Invasive pneumococcal pneumonia with massive empyema: a case report / Tin Nwe Latt and Noor Shafina Mohd Nor

Although the use of appropriate antibiotics has significantly improved the outcome of pneumonia, severe complications are still encountered. We report here of a case with invasive pneumococcal pneumonia with massive empyema. A 2-year-4-month old girl presented with fever for 8 days and intermittent cough for 2 weeks. On examination, reduced air entry with dullness on percussion was noted on the left lung. Chest ultrasound revealed moderate to gross pleural effusion with septations, for which left thoraco-centesis with insertion of pigtail tube was performed. Streptococcus pneumoniae was detected via polymerase chain reaction (PCR) test in the pleural fluid. Intravenous (IV) benzylpenicillin and ceftriaxone were given together with one course (5 days) of intrapleural urokinase to breakdown the septations. Timely and appropriate management of pneumonia including the use of thrombolytic agent is vital to ensure optimal outcome and reduce the need of invasive procedures in cases with massive empyema. Public awareness of pneumococcal vaccination is also essential as a part of preventive measures

The impacts of intrauterine Bisphenol A exposure on pregnancy and expression of miRNAs related to heart development and diseases in animal model

This study aimed to examine the impact of BPA exposure on pregnancy and foetuses on cardiac tissues and the expression of cardiac microRNAs (miRNAs) related to heart development and diseases. Pregnancy is known to be the “critical windows” in determining the offspring physical and cells development in their life after birth. The increment of the risk of cardiovascular disease (CVD) in a later stage of life has been reported by few studies demonstrated from prenatal exposure of BPA. BPA has been shown to alter miRNAs expression profiles for organ development, regeneration and metabolic functions. These alterations have been associated with the risk of CVDs. However, the associations between pregnancy outcomes and miRNAs expression in cardiac of mother- and foetuses-exposed to BPA are still not entirely explored. In BPA-exposed pregnant rat groups, a significant weight gained was observed in comparison to control (p < 0.05). Interestingly, significant changes in systolic and diastolic blood pressure between the first and third trimester of BPA-exposed pregnant rats were also observed (p < 0.05). In BPA-exposed pregnant rats, miR-499-5p was significantly altered in the heart (p < 0.01). Meanwhile, altered miR-17-5p, -208-3p, and -210-3p expressions were observed in all heart of the foetuses from BPA-exposed pregnant rats (p < 0.05). In H&E staining, BPA-exposed foetal hearts showed a sign of fibrosis while BPA-exposed pregnant rats showed muscle remnant. Masson trichrome staining further confirmed the presence of fibrosis observed in BPA-exposed foetal heart and reduced expression of cardiac troponin I (cTnI) was also observed in BPA-exposed foetal heart. In summary, altered cardiac miRNAs with histological changes were observed in both mother- and foetus-exposed BPA These findings put forward the importance of future work to further understand how prenatal BPA exposure affect foetuses in their later stage of life

Familial hypercholesterolaemia in children and adolescents from 48 countries: a cross-sectional study

Background: Approximately 450 000 children are born with familial hypercholesterolaemia worldwide every year, yet only 2·1% of adults with familial hypercholesterolaemia were diagnosed before age 18 years via current diagnostic approaches, which are derived from observations in adults. We aimed to characterise children and adolescents with heterozygous familial hypercholesterolaemia (HeFH) and understand current approaches to the identification and management of familial hypercholesterolaemia to inform future public health strategies. Methods: For this cross-sectional study, we assessed children and adolescents younger than 18 years with a clinical or genetic diagnosis of HeFH at the time of entry into the Familial Hypercholesterolaemia Studies Collaboration (FHSC) registry between Oct 1, 2015, and Jan 31, 2021. Data in the registry were collected from 55 regional or national registries in 48 countries. Diagnoses relying on self-reported history of familial hypercholesterolaemia and suspected secondary hypercholesterolaemia were excluded from the registry; people with untreated LDL cholesterol (LDL-C) of at least 13·0 mmol/L were excluded from this study. Data were assessed overall and by WHO region, World Bank country income status, age, diagnostic criteria, and index-case status. The main outcome of this study was to assess current identification and management of children and adolescents with familial hypercholesterolaemia. Findings: Of 63 093 individuals in the FHSC registry, 11 848 (18·8%) were children or adolescents younger than 18 years with HeFH and were included in this study; 5756 (50·2%) of 11 476 included individuals were female and 5720 (49·8%) were male. Sex data were missing for 372 (3·1%) of 11 848 individuals. Median age at registry entry was 9·6 years (IQR 5·8-13·2). 10 099 (89·9%) of 11 235 included individuals had a final genetically confirmed diagnosis of familial hypercholesterolaemia and 1136 (10·1%) had a clinical diagnosis. Genetically confirmed diagnosis data or clinical diagnosis data were missing for 613 (5·2%) of 11 848 individuals. Genetic diagnosis was more common in children and adolescents from high-income countries (9427 [92·4%] of 10 202) than in children and adolescents from non-high-income countries (199 [48·0%] of 415). 3414 (31·6%) of 10 804 children or adolescents were index cases. Familial-hypercholesterolaemia-related physical signs, cardiovascular risk factors, and cardiovascular disease were uncommon, but were more common in non-high-income countries. 7557 (72·4%) of 10 428 included children or adolescents were not taking lipid-lowering medication (LLM) and had a median LDL-C of 5·00 mmol/L (IQR 4·05-6·08). Compared with genetic diagnosis, the use of unadapted clinical criteria intended for use in adults and reliant on more extreme phenotypes could result in 50-75% of children and adolescents with familial hypercholesterolaemia not being identified. Interpretation: Clinical characteristics observed in adults with familial hypercholesterolaemia are uncommon in children and adolescents with familial hypercholesterolaemia, hence detection in this age group relies on measurement of LDL-C and genetic confirmation. Where genetic testing is unavailable, increased availability and use of LDL-C measurements in the first few years of life could help reduce the current gap between prevalence and detection, enabling increased use of combination LLM to reach recommended LDL-C targets early in life

Congenital Adrenal Hyperplasia: Diagnostic Pitfalls in Prolonged Neonatal Jaundice

Congenital Adrenal Hyperplasia (CAH) is a genetic disorder that leads to cortisol deficiency. However, prolonged neonatal jaundice is a rare presentation of CAH. The pathophysiology of hyperbilirubinemia in CAH is still ill-defined. Plausible causes are related to the synthesis of bile, maturity of the liver and adrenal function. This case reported a neonate who presented with severe prolonged jaundice that lasted for more than a month. A short Synacthen test confirmed diagnosis of CAH. He was started on steroid replacement. He had regular follow-up under paediatric endocrinologist and primary care physician for long-term monitoring and overall health care. This case demonstrates the importance of recognizing the clinical and biochemical features of CAH for early detection and referral. Long-term follow-up and monitoring is necessary due to the risk of complications and side effects of medications. This is the first case of CAH presented with persistent hyperbilirubinemia to be reported from Malaysia. The case describes the difficult workup that has been encountered in the patient’s care and management

Congenital Adrenal Hyperplasia: Diagnostic Pitfalls in Prolonged Neonatal Jaundice

Congenital Adrenal Hyperplasia (CAH) is a genetic disorder that leads to cortisol deficiency. However, prolonged neonatal jaundice is a rare presentation of CAH. The pathophysiology of hyperbilirubinemia in CAH is still ill-defined. Plausible causes are related to the synthesis of bile, maturity of the liver and adrenal function. This case reported a neonate who presented with severe prolonged jaundice that lasted for more than a month. A short Synacthen test confirmed diagnosis of CAH. He was started on steroid replacement. He had regular follow-up under paediatric endocrinologist and primary care physician for long-term monitoring and overall health care. This case demonstrates the importance of recognizing the clinical and biochemical features of CAH for early detection and referral. Long-term follow-up and monitoring is necessary due to the risk of complications and side effects of medications. This is the first case of CAH presented with persistent hyperbilirubinemia to be reported from Malaysia. The case describes the difficult workup that has been encountered in the patient’s care and management

The Current Findings on the Impact of Prenatal BPA Exposure on Metabolic Parameters: In Vivo and Epidemiological Evidence

Metabolic syndrome (MS) is a multifactorial disease entity and is not fully understood. Growing evidence suggests that early exposure to bisphenol A (BPA) is a significant risk factor for the development of metabolic diseases. BPA is a monomer used in the manufacturing of polycarbonate plastics, thermal receipt paper, and epoxy resins. Owing to its widespread use, BPA has been detected in human fluids and tissues, including blood, placental breast milk, and follicular fluid. In the present review, we aimed to review the impact of prenatal exposure to different doses of BPA on metabolic parameters as determined by in vivo and epidemiological studies. The PubMed, Scopus, and Web of Science electronic databases were searched to identify articles published during a period of 15 years from 2006 to 2021, and 29 studies met the criteria. Most studies demonstrated that prenatal exposure to low BPA concentrations correlated with alterations in metabolic parameters in childhood and an increased risk of metabolic diseases, such as obesity and type 2 diabetes mellitus (T2DM), in adulthood. Therefore, prenatal exposure to low doses of BPA may be associated with an increased risk of obesity and T2DM in a sex-specific manner

Prenatal Bisphenol a Exposure and Postnatal Trans Fat Diet Alter Small Intestinal Morphology and Its Global DNA Methylation in Male Sprague-Dawley Rats, Leading to Obesity Development

In this study, we aimed to determine whether a postnatal trans fat diet (TFD) could aggravate prenatal bisphenol A (BPA) exposure effects on offspring&rsquo;s small intestine and adulthood obesity, due to the relatively sparse findings on how the interaction between these two variables interrupt the small intestinal cells. Twelve pregnant rats were administered with either unspiked drinking water (control; CTL) or BPA-spiked drinking water throughout pregnancy. Twelve weaned pups from each pregnancy group were then given either a normal diet (ND) or TFD from postnatal week (PNW) 3 until PNW14, divided into control offspring on normal diet (CTL-ND), BPA-exposed offspring on normal diet (BPA-ND), control offspring on trans fat diet (CTL-TFD), and BPA offspring on trans fat diet (BPA-TFD) groups. Body weight (BW), waist circumference, and food and water intake were measured weekly in offspring. At PNW14, small intestines were collected for global DNA methylation and histological analyses. Marked differences in BW were observed starting at PNW9 in BPA-TFD (389.5 &plusmn; 10.0 g; p &lt; 0.05) relative to CTL-ND (339.0 &plusmn; 7.2 g), which persisted until PNW13 (505.0 &plusmn; 15.6 g). In contrast, water and food intake between offspring were significantly different (p &lt; 0.01&ndash;0.05) at earlier ages only (PNW4&ndash;6 and PNW7&ndash;9, respectively). Furthermore, substantial differences in the general parameters of the intestinal structures were exclusive to ileum crypt length alone, whereby both BPA-ND (150.5 &plusmn; 5.1 &mu;m; p &lt; 0.001), and BPA-TFD (130.3 &plusmn; 9.9 &mu;m; p &lt; 0.05) were significantly longer than CTL-ND (96.8 &plusmn; 8.9 &mu;m). Moreover, BPA-ND (2.898 &plusmn; 0.147%; p &lt; 0.05) demonstrated global small intestinal hypermethylation when compared to CTL-ND and CTL-TFD (1.973 &plusmn; 0.232% and 1.913 &plusmn; 0.256%, respectively). Prenatal BPA exposure may significantly affect offspring&rsquo;s physiological parameters and intestinal function. Additionally, our data suggest that there might be compensatory responses to postnatal TFD in the combined BPA prenatal group (BPA-TFD)

Comparable Enhanced Prothrombogenesis in Simple Central Obesity and Metabolic Syndrome

Objective. There is limited data comparing prothrombogenic or fibrinolysis biomarkers (tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1)) simultaneously in subjects with Metabolic Syndrome (MS), simple central obesity without MS (COB) and normal controls (NC). We investigated the concentrations of fibrinolysis biomarkers in subjects with MS, COB and NC. Methods. A cross-sectional study involving 503 drug naive subjects (163 males, aged 30–65 years old (mean age ± SD = 47.4 ± 8.3 years)) divided into MS, COB and NC groups. COB was defined as central obesity (waist circumference (WC) males ≥90 cm, females ≥80 cm) in the absence of MS according to the International Diabetes Federation 2006. Fasting blood levels of tPA and PAI-1were analyzed. Results. MS and COB had significantly higher concentration of all biomarkers compared to NC. The MS group had significantly higher concentration of tPA and PAI-1 compared to COB. WC and HDL-c had significant correlation with all biomarkers (tPA p<0.001, PAI-1 p<0.001). Fasting plasma glucose and diastolic blood pressure were independent predictors after correcting for confounding factors. Conclusion. Central obesity with or without MS both demonstrated enhanced prothrombogenesis. This suggests that simple obesity possibly increases the risk of coronary artery disease in part, via increased susceptibility to thrombogenesis

The effects of trans fat diet intake on metabolic parameters and pancreatic tissue in offspring of prenatal bisphenol A exposed rats

Abstract Bisphenol A (BPA) is a plasticiser used in the manufacturing of many products and its effects on human health remain controversial. Up till now, BPA involvement in metabolic syndrome risk and development is still not fully understood. In this study, we aimed to investigate the effect of prenatal BPA exposure with postnatal trans-fat diet intake on metabolic parameters and pancreatic tissue histology. Eighteen pregnant rats were divided into control (CTL), vehicle tween 80 (VHC), and BPA (5 mg/kg/day) from gestational day (GD) 2 until GD 21, then their weaning rat’s offspring were fed with normal diet (ND) or trans-fat diet (TFD) from postnatal week (PNW) 3 until PNW 14. The rats were then sacrificed and the blood (biochemical analysis) and pancreatic tissues (histological analysis) were collected. Glucose, insulin, and lipid profile were measured. The study has shown that there was no significant difference between groups with regard to glucose, insulin, and lipid profiles (p > 0.05). All pancreatic tissues showed normal architecture with irregular islets of Langerhans in TFD intake groups compared to offspring that consumed ND. Furthermore, the pancreatic histomorphometry was also affected whereby the study findings revealed that there was a significant increase in the mean number of pancreatic islets in rats from BPA-TFD group (5.987 ± 0.3159 islets/field, p = 0.0022) compared to those fed with ND and BPA non-exposed. In addition, the results have found that prenatal BPA exposure resulted in a significant decrease in the pancreatic islets diameter of the BPA-ND group (183.3 ± 23.28 µm, p = 0.0022) compared to all other groups. In conclusion, prenatal BPA exposure with postnatal TFD in the offspring may affect glucose homeostasis and pancreatic islets in adulthood, and the effect may be more aggravated in late adulthood