possible to explore inflammation of choroidal vessels and of scleral vasculitis in addition to retinal vasculitis, contributing to the global concept of ocular vasculitis. It has been shown, in particular, that the choriocapillaris, a vascular structure adjacent to the retina, can be the site of a primary inflammatory vasculopathy unrecognized so far. Most of the recent articles cited, however, deal not so much with new findings but with the integration of ocular pathologic changes into the systemic diseases they are part of. New knowledge about disease mechanisms and novel therapeutic modalities with biologic agents cited in this review are coming from other fields but have contributed to progress in the management of ocular vasculitis. SUMMARY: New investigational techniques of vasculitis in ocular structures other than the retina have contributed to the development of the global concept of ocular vasculitis. This review shows the importance of promoting a comprehensive and global classification of ocular vasculitis compatible with the concepts accepted for systemic vasculitis to contribute to its multidisciplinary approach.

Diagnostic Techniques, Ophthalmological↗

Improvement of spatial contrast sensitivity threshold after surgical reduction of intraocular pressure in unilateral high-tension glaucoma.

PURPOSE: To measure the effect of a surgical reduction of IOP on the spatial contrast sensitivity threshold in eyes showing a considerably increased IOP but no glaucomatous visual field defect, on white-on-white computer-assisted static perimetry. METHODS: Prospective clinical trial, lasting 36 months; 10 consecutive subjects with untreated IOP > or = 30 mmHg in one eye and < or =18 mmHg in the fellow eye, no evidence of field damage in both eyes, best corrected visual acuity > or =20/20 in both eyes, and scheduled for a primary trabeculectomy in the eye showing a high IOP. The spatial contrast sensitivity threshold was measured before surgery and at each follow-up visit. RESULTS: Preoperative spatial contrast sensitivity was worse in those eyes bearing a high IOP relative to the normal fellow eyes (paired samples t-test, P <0.0005). An improvement of contrast sensitivity threshold, exceeding the 95% confidence limits of the preoperative test-retest variability, was observed at 3, 6, and 12 cyc/deg in each surgical eye at the end of follow-up. No change was observed in the fellow untreated normal eyes. The improvement correlated directly with the amount of decrease in pressure obtained by surgery. CONCLUSIONS: Eyes with no field defects on white-on-white computer-assisted static perimetry, but bearing a IOP > or = 30 mmHg, show a decreased spatial contrast sensitivity. A surgically obtained reduction of IOP is paralleled by an improvement of spatial contrast sensitivity.

Adult↗

Interleukin-6 promoter polymorphism at position -174 in giant cell arteritis.

OBJECTIVE: To investigate potential associations between the -174 G/C interleukin-6 (IL-6) promoter polymorphism and susceptibility to and clinical features of giant cell arteritis (GCA), particularly in patients with or without polymyalgia rheumatica (PMR) and with or without ischemic complications. METHODS: One hundred and twenty-six patients with biopsy-proven GCA who were residents in Reggio Emilia, Italy, and 112 population-based controls from the same geographic area were genotyped for IL-6 polymorphism at position -174 by molecular methods. Patients were divided in subgroups according to presence or absence of PMR and ischemic complications (visual loss, jaw claudication, cerebrovascular accidents, aortic arch syndrome). RESULTS: Distribution of the G/C 174 genotype was similar in patients with GCA and controls. No significant associations with the IL-6 promoter polymorphism at position -174 were found when GCA patients with or without PMR or with or without ischemic complications were compared. Further, IL-6 genotypes did not significantly affect levels of C-reactive protein or other inflammatory markers at diagnosis. CONCLUSION: Our findings show that the 174 G/C promoter IL-6 polymorphism does not seem to be implicated in susceptibility to and clinical expression of GCA.

Aged↗

Effect of bimatoprost on patients with primary open-angle glaucoma or ocular hypertension who are nonresponders to latanoprost.

PURPOSE: To test the efficacy of bimatoprost 0.03% 2D for lowering intraocular pressure (IOP) in patients affected by primary open-angle glaucoma or ocular hypertension who did not respond to treatment with latanoprost 0.005% 2D. DESIGN: Prospective, randomized clinical trial with a cross over design (two 30-day treatment phases with a 30-day washout phase in between). PARTICIPANTS: Fifteen patients were enrolled. Random allocation to treatment to a single eye only of every subject. ELIGIBILITY CRITERIA: (1) IOP > 22 mmHg in both eyes on current treatment (on three separate readings > 24 hours apart), (2) angle wide open in both eyes, (3) no pseudoexfoliation and/or pigment dispersion in either eye, (4) documented medical history consistent with < 10% IOP decrease in both eyes on 2-month treatment with latanoprost 0.005% every day. METHOD: The following variables were measured at each study visit: (1) IOP (Goldmann applanation tonometry, 5 readings, 8 AM, 12 noon, 4 PM, 8 PM, and 12 midnight); (2) visual acuity (Early Treatment of Diabetic Retinopathy Study chart, logarithm of the minimum angle of resolution); (3) estimate of conjunctival hyperemia based on 5 standard photographs (graded as "none," "trace," "mild," "moderate," and "severe"). MAIN OUTCOME MEASURE: IOP. RESULTS: IOP data (mean and standard deviation) were the following: baseline = 24.7 +/- 0.9 mmHg, after washout = 24.8 +/- 1.1 mmHg, after latanoprost phase = 24.1 +/- 0.9 mmHg, after bimatoprost phase = 18.1 +/- 1.7 mmHg. IOP on bimatoprost proved lower than both baseline (P < 0.0001) and latanoprost (P = 0.0001). Thirteen of 15 patients showed a > or =20% IOP decrease with bimatoprost treatment. None of the 15 patients showed a > or =20% decrease of IOP after 30 days of latanoprost treatment. No significant IOP changes were observed in the fellow untreated eye in each patient throughout the study. Trace-to-mild conjunctival hyperemia was recorded more often with bimatoprost phase (P = 0.035). CONCLUSIONS: Thirteen of 15 patients, who were nonresponders to latanoprost, 0.005%, 2D, were successfully treated with bimatoprost, 0.03%, 2D. Bimatoprost treatment was associated with a higher incidence of trace-to-mild conjunctival hyperemia than latanoprost.

Amides↗

Effect of a drug combination treatment on ocular perfusion in recurrent idiopathic intermediate uveitis.

PURPOSE: To test the effect of a drug combination therapy on ocular perfusion in human eyes affected by idiopathic intermediate uveitis. METHODS: Seven patients (12 eyes) showing active signs of intermediate uveitis, with at least two more similar episodes reported within the previous 12 months, were enrolled in a prospective case series. Two fellow healthy eyes of two of the enrolled patients were studied as internal controls. Color Doppler imaging of the central retinal artery (CRA), the ophthalmic artery (OA), and the posterior ciliary arteries (PCAs) was performed at the time of enrollment, and at 6 and 12 months after starting treatment with oral fluorocortolone, cyclosporine, and parenteral methotrexate. The best-corrected visual acuity was concurrently measured as a second parameter. RESULTS: In the 12 affected eyes, the mean visual acuity (+/-SD) improved from 0.15(+/-0.12) to 0.04(+/-0.18) LogMAR (paired samples Student's t-test: p = 0.015). The resistivity index (RI +/- SD) of the CRA decreased from 0.81(+/-0.13) to 0.71(+/-0.13)(p = 0.0091). Further, the variation of the RI in the PCAs reached a borderline significance (p = 0.062), decreasing from 0.71(+/-0.12) to 0.61(+/-0.12). No significant changes were observed in the OA. Moreover, eyes showing a visual improvement of > or =0.1 (LogMAR) were more likely to show a > or =10% improvement of the RI for the CRA (Fisher's exact test: p = 0.018; power = 90%; alpha probability = 5%; odds ratio = 2,4). CONCLUSIONS: In eyes affected by idiopathic intermediate uveitis, treated with a systemic drug combination therapy, the improvement of the visual acuity seems to correlate with a proportional improvement of the retrobulbar circulation.

Adult↗

Replacing maximum-tolerated medications with latanoprost versus adding latanoprost to maximum-tolerated medications: a two-center randomized prospective trial.

PURPOSE: To compare the replacement of every drug with latanoprost 0.005% once a day in glaucomatous eyes with poorly controlled intraocular pressure upon combination therapy, versus addition of latanoprost to the pre-existing treatment. PATIENTS AND METHODS STUDY DESIGN: prospective, investigator-masked, two-center, randomized clinical trial lasting 3 months. ELIGIBILITY CRITERIA: open-angle glaucoma; IOP > or = 21 mm Hg upon the combination of a non-selective beta-blocker with pilocarpine or dorzolamide or both; no previous bulbar surgery; and prior glaucoma therapy lasting at least 2 years. Two treatment arms: (1) addition of latanoprost 0.005% QD to the pre-existing therapy [group A]; (2) substitution with latanoprost alone [group B]. RESULTS: One hundred thirty-six eyes (68 eyes/treatment group) were randomized according to intraocular pressure level and the number of adjunctive medications to beta blocker. Both treatments provided a significant IOP decrease over baseline (from 23.5 +/- 1.4 to 19.7 +/- 1.9 mm Hg in group A, (P < 0.001); from 23.2 +/- 1.3 to 20.1 +/- 2.2 mm Hg in group B (P < 0.001), paired Student t test). At the end of the follow-up period, group A showed a higher number of intraocular readings less than or equal to 18 mm Hg than group B (42.6% vs. 30.8%; Fisher exact test: P = 0.018). CONCLUSIONS: In eyes showing an intraocular pressure greater than 21 mm Hg upon combination therapy, the substitution of the pre-existing treatment with latanoprost can provide a significant IOP decrease. However, adding latanoprost to the pre-existing therapy is more likely to achieve a target intraocular pressure less than or equal to 18 mm Hg.

Adrenergic beta-Antagonists↗

Autoimmune uveitis in children: clinical correlation between antinuclear antibody positivity and ocular recurrences.

OBJECTIVE: The aim of this study was to identify the correlation between antinuclear antibody (ANA) titre and the onset and clinical course of uveitis in children with juvenile idiopathic arthritis (JIA) or without any other systemic autoimmune disease, i.e., idiopathic uveitis (IU). METHODS: Twenty-two patients affected by uveitis were examined. Ten had JIA-associated uveitis, 12 had IU. Follow-up ranged from 7 to 101 months. The ANA were titrated three times per year and additionally in case of ocular recurrences. All patients were treated with immunosuppressive drug combination therapy (IDCT). RESULTS: JIA-associated uveitis: ocular recurrences were noted in three ANA-positive patients and in one ANA-negative patient. IU uveitis: ocular recurrences were noted in one ANA-positive and in one ANA-negative patient. No significant rise in ANA titre was noted in either group during uveitis recurrence. CONCLUSIONS: (1) ANA had no value in predicting the recurrence of uveitis. (2) IDCT does not influence ANA production.

Age Distribution↗

Assessment and classification of choroidal vasculitis in posterior uveitis using indocyanine green angiography.

BACKGROUND: By allowing one to detect fluorescence beyond the retinal pigment epithelium, indocyanine green angiography (ICGA) has made it possible to analyse the choroidal vessels. Our aim was to characterize choroidal vasculitis in posterior uveitis using ICGA. METHODS: Charts of active posterior uveitis patients with a specific diagnosis seen in the different centers participating in the study who had undergone dual fluorescein and ICG angiography were reviewed. The type of inflammatory involvement of the choroidal circulation at entry and the treatment response on follow-up angiograms were analysed. RESULTS: A total of 129 patients were analysed. Choroidal vasculitis could be subdivided into two main patterns: (1) primary inflammatory choriocapillaropathy and (2) stromal inflammatory vasculopathy. The first pattern consisted of hypofluorescent areas up to the late phase of angiography characteristic for choriocapillaris non-perfusion and included entities such as multiple evanescent white dot syndrome (MEWDS), acute posterior multifocal placoid pigment epitheliopathy (APMPPE), multifocal choroiditis (MC), ampiginous choroidopathy and serpiginous choroidopathy. The second pattern consisted of fuzzy indistinct appearance of vessels in the intermediate angiographic phase and diffuse choroidal hyperfluorescence in the late phase indicating inflammatory vasculopathy of larger choroidal vessels. This pattern was found in all cases of active Vogt-Koyanagi-Harada disease, ocular sarcoidosis and tuberculosis and birdshot chorioretinopathy. In Behçet's uveitis of recent onset, choriocapillaris perfusion delay and fuzzy choroidal vessels without diffuse late choroidal hyperfluorescence was found. In posterior scleritis, enlargement of vorticous veins was an additionnal ICGA sign. Stromal inflammatory vasculopathy always responded to anti-inflammatory therapy. A third group of patients with severe retinal or choroidal inflammation presented with associated secondary inflammatory choriocapillaropathy angiographically identical to the primary involvement. CONCLUSIONS: ICGA allowed the hitherto impossible characterization of inflammatory involvement of the choroidal vessels, showing either predominant inflammation of the choriocapillaris or predominant inflammation of the stromal choroidal vessels with or without secondary choriocapillaritis. ICGA will be indispensable for the correct evaluation and follow-up of posterior inflammation with suspected choroidal involvement.

Angiography↗

Cogan syndrome.

PURPOSE: To lead ophthalmologists to consider Cogan syndrome when managing a patient presenting with keratitis or other ocular inflammation accompanied by sensorineural hearing loss. METHODS: Seven patients affected by Cogan syndrome were studied: two males and five females, ranging from 27 to 65 years of age (mean age: 41 years). Subjects were evaluated for a period ranging from 22 to 46 months (mean follow up time: 29.2 months). All patients were treated with immunosuppressive drug combination therapy (IDCT). RESULTS: Three patients were affected by classic Cogan syndrome (i.e., vestibuloauditory symptoms and later sensorineural hearing loss and interstitial keratitis). Four patients presented atypical Cogan syndrome (i.e., sensorineural hearing loss and chronic ocular inflammation such as uveitis, scleritis, conjunctivitis, retinal vasculitis, etc.). Four of these patients had a late diagnosis. Two of them were diagnosed when they already had a cochlear implant, one with bilateral deafness underwent cochlear implantation 1 year after the beginning of IDCT, one had severe bilateral hearing loss that improved during the first year of IDCT, and then rapidly worsened to total deafness in 1 month following an episode of severe systemic hypotension. Three patients who had an early diagnosis of Cogan syndrome had no worsening of vestibuloauditory dysfunction during the follow up period. CONCLUSION: Diagnosis of Cogan syndrome should not be overlooked by ophthalmologists in all patients with recurrent ocular inflammatory disease associated with vestibuloauditory symptoms. Early diagnosis is essential to commence the appropriate immunosuppressive therapy that may prevent permanent hearing loss and ocular dysfunction.

Adult↗