Adherence to a gluten-free diet in celiac disease patients from Paraguay.

INTRODUCTION AND AIM: The treatment for celiac disease is a gluten-free diet that should be strictly and permanently carried out. Our aims were to determine adherence to the gluten-free diet and the risk factors for non-adherence. MATERIALS AND METHODS: An observational, cross-sectional, comparative study was conducted. It included individuals of both sexes and of any age that presented with celiac disease, lived in Paraguay from January to April 2021, and agreed to participate in the survey. Incomplete questionnaires were excluded. Non-probabilistic convenience sampling was utilized. Adherence was measured using the Leffler questionnaire. The study was approved by the Ethics Committee of the Universidad Privada del Este. RESULTS: The sample consisted of 371 respondents, 322 (87%) of whom were adults, with a mean age of 38 ±â€¯12 years, and 49 (13%) of whom were children and adolescents, with a mean age of 10 ±â€¯5 years. Female sex was predominant (85%). Adherence to the gluten-free diet was detected in 59% of the adults and 73% of the children and adolescents. The factors significantly associated with adherence included belonging to the child and adolescent age group and having had the diagnosis for a longer time: 9 ±â€¯8 years for the adherence group and 7 ±â€¯8 years for the non-adherence group. CONCLUSIONS: The present study demonstrated the frequency of adherence to the gluten-free diet in celiac patients in Paraguay. Psychologic and nutritional support is recommended for individuals with celiac disease that do not adhere to their treatment.

Neuroprotective effects of brimonidine against transient ischemia-induced retinal ganglion cell death: a dose response in vivo study.

The purpose of this study was to investigate the dose-response effects of topically administered brimonidine (BMD) on retinal ganglion cell (RGC) survival, short and long periods of time after transient retinal ischemia. In adult Sprague-Dawley rats, RGCs were retrogradely labeled with the fluorescent tracer fluorogold (FG) applied to both superior colliculi. Seven days later, the left ophthalmic vessels were ligated for 90 min. One hr prior to retinal ischemia, two 5 microl drops of saline alone or saline containing 0.0001, 0.001, 0.01 or 0.1% BMD were instilled on the left eye. Rats were processed 7, 14 or 21 days later and densities of surviving RGCs were estimated by counting FG-labeled RGCs in 12 standard regions of each retina. The following have been found. (1) Seven days after 90 min of transient ischemia there is loss of approximately 46% of the RGC population. (2) topical pre-treatment with BMD prevents ischemia-induced RGC death in a dose-dependent manner. Administration of 0.0001% BMD resulted in the loss of approximately 37% of the RGC population and had no significant neuroprotective effects. Administration of higher concentrations of BMD (0.001 or 0.01%) resulted in the survival of 76 or 90%, respectively, of the RGC population, and 0.1% BMD fully prevented RGC death in the first 7 days after ischemia. (3) Between 7 and 21 days after ischemia there was an additional slow cell loss of approximately 25% of the RGC population. Pre-treatment with 0.1% BMD also reduced significantly this slow cell death. These results indicate that the neuroprotective effects of BMD, when administered topically, are dose-dependent and that the 0.1% concentration achieves optimal neuroprotective effects against the early loss of RGCs. Furthermore, this concentration is also effective to diminish the protracted loss of RGCs that occurs with time after transient ischemia.

Brimonidine's neuroprotective effects against transient ischaemia-induced retinal ganglion cell death.

PURPOSE: Brimonidine is a lowering pressure agent currently used in glaucoma. This chronic degenerative condition is characterised by neuronal death, and an agent which offers neuroprotection may slow down or impede the progression of neuronal cell death. METHODS: The effects of brimonidine (BMD) on the short- and long-term survival of retinal ganglion cells (RGCs) after transient retinal ischaemia are reported here using a rat model. The fluorescent tracer Fluorogold (FG) was applied to both superior colliculi to retrogradely label RGCs. A ninety-minute period of ischaemia was induced and densities of surviving RGCs were estimated over time by counting FG-labelled RGCs in 12 standard regions of each retina. RESULTS: Seven days after inducing transient ischaemia, there was loss of approximately half of the RGC population. Topical pre-treatment with 0.1% or 0.5% BMD prevented ischaemia-induced RGC death. CONCLUSIONS: These results indicate that optimal neuroprotective effects against the early loss of RGCs are seen with 0.1% or 0.5% BMD. Ischaemia-induced RGC loss continued between day 7 and day 21 in the vehicle treated groups and amounted to approximately 25% of the RGC population. Topical pre-treatment with 0.1% or 0.5% BMD was also effective in reducing the slow loss of RGCs.