MyMedR

Sulphone resistance in leprosy. A review of one hundred proven clinical cases

Pearson JM, Rees RJ, Waters MF

Lancet, 1975 Jul 12;2(7924):69-72.

An account is given of the first hundred consecutive proven cases of sulphone resistance in leprosy, detected in Malaysia between 1963 and 1974. Proof of resistance was clinical in eighty patients and was obtained by drug-sensitivity testing in mice in ninety-six patients; 76 cases were proved both clinically and experimentally, and there was no discrepancy between the two methods. Sulphone resistance was confined to patients with lepromatous-type leprosy--i.e., patients with a large bacterial population. Clinical evidence of relapse due to drug resistance appeared 5-24 years after the start of sulphone treatment. Low dosage favoured the appearance of resistance; therefore regular treatment of lepromatous leprosy with dapsone in full dosage is recommended. The attainment of "skin smears negative for leprosy bacilli" is no test of cure of lepromatous leprosy.

Sudan's maternal health needs urgent attention amid armed conflict

Olaleye SO, Aroyewun TF, Osman RA

Lancet, 2023 Sep 09;402(10405):848-849.

PMID: 37689405 DOI: 10.1016/S0140-6736(23)01697-5

Substitution treatment in Malaysia

Noordin NM, Merican MI, Rahman HA, Lee SS, Ramly R

Lancet, 2008 Sep 27;372(9644):1149-50.

PMID: 18926274 DOI: 10.1016/S0140-6736(08)61479-8

Still relevant: the 75th anniversary of the Universal Declaration of Human Rights

Kamarulzaman A, Maleche A, Beyrer C

Lancet, 2023 Dec 09;402(10418):2171-2173.

PMID: 38070941 DOI: 10.1016/S0140-6736(23)02653-3

Fulltext Statement in support of the scientists, public health professionals, and medical professionals of China combatting COVID-19

Calisher C, Carroll D, Colwell R, Corley RB, Daszak P, Drosten C, et al.

Lancet, 2020 03 07;395(10226):e42-e43.

PMID: 32087122 DOI: 10.1016/S0140-6736(20)30418-9

Southeast Asian countries vie with each other to woo foreign patients

Choo V

Lancet, 2002 Sep 28;360(9338):1004.

PMID: 12383679

Fulltext Smoking prevalence and attributable disease burden in 195 countries and territories, 1990-2015: a systematic analysis from the Global Burden of Disease Study 2015

GBD 2015 Tobacco Collaborators

Lancet, 2017 May 13;389(10082):1885-1906.

PMID: 28390697 DOI: 10.1016/S0140-6736(17)30819-X

BACKGROUND: The scale-up of tobacco control, especially after the adoption of the Framework Convention for Tobacco Control, is a major public health success story. Nonetheless, smoking remains a leading risk for early death and disability worldwide, and therefore continues to require sustained political commitment. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) offers a robust platform through which global, regional, and national progress toward achieving smoking-related targets can be assessed.
METHODS: We synthesised 2818 data sources with spatiotemporal Gaussian process regression and produced estimates of daily smoking prevalence by sex, age group, and year for 195 countries and territories from 1990 to 2015. We analysed 38 risk-outcome pairs to generate estimates of smoking-attributable mortality and disease burden, as measured by disability-adjusted life-years (DALYs). We then performed a cohort analysis of smoking prevalence by birth-year cohort to better understand temporal age patterns in smoking. We also did a decomposition analysis, in which we parsed out changes in all-cause smoking-attributable DALYs due to changes in population growth, population ageing, smoking prevalence, and risk-deleted DALY rates. Finally, we explored results by level of development using the Socio-demographic Index (SDI).
FINDINGS: Worldwide, the age-standardised prevalence of daily smoking was 25·0% (95% uncertainty interval [UI] 24·2-25·7) for men and 5·4% (5·1-5·7) for women, representing 28·4% (25·8-31·1) and 34·4% (29·4-38·6) reductions, respectively, since 1990. A greater percentage of countries and territories achieved significant annualised rates of decline in smoking prevalence from 1990 to 2005 than in between 2005 and 2015; however, only four countries had significant annualised increases in smoking prevalence between 2005 and 2015 (Congo [Brazzaville] and Azerbaijan for men and Kuwait and Timor-Leste for women). In 2015, 11·5% of global deaths (6·4 million [95% UI 5·7-7·0 million]) were attributable to smoking worldwide, of which 52·2% took place in four countries (China, India, the USA, and Russia). Smoking was ranked among the five leading risk factors by DALYs in 109 countries and territories in 2015, rising from 88 geographies in 1990. In terms of birth cohorts, male smoking prevalence followed similar age patterns across levels of SDI, whereas much more heterogeneity was found in age patterns for female smokers by level of development. While smoking prevalence and risk-deleted DALY rates mostly decreased by sex and SDI quintile, population growth, population ageing, or a combination of both, drove rises in overall smoking-attributable DALYs in low-SDI to middle-SDI geographies between 2005 and 2015.
INTERPRETATION: The pace of progress in reducing smoking prevalence has been heterogeneous across geographies, development status, and sex, and as highlighted by more recent trends, maintaining past rates of decline should not be taken for granted, especially in women and in low-SDI to middle-SDI countries. Beyond the effect of the tobacco industry and societal mores, a crucial challenge facing tobacco control initiatives is that demographic forces are poised to heighten smoking's global toll, unless progress in preventing initiation and promoting cessation can be substantially accelerated. Greater success in tobacco control is possible but requires effective, comprehensive, and adequately implemented and enforced policies, which might in turn require global and national levels of political commitment beyond what has been achieved during the past 25 years.
FUNDING: Bill & Melinda Gates Foundation and Bloomberg Philanthropies.
Malaysian Collaborators: Southern University College, Skudai, Malaysia (Y J Kim PhD); University of Science Malaysia, Kubang Kerian, Malaysia (K I Musa MD); International Medical University, Kuala Lumpur, Malaysia (C T Sreeramareddy MD)

Fulltext Shifting gender barriers in immunisation in the COVID-19 pandemic response and beyond

Nassiri-Ansari T, Atuhebwe P, Ayisi AS, Goulding S, Johri M, Allotey P, et al.

Lancet, 2022 Jul 02;400(10345):24.

PMID: 35780789 DOI: 10.1016/S0140-6736(22)01189-8

Shared commitment to women's health abroad and at home

Sebelius K

Lancet, 2013 May 18;381(9879):1689.

PMID: 23683615 DOI: 10.1016/S0140-6736(13)60905-8

Fulltext Sex-disaggregated data in COVID-19 vaccine trials

Vijayasingham L, Bischof E, Wolfe J, Gender and COVID-19 Research Agenda-setting Initiative

Lancet, 2021 Mar 13;397(10278):966-967.

PMID: 33684351 DOI: 10.1016/S0140-6736(21)00384-6

Seeding a planetary health education revolution: institutional sign-on challenge

Howard C, Moineau G, Poitras J, Redvers N, Mahmood J, Eissa M, et al.

Lancet, 2023 Dec 09;402(10418):2173-2176.

PMID: 38000382 DOI: 10.1016/S0140-6736(23)02526-6

Fulltext Science, not speculation, is essential to determine how SARS-CoV-2 reached humans

Calisher CH, Carroll D, Colwell R, Corley RB, Daszak P, Drosten C, et al.

Lancet, 2021 Jul 17;398(10296):209-211.

PMID: 34237296 DOI: 10.1016/S0140-6736(21)01419-7

Satiation or satiety? More than mere semantics - Authors' reply

Carbone MF, Mahadeva S, Lacy BE, Talley NJ, Ford AC

Lancet, 2021 03 20;397(10279):1061.

PMID: 33743867 DOI: 10.1016/S0140-6736(21)00239-7

Satay and Salmonella and listeria infection

Arumugaswamy RK, Ali GR, ab Hamid SN

Lancet, 1993 Jul 24;342(8865):247.

PMID: 8100972

Safeguarding human health in the Anthropocene epoch: report of The Rockefeller Foundation-Lancet Commission on planetary health

Whitmee S, Haines A, Beyrer C, Boltz F, Capon AG, de Souza Dias BF, et al.

Lancet, 2015 Nov 14;386(10007):1973-2028.

PMID: 26188744 DOI: 10.1016/S0140-6736(15)60901-1

Robert Barr MacGregor

Lancet, 1980 Jan 19;1(8160):162.

PMID: 6101506

Rivaroxaban with or without aspirin in patients with stable coronary artery disease: an international, randomised, double-blind, placebo-controlled trial

Connolly SJ, Eikelboom JW, Bosch J, Dagenais G, Dyal L, Lanas F, et al.

Lancet, 2018 01 20;391(10117):205-218.

PMID: 29132879 DOI: 10.1016/S0140-6736(17)32458-3

BACKGROUND: Coronary artery disease is a major cause of morbidity and mortality worldwide, and is a consequence of acute thrombotic events involving activation of platelets and coagulation proteins. Factor Xa inhibitors and aspirin each reduce thrombotic events but have not yet been tested in combination or against each other in patients with stable coronary artery disease.

METHODS: In this multicentre, double-blind, randomised, placebo-controlled, outpatient trial, patients with stable coronary artery disease or peripheral artery disease were recruited at 602 hospitals, clinics, or community centres in 33 countries. This paper reports on patients with coronary artery disease. Eligible patients with coronary artery disease had to have had a myocardial infarction in the past 20 years, multi-vessel coronary artery disease, history of stable or unstable angina, previous multi-vessel percutaneous coronary intervention, or previous multi-vessel coronary artery bypass graft surgery. After a 30-day run in period, patients were randomly assigned (1:1:1) to receive rivaroxaban (2·5 mg orally twice a day) plus aspirin (100 mg once a day), rivaroxaban alone (5 mg orally twice a day), or aspirin alone (100 mg orally once a day). Randomisation was computer generated. Each treatment group was double dummy, and the patients, investigators, and central study staff were masked to treatment allocation. The primary outcome of the COMPASS trial was the occurrence of myocardial infarction, stroke, or cardiovascular death. This trial is registered with ClinicalTrials.gov, number NCT01776424, and is closed to new participants.

FINDINGS: Between March 12, 2013, and May 10, 2016, 27 395 patients were enrolled to the COMPASS trial, of whom 24 824 patients had stable coronary artery disease from 558 centres. The combination of rivaroxaban plus aspirin reduced the primary outcome more than aspirin alone (347 [4%] of 8313 vs 460 [6%] of 8261; hazard ratio [HR] 0·74, 95% CI 0·65-0·86, p<0·0001). By comparison, treatment with rivaroxaban alone did not significantly improve the primary outcome when compared with treatment with aspirin alone (411 [5%] of 8250 vs 460 [6%] of 8261; HR 0·89, 95% CI 0·78-1·02, p=0·094). Combined rivaroxaban plus aspirin treatment resulted in more major bleeds than treatment with aspirin alone (263 [3%] of 8313 vs 158 [2%] of 8261; HR 1·66, 95% CI 1·37-2·03, p<0·0001), and similarly, more bleeds were seen in the rivaroxaban alone group than in the aspirin alone group (236 [3%] of 8250 vs 158 [2%] of 8261; HR 1·51, 95% CI 1·23-1·84, p<0·0001). The most common site of major bleeding was gastrointestinal, occurring in 130 [2%] patients who received combined rivaroxaban plus aspirin, in 84 [1%] patients who received rivaroxaban alone, and in 61 [1%] patients who received aspirin alone. Rivaroxaban plus aspirin reduced mortality when compared with aspirin alone (262 [3%] of 8313 vs 339 [4%] of 8261; HR 0·77, 95% CI 0·65-0·90, p=0·0012).

INTERPRETATION: In patients with stable coronary artery disease, addition of rivaroxaban to aspirin lowered major vascular events, but increased major bleeding. There was no significant increase in intracranial bleeding or other critical organ bleeding. There was also a significant net benefit in favour of rivaroxaban plus aspirin and deaths were reduced by 23%. Thus, addition of rivaroxaban to aspirin has the potential to substantially reduce morbidity and mortality from coronary artery disease worldwide.

FUNDING: Bayer AG.

Rethinking health-care systems: a focus on chronicity

Allotey P, Reidpath DD, Yasin S, Chan CK, de-Graft Aikins A

Lancet, 2011 Feb 5;377(9764):450-1.

PMID: 21074257 DOI: 10.1016/S0140-6736(10)61856-9

Fulltext Remdesivir and three other drugs for hospitalised patients with COVID-19: final results of the WHO Solidarity randomised trial and updated meta-analyses

WHO Solidarity Trial Consortium

Lancet, 2022 May 21;399(10339):1941-1953.

PMID: 35512728 DOI: 10.1016/S0140-6736(22)00519-0

BACKGROUND: The Solidarity trial among COVID-19 inpatients has previously reported interim mortality analyses for four repurposed antiviral drugs. Lopinavir, hydroxychloroquine, and interferon (IFN)-β1a were discontinued for futility but randomisation to remdesivir continued. Here, we report the final results of Solidarity and meta-analyses of mortality in all relevant trials to date.

METHODS: Solidarity enrolled consenting adults (aged ≥18 years) recently hospitalised with, in the view of their doctor, definite COVID-19 and no contraindication to any of the study drugs, regardless of any other patient characteristics. Participants were randomly allocated, in equal proportions between the locally available options, to receive whichever of the four study drugs (lopinavir, hydroxychloroquine, IFN-β1a, or remdesivir) were locally available at that time or no study drug (controls). All patients also received the local standard of care. No placebos were given. The protocol-specified primary endpoint was in-hospital mortality, subdivided by disease severity. Secondary endpoints were progression to ventilation if not already ventilated, and time-to-discharge from hospital. Final log-rank and Kaplan-Meier analyses are presented for remdesivir, and are appended for all four study drugs. Meta-analyses give weighted averages of the mortality findings in this and all other randomised trials of these drugs among hospital inpatients. Solidarity is registered with ISRCTN, ISRCTN83971151, and ClinicalTrials.gov, NCT04315948.

FINDINGS: Between March 22, 2020, and Jan 29, 2021, 14 304 potentially eligible patients were recruited from 454 hospitals in 35 countries in all six WHO regions. After the exclusion of 83 (0·6%) patients with a refuted COVID-19 diagnosis or encrypted consent not entered into the database, Solidarity enrolled 14 221 patients, including 8275 randomly allocated (1:1) either to remdesivir (ten daily infusions, unless discharged earlier) or to its control (allocated no study drug although remdesivir was locally available). Compliance was high in both groups. Overall, 602 (14·5%) of 4146 patients assigned to remdesivir died versus 643 (15·6%) of 4129 assigned to control (mortality rate ratio [RR] 0·91 [95% CI 0·82-1·02], p=0·12). Of those already ventilated, 151 (42·1%) of 359 assigned to remdesivir died versus 134 (38·6%) of 347 assigned to control (RR 1·13 [0·89-1·42], p=0·32). Of those not ventilated but on oxygen, 14·6% assigned to remdesivir died versus 16·3% assigned to control (RR 0·87 [0·76-0·99], p=0·03). Of 1730 not on oxygen initially, 2·9% assigned to remdesivir died versus 3·8% assigned to control (RR 0·76 [0·46-1·28], p=0·30). Combining all those not ventilated initially, 11·9% assigned to remdesivir died versus 13·5% assigned to control (RR 0·86 [0·76-0·98], p=0·02) and 14·1% versus 15·7% progressed to ventilation (RR 0·88 [0·77-1·00], p=0·04). The non-prespecified composite outcome of death or progression to ventilation occurred in 19·6% assigned to remdesivir versus 22·5% assigned to control (RR 0·84 [0·75-0·93], p=0·001). Allocation to daily remdesivir infusions (vs open-label control) delayed discharge by about 1 day during the 10-day treatment period. A meta-analysis of mortality in all randomised trials of remdesivir versus no remdesivir yielded similar findings.

INTERPRETATION: Remdesivir has no significant effect on patients with COVID-19 who are already being ventilated. Among other hospitalised patients, it has a small effect against death or progression to ventilation (or both).

FUNDING: WHO.

Recognising patients' rights: patchy progress

Kaur S, Herxheimer A

Lancet, 1994 Jan 15;343(8890):132.

PMID: 7904000

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