Mejiahunter1942
Warfarin requires strict monitoring by measuring prothrombin time (PT), international normalized ratio (INR), and time in therapeutic range (TTR). Several factors can lead to poor PT/INR control including vitamin K status, medication adherence, knowledge, and quality of life. The present study aims to assess patient adherence to warfarin treatment and its correlation with INR control.
A cross-sectional study was conducted between October 2017 and January 2018 at Tripoli University Hospital. Data were collected by structured questionnaires which included; demographic and clinical characteristics, the Oral Anticoagulation Knowledge (OAK) test, and the Morisky Medication Adherence Scale (MMAS-8).
The final analysis included 88 out of 140 patients (73.33%). There were significant differences in age range, gender, marital status, and education level between the 2 groups (poor knowledge and adequate knowledge) (p < 0.05). selleck products There was a significant positive correlation between OAK test score and TTR. Overall, 76.2% of patients were adherent to warfarin (MMAS score ≥6) and 20.45% of patients were of high adherence (MMAS score of 8). The median score was 6 (IQR 6-7). A statistically significant, strong positive correlation between adherence to medication and TTR as an indicator of INR control was found (rs[86] = 0.472, p < 0.0001).
The study addressed and identified several areas for future improvement of patient outcomes. The implementation of new approaches to enhance patient knowledge and adherence is warranted, and measures to provide treatment for all patients that require it are needed, to improve outcomes and decrease adverse drug effects.
The study addressed and identified several areas for future improvement of patient outcomes. The implementation of new approaches to enhance patient knowledge and adherence is warranted, and measures to provide treatment for all patients that require it are needed, to improve outcomes and decrease adverse drug effects.Trisomy 14 (T14) mosaicism is a rare chromosomal condition characterised by various clinical features, including developmental delay, growth impairment, and dysmorphism. Here, we report on a 12-year-old female referred for cytogenetic analysis due to short stature. Standard GTG-banding analysis on the patient's peripheral blood revealed mosaic Τ14 in the form of an i(14)(q10) in 3% of cells. Furthermore, a small supernumerary marker chromosome (sSMC) had been detected in the first trimester of pregnancy in chorionic villus sampling. A skin biopsy in the patient revealed the presence of a metacentric sSMC in 100% of cells. Cytogenetic and FISH studies showed that it was a de novo metacentric bisatellited sSMC derived from chromosomes 14 or 22. Oligonucleotide array-CGH using skin cells revealed no copy number variations. Studies for uniparental disomy 14 by microsatellite analysis confirmed biparental inheritance. To the best of our knowledge, this is the second report of a patient with 2 abnormal cell lines involving chromosome 14 in different tissues, one with mosaic T14 in the form of i(14)(q10) and one with an sSMC derived from chromosome 14, present in blood and skin, respectively. A rare mechanism of trisomy rescue events is proposed to explain the presence of the different cell lines in the tissues examined. This case highlights the importance of providing the cytogenetics laboratory with adequate clinical data to test for low mosaicism and analyse different tissues if necessary, thus contributing to the suitable clinical management of the patient.Biological agents have had an increased usage during the past years, also in pediatric population. Monoclonal antibodies can cause adverse drug reactions with different pathomechanisms, including type I IgE-mediated hypersensitivity reactions (HR). In this report, we describe 2 children who had a diagnosis of anaphylaxis to rituximab (RTX), confirmed by positive in vivo tests in both cases and elevated tryptase value in one case. We also made a review of the few cases of HR to RTX in pediatric population reported in literature and discuss differential diagnosis and utility of allergy investigations.
The pathophysiology of renal disease progression in autosomal-dominant polycystic kidney disease (ADPKD) involves not only cystogenesis but also endothelial dysfunction, leading to the activation of inflammatory and fibrotic pathways. This study evaluated the levels of biomarkers related to osmoregulation, immune system activation, and tubular injury in ADPKD patients with impaired or preserved renal function.
This study included 26 ADPKD patients with modestly impaired renal function (estimated glomerular filtration rate [eGFR] 45-70 mL/min/1.73 m2; Group A), 26 age- and sex-matched ADPKD patients with relatively preserved renal function (eGFR >70 mL/min/1.73 m2; Group B), and 26 age- and sex-matched controls (Group C). Serum levels of copeptin, the inflammasome nucleotide-binding and oligomerization domain-like receptors pyrin domain-containing protein 3 (NLRP3), and soluble urokinase-type plasminogen activator receptor (suPAR) were measured with ELISA techniques.
Patients in Group A had higher levon, even in the early stages of ADKPD.
This study showed that ADPKD patients with impaired and preserved renal function had higher copeptin, NLRP3, and suPAR levels than controls. Such findings support that cystogenesis and inflammation are associated with endothelial dysfunction, even in the early stages of ADKPD.
We previously reported that nonsteroidal anti-inflammatory drugs (NSAIDs) induced small intestinal damage through nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome-dependent interleukin-1β secretion in mice. Our further study demonstrated that colchicine, a therapeutic agent for gout, significantly suppressed NSAID-induced small intestinal damage by inhibiting NLRP3 inflammasome activation in mice. However, clinical efficacy of colchicine for NSAID-induced small intestinal damage has not been established.
We examined the clinical efficacy of colchicine in patients with NSAID-induced severe small intestinal damage as an animal-to-human translational research.
This is a single-center, single-arm, prospective pilot study. From February 2017 to March 2019, we performed video capsule endoscopy (VCE) to screen 10 patients who took NSAIDs continuously for more than 3 months, and 7 of those with severe small intestinal damage were enrolled. Participants were treated with oral colchicine 0.