1. Patients randomized to use of two doses of ursodeoxycholic acid (UDCA) along with phototherapy had significantly reduced total serum bilirubin (TSB) levels at 48 hours after hospitalization and at discharge compared to those receiving only phototherapy.Â
2. Length of stay in hospital was significantly reduced for the experimental group, and an adequate safety profile for UDCA was established.Â
Evidence Rating Level: 1 (Excellent)
Hyperbilirubinemia affects half of term infants and most preterm infants, ranking it among the most common of neonatal disorders. The severity of hyperbilirubinemia indicates whether a neonate requires therapy (most commonly phototherapy). However, few pharmacological agents have been used to clinically treat the condition. UDCA is a hydrophilic bile acid that is naturally synthesized in the gallbladder and due to its hydrophilic nature, it more efficiently replaces hydrophobic acids and facilitates bile outflow from the liver/gallbladder. It also reverses the apoptosis of indirect bilirubin. Its use as a pharmacotherapy has not been fully elucidated and there is a need to better understand potential side effects. Thus, the current study sought to examine the effects of phototherapy along with UCDA on TSB levels and length of hospitalization. The current randomized single-blinded controlled clinical trial included 106 term, appropriate-for-gestational-age, breastfed neonates between three to seven days of age with 14-20 mg/dL TSB. Those receiving UDCA (n = 53) were given two doses of 10 mg/kg/day with phototherapy, compared to controls (n = 53) who only received phototherapy. At hospital discharge, TSB in the intervention group decreased significantly compared to the control group (p = .001). While no difference in bilirubin was observed between the groups at 12 and 24 hours into hospitalization, by 48 hours the TSB was significantly lower in the intervention group (p = .009). Length of stay in hospital was also significantly lower in the intervention group compared to controls (p = .038; 38.49 hours versus 43.52 hours, respectively). Most reassuringly, there were no differences in side effects observed between the groups, which suggests an acceptable safety profile for the medication. Future studies should replicate the protocol with preterm infants and should explore results for infants with additional risk factors (e.g., ABO & Rhesus incompatibility, G6PD-deficiency, and infants of diabetic mothers).
Antiplatelet Therapy, Abdominal Aortic Aneurysm Progression, and Clinical Outcomes
1. In a retrospective cohort of 3435 adults, the progression of abdominal aortic aneurysm (AAA) slowed significantly for those taking aspirin compared to those not taking aspirin.Â
2. Composite rates of rupture, repair, and dissection did not differ over a 10-year period.Â
Evidence Rating Level: 2 (Good)
AAA is a relatively common cardiovascular cause of mortality, and although risk factors for the condition are established, very few pharmacotherapies have been established in decreasing risk of rupture and limiting its progression. However, preclinical studies have raised questions as to whether biomechanical platelet activation in disturbed flow environments are pathophysiologic in AAA. The current retrospective cohort study sought to investigate the association of aspirin, an antiplatelet therapy, with AAA long-term outcomes. A total of 3435 adults’ medical records (mean [SD] age 73.7 [9.0] years; 77.5% men) were reviewed to assess aspirin use/dosage as it relates to AAA diameter, the need for repair or dissection, and survival. All-cause mortality, major bleeds, and composite outcomes of dissection, rupture, or repair after ten years between patients taking aspirin and not taking aspirin did not differ significantly (ps > .05). However, aspirin use was found to be associated with slower progression of AAA annually (2.8 vs 3.8 mm per year; p = .001). The relationship between aspirin use and slowed progression remained significant for non-smokers and makes (Ps for interactions < .05). Aspiring was additionally not associated with more adverse events than non-aspirin use in this cohort (p > .05). These findings may suggest that aspirin could be beneficial in slowing AAA progression, particularly for specific patient groups. However, further prospective research that takes specific precautions to control for the variability in ultrasonography measurements should be considered.
The association between systemic inflammation markers and the prevalence of hypertension
1. Higher scores for systemic inflammatory markers including the systemic immune inflammation index (SII), system inflammation response index (SIRI), and aggregate index of systemic inflammation (AISI) were significantly associated with risk for hypertension.
2. There was also a significant difference in mean arterial pressures (MAP) in patients with higher quartile scores for the above markers. Â
Evidence Rating Level: 2 (Good)
Hypertension is itself a potent risk factor for several adverse cardiovascular outcomes, representing an important public health concern globally. Recent literature has produced quantifiable markers in peripheral blood cell lines related to systemic inflammation; the SII, SIRI, and AISI have each been established as such markers. This large-scale cross-sectional study analyzed data belonging to 119,664 individuals (aged 20 to 85 years old [median age 49 years], 48.44% male) derived from the National Health and Nutrition Examination Survey (NHANES) with the purpose of establishing association between SII, AISI, and SIRI scores with hypertension. There was a significant association between higher SII, SIRI, and AISI scores in hypertensive patients compared to those without hypertension, with each unit increase in logarithmically converted quartiles for each marker (logSII, logAISI, logSIRI) resulting in increased risk for hypertension by 20.3%, 20.1%, and 23.7%, respectively. The highest quartile for each of these systemic inflammation markers yielded a 1.11-fold, 1.14-fold, and 1.19-fold increase in risk for hypertension, respectively. There was also a negative correlation between mean arterial pressure (MAP) and logSII, logSIRI, and logAISI. The highest odds ratios for hypertension were associated with the SIRI, suggesting that it may be the most effective systemic inflammatory marker for identifying HTN. Overall, these results indicate that systemic markers for inflammation could serve useful in stratifying one’s risk for developing hypertension.
1. This prospective study found that low eosinophil counts were significantly associated with acute bacterial infection in older adults, and was more sensitive than a CIBLE score of > 87, but less specific.Â
2. The eosinopenia cutoff established was < .01 g/L in this study.Â
Evidence Rating Level: 2 (Good)
Sepsis is significantly associated with increased age, as is the incidence of bacterial infection. Oftentimes, older patients present atypically, typical inflammatory markers are not as reliable in this population, and they can be afflicted by distinct pathogens compared to their younger counterparts. The literature has suggested the association of eosinopenia in the acute stages of infection, with reliable sensitivity and specificity for bacterial infection. The current prospective study investigated the value of the eosinophil count in 156 older adult patients (≥ 75 years, mean 88.7, SD 5.9) with acute bacterial infections with fever (≥ 38 degrees Celsius) or inflammation (white blood cell [WBC] count > 10 g/L, C-reactive protein [CRP] > 20 mg/L). Of those with bacterial infections, pulmonary infections and urinary tract infections were most diagnosed conditions. Low eosinophil count (< .01 g/L) was found to be independently associated with acute bacterial infection (p < .001). Additionally, eosinophil counts below 0.01 g/L were more specific (84%) than a high CIBLE score (72%) for acute bacterial infection but were less sensitive (49%) than CIBLE scores (62%), which are composite scores that include: age, CRP, temperature, chronic obstructive pulmonary disease (COPD), and eosinophil/granulocyte ratios. The area-under-the-curve (AUC) was comparable between the two. Overall, these results indicate that eosinophil counts could prove useful as an accessible and inexpensive tool in the overall clinical picture and diagnosis of bacterial infection. Future studies should apply this protocol in multicentre trials to ensure generalizability.
Statin use and the risk of venous thromboembolism in women taking hormone therapy
1. In this case-control study, the use of statins in menopausal women concurrently with hormone therapy (HT) significantly reduced the risk of VTE.Â
2. The response was dose-dependent, with high-intensity statins providing a higher reduction in VTE risk compared with low- to -medium intensity statins.Â
Evidence Rating Level: 3 (Average)
Menopausal symptoms can have debilitating impacts on women’s quality of life, and although hormone therapy (HT) can be effective, concerns surrounding increased risk for complications (such as the doubled risk for VTE) are a barrier to the initiation of HT. The anti-inflammatory and antithrombotic benefits of statins in reducing the risk for VTE have been established, but their potential role in mediating VTE risk for postmenopausal women on HT has not been established in the US, nor has it been re-established in the recently changing landscape of HT (e.g., there has been a decrease in estrogen products use in the past decade, and research has not included women on higher-risk combined hormonal contraceptives). The current case-control study analyzed databases of over 223,000 women aged 50 to 64 (mean [SD] age, 57.5 [4.4] years), with controls matching VTE cases in a 10:1 ratio. It was found that overall, recent HT exposure was associated with 51% increased risk for VTE compared to those with no recent HT (OR, 1.51; 95% CI, 1.43-1.60). Current statin use was associated with a decreased risk (12%) of VTE for women on HT compared to those using no statins (OR, 0.88; 95% CI, 0.84-0.93). Overall, individuals taking HT with statins had an 18% lower risk of VTE than those on HT without statins, and there was a dose-dependent response where high-intensity statin use (atorvastatin ≥40 mg or rosuvastatin ≥20 mg) was associated with a 31% reduction in VTE risk compared to low- to medium- intensity statin therapy which (16% decreased risk). These results indicate that HT may not be contraindicated in women taking statins and suggest that they may actually counteract some of the associated risks of VTE and cardiovascular complications while on HT.
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