Effectiveness of the Dexamethasone Intravitreal Implant for Treatment of Patients with Diabetic Macular Oedema

Diabetic macular oedema (DMO) is a leading cause of vision loss in the working-age population worldwide. Corticosteroid drugs have been demonstrated to inhibit the expression of both the vascular endothelial growth factor (VEGF) gene and other anti-inflammatory mediators, such as prostaglandins. Triamcinolone, fluocinolone and dexamethasone are the main steroids that have been studied for the treatment of macular oedema. Over the last few years, several studies have suggested an important role for dexamethasone in the management of DMO. The dexamethasone intravitreal implant (DEX implant) (Ozurdex®; Allergan, Inc., Irvine, CA) is a novel approach approved by the US Food and Drug Administration (FDA) and by the EU for the intravitreal treatment of macular oedema after branch or central retinal vein occlusion, and for the treatment of non-infectious uveitis affecting the posterior segment of the eye. We reviewed manuscripts that had investigated the pharmacokinetics, efficacy and safety of the DEX implant regarding DMO treatment.

Long-Term Lamivudine Treatment of Children with Chronic Hepatitis B: Durability of Therapeutic Responses and Safety

Lamivudine has been demonstrated safe and efficacious in the short term in a large cohort of children with chronic hepatitis B (CHB), but optimal duration of treatment has not been elucidated and limited data on the safety of long-term lamivudine administration have been reported. In addition, the durability of favourable therapeutic outcomes after lamivudine therapy in children has not been well characterized. The aim of this study was to examine the safety of lamivudine and the durability of clinical responses in a group of children who received up to 3 years of treatment for CHB. One hundred and fifty-one children from centres in nine countries who had previously received lamivudine in a large prospective trial were enrolled. During the first year, children had been randomized to either lamivudine or placebo treatment. Subsequently, in a separate extension study, those who remained hepatitis B e antigen (HBeAg) positive were given lamivudine for up to 2 years and those who were HBeAg negative were observed for additional 2 years. Results of these studies have been previously reported. In this study, these children were followed for 2 additional years. Data gathered from medical record review included weight, height, signs and symptoms of hepatitis, alanine aminotransferase (ALT) levels, serologic markers, hepatitis B virus (HBV) DNA levels and serious adverse events (SAEs). Other pharmacological treatments for CHB were allowed according to the practices of individual investigators and were documented. Subjects were divided into two groups for analysis, those who had achieved virological response (VR), defined as HBeAg negative and undetectable HBV DNA by the bDNA assay by the end of the extension study at 3 years, and those who had not. In those who had achieved VR by the end of the extension study, long-term durability of HBeAg seroconversion was 82% and >90% in those who had received lamivudine for 52 weeks and at least 2 years respectively. This compares to 75% for those who had achieved seroconversion after placebo. In those who had not achieved VR by the end of the extension study, an additional 11% did so by the end of the study; they had all received lamivudine in the previous trial, and none had received further treatment during the study. Eight children lost hepatitis B surface antigen during the study and all had received lamivudine at some point during the previous trials. Evaluation of safety data revealed no SAEs related to lamivudine. There was no effect of treatment on weight or height z scores. Clinically benign ALT flares (>10 times normal) were seen in 2% of children. Favourable outcomes from lamivudine treatment of CHB in children are maintained for at least several years after completion of treatment. Up to 3 years of lamivudine treatment is safe in children.

Treatment of a nineteenth century male portrait in oil including the characterisation of materials, technique and a study of the lead soap aggregation in the paint composite

Dissertação para obtenção do Grau de Mestre em Conservação e Restauro

Malaria in humait a county, state of Amazonas, Brazil. XIX - evaluation of clindamycin for the treatment of patients with Plasmodium falciparum infection

A total of 207 patients with malaria caused by Plasmodium falciparum were submitted to 5 different treatment schedules with clindamycin from 1981 to 1984: A - 89 patients were treated intravenously and orally, or intramuscularly and orally with 20 mg/kg/day divided into two daily applications for 5 to 7 days; B-40 patients were treated orally with 20 mg/kg/day divided into two daily doses for 5 to 7 days; C-27 patients were treated with 20 mg/kg/day intravenously or orally divided into two daily applications for 3 days; D-16 patients were treated orally and/or intravenously with a single daily dose of 20 to 40 mg/kg/day for 5 to 7 days; E-35 patients were treated orally with 5 mg/kg/day divided into two doses for 5 days. Patients were examined daily during treatment and reexamined on the 7th, 24th, 21st, 28th and 35th day both clinically and parasitologically (blood test). Eighty three (40.1%) had moderate or severe malaria, and 97 (46.8%) had shown resistance to chloroquine or to the combination ofsulfadoxin and pyrimethamine. The proportion of cured patients was higher than 95% among patients submitted to schedules A and B. Side effects were only occasional and of low intensity. Three deaths occurred (1.4%), two of them involving patients whose signs and symptoms were already very severe when treatment was started. Thus, clindamycin proved to be very useful in the treatment of patients with malaria caused by Plasmodium falciparum and we recommend schedule A for moderate and severe cases and Bfor initial cases.

Reduction of morbidity in hepatosplenic Schistosomiasis mansoni after treatment with praziquantel: a long term study

Forty-two with hepatosplenic patients treated with praziquantel and followed up for 5 years. One half of the patients received a single 30 mg/kg dose and the other half, two doses of 25 mg/kg given 4 hrs apart. According to Hoffman and Kato-Katz stool exams, an 83.3% cure rate, was observed after twelve months. Stool egg counts in cases of incomplete cure were greatly reduced. Liver function, as assessed by serum levels of aspartate aminotransferase, alanine aminotransferase, gamma glutamyltransferase and alkaline phosphatase activities as well as albumin and gamma globulin showed marked improvement after one year. Hepatomegaly was reduced in 81.0% of patients and splenomegaly in 78.8%. Spleen regression was complete in 15.1% of the total, and in 18.5% of those with compensated hepatosplenic disease. As a result of these observations, the authors recomend early treatment with anti-schistosomal medication, either oxamniquine or praziquantel, to halt progression of disease and reduce splenomegaly.

Specific treatment of hepatosplenic schistosomiasis can increase T-lymphocyte reactivity

It has been recognized that Schistosoma mansoni infection causes depression of T-cell responsiveness. In this study we have evaluated whether immunodepression associated to schistosomiasis could be reverted by specific treatment. T-cell immune response was assessed by means of intradermal tests using recall antigens in a group of 22 patients with hepatosplenic schistosomiasis, one year after treatment with oxamniquine and compared with a group of untreated hepatosplenic patients. Only 27% of treated patients presented complete anergy to all tested antigens, in marked contrast to 80% unresponsiveness showed by hepatosplenic patients without treatment. Although most of the treated individuals showed some response to the tested antigens, in some individuals this unresponsiveness still persisted after treatment. Anergy was not found in any normal individual of the control group. It was concluded that Schistosoma mansoni infected patients may recover their normal immune responsiveness after the elimination of the worm by treatment

Pre-treatment of different types of lignocellulosic biomass using ionic liquids

Dissertação apresentada na Faculdade de Ciências e Tecnologia da Universidade Nova de Lisboa para obtenção do grau Mestre em Biotecnologia

Schistosoma mansoni in mice: modulation of granulomatous response after reinfection and chemotherapeutic treatment

Mice previously infected with Schistosoma mansoni, and cured by specific treatment (400mg/kg oxamniquine, p. o.) in the chronic phase of the disease, were reinfected 20 days after treatment to assess their capacityfor modulation ofthe granulomatous response. Histopathologic examination of the animals ' liver, at 60 days after reinfection, evidenced the presence of typical granulomas of the chronic phase in most animals. This infer that the capacity for modulation of the granulomatous response had been maintained, thus preventing a new acute phase of the disease. Conversely, a group of previously infected mice, untreated and submitted to reinfection, showed reactivation of the granulomatous response in 50% of the animals. The possible implications of these findings in human schistosomiasis mansoni are discussed.

Micropollutant bioremoval in wastewater treatment systems: from microbial population structure to function

Dissertation presented to obtain the Ph.D degree in Biology

Treatment of T. cruzi infected human platelet concentrates with aminomethyltrimethyl psoralen (AMT) and ultravioleta (UV-A) light: preliminary results

The present measures adopted to prevent transfusion-associated Chagas' disease include screening of blood donors. and/or the inactivation of T. cruzi in collected blood using gentian violet (GV) as a trypanocidal agent. In this study, we investigated the efficacy of the combined use of AMT and UV-A in inactirating T. cruzi in infected human platelet cuncentrates. Human platelet concentrates were infected with T. cruzi (2x10/ml) of the Y strain transfered to PL 269 (Fenwal Laboratories) containers and treated with GV (250řg,/ml). and ascorbic acid (1 mg/ml); GV. ascorbic acid and UV-A; GV and UV-A; AMT (40/tG/ml) and ascorbic acid; AMT, ascorbic acid and UV-A; AMT and UV-A; UV-A alone; and untreated (control). All UV-A treated platelet concentrates were exposed to UV-A doses of 24, 92, 184, 276, 368 and 644 kj/m². and the microscopical research of active T. cruzi was performed, using the microhematocrit technique, 1, 6 and 24 hours after each treatment. A high number of active forms of T. cruzi was observed in all condictions, except when GV was used as the trypanocidal agent, providing evidence of the failure of AMT and UV-A in inactivating T cruzi in infected human platelet concentrates.

Plants used in the treatment of leishmanial ulcers due to Leishmania (Viannia) braziliensis in an endemic area of Bahia, Brazil

This paper records the plants used in the treatment of cutaneous leishmaniasis due to Leishmania (Viannia) braziliensis (L(V)b) among the rural population of a cocoa- producing coastal area of Bahia state, Brazil. An enquiry conducted among a hundred patients identified 49 plant species used to treat skin ulceration caused by this Leishmania species. The principal plants used are caju-branco (Anacardium occidentale - Anacardiaceae), used by 65% of the population, folha-fogo (Clidemia hirta - Melastomataceae) 39%, alfavaca-grossa (Plectranthus amboinicus - Lamiaceae) 33%, mastruz (Chenopodium ambrosioides - Chenopodiaceae) 31%, erva-de-santa-maria (Solatium americanum - Solanaceae) (25%) and transagem (Plantago major - Plantaginaceae.) 2%.

Histopathology of human American cutaneous leishmaniasis before and after treatment

Chemical therapy for the treatment of leishmaniasis is still inadequate, and a number of drugs and therapeutic programs are being tested. Besides treatment, the ultimate goal is an effective cure, and histopathological analyses of the lesion cicatrices constitute an important measure of treatment success, or otherwise, in this respect. In this paper, we describe histopathological patterns in cases of American cutaneous leishmaniasis in 32 patients from the municipality of Caratinga, Minas Gerais, Brazil, before and after treatment with the following therapeutic methodos: l) leishvacin + glucantime; 2) leishvacin + BCG associated with glucantime; 3) glucantime; 4) leishvacin + BCG. Lesion fragments were collected from all patients by biopsy prior to, and approximately 30 days after, each treatment which resulted in a clinical diagnosis of cure. Following the analysis of slides, the preparations were described from a histopathological point of view and grouped taking into account the prevalence or significance of the characteristic elements. This process resulted in the following classification: 1. exsudative reaction (ER); 2. exsudative giant cell reaction (EGCR); 3. exsudative productive reaction (EPR); 4. exsudative productive giant cell reaction (EPGCR); 5. exsudative productive necrotic reaction (EPNR); 6. necrotic exsudative reaction (NER); 7. productive exsudative reaction (PER), 8. productive giant cell reaction (PGCR); 9. productive exsudative giant cell reaction (PEGCR); 10. productive exsudative giant cell granulomatous reaction (PEGCGR); 11. productive reaction (PR) and 12. productive cicatricial (cure) reaction (PCR). After this analysis, it was noted that clinical cure did not always coincide with histopathological cure.