Delphi study to identify consensus on patient selection for hydrogel rectal spacer use during radiation therapy for prostate cancer in the UK.

OBJECTIVES: To identify consensus on patient prioritisation for rectal hydrogel spacer use during radiation therapy for the treatment of prostate cancer in the UK. DESIGN: Delphi study consisting of two rounds of online questionnaires, two virtual advisory board meetings and a final online questionnaire. SETTING: Radical radiation therapy for localised and locally advanced prostate cancer in the UK. PARTICIPANTS: Six leading clinical oncologists and one urologist from across the UK. INTERVENTIONS: Rectal hydrogel spacer. PRIMARY AND SECONDARY OUTCOME MEASURES: None reported. RESULTS: The panel reached consensus on the importance of minimising toxicity for treatments with curative intent and that even low-grade toxicity-related adverse events can significantly impact quality of life. There was agreement that despite meeting rectal dose constraints, too many patients experience rectal toxicity and that rectal hydrogel spacers in eligible patients significantly reduces toxicity-related adverse events. However, as a consequence of funding limitations, patients need to be prioritised for spacer use. A higher benefit of spacers can be expected in patients on anticoagulation and in patients with diabetes or inflammatory bowel disease, but consensus could not be reached regarding patient groups expected to benefit less. While radiation therapy regimen is not a main factor determining prioritisation, higher benefit is expected in ultrahypofractionated regimens. CONCLUSION: There is a strong and general agreement that all patients with prostate cancer undergoing radical radiation therapy have the potential to benefit from hydrogel spacers. Currently, not all patients who could potentially benefit can access hydrogel spacers, and access is unequal. Implementation of the consensus recommendations would likely help prioritise and equalise access to rectal spacers for patients in the UK.

Metastatic Anorectal Melanoma Presenting as Seizures: An Infrequent Culprit.

Anorectal malignant melanoma is a rare culprit of malignancies in the anorectal region. With a presentation that mimics the vastly more common colorectal tumours, clinical misdiagnosis and diagnostic delays often occur, contributing to a dismal prognosis. The authors report a case of metastatic anorectal malignant melanoma presenting as seizures. Though our standard diagnostic pathway for suspected anorectal malignancies was followed, and despite the patient having computerized tomography (CT) of the head earlier, this presentation nonetheless led to a prolongation of time needed to reach histological diagnosis and delay in commencing definitive treatment. It also highlights the paucity of research into the pathophysiology and management of this infrequent but aggressive disease, and the need for raising awareness about this condition to the medical community so that it is considered as a plausible differential diagnosis from the outset and diagnostic pathways adjusted accordingly.

Drug-induced Sarcoid Uveitis with Biologics.

PURPOSE/OBJECTIVES: to evaluate new onset uveitis or reactivated uveitis by biologic agents and characterize their features. MATERIALS AND METHODS: This is a multicenter, retrospective case series. Patients under biologic therapy were included if they developed uveitis for the first time or experienced intraocular inflammation which was different in location or laterality to previous inflammation. RESULTS: Sixteen patients were identified. The underlying disorders included ankylosing spondylitis, juvenile idiopathic arthritis, rheumatoid arthritis, and Behçet's Disease. The biologic agents associated with a first episode of uveitis (n = 11) or with a new recurrence of uveitis (n = 5) were etanercept, adalimumab, abatacept, infliximab, and golimumab. Sarcoidosis based on bihilar lymphadenopathy, other computer tomography-findings, or biopsy was diagnosed in five patients under therapy with etanercep, adalimumab, and abatacept. Additionally, seven patients developed clinical changes in their uveitis pattern, suggesting sarcoid uveitis. CONCLUSIONS: Biologic treatment-induced uveitis often presents as granulomatous disease.

Disease Expression and Familial Transmission of Fuchs Endothelial Corneal Dystrophy With and Without CTG18.1 Expansion.

Purpose: To characterize inheritance, penetrance, and trinucleotide repeat expansion stability in Fuchs endothelial corneal dystrophy (FECD). Methods: One thousand unrelated and related subjects with and without FECD were prospectively recruited. CTG18.1 repeat length (CTG18.1L) was determined via short tandem repeat assay and Southern blotting of leukocyte DNA. Multivariable logistic regression and generalized estimating equation models were employed. Results: There were 546 unrelated FECD cases (67.6% female; 70 ± 10 years) and 235 controls (63.8% female; 73 ± 8 years; all ≥ 50 years). CTG18.1 expansion (CTG18.1exp+) was observed in 424 (77.7%) cases and 18 (7.7%) controls (P = 2.48 × 10-44). CTG18.1 expansion was associated with FECD severity (P = 5.62 × 10-7). The family arm of the study included 331 members from 112 FECD-affected families; 87 families were CTG18.1exp+. Autosomal dominant inheritance with variable expression of FECD was observed, regardless of expansion status. FECD penetrance of CTG18.1 expansion increased with age, ranging from 44.4% in the youngest (19-46 years) to 86.2% in the oldest (64-91 years) age quartiles. Among 62 parent-offspring transmissions of CTG18.1exp+, 48 (77.4%) had a change in CTG18.1L ≤ 10 repeats, and eight (12.9%) were ≥50 repeats, including five large expansions (∼1000-2000 repeats) that contracted. Among 44 offspring who did not inherit the CTG18.1exp+ allele, eight (18.2%) exhibited FECD. Conclusions: CTG18.1 expansion was highly associated with FECD but demonstrated incomplete penetrance. CTG18.1L instability occurred in a minority of parent-offspring transmissions, with large expansions exhibiting contraction. The observation of FECD without CTG18.1 expansion among family members in CTG18.1exp+ families highlights the complexity of the relationship between the FECD phenotype and CTG18.1 expansion.

No clinically significant association between CFH and ARMS2 genotypes and response to nutritional supplements: AREDS report number 38.

OBJECTIVE: To determine whether genotypes at 2 major loci associated with late age-related macular degeneration (AMD), complement factor H (CFH) and age-related maculopathy susceptibility 2 (ARMS2), influence the relative benefits of Age-Related Eye Disease Study (AREDS) supplements. DESIGN: Unplanned retrospective evaluation of a prospective, randomized, placebo-controlled clinical trial of vitamins and minerals for the treatment of AMD. SUBJECTS: AREDS participants (mean age, 69 years) who were at risk of developing late AMD and who were randomized to the 4 arms of AREDS supplement treatment. METHODS: Analyses were performed using the Cox proportional hazards model to predict progression to late AMD (neovascular or central geographic atrophy). Statistical models, adjusted for age, gender, smoking status, and baseline AMD severity, were used to examine the influence of genotypes on the response to therapy with 4 randomly assigned arms of AREDS supplement components: placebo, antioxidants (vitamin C, vitamin E, ß-carotene), zinc, or a combination. MAIN OUTCOME MEASURES: The influence of the genotype on the relative treatment response to the randomized components of the AREDS supplement, measured as progression to late AMD. RESULTS: Of the 1237 genotyped AREDS participants of white ethnicity, late AMD developed in 385 (31.1%) during the mean follow-up of 6.6 years. As previously demonstrated, CFH genotype (P = 0.005), ARMS2 (P< 0.0001), and supplement were associated individually with progression to late AMD. An interaction analysis found no evidence that the relative benefits of AREDS supplementation varied by genotype. Analysis of (1) CFH rs1061170 and rs1410996 combined with ARMS2 rs10490924 with the 4 randomly assigned arms of AREDS supplement and (2) analysis of the combination of CFH rs412852 and rs3766405 with ARMS2 c.372_815del443ins54 with the AREDS components resulted in no interaction (P = 0.06 and P = 0.45, respectively, before multiplicity adjustment). CONCLUSIONS: The AREDS supplements reduced the rate of AMD progression across all genotype groups. Furthermore, the genotypes at the CFH and ARMS2 loci did not statistically significantly alter the benefits of AREDS supplements. Genetic testing remains a valuable research tool, but these analyses suggest it provides no benefits in managing nutritional supplementation for patients at risk of late AMD.

Does prostate HistoScanning™ play a role in detecting prostate cancer in routine clinical practice? Results from three independent studies.

OBJECTIVES: To evaluate the ability of prostate HistoScanning™ (PHS; Advanced Medical Diagnostics, Waterloo, Belgium) to detect, characterize and locally stage prostate cancer, by comparing it with transrectal ultrasonography (TRUS)-guided prostate biopsies, transperineal template prostate biopsies (TTBs) and whole-mount radical prostatectomy specimens. SUBJECTS AND METHODS: Study 1. We recruited 24 patients awaiting standard 12-core TRUS-guided biopsies of the prostate to undergo PHS immediately beforehand. We compared PHS with the TRUS-guided biopsy results in terms of their ability to detect cancer within the whole prostate and to localize it to the correct side and to the correct region of the prostate. Lesions that were suspicious on PHS were biopsied separately. Study 2. We recruited 57 patients awaiting TTB to have PHS beforehand. We compared PHS with the TTB pathology results in terms of their ability to detect prostate cancer within the whole gland and to localize it to the correct side and to the correct sextant of the prostate. Study 3. We recruited 24 patients awaiting radical prostatectomy for localized prostate cancer to undergo preoperative PHS. We compared PHS with standardized pathological analysis of the whole-mount prostatectomy specimens in terms of their measurement of total tumour volume within the prostate, tumour volume within prostate sextants and volume of index lesions identified by PHS. RESULTS: The PHS-targeted biopsies had an overall cancer detection rate of 38.1%, compared with 62.5% with standard TRUS-guided biopsies. The sensitivity and specificity of PHS for localizing tumour to the correct prostate sextant, compared with standard TRUS-guided biopsies, were 100 and 5.9%, respectively. The PHS-targeted biopsies had an overall cancer detection rate of 13.4% compared with 54.4% for standard TTB. PHS had a sensitivity and specificity for cancer detection in the posterior gland of 100 and 13%, respectively, and for the anterior gland, 6 and 82%, respectively. We found no correlation between total tumour volume estimates from PHS and radical prostatectomy pathology (Pearson correlation coefficient -0.096). Sensitivity and specificity of PHS for detecting tumour foci ≥0.2 mL in volume were 63 and 53%. CONCLUSIONS: These three independent studies in 105 patients suggest that PHS does not reliably identify and characterize prostate cancer in the routine clinical setting.

Seven new loci associated with age-related macular degeneration.

Age-related macular degeneration (AMD) is a common cause of blindness in older individuals. To accelerate the understanding of AMD biology and help design new therapies, we executed a collaborative genome-wide association study, including >17,100 advanced AMD cases and >60,000 controls of European and Asian ancestry. We identified 19 loci associated at P < 5 × 10(-8). These loci show enrichment for genes involved in the regulation of complement activity, lipid metabolism, extracellular matrix remodeling and angiogenesis. Our results include seven loci with associations reaching P < 5 × 10(-8) for the first time, near the genes COL8A1-FILIP1L, IER3-DDR1, SLC16A8, TGFBR1, RAD51B, ADAMTS9 and B3GALTL. A genetic risk score combining SNP genotypes from all loci showed similar ability to distinguish cases and controls in all samples examined. Our findings provide new directions for biological, genetic and therapeutic studies of AMD.

Administration of repeat intravitreal anti-VEGF drugs by retina specialists in an injection-only clinic for patients with exudative AMD: patient acceptance and safety.

PURPOSE: To report patient acceptance and safety of repeated intravitreal injections of anti-VEGF agents for exudative AMD, by retina specialists, without an eye examination before every injection. METHODS: Retrospective chart review. 115 eyes (110 patients) with exudative AMD underwent repeated intravitreal anti-VEGF injections with limited interval examination and diagnostic testing. Medication, laterality, number of injection cycles started and completed, number of injections per injection cycle, subjective visual changes, pre- and post-injection visual acuity (VA), pre- and post-injection intraocular pressure (IOP), nurse- and patient-initiated phone calls, emergency (non-scheduled) clinic visits, complications, new diagnoses, and patient complaints after each injection were recorded. The main outcome measures were complications and patient complaints. RESULTS: 396 injections were administered in the injection clinic to 110 patients in 175 injection cycles (range: 0 to 5 injections per cycle). Of 175 injection cycles, there were 134 uninterrupted cycles and 41 interrupted cycles where an eye exam was performed. Fourteen new diagnoses were made: six during emergency visits, three at injection clinic appointments, and five at the next full examination after completion of a prescribed injection clinic cycle. CONCLUSIONS: Administration of anti-VEGF injections in a designated injection clinic, by retina specialists, according to a prescribed schedule, and with limited pre-injection testing, for patients with wet AMD, is well-tolerated.

Genome-wide association analyses of genetic, phenotypic, and environmental risks in the age-related eye disease study.

PURPOSE: To present genome-wide association analyses of genotypic and environmental risks on age-related macular degeneration (AMD) using 593 subjects from the age-related eye disease study (AREDS), after adjusting for population stratification and including questionable controls. METHODS: Single nucleotide polymorphism (SNP) associations with AMD for the non-Hispanic white population were investigated using a log-additive model after adjusting for population stratification. Replication of possible SNP-disease association was performed by genotyping an independent group of 444 AMD case and 300 control subjects. Logistic regression models were used to assess interaction effects between smoking and SNPs associated with AMD. Independent genetic risk effects among the disease-associated SNPs were also investigated using multiple logistic regression models. RESULTS: Population stratification was observed among the individuals having a self-reported race of non-Hispanic white. Risk allele frequencies at established AMD loci demonstrated that questionable control subjects were similar to control subjects in the AREDS, suggesting that they could be used as true controls in the analyses. Genetic loci (complement factor H [CFH], complement factor B [CFB], the age-related maculopathy susceptibility 2 locus containing the hypothetical gene [LOC387715]/the high-temperature requirement A-1 [HTRA1], and complement component 3 [C3]) that were already known to be associated with AMD were identified. An additional 26 novel SNPs potentially associated with AMD were identified, but none were definitely replicated in a second independent group of subjects. Smoking did not interact with known AMD loci, but was associated with late AMD. Statistically independent genetic signals were observed within the Pleckstrin homology domain-containing family A member 1 (PLEKHA1) region near LOC387715/HTRA1 and within a haplotype spanning exon 19 of the C3 gene. CONCLUSIONS: Population stratification among Caucasian subjects from the multicentered AREDS was observed, suggesting that it should be adjusted for in future studies. The AREDS questionable control subjects can be used as control subjects in the AREDS genome-wide association study (GWAS). Smoking was an independent risk factor for advanced AMD in the AREDS subjects. There continues to be evidence that the 10q26 (age-related maculopathy susceptibility 2 gene [ARMS2]) locus spanning PLEKHA1-LOC387715-HTRA1 and the C3 gene may contain multiple independent genetic risks contributing to AMD.

Same-day triple therapy with photodynamic therapy, intravitreal dexamethasone, and bevacizumab in wet age-related macular degeneration.

PURPOSE: To report the results of same-day triple therapy with reduced fluence photodynamic therapy, intravitreal dexamethasone, and bevacizumab in patients with neovascular age-related macular degeneration. METHODS: Retrospective case series. Records of patients who received same-day triple therapy with reduced fluence photodynamic therapy (25 J/cm), intravitreal dexamethasone (200 microg), and intravitreal bevacizumab (1.25 mg) were reviewed. All patients had neovascular subfoveal age-related macular degeneration with at least 1 year of follow-up. Snellen visual acuity (VA), central macular thickness on optical coherence tomography, intraocular pressure, and endophthalmitis occurrence were recorded. RESULTS: The 31 patients were observed for a mean of 13.7 months. In all patients, mean baseline VA was 20/80 and vision at final follow-up was 20/60 (P = 0.69). In patients who received previous treatment for exudative age-related macular degeneration (n = 18), mean baseline VA was 20/100 and vision at final follow-up (mean, 13.7 months) was 20/100 (P = 0.31). In treatment-naïve patients (n = 13), mean baseline VA was 20/60 and vision at final follow-up (mean, 13.5 months) was 20/40 (P = 0.31). In all patients, mean central macular thickness was 293 mum at baseline and 245 mum at final follow-up (P = 0.053). In previously treated patients (n = 18), mean central macular thickness was 325 mum at baseline and 265 mum at final follow-up (P = 0.10). In treatment-naïve patients, mean central macular thickness was 249 mum at baseline (n = 13) and 218 mum at final follow-up (P = 0.34). Previously treated patients required more antivascular endothelial growth factor injections (mean = 3.6) than treatment-naïve patients (mean = 0.8), but the mean number of repeat triple therapy treatments was 0.3 in both groups. Changes in intraocular pressure and endophthalmitis were not observed during follow-up. CONCLUSION: Same-day triple therapy maintained VA and decreased macular thickness in patients with and without previous antivascular endothelial growth factor therapy. Triple therapy may reduce the number of antivascular endothelial growth factor injections in some patients and stabilize vision in some patients not responding to antivascular endothelial growth factor therapy.

Bilateral simultaneous intravitreal injections in the office setting.

PURPOSE: To report the outcomes and complications of bilateral simultaneous intravitreal injections performed in the office. DESIGN: Retrospective case series. METHODS: Records of 35 patients receiving simultaneous bilateral intravitreal injections between November 2007 and November 2008 were reviewed. Data collected included indication for injection, preinjection and postinjection intraocular pressure (IOP), preinjection and postinjection visual acuity (VA), and complications/complaints after each injection. RESULTS: A total of 208 injections were administered to 35 patients, with a mean of 5.9 injections per patient (range, 2 to 14; standard deviation [SD], 3.68). One hundred and thirty-three eyes received bevacizumab (Avastin; Genentech Inc, South San Francisco, California, USA) alone, 14 received bevacizumab plus preservative-free intravitreal triamcinolone or Triescence (Kenalog; Bristol-Myers Squibb Co, New York, New York, USA), 56 received ranibizumab (Lucentis; Genentech Inc), and 5 received bevacizumab plus dexamethasone (Decadron; Merck, Whitehouse Station, New Jersey, USA). Mean time of postinjection follow-up was 39 days. Postinjection VA follow-up measurements were available for 194 injections. The indication for initiating therapy was choroidal neovascularization from age-related macular degeneration (49 eyes), diabetic macular edema (ME) (13 eyes), proliferative diabetic retinopathy (4 eyes), ME attributable to retinal vein occlusion (2 eyes), and ME attributable to autoimmune retinopathy (2 eyes). The mean VA before each injection was 20/96 and at the next follow-up was 20/91 (P = .40). One patient had a painless, culture-negative endophthalmitis in 1 eye 3 days after bilateral bevacizumab; at 1 year VA improved from 20/400 to 20/80. CONCLUSIONS: Simultaneous bilateral intravitreal injections in the office are well tolerated. A separate povidone-iodine preparation, speculum, needle, and syringe were used for each eye. None of the patients requested alternating unilateral injections, after receiving bilateral injections. Patients should be counseled as to the risk of complications.

Infectious endophthalmitis after intravitreal injection of antiangiogenic agents.

PURPOSE: To evaluate the rate of infectious endophthalmitis associated with intravitreal injection of bevacizumab, ranibizumab, and pegaptanib sodium. METHODS: A retrospective review of patients who received intravitreal injections of bevacizumab, ranibizumab, and pegaptanib sodium was undertaken. Cases of clinical diagnoses of endophthalmitis or suspected endophthalmitis resulting from intravitreal injection were identified and reviewed. From these data, the risk per injection was estimated. RESULTS: Three patients developed endophthalmitis after the intravitreal injection. The risk per injection was 0.00077 (0.077%). The rate of endophthalmitis was 1 per 1,291 injections. CONCLUSION: A similar risk of endophthalmitis per injection compared with some trials was obtained in this study. Although no definite risk factors could be identified, intravitreal injections performed by nonretina specialist physicians may be a risk factor for the development of endophthalmitis.

Complement component 3 (C3) haplotypes and risk of advanced age-related macular degeneration.

PURPOSE: Nonsynonymous coding single nucleotide polymorphisms (nsSNPs) in complement component 3 (C3) alter the risk of age-related macular degeneration (AMD). This was a study of the effect of haplotypes across C3 on AMD risk. METHODS: Nine SNPs tagging haplotypes across C3 were genotyped on 738 subjects at the Mayo Clinic. Haplotype analyses were performed with and without conditioning on individual SNPs. Replication studies were performed using 1541 subjects from the age-related eye disease study (AREDS). RESULTS: Two nsSNPs located 5125 bp apart in the 5' end of C3 showed the highest association (rs1047286 or P314L, P = 9.2E-05; rs2230199 or R102G, P = 4.1E-05) with AMD. The minor alleles of both SNPs tagged a single risk haplotype. The effects of the two nsSNPs could not be distinguished due to high linkage disequilibrium. The risk SNPs preferentially promoted the development of advanced AMD relative to early AMD in both the Mayo and AREDS subjects. Haplotypes in the 3' end of the C3 locus were associated with AMD in both the Mayo and AREDS subjects. The effect persisted after conditioning on the nsSNPs only in the Mayo subjects. No interaction was found between rs2230199 and smoking or other AMD loci. CONCLUSIONS: nsSNPs in C3 increased the risk of developing AMD 1.8-fold for 1 risk allele or 2.4-fold for two risk alleles and were preferentially associated with advanced AMD. Further study is needed to determine whether haplotypes in the 3' end of C3 have an independent association with AMD.

Focal radiation therapy for patients with persistent/recurrent pituitary adenoma, despite previous radiotherapy.

With the stricter endocrine definitions of cure following conventionally planned and fractionated radiotherapy for functioning pituitary adenomas, together with the move in the profession (since the advent of high quality MRI) to postpone radiation therapy until macroscopic disease appears after surgery, it is now realised that cure rates following conventional radiotherapy approximate three out of four rather than the >90% cited for more than a decade. Patients with persistent active tumours may be successfully further treated by focal radiation therapy by one of the stereotactic focal techniques. We have experience of such re-treatment radiation therapy in 50 patients. With careful case selection, we here demonstrate that in acromegaly, for example, normalisation of both GH and IGF levels may be achieved in 37-58% of these previously irradiated patients with low risk of late morbidity. Unquestionably, growth delay occurs in many cases but the long term tumour control rate has yet to be established.

Noninfectious endophthalmitis occurring after intravitreal triesence injection.

PURPOSE: To report a case of noninfectious endophthalmitis occurring after intravitreal Triesence (preservative-free triamcinolone acetonide) injection. METHOD: Case report. RESULTS: A 62-year-old patient with macular edema occurring after cataract surgery received 0.1 mL (4 mg) of intravitreal Triesence to the left eye. His vision was 20/60. One day later, he presented with a decrease in vision to light perception upon awakening. He denied ocular pain, and the eye was not red. Clinical examination was remarkable for orbital proptosis, minimal fibrin on the anterior chamber intraocular lens, and a white hypopyon. There was no view of the retina due to vitreous opacities. A vitreous tap and injection of intravitreal Ceftazidime and Vancomycin were performed. Microbiology showed no organisms on gram stain, and the cultures were negative. The endophthalmitis resolved, and the patient recovered vision to 20/70. CONCLUSIONS: Noninfectious endophthalmitis can occur after preservative-free commercially available intravitreal Triesence. This case suggests that noninfectious endophthalmitis can occur in the absence of the benzyl alcohol found in preserved preparations of Kenalog.

Persisent ocular hypertension following intravitreal ranibizumab.

BACKGROUND: To describe the occurrence of ocular hypertension in four patients following injection of ranibizumab intravitreally. METHODS: Case series. RESULTS: Four patients had high intraocular pressure after intravitreal ranibizumab 0.5 mg. Ocular hypertension occurred 1 month after the second ranibizumab injection in patients 1 and 3, and 1 month after the first ranibizumab in patient 2. In patient 4, it occurred several hours after the first ranibizumab injection. In all patients, the IOP increase was sustained across several visits, requiring control with topical glaucoma therapy, and in two cases the addition of a systemic carbonic anhydrase inhibitor. None of the patients had a previous history of glaucoma, ocular hypertension or IOP asymmetry and the IOP was as high as 30, 34, 46, and 50 mmHg in the four patients. CONCLUSION: Severe and sustained ocular hypertension may occur after intravitreal ranibizumab. Although the mechanism of the pressure rise is unknown, all eyes in our series were controlled with medical therapy.

Intraocular inflammation following intravitreal injection of bevacizumab.

BACKGROUND: Injection of drugs into the vitreous can lead to intraocular inflammation through infectious and non-infectious processes. Failure to recognize an eye with anterior chamber and vitreous cell as sterile inflammation can lead to unnecessary treatment for endophthalmitis. METHODS: Four cases of uveitis following intravitreal bevacizumab (Avastin) for exudative age-related macular degeneration are described followed by review of the literature. RESULTS: Four patients presented with uveitis. Two patients presented with pain and red eye associated with iritis and two patients with vitritis, several days following intravitreal injection of bevacizumab. No paracentesis was performed and no corneal epithelial defect was created. Both patients with iritis were presumed to have sterile intraocular inflammation since the anterior chamber cell was much greater than the vitreous cell and resolved with cycloplegic and topical corticosteroid therapy. The third patient presented only with vitreous cell which resolved without therapy. The fourth patient had anterior chamber cell and vitreous cell with clumps, which resolved with topical prednisolone acetate. The inflammation resolved in all cases within 1 to 2 weeks. CONCLUSION: There are few published cases of uveitis following bevacizumab. With its rising use, it is important to be aware of its potential to be associated with intraocular inflammation.

Molecular genetics of AMD and current animal models.

During the past few years systematic investigation into the epidemiology, genetics, and pathophysiology of age-related macular degeneration (AMD) has provided important new insight into this leading cause of vision loss in older persons. These studies provide a view of AMD as a complex trait influenced by well-established genetic and environmental risks that leads to the deposition of inflammatory deposits in the outer retina. This maculopathy leads to visual dysfunction through a variety of mechanisms and complications that can be observed in both humans and animal models. In this review, the risks associated with AMD in humans and the animal models used to study AMD and its complications will be summarized. No effort has been made to perform a comprehensive citation of all areas of AMD genetics and animal models, but rather a selection of observations and supporting references illustrative of the current state of the field is presented.