Acute necrotising ulcerative gingivitis in an immunocompromised young adult.
Ontology highlight
ABSTRACT:
SUBMITTER: Hu J
PROVIDER: S-EPMC4577715 | biostudies-other | 2015 Sep
REPOSITORIES: biostudies-other
Publications
Acute necrotising ulcerative gingivitis in an immunocompromised young adult.
Hu Jessie J Kent Paul P Lennon Joshua M JM Logan Latania K LK
BMJ case reports 20150916
Acute necrotising ulcerative gingivitis is an acute onset disease characterised by ulceration, necrosis, pain and bleeding in gingival surfaces. It is predominantly seen in severely malnourished children and young adults with advanced HIV infection. We present a unique presentation in a young adult with high-grade osteogenic sarcoma. ...[more]
Similar Datasets
Project description:AIM: To report promoted healing of acute ulcerative and necrotising herpetic keratitis after amniotic membrane transplantation (AMT). METHODS: Retrospective, non-comparative case series of seven patients with acute ulcerative and necrotising herpetic stromal keratitis. Single or multilayer AMT with epithelial side facing up was performed. The main outcome measures were wound healing of the corneal ulcers and decrease of stromal inflammation. RESULTS: The mean follow up was 10.7 (SEM 1.4) months (range 5-15 months). AMT was performed once in five cases, and twice in further two. Improvement of stromal inflammation was noted within 16.4 (2.5) days (range 7-28 days). Epithelial defects healed within a mean of 17 (2.7) days (range 7-28 days). Vision improved in all but two patients. No serious side effects occurred during the follow up. CONCLUSIONS: Although performed in an uncontrolled and non-randomised series of patients, these findings indicate that the AMT shows promise in selected cases for the restoration of ocular surface integrity, reduction of stromal inflammation, and improvement of vision in acute ulcerative and necrotising herpetic keratitis.
| S-EPMC1920776 | biostudies-other
Project description:Acute respiratory failure occurs in up to half of patients with haematological malignancies and 15% of those with solid tumours or solid organ transplantation. Mortality remains high. Factors associated with mortality include a need for invasive mechanical ventilation, organ dysfunction, older age, frailty or poor performance status, delayed intensive care unit admission, and acute respiratory failure due to an invasive fungal infection or unknown cause. In addition to appropriate antibacterial therapy, initial clinical management aims to restore oxygenation and predict the most probable cause based on variables related to the underlying disease, acute respiratory failure characteristics, and radiographic findings. The cause of acute respiratory failure must then be confirmed using the most efficient, least invasive, and safest diagnostic tests. In patients with acute respiratory failure of undetermined cause, a standardised diagnostic investigation should be done immediately at admission before deciding whether to perform more invasive diagnostic procedures or to start empirical treatments. Collaborative and multidisciplinary clinical and research networks are crucial to improve our understanding of disease pathogenesis and causation and to develop less invasive diagnostic strategies and more targeted treatment options.
| S-EPMC7185453 | biostudies-literature
Project description:Coronavirus is a severe infectious disease (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has led to increased mortality worldwide. Multiple reports have been published citing that gastrointestinal symptoms are common in patients with COVID-19 infection. It has also been found that the ACE2 receptor of SARS-CoV-2 is expressed more in the pancreas than the lungs. Despite this, little attention has been paid to the extent and details of pancreatic injury caused by COVID-19. Lack of awareness regarding the COVID-19 status of patients presenting with pancreatitis may expose healthcare workers to SARS-CoV-2 while performing interventions to manage complications of pancreatitis such as necrosis. We report a case of COVID-19-induced acute necrotising pancreatitis in the absence of any known risk factors.
| S-EPMC7477985 | biostudies-literature
Project description:The objectives of this review were to discuss standard and investigational treatment strategies for adolescent and young adult with acute myeloid leukemia, excluding acute promyelocytic leukemia. Acute myeloid leukemia (AML) in adolescent and young adult patients (AYAs) may need a different type of therapy than those currently used in children and older patients. As soon as AML is diagnosed, AYA patient should be offered to participate in well-designed clinical trials. The standard treatment approach for AYAs with AML is remission induction chemotherapy with an anthracycline/cytarabine combination, followed by either consolidation chemotherapy or stem cell transplantation, depending on the ability of the patient to tolerate intensive treatment and cytogenetic features. Presently, continuing progress of novel drugs targeting specific pathways in acute leukemia may bring AML treatment into a new era.
| S-EPMC4470138 | biostudies-literature
Project description:The oral treponeme bacterium Treponema sp. OMZ 838 was originally isolated from a human necrotizing ulcerative gingivitis (NUG) lesion. Its taxonomic status remains uncertain. The complete genome sequence length was determined to be 2,708,067 bp, with a G+C content of 44.58%, and 2,236 predicted coding DNA sequences (CDS).
| S-EPMC4276824 | biostudies-literature
Project description:ObjectivesWe here investigated whether experimental gingivitis enhances systemic markers of inflammation which are also known as surrogate markers of atherosclerotic plaque development.BackgroundGingivitis is a low-level oral infection induced by bacterial deposits with a high prevalence within Western populations. A potential link between the more severe oral disease periodontitis and cardiovascular disease has already been shown.Methods37 non-smoking young volunteers with no inflammatory disease or any cardiovascular risk factors participated in this single-subject interventional study with an intra-individual control. Intentionally experimental oral inflammation was induced by the interruption of oral hygiene for 21 days, followed by a 21-days resolving phase after reinitiation of oral hygiene. Primary outcome measures at baseline, day 21 and 42 were concentrations of hsCRP, IL-6, and MCP-1, as well as adhesion capacity and oxLDL uptake of isolated blood monocytes.ResultsThe partial cessation of oral hygiene procedures was followed by the significant increase of gingival bleeding (34.0%, P<0.0001). This local inflammation was associated with a systemic increase in hsCRP (0.24 mg/L, P?=?0.038), IL-6 (12.52 ng/L, P?=?0.0002) and MCP-1 (9.10 ng/l, P?=?0.124) in peripheral blood samples between baseline and day 21, which decreased at day 42. Monocytes showed an enhanced adherence to endothelial cells and increased foam cell formation after oxLDL uptake (P<0.050) at day 21 of gingivitis.ConclusionsBacterial-induced gingival low-level inflammation induced a systemic increase in inflammatory markers. Dental hygiene almost completely reversed this experimental inflammatory process, suggesting that appropriate dental prophylaxis may also limit systemic markers of inflammation in subjects with natural gingivitis. International Clinical Trials Register Platform of the World Health Organization, registry number: DRKS00003366, URL: http://apps.who.int/trialsearch/Default.aspx.
| S-EPMC3567060 | biostudies-literature
Project description:The purpose of this study was to examine the effect of resistance exercise (RE) intensity on acute hyperglycemia, in young adult males. Thirteen males (age 23.43 ± 2.18 years, height 175.16 ± 10.44 cm, weight 77.02 ± 8.91 kg, body fat 20 ± 0.03%) participated in three randomized testing sessions, each separated by 96 h. The three testing conditions were: control (CON; induction of hyperglycemia with no-exercise), high (HI; induction of hyperglycemia followed by high-intensity RE: 5 × 4, 90% 1-repetition maximum (1-RM)), and moderate (MO; induction of hyperglycemia followed by low-intensity RE: 3 × 14, 65% 1-RM). In all three testing conditions, participants orally ingested a D100 (100 g/10 oz) glucose beverage at a dosage of 2 g glucose/kg body weight and capillary blood was obtained for plasma glucose and insulin analysis at 0 (fasting), 30, 60, 90 and 120 min, following glucose ingestion. At 30-min post-ingestion in the HI and MO conditions, participants began the respective RE protocols. Acute hyperglycemia was achieved throughout all three 2-h testing conditions; mean 2-h plasma glucose levels during CON (7.1 ± 1.3 mmol?L-1), MO (7.5 ± 0.6 mmol?L-1) and HI (8.2 ± 1.9 mmol?L-1) were all significantly (p < 0.05) greater than mean fasting plasma glucose (5.6 ± 0.46 mmol?L-1). Plasma glucose and insulin did not differ (p < 0.05) between treatment conditions at any times points over the 120 min, however, 2-h glucose area under the curve in the HI condition was significantly greater (p < 0.05) than CON and MO. In conclusion, this study indicates that hyperglycemia, induced prior to RE, may be exacerbated by high-intensity RE.
| S-EPMC7552604 | biostudies-literature
Project description:Genetic alterations that activate NOTCH1 signaling and T cell transcription factors, coupled with inactivation of the INK4/ARF tumor suppressors, are hallmarks of T-lineage acute lymphoblastic leukemia (T-ALL), but detailed genome-wide sequencing of large T-ALL cohorts has not been carried out. Using integrated genomic analysis of 264 T-ALL cases, we identified 106 putative driver genes, half of which had not previously been described in childhood T-ALL (for example, CCND3, CTCF, MYB, SMARCA4, ZFP36L2 and MYCN). We describe new mechanisms of coding and noncoding alteration and identify ten recurrently altered pathways, with associations between mutated genes and pathways, and stage or subtype of T-ALL. For example, NRAS/FLT3 mutations were associated with immature T-ALL, JAK3/STAT5B mutations in HOXA1 deregulated ALL, PTPN2 mutations in TLX1 deregulated T-ALL, and PIK3R1/PTEN mutations in TAL1 deregulated ALL, which suggests that different signaling pathways have distinct roles according to maturational stage. This genomic landscape provides a logical framework for the development of faithful genetic models and new therapeutic approaches.
| S-EPMC5535770 | biostudies-literature
Project description:A 21-year-old man with no known medical history presented with substernal chest pain. Serial 12-lead electrocardiography showed dynamic ST-segment elevations in the anterolateral leads. Emergent coronary angiography revealed diffuse coronary aneurysmal disease and thrombotic occlusion of the left anterior descending coronary artery. The patient underwent urgent coronary artery bypass grafting. Subsequent imaging showed intracerebral aneurysms that involved his right and left middle cerebral arteries. The incidence, multiple causes, and proposed mechanisms of coronary artery aneurysmal formation are discussed, as is the rare association of these lesions with extracardiac arterial aneurysms.This association between coronary and extracardiac aneurysms is a phenomenon that warrants further study to determine its prevalence and possible causes. Findings could influence recommendations for further screening of patients diagnosed with coronary aneurysmal disease.
| S-EPMC3368465 | biostudies-literature
Project description:BackgroundTreatment on risk adapted intensive pediatric protocols has improved outcome for teenagers and young adults (TYA) with T-cell acute lymphoblastic leukemia (T-ALL). Understanding the biology of disease in this age group and the genetic basis of relapse is a key goal as patients with relapsed/refractory disease have poor outcomes with conventional chemotherapy and novel molecular targets are required. This study examines the question of whether TYA T-ALL has a specific biological-molecular profile distinct from pediatric or adult T-ALL.MethodsGenomic characterization was undertaken of a retrospective discovery cohort of 80 patients aged 15-26 years with primary or relapsed T-ALL, using a combination of Genome-Wide Human SNP Array 6.0, targeted gene mutation and promoter methylation analyses. Findings were confirmed by MLPA, real-time quantitative PCR, and FISH. Whole Exome Sequencing was performed in 4 patients with matched presentation and relapse to model clonal evolution. A prevalence analysis was performed on a final data set of 1,792 individual cases to identify genetic lesions with age specific frequency patterns, including 972 pediatric (1-14 years), 439 TYA (15-24 years) and 381 adult (≥25 years) cases. These cases were extracted from 19 publications with comparable genomic data identified through a PubMed search.ResultsGenomic characterization of this large cohort of TYA T-ALL patients identified recurrent isochromosome 7q i(7q) in our discovery cohort (n = 3). Prevalence analysis did not identify any age specific genetic abnormalities. Genomic analysis of 6 pairs of matched presentation - relapsed T-ALL established that all relapses were clonally related to the initial leukemia. Whole exome sequencing analysis revealed recurrent, targetable, mutations disrupting NOTCH, PI3K/AKT/mTOR, FLT3, NRAS as well as drug metabolism pathways.ConclusionsAll genetic aberrations in TYA T-ALL occurred with an incidence similar or intermediate to that reported in the pediatric and adult literature, demonstrating that overall TYA T-ALL exhibits a transitional genomic profile. Analysis of matched presentation - relapse supported the hypothesis that relapse is driven by the Darwinian evolution of sub-clones associated with drug resistance (NT5C2 and TP53 mutations) and re-iterative mutation of known key T-ALL drivers, including NOTCH1.
| S-EPMC8290240 | biostudies-literature