ABSTRACT
Background: Scientific information on the impact of malaria on the risk of developing type 2 diabetes mellitus (T2DM) after recovery from the coronavirus disease 2019 (COVID-19) is limited in the Ghanaian context. The purpose of this study was to examine the association between selected risk markers of T2DM in falciparum malaria patients post-COVID-19 or not at a tertiary hospital in Ghana. Methodology: This was a descriptive cross-sectional comparative study of 38-recovered COVID-19 adult participants with malaria and 40 unexposed COVID-19 adults with malaria at the Tamale Teaching Hospital, Ghana. Demographic, anthropometric and levels of glucose, insulin, C-reactive protein and lipid profiles were measured in the two groups of participants under fasting conditions. Parasitaemia was assessed microscopically but insulin resistance and beta-cell function were assessed by the homeostatic model. Results: The COVID-19 exposed participants were older (p=0.035) with lower parasitaemia (p=0.025) but higher mean levels of insulin, insulin resistance, and beta-cell function compared with their unexposed counterparts (p<0.05). Parasitaemia correlated positively with a number of the measured indices of diabetogenic risk markers in the COVID-19 exposed group only, and predicted (Adjusted R2=0.751; p=0.031) by beta-cell function, C-reactive protein and triglycerides with the model explaining about 75% of the observed variation. Parasitaemia could only be predicted (Adjusted R2=0.245; p=0.002) by C-reactive protein with the model explaining just about a quarter of the observed variation in the COVID-19 unexposed group. Insulin resistance and sub-optimal beta-cell function were detected in both groups of participants. Conclusion: Falciparum malaria is associated with risk markers for development of T2DM irrespective of COVID-19 exposure. Insulin resistance, inflammation and sub-optimal beta-cell secretory function may drive the risk. The observed diabetogenic risk is higher in the recovered COVID-19 participants.
Subject(s)
Humans , Male , Female , Malaria, Falciparum , Diabetes Mellitus, Type 2 , COVID-19 , Inflammation , Risk FactorsABSTRACT
Bajo la teoría de vía aérea unificada, se ha observado que el asma y la rinosinusitis crónica (RSC) tienen una estrecha relación, con efectos importantes de una enfermedad sobre el control de la otra. El objetivo de esta revisión bibliográfica es clarificar cómo ambas enfermedades se relacionan desde su origen, epidemiología, fisiopatología y tratamiento. Sabemos que la presencia de RSC se asocia con peores resultados del asma, mayor frecuencia de exacerbaciones, hospitalizaciones y mayor uso de corticoides sistémicos. Varios mecanismos parecen tener un rol en la disfunción de la vía aérea inferior en pacientes con RSC, dentro de los cuales se plantea que la respuesta inflamatoria en común de tipo Th2 juega un papel principal. Existe amplia literatura respecto al efecto que tiene el tratamiento de la RSC en el control del asma, en esta revisión se expondrá la evidencia disponible del tratamiento médico con corticoides nasales, montelukast y macrólidos, así como también del tratamiento quirúrgico de la RSC y el uso de biológicos.
Under the unified airway theory, asthma and chronic rhinosinusitis (CRS) have a close relationship, with significant effects of one disease on the control of the other. This bibliographic review aims to clarify how both diseases relate to each other from their origin, epidemiology, pathophysiology, and treatment. CRS is associated with worse asthma outcomes, higher frequency of exacerbations, hospitalizations, and increased use of systemic corticosteroids. Several mechanisms play a role in lower airway dysfunction in patients with CRS, among which the common Th2-type inflammatory response plays a substantial role. There is extensive literature regarding the effect of the treatment of CRS in the control of asthma. We present the available evidence regarding the effect of medical treatment with nasal corticosteroids, montelukast, and macrolides, as well as the surgical treatment and use of biologics.
Subject(s)
Humans , Asthma/physiopathology , Asthma/epidemiology , Sinusitis/physiopathology , Sinusitis/epidemiology , Rhinitis/physiopathology , Rhinitis/epidemiology , Chronic DiseaseABSTRACT
Objective:To investigate the clinical efficacy and safety of Dupilumab on the treatment of asthma combined with atopic dermatitis (AD) and other type 2 inflammatory co-morbidities in children.Methods:Clinical data of children with asthma combined with AD, allergic rhinitis (AR) type 2 inflammatory co-morbidities who received Dupilumab treatment for 16 weeks or longer in the Pediatric Asthma and Allergy Clinic of the Second Hospital of Tianjin Medical University from April 1, 2021 to September 1, 2022 were retrospectively analyzed.The efficacy and safety of Dupilumab on the treatment of asthma combined with AD and AR in children were assessed by comparing clinical symptoms before and after 16 weeks of treatment, changes in the dosage of inhaled corticosteroids (ICS), lung function, fractional exhaled nitric oxide (FeNO), and peripheral blood eosinophil (EOS) count, and the incidence of adverse events, respectively.The correlation between the efficacy on AD, AR and asthma was assessed.Quantitative indicators that were normally distributed were compared by the paired samples t-test; otherwise, they were compared by rank- sum test.The correlation between different indicators was compared by Spearman rank correlation test. Results:(1) Ten children with asthma combined with AD, AR were recruited, including 8 males and 2 females, with the mean age of 9 (4-14) years.Three children were previously treated with subcutaneous immunotherapy (SCIT) prior to Dupilumab treatment, and 1 child was transferred to Dupilumab treatment because of a poor responsiveness to Omalizumab.(2) Improvement of asthma: after 16 weeks of treatment, asthma symptoms were well controlled in the 10 children, and none of them had acute asthma attacks.The childhood asthma control test for children and asthma control questionnaire findings were significantly improved from baseline (all P<0.05). Forced expiratory volume in the first second to the predicted value was significantly improved from baseline ( P<0.05). The dosage of ICS [all converted to Beclomethasone Dipropionate, 0 (0, 125.00) μg/d vs.400.00 (200.00, 400.00) μg/d] and FeNO level [11.00(9.00, 19.25)×10 -9vs.38.00(18.25, 56.75)×10 -9] significantly decreased from baseline (all P<0.05). Serum T-IgE testing before and after treatment were performed in 3 children, which were significantly reduced at 16 weeks of treatment compared with baseline (case 1: 2 759 kU/L vs.>5 000 kU/L; case 2: 1 432 kU/L vs.3 546 kU/L; case 3: 655 kU/L vs.1 000 kU/L, all P<0.05). (3) Improvement of asthma co-morbidities: The scoring atopic dermatitis scores, and patient-oriented eczema measure scores at each time point of follow-up decreased significantly compared with baseline (all P<0.001). The overall peripheral blood EOS count increased during the treatment period compared with baseline[1.18(0.62, 1.51)×10 9/L vs.1.01(0.54, 1.90)×10 9/L, P=0.444], although no significant difference was detected.Visual analog scale and total rhinitis medication scores decreased significantly compared with baseline (all P<0.05). (4) There was a positive correlation between baseline AD severity and the therapeutic efficacy on asthma ( r=0.697, P=0.025). (5) Safety: during the treatment, one case developed bilateral conjunctivitis and one developed bilateral bulbar conjunctival hemosiderosis, both of whom were improved after symptomatic treatment. Conclusions:Dupilumab treatment significantly improves clinical symptoms of asthma, AD and AR in children with asthma combined with AD, AR type 2 inflammatory co-morbidities, which also reduces ICS dosage, FeNO level, rhinitis medication and serum T-IgE level, and improve pulmonary function, with a good safety profile.It is a promising treatment to children with type 2 inflammatory disease who have a poor Omalizumab efficacy, and its combination with SCIT is a favorable etiologic treatment.
ABSTRACT
Chronic rhinosinusitis（CRS） is an inflammatory disease involving the mucosa of the nasal and paranasal sinuses for more than 12 weeks and can be classified as CRS with nasal polyp（CRSwNP） and CRS without nasal polyp（CRSsNP） depending on the phenotype. Clinical treatments reveal significant differences in disease prognosis and improvement in quality of life in patients with the same clinical phenotype. Inflammatory cells infiltration and inflammatory mediators are important factors driving CRS endotypes. In particular, CRS with predominantly eosinophilic infiltration and type 2 CRS present severe clinical symptoms, comorbidities, and high recurrence rates. CRS endotype-oriented treatment methods may better contribute to improving patient prognosis and quality of life. This article summarizes the current progress of CRS endotype research and reviews the endotype-oriented treatment options.
Subject(s)
Humans , Rhinitis/therapy , Nasal Polyps/diagnosis , Quality of Life , Sinusitis/diagnosis , Eosinophilia , Chronic DiseaseABSTRACT
@#Asthma is a chronic inflammatory airway disease, for which the cornerstone of asthma therapy is inhaled corticosteroids. However, long term clinical outcomes are variable, and not all patients respond optimally to corticosteroids. Underpinning this observation is that asthma is a heterogeneous disease consisting of phenotypes that are driven by different inflammatory pathways. In this article, we will discuss the different inflammatory mechanisms of asthma to better define patient characteristics and help improve patient outcomes with newer specific-targeted asthma therapies.
ABSTRACT
@#Asthma is a chronic inflammatory airway disease, for which the cornerstone of asthma therapy is inhaled corticosteroids. however, long term clinical outcomes are variable, and not all patients respond optimally to corticosteroids. Underpinning this observation is that asthma is a heterogeneous disease consisting of phenotypes that are driven by different inflammatory pathways. In this article, we will discuss the different inflammatory mechanisms of asthma to better define patient characteristics and help improve patient outcomes with newer specific-targeted asthma therapies.
ABSTRACT
@#Asthma is a chronic inflammatory airway disease, for which the cornerstone of asthma therapy is inhaled corticosteroids. however, long term clinical outcomes are variable, and not all patients respond optimally to corticosteroids. Underpinning this observation is that asthma is a heterogeneous disease consisting of phenotypes that are driven by different inflammatory pathways. In this article, we will discuss the different inflammatory mechanisms of asthma to better define patient characteristics and help improve patient outcomes with newer specific-targeted asthma therapies.
ABSTRACT
Persistent asthma has long been treated with inhaled corticosteroids (CSs), as the mainstay of therapy. However, their efficacy in patients with more severe disease is limited, which led to the incorporation of poor response to ICSs (and thereby use of high doses of ICS) into recent definitions of severe asthma. Several studies have suggested that severe asthma might consist of several different phenotypes, each with ongoing symptoms and health care utilization, despite the use of high doses of ICS, usually in combination with a second or third controller. Several new therapies have been approved for severe asthma. Long-acting muscarinic agents have recently been approved as an additional controller agent and appear to improve lung function, although their effect on symptoms and exacerbations is less. Although bronchial thermoplasty (BT) has emerged as a therapy for severe asthma, little is understood regarding the appropriate selection of these patients. Considerable data have emerged to support the presence of a group of patients with severe asthma who have ongoing Type 2 inflammation. These patients appear to respond to targeted biologic approaches which are at the current time mostly investigational. In contrast, few effective therapies for patients with less or no evidence for Type 2 inflammation have emerged. Many new and exciting therapies are at the forefront for severe asthma therapy and, in conjunction with precision medicine approaches to identify the group of patients likely to respond to these approaches, will change the way we think about treating severe asthma.