Corrigendum

This correction is being published to correct the name of author

Clearing the myths of time: Tuskegee revisited

More than a quarter of black Americans questioned in a recent survey believe that AIDS was produced in a laboratory, and 16% believe that it was created by the US government to control the black population. In attempting to explain why such mistaken notions are so widely held, Laura Bogart, lead author of the study, says: “Conspiracy beliefs stem from current and historical discrimination against blacks in our healthcare system, including the Tuskegee syphilis study”. The Tuskegee study has become the archetype of unethical research and racism in medicine. However, by citing Tuskegee, is Bogart merely invoking one set of conspiracy beliefs to explain another? Between 1932 and 1972, the US Public Health Service (USPHS) studied 600 black men, 399 with untreated latent syphilis and 201 uninfected controls, living around Tuskegee, Macon County, Alabama. Although there was no study protocol, the purpose of the Tuskegee experiments seems to have been to observe patients with untreated latent syphilis to autopsy and verify the presence or absence of syphilitic destructive lesions. According to a detailed analysis of the Tuskegee study by Robert M White in Archives of Internal Medicine, USPHS officers believed that the study “should forever dispel the rather general belief that syphilis is a disease of small consequence to the negro”

Corrigendum: Treatments of Advanced Non‑Small Cell Lung Cancer (NSCLC) in an Italian Center: Drug Utilization and the Treatment Costs of Innovative Drugs

There was an error in Discussion section at page 36 in this article by Piantedosi et al. [Farmeconomia. Health economics and therapeutic pathways 2019; 20(1): 27-41; https://doi.org/10.7175/fe.v20i1.1376]. The online version has been corrected on June 5, 201

Corrigendum: An Integrated Management Model of Patients With Atrial Fibrillation: The Experience of the Local Health Unit Tuscany North-West

There was an error in the description of GLORIA-AF registry program at page 10 in this Supplement by Casolo et al. [Farmeconomia. Health economics and therapeutic pathways 2019; 20(Suppl 1): 3-16; https://doi.org/10.7175/fe.v20i1S.1454]. The online version has been corrected on February 12, 2020

Erratum: Effectiveness of Long-Acting Injectable Antipsychotics in Schizophrenia: A Literature Review and Bayesian Meta-Analysis Informing Economic Considerations

There was an error in the relapse rate reduction reported in Figure 2 in this article by Zaniolo et al. [Farmeconomia. Health economics and therapeutic pathways 2019; 20: 13-24; https://doi.org/10.7175/fe.v20i1.1393]. The online version has been corrected on 13 February 2019

Type 2 myocardial infarction: the chimaera of cardiology?

The term type 2 myocardial infarction first appeared as part of the universal definition of myocardial infarction. It was introduced to cover a group of patients who had elevation of cardiac troponin but did not meet the traditional criteria for acute myocardial infarction although they were considered to have an underlying ischaemic aetiology for the myocardial damage observed. Since first inception, the term type 2 myocardial infarction has always been vague. Although attempts have been made to produce a systematic definition of what constitutes a type 2 myocardial infarction, it has been more often characterised by what it is not rather than what it is. Clinical studies that have used type 2 myocardial infarction as a diagnostic criterion have produced disparate incidence figures. The range of associated clinical conditions differs from study to study. Additionally, there are no agreed or evidence-based treatment strategies for type 2 myocardial infarction. The authors believe that the term type 2 myocardial infarction is confusing and not evidence-based. They consider that there is good reason to stop using this term and consider instead the concept of secondary myocardial injury that relates to the underlying pathophysiology of the primary clinical condition

Withdrawal of antihypertensive medication: a systematic review

Although antihypertensive medication is usually continued indefinitely, observations during wash-out phases in hypertension trials have shown that withdrawal of antihypertensive medication might be well tolerated to do in a considerable proportion of people. A systematic review was completed to determine the proportion of people remaining normotensive for 6 months or longer after cessation of antihypertensive therapy and to investigate the safety of withdrawal. The mean proportion adjusted for sample size of people remaining below each study's threshold for hypertension treatment was 0.38 at 6 months [95% confidence interval (CI) 0.37–0.49; 912 participants], 0.40 at 1 year (95% CI 0.40–0.40; 2640 participants) and 0.26 at 2 years or longer (95% CI 0.26–0.27; 1262 participants). Monotherapy, lower blood pressure before withdrawal and body weight were reported as predictors for successful withdrawal. Adverse events were more common in those who withdrew but were minor and included headache, joint pain, palpitations, oedema and a general feeling of being unwell. Prescribers should consider offering patients with well controlled hypertension a trial of withdrawal of antihypertensive treatment with subsequent regular blood pressure monitoring

Angiotensin-converting enzyme defines matrikine-regulated inflammation and fibrosis

The neutrophil chemoattractant proline-glycine-proline (PGP) is generated from collagen by matrix metalloproteinase-8/9 (MMP-8/9) and prolyl endopeptidase (PE), and it is concomitantly degraded by extracellular leukotriene A4 hydrolase (LTA4H) to limit neutrophilia. Components of cigarette smoke can acetylate PGP, yielding a species (AcPGP) that is resistant to LTA4H-mediated degradation and can, thus, support a sustained neutrophilia. In this study, we sought to elucidate if an antiinflammatory system existed to degrade AcPGP that is analogous to the PGP-LTA4H axis. We demonstrate that AcPGP is degraded through a previously unidentified action of the enzyme angiotensin-converting enzyme (ACE). Pulmonary ACE is elevated during episodes of acute inflammation, as a consequence of enhanced vascular permeability, to ensure the efficient degradation of AcPGP. Conversely, we suggest that this pathway is aberrant in chronic obstructive pulmonary disease (COPD) enabling the accumulation of AcPGP. Consequently, we identify a potentially novel protective role for AcPGP in limiting pulmonary fibrosis and suggest the pathogenic function attributed to ACE in idiopathic pulmonary fibrosis (IPF) to be a consequence of overzealous AcPGP degradation. Thus, AcPGP seemingly has very divergent roles: it is pathogenic in its capacity to drive neutrophilic inflammation and matrix degradation in the context of COPD, but it is protective in its capacity to limit fibrosis in IPF