Purpose Although classically classified as a non-inflammatory condition, an inflammatory basis for keratoconus (KC) appears to be a growing evidence. Recently, it has been shown that KC patients have an increased choroidal thickness (CT). Among inflammatory disorders, atopy has been associated with KC development; therefore, the aim of this study was to evaluate if the increased CT in patients with KC is related to atopy. Methods This is an analytical cross-sectional study of patients with KC. Patients were classified as atopic and non-atopic according to their atopy history (allergic rhinoconjunctivitis (AR), asthma (AA) and/or atopic dermatitis (AD)) and were also classified based on their eye rubbing habits. Choroidal profile of all subjects was evaluated using a Spectralis optical coherence tomography (OCT) device with enhanced depth imaging (EDI) mode. CT was measured and compared between groups at the center of the fovea and at 500 µm intervals along a horizontal section. A multivariable analysis, adjusted for sex, age, spherical equivalent, history of medication and atopy, was performed to assess the influence of atopy in CT. Results Of the 80 patients included, 51 were atopic and 29 non-atopic. Atopic patients showed a thicker choroid in every measured location than the non-atopic patients (mean subfoveal CT 391.53 µm vs 351.17 µm, respectively), although the differences were not statistically different. The multivariable analysis revealed that being atopic makes the choroid statistically thicker, on average, 55.14 µm, when compared to non-atopic patients (p=0.043). Furthermore, patients who are frequent eye rubbers have significantly thicker choroids than non-rubbers (p=0.004). Conclusion Although some results do not reach statistical significance, atopic KC patients seem to have thicker choroids compared with non-atopic KC patients, suggesting a possible role for atopy in the choroidal profile of KC. This constitutes a completely new sight in this field of research that needs further investigation.
BackgroundImmunophenotypic analysis of the bone marrow (BM) cells has proven to be helpful in the diagnosis of Myelodysplastic Syndromes (MDS). However, the usefulness of flow cytometry (FCM) for the detection of myelodysplasia in the peripheral blood (PB) still needs to be investigated. The aim of this pilot study was to evaluate the value of FCM-based PB neutrophil and monocyte immunophenotyping for the diagnosis of lower risk MDS (LR-MDS).MethodsWe evaluated by 8-color FCM the expression of multiple cell surface molecules (CD10, CD11b, CD11c, CD13, CD14, CD15, CD16, CD34, CD45, CD56, CD64 and HLA-DR) in PB neutrophils and monocytes from a series of 14 adult LR-MDS patients versus 14 normal individuals.ResultsPeripheral blood neutrophils from patients with LR-MDS frequently had low forward scatter (FSC) and side scatter (SSC) values and low levels of CD11b, CD11c, CD10, CD16, CD13 and CD45 expression, in that order, as compared to normal neutrophils. In addition, patients with LR-MDS commonly display a higher fraction of CD14+CD56+ and a lower fraction of CD14+CD16+ monocytes in the PB. Based on these results, we proposed an immunophenotyping score based on which PB samples from patients with LR-MDS could be distinguished from normal PB samples with a sensitivity 93% and a specificity of 100%. In addition, we used this score to construct the MDS Thermometer, a screening tool for detection and monitoring of MDS in the PB in clinical practice.ConclusionsPeripheral blood neutrophil and monocyte immunophenotyping provide useful information for the diagnosis of LR-MDS, as a complement to cytomorphology. If validated by subsequent studies in larger series of MDS patients and extended to non-MDS patients with cytopenias, our findings may improve the diagnostic assessment and avoid invasive procedures in selected groups of MDS patients.Electronic supplementary materialThe online version of this article (10.1186/s12878-018-0101-8) contains supplementary material, which is available to authorized users.
Summary: Periodic limb movements (PLMs) may occur as a primary condition or be associated with other pathologies, such as sleep disorders. However, PLMs have not been described in comatose patients. We report the case of a 66-year-old man, with no history of sleep disorders, who presented PLMs during coma caused by an extensive right hemispheric abscess inducing midline shift. These movements were further characterized by video and electromyographic recordings, which displayed bilateral periodic bursts of the tibialis anterior muscles, occurring every 7 to 15 seconds, with no concomitant electroencephalographic correlate. After a long period of hospitalization, the patient eventually regained consciousness and PLMs seem to persist, only in sleep. To the best of our knowledge, this is the first report showing that PLMs may be observed in a setting where the networks supporting consciousness are lost, namely in a coma of structural etiology.
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