|
Why COVID-19 is less frequent and severe in children: a narrative review
|
|
Reza Sinaei, Sara Pezeshki, Saeedeh Parvaresh, Roya Sinaei |
|
Background: Despite the streaks of severity, severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection is, in general, less frequent and severe in children than in adults. We searched for causal evidence of this mystery.
Data sources: An extensive search strategy was designed to identify papers on coronavirus disease 2019 (COVID-19). We searched Ovid MEDLINE, PubMed, EMBASE databases, and Cochrane library and carried out a review on the causes of this dilemma.
Results: Our searches produced 81 relevant articles. The review showed that children accounted for a lower percentage of reported cases, and they also experienced less severe illness courses. Some potential explanations, including the tendency to engage the upper airway, the different expression in both receptors of angiotensin-converting enzyme and renin-angiotensin system, a less vigorous immune response, the lower levels of interleukin (IL)-6, IL-10, myeloperoxidase, and P-selectin and a higher intracellular adhesion molecule-1, a potential protective role of lymphocytes, and also lung infiltrations might have protective roles in the immune system-respiratory tract interactions. Finally, what have shed light on this under representation comes from two studies that revealed high-titer immunoglobulin-G antibodies against respiratory syncytial virus and mycoplasma pneumonia, may carry out cross-protection against SARS-CoV-2 infection, just like what suggested about the vaccines. Conclusions: These results require an in-depth look. Properties of the immune system including a less vigorous adaptive system beside a preliminary potent innate response and a trained immunity alongside a healthier respiratory system, and their interactions, might protect children against SARS-CoV-2 infection. However, further studies are needed to explore other possible causes of this enigma. |
|
[Abstract] [Full Text] [PDF]
|
|
Assessment of left-ventricular diastolic function in pediatric intensive-care patients: a review of parameters and indications compared with those for adults
|
|
Morgan Recher, Astrid Botte, Jerome Soquet, Jean-Benoit Baudelet, François Godart, Stephane Leteurtre |
|
Background: The incidence of diastolic heart failure has increased over time. The evaluation of left-ventricular diastolic function is complex, ongoing, and remains poorly performed in pediatric intensive-care patients. This study aimed to review the literature and to provide an update on the evaluation of left-ventricular diastolic function in adults and children in intensive care.
Data sources: We searched data from PubMed/Medline. Thirty-two studies were included. Four pragmatic questions were identified: (1) What is the physiopathology of diastolic dysfunction? (2) Which tools are required to evaluate diastolic function? (3) What are the echocardiographic criteria needed to evaluate diastolic function? (4) When should diastolic function be evaluated in pediatric intensive care?
Results: Early diastole allows characterization of relaxation, whereas compliance assessments and filling pressures are evaluated during late diastole. The evolution of diastolic function differs between adults and children. Unlike in adults, decreased compliance occurs at the same time as delayed relaxation in children. Diastolic function can be evaluated by Doppler echocardiography. The echocardiographic criteria for ventricular relaxation include the E wave, E/A wave ratio, and isovolumic relaxation time. Ventricular compliance can be assessed by the E/e¡¯ wave ratio, atrial volume, and Ap wave duration during pulmonary vein flow. In adult intensive-care patients, the E/e¡¯ ratio can be used as an index of tolerance for volume expansion in septic patients and to adjust the inotropic support. Conclusions: Clinical studies would allow some of these parameters to be validated for use in children in intensive care. |
|
[Abstract] [Full Text] [PDF]
|
|
Bartter¡¯s syndrome: clinical findings, genetic causes and therapeutic approach
|
|
Flavia Cristina Carvalho Mrad, S¨ªlvia Bouissou Morais Soares, Luiz Alberto Wanderley de Menezes Silva, Pedro Versiani dos Anjos Menezes, Ana Cristina Simões-e-Silva |
|
Background: Bartter¡¯s syndrome (BS) is a rare group of salt losing tubulopathies due to the impairment of transport mechanisms at the thick ascending limb of the Henle¡¯s loop.
Data sources: Literature reviews and original research articles were collected from database, including PubMed and Scopus.
Results: According to the time of onset and symptoms, BS can be classified into antenatal and classic BS. Molecular studies have identified different subtypes of BS. BS types I, II and III are caused by mutations on genes encoding the luminal Na+¨CK+¨C2Cl- co-transporter, the luminal K+ channel ROMK, and the basolateral chloride channel ClC-Kb (CLCNKB), respectively. Loss-of-function mutations of Barttin CLCNK type accessory beta subunit cause BS type IVa. Simultaneous mutations of CLCNKB and CLCNKA cause BS type IVb. BS type V consists in a novel transient form characterized by antenatal presentation due to mutations in the MAGE family member D2. Severe gain-of-function mutations of the extracellular calcium sensing receptor gene can result in an autosomal dominant condition of BS. Main clinical and biochemical alterations in BS include polyuria, dehydration, hypokalemia, hypochloremic metabolic alkalosis, hyperreninemia, high levels of prostaglandins, normal or low blood pressure, hypercalciuria and failure to thrive. Treatment focuses mainly at correcting dehydration and electrolyte disturbances and in measures to reduce polyuria, including the use of nonsteroidal anti-inflammatory medications to control excessive renal prostaglandin E2 production. Conclusions: Early diagnosis and treatment of BS may prevent long-term consequences such as growth failure, nephrocalcinosis and end-stage renal disease. |
|
[Abstract] [Full Text] [PDF]
|
|
Intestinal microbiota and juvenile idiopathic arthritis: current understanding and future prospective
|
|
Le Xin, Feng He, Sen Li, Zhi-Xuan Zhou, Xiao-Lin Ma |
|
Background: Juvenile idiopathic arthritis (JIA) characterized by arthritis of unknown origin is the most common childhood chronic rheumatic disease, caused by both host genetic factors and environmental triggers. Recent evidence has mounted to focus on the intestinal microbiota, a potentially recognized set of environmental triggers affecting JIA development. Here we offer an overview of recently published animal and human studies that support the impact of intestinal microbiota in JIA.
Data sources: We searched PubMed for animal and human studies publications with the search terms ¡°intestinal microbiota or gut microbiota¡± and ¡°juvenile idiopathic arthritis or juvenile chronic arthritis or juvenile rheumatoid arthritis or childhood rheumatoid arthritis or pediatric rheumatoid arthritis¡±.
Results: Several comparative studies have demonstrated that intestinal microbial alterations might be triggers in disease pathogenesis. Alternatively, a slice of studies has suggested environmental triggers in early life might disrupt intestinal microbial colonization, including cesarean section, formula feeding, and antibiotic exposure. Aberrant intestinal microbiota may infl uence the development of JIA by mediating host immune programming and by altering mucosal permeability. Conclusions: Specific microbial factors may contribute to the pathogenesis of JIA. Intensive studies, however, are warranted to investigate the causality between intestinal dysbiosis and JIA and the mechanisms behind these epidemiologic relationships. Studies are also needed to design the best interventional administrations to restore balanced intestinal microbial communities. |
|
[Abstract] [Full Text] [PDF]
|
|
Dent disease: classification, heterogeneity and diagnosis
|
|
Yan-Yan Jin, Li-Min Huang, Xiao-Fang Quan, Jian-Hua Mao |
|
Background: Dent disease is a rare tubulopathy characterized by manifestations of proximal tubular dysfunction, which occurs almost exclusively in males. It mainly presents symptoms in early childhood and may progress to end-stage renal failure between the 3rd and 5th decades of human life. According to its various genetic basis and to clinical signs and symptoms, researchers define two forms of Dent disease (Dent diseases 1 and 2) and suggest that these forms are produced by mutations in the CLCN5 and OCRL genes, respectively. Dent diseases 1 and 2 account for 60% and 15% of all Dent disease cases, and their genetic cause is generally understood. However, the genetic cause of the remaining 25% of Dent disease cases remains unidentified.
Data sources: All relevant peer-reviewed original articles published thus far have been screened out from PubMed and have been referenced.
Results: Genetic testing has been used greatly to identify mutation types of CLCN5 and OCRL gene, and next-generation sequencing also has been used to identify an increasing number of unknown genotypes. Gene therapy may bring new hope to the treatment of Dent disease. The abuse of hormones and immunosuppressive agents for the treatment of Dent disease should be avoided to prevent unnecessary harm to children. Conclusions: The current research progress in classification, genetic heterogeneity, diagnosis, and treatment of Dent disease reviewed in this paper enables doctors and researchers to better understand Dent disease and provides a basis for improved prevention and treatment. |
|
[Abstract] [Full Text] [PDF]
|
|
Advance in the understanding of vasovagal syncope in children and adolescents
|
|
Hong-Xia Li, Lu Gao, Yue Yuan |
|
Background: Vasovagal syncope (VVS) accounts for 60-80% of cases of neurally mediated syncope. VVS results from acute orthostatic intolerance and recurrent syncopal attacks, which can seriously affect an individual¡¯s quality of life. In addition, some children even experience trauma during attacks. Therefore, it is particularly important to clarify the pathogenesis of VVS. The aim of our study is to reveal the latest research progress of VVS.
Data sources: Literature that involved the pathogenesis of VVS were selected from Cochrane Library (1990-2019), EMBASE (1991-2019) and PubMed (1968-2019) databases.
Results: Hypovolemia, autonomic dysfunction, vasomotor dysfunction, baroreceptor reflex abnormalities, endothelial dysfunction, serotonin surges, and gut microbiota were involved in the underlying mechanism of VVS. Conclusions: VVS is not always a benign prognosis. Various aspects were involved in its pathogenesis. Bezold-Jarish reflex, dysfunction of the autonomic nervous system, genetic factors and so on played important roles in VVS; however, the mechanism remains unclear. |
|
[Abstract] [Full Text] [PDF]
|
|
Current status of fecal calprotectin as a diagnostic or monitoring biomarker for cow¡¯s milk protein allergy in children: a scoping review
|
|
Li-Jing Xiong, Xiao-Li Xie, Yang Li, Xiao-Zhi Deng |
|
Background: There are few approved biomarkers for diagnosis and monitoring of cow¡¯s milk protein allergy (CMPA), thus the oral food challenge remains to be the golden diagnostic standard. A potential biomarker is fecal calprotectin, a cytosolic protein, elevating in the presence of intestinal mucosal inflammation. We aimed to undertake a scoping review of the evidence pertaining to the current status of fecal calprotectin used for diagnosis and monitoring CMPA in children, and tried to indicate the aspects needed to be concerned in the future investigations and researches.
Methods: A scoping review was performed using the literature searched from PUBMED, EMBASE, and Web of Science Databases until July 2019 on the studies about the application of fecal calprotectin as a biomarker of CMPA in children. Studies were examined according to the inclusion and exclusion criteria. Data were extracted, and a narrative synthesis was conducted to summarize and analyze.
Results: Thirteen studies with different study design embracing 1238 children were included. The age range was from infants to adolescents. Most children with CMPA presented gastrointestinal symptoms, among which hematochezia was most common. Amount of data suggested that infants with CMPA represented elevated levels of fecal calprotectin, particularly with distinct significance in non-IgE-mediated CMPA groups. Decreases of fecal calprotectin after elimination diet were demonstrated in enrolled studies. However, no matter in the CMPA positive or negative groups, the changes of fecal calprotectin before or after challenge showed no significance. Contradictory results were generated from studies on the role of fecal calprotectin in predicting allergic disease. Conclusions: Available evidence is not sufficient to confirm the utilization of fecal calprotectin both in diagnosis and monitoring of CMPA and predicting for allergic disease. More clinical and bench researches with elaborate design should be conducted and the exact cut-off values of fecal calprotectin in different groups remain to be determined. |
|
[Abstract] [Full Text] [PDF]
|
|