Global review of COVID-19 mitigation strategies and their impact on cancer service disruptions.

During the COVID-19 pandemic, countries adopted mitigation strategies to reduce disruptions to cancer services. We reviewed their implementation across health system functions and their impact on cancer diagnosis and care during the pandemic. A systematic search was performed using terms related to cancer and COVID-19. Included studies reported on individuals with cancer or cancer care services, focusing on strategies/programs aimed to reduce delays and disruptions. Extracted data were grouped into four functions (governance, financing, service delivery, and resource generation) and sub-functions of the health system performance assessment framework. We included 30 studies from 16 countries involving 192,233 patients with cancer. Multiple mitigation approaches were implemented, predominantly affecting sub-functions of service delivery to control COVID-19 infection via the suspension of non-urgent cancer care, modified treatment guidelines, and increased telemedicine use in routine cancer care delivery. Resource generation was mainly ensured through adequate workforce supply. However, less emphasis on monitoring or assessing the effectiveness and financing of these strategies was observed. Seventeen studies suggested improved service uptake after mitigation implementation, yet the resulting impact on cancer diagnosis and care has not been established. This review emphasizes the importance of developing effective mitigation strategies across all health system (sub)functions to minimize cancer care service disruptions during crises. Deficiencies were observed in health service delivery (to ensure equity), governance (to monitor and evaluate the implementation of mitigation strategies), and financing. In the wake of future emergencies, implementation research studies that include pre-prepared protocols will be essential to assess mitigation impact across cancer care services.

Quantitative estimates of preventable and treatable deaths from 36 cancers worldwide: a population-based study.

BACKGROUND: Cancer is a leading cause of premature mortality globally. This study estimates premature deaths at ages 30-69 years and distinguishes these as deaths that are preventable (avertable through primary or secondary prevention) or treatable (avertable through curative treatment) in 185 countries worldwide. METHODS: For this population-based study, estimated cancer deaths by country, cancer, sex, and age groups were retrieved from the International Agency for Research on Cancer's GLOBOCAN 2020 database. Crude and age-adjusted cancer-specific years of life lost (YLLs) were calculated for 36 cancer types. FINDINGS: Of the estimated all-ages cancer burden of 265·6 million YLLs, 182·8 million (68·8%) YLLs were due to premature deaths from cancer globally in 2020, with 124·3 million (68·0%) preventable and 58·5 million (32·0%) treatable. Countries with low, medium, or high human development index (HDI) levels all had greater proportions of YLLs at premature ages than very high HDI countries (68·9%, 77·0%, and 72·2% vs 57·7%, respectively). Lung cancer was the leading contributor to preventable premature YLLs in medium to very high HDI countries (17·4% of all cancers, or 29·7 million of 171·3 million YLLs), whereas cervical cancer led in low HDI countries (26·3% of all preventable cancers, or 1·83 million of 6·93 million YLLs). Colorectal and breast cancers were major treatable cancers across all four tiers of HDI (25·5% of all treatable cancers in combination, or 14·9 million of 58·5 million YLLs). INTERPRETATION: Alongside tailored programmes of early diagnosis and screening linked to timely and comprehensive treatment, greater investments in risk factor reduction and vaccination are needed to address premature cancer inequalities. FUNDING: Erasmus Mundus Exchange Programme and the International Agency for Research on Cancer. TRANSLATIONS: For the German, French, Spanish and Chinese translations of the abstract see Supplementary Materials section.

Case Report: Bocavirus Infection Radiologically Resembling a Congestive Heart Failure in a Patient with Metastatic Castration-Resistant Prostate Cancer.

Background: Human bocavirus (HBoV) is a viral pathogen from the genus Bocaparvovirus (family Parvoviridae, subfamily Parvovirinae) discovered in 2005. Most of available literature is about HBoV in children and adults with hematological malignancies and in otherwise healthy children with respiratory infections. Information regarding infection in the adult population with solid tumors is scarce. Case Report: We report the case of a 51-year-old male with metastatic castration resistant prostate cancer undergoing chemotherapy treatment who presented with fever, dyspnea, dry cough, and pleuritic pain. Imaging techniques showed signs of congestive heart failure. Symptoms, laboratory tests and echocardiography revealed a more probable infectious etiology. Antibiotic therapy was started. A polymerase chain reaction (PCR) test of nasopharyngeal exudate for respiratory viruses was positive for HBoV. The rest of the microbiological tests were negative. Bronchoalveolar lavage (BAL) was performed. Bacterial culture of BAL was negative while respiratory virus PCR confirmed positivity for HBoV. Antibiotic therapy was discontinued. The patient gradually recovered. Conclusions: Emerging infectious diseases are a notorious threat for immunocompromised populations such as solid tumor patients. This case is unique because to our knowledge this is the first case report article of HBoV in a solid tumor patient and because imaging techniques exhibited signs of congestive heart failure that did not correlate with the rest of the tests. It shows that unusual pathogens should be considered when managing serious clinical complications with uncommon presentations in cancer patients. Notable diagnostic efforts should be made to reach a diagnosis in these cases.

Coexistence of calcified- and lipid-containing plaque components and their association with incidental rupture points in acute coronary syndrome-causing culprit lesions: results from the prospective OPTICO-ACS study.

AIMS: Rupture of the fibrous cap (RFC) represents the main pathophysiological mechanism causing acute coronary syndromes (ACS). Destabilization due to plaque biomechanics is considered to be importantly involved, exact mechanisms triggering plaque ruptures are, however, unknown. This study aims at characterizing the relation between plaque components and rupture points at ACS-causing culprit lesions in a large cohort of ACS-patients assessed by high-resolution intracoronary imaging. METHODS AND RESULTS: Within the prospective, multicentric OPTICO-ACS study program, the ACS-causing culprit plaques of 282 consecutive patients were investigated following a standardized optical coherence tomography (OCT) imaging protocol. Each pullback was assessed on a frame-by-frame basis for the presence of lipid components (LC), calcium components (CC), and coexistence of both LC and CC (LCC) by two independent OCT-core labs. Of the 282 ACS-patients, 204 patients (72.3%) presented with ACS caused by culprit lesions with rupture of the fibrous cap (RFC-ACS) and 27.7% patients had ACS caused by culprit lesions with intact fibrous cap (IFC-ACS). When comparing RFC-ACS to IFC-ACS, a preferential occurrence of all three plaque components (LC, CC, and LCC) in RFC-ACS became apparent (P < 0.001). Within ruptured culprit lesions, the zone straight at the rupture point [extended rupture zone (RZ)] was characterized by similar (24.7% vs. 24.0%; P = ns) calcium content when compared with the proximal and distal border of the culprit lesion [border zone (BZ)]. The RZ displayed a significantly higher amount of both, LC (100% vs. 69.8%; P < 0.001) and LCC (22.7% vs. 6.8%; P < 0.001), when compared with the BZ. The relative component increase towards the RZ was particularly evident for LCC (+233.8%), while LC showed only a modest increase (+43.3%). CONCLUSIONS: Calcified- and lipid-containing components characterize ruptured fibrous cap ACS-causing culprit lesions. Their coexistence is accelerated directly at the ruptured point, suggesting a pathophysiological contribution in the development of RFC-ACS.