Higher infliximab trough levels are associated with perianal fistula healing in patients with Crohn's disease.

BACKGROUND: Infliximab has been found to be efficacious in the treatment of fistulas in the setting of Crohn's disease, even though some patients do not benefit from therapy. AIM: To assess the correlation between perianal fistula healing and trough levels of infliximab. METHODS: In this cross-sectional study, we identified patients with Crohn's disease who had perianal fistulas and were treated with infliximab for at least 24 weeks. We excluded patients who underwent a faecal diversion procedure or proctectomy. Predictive variables included demographics, disease phenotype, disease activity, infliximab levels, anti-infliximab antibodies. The primary outcome was fistula healing defined as the absence of drainage. The secondary outcome was complete fistula closure and mucosal healing. RESULTS: 117 patients were included. Patients with fistula healing had significantly higher median serum infliximab levels when compared to those with active fistulas [15.8 vs. 4.4 µg/mL, respectively (P < 0.0001)]. There was an incremental gain in fistula healing with higher infliximab levels. The AUC for the association between fistula healing and infliximab levels was 0.82 (P < 0.0001), while the AUC for the association of infliximab levels and fistula closure was 0.69 (P = 0.014). Patients with anti-infliximab antibodies had a lower chance of achieving fistula healing (OR: 0.04 [95%CI: 0.005-0.3], P < 0.001). CONCLUSIONS: There is a significant association between serum infliximab levels and rates of fistula healing. Achieving infliximab levels ≥10.1 mcg/mL in patients with Crohn's disease and perianal fistulas may improve outcomes as part of a treat-to-target strategy.

The incidence and risk factors for developing depression after being diagnosed with inflammatory bowel disease: a cohort study.

BACKGROUND: Studies have found that depression is more frequent in patients with inflammatory bowel disease (IBD) than the general population. Clinicians are now trying to pinpoint risk factors for psychological impairment in the IBD population. AIMS: To examine the demographic and phenotypic variables associated with the development of depression among a diverse cohort of IBD patients. We also sought to describe psychotropic therapy prescribed to IBD patients. METHODS: We conducted a retrospective cohort study including patients with Crohn's disease (CD) and ulcerative colitis (UC) without a prior psychiatric diagnosis and followed in the gastroenterology clinics of the private university hospital and public safety net hospital at a large academic centre in Miami (Florida). Predictive variables included demographic characteristics, IBD phenotype, exposure to IBD medications, history of a surgical stoma or seton placement, extra-intestinal manifestations, laboratory indices, aggressive disease and disease activity (based on imaging and endoscopic parameters). Proportional hazard regression models and stepwise Cox regression analysis were used for statistical analysis. RESULTS: Independent predictors of depression were female gender [HR: 1.3 (95% CI: 1.1-1.7), P = 0.01], aggressive disease [HR: 1.4 (95% CI: 1.02-1.9), P = 0.03] and active disease [HR: 1.5 (95% CI: 1.1-2.0), P = 0.04]. In the group that did develop a depressive disorder, 65% received pharmacologic therapy with one or more psychotropic agents. CONCLUSIONS: We found female gender, aggressive disease and increased endoscopic/radiological activity to be independently associated with the development of depression in inflammatory bowel disease.

Early clinical experience with adalimumab in treatment of inflammatory bowel disease with infliximab-treated and naïve patients.

BACKGROUND: Adalimumab, at an induction dose of 160/80 mg followed by 40 mg every other week is approved for treatment of refractory Crohn's disease (CD) and for patients with loss of response to infliximab. AIM: To evaluate the indications for adalimumab, the proportion of inflammatory bowel disease patients who require dose escalation and to identify whether this strategy is effective in inducing or maintaining remission. METHODS: Patients prescribed adalimumab for CD were identified and included for analysis, if they had follow-up of at least 6 weeks. Adalimumab dose was escalated if patients had return of symptoms prior to next dose. Clinical judgment was used to determine severity of disease. A second GI physician confirmed disease severity as determined by the first physician. RESULTS: A total of 48 out of 60 patients met inclusion criteria. Adalimumab was used to treat CD in 47/48 (98%) and ulcerative colitis in one (2%). Most patients had moderate 30/48 (63%) or severe 17/48 (35%) disease. Prior infliximab exposure was present in 42/48 (88%). Adalimumab dose escalation occurred in 14/48 (29%) within an average time of 2.2 months (s.d. 1.5 months). A majority of patients who required dose escalation, nine of 14 (64%) did not improve clinically. Steroids could be discontinued in three of 16 (18.8%). Clinical improvement was noted in 21/48 (43.8%) and one of 48 (2%) patients achieved clinical remission. Adverse drug reactions necessitated drug discontinuation in four of 48 (8%) of patients. CONCLUSIONS: This retrospective review from a single academic medical centre suggests that a minority of patients, who cannot be maintained on 40 mg every other week, of adalimumab benefit from an increased dose. This suggests the need for a treatment with an alternative mode of action in anti-TNF failures.

Role of Toll-like receptors in gastrointestinal malignancies.

Mounting evidence supports the tenet that innate immune responses to luminal microbes participate in the development of gastrointestinal malignancies. The gastrointestinal tract is relatively unique in that it has evolved in the presence of diverse enteric microflora. Intestinal flora is required to develop a normal adaptive immune response in the periphery. With the characterization of the innate immune system, we have begun to understand the adaptations the intestine has made to the microbiota. The interaction between the microbiota and the intestinal mucosa through Toll-like receptors (TLRs) is required to maintain intestinal homeostasis. In particular, intestinal epithelial cells and lamina propria mononuclear cells such as antigen-presenting cells and T cells must respond to breaches in the mucosal barrier by activating TLR-dependent pathways that result in increased epithelial proliferation, wound healing and recruitment of acute inflammatory cells. In the setting of chronic inflammation such as Helicobacter pylori (H. pylori) infection in the stomach or idiopathic inflammatory bowel disease, the process of repair may eventually result in carcinogenesis. The following review highlights human and animal data that support a role for innate immune responses and TLRs specifically in promoting gastrointestinal malignancies. Candidate pathways linking TLRs to gastrointestinal malignancies include activation of nuclear factor-kappaB and cyclooxygenase-2. Studying the link between innate immune signaling and gastrointestinal malignancies offers the possibility to identify novel ways to both prevent and treat gastrointestinal cancer.

TLR4 signalling in the intestine in health and disease.

The colonic epithelium is lined along its apical membrane with approximately 10(14) bacteria/g of tissue. Commensal bacteria outnumber mammalian cells in the gut severalfold. The reason for this degree of commensalism probably resides in the recent recognition of the microbiome as an important source of metabolic energy in the setting of poorly digestible nutrients. As in many themes in biology, the host may have sacrificed short-term benefit, i.e. nutritional advantages, for long-term consequences, such as chronic inflammation or colon cancer. In the present review, we examine the role of TLR (Toll-like receptor) signalling in the healthy host and the diseased host. We pay particular attention to the role of TLR signalling in idiopathic IBD (inflammatory bowel disease) and colitis-associated carcinogenesis. In general, TLR signalling in health contributes to homoeostatic functions. These include induction of antimicrobial peptides, proliferation and wound healing in the intestine. The pathogenesis of IBD, ulcerative colitis and Crohn's disease may be due to increased TLR or decreased TLR signalling respectively. Finally, we discuss the possible role of TLR signalling in colitis-associated neoplasia.

The effect of adrenalectomy on Fos expression in vasopressinergic and oxytocinergic neurons in response to stress in the rat.

This study evaluated the responses of vasopressin (AVP) and oxytocin (OT) neurons to alterations in hypothalamo-pituitary axis activity by adrenalectomy (ADX) or after restraint stress compared with basal conditions. Wistar male rats were perfuse-fixed by cardiac perfusion under anesthesia 3 h, 1, 3 and 14 days after ADX or Sham surgery. Coronal hypothalamic sections were used for evaluation of Fos, AVP and OT expression by immunohistochemistry. Under basal conditions and after stress, Fos-AVP double labeling showed no difference in the magnocellular subdivisions of the paraventricular nuclei (PVN) or in the supraoptic nuclei (SON), suggesting that the magnocellular AVP system is unlikely to contribute to ACTH secretion after restraint in both Sham and ADX rats. Fos-AVP double labeling in the parvocellular medial paraventricular nucleus (PaMP) in ADX groups was increased after 3 h in basal conditions, and in all periods after restraint stress. There were no differences between Sham and ADX groups in Fos-OT double labeling in any subdivision of the PVN; however, in the SON, the number of Fos-OT double labeled cells was increased at all time-points after stress in the ADX group. Fos expression was increased in the PaMP after 3 h and after restraint stress in the Sham and ADX groups, especially in the ADX group. In conclusion, Fos expression in different cell populations of the PVN can be differentially regulated by short- and long-term absence of glucocorticoid negative feedback and also by stress-related excitatory and/or inhibitory neural inputs. The Fos-AVP double labeling findings in the PaMP also indicate a minor participation of these vasopressinergic neurons in the regulation of the HPA axis after ADX.

Time course of vasopressin and oxytocin secretion after stress in adrenalectomized rats.

To characterize the participation of vasopressin (AVP) and oxytocin (OT) in hypothalamus-pituitary-adrenal regulation after adrenalectomy (ADX), we evaluated corticosterone, ACTH, AVP and OT plasma concentrations and AVP and OT content of the paraventricular nucleus (PVN) at different periods (3 h, 1, 3, 7 and 14 days) in sham or ADX rats under basal conditions and after immobilization stress. ADX animals showed undetectable corticosterone levels, while sham animals showed a marked increase in corticosterone and ACTH 3 h after surgery, then lowering to basal control levels. ADX rats showed high basal ACTH levels with a triphasic response without changes after immobilization. After three hours, the ADX group showed higher OT levels than the sham group. OT was increased after immobilization stress in sham and ADX groups. AVP plasma levels did not change throughout the basal or stress studies in either group. There was a decrease in hypothalamic AVP content 1 and 3 days after ADX under basal and stress conditions. Plasma osmolality showed a significant decrease in the ADX group at 3, 7, and 14 days. In conclusion, there are different pituitary-adrenal axis set points after removal of the glucocorticoid negative feedback. The role of vasopressinergic and oxytocinergic neurons in the ACTH secretion after ADX or immobilization stress appears to differ. Magnocellular AVP is unlikely to contribute to ACTH secretion in response to ADX or immobilization stress. On the other hand, OT is elicited by immobilization stress and might contribute to the ACTH secretion during short-term ADX.

Measurement of vitamin D levels in inflammatory bowel disease patients reveals a subset of Crohn's disease patients with elevated 1,25-dihydroxyvitamin D and low bone mineral density.

OBJECTIVES: Many patients with Crohn's disease (CD) have low bone mineral density (BMD) that may not be solely attributable to glucocorticoid use. We hypothesised that low BMD in patients with CD is associated with elevated circulating levels of the active form of vitamin D, 1,25-dihydroxyvitamin D (1,25(OH)(2)D). We further hypothesised that this was secondary to increased synthesis of 1,25(OH)(2)D by inflammatory cells in the intestine. The aim of this study was to examine the relationship between 1,25(OH)(2)D levels and BMD in patients with CD. METHODS: An IRB approved retrospective review of medical records from patients with CD (n = 138) or ulcerative colitis (UC, n = 29). Measurements of vitamin D metabolites and immunoreactive parathyroid hormone (iPTH) were carried out. BMD results were available for 88 CD and 20 UC patients. Immunohistochemistry or real time reverse transcription-polymerase chain reaction (RT-PCR) for the enzyme 1alpha-hydroxylase was performed on colonic biopsies from patients with CD (14) or UC (12) and normal colons (4). RESULTS: Inappropriately high levels of serum 1,25(OH)(2)D (>60 pg/ml) were observed in 42% of patients with CD compared with only 7% in UC, despite no differences in mean iPTH. Serum 1,25(OH)(2)D levels were higher in CD (57 pg/ml) versus UC (41 pg/ml) (p = 0.0001). In patients with CD, there was a negative correlation between 1,25(OH)(2)D levels and lumbar BMD (r = -0.301, p = 0.005) independent of therapeutic glucocorticoid use. 1,25(OH)(2)D levels also correlated with CD activity. Lastly, immunohistochemistry and RT-PCR demonstrated increased expression of intestinal 1alpha-hydroxylase in patients with CD. CONCLUSIONS: These data demonstrate that elevated 1,25(OH)(2)D is more common in CD than previously appreciated and is independently associated with low bone mineral density. The source of the active vitamin D may be the inflamed intestine. Treatment of the underlying inflammation may improve metabolic bone disease in this subgroup of patients.

Phosphatidylinositol 3-kinase-dependent pathways oppose Fas-induced apoptosis and limit chloride secretion in human intestinal epithelial cells. Implications for inflammatory diarrheal states.

The epithelial lining of the intestine serves as a barrier to lumenal bacteria and can be compromised by pathologic Fas-mediated epithelial apoptosis. Phosphatidylinositol (PI)3-kinase signaling has been described to limit apoptosis in other systems. We hypothesized that PI3-kinase-dependent pathways regulate Fas-mediated apoptosis and barrier function in intestiynal epithelial cells (IEC). IEC lines (HT-29 and T84) were exposed to agonist anti-Fas antibody in the presence or absence of chemical inhibitors of PI3-kinase (LY294002 and wortmannin). Apoptosis, barrier function, changes in short circuit current (DeltaI(sc)), and expression of adhesion molecules were assessed. Inhibition of PI3-kinase strongly sensitized IEC to Fas-mediated apoptosis. Expression of constitutively active Akt, a principal downstream effector of the PI3-kinase pathway, protected against Fas-mediated apoptosis to an extent that was comparable with expression of a genetic caspase inhibitor, p35. PI3-kinase inhibition sensitized to apoptosis by increasing and accelerating Fas-mediated caspase activation. Inhibition of PI3-kinase combined with cross-linking Fas was associated with increased permeability to molecules that were <400 Da but not those that were >3,000 Da. Inhibition of PI3-kinase resulted in chloride secretion that was augmented by cross-linking Fas. Confocal analyses revealed polymerization of actin and maintenance of epithelial cell adhesion molecule-mediated interactions in monolayers exposed to anti-Fas antibody in the context of PI3-kinase inhibition. PI3-kinase-dependent pathways, especially Akt, protect IEC against Fas-mediated apoptosis. Inhibition of PI3-kinase in the context of Fas signaling results in increased chloride secretion and barrier dysfunction. These findings suggest that agonists of PI3-kinase such as growth factors may have a dual effect on intestinal inflammation by protecting epithelial cells against immune-mediated apoptosis and limiting chloride secretory diarrhea.

An open-label pilot study using thioguanine as a therapeutic alternative in Crohn's disease patients resistant to 6-mercaptopurine therapy.

BACKGROUND AND AIMS: A substantial number of patients with inflammatory bowel disease (IBD) fail to achieve a complete clinical response with 6-mercaptopurine (6-MP) and azathioprine (AZA). Inability to achieve therapeutic 6-thioguanine nucleotide (6-TGN) levels due to the preferential overproduction of 6-methylmercaptopurine ribonucleotides (6-MMPR) upon dose escalation characterizes a newly described subgroup of IBD patients resistant to 6-MP/AZA therapy. Treatment with 6-thioguanine (6-TG), a related thiopurine, which forms 6-TGNs more directly may be beneficial in such patients. This pilot study evaluated the safety, tolerance, and efficacy of 6-TG in the subgroup of Crohn's disease (CD) patients failing to attain adequate disease control with traditional 6-MP/AZA therapy. METHODS: Ten CD patients with preferential 6-MMPR production upon 6-MP/AZA dose escalation were enrolled in an open-label pilot study. Seven of 10 patients had experienced dose-related 6-MP toxicities. RESULTS: Seventy percent of the patients (7 of 10) responded or were in remission at week 16. Clinical response was evident by week 4 in most. 6-TGN levels were nine-fold higher with 6-TG treatment than with 6-MP, whereas 6-MMPR levels were undetectable. No patient developed a recurrence of hepatic or hematological toxicity. CONCLUSIONS: 6-TG was a safer and more efficacious thiopurine in this subgroup of IBD patients resistant to 6-MP therapy. Larger controlled trials are warranted to further evaluate both the short- and long-term safety and efficacy in this subgroup of patients as well as a broader spectrum of IBD patients.

Modulation of barrier function during Fas-mediated apoptosis in human intestinal epithelial cells.

BACKGROUND & AIMS: Intestinal epithelial cell apoptosis occurs continually without apparent permeability defects and is increased in response to intestinal inflammation. We hypothesized that increased, immune-mediated apoptosis during inflammation might result in barrier dysfunction of the epithelium. METHODS: T84 cells were cultured as a polarized monolayer and exposed to agonist antibody to Fas. Barrier function was assessed by transepithelial resistance and permeability measurements. Immunofluorescent staining was used to examine junctional protein expression. RESULTS: Fas expression is predominantly basolateral in polarized T84 monolayers. Basolateral cross-linking of the Fas receptor resulted in T84 cell apoptosis and a loss of 50% of the cells within 24 hours. Apoptosis was coincident with a decrease in transepithelial electrical resistance and increased flux of small but not large molecules. Preservation of barrier function was associated with dramatic rearrangement of tight junctions and desmosomal junctions in apoptotic monolayers. E-cadherin-mediated cell contact was maintained between intact cells in the monolayer, thus sealing gaps created by apoptotic cells. Apoptosis and barrier dysfunction could be prevented by caspase inhibition. CONCLUSIONS: Immune-mediated apoptosis of intestinal epithelial cells may contribute to the permeability defects associated with inflammatory conditions of the bowel, but the intestinal epithelium is remarkably resilient in the face of apoptosis.

Efficacy of mycophenolate mofetil in patients failing 6-mercaptopurine or azathioprine therapy for Crohn's disease.

Mycophenolate mofetil (MMF) is a novel immunomodulator that may be effective in the treatment of chronic active and perianal Crohn's disease (CD). The aim of this study is to assess the efficacy of MMF in CD patients who failed or were intolerant of 6-mercaptopurine (6-MP) or azathioprine (AZA). Eleven CD patients were treated with MMF after a failed course of 6-MP/AZA, and their records reviewed retrospectively. Reasons for 6-MP/AZA intolerance or failure were recorded. Response to MMF was determined by calculation of the Harvey-Bradshaw index and ability to taper steroids. Adverse reactions to MMF were recorded. Eleven patients were identified who failed a previous trial of 6-MP/AZA and other immunomodulators and required immunomodulator therapy. Of 11 patients who started MMF, four had early adverse reactions within 8 weeks and stopped the medication. Of the remaining seven patients who took MMF for at least 8 weeks, one had a complete response, two had a partial response, and four had no response to the medication. In patients who failed 6-MP/AZA, MMF was of benefit in 3 of 11 patients with only one complete responder. This lower-than-expected response rate may indicate that patients who are resistant to 6-MP or AZA may also be resistant to MMF.

Toxoplasmose ocular em Venda Nova do Imigrante, ES, Brasil / Ocular toxoplasmosis at Venda Nova do Imigrante, ES, Brasil

Realizamos um estudo amostral populacional para melhor conhecer a prevalência de toxoplasmose ocular em Venda Nova do Imigrante, ES e compará-la co a prevalência de lesöes em outras regiöes do Brasil. De 1074 pessoas examinadas , 11.27 por cento foram diagnosticadas como portadoras de toxoplasmose ocular, baseado em achados fundoscópicos. Esta prevalência foi superior à existente nos Estados Unidos (0.6 por cento) e em Säo Paulo (9 por cento), mas inferior à de Erechin, RS (17.7 por cento). Foram encontrados quatro casos familiares (2 famílias com dois irmäos näo gêmeos e 2 famílias com casos de mäes e filhos afetados), sugerindo toxoplasmose adquirida. A acuidade visual foi igual ou inferior a 20/200 em 7 por cento dos olhos com lesöes oculares devido a presença de lesöes maculares.

Prospective and controlled study of ophthalmopathy after radioiodine therapy for Graves' hyperthyroidism.

The effects of radioiodine (131I) therapy for hyperthyroidism on the ocular process of Graves' disease is controversial. In order to evaluate the outcome of ophthalmopathy after radioiodine therapy for thyrotoxicosis we studied prospectively 30 Graves' hyperthyroid patients, 22 submitted to radioiodine (131I) treatment (group A) and 8 treated with antithyroid drugs (group B). All patients were evaluated by clinical ophthalmologic examination, and ocular proptosis (OP) was measured with both a Hertel exophthalmometer (HE) and computed tomography (CT) before and 4 to 7 months after therapy. No statistical difference was obtained between pre- and post-treatment OP measurements in each eye in either group, and we did not observe worsening in the ophthalmopathy of patients treated with drugs or radioiodine. After therapy, there was an improvement in the clinical signs of ophthalmopathy in 59% of group A and in 37.5% of group B patients. We found a significant correlation between OP measured by HE and by CT. CT findings showed an increase in orbital fat and/or muscle thickening in all patients at baseline, proving to be a useful procedure for ophthalmologic diagnosis in doubtful cases. No patient in either group developed hypothyroidism or elevated TSH levels during the study period; this may explain our good results in the evolution of Graves' ophthalmopathy after treatment with 131I and antithyroid drugs. Euthyroidism seems to be an important factor in the outcome of ophthalmopathy after therapy, whatever the mode of treatment chosen to achieve it.

Achados oftalmológicos em AIDS: avaliaçäo de 445 casos atendidos em um ano / Ophtalmological manifestations in AIDS: evaluation of 445 patients in one year

Os autores avaliaram 445 pacientes HIV positivos e identificaram as manifestaçöes oftalmológicas presentes nesses pacientes. OBJETIVO. Identificar e correlacionar as alteraçöes oftalmológicas com dados de literatura, bem como correlacioná-las com as diversas manifestaçöes clínicas presentes na síndrome. MÉTODOS. Foram estudados 445 pacientes ambulatoriais HIV (com 66 por cento e sem 34 por cento AIDS), sendo 87 por cento do sexo masculino e 58,2 por cento homossexuais, no período de um ano, atendidos na Escola Paulista de Medicina, Hospital Säo Paulo. RESULTADOS. Do total de pacientes examinados, 52 por cento apresentaram alteraçöes oculares secundárias à infecçäo pelo HIV ao primeiro exame (27 por cento bilaterais). A retinite por citomegalovírus esteve presente em 25 por cento deles, seguida por toxoplasmose ocular (8,5 por cento), retinite por herpes (3,6 por cento), papiledema (2,2 por cento), atrofia óptica (1,6 por cento), phthisis bulbi (1,5 por cento), coroidite multifocal (1,2 por cento), hemorragia retiniana (0,9 por cento), uveíte por sífilis (0,6 por cento) e oclusäo da veia central da retina (0,2 por cento). CONCLUSAO. Nossos dados estäo de acordo com a literatura mundial, com exceçäo feita à retinocoroidite por toxoplasmose, que mostrou muito maior freqüência em nosso meio, se comparada à da literatura. Pudemos observar, também, uma alta taxa de descolamento de retina secundário à inflamaçäo intra-ocular. Nenhum caso de coroidite por Pneumocystis carinii foi diagnosticado nessa época

Cérato-conjuntivite por microsporídeo em AIDS: descriçäo do primeiro caso brasileiro e revisäo da literatura / Microsporidial kerato-conjunctivitis in AIDS: description of the brazilian first case and literature review

Relato do conhecimento dos autores sobre o primeiro caso diagnosticado na América do Sul

Arachidonic acid cascade and platelet-activating factor in the network of eye inflammatory mediators: therapeutic implications in uveitis.

The cellular and biochemical events triggered by uveitis involve a complex array of cells and a heterogeneous network of mediators of intraocular inflammation. Resident cells are activated and inflammatory cells are recruited. Chemical mediators from the arachidonic acid cascade, prostaglandins, hydroxyeicosatetraenoic acids, and leukotrienes, are formed. Several of these metabolites are modulators of cellular functions, but when generated in sustained, excessive amounts, they contribute to enhanced vascular permeability and to the onset of pathophysiological responses. Another very active membrane-derived mediator is platelet-activating factor. This important mediator of immune and inflammatory responses may play a central role in uveitis due to cell priming, since interleukin-1, tumor necrosis factor, and other as yet unidentified mediators are also being generated. The concomitant accumulation of these networks of mediators in various parts of the uveal tract leads to spreading of the intraocular inflammatory response and cellular damage. At both early and late stages of uveitis, the generation of free radicals is also a major contributor to the impairment of function. Free radicals are generated in two distinct sites: in the oxidative burst of recruited white cells and in free radical formation and lipid peroxidation in resident cells. The identification of the cellular events that lead to the accumulation of networks of mediators of inflammation and their effects has important therapeutic implications in uveitis.

Ultrasonic fragmentation of cataract in uveitis.

Thirty-nine eyes with uveitis from various causes, and complicated by cataract and vitreous opacification, underwent pars plana lensectomy and vitrectomy by ultrasonic fragmentation. Anatomical results were excellent, with clearing of all lens and vitreous opacities in all eyes. Visual results showed that there was no exacerbation and no recurrence of uveitis. Visual results depended mainly on the presence of previous damage of the uveitis to the retina and optic nerve. Visual results did not depend on the presence of uveitis activity at the time of the surgery. Complications that occurred were cystoid macular edema, which was present in 17.94% of the eyes and diagnosed in some eyes at the surgery, retinal detachment in one eye (2.56%), sterile hypopyon in one eye (2.56%), and ultrasonic lesion of the retina in one eye (2.56%). Visions of 20/20 to 20/40 were obtained in 23% of the eyes, 20.5% had vision between 20/50 and 20/80, and 56.4% had vision of 20/100 or less. The good results justify the surgical intervention in cases of cataracts associated with uveitis. Pars plana lensectomy and vitrectomy appears to be the procedure of choice in removal of cataracts secondary to uveitis.