Lost to follow-up of patients who received intravitreal anti-vascular endothelial growth factor therapy to treat four different retina disorders in an individual center in Brazil.

Objectives: To identify risk factors for loss to follow-up in periodic intravitreal anti-vascular endothelial growth factor injections for the treatment patients with diabetic macular edema, subretinal neovascularization, age-related macular degeneration, and retinal vein occlusion in a single eye center in São Paulo, Brazil. Methods: This was a retrospective longitudinal study that gathered information from 992 patients who required intravitreal anti-vascular endothelial growth factor drugs over 6 months. The authors included age, eye disease, laterality, monthly income, distance, and payment mode as risk factors. Results: Two hundred and seventy patients (29.93%) were lost to follow-up. Multivariate analysis showed age, monthly income, eye involvement, and type of medical assistance independently associated with loss to follow-up. The odds of loss to follow-up were greater among older patients than those less than 50 years (reference), p < 0.001. The odds of loss to follow-up were greater among patients who received unilateral treatment than those who received bilateral injections (p = 0.013). Concerning gross monthly income, there were no differences in the odds of the four salary strata; the data also indicate an absence of difference in the three strata of patients' distance to the clinic. Considering the diagnosis, only age-related macular degeneration showed greater odds of loss to follow-up (p = 0.016). Finally, the data suggest greater odds of loss to follow-up in private patients than in those on a health care plan (p < 0.001). Conclusion: Loss to follow-up is paramount because many patients may remain unassisted concerning their eye diseases. Identifying the risk factors is crucial to enforcing measures to increase adherence and the long-term success of the treatment.

A Retrospective Comparison of Ahmed Glaucoma Valve Implants with or without Ologen Collagen Matrix.

Purpose: To study the effects of Ologen collagen matrix on the outcomes of the Ahmed glaucoma valve implant. Study Design: Retrospective case-control multicenter study, conducted at four centers, comparing the 6-month outcomes of Ahmed valve implants with or without Ologen. Participants: The study included 125 eyes in a 4:1 pairing (25 patients with Ologen matched to 100 patients without Ologen). Intervention: Ologen was placed over the Ahmed plate in the study group. Success was defined as an intraocular pressure (IOP) ≤ 21 mmHg either with no medication (complete success) or regardless of medications (qualified success). Other outcomes included IOP variation, eye drop use, and surgical complications. Results: Overall, the IOP decreased from 30.72 ± 9.08 to 16.14 ± 4.79 mmHg (p=0.0001). Of the 125 eyes, 26 achieved complete success and 94 achieved qualified success. There was no difference in complete success between the groups (p=0.12); however, there was a difference in qualified success (p=0.01), with better results in the no-Ologen group (80% vs 56%). There were no differences in the decrease in medications (p=0.06), as well as the incidence of complications (p=0.69). Although the need for postoperative surgical reintervention was higher in the no-Ologen group (13% vs 4%), the difference was not significant (p=0.2). Conclusion: The reductions in IOP and number of medications were similar in both groups after 6 months, with similar complication rates. The qualified success rate was lower in the Ologen group, but further studies are needed to clarify the role of Ologen in Ahmed valve implants.

Angiotensin II type 1 and 2 receptors and lymphatic vessels modulate lung remodeling and fibrosis in systemic sclerosis and idiopathic pulmonary fibrosis.

OBJECTIVE: To validate the importance of the angiotensin II receptor isotypes and the lymphatic vessels in systemic sclerosis and idiopathic pulmonary fibrosis. METHODS: We examined angiotensin II type 1 and 2 receptors and lymphatic vessels in the pulmonary tissues obtained from open lung biopsies of 30 patients with systemic sclerosis and 28 patients with idiopathic pulmonary fibrosis. Their histologic patterns included cellular and fibrotic non-specific interstitial pneumonia for systemic sclerosis and usual interstitial pneumonia for idiopathic pulmonary fibrosis. We used immunohistochemistry and histomorphometry to evaluate the number of cells in the alveolar septae and the vessels stained by these markers. Survival curves were also used. RESULTS: We found a significantly increased percentage of septal and vessel cells immunostained for the angiotensin type 1 and 2 receptors in the systemic sclerosis and idiopathic pulmonary fibrosis patients compared with the controls. A similar percentage of angiotensin 2 receptor positive vessel cells was observed in fibrotic non-specific interstitial pneumonia and usual interstitial pneumonia. A significantly increased percentage of lymphatic vessels was present in the usual interstitial pneumonia group compared with the non-specific interstitial pneumonia and control groups. A Cox regression analysis showed a high risk of death for the patients with usual interstitial pneumonia and a high percentage of vessel cells immunostained for the angiotensin 2 receptor in the lymphatic vessels. CONCLUSION: We concluded that angiotensin II receptor expression in the lung parenchyma can potentially control organ remodeling and fibrosis, which suggests that strategies aimed at preventing high angiotensin 2 receptor expression may be used as potential therapeutic target in patients with pulmonary systemic sclerosis and idiopathic pulmonary fibrosis.

Angiotensin II type 1 and 2 receptors and lymphatic vessels modulate lung remodeling and fibrosis in systemic sclerosis and idiopathic pulmonary fibrosis

OBJECTIVE: To validate the importance of the angiotensin II receptor isotypes and the lymphatic vessels in systemic sclerosis and idiopathic pulmonary fibrosis. METHODS: We examined angiotensin II type 1 and 2 receptors and lymphatic vessels in the pulmonary tissues obtained from open lung biopsies of 30 patients with systemic sclerosis and 28 patients with idiopathic pulmonary fibrosis. Their histologic patterns included cellular and fibrotic non-specific interstitial pneumonia for systemic sclerosis and usual interstitial pneumonia for idiopathic pulmonary fibrosis. We used immunohistochemistry and histomorphometry to evaluate the number of cells in the alveolar septae and the vessels stained by these markers. Survival curves were also used. RESULTS: We found a significantly increased percentage of septal and vessel cells immunostained for the angiotensin type 1 and 2 receptors in the systemic sclerosis and idiopathic pulmonary fibrosis patients compared with the controls. A similar percentage of angiotensin 2 receptor positive vessel cells was observed in fibrotic non-specific interstitial pneumonia and usual interstitial pneumonia. A significantly increased percentage of lymphatic vessels was present in the usual interstitial pneumonia group compared with the non-specific interstitial pneumonia and control groups. A Cox regression analysis showed a high risk of death for the patients with usual interstitial pneumonia and a high percentage of vessel cells immunostained for the angiotensin 2 receptor in the lymphatic vessels. CONCLUSION: We concluded that angiotensin II receptor expression in the lung parenchyma can potentially control organ remodeling and fibrosis, which suggests that strategies aimed at preventing high angiotensin 2 receptor expression may be used as potential therapeutic target in patients with pulmonary systemic sclerosis and idiopathic pulmonary fibrosis. .

Clinical manifestations and pulmonary histopathological analysis related to different diseases in patients with fatal pulmonary thromboembolism: an autopsy study.

BACKGROUND: To correlate underlying diseases, in autopsies of patients with pulmonary thromboembolism (PTE) to histological findings and manifestations reviewed in the medical records. METHODS: The autopsy records between 2001 and 2008 of 291 patients whose cause of death was PTE were reviewed. The following data were obtained: age, sex, clinical "in vivo" manifestations, postmortem pathological patterns, and main associated underlying diseases, cancers, and surgeries performed in the last hospitalization. The pulmonary histopathological changes were categorized as diffuse alveolar damage, pulmonary edema, alveolar hemorrhage, and lymphoid interstitial pneumonia. Odds ratios of positive relations were obtained by logistic regression and were considered significant when P<0.05. RESULTS: The median age was 64 years old. About 64% of patients presented cardiovascular illness associated with PTE. The most prevalent pulmonary finding was pulmonary edema. Only 13% of cases had clinical suspicion of PTE. Acute respiratory failure was positively related to pulmonary edema, alveolar hemorrhage, and diffuse alveolar damage as well as hemodynamic instability to alveolar hemorrhage and diffuse alveolar damage. CONCLUSION: We found important relations between clinical data and histological findings of patients with fatal PTE. A greater understanding of the pulmonary physiopathological mechanisms involved with each disease associated to PTE could improve its diagnosis and treatment.

Manifestações clínicas e análise histopatológica pulmonar relacionadas a diferentes doenças em pacientes com tromboembolismo pulmonar fatal – um estudo em autópsias / Clinical manifestations and pulmonary histopathological analysis related to different diseases in patients with fatalpulmonary thromboembolism – an autopsy study

Introdução: Tromboembolismo pulmonar (TEP) é uma das mais graves complicações dentre pacientes hospitalizados e permanece subdiagnosticado. Ainda hoje, sua fisiopatologia não está completamente elucidada. Objetivos: Correlacionar comorbidades, neoplasias, cirurgias e achados histológicos às manifestações clínicas associadas ao TEP. Métodos: Entre 2001 a 2008, foram revisadas 291 autópsias de pacientes cuja causa de morte foi TEP. Os seguintes dados foram obtidos: idade, sexo, manifestações clínicas, achados histológicos e principais doenças de base/comorbidades, neoplasias e cirurgias da última internação. Os achados histológicos foram categorizados em: dano alveolar difuso (DAD), edema agudo de pulmão (EAP), hemorragia intra alveolar (HIA) e pneumonia intersticial linfo-plasmocítica (PILP). Odds ratios foram obtidas por regressão logística e foram consideradas significativas quando p < 0,05. Resultados: A mediana de idade foi 64 anos. Cerca de 64% dos pacientes apresentava doenças cardiovasculares. O achado pulmonar mais prevalente foi EAP. Apenas 13% dos casos apresentaram suspeita clínica. Insuficiência respiratória esteve associada a EAP, HIA e DAD; assim como instabilidade hemodinâmica a HIA e DAD. Conclusões: Foram encontradas importantes associações entre achados clínicos e histológicos em pacientes com TEP. A compreensão dos mecanismos fisiopatológicos envolvidos com cada doença associada a TEP pode auxiliar no diagnóstico e no tratamento da doença.

Introduction: Pulmonary thromboembolism (PTE) is one of the most fatal complications among hospitalized patients and remains undiagnosed. Its physiopathology and its epidemiology aren’t widely known in literature. Objectives: To correlate underlying diseases, different cancers and surgeries to histological findings and in-vivo manifestations associated to fatal PTE from autopsy reports. Methods: From 2,001 to 2,008, were reviewed 291 autopsies of patients whose cause of death was PTE. The following data were obtained: age, sex, clinical invivo manifestations, post-mortem pathological patterns and mainassociated underlying diseases, cancers and surgeries performed in last hospitalization. The pulmonary histopathological changes were categorized in: diffuse alveolar damage (DAD), pulmonary edema (PE), alveolar hemorrhage (AH) and lympho/plasmacytic interstitial pneumonia (LPIP). Odds ratios of positive relations were obtained by logistic regression and were considered significative when p < 0.05. Results: The median age was 64 years. 64% ofpatients presented cardiovascular illness associated to PTE. The most prevalent pulmonary finding was PE. Only 13% of cases had clinical suspect. Acute respiratory failure was positively related to PE, AH and DAD; as well hemodynamic instability to AH and DAD. Conclusions: We found important relations between clinical data and histological findings of fatal PTE patients. The understanding of pulmonary physiopathological mechanism involved with eachPTE-associated disease can improve diagnosis in order to offer prompt treatment and reduce mortality.

Manifestação rara de edema agudo de pulmão associado à miocardite lúpica aguda - relato de caso / Unusual clinical manifestation of acute pulmonary edema associated to acute lupic myocarditis - case report

O lupus eritematoso sistêmico (LES) é a mais comum das doenças auto-imunes sistêmicas. Embora os rins classicamente sejam os órgãos mais acometidos no LES, o coração também pode ser afetado de forma significativa. Entretanto, a ocorrência de edema agudo de pulmão associado à miocardite lúpica é rara e de tratamento imunossupressor específico ainda incerto. O presente relato de caso revisa a literatura quanto a manifestações lúpicas do sistema cardiopulmonar, seu diagnóstico e tratamento, e descreve uma paciente lúpica jovem que evoluiu com edema agudo de pulmão decorrente de uma miopericardite lúpica aguda. O rápido diagnóstico pôde permitir o emprego da terapêutica imunossupressora adequada com reversão completa da disfunção miocárdica. Em pacientes jovens com quadro sugestivo de edema agudo de pulmão, o diagnóstico de LES deve ser considerado. O uso de pulsoterapia com corticóide endovenoso mostrou-se eficaz e seguro para o tratamento da manifestação cardíaca extrema.

Systemic lupus erythematosus is the most common systemic autoimmune disease. Although kidneys are the mainorgans affected, heart may suffer injury too. However, acute pulmonary edema associated to lupic myocarditis is rare and its specific immunosuppressive treatment is still undefined. The present case report reviews literature about lupic manifestations in heart and lungs, their diagnosis and treatment, and describes an young lupic patient that had pulmonary edema due toacute lupic myopericarditis. Prompt diagnosis enabled correct immunosuppressive therapy that resulted in a complete reversion of myocardial disfunction. Lupus is a possible diagnosis in young patients with pulmonary edema. The use of intravenous pulse therapy with corticosteroids was safe and efficient to healing of this severe myocardial manifestation.

Artrite reumatóide e doença cardiovascular na atualidade: o que sabemos sobre essa associação e o que podemos fazer pelo paciente? / Rheumatoid arthritis and cardiovascular disease: what do we know about this relationship and how can we treat affected patients nowadays?

O interesse em doenças auto-imunes vem crescendo a cada ano, principalmente sobre sua relação com doenças cardiovasculares. Especificamente a artrite reumatóide vem sendo considerada um fator de risco independente para doença arterial coronária nos últimos anos. Diversos estudos foram realizados recentemente com o objetivo de esclarecer pontos cruciais na estratificação de risco desses pacientes e no seu respectivo tratamento medicamentoso adequado. Novas terapias específicas da doença reumatóide ainda estão em estudo, e prometem reduzir o risco cardiovascular a longo prazo. Desse modo, realizamos uma revisão bibliográfica ampla, utilizando as principais bases de dados nacionais e internacionais, com o objetivo de salientar a importância de mecanismos ateroscleróticos e inflamatórios sobre a doença arterial coronária. Além disso, frente às atuais evidências, sugerimos estratégias de estratificação de risco e tratamento da doença arterial coronária em pacientes com artrite reumatóide.

The interest in auto-immune diseases has been grown, mainly about cardiovascular illnesses. Rheumatoid arthritis has been considered an independent risk factor for coronary arterial disease in last years. Recently, different studies have been performed in order to better clarify crucial points in risk stratification and correct treatment for patients with rheumatoid arthritis. New specific therapies have been studying and promising reduction of cardiovascular risk. Thereby, we made a bibliographic revision to show the importance of atherosclerotic and inflammatory mechanisms in coronary artery disease. Furthermore, wesuggested different strategies to establish risk stratification andtreatment of cardiovascular diseases in patients with rheumatoid arthritis.

Diagnóstico post-mortem de infarto agudo do miocárdio em pacientes com insuficiência respiratória aguda - análise demográfica, etiológica e histológica pulmonar / Post-mortem diagnosis of acute myocardial infarction in patients with acute respiratory failure - demographic,etiologic and histological pulmonary analysis

Introdução: A insuficiência respiratória aguda (IRA) está presente em 5% dos pacientes com infarto agudo do miocárdio (IAM) e é associada à mortalidade de 20% a 30% nesses pacientes. Não está claro o papel da inflamação relacionada ao edemaagudo de pulmão (EAP) na gênese da IRA pós IAM. Objetivos: Descrever os dados demográficos, etiológicos e os achados histológicos pulmonares em autópsias realizadas entre 1990 e 2008, de pacientes que morreram por IRA, sem diagnóstico in-vivo de IAM. Métodos: Este estudo considerou 4223 autópsias de pacientes que morreram de IRA nos quais só foi definida postmortem sua causa de morte. O diagnóstico de IAM foi feito porautópsia em 218 (4,63%) pacientes, dos quais foram obtidos: idade, sexo e principais doenças associadas. Os achados pulmonares histológicos foram classificados em: dano alveolar difuso (DAD), edema agudo de pulmão (EAP), hemorragia alveolar (HA) e pneumonia intersticial linfo-plasmocitária (PILP). A probabilidade de IAM desenvolver determinado tipo de achado histopatológico pulmonar foi calculada por regressão logística. Resultados: Foram observados 147 homens, e a mediana de idade foi 64 anos. A análise histopatológica pulmonar mostrou, em ordem decrescente: EAP (72,9%), DAD, PILP e HIA. Broncopneumonia bacteriana esteve presente em 11,9%, hipertensão arterial sistêmica em 10,1%, miocardiopatia dilatada em 6,9%, tromboembolismo pulmonar em 6,0%, cardiomiopatia hipertrófica em 4,6%, doença pulmonar obstrutiva crônica em 3,7% e diabetes mellitusem 3,7% dos pacientes. A análise multivariada demonstrou associação significativamente positiva de IAM com EAP e DAD. Conclusões: Pela primeira vez na literatura, demonstramos, pormeio de autópsias, que em pacientes com IRA que evoluem à óbito sem diagnóstico estabelecido, IAM esteve presente em aproximadamente 5% dos casos. Nós observamos importantecomponente inflamatório na histologia pulmonar, nunca antes sugerido...

Introduction: Acute respiratory failure (ARF) is present in 5% of the patients with acute myocardial infarction (AMI) and is responsible for 20% to 30% of the mortality post-AMI. It is unclearthe role of inflammation correlated with pulmonary edema (PE) as a cause of ARF post-AMI. Objectives: Describe the demographic, etiologic data and histological pulmonary findings in autopsies of patients dead due to ARF with non-diagnosis AMI during lifebetween 1,990 and 2,008. Methods: This study considers 4,223 autopsies of patients who died of ARF without cause of death related during life. The diagnosis of AMI was performed in 218(4.63%) patients, and were obtained: age, sex and major associated diseases. Pulmonary histopathology was categorized as: diffuse alveolar damage (DAD); pulmonary edema (PE); alveolarhemorrhage (AH);and lympho-plamacytic interstitial pneumonia(LPIP). Odds ratio of AMI developing specific histopathology was determined by logistic regression. Results: Were observed 147 men and mean age was 64 years. Pulmonary histopathology showed, in descending order: PE (72.9%), DAD, LPIP and HA. Bacterialbronchopneumonia was present in 11.9%, systemic arterial hypertension in 10.1%, dilated cardiomyopathy in 6.9%, pulmonary embolism in 6.0%, hypertrophic cardiomyopathy in 4.6%, chronic obstructive pulmonary disease in 3.7% and diabetes mellitus in 3.7% of patients. Multivariate analysis demonstrated significantly positive association of IAM with PE and with DAD. Conclusions: For the first time we demonstrated that in autopsies of patients with ARF as cause of death, the diagnosis of AMI was present in about 5%. We observed important inflammatory response in pulmonaryhistology as never suggested before...