Age-related macular degeneration (AMD) is an eye disease causing damage to the macular region of the retina where most of the photoreceptors responsible for central visual acuity are located. MicroRNAs (miRNAs) are small single-stranded non-coding RNA molecules that negatively regulate genes by silent post-transcriptional gene expressions. Previous studies have shown that changes in specific miRNAs are involved in the pathogenesis of eye diseases, including AMD. Altered expressions of miRNAs are related to disturbances of regulating oxidative stress, inflammation, angiogenesis, apoptosis and phagocytosis, which are known factors in the pathogenesis of AMD. Moreover, dysregulation of miRNA is involved in drusen formation. Thus, miRNAs may be used as potential molecular biomarkers for the disease and, furthermore, tailoring therapeutics to particular disturbances in miRNAs may, in the future, offer hope to prevent irreversible vision loss. In this review, we clarify the current state of knowledge about the influence of miRNA on the pathogenesis, diagnosis and treatment of AMD. Our study material consisted of publications, which were found in PubMed, Google Scholar and Embase databases using “Age-related macular degeneration”, “miRNA”, “AMD biomarkers”, “miRNA therapeutics” and “AMD pathogenesis” as keywords. Paper search was limited to articles published from 2011 to date. In the section “Retinal, circulating and vitreous body miRNAs found in human studies”, we limited the search to studies with patients published in 2016–2021.
Corneal transplantation is the most effective treatment for corneal blindness. Standard planned keratoplasties have a high success rate. Conditions such as active inflammation at the time of surgery, the presence of ocular surface disease, previous graft disease, or neovascularization make them more susceptible to rejection. These are so-called high-risk corneal transplantations. In our study, we selected 52 patients with a higher risk of graft rejection. A total of 78 procedures were performed. The main indications for the first keratoplasty were infections (59.6%) and traumas (21.2%). Visual acuity (VA) significantly improved from 2.05 logMAR on the day of keratoplasty to 1.66 logMAR in the latest examination (p = 0.003). An analysis of the graft survival showed a 1-year survival of 54% and a 5-year survival of 19.8% of grafts. The mean observation time without complications after the first, second, and third surgery was 23, 13, and 14 months, respectively. The best results were noted among patients with infectious indications for keratoplasty (p = 0.001). Among them, those with bacterial infection had the best visual outcomes (p = 0.047).
Hyperinsulinaemic hypoglycaemia (HH) is the most common cause of persistent hypoglycaemia in infants and children with incidence estimated at 1 per 50,000 live births. Congenital hyperinsulinism (CHI) is symptomatic mostly in early infancy and the neonatal period. Symptoms range from ones that are unspecific, such as poor feeding, lethargy, irritability, apnoea and hypothermia, to more serious symptoms, such as seizures and coma. During clinical examination, newborns present cardiomyopathy and hepatomegaly. The diagnosis of CHI is based on plasma glucose levels <54 mg/dL with detectable serum insulin and C-peptide, accompanied by suppressed or low serum ketone bodies and free fatty acids. The gold standard in determining the form of HH is fluorine-18-dihydroxyphenyloalanine PET ((18)F-DOPA PET). The first-line treatment of CHI is diazoxide, although patients with homozygous or compound heterozygous recessive mutations responsible for diffuse forms of CHI remain resistant to this therapy. The second-line drug is the somatostatin analogue octreotide. Other therapeutic options include lanreotide, glucagon, acarbose, sirolimus and everolimus. Surgery is required in cases unresponsive to pharmacological treatment. Focal lesionectomy or near-total pancreatectomy is performed in focal and diffuse forms of CHI, respectively. To prove how difficult the diagnosis and management of CHI is, we present a case of a patient admitted to our hospital.
COVID-19 neurological manifestations vary from mild symptoms, such as fatigue, to severe complications. This article presents a case of a 15-year-old male with multiple brain abscesses, meningitis, massive sinusitis and saggital sinus thrombosis. SARS-CoV-2 IgM and IgG antibodies were increased, while blood and CSF cultures, anti-HSV antibodies and IGRA were negative. The patient responded well to the initial treatment with broad-spectrum antibiotics, glucocorticoids and intravenous immunoglobulins. After two weeks, his clinical state sudd0enly collapsed, with the progression of purulent lesions in the MRI. Urgent craniotomy was performed. A follow-up MRI confirmed regression of the purulent lesions. Negative blood and CSF cultures, as well as insufficiency of the broad-spectrum antibiotic therapy, suggested an atypical or opportunistic CNS infection, characteristic of immunocompromised patients. This strengthens the hypothesis that SARS-CoV-2 infection may lead to decreased immunocompetence.
Introduction: Age-related macular degeneration (AMD) is the most common cause of central vision loss in elderly people over 50 years of age. It is characterized by the presence of drusen on the fundus and may be associated with choroidal neovascularization (CNV) or geographic atrophy. AMD is a condition caused by many factors including environmental, genetic, and vascular. Currently, it affects over 25 million people worldwide, but with the progressive aging of the population, the incidence of the disease is increasing. Disease is therefore an important issue in geriatrics.Case report: A 75-year-old patient was referred to the General and Pediatric Ophthalmology Clinic of the Medical University of Lublin due to the three-week deterioration of visual acuity in the left eye. The visual acuity of the left eye was: counting fingers at a distance of 1.5 m. Initial cataracts of this eye and wet AMD were diagnosed. In July 2018. an injection of ranibizumab was administered into the vitreous humor of the left eye. After achieving an improvement in visual acuity to 0.2 (on Snellen charts), in September the patient was qualified to the Drug Program for the treatment of the wet form of AMD. From September to October 2019. the patient received 9 doses of ranibizumab. In October 2019. visual acuity improved to 0.4. In November, due to the unsatisfactory results of the therapy, the drug was changed to aflibercept. The patient received a total of 3 injections of this drug and his visual acuity improved to a value of 0.7. The last injection was given in July 2020 and the clinical condition and visual acuity stabilized. After the end of the drug program, the patient regularly shows up for checkups, and the visual acuity of the left eye has normalized since July 2020. and is now 0.4 (due in part to atrophic changes and scarring).Conclusions: Treatment of the wet form of AMD is a difficult and lengthy process. Early diagnosis of the disease, starting treatment as soon as possible, regular checkups and cooperation with the patient are very important for the success of the therapy. During 3 years of treatment, the patient experienced a significant improvement in visual acuity for one year. The treatment allowed the disease progression to slow down. The morphological condition of the retina improved. The applied treatment and management of the elderly patient turned out to be effective, and the achieved effects of the therapy are satisfactory.
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