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Systemic lupus erythematosus (SLE), a multisystem autoimmune inflammatory disease, may involve any organs, including the liver. Liver involvement in SLE is not part of the American College of Rheumatology criteria and is relatively rare. Liver disease is usually mild, manifesting as subtle elevation of liver enzymes. Jaundice and hepatomegaly can be seen in some patients; advanced liver disease with cirrhosis is extremely rare. VVD214 Precise pathology remains obscure. SLE may cause non-specific changes, including hepatocellular, cholestatic, or vascular changes. Alcohol, drugs, viral infections, metabolic disorders, autoimmune hepatitis, and other common causes of liver dysfunction should be excluded. Corticosteroids may expedite the recovery process, but may lead to non-alcoholic fatty liver disease and liver damage. Several large-scale multicentre studies have shown that liver involvement is not the major cause of morbidity and mortality in SLE patients. In this review, we discuss the pathogenesis, diagnosis, differential diagnosis, clinical manifestations, management, complications, and prognosis of lupus hepatitis.

To report the ultrasound biomicroscopic features of normal lower eyelid structures.

Thirty lower eyelids of fifteen healthy adults were randomized and prospectively subjected to Ultrasound Biomicroscopy (Quantel Aviso with 50MHz transducer) by two independent observers (an ophthalmologist and an optometrist). The measurements were performed in upgaze, with the probe perpendicular to the lower eyelid margin in the mid-pupillary line, two limbal lines, and two canthal lines. The tarsus, orbicularis, capsulopalpebral fascia, and retractor-conjunctiva complex were assessed for two parameters echogenicity (hyper/hypoechoic) and measurement in millimeters.

Mean age was 25years (range 20-39years), 15 (50%) were right lower eyelids and 8 were males. The first layer, skin-orbicularis complex appeared hyperechoic. The second layer was hypoechoic band which represents the tarsal plate superiorly and capsulopalpebral fascia inferiorly. This was noted to be continuous and of almost uniform thickness in the normal eyelids. The glandular structure of meibomian glands was identified in 100% cases. The hyperechoic layer below the capsulopalpebral fascia is the retractor-conjunctiva complex. The mean thickness of pretarsal and pre-septal orbicularis was 0.68±0.18 mm and 0.89±0.16 mm, respectively. The tarsal plate measured 0.57±0.12 mm, capsulopalpebral fascia 0.42±0.13 mm and the retractor-conjunctiva complex 0.79±0.18 mm. On Bland-Altman analysis, the majority of the measurements had mean agreements between -0.14 mm and +0.12 mm. Anatomical differentiation was not useful in the canthal region.

Echogenicity and thickness of normal lower eyelid structures as measured by UBM are reported. The test is non-invasive, with a good inter-observer agreement.

Echogenicity and thickness of normal lower eyelid structures as measured by UBM are reported. The test is non-invasive, with a good inter-observer agreement.Objective To determine the clinical relevance and frequency of BEST1 and PRPH2 mutations in a clinically diagnosed adult-onset vitelliform macular dystrophy (AVMD) group with Caucasian ethnicity. Methods The study comprised 24 patients who had been diagnosed with AVMD via indirect fundus ophthalmoscopy and presented with a dome-shaped appearance between the retinal pigment epithelium and photoreceptors on their spectral-domain optical coherence tomography. They had lesion hyper- autofluorescence on their fundus autofluorescence images and were also investigated for BEST1 and PRPH2 mutations for a probable molecular aetiology. Results No pathogenic or likely pathogenic mutation was detected in the BEST1 and PRPH2 genes of any of the clinically diagnosed AVDM patients. A heterozygous NM_000322.5c.938C>T (p.Pro313Leu) variant of the PRPH2 gene was detected in 2 non-consanguineous patients. According to current guidelines, this variant was classified as a 'variant of uncertain significance'. Conclusion In conclusion, AVMD is a genotypic and phenotypic heterogeneous disease. The genetic aetiology could not be explained by sequencing BEST1 and PRPH2 genes in the AVMD patients; however, the variant of PRPH2 could be a cause of predisposition relevant to the phenotype.

Preterm delivery (PTD) represents the leading cause of neonatal death and disability. Among risk factors for PTD, maternal obesity (MO) is becoming an ever more relevant condition in developed countries, although the mechanisms relating this condition to higher risk of PTD is not clear. Aim of this narrative review is to summarize evidences from clinical and translational research showing how MO might negatively impact on pregnancy and neonatal outcomes, particularly, by increasing the risk of PTD.

We performed comprehensive review of the literature in PubMed and Google Scholar databases for studies from 1998 to 2018 linking MO to PTD and inflammation.

Chronic inflammatory status associated to increased synthesis of adipokines and cytokines from fat tissue has been shown in obesity. Obese women have a higher risk of both spontaneous and medically induced PTD. In about 50% of cases of spontaneous PTD, an infection-induced chorion amnionitis can be detected while in the remaining 50% a sterile inflammatory response has been described. Activation of uterine innate immunity system in intra-amniotic cavity and in chorioamniotic membranes might represent the missing link between MO and the pathogenesis of PTD.

Tissue inflammation might represent the pathogenic link between MO and increased occurrence of PTD. The achievement of pre-pregnancy normal maternal weight and body mass index is a fundamental aim of public health to reduce the incidence of PTD and get optimal reproductive outcomes.

Tissue inflammation might represent the pathogenic link between MO and increased occurrence of PTD. The achievement of pre-pregnancy normal maternal weight and body mass index is a fundamental aim of public health to reduce the incidence of PTD and get optimal reproductive outcomes.Introduction Ejaculatory dysfunction is a common complication of surgeries for benign prostatic obstruction. It causes a clear deterioration in quality of life. Techniques have been developed to attempt to preserve antegrade ejaculation (AE). Our objective was to analyze results of ejaculatory function using an AE preservation technique during anatomical vaporization with XPS 180-W. Methods Between 2017 and 2019, sexually active patients were treated using this technique by the same surgical team. A questionnaire (MSHQ-EjD Short Form) was mailed, patients who did not answer were contacted by phone or personally during follow-up. Responses were analyzed. Voiding function was evaluated using International Prostatic Symptoms Score (IPSS), Qmax, and postvoid residual volume. t-Test for paired samples was used to compare conformity of patients with and without AE and voiding results. A p  less then  0.05 was considered statistically significant. Results In total, 77 of 112 patients (68.8%) completed questionnaires and were included.

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