185 research outputs found
Global, regional, and national mortality among young people aged 10–24 years, 1950–2019: a systematic analysis for the Global Burden of Disease Study 2019
- Author
- Abd-Allah F
- Abdoli A
- Abdollahi M
- Abdullah KH
- Abedi A
- Abolhassani H
- Abreu LG
- Abrigo MRM
- Abu-Gharbieh E
- Abushouk AI
- Adebayo OM
- Adekanmbi V
- Adham D
- Advani SM
- Afshari K
- Agrawal A
- Ahmad T
- Ahmadi K
- Ahmed AE
- Aji B
- Akombi-Inyang B
- Al-Aly Z
- Al-Hajj S
- Al-Mekhlafi HM
- Al-Raddadi RM
- Alahdab F
- Alam K
- Alanezi FM
- Alanzi TM
- Alcalde-Rabanal JE
- Alemu BW
- Alhassan RK
- Ali S
- Alicandro G
- Alijanzadeh M
- Aljunid SM
- Almasi-Hashiani A
- Almasri NA
- Alonso J
- Altirkawi KA
- Alvis-Guzman N
- Amare AT
- Amini S
- Aminorroaya A
- Amit AML
- Amugsi DA
- Ancuceanu R
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- Andrei CL
- Androudi S
- Ansari F
- Ansari I
- Antonio CAT
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- Ausloos M
- Avenyo EK
- Avila-Burgos L
- Ayano G
- Aynalem YA
- Azari S
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- Bakkannavar SM
- Bali AO
- Banach M
- Banik PC
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- Bedi N
- Beghi E
- Bekuma TT
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- Berhe AK
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- Bhardwaj N
- Bhardwaj P
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- Chandan JS
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- Varughese S
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- Vu GT
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- Wu C
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- Yano Y
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- Yip P
- Yonemoto N
- Yoon S-J
- Younis MZ
- Yousefinezhadi T
- Yu C
- Yu Y
- Yuce D
- Zaidi SS
- Zamani M
- Zamanian M
- Zarafshan H
- Zarei A
- Zastrozhin MS
- Zhang Y
- Zhang Z-J
- Zhao X-JG
- Zhu C
- Ärnlöv J
- Øverland S
- Publication venue
- eCommons@AKU
- Publication date
- 01/01/2021
- Field of study
Summary: Background Documentation of patterns and long-term trends in mortality in young people, which reflect huge changes in demographic and social determinants of adolescent health, enables identification of global investment priorities for this age group. We aimed to analyse data on the number of deaths, years of life lost, and mortality rates by sex and age group in people aged 10–24 years in 204 countries and territories from 1950 to 2019 by use of estimates from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019. Methods We report trends in estimated total numbers of deaths and mortality rate per 100 000 population in young people aged 10–24 years by age group (10–14 years, 15–19 years, and 20–24 years) and sex in 204 countries and territories between 1950 and 2019 for all causes, and between 1980 and 2019 by cause of death. We analyse variation in outcomes by region, age group, and sex, and compare annual rate of change in mortality in young people aged 10–24 years with that in children aged 0–9 years from 1990 to 2019. We then analyse the association between mortality in people aged 10–24 years and socioeconomic development using the GBD Socio-demographic Index (SDI), a composite measure based on average national educational attainment in people older than 15 years, total fertility rate in people younger than 25 years, and income per capita. We assess the association between SDI and all-cause mortality in 2019, and analyse the ratio of observed to expected mortality by SDI using the most recent available data release (2017). Findings In 2019 there were 1·49 million deaths (95% uncertainty interval 1·39–1·59) worldwide in people aged 10–24 years, of which 61% occurred in males. 32·7% of all adolescent deaths were due to transport injuries, unintentional injuries, or interpersonal violence and conflict; 32·1% were due to communicable, nutritional, or maternal causes; 27·0% were due to non-communicable diseases; and 8·2% were due to self-harm. Since 1950, deaths in this age group decreased by 30·0% in females and 15·3% in males, and sex-based differences in mortality rate have widened in most regions of the world. Geographical variation has also increased, particularly in people aged 10–14 years. Since 1980, communicable and maternal causes of death have decreased sharply as a proportion of total deaths in most GBD super-regions, but remain some of the most common causes in sub-Saharan Africa and south Asia, where more than half of all adolescent deaths occur. Annual percentage decrease in all-cause mortality rate since 1990 in adolescents aged 15–19 years was 1·3% in males and 1·6% in females, almost half that of males aged 1–4 years (2·4%), and around a third less than in females aged 1–4 years (2·5%). The proportion of global deaths in people aged 0–24 years that occurred in people aged 10–24 years more than doubled between 1950 and 2019, from 9·5% to 21·6%. Interpretation Variation in adolescent mortality between countries and by sex is widening, driven by poor progress in reducing deaths in males and older adolescents. Improving global adolescent mortality will require action to address the specific vulnerabilities of this age group, which are being overlooked. Furthermore, indirect effects of the COVID-19 pandemic are likely to jeopardise efforts to improve health outcomes including mortality in young people aged 10–24 years. There is an urgent need to respond to the changing global burden of adolescent mortality, address inequities where they occur, and improve the availability and quality of primary mortality data in this age group
Impact of opioid-free analgesia on pain severity and patient satisfaction after discharge from surgery: multispecialty, prospective cohort study in 25 countries
- Author
- Aamir Faiqa Binte
- Aamir Syed Roohan
- Ababneh Adnan
- Abbal Muhammad Anas
- Abbas Ahmed M
- Abbas Mostafa
- Abd-Albain Montasir A
- Abdalei Abdulwahab
- Abdalla Ahmed
- Abdalla Ahmed Yassir
- Abdalla Mohamed Galal Ali
- Abdalla Zainab
- Abdallah Mohamed M
- Abdalmahmoud Noon Ezzeldien
- Abdalsadeg Rowa
- Abdelaal Ahmed M
- Abdelbagi Alnazeer Y
- Abdelbaky Mostafa
- Abdelbaset Doaa
- AbdElbaset Esraa
- Abdelbast Menhag
- Abdelfatah Mohammed Abdelnasser
- Abdelgawad Samia
- Abdelhamid Mohamed M
- Abdeljaber Mahmoud
- Abdelkhalig Mubarak
- Abdelmaksoud Mohamed
- Abdelmeguid Rana
- Abdelmelek Dhia Errahmane
- Abdelnaeam Samah
- Abdelnasser Mohammad K
- Abdelrahim Najwa
- Abdelrahman Amira
- Abdelrahman Ayman
- Abdelsalam Hebatalla
- Abdelsamed Enas Abdelbaset
- Abdelwahab Khaled
- Abdoun Meriem
- Abdulali Fatima
- Abdulaziz Mohamed
- Abdulla Dheba Almukhtar
- Abdullah Bahiyah
- Abdullah Bahiyah
- Abdullah Walaa
- Abdullahi Habiba Ibrahim
- Abdulrahman Ahmed
- Abdulrasheed Lubabatu
- Abdulwahed Eman
- Abdulwahed Eman
- Abeysirigunawardana Dewmi
- Abidin Muhammad Fihmi Zainal
- Abiola Olukayode
- Abiyere Henry
- Abodina Ahmed Mohammed
- Aboelela Reham
- AboElfarh Hadeer Elsaeed
- Aboudlal Husein
- AbouHiekal Osama
- Aboulfotouh Ahmed
- Abozid Anwaar
- Abubaker Noora
- Abubaker Noora
- Abufanas Asma
- Abughanima Mahmoud
- Abuhashem Shehab
- Abulafia Daniel
- Abushaala Fatima
- Abushanab Khaled
- AbuShawareb Issa
- Abuuqteish Hamza
- Abuzaho Amany
- Achem Arome
- Adam Eithar
- Adam Mohammed
- Adam Mohammed A
- Addalla Mohamed
- Addley Jordan
- Adeleye Gbadebo
- Adeniyi Adebayo
- Adewole Nathaniel
- Adeyemo Olabisi
- Adeyeye Ademola
- Adeyeye Ademola
- Adly Michael
- Adnan Siti Nasyirah Nisya
- Ads Adel Mohamed
- Ads Alaa Mohamed
- Adze Joel Amwe
- Afeikhena Ehis
- Agida Teddy
- Agilla Hamza
- Agnew Emilie
- Agu Joy Onyekachi
- Ahmad Zatul Akmar
- Ahmed Abdalla
- Ahmed Ahmed
- Ahmed Ahmed
- Ahmed Alaaaldeen
- Ahmed Entisar
- Ahmed Habeeba
- Ahmed Hatem
- Ahmed Reem
- Ahmed Rehab
- Ahmed Rihab
- Ahmed Rogia Ahmed Abdalla
- Ahmed Ruaa
- Ahmed Sharwany
- Ahmed Uzair
- Ahmed Wahiba
- Ahmeed Sultan
- Airede Lydia Regina
- Aitchison Lori
- Ajredini Mirac
- Ajulo Adeshina A
- Akaba Godwin
- Akasha Mazin
- Akbar Maha Ghulam
- Akbuz Seyma Orcan
- Akdere Hakan
- Akın Bilge
- Akkaya Ege Nur
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- Akwaisah Ayoub
- Al Hammoud Amr
- Al Rawashdeh Toka
- Al-Baw Mahmoud
- Al-Dahdouh Mosheer
- Al-Haek Safa’
- Al-Hazaimeh Mo'ath
- Al-issawi Dima
- Al-Issawi Subhi
- Al-jammal Maryam
- Al-Juaifari Maytham A
- Al-Mwajeh Tesneem
- Al-Omary Sohaib
- Al-Quossi Mohammed
- Al-Shambaty Yasir Babkir Ali
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- Alhashimi Abdulhadi Mohammed Alhadi
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- Ali Ahmed
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- Alkazali Mustafa
- Alkchr Hayat Ben Hasan Mohamed A A
- Alkhatib Abed Alazeez
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- Alsori Mohamed
- Alsoudani Ali
- Altabbaa Hashem
- Altahir Mohamed
- Altair Mawadda
- Altaweel Ahmad
- Altughar Bushra
- Alvarez Matias
- Alvarez-Lozada Luis Adrian
- Alvarez-Lozada Luis Adrian
- Alwahaib Anas
- Alwash Mohammed
- Alzarga Ali
- Alzarouq Ebtisam
- Alzarroug Amal
- Alzghoul Bader
- Alzyoud Osama
- Amarasekara Mishka
- Amary Marwa
- Ametov Amet
- Amin Mostafa K
- Aminu Bashiru
- Aminu Muhammad Baffah
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- Amro Dana
- Ananthapadmanabhan Shravankrishna
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- Ather M Hammad
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- Atiq Tabish
- Atta Raneem
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- Rasheed Ayat
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- Shah Jainil
- Shahat Mohammed A
- Shaheen Nourhan
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- Yaghmour Jamal
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- Yildirim Yasemin
- Yildiz Ahmet
- Yıldız Berkay
- Yilmaz Hakan
- Yin Chonghao
- Ying Geoffrey
- Yodkitydomying Chatnapa
- Yong Nathania
- Yoon Si Woo
- You Ha Seong
- Young Simon
- Young Stevie
- Younus Khadijah
- Yousif Fatima Imad
- Yousri Mohamed
- Youssef Ahmed A
- Youssef Arkan
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- Yuan Grace
- Yue Bosco
- Yue Tiffany
- Yunos Mohamed Haseef Mohamed
- Yusuf Stephen
- Yuzgec Ayse Nilufer
- Zachomitros Fotios
- Zaed Moahmed
- Zafar Fatima
- Zaghloul Ahmed
- Zaheer Adil
- Zaidi Faseeh
- Zain Ahmad
- Zakaria Ahmed
- Zakaria Andee Dzulkarnaen
- Zakaria Mohd Zaim
- Zalloum Jihad
- Zamanbandhon Bushra
- Zambon Mattia
- Zapsalis Konstantinos
- Zargar Kamran
- Zarzour Mohamed A
- Zeng Raymond
- Zeng Raymond
- Zengin Kagan
- Zertuche Juventino Tadeo Guerrero
- Zhang Caitlin
- Zhang Edward
- Zhang Shane
- Zhang Yichi
- Zhao Hailin
- Zheng Helen
- Zhou Karen
- Zhou Yida
- Ziergiebel Felix
- Zou Peishan
- Zuylekom Kate Van
- Zuylekom Katie Van
- Zwain Yasir Adnan
- Zyul'korneeva Sof'ya
- Aladna Abdallah
- Aljoumaa Abdullah
- Nawfal Hamdi
- Niazi Ammar
- Publication venue
- Publication date
- 01/01/2024
- Field of study
Background: Balancing opioid stewardship and the need for adequate analgesia following discharge after surgery is challenging. This study aimed to compare the outcomes for patients discharged with opioid versus opioid-free analgesia after common surgical procedures.Methods: This international, multicentre, prospective cohort study collected data from patients undergoing common acute and elective general surgical, urological, gynaecological, and orthopaedic procedures. The primary outcomes were patient-reported time in severe pain measured on a numerical analogue scale from 0 to 100% and patient-reported satisfaction with pain relief during the first week following discharge. Data were collected by in-hospital chart review and patient telephone interview 1 week after discharge.Results: The study recruited 4273 patients from 144 centres in 25 countries; 1311 patients (30.7%) were prescribed opioid analgesia at discharge. Patients reported being in severe pain for 10 (i.q.r. 1-30)% of the first week after discharge and rated satisfaction with analgesia as 90 (i.q.r. 80-100) of 100. After adjustment for confounders, opioid analgesia on discharge was independently associated with increased pain severity (risk ratio 1.52, 95% c.i. 1.31 to 1.76; P < 0.001) and re-presentation to healthcare providers owing to side-effects of medication (OR 2.38, 95% c.i. 1.36 to 4.17; P = 0.004), but not with satisfaction with analgesia (beta coefficient 0.92, 95% c.i. -1.52 to 3.36; P = 0.468) compared with opioid-free analgesia. Although opioid prescribing varied greatly between high-income and low- and middle-income countries, patient-reported outcomes did not.Conclusion: Opioid analgesia prescription on surgical discharge is associated with a higher risk of re-presentation owing to side-effects of medication and increased patient-reported pain, but not with changes in patient-reported satisfaction. Opioid-free discharge analgesia should be adopted routinely
Global burden of 369 diseases and injuries in 204 countries and territories, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019
- Author
- Abbafati C
- Abbas KM
- Abbasi M
- Abbasi-Kangevari M
- Abbasifard M
- Abbastabar H
- Abd El Razek HM
- Abd El Razek MM
- Abd-Allah F
- Abdelalim A
- Abdollahi M
- Abdollahpour I
- Abdulkader RS
- Abdullah KH
- Abedi A
- Abedi P
- Abegaz KH
- Abolhassani H
- Abosetugn AE
- Aboyans V
- Abrams EM
- Abreu LG
- Abrigo MRM
- Abu Haimed AK
- Abu-Gharbieh E
- Abu-Raddad LJ
- Abualhasan A
- Abushouk AI
- Acebedo A
- Ackerman IN
- Adabi M
- Adair T
- Adamu AA
- Adebayo OM
- Adedeji IA
- Adekanmbi V
- Adelson JD
- Adeoye AM
- Adetokunboh OO
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- Umeokonkwo CD
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- Valdez PR
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- Wickramasinghe ND
- Wiens KE
- Wijeratne T
- Wilner LB
- Wilson S
- Wiysonge CS
- Wojtyniak B
- Woldu G
- Wolfe CDA
- Wondmeneh TG
- Wondmieneh AB
- Wool EE
- Wozniak SS
- Wu A-M
- Wu C
- Wu J
- Wunrow HY
- Xie Y
- Xu G
- Xu R
- Yadgir S
- Yamada T
- Yamagishi K
- Yaminfirooz M
- Yano Y
- Yaya S
- Yazdi-Feyzabadi V
- Yearwood JA
- Yeheyis TY
- Yeshitila YG
- Yilgwan CS
- Yilma MT
- Yip P
- Yonemoto N
- Yoon S-J
- York HW
- Younis MZ
- Younker TP
- Yousefi B
- Yousefi Z
- Yousefifard M
- Yousefinezhadi T
- Yousuf AY
- Yu C
- Yu Y
- Yuan C-W
- Yuce D
- Yusefzadeh H
- Zadey S
- Zahabi SS
- Zaidi SS
- Zaki L
- Zaki MES
- Zakzuk J
- Zamani M
- Zamanian M
- Zandian H
- Zangeneh A
- Zarafshan H
- Zastrozhin MS
- Zewdie KA
- Zhang J
- Zhang Y
- Zhang Z-J
- Zhao JT
- Zhao X-JG
- Zhao Y
- Zheleva B
- Zheng P
- Zhou M
- Zhu C
- Ziapour A
- Zimsen SRM
- Zlavog BS
- Zodpey S
- Publication venue
- 'Elsevier BV'
- Publication date
- 17/10/2020
- Field of study
Five insights from the Global Burden of Disease Study 2019
- Author
- Abbafati C
- Abbas KM
- Abbasi M
- Abbasi-Kangevari M
- Abbasifard M
- Abbastabar H
- Abd El Razek HM
- Abd El Razek MM
- Abd-Allah F
- Abdelalim A
- Abdollahi M
- Abdollahpour I
- Abdulkader RS
- Abdullah KH
- Abedi A
- Abedi P
- Abegaz KH
- Abolhassani H
- Abosetugn AE
- Aboyans V
- Abrams EM
- Abreu LG
- Abrigo MRM
- Abu Haimed AK
- Abu-Gharbieh E
- Abu-Raddad LJ
- Abualhasan A
- Abushouk AI
- Acebedo A
- Ackerman IN
- Adabi M
- Adair T
- Adamu AA
- Adebayo OM
- Adedeji IA
- Adekanmbi V
- Adelson JD
- Adeoye AM
- Adetokunboh OO
- Adham D
- Advani SM
- Afarideh M
- Afshari M
- Afshin A
- Agardh EE
- Agarwal G
- Agasthi P
- Agesa KM
- Aghaali M
- Aghamir SMK
- Agrawal A
- Ahmad T
- Ahmadi A
- Ahmadi K
- Ahmadi M
- Ahmadieh H
- Ahmadpour E
- Ahmed MB
- Aji B
- Akalu TY
- Akinyemi RO
- Akinyemiju T
- Akombi B
- Akunna CJ
- Al-Aly Z
- Al-Mekhlafi HM
- Al-Raddadi RM
- Alahdab F
- Alam K
- Alam N
- Alam S
- Alam T
- Alanezi FM
- Alanzi TM
- Albertson SB
- Alcalde-Rabanal JE
- Alema NM
- Alemu BW
- Alemu YM
- Alhabib KF
- Alhassan RK
- Ali M
- Ali S
- Alicandro G
- Alijanzadeh M
- Alinia C
- Alipour V
- Alizade H
- Aljunid SM
- Alla F
- Allebeck P
- Almadi MAH
- Almasi A
- Almasi-Hashiani A
- Almasri NA
- Almulhim AM
- Alonso J
- Altirkawi KA
- Alumran AK
- Alvis-Guzman N
- Alvis-Zakzuk NJ
- Amare AT
- Amare B
- Amini S
- Amini-Rarani M
- Aminorroaya A
- Amiri F
- Amit AML
- Amugsi DA
- Amul GGH
- Anbesu EW
- Ancuceanu R
- Anderlini D
- Anderson JA
- Andrei CL
- Andrei T
- Androudi S
- Angus C
- Anjomshoa M
- Ansari F
- Ansari I
- Ansari-Moghaddam A
- Antonazzo IC
- Antonio CAT
- Antony CM
- Antriyandarti E
- Anvari D
- Anwer R
- Appiah SCY
- Arab-Zozani M
- Arabloo J
- Aravkin AY
- Arba AAK
- Aremu O
- Ariani F
- Aripov T
- Armoon B
- Arnlov J
- Arowosegbe OO
- Aryal KK
- Arzani A
- Asaad M
- Asadi-Aliabadi M
- Asadi-Pooya AA
- Asgari S
- Asghari B
- Ashbaugh C
- Assmus M
- Atafar Z
- Athari SS
- Atnafu DD
- Atout MMW
- Atre SR
- Atteraya MS
- Ausloos F
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- Field of study
The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 provides a rules-based synthesis of the available evidence on levels and trends in health outcomes, a diverse set of risk factors, and health system responses. GBD 2019 covered 204 countries and territories, as well as first administrative level disaggregations for 22 countries, from 1990 to 2019. Because GBD is highly standardised and comprehensive, spanning both fatal and non-fatal outcomes, and uses a mutually exclusive and collectively exhaustive list of hierarchical disease and injury causes, the study provides a powerful basis for detailed and broad insights on global health trends and emerging challenges. GBD 2019 incorporates data from 281 586 sources and provides more than 3.5 billion estimates of health outcome and health system measures of interest for global, national, and subnational policy dialogue. All GBD estimates are publicly available and adhere to the Guidelines on Accurate and Transparent Health Estimate Reporting. From this vast amount of information, five key insights that are important for health, social, and economic development strategies have been distilled. These insights are subject to the many limitations outlined in each of the component GBD capstone papers.Peer reviewe
Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases
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- A Abbott
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- The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group
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- Publication venue
- Publication date
- 09/08/2008
- Field of study
The production of peroxide and superoxide is an inevitable consequence of
aerobic metabolism, and while these particular "reactive oxygen species" (ROSs)
can exhibit a number of biological effects, they are not of themselves
excessively reactive and thus they are not especially damaging at physiological
concentrations. However, their reactions with poorly liganded iron species can
lead to the catalytic production of the very reactive and dangerous hydroxyl
radical, which is exceptionally damaging, and a major cause of chronic
inflammation. We review the considerable and wide-ranging evidence for the
involvement of this combination of (su)peroxide and poorly liganded iron in a
large number of physiological and indeed pathological processes and
inflammatory disorders, especially those involving the progressive degradation
of cellular and organismal performance. These diseases share a great many
similarities and thus might be considered to have a common cause (i.e.
iron-catalysed free radical and especially hydroxyl radical generation). The
studies reviewed include those focused on a series of cardiovascular, metabolic
and neurological diseases, where iron can be found at the sites of plaques and
lesions, as well as studies showing the significance of iron to aging and
longevity. The effective chelation of iron by natural or synthetic ligands is
thus of major physiological (and potentially therapeutic) importance. As
systems properties, we need to recognise that physiological observables have
multiple molecular causes, and studying them in isolation leads to inconsistent
patterns of apparent causality when it is the simultaneous combination of
multiple factors that is responsible. This explains, for instance, the
decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference
Measurement and interpretation of same-sign W boson pair production in association with two jets in pp collisions at s = 13 TeV with the ATLAS detector
- Author
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- Åkesson TPA
- Öncel ÖO
- Ženiš T
- Živković L
- Publication venue
- Springer Nature
- Publication date
- 01/04/2024
- Field of study
This paper presents the measurement of fducial and diferential cross sections for both the inclusive and electroweak production of a same-sign W-boson pair in association with two jets (W±W±jj) using 139 fb−1 of proton-proton collision data recorded at a centre-of-mass energy of √s = 13 TeV by the ATLAS detector at the Large Hadron Collider. The analysis is performed by selecting two same-charge leptons, electron or muon, and at least two jets with large invariant mass and a large rapidity diference. The measured fducial cross sections for electroweak and inclusive W±W±jj production are 2.92 ± 0.22 (stat.) ± 0.19 (syst.)fb and 3.38±0.22 (stat.)±0.19 (syst.)fb, respectively, in agreement with Standard Model predictions. The measurements are used to constrain anomalous quartic gauge couplings by extracting 95% confdence level intervals on dimension-8 operators. A search for doubly charged Higgs bosons H±± that are produced in vector-boson fusion processes and decay into a same-sign W boson pair is performed. The largest deviation from the Standard Model occurs for an H±± mass near 450 GeV, with a global signifcance of 2.5 standard deviations
Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy
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- Abdallah J
- Abdul Ghani R
- Abdul Kadir K
- Abdullah R
- Abejuela Z
- Abouglila K
- Abraham O
- Abrahamsen I
- Abraira Munoz Ld
- Abramowitz M
- Abusnana S
- Accini Mendoza Jl
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- Ahmed F
- Ahuad Guerrero Ra
- Aiello J
- Ainsworth P
- Aizenberg D
- Akiyama H
- Akright L
- Akyea-Djamson A
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- Zateyshshikov D
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- Zinman B
- Zinman Bernard
- Zlova T
- Zsom M
- Zub L
- Zykova T
- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2019
- Field of study
BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to 300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m 2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years
Combination of searches for heavy spin-1 resonances using 139 fb−1 of proton-proton collision data at s = 13 TeV with the ATLAS detector
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- Aakvaag E
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- Abicht NJ
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- Zhou H
- Zhou N
- Zhou Y
- Zhou Y
- Zhu CG
- Zhu J
- Zhu Y
- Zhu Y
- Zhuang X
- Zhukov K
- Zimine NI
- Zinsser J
- Ziolkowski M
- Zoccoli A
- Zoch K
- Zorbas TG
- Zormpa O
- Zou W
- Zwalinski L
- Åkesson TPA
- Öncel ÖO
- Ženiš T
- Živković L
- Publication venue
- Springer Nature
- Publication date
- 19/04/2024
- Field of study
A combination of searches for new heavy spin-1 resonances decaying into different pairings of W, Z, or Higgs bosons, as well as directly into leptons or quarks, is presented. The data sample used corresponds to 139 fb−1 of proton-proton collisions at
= 13 TeV collected during 2015–2018 with the ATLAS detector at the CERN Large Hadron Collider. Analyses selecting quark pairs (qq, bb,
, and tb) or third-generation leptons (τν and ττ) are included in this kind of combination for the first time. A simplified model predicting a spin-1 heavy vector-boson triplet is used. Cross-section limits are set at the 95% confidence level and are compared with predictions for the benchmark model. These limits are also expressed in terms of constraints on couplings of the heavy vector-boson triplet to quarks, leptons, and the Higgs boson. The complementarity of the various analyses increases the sensitivity to new physics, and the resulting constraints are stronger than those from any individual analysis considered. The data exclude a heavy vector-boson triplet with mass below 5.8 TeV in a weakly coupled scenario, below 4.4 TeV in a strongly coupled scenario, and up to 1.5 TeV in the case of production via vector-boson fusion
The clinical and genetic spectrum of autosomal-recessive TOR1A-related disorders.
- Author
- Abedini S
- Abicht A
- Ahangari N
- Akhondian J
- Al-Hertani W
- Al-Sannaa NA
- Alavi S
- AlShamsi AM
- Alvi JR
- Andrew EH
- Ashrafzadeh F
- Baker J
- Bauer P
- Bedoukian E
- Benezit A
- Berger SI
- Bhambhani V
- Bruel A-L
- Calderwood L
- Christodoulou J
- Chung WK
- Collins F
- Dafsari HS
- Day-Salvatore D-L
- Doosti M
- Ebrahimi-Fakhari D
- Efthymiou S
- Eshaghian S
- Faure J
- Gallati S
- Ghavideldarestani M
- Ghazavi M
- Gomez-Ospina N
- Goodchild R
- Gulec EY
- Hashemi N
- Henderson LB
- Herman I
- Houlden H
- Ibrahim S
- Idleburg MJ
- Imannezhad S
- Jungbluth H
- Karimiani EG
- Kariminejad A
- Keena BA
- Lau T
- Lek M
- Lemke JR
- Levandoski KM
- Li C
- Lochmüller H
- Lupski JR
- Madan-Khetarpal S
- Marinakis NM
- Maroofian R
- Martínez-González MJ
- McRae A
- Melki J
- Menezes MJ
- Millan F
- Mirzadeh HS
- Mohammadi MH
- Moreno-De-Luca A
- Morrow MM
- Moutton S
- Offiah AC
- Oppermann H
- Ortigoza-Escobar JD
- Pascher MT
- Pehlivan D
- Peter M
- Platzer K
- Rahimian E
- Rendu J
- Rieubland C
- Saffari A
- Safi M
- Salpietro V
- Sandra W
- Sedighzadeh S
- Senderek J
- Shahrooei M
- Siddharth A
- Siu VM
- Skraban CM
- Smitka M
- Sofocleous C
- Strom TM
- Sultan T
- Suri M
- Tajsharghi H
- Tarnopolsky M
- Toosi MB
- Torbati PN
- Veltra D
- Vogel M
- Weis D
- Wentzensen IM
- Zackai EH
- Zifarelli G
- Publication venue
- Oxford University Press
- Publication date
- 01/08/2023
- Field of study
In the field of rare diseases, progress in molecular diagnostics led to the recognition that variants linked to autosomal-dominant neurodegenerative diseases of later onset can, in the context of biallelic inheritance, cause devastating neurodevelopmental disorders and infantile or childhood-onset neurodegeneration. TOR1A-associated arthrogryposis multiplex congenita 5 (AMC5) is a rare neurodevelopmental disorder arising from biallelic variants in TOR1A, a gene that in the heterozygous state is associated with torsion dystonia-1 (DYT1 or DYT-TOR1A), an early-onset dystonia with reduced penetrance. While 15 individuals with AMC5-TOR1A have been reported (less than 10 in detail), a systematic investigation of the full disease-associated spectrum has not been conducted. Here, we assess the clinical, radiological and molecular characteristics of 57 individuals from 40 families with biallelic variants in TOR1A. Median age at last follow-up was 3 years (0-24 years). Most individuals presented with severe congenital flexion contractures (95%) and variable developmental delay (79%). Motor symptoms were reported in 79% and included lower limb spasticity and pyramidal signs, as well as gait disturbances. Facial dysmorphism was an integral part of the phenotype, with key features being a broad/full nasal tip, narrowing of the forehead and full cheeks. Analysis of disease-associated manifestations delineated a phenotypic spectrum ranging from normal cognition and mild gait disturbance to congenital arthrogryposis, global developmental delay, intellectual disability, absent speech and inability to walk. In a subset, the presentation was consistent with foetal akinesia deformation sequence with severe intrauterine abnormalities. Survival was 71%, with higher mortality in males. Death occurred at a median age of 1.2 months (1 week-9 years), due to respiratory failure, cardiac arrest or sepsis. Analysis of brain MRI studies identified non-specific neuroimaging features, including a hypoplastic corpus callosum (72%), foci of signal abnormality in the subcortical and periventricular white matter (55%), diffuse white matter volume loss (45%), mega cisterna magna (36%) and arachnoid cysts (27%). The molecular spectrum included 22 distinct variants, defining a mutational hotspot in the C-terminal domain of the Torsin-1A protein. Genotype-phenotype analysis revealed an association of missense variants in the 3-helix bundle domain to an attenuated phenotype, while missense variants near the Walker A/B motif as well as biallelic truncating variants were linked to early death. In summary, this systematic cross-sectional analysis of a large cohort of individuals with biallelic TOR1A variants across a wide age-range delineates the clinical and genetic spectrum of TOR1A-related autosomal-recessive disease and highlights potential predictors for disease severity and survival
Measuring universal health coverage based on an index of effective coverage of health services in 204 countries and territories, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019
- Author
- Abbafati C
- Abbastabar H
- Abd-Allah F
- Abdollahi M
- Abedi A
- Abolhassani H
- Abosetugn AE
- Abreu LG
- Abrigo MRM
- Abu Haimed AK
- Abushouk AI
- Adabi M
- Adebayo OM
- Adekanmbi V
- Adelson JD
- Adetokunboh OO
- Adham D
- Advani SM
- Afshin A
- Agarwal G
- Agasthi P
- Aghamir SMK
- Agrawal A
- Ahmad T
- Akinyemi RO
- Al-Aly Z
- Al-Mekhlafi HM
- Al-Raddadi RM
- Alahdab F
- Alam K
- Albertson SB
- Alemu YM
- Alhassan RK
- Ali M
- Ali S
- Alipour V
- Aljunid SM
- Alla F
- Almadi MAH
- Almasi A
- Almasi-Hashiani A
- Almasri NA
- Almulhim AM
- Alonso J
- Altirkawi KA
- Alvis-Guzman N
- Alvis-Zakzuk NJ
- Amini S
- Amini-Rarani M
- Amiri F
- Amit AML
- Amugsi DA
- Ancuceanu R
- Anderlini D
- Andrei CL
- Androudi S
- Ansari F
- Ansari-Moghaddam A
- Antonio CAT
- Antony CM
- Antriyandarti E
- Anvari D
- Anwer R
- Arab-Zozani M
- Arabloo J
- Aravkin AY
- Aremu O
- Arnlov J
- Asaad M
- Asadi-Aliabadi M
- Asadi-Pooya AA
- Ashbaugh C
- Athari SS
- Atout MMW
- Ausloos M
- Avila-Burgos L
- Ayano G
- Ayanore MA
- Aynalem GL
- Aynalem YA
- Ayza MA
- Azari S
- Azzopardi PS
- Babaee E
- Babaee E
- Badiye AD
- Badiye AD
- Bahrami MA
- Bahrami MA
- Baig AA
- Bakhshaei MH
- Bakhtiari A
- Bakkannavar SM
- Balachandran A
- Balassyano S
- Bali AO
- Banach M
- Banerjee SK
- Banik PC
- Bante AB
- Bante SA
- Barker-Collo SL
- Barnighausen TW
- Barrero LH
- Barthelemy CM
- Bassat Q
- Basu S
- Baune BT
- Bayati M
- Baye BA
- Bedi N
- Beghi E
- Behzadifar M
- Bekuma TTT
- Bell ML
- Bensenor IM
- Berman AE
- Bernabe E
- Bernstein RS
- Bhagavathula AS
- Bhandari D
- Bhardwaj P
- Bhat AG
- Bhattacharyya K
- Bhattarai S
- Bhutta ZA
- Bijani A
- Bikbov B
- Bilano V
- Bin Zaman S
- Biondi A
- Birihane BM
- Bockarie MJ
- Bohlouli S
- Bojia HA
- Bolla SRR
- Boloor A
- Brady OJ
- Braithwaite D
- Briant PS
- Briggs AM
- Briko NI
- Busse R
- Butt ZA
- Cahuana-Hurtado L
- Camera LA
- Car LT
- Cardenas R
- Carreras G
- Carrero JJ
- Carvalho F
- Castaldelli-Maia JM
- Castaneda-Orjuela CA
- Castelpietra G
- Castro F
- Catala-Lopez F
- Causey K
- Cederroth CR
- Cercy KM
- Cerin E
- Chandan JS
- Chang AY
- Charan J
- Chattu VK
- Chaturvedi S
- Chin KL
- Cho DY
- Choi J-YJ
- Christensen H
- Chu D-T
- Chung MT
- Ciobanu LG
- Cirillo M
- Comfort H
- Compton K
- Cortesi PA
- Costa VM
- Cousin E
- Cuong TN
- da Silva DD
- Dahlawi SMA
- Damiani G
- Dandona L
- Dandona R
- Darshan BB
- Darwesh AM
- Daryani A
- Dash AP
- Davey G
- Davila-Cervantes CA
- Davletov K
- De Neve J-W
- Denova-Gutierrez E
- Deribe K
- Dervenis N
- Desai R
- Dharmaratne SD
- Dhungana GP
- Dianatinasab M
- Diaz D
- Diep NN
- Dippenaar IN
- Dorostkar F
- Doshmangir L
- Duncan BB
- Duraes AR
- Eagan AW
- Edvardsson D
- El Sayed I
- El Tantawi M
- Elgendy IY
- Elyazar IRF
- Eskandari K
- Eskandarieh S
- Esmaeilnejad S
- Esteghamati A
- Ezekannagha O
- Farag T
- Farahmand M
- Faraon EJA
- Farioli A
- Faris PS
- Faro A
- Fazlzadeh M
- Feigin VL
- Fernandes E
- Ferrara P
- Feyissa GT
- Filip I
- Fischer F
- Fisher JL
- Flor LS
- Foigt NA
- Folayan MO
- Fomenkov AA
- Foroutan M
- Francis JM
- Fu W
- Fukumoto T
- Fullman N
- Furtado JM
- Gad MM
- Gaidhane AM
- Gakidou E
- Galles NC
- Gallus S
- Gardner WM
- Geberemariyam BS
- Gebrehiwot AM
- Gebremeskel GG
- Gebremeskel LG
- Gela JD
- Gesesew HA
- Ghadiri K
- Ghafourifard M
- Ghashghaee A
- Ghith N
- Gholamian A
- Gilani SA
- Gill PS
- Gill TK
- Ginindza TG
- Gitimoghaddam M
- Giussani G
- Glagn M
- Gnedovskaya EV
- Godinho MA
- Goharinezhad S
- Gopalani SV
- Goudarzian AH
- Goulart BNG
- Gubari MIM
- Guimaraes RA
- Guled RA
- Gultie T
- Guo Y
- Gupta R
- Gupta R
- Hafezi-Nejad N
- Hafiz A
- Haile TG
- Hamadeh RR
- Hameed S
- Hamidi S
- Han C
- Han H
- Handiso DW
- Hanif A
- Hankey GJ
- Hanson SW
- Haro JM
- Hasaballah AI
- Hasan MM
- Hashi A
- Hassan A
- Hassan S
- Hassanipour S
- Hassankhani H
- Havmoeller RJ
- Hay SI
- Hayat K
- Heidari G
- Heidari-Soureshjani R
- Hendrie D
- Herteliu C
- Hird TR
- Ho HC
- Hoa TD
- Hole MK
- Holla R
- Hoogar P
- Hopf KP
- Horita N
- Hossain N
- Hosseini M
- Hosseinzadeh M
- Hostiuc M
- Hostiuc S
- Househ M
- Hsieh VC-R
- Hu G
- Huda TM
- Humayun A
- Huong LTN
- Hwang B-F
- Iavicoli I
- Ibitoye SE
- Ikeda N
- Ilesanmi OS
- Ilic IM
- Ilic MD
- Inbaraj LR
- Iqbal U
- Irvani SSN
- Irvine CMS
- Islam MM
- Islam SMS
- Islami F
- Iso H
- Iwu CCD
- Iwu CJ
- Jaafari J
- Jabbari SHY
- Jadidi-Niaragh F
- Jafarinia M
- Jahagirdar D
- Jahani MA
- Jahanmehr N
- Jakovljevic M
- Janjani H
- Javaheri T
- Jayatilleke AU
- Jenabi E
- Jha RP
- Jha V
- Ji JS
- Jia P
- John-Akinola YO
- Jonas JB
- Joukar F
- Jozwiak JJ
- Jurisson M
- Kabir Z
- Kafil HS
- Kalankesh LR
- Kalhor R
- Kalhori RP
- Kamath AM
- Kanchan T
- Kapoor N
- Karanikolos M
- Karimi SM
- Kassebaum NJ
- Katikireddi SV
- Kayode GA
- Keiyoro PN
- Khader YS
- Khammarnia M
- Khan EA
- Khan M
- Khaneghah AM
- Khang Y-H
- Khatab K
- Khater AM
- Khater MM
- Khatib MN
- Khayamzadeh M
- Khubchandani J
- Kianipour N
- Kim Y-E
- Kim YJ
- Kimokoti RW
- Kinfu Y
- Kisa A
- Kissimova-Skarbek K
- Kivimaki M
- Kneib CJ
- Knight M
- Kocarnik JM
- Kochhar S
- Kohler S
- Kopec JA
- Korotkova AV
- Korshunov VA
- Kosen S
- Kotlo A
- Koul PA
- Koyanagi A
- Krishan K
- Krohn KJ
- Kugbey N
- Kulkarni V
- Kumar GA
- Kumar M
- Kumar N
- Kurmi OP
- Kusuma D
- Kyu HH
- La Vecchia C
- Lacey B
- Lal DK
- Lalloo R
- Landires I
- Lansingh VC
- Larsson AO
- Lasrado S
- Lau KM-M
- Lauriola P
- Lazarus JV
- Ledesma JR
- Lee PH
- Lee SWH
- Leever AT
- LeGrand KE
- Leigh J
- Leonardi M
- Li S
- Lim L-L
- Lim SS
- Liu X
- Logroscino G
- Lopez AD
- Lopukhov PD
- Lotufo PA
- Lozano R
- Lu A
- Luciano Caetano dos Santos F
- Ma J
- Madadin M
- Mahasha PW
- Mahmoudi M
- Majeed A
- Malagon-Rojas JN
- Maleki S
- Malta DC
- Mansouri B
- Mansournia MA
- Martini S
- Martins-Melo FR
- Martopullo I
- Massenburg BB
- Mastrogiacomo CI
- Mathur MR
- Matin BK
- McAlinden C
- McKee M
- Medina-Solis CE
- Meharie BG
- Mehndiratta MM
- Mehri F
- Mehrotra R
- Mekonnen T
- Melese A
- Memiah PTN
- Mendoza W
- Menezes RG
- Mensah GA
- Meretoja A
- Meretoja TJ
- Mestrovic T
- Mezerji NMG
- Miazgowski B
- Michalek IM
- Mirrakhimov EM
- Mirzaei M
- Mirzaei-Alavijeh M
- Mitchell PB
- Moazen B
- Moghadam TZ
- Moghadaszadeh M
- Mohamadi E
- Mohammad DK
- Mohammad Y
- Mohammadian-Hafshejani A
- Mohammed JA
- Mohammed S
- Mokdad AH
- Monasta L
- Mondello S
- Moradi M
- Moradi-Lakeh M
- Moradzadeh R
- Moraga P
- Morgado-da-Costa J
- Morrison SD
- Mosapour A
- Mosser JF
- Mumford JE
- Muriithi MK
- Murray CJL
- Mustafa G
- Nabhan AF
- Naderi M
- Nagaraja SB
- Nagarajan AJ
- Naghavi M
- Naghshtabrizi B
- Naimzada MD
- Nangia V
- Nansseu JR
- Nasab EM
- Nayak VC
- Nazari J
- Ndejjo R
- Negoi I
- Negoi RI
- Neupane S
- Ngari KN
- Nguefack-Tsague G
- Ngunjiri JW
- Nnaji CA
- Nomura S
- Norheim OF
- Noubiap JJ
- Nowak C
- Nunez-Samudio V
- Ogbo FA
- Oghenetega OB
- Oh I-H
- Oiu AO
- Okunga EW
- Oladnabi M
- Olagunju AT
- Olusanya BO
- Olusanya JO
- Oluwasanu MM
- Omer MO
- Ong KL
- Onwujekwe OE
- Ortega-Altamirano DV
- Ortiz A
- Ostojic SM
- Otstavnov N
- Otstavnov SS
- Overland S
- Owolabi MO
- Padubidri JR
- Pakhale S
- Palladino R
- Pana A
- Panda-Jonas S
- Pangaribuan HU
- Pathak M
- Patton GC
- Paudel S
- Pease SA
- Peden AE
- Pennini A
- Peprah EK
- Pereira J
- Pigott DM
- Pilgrim T
- Pilz TM
- Pinheiro M
- Piradov MA
- Pirsaheb M
- Pokhrel KN
- Postma MJ
- Pourjafar H
- Pourmalek F
- Pourshams A
- Prada SI
- Pribadi DRA
- Pupillo E
- Quazi Syed Z
- Quintanilla BPA
- Radfar A
- Rafiee A
- Rafiei A
- Raggi A
- Rahim F
- Rahman MA
- Rajabpour-Sanati A
- Rana SM
- Ranabhat CL
- Rao SJ
- Rasella D
- Rashedi V
- Rath GK
- Rathi P
- Rawaf DL
- Rawaf S
- Rawal L
- Rawassizadeh R
- Razo C
- Renjith V
- Renzaho AMN
- Reshmi B
- Rezaei N
- Riahi SM
- Ribeiro DC
- Rickard J
- Roberts NLS
- Roever L
- Romoli M
- Ronfani L
- Roshandel G
- Rubagotti E
- Rwegerera GM
- Sabour S
- Sachdev PS
- Saddik B
- Sadeghi E
- Sadeghi M
- Safari Y
- Sagar R
- Sahebkar A
- Sahraian MA
- Sajadi SM
- Salahshoor MR
- Salem H
- Salem MR
- Salomon JA
- Samy AM
- Sanabria J
- Santric-Milicevic MM
- Saraswathy SYI
- Sarmiento-Suarez R
- Sartorius B
- Sarveazad A
- Sathian B
- Sathish T
- Sattin D
- Savic M
- Sawyer SM
- Saxena D
- Sbarra AN
- Schaeffer LE
- Schiavolin S
- Schmidt MI
- Schutte AE
- Schwebel DC
- Schwendicke F
- Seedat S
- Sha F
- Shahabi S
- Shaheen AA
- Shaikh MA
- Shamsizadeh M
- Shannawaz M
- Sharafi K
- Sharara F
- Sharifi H
- Shaw DH
- Sheikh A
- Sheikhtaheri A
- Shetty BSK
- Shibuya K
- Shiferaw WS
- Shigematsu M
- Shin JI
- Shiri R
- Shirkoohi R
- Shivakumar KM
- Shrime MG
- Shuval K
- Siabani S
- Sierpinski R
- Sigfusdottir ID
- Sigurvinsdottir R
- Silva DAS
- Silva JP
- Simonetti B
- Simpson KE
- Singh JA
- Singh P
- Sinha DN
- Skryabin VY
- Smith EUR
- Sofia e Sa Farinha C
- Soheili A
- Soltani S
- Soofi M
- Sorensen RJD
- Soriano JB
- Sorrie MB
- Soyiri IN
- Spurlock EE
- Sreeramareddy CT
- Stanaway JD
- Steel N
- Stein C
- Stokes MA
- Sufiyan MB
- Suleria HAR
- Sultan I
- Szumowski L
- Tabares-Seisdedos R
- Tabuchi T
- Tadakamadla SK
- Taddele BW
- Tadesse DB
- Taherkhani A
- Tamiru AT
- Tanser FC
- Tareque MI
- Tarigan IU
- Teagle WL
- Tediosi F
- Tefera YG
- Tela FGG
- Tessema ZT
- Thakur B
- Titova MV
- Tonelli M
- Topor-Madry R
- Topouzis F
- Toroudi HP
- Tovani-Palone MR
- Tran BX
- Travillian RS
- Troeger CE
- Uddin R
- Ullah I
- Umeokonkwo CD
- Unnikrishnan B
- Upadhyay E
- Uthman OA
- Vacante M
- Valdez PR
- Varughese S
- Vasankari TJ
- Vasseghian Y
- Venketasubramanian N
- Violante FS
- Vlassov V
- Vollset SE
- Vongpradith L
- Vos T
- Waheed Y
- Walters MK
- Wamai RG
- Wang H
- Wang Y-P
- Weintraub RG
- Weiss J
- Werdecker A
- Westerman R
- Wilner LB
- Woldu G
- Wolfe CDA
- Wu A-M
- Xie Y
- Xu R
- Yamagishi K
- Yano Y
- Yaya S
- Yazdi-Feyzabadi V
- Yearwood JA
- Yeshitila YG
- Yip P
- Yonemoto N
- Younis MZ
- Yousefi Z
- Yousefinezhadi T
- Yusefzadeh H
- Zadey S
- Zaidi SS
- Zaki L
- Zamani M
- Zamanian M
- Zandian H
- Zastrozhin MS
- Zewdie KA
- Zhang Y
- Zhao X-JG
- Zhao Y
- Zheng P
- Zhu C
- Ziapour A
- Zlavog BS
- Zodpey S
- Publication venue
- 'Elsevier BV'
- Publication date
- 01/01/2020
- Field of study
Background Achieving universal health coverage (UHC) involves all people receiving the health services they need, of high quality, without experiencing financial hardship. Making progress towards UHC is a policy priority for both countries and global institutions, as highlighted by the agenda of the UN Sustainable Development Goals (SDGs) and WHO's Thirteenth General Programme of Work (GPW13). Measuring effective coverage at the health-system level is important for understanding whether health services are aligned with countries' health profiles and are of sufficient quality to produce health gains for populations of all ages. Methods Based on the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019, we assessed UHC effective coverage for 204 countries and territories from 1990 to 2019. Drawing from a measurement framework developed through WHO's GPW13 consultation, we mapped 23 effective coverage indicators to a matrix representing health service types (eg, promotion, prevention, and treatment) and five population-age groups spanning from reproductive and newborn to older adults (≥65 years). Effective coverage indicators were based on intervention coverage or outcome-based measures such as mortality-to-incidence ratios to approximate access to quality care; outcome-based measures were transformed to values on a scale of 0–100 based on the 2·5th and 97·5th percentile of location-year values. We constructed the UHC effective coverage index by weighting each effective coverage indicator relative to its associated potential health gains, as measured by disability-adjusted life-years for each location-year and population-age group. For three tests of validity (content, known-groups, and convergent), UHC effective coverage index performance was generally better than that of other UHC service coverage indices from WHO (ie, the current metric for SDG indicator 3.8.1 on UHC service coverage), the World Bank, and GBD 2017. We quantified frontiers of UHC effective coverage performance on the basis of pooled health spending per capita, representing UHC effective coverage index levels achieved in 2019 relative to country-level government health spending, prepaid private expenditures, and development assistance for health. To assess current trajectories towards the GPW13 UHC billion target—1 billion more people benefiting from UHC by 2023—we estimated additional population equivalents with UHC effective coverage from 2018 to 2023. Findings Globally, performance on the UHC effective coverage index improved from 45·8 (95% uncertainty interval 44·2–47·5) in 1990 to 60·3 (58·7–61·9) in 2019, yet country-level UHC effective coverage in 2019 still spanned from 95 or higher in Japan and Iceland to lower than 25 in Somalia and the Central African Republic. Since 2010, sub-Saharan Africa showed accelerated gains on the UHC effective coverage index (at an average increase of 2·6% [1·9–3·3] per year up to 2019); by contrast, most other GBD super-regions had slowed rates of progress in 2010–2019 relative to 1990–2010. Many countries showed lagging performance on effective coverage indicators for non-communicable diseases relative to those for communicable diseases and maternal and child health, despite non-communicable diseases accounting for a greater proportion of potential health gains in 2019, suggesting that many health systems are not keeping pace with the rising non-communicable disease burden and associated population health needs. In 2019, the UHC effective coverage index was associated with pooled health spending per capita (r=0·79), although countries across the development spectrum had much lower UHC effective coverage than is potentially achievable relative to their health spending. Under maximum efficiency of translating health spending into UHC effective coverage performance, countries would need to reach 1398pooledhealthspendingpercapita(US adjusted for purchasing power parity) in order to achieve 80 on the UHC effective coverage index. From 2018 to 2023, an estimated 388·9 million (358·6–421·3) more population equivalents would have UHC effective coverage, falling well short of the GPW13 target of 1 billion more people benefiting from UHC during this time. Current projections point to an estimated 3·1 billion (3·0–3·2) population equivalents still lacking UHC effective coverage in 2023, with nearly a third (968·1 million [903·5–1040·3]) residing in south Asia. Interpretation The present study demonstrates the utility of measuring effective coverage and its role in supporting improved health outcomes for all people—the ultimate goal of UHC and its achievement. Global ambitions to accelerate progress on UHC service coverage are increasingly unlikely unless concerted action on non-communicable diseases occurs and countries can better translate health spending into improved performance. Focusing on effective coverage and accounting for the world's evolving health needs lays the groundwork for better understanding how close—or how far—all populations are in benefiting from UHC. Funding Bill & Melinda Gates Foundation
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