Background Iron-deficiency anemia (IDA) is common in children with inflammatory bowel disease (IBD); however, oral iron supplements are commonly associated with poor compliance due to gastrointestinal side effects. We compared the effect of lactoferrin versus oral ferrous sulfate for the treatment of IDA in children with IBD. Methods Ninety-two IBD children with IDA were included but only 80 children completed the study and they were randomized into two groups: ferrous sulfate group (n = 40) who received ferrous sulfate 6 mg/kg/day for 3 months and lactoferrin group (n = 40) who received lactoferrin 100 mg/day for 3 months. Complete blood count, serum iron, total iron-binding capacity (TIBC), transferrin saturation (TS), serum ferritin, interleukin-6 (IL-6), and hepcidin 25 were measured before and after the treatment. Results Hemoglobin (Hb), mean corpuscular volume, serum iron, TS, and serum ferritin significantly increased, while TIBC decreased significantly after the administration of either ferrous sulfate or lactoferrin compared to their baseline data. In addition, lactoferrin significantly increased Hb, serum iron, TS, and serum ferritin compared to ferrous sulfate. Moreover, lactoferrin significantly decreased IL-6 and hepcidin levels. Conclusion Lactoferrin is a promising effective treatment with fewer side effects than oral elemental iron in children with IBD and IDA. Clinical trial registration The study was registered at www.pactr.org (PACTR202002763901803). Impact Iron-deficiency anemia (IDA) in children with inflammatory bowel disease (IBD) is treated with oral iron therapy; however, oral iron supplements are commonly associated with poor compliance due to gastrointestinal side effects. To the best of our knowledge, our study was the first in pediatrics that compared the effect of lactoferrin versus oral ferrous sulfate as an iron supplement for the treatment of IDA in children with IBD. We found that lactoferrin is a promising effective treatment with fewer side effects than oral elemental iron in children with IBD and IDA.
Background Hepatic encephalopathy exacerbates the morbidity, delays hospital discharge, and increases the rate of readmissions of cirrhotic patients, particularly those are admitted by acute variceal bleeding. We evaluated the performance of albumin-bilirubin score in prediction of hepatic encephalopathy in cirrhotic patients with acute variceal bleeding, in comparison to Child-Pugh and MELD scores. This prospective cohort study was conducted on 250 cirrhotic patients who were consecutively presented by acute variceal bleeding in the period from January to December 2020 at Tanta university emergency hospital. Albumin-bilirubin, Child-Pugh, and MELD scores were measured at admission, and then all patients were followed up for 4 weeks after endoscopic bleeding control for possible occurrence of hepatic encephalopathy Results Albumin-bilirubin, Child-Pugh, and MELD scores had significant performances in prediction of hepatic encephalopathy in cirrhotic patients with acute variceal bleeding; in this regard, albumin-bilirubin score had the highest accuracy (AUC 0.858, CI 0.802-0.914, sig 0.000) followed by Child-Pugh score (AUC 0.654, CI 0.574–0.735, sig 0.001) and then MELD score (AUC 0.602, CI 0.519–0.686, sig 0.031). The cumulative incidence of hepatic encephalopathy in cirrhotic patients with albumin-bilirubin grade 3 was found to be significantly more than that present in albumin-bilirubin grade 2; most of these hepatic encephalopathy cases occurred in the first 2 weeks of follow-up period. Conclusions Albumin-bilirubin score has a significant performance in risk prediction of hepatic encephalopathy in cirrhotic patients with acute variceal bleeding better than Child-Pugh and MELD scores. Albumin-bilirubin grades could be used as a risk stratifying tool to triage cirrhotic patients who will benefit from early discharge after bleeding control and those patients who will benefit from prophylactic measures for hepatic encephalopathy.
Background and Aim Esophagogastroduodenoscopy (EGD) is the gold standard tool in both screening/diagnosis and management of varices in cirrhotic patients; however, its invasive nature may be uncomfortable to some patients, and in addition, it may be unavailable in some centers that cannot afford it. Therefore, to decrease the economic and physical burden on patients, multiple noninvasive clinical, laboratory, and radiological parameters are evaluated as triage screening predictors of varices before patients' referral to endoscopy. In this respect, we tried to evaluate the validity of portal vein velocity (PVV) as a noninvasive screening tool of esophageal varices (EV). Methods One hundred thirty‐five cirrhotic patients were consecutively enrolled in this cross‐sectional study. All patients were evaluated independently and blindly by EGD as the gold standard and then by Doppler ultrasound on portal vein (PV). Results Univariate regression showed significant coefficients for PVV, platelet (PLT), albumin, bilirubin, international normalized ratio (INR), portal vein diameter, and ascites; however, multivariable regression showed significant coefficients only for PVV, PLT, and albumin; ( P = 0.000, 0.000, and 0.006, respectively). Area under the receiver operating characteristic curve (AUROC), sensitivity, specificity, LR+, and LR− values were then calculated and validated using bootstrap analysis. PVV was more accurate than other evaluated parameters (AUROC: 0.927 and P = 0.000). The most accurate rule out cutoff value for PVV was ≥19 cm/s with the sensitivity of 97% and LR− of 0.05. Conclusion PVV may be useful as a noninvasive triage test for selection of the high‐risk cirrhotic patients who should be referred to and could benefit from EGD. We could highlight using PVV to rule out EV at a cutoff value ≥19 cm/s, reserving EGD only for patients with the PVV value <19 cm/s.
Introduction: The onset of the Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) is caused by acquired somatic mutations in target myeloid genes “driver mutations”. The CCL2 gene is overexpressed by non-Hodgkin lymphomas and multiple solid tumors. Aim of the study: to evaluate the possible association of CCL2 rs1024611 SNP and its expression level and the risk of developing Philadelphia-negative MPNs. Patients and methods: A total of 128 newly diagnosed Philadelphia-negative MPN patient and 141 healthy subjects were evaluated for the genotype distribution of CCL2 rs1024611 and CCL2 expression levels. Results: The CCL2 rs1024611 G/G genotype was more frequent and significantly frequent among PMF and Post-PV/ET-MF patients and the mean CCL2 expression levels were significantly higher in PMF and Post-PV/ET-MF compared to the healthy subjects. The CCL2 rs1024611 SNP was significantly correlated to the CCL2 gene expression level and fibrosis grade. ROC analysis for the CCL2 gene expression level that discriminates MF patients from PV + ET patients revealed a sensitivity of 80.43% and a specificity of 73.17% with an AUC of 0.919 (p < 0.001). Conclusion: The CCL2 rs1024611 polymorphism could be an independent risk factor for developing MF (PMF and Post-PV/ET-MF). Moreover, CCL2 gene expression could be potential genetic biomarker of fibrotic progression.
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