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TNF inhibitors (TNFi) have revolutionized the therapeutic management of various chronic immune-mediated inflammatory diseases. Despite their known benefits, these therapies are related to paradoxical adverse effects (PAEs), including paradoxical psoriasis (PP). Although the underlying mechanism remains somewhat unclear, some theories suggest that genetic factors, particularly certain single-nucleotide polymorphisms (SNPs), may play an important role. The present review aimed to research and analyze recent findings regarding the pathomechanisms involved in the appearance of PP and the association between various genetic factors and PP in individuals treated with TNFi. We performed a literature search and found that certain genes (IL23R, TNF, FBXL19, CTLA4, SLC12A8, TAP1) are strongly associated with the occurrence of PP in pediatric and adult patients during therapy with TNFi. The identification of the specific SNPs involved in the appearance of PP and other PAEs in patients treated with TNFi for various diseases and in different populations may later favor the recognition of those patients at a high risk of developing such adverse effects and could guide personalized therapeutic strategies in future years.
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Polimorfismo de Nucleótido Simple , Psoriasis , Inhibidores del Factor de Necrosis Tumoral , Humanos , Psoriasis/genética , Psoriasis/tratamiento farmacológico , Inhibidores del Factor de Necrosis Tumoral/uso terapéutico , Inhibidores del Factor de Necrosis Tumoral/efectos adversos , Predisposición Genética a la Enfermedad , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Factor de Necrosis Tumoral alfa/genéticaRESUMEN
Rheumatoid arthritis (RA) is a chronic autoimmune condition frequently found in rheumatological patients that sometimes raises diagnosis and management problems. The pathogenesis of the disease is complex and involves the activation of many cells and intracellular signaling pathways, ultimately leading to the activation of the innate and acquired immune system and producing extensive tissue damage. Along with joint involvement, RA can have numerous extra-articular manifestations (EAMs), among which lung damage, especially interstitial lung disease (ILD), negatively influences the evolution and survival of these patients. Although there are more and more RA-ILD cases, the pathogenesis is incompletely understood. In terms of genetic predisposition, external environmental factors act and subsequently determine the activation of immune system cells such as macrophages, neutrophils, B and T lymphocytes, fibroblasts, and dendritic cells. These, in turn, show the ability to secrete molecules with a proinflammatory role (cytokines, chemokines, growth factors) that will produce important visceral injuries, including pulmonary changes. Currently, there is new evidence that supports the initiation of the systemic immune response at the level of pulmonary mucosa where the citrullination process occurs, whereby the autoantibodies subsequently migrate from the lung to the synovial membrane. The aim of this paper is to provide current data regarding the pathogenesis of RA-associated ILD, starting from environmental triggers and reaching the cellular, humoral, and molecular changes involved in the onset of the disease.
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Artritis Reumatoide , Enfermedades Pulmonares Intersticiales , Humanos , Artritis Reumatoide/metabolismo , Artritis Reumatoide/inmunología , Artritis Reumatoide/patología , Artritis Reumatoide/etiología , Enfermedades Pulmonares Intersticiales/etiología , Enfermedades Pulmonares Intersticiales/inmunología , Enfermedades Pulmonares Intersticiales/metabolismo , Enfermedades Pulmonares Intersticiales/patología , Pulmón/patología , Pulmón/inmunología , Pulmón/metabolismo , Animales , Autoanticuerpos/inmunologíaRESUMEN
Background: The global epidemic of noncommunicable diseases (NCDs) is increasing. Current assessments that monitor capacity to address NCDs are often externally led and do not facilitate country planning. The Noncommunicable Disease Capacity Assessment and Planning (N-CAP) Process assists ministries of health and other governmental and non-governmental stakeholders to assess, prioritize, and plan how to address NCDs and other public health threats. This paper describes the development of this tool. Materials and methods: Driven by ministries of health, the N-CAP Process engages new and existing stakeholders in three activities: Stakeholder Mapping; Strengths, Weaknesses, Opportunities, and Threats Workshop; and N-CAP Workshop that uses Discussion Guides to lead in-depth assessment and planning. Standard Operating Procedures, a library of Discussion Guides based on common NCD themes, and an open-access e-learning course are available. Results: The N-CAP Process outcome is a prioritized plan of how to improve the country's public health functions. Adaptations to the tool were made after piloting in Jordan and Iraq. Conclusion: The N-CAP Process helps countries engage various stakeholders to identify gaps and create collaborative, country-specific strategies to effectively respond to NCDs, a leading public health threat. The pilots sparked interest from other countries and underscored its potential for broader implementation to combat the rising global burden of NCDs.
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Enfermedades no Transmisibles , Salud Pública , Enfermedades no Transmisibles/prevención & control , Enfermedades no Transmisibles/epidemiología , Humanos , Jordania , Creación de Capacidad , Salud Global , Participación de los InteresadosRESUMEN
Rheumatoid arthritis (RA) is a systemic immune-mediated disease that, in addition to the articular involvement, can have extra-articular manifestations. Even though liver damage in RA is not very common, associated autoimmune liver diseases (AILDs) may occur. The most common AILD associated with RA is primary biliary cirrhosis (PBC), followed by autoimmune hepatitis (AIH) and primary sclerosing cholangitis (PSC). There are common underlying mechanisms that play a role in the emergence of autoimmunity and inflammation in both rheumatic and autoimmune liver diseases. Genetic studies have revealed the existence of several common disease-associated genes shared between RA and AILDs, and infectious triggers, particularly those associated with recurrent or complicated urinary tract infections, are also speculated to be potential triggers for these conditions. Moreover, these diseases share common serologic patterns characterized by the presence of specific autoantibodies and hyper-gammaglobulinemia. In this study, we focus on reviewing the association between RA and AILDs regarding the prevalence and possible etiopathogenic link.
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Artritis Reumatoide , Hepatitis Autoinmune , Hepatopatías , Humanos , Artritis Reumatoide/complicaciones , Hepatitis Autoinmune/complicaciones , Inflamación , Autoinmunidad , Hepatopatías/etiologíaRESUMEN
Relapsing polychondritis is a chronic autoimmune inflammatory condition characterized by recurrent episodes of inflammation at the level of cartilaginous structures and tissues rich in proteoglycans. The pathogenesis of the disease is complex and still incompletely elucidated. The data support the important role of a particular genetic predisposition, with HLA-DR4 being considered an allele that confers a major risk of disease occurrence. Environmental factors, mechanical, chemical or infectious, act as triggers in the development of clinical manifestations, causing the degradation of proteins and the release of cryptic cartilage antigens. Both humoral and cellular immunity play essential roles in the occurrence and perpetuation of autoimmunity and inflammation. Autoantibodies anti-type II, IX and XI collagens, anti-matrilin-1 and anti-COMPs (cartilage oligomeric matrix proteins) have been highlighted in increased titers, being correlated with disease activity and considered prognostic factors. Innate immunity cells, neutrophils, monocytes, macrophages, natural killer lymphocytes and eosinophils have been found in the perichondrium and cartilage, together with activated antigen-presenting cells, C3 deposits and immunoglobulins. Also, T cells play a decisive role in the pathogenesis of the disease, with relapsing polychondritis being considered a TH1-mediated condition. Thus, increased secretions of interferon γ, interleukin (IL)-12 and IL-2 have been highlighted. The "inflammatory storm" formed by a complex network of pro-inflammatory cytokines and chemokines actively modulates the recruitment and infiltration of various cells, with cartilage being a source of antigens. Along with RP, VEXAS syndrome, another systemic autoimmune disease with genetic determinism, has an etiopathogenesis that is still incompletely known, and it involves the activation of the innate immune system through different pathways and the appearance of the cytokine storm. The clinical manifestations of VEXAS syndrome include an inflammatory phenotype often similar to that of RP, which raises diagnostic problems. The management of RP and VEXAS syndrome includes common immunosuppressive therapies whose main goal is to control systemic inflammatory manifestations. The objective of this paper is to detail the main etiopathogenetic mechanisms of a rare disease, summarizing the latest data and presenting the distinct features of these mechanisms.
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Síndromes Mielodisplásicos , Policondritis Recurrente , Enfermedades Cutáneas Genéticas , Humanos , Policondritis Recurrente/diagnóstico , Policondritis Recurrente/patología , Autoinmunidad , Colágeno , InflamaciónRESUMEN
Despite the high burden of hyperlipidemia and the effectiveness of treatment, evidence suggests that the accessibility of hyperlipidemia medicines can be low in many low- and middle-income countries (LMICs). The aim of this study was to identify common barriers to the accessibility of medicines for hyperlipidemia in LMICs. A multimethod analysis and multiple data sources were used to assess the accessibility and barriers of medicines for hyperlipidemia in selected LMICs. The overall median availability of statins for hyperlipidemia in public facilities was 0% and 5.4%, for originators and generics, respectively. In private facilities, median availability was 13.3% and 35.9%, for originators and generics, respectively. Statin availability was lowest in Africa and South-East Asia. Private facilities generally had higher availability than public facilities. Statins are less affordable in lower-income countries, costing around 6 days' wages per month. Originator statins are less affordable than generics in countries of all income-levels. The median cost for statin medications per month ranges from a low of $1 in Kenya to a high of $62 in Mexico, with most countries having a median monthly cost between $3.6 and $17.0. The key informant interviews suggested that accessibility to hyperlipidemia medicines in LMICs faces barriers in multiple dimensions of health systems. The availability and affordability of statins are generally low in LMICs. Several steps could be implemented to improve the accessibility of hyperlipidemia medicines, including private sector engagement, physician education, investment in technology, and enhancement of health systems.
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INTRODUCTION: Despite a growing body of scholarly research on the risks of severe COVID-19 associated with diabetes, hypertension and obesity, there is a need for estimating pooled risk estimates with adjustment for confounding effects. We conducted a systematic review and meta-analysis to estimate the pooled adjusted risk ratios of diabetes, hypertension and obesity on COVID-19 mortality. METHODS: We searched 16 literature databases for original studies published between 1 December 2019 and 31 December 2020. We used the adapted Newcastle-Ottawa Scale to assess the risk of bias. Pooled risk ratios were estimated based on the adjusted effect sizes. We applied random-effects meta-analysis to account for the uncertainty in residual heterogeneity. We used contour-funnel plots and Egger's test to assess possible publication bias. RESULTS: We reviewed 34 830 records identified in literature search, of which 145 original studies were included in the meta-analysis. Pooled adjusted risk ratios were 1.43 (95% CI 1.32 to 1.54), 1.19 (95% CI 1.09 to 1.30) and 1.39 (95% CI 1.27 to 1.52) for diabetes, hypertension and obesity (body mass index ≥30 kg/m2) on COVID-19 mortality, respectively. The pooled adjusted risk ratios appeared to be stronger in studies conducted before April 2020, Western Pacific Region, low- and middle-income countries, and countries with low Global Health Security Index scores, when compared with their counterparts. CONCLUSIONS: Diabetes, hypertension and obesity were associated with an increased risk of COVID-19 mortality independent of other known risk factors, particularly in low-resource settings. Addressing these chronic diseases could be important for global pandemic preparedness and mortality prevention. PROSPERO REGISTRATION NUMBER: CRD42021204371.
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COVID-19 , Diabetes Mellitus , Hipertensión , Humanos , Diabetes Mellitus/epidemiología , Hipertensión/epidemiología , Obesidad/epidemiología , Factores de RiesgoRESUMEN
Systemic lupus erythematosus (SLE) is an autoimmune disorder known for its complex pathogenesis, in which cytokines play an essential role. It seems that the modulation of these cytokines may impact disease progression, being considered potential biomarkers. Thus, TNF (tumor necrosis factor)-α and IL (interleukin)-17 are molecules of great interest in SLE. TNF-α plays a dual role in SLE, with both immunosuppressive and proinflammatory functions. The role of IL-17 is clearly described in the pathogenesis of SLE, having a close association with IL-23 in stimulating the inflammatory response and consecutive tissue destruction. It appears that patients with elevated levels of these cytokines are associated with high disease activity expressed by the SLE disease activity index (SLEDAI) score, although some studies do not confirm this association. However, TNF-α and IL-17 are found in increased titers in lupus patients compared to the general population. Whether inhibition of these cytokines would lead to effective treatment is under discussion. In the case of anti-TNF-α therapies in SLE, the possibility of ATIL (anti-TNF-induced lupus) is a serious concern that limits their use. The use of anti-IL-17 therapies in SLE is a promising option, but not yet approved. Future studies of these cytokines in large cohorts will provide valuable information for the management of SLE.
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Citocinas , Lupus Eritematoso Sistémico , Humanos , Factor de Necrosis Tumoral alfa , Interleucina-17 , Inhibidores del Factor de Necrosis TumoralRESUMEN
Cardiovascular diseases (CVD), principally ischemic heart disease (IHD) and stroke, are the leading causes of death (18. 6 million deaths annually) and disability (393 million disability-adjusted life-years lost annually), worldwide. High blood pressure is the most important preventable risk factor for CVD and deaths, worldwide (10.8 million deaths annually). In 2016, the World Health Organization (WHO) and the United States Centers for Disease Control (CDC) launched the Global Hearts initiative to support governments in their quest to prevent and control CVD. HEARTS is the core technical package of the initiative and takes a public health approach to treating hypertension and other CVD risk factors at the primary health care level. The HEARTS Partner Forum, led by WHO, brings together the following 11 partner organizations: American Heart Association (AHA), Center for Chronic Disease Control (CCDC), International Society of Hypertension (ISH), International Society of Nephrology (ISN), Pan American Health Organization (PAHO), Resolve to Save Lives (RTSL), US CDC, World Hypertension League (WHL), World Heart Federation (WHF) and World Stroke Organization (WSO). The partners support countries in their implementation of the HEARTS technical package in various ways, including providing technical expertise, catalytic funding, capacity building and evidence generation and dissemination. HEARTS has demonstrated the feasibility and acceptability of a public health approach, with more than seven million people already on treatment for hypertension using a simple, algorithmic HEARTS approach. Additionally, HEARTS has demonstrated the feasibility of using hypertension as a pathfinder to universal health coverage and should be a key intervention of all basic benefit packages. The partner forum continues to find ways to expand support and reinvigorate enthusiasm and attention on preventing CVD. Proposed future HEARTS Partner Forum activities are related to more concrete information sharing between partners and among countries, expanded areas of partner synergy, support for implementation, capacity building, and advocacy with country ministries of health, professional societies, academy and civil societies organizations. Advancing toward the shared goals of the HEARTS partners will require a more formal, structured approach to the forum and include goals, targets and published reports. In this way, the HEARTS Partner Forum will mirror successful global partnerships on communicable diseases and assist countries in reducing CVD mortality and achieving global sustainable development goals (SDGs).
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Enfermedades Cardiovasculares , Hipertensión , Accidente Cerebrovascular , Estados Unidos , Humanos , Hipertensión/prevención & control , Enfermedades Cardiovasculares/prevención & control , Factores de RiesgoRESUMEN
The pathologic triangle formed by chronic heart failure (HF), chronic kidney disease (CKD), and anemia carries high morbidity and mortality rates and decreases quality of life. Anemia represents a common condition in patients with advanced HF and CKD, with a total prevalence in cardiorenal syndrome (CRS) ranging from 5% to 55%. Searching for a pragmatic approach for these patients with guided and disease-specific recommendations beyond just targeted hemoglobin therapeutic behavior represents the core of research for ongoing clinical trials. It is well known that the prevalence of anemia increases with the advancement of CKD and HF. The physiopathological mechanisms of anemia, such as the reduction of endogenous erythropoietin and the decrease in oxygen transport, are leading to tissue hypoxia, peripheral vasodilation, stimulating neurohormonal activity, and maintenance of the progressive renal and cardiac dysfunction. Given the challenges with the treatment options for patients with cardiorenal anemia syndrome (CRSA), new therapeutic agents such as hypoxia-inducible factor-prolyl hydroxylase domain inhibitors (HIF-PH) or hepcidin antagonists are emerging in the light of recent research. This review summarizes the potential therapeutic tools for anemia therapy in the cardiorenal population.
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Interstitial lung disease (ILD) is a severe and frequent manifestation of connective tissue diseases (CTD). Due to its debilitating potential, it requires serious evaluation and treatment. The prevalence of ILD in systemic lupus erythematosus (SLE) is still controversial. Therefore, in order to establish the diagnosis of ILD, an overlap syndrome must be excluded. Increasing the identification of SLE-associated ILD cases should become a target. To treat this complication, various therapies are now being proposed. To date, no placebo-controlled studies were conducted. Regarding another CTD, systemic sclerosis (SSc), SSc-associated ILD is considered one of the leading causes of mortality. The incidence of ILD varies among disease subtypes, being influenced by diagnostic method, but also by disease duration. Due to the high prevalence of this complication, all SSc patients should be investigated for ILD at the time of SSc diagnosis and during the course of the disease. Fortunately, progress was made in terms of treatment. Nintedanib, a tyrosine kinases inhibitor, showed promising results. It appeared to decrease the rate of progression of ILD compared to placebo. This review aimed to provide up-to-date findings related to SLE-associated ILD and SSc-associated ILD, in order to raise awareness of their diagnosis and management.
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Enfermedades del Tejido Conjuntivo , Enfermedades Pulmonares Intersticiales , Lupus Eritematoso Sistémico , Esclerodermia Sistémica , Humanos , Enfermedades Pulmonares Intersticiales/diagnóstico , Enfermedades Pulmonares Intersticiales/tratamiento farmacológico , Enfermedades Pulmonares Intersticiales/etiología , Lupus Eritematoso Sistémico/complicaciones , Lupus Eritematoso Sistémico/diagnóstico , Lupus Eritematoso Sistémico/tratamiento farmacológico , Esclerodermia Sistémica/complicaciones , Esclerodermia Sistémica/diagnóstico , Esclerodermia Sistémica/terapia , Enfermedades del Tejido Conjuntivo/complicaciones , PulmónAsunto(s)
Enfermedades Cardiovasculares , Enfermedades no Transmisibles , Humanos , Países en Desarrollo , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/prevención & control , Enfermedades no Transmisibles/epidemiología , Enfermedades no Transmisibles/prevención & control , Atención a la Salud , Salud GlobalRESUMEN
The global COVID-19 response focused heavily on nonpharmaceutical interventions (NPIs) until vaccines became available. Even where vaccination coverage is low, over time governments have become increasingly reluctant to use NPIs. Inequities in vaccine and treatment accessibility and coverage, differences in vaccine effectiveness, waning immunity, and immune-escape variants of concern of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reinforce the long-term need for mitigation. Initially, the concept of NPIs, and mitigation more broadly, was focused on prevention of SARS-CoV-2 transmission; however, mitigation can and has done more than prevent transmission. It has been used to address the clinical dimensions of the pandemic as well. The authors propose an expanded conceptualization of mitigation that encompasses a continuum of community and clinical mitigation measures that can help reduce infection, illness, and death from COVID-19. It can further help governments balance these efforts and address the disruptions in essential health services, increased violence, adverse mental health outcomes, and orphanhood precipitated by the pandemic and by NPIs themselves. The COVID-19 pandemic response revealed the benefits of a holistic and layered mitigation approach to public health emergencies from the outset. Lessons learned can inform the next phases of the current pandemic response and planning for future public health emergencies.
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COVID-19 , Urgencias Médicas , Salud Pública , Humanos , COVID-19/epidemiología , COVID-19/prevención & control , Pandemias , SARS-CoV-2RESUMEN
Adult-onset Still's disease (AOSD) is a systemic inflammatory disorder with an unknown cause characterized by high-spiking fever, lymphadenopathy, hepatosplenomegaly, hyperferritinemia, and leukocytosis. The clinical course can be divided into three significant patterns, each with a different prognosis: Self-limited or monophasic, intermittent or polycyclic systemic, and chronic articular. Two criteria sets have been validated. The Yamaguchi criteria are the most generally used, although the Fautrel criteria offer the benefit of adding ferritin and glycosylated ferritin values. AOSD's pathogenesis is not yet completely understood. Chemokines and pro-inflammatory cytokines, including interferon (IFN)-γ, tumor necrosis factor α (TNFα), interleukin (IL)-1, IL-6, IL-8, and IL-18, play a crucial role in the progression of illness, resulting in the development of innovative targeted therapeutics. There are no treatment guidelines for AOSD due to its rarity, absence of controlled research, and lack of a standard definition for remission and therapy objectives. Non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids (CS), and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) are used in AOSD treatment. Biological therapy, including IL-1, IL-6, IL-18, and IL-17 inhibitors, as well as TNFα or Janus-kinases (JAKs) inhibitors, is administered to patients who do not react to CS and csDMARDs or achieve an inadequate response.
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Antirreumáticos , Enfermedad de Still del Adulto , Adulto , Humanos , Enfermedad de Still del Adulto/diagnóstico , Enfermedad de Still del Adulto/tratamiento farmacológico , Interleucina-18 , Factor de Necrosis Tumoral alfa/uso terapéutico , Interleucina-6 , Antirreumáticos/uso terapéutico , Corticoesteroides/uso terapéutico , Interleucina-1/uso terapéuticoRESUMEN
Cardiovascular diseases (CVD) are one of the leading causes of high mortality in patients with systemic lupus erythematosus (SLE). The Framingham risk score and other traditional risk factors do not fully reflect the CVD risk in SLE patients. Therefore, in order to stratify these high-risk patients, additional biomarkers for subclinical CVD are needed. The mechanisms of atherogenesis in SLE are still being investigated. During the past decades, many reports recognized that inflammation plays a crucial role in the development of atherosclerosis. The aim of this report is to present novel proinflammatory and pro-atherosclerotic risk factors that are closely related to SLE inflammation and which determine an increased risk for the occurrence of early cardiovascular events.
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Aterosclerosis , Enfermedades Cardiovasculares , Lupus Eritematoso Sistémico , Humanos , Aterosclerosis/etiología , Aterosclerosis/epidemiología , Lupus Eritematoso Sistémico/complicaciones , Factores de Riesgo , Enfermedades Cardiovasculares/epidemiología , Inflamación/complicaciones , BiomarcadoresRESUMEN
Systemic lupus erythematosus (SLE) is a chronic, multifactorial autoimmune disease with complex pathogenesis characterized by the imbalance of pro-inflammatory and anti-inflammatory cytokines. Janus kinases (JAKs), intracellular non-receptor tyrosine kinases, are essential for signal pathways of many cytokines. The JAK signal transducers and activators of transcription (STAT) pathways consist of four JAK kinases and seven STATs family members. The dysregulation of JAK-STAT pathways represents an important process in the pathogenesis of SLE. Thus, the use of therapies that target specific signaling pathways would be a challenge in SLE. It is well known that JAK inhibitors have real potential for the treatment of rheumatic diseases, but their efficacy in the treatment of SLE remains to be determined. JAK inhibitors are currently being investigated in phase II and III trials and are considered to become the next stage in SLE therapy. In this review, we report the current data regarding the efficacy of JAK inhibitors in SLE. The development of clinically useful kinase inhibitors might improve upon traditional therapeutic strategies.
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Inhibidores de las Cinasas Janus , Lupus Eritematoso Sistémico , Antiinflamatorios/uso terapéutico , Citocinas/metabolismo , Humanos , Inhibidores de las Cinasas Janus/farmacología , Inhibidores de las Cinasas Janus/uso terapéutico , Quinasas Janus/metabolismo , Lupus Eritematoso Sistémico/tratamiento farmacológico , Factores de Transcripción STAT/metabolismo , TirosinaRESUMEN
Systemic sclerosis (SSc) is a complex autoimmune disease characterized by heterogeneous changes involving numerous organs and systems. The currently available data indicate that muscle injury (both smooth and striated muscles) is widespread and leads to significant morbidity, either directly or indirectly. From the consequences of smooth muscle involvement in the tunica media of blood vessels or at the level of the digestive tract, to skeletal myopathy (which may be interpreted strictly in the context of SSc, or as an overlap with idiopathic inflammatory myopathies), muscular injury in scleroderma translates to a number of notable clinical manifestations. Heart involvement in SSc is heterogenous depending on the definition used in the various studies. The majority of SSc patients experience a silent form of cardiac disease. The present review summarizes certain important features of myocardial, as well as smooth and skeletal muscle involvement in SSc. Further research is needed to fully describe and understand the pathogenic pathways and the implications of muscle involvement in scleroderma.
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Enfermedades Musculares , Esclerodermia Sistémica , Humanos , Músculo Esquelético/patología , Músculo Liso/patología , Enfermedades Musculares/patología , Miocardio/patología , Esclerodermia Sistémica/patologíaRESUMEN
Noncommunicable diseases (NCDs) are the leading cause of death in the world, and 80% of all NCD deaths occur in low- and middle-income countries (LMICs). The COVID-19 pandemic has demonstrated that patients with NCDs are at increased risk of becoming severely ill from the virus. Disproportionate investment in vertical health programs can result in health systems vulnerable to collapse when resources are strained, such as during pandemics. Although NCDs are largely preventable, globally there is underinvestment in efforts to address them. Integrating health systems to collectively address NCDs and infectious diseases through a wide range of services in a comprehensive manner reduces the economic burden of healthcare and strengthens the healthcare system. Health system resiliency is essential for health security. In this article, we provide an economically sound approach to incorporating NCDs into routine healthcare services in LMICs through improved alignment of institutions that support prevention and control of both NCDs and infectious diseases. Examples from Zambia's multisector interventions to develop and support a national NCD action plan can inform and encourage LMIC countries to invest in systems integration to reduce the social and economic burden of NCDs and infectious diseases.
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COVID-19 , Enfermedades Transmisibles , Enfermedades no Transmisibles , COVID-19/prevención & control , Enfermedades Transmisibles/epidemiología , Enfermedades Transmisibles/terapia , Países en Desarrollo , Humanos , Enfermedades no Transmisibles/epidemiología , Enfermedades no Transmisibles/prevención & control , Pandemias , Zambia/epidemiologíaRESUMEN
Cardiorenal syndrome encompasses complex multifactorial facets and carries significant morbidity and mortality worldwide. The bi-directional relationship between the heart and kidneys, where dysfunction in one organ worsens the function of the other, has been the leading motor for research in the last few years. In the pathophysiological process, small noncoding RNAs, epigenetics, vascular growth factors, oxidative stress, hemodynamic factors, and biomarkers play a pivotal role in the development of cardiorenal syndrome. It is therefore important to elucidate all the mechanisms in order to provide diagnostic and treatments tools. This review summarizes the hemodynamic and non-hemodynamic pathways along with biomarkers that could be the next target for diagnosis, treatment, and prognosis in cardiorenal syndrome.
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Hyperlipidemia is a risk factor for cardiovascular disease - the leading cause of death globally. Increased understanding of the cost-effectiveness of hyperlipidemia treatment in low- and middle-income countries can guide approaches to hyperlipidemia management in resource-limited environments. We conducted a systematic review of the evidence on the cost-effectiveness of hyperlipidemia medication treatment in low- and middle-income countries using studies published between January 2010 and April 2020. We abstracted study details, including study design, treatment setting, intervention type, health metrics, costs standardized to constant 2019 US dollars, and cost-effectiveness measures including average and incremental cost-effectiveness ratios. Comparisons across studies suggested that treatment via polypill is generally more cost-effective than statin-only therapy, and that primary prevention is more cost-effective than secondary prevention. Treating hyperlipidemia at a threshold of 5.7 mmol/l comes at a higher cost per disability-adjusted life-years averted than at a threshold of 6.2 mmol/l. Most pharmacological treatment strategies for hyperlipidemia were found to be cost-effective in most of the examined low- and middle-income countries.