Key clinical point: Aromatase inhibitor vs. tamoxifen reduced the risk for breast cancer (BC) recurrence in premenopausal women with early-stage, estrogen receptor-positive (ER+) BC receiving ovarian suppression.

Major finding: Aromatase inhibitor vs. tamoxifen was associated with significantly reduced rates of BC recurrence during the first 4 years of follow-up (risk ratio [RR] 0.68; P < .0001) and distant recurrence (RR 0.83; P = .018). No significant differences in breast cancer mortality, death without recurrence, or all-cause mortality were observed between the treatment groups.

Study details: Findings are a meta-analysis of 4 phase 3 trials (ABCSG-XII, TEXT, SOFT, and HOBOE) including 7,030 premenopausal women with ER+ BC who were randomly assigned to aromatase inhibitors (anastrozole, exemestane, or letrozole) or tamoxifen for 3 or 5 years, all in combination with ovarian suppression or ablation.

Disclosures: This study was funded by the Cancer Research UK and UK Medical Research Council. The authors declared serving as leaders and fiduciaries or receiving grants, consulting fees, travel support, or honoraria from several sources.

Source: Early Breast Cancer Trialists' Collaborative Group. Lancet Oncol. 2022 (Feb 3). Doi: 10.1016/S1470-2045(21)00758-0.

Key clinical point: Aromatase inhibitor vs. tamoxifen reduced the risk for breast cancer (BC) recurrence in premenopausal women with early-stage, estrogen receptor-positive (ER+) BC receiving ovarian suppression.

Major finding: Aromatase inhibitor vs. tamoxifen was associated with significantly reduced rates of BC recurrence during the first 4 years of follow-up (risk ratio [RR] 0.68; P < .0001) and distant recurrence (RR 0.83; P = .018). No significant differences in breast cancer mortality, death without recurrence, or all-cause mortality were observed between the treatment groups.

Study details: Findings are a meta-analysis of 4 phase 3 trials (ABCSG-XII, TEXT, SOFT, and HOBOE) including 7,030 premenopausal women with ER+ BC who were randomly assigned to aromatase inhibitors (anastrozole, exemestane, or letrozole) or tamoxifen for 3 or 5 years, all in combination with ovarian suppression or ablation.

Disclosures: This study was funded by the Cancer Research UK and UK Medical Research Council. The authors declared serving as leaders and fiduciaries or receiving grants, consulting fees, travel support, or honoraria from several sources.

Source: Early Breast Cancer Trialists' Collaborative Group. Lancet Oncol. 2022 (Feb 3). Doi: 10.1016/S1470-2045(21)00758-0.

Key clinical point: Aromatase inhibitor vs. tamoxifen reduced the risk for breast cancer (BC) recurrence in premenopausal women with early-stage, estrogen receptor-positive (ER+) BC receiving ovarian suppression.

Major finding: Aromatase inhibitor vs. tamoxifen was associated with significantly reduced rates of BC recurrence during the first 4 years of follow-up (risk ratio [RR] 0.68; P < .0001) and distant recurrence (RR 0.83; P = .018). No significant differences in breast cancer mortality, death without recurrence, or all-cause mortality were observed between the treatment groups.

Study details: Findings are a meta-analysis of 4 phase 3 trials (ABCSG-XII, TEXT, SOFT, and HOBOE) including 7,030 premenopausal women with ER+ BC who were randomly assigned to aromatase inhibitors (anastrozole, exemestane, or letrozole) or tamoxifen for 3 or 5 years, all in combination with ovarian suppression or ablation.

Disclosures: This study was funded by the Cancer Research UK and UK Medical Research Council. The authors declared serving as leaders and fiduciaries or receiving grants, consulting fees, travel support, or honoraria from several sources.

Source: Early Breast Cancer Trialists' Collaborative Group. Lancet Oncol. 2022 (Feb 3). Doi: 10.1016/S1470-2045(21)00758-0.

Key clinical point: Protein-truncating variants (PTV) of 9 breast cancer (BC) risk genes showed substantial differences in tumor pathology and were generally associated with triple-negative (TN) or high-grade disease.

Major finding: BRCA1 showed the highest association for TN disease (odds ratio [OR] 55.32; 95% CI 40.51-75.55) and ATM variants for the hormone receptor-positive (HR+) erb-b2 receptor tyrosine kinase 2-negative (ERBB2−) high-grade subtype (OR 4.99; 95% CI 3.68-6.76). RAD51C (OR 6.19; 95% CI 3.17-12.12), RAD51D (OR 6.19; 95% CI 2.99-12.79), and BARD1 (OR 10.05; 95% CI 5.27-19.19) were most strongly associated with TN disease. PALB2 PTVs showed higher ORs for HR+ERBB2− high-grade subtype (OR 9.43; 95% CI 6.24- 14.25) and TN disease (OR 8.05; 95% CI 5.17-12.53).

Study details: This was a case-control analysis of the BRIDGES study including 42,680 patients with BC who were matched with 46,387 healthy controls.

Disclosures: This study was funded by the European Union Horizon 2020 research and innovation program, Wellcome Trust, and several other sources. The authors declared receiving grants, honorariums, personal fees, or awards from several sources.

Source: Breast Cancer Association Consortium. JAMA Oncol. 2022 (Jan 27). Doi: 10.1001/jamaoncol.2021.6744.

Key clinical point: Protein-truncating variants (PTV) of 9 breast cancer (BC) risk genes showed substantial differences in tumor pathology and were generally associated with triple-negative (TN) or high-grade disease.

Major finding: BRCA1 showed the highest association for TN disease (odds ratio [OR] 55.32; 95% CI 40.51-75.55) and ATM variants for the hormone receptor-positive (HR+) erb-b2 receptor tyrosine kinase 2-negative (ERBB2−) high-grade subtype (OR 4.99; 95% CI 3.68-6.76). RAD51C (OR 6.19; 95% CI 3.17-12.12), RAD51D (OR 6.19; 95% CI 2.99-12.79), and BARD1 (OR 10.05; 95% CI 5.27-19.19) were most strongly associated with TN disease. PALB2 PTVs showed higher ORs for HR+ERBB2− high-grade subtype (OR 9.43; 95% CI 6.24- 14.25) and TN disease (OR 8.05; 95% CI 5.17-12.53).

Study details: This was a case-control analysis of the BRIDGES study including 42,680 patients with BC who were matched with 46,387 healthy controls.

Disclosures: This study was funded by the European Union Horizon 2020 research and innovation program, Wellcome Trust, and several other sources. The authors declared receiving grants, honorariums, personal fees, or awards from several sources.

Source: Breast Cancer Association Consortium. JAMA Oncol. 2022 (Jan 27). Doi: 10.1001/jamaoncol.2021.6744.

Key clinical point: Protein-truncating variants (PTV) of 9 breast cancer (BC) risk genes showed substantial differences in tumor pathology and were generally associated with triple-negative (TN) or high-grade disease.

Major finding: BRCA1 showed the highest association for TN disease (odds ratio [OR] 55.32; 95% CI 40.51-75.55) and ATM variants for the hormone receptor-positive (HR+) erb-b2 receptor tyrosine kinase 2-negative (ERBB2−) high-grade subtype (OR 4.99; 95% CI 3.68-6.76). RAD51C (OR 6.19; 95% CI 3.17-12.12), RAD51D (OR 6.19; 95% CI 2.99-12.79), and BARD1 (OR 10.05; 95% CI 5.27-19.19) were most strongly associated with TN disease. PALB2 PTVs showed higher ORs for HR+ERBB2− high-grade subtype (OR 9.43; 95% CI 6.24- 14.25) and TN disease (OR 8.05; 95% CI 5.17-12.53).

Study details: This was a case-control analysis of the BRIDGES study including 42,680 patients with BC who were matched with 46,387 healthy controls.

Disclosures: This study was funded by the European Union Horizon 2020 research and innovation program, Wellcome Trust, and several other sources. The authors declared receiving grants, honorariums, personal fees, or awards from several sources.

Source: Breast Cancer Association Consortium. JAMA Oncol. 2022 (Jan 27). Doi: 10.1001/jamaoncol.2021.6744.

Key clinical point: A regimen consisting of docetaxel and capecitabine (TX) followed by cyclophosphamide, epirubicin, and capecitabine (CEX) vs. only docetaxel followed by cyclophosphamide, epirubicin, and fluorouracil (T-CEF) prolonged recurrence-free survival (RFS) in patients with non- BRCA1-like early triple-negative breast cancer (TNBC).

Major finding: Overall, patients assigned to TX-CEX vs. T-CEF arms had higher RFS (hazard ratio [HR] 0.39; P = .01), with the capecitabine-containing chemotherapy being significantly more effective than conventional chemotherapy in patients with non-BRCA1-like tumor (HR 0.23; P < .01) but not in patients with BRCA1-like tumor (HR 0.66; P = .42).

Study details: Findings are from the open-label, phase 3 FinXX study including 202 patients with early TNBC who were randomly assigned to TX-CEX or T-CEF arms.  BRCA1-like status was obtained for 129 patients.

Disclosures: This work was supported by the Dutch Cancer Society. The authors declared serving as board members and employees or receiving fees, grants, nonfinancial, and research support from several sources.

Source: de Boo LW et al. Br J Cancer. 2022 (Feb 5). Doi: 10.1038/s41416-022-01711-y.

Key clinical point: A regimen consisting of docetaxel and capecitabine (TX) followed by cyclophosphamide, epirubicin, and capecitabine (CEX) vs. only docetaxel followed by cyclophosphamide, epirubicin, and fluorouracil (T-CEF) prolonged recurrence-free survival (RFS) in patients with non- BRCA1-like early triple-negative breast cancer (TNBC).

Major finding: Overall, patients assigned to TX-CEX vs. T-CEF arms had higher RFS (hazard ratio [HR] 0.39; P = .01), with the capecitabine-containing chemotherapy being significantly more effective than conventional chemotherapy in patients with non-BRCA1-like tumor (HR 0.23; P < .01) but not in patients with BRCA1-like tumor (HR 0.66; P = .42).

Study details: Findings are from the open-label, phase 3 FinXX study including 202 patients with early TNBC who were randomly assigned to TX-CEX or T-CEF arms.  BRCA1-like status was obtained for 129 patients.

Disclosures: This work was supported by the Dutch Cancer Society. The authors declared serving as board members and employees or receiving fees, grants, nonfinancial, and research support from several sources.

Source: de Boo LW et al. Br J Cancer. 2022 (Feb 5). Doi: 10.1038/s41416-022-01711-y.

Key clinical point: A regimen consisting of docetaxel and capecitabine (TX) followed by cyclophosphamide, epirubicin, and capecitabine (CEX) vs. only docetaxel followed by cyclophosphamide, epirubicin, and fluorouracil (T-CEF) prolonged recurrence-free survival (RFS) in patients with non- BRCA1-like early triple-negative breast cancer (TNBC).

Major finding: Overall, patients assigned to TX-CEX vs. T-CEF arms had higher RFS (hazard ratio [HR] 0.39; P = .01), with the capecitabine-containing chemotherapy being significantly more effective than conventional chemotherapy in patients with non-BRCA1-like tumor (HR 0.23; P < .01) but not in patients with BRCA1-like tumor (HR 0.66; P = .42).

Study details: Findings are from the open-label, phase 3 FinXX study including 202 patients with early TNBC who were randomly assigned to TX-CEX or T-CEF arms.  BRCA1-like status was obtained for 129 patients.

Disclosures: This work was supported by the Dutch Cancer Society. The authors declared serving as board members and employees or receiving fees, grants, nonfinancial, and research support from several sources.

Source: de Boo LW et al. Br J Cancer. 2022 (Feb 5). Doi: 10.1038/s41416-022-01711-y.

Key clinical point: Adding carboplatin to neoadjuvant paclitaxel followed by doxorubicin and cyclophosphamide improved long-term event-free survival (EFS) along with a manageable safety profile in patients with triple-negative breast cancer (TNBC).

Major finding: Patients receiving carboplatin+veliparib+paclitaxel vs. paclitaxel showed significant improvements in EFS (hazard ratio [HR] 0.63; P = .02), whereas EFS was not significntly different among patients assigned to carboplatin+veliparib+paclitaxel vs. carboplatin+paclitaxel (HR 1.12; P = .62). Rates of treatment-emergent and post-treatment-emergent adverse events and secondary malignancies were similar across treatment groups.

Study details: Findings are based on the 4.5-year follow-up data from the phase 3 BrighTNess trial including 634 patients with stage II-III TNBC who were randomly assigned to receive carboplatin+veliparib, carboplatin+veliparib placebo, or carboplatin placebo+veliparib placebo, all in combination with paclitaxel.

Disclosures: This study was supported by AbbVie. Some authors declared serving on the advisory board and speaker’s bureau or receiving travel funds, writing support, honoraria, research funds, and consulting fees from several sources including AbbVie. D Maag declared being an employee or stockholder of AbbVie.

Source: Geyer CE Jr et al. Ann Oncol. 2022 (Jan 27). Doi: 10.1016/j.annonc.2022.01.009.

Key clinical point: Adding carboplatin to neoadjuvant paclitaxel followed by doxorubicin and cyclophosphamide improved long-term event-free survival (EFS) along with a manageable safety profile in patients with triple-negative breast cancer (TNBC).

Major finding: Patients receiving carboplatin+veliparib+paclitaxel vs. paclitaxel showed significant improvements in EFS (hazard ratio [HR] 0.63; P = .02), whereas EFS was not significntly different among patients assigned to carboplatin+veliparib+paclitaxel vs. carboplatin+paclitaxel (HR 1.12; P = .62). Rates of treatment-emergent and post-treatment-emergent adverse events and secondary malignancies were similar across treatment groups.

Study details: Findings are based on the 4.5-year follow-up data from the phase 3 BrighTNess trial including 634 patients with stage II-III TNBC who were randomly assigned to receive carboplatin+veliparib, carboplatin+veliparib placebo, or carboplatin placebo+veliparib placebo, all in combination with paclitaxel.

Disclosures: This study was supported by AbbVie. Some authors declared serving on the advisory board and speaker’s bureau or receiving travel funds, writing support, honoraria, research funds, and consulting fees from several sources including AbbVie. D Maag declared being an employee or stockholder of AbbVie.

Source: Geyer CE Jr et al. Ann Oncol. 2022 (Jan 27). Doi: 10.1016/j.annonc.2022.01.009.

Key clinical point: Adding carboplatin to neoadjuvant paclitaxel followed by doxorubicin and cyclophosphamide improved long-term event-free survival (EFS) along with a manageable safety profile in patients with triple-negative breast cancer (TNBC).

Major finding: Patients receiving carboplatin+veliparib+paclitaxel vs. paclitaxel showed significant improvements in EFS (hazard ratio [HR] 0.63; P = .02), whereas EFS was not significntly different among patients assigned to carboplatin+veliparib+paclitaxel vs. carboplatin+paclitaxel (HR 1.12; P = .62). Rates of treatment-emergent and post-treatment-emergent adverse events and secondary malignancies were similar across treatment groups.

Study details: Findings are based on the 4.5-year follow-up data from the phase 3 BrighTNess trial including 634 patients with stage II-III TNBC who were randomly assigned to receive carboplatin+veliparib, carboplatin+veliparib placebo, or carboplatin placebo+veliparib placebo, all in combination with paclitaxel.

Disclosures: This study was supported by AbbVie. Some authors declared serving on the advisory board and speaker’s bureau or receiving travel funds, writing support, honoraria, research funds, and consulting fees from several sources including AbbVie. D Maag declared being an employee or stockholder of AbbVie.

Source: Geyer CE Jr et al. Ann Oncol. 2022 (Jan 27). Doi: 10.1016/j.annonc.2022.01.009.

Key clinical point: Pyrotinib+capecitabine showed intracranial objective response and was well tolerated in patients with human epidermal growth factor receptor 2-positive (HER2+) metastatic breast cancer (BC) and brain metastases in the PERMEATE phase 2 study.

Major finding: The intracranial objective response rate was 74.6% (95% CI 61.6%-85.0%) in radiotherapy-naive patients and 42.1% (95% CI 20.3%-66.5%) in patients with progressive disease after whole-brain radiotherapy. Common grade 3 treatment-emergent adverse events were diarrhea and decreased white blood cell count. No treatment-related deaths were reported.

Study details: Findings are from the single-arm, phase 2 PERMEATE study including 78 patients with HER2+ BC and brain metastases who were either radiotherapy-naive or had progressive disease after radiotherapy. Patients received 400 mg pyrotinib once daily and 1000 mg/m² capecitabine twice daily for 14 days, followed by 7 days off during each 21-day cycle.

Disclosures: This study was funded by the National Cancer Centre Climbing Foundation Key Project of China and Jiangsu Hengrui Pharmaceuticals. The authors declared no conflicts of interest.

Source: Yan M et al. Lancet Oncol. 2022 (Jan 24). Doi: 10.1016/S1470-2045(21)00716-6.

Key clinical point: Pyrotinib+capecitabine showed intracranial objective response and was well tolerated in patients with human epidermal growth factor receptor 2-positive (HER2+) metastatic breast cancer (BC) and brain metastases in the PERMEATE phase 2 study.

Major finding: The intracranial objective response rate was 74.6% (95% CI 61.6%-85.0%) in radiotherapy-naive patients and 42.1% (95% CI 20.3%-66.5%) in patients with progressive disease after whole-brain radiotherapy. Common grade 3 treatment-emergent adverse events were diarrhea and decreased white blood cell count. No treatment-related deaths were reported.

Study details: Findings are from the single-arm, phase 2 PERMEATE study including 78 patients with HER2+ BC and brain metastases who were either radiotherapy-naive or had progressive disease after radiotherapy. Patients received 400 mg pyrotinib once daily and 1000 mg/m² capecitabine twice daily for 14 days, followed by 7 days off during each 21-day cycle.

Disclosures: This study was funded by the National Cancer Centre Climbing Foundation Key Project of China and Jiangsu Hengrui Pharmaceuticals. The authors declared no conflicts of interest.

Source: Yan M et al. Lancet Oncol. 2022 (Jan 24). Doi: 10.1016/S1470-2045(21)00716-6.

Key clinical point: Pyrotinib+capecitabine showed intracranial objective response and was well tolerated in patients with human epidermal growth factor receptor 2-positive (HER2+) metastatic breast cancer (BC) and brain metastases in the PERMEATE phase 2 study.

Major finding: The intracranial objective response rate was 74.6% (95% CI 61.6%-85.0%) in radiotherapy-naive patients and 42.1% (95% CI 20.3%-66.5%) in patients with progressive disease after whole-brain radiotherapy. Common grade 3 treatment-emergent adverse events were diarrhea and decreased white blood cell count. No treatment-related deaths were reported.

Study details: Findings are from the single-arm, phase 2 PERMEATE study including 78 patients with HER2+ BC and brain metastases who were either radiotherapy-naive or had progressive disease after radiotherapy. Patients received 400 mg pyrotinib once daily and 1000 mg/m² capecitabine twice daily for 14 days, followed by 7 days off during each 21-day cycle.

Disclosures: This study was funded by the National Cancer Centre Climbing Foundation Key Project of China and Jiangsu Hengrui Pharmaceuticals. The authors declared no conflicts of interest.

Source: Yan M et al. Lancet Oncol. 2022 (Jan 24). Doi: 10.1016/S1470-2045(21)00716-6.

Updated guidance for health care providers on multisystem inflammatory syndrome in children (MIS-C) recognizes the evolving nature of the disease and offers strategies for pediatric rheumatologists, who also may be asked to recommend treatment for hyperinflammation in children with acute COVID-19.

Guidance is needed for many reasons, including the variable case definitions for MIS-C, the presence of MIS-C features in other infections and childhood rheumatic diseases, the extrapolation of treatment strategies from other conditions with similar presentations, and the issue of myocardial dysfunction, wrote Lauren A. Henderson, MD, MMSC, of Boston Children’s Hospital, and members of the American College of Rheumatology MIS-C and COVID-19–Related Hyperinflammation Task Force.

However, “modifications to treatment plans, particularly in patients with complex conditions, are highly disease, patient, geography, and time specific, and therefore must be individualized as part of a shared decision-making process,” the authors said. The updated guidance was published in Arthritis & Rheumatology.
 

Update needed in wake of Omicron

“We continue to see cases of MIS-C across the United States due to the spike in SARS-CoV-2 infections from the Omicron variant,” and therefore updated guidance is important at this time, Dr. Henderson told this news organization.

“MIS-C remains a serious complication of COVID-19 in children and the ACR wanted to continue to provide pediatricians with up-to-date recommendations for the management of MIS-C,” she said.

“Children began to present with MIS-C in April 2020. At that time, little was known about this entity. Most of the recommendations in the first version of the MIS-C guidance were based on expert opinion,” she explained. However, “over the last 2 years, pediatricians have worked very hard to conduct high-quality research studies to better understand MIS-C, so we now have more scientific evidence to guide our recommendations.

“In version three of the MIS-C guidance, there are new recommendations on treatment. Previously, it was unclear what medications should be used for first-line treatment in patients with MIS-C. Some children were given intravenous immunoglobulin while others were given IVIg and steroids together. Several new studies show that children with MIS-C who are treated with a combination of IVIg and steroids have better outcomes. Accordingly, the MIS-C guidance now recommends dual therapy with IVIg and steroids in children with MIS-C.”

Diagnostic evaluation

The guidance calls for maintaining a broad differential diagnosis of MIS-C, given that the condition remains rare, and that most children with COVID-19 present with mild symptoms and have excellent outcomes, the authors noted. The range of clinical features associated with MIS-C include fever, mucocutaneous findings, myocardial dysfunction, cardiac conduction abnormalities, shock, gastrointestinal symptoms, and lymphadenopathy.

Some patients also experience neurologic involvement in the form of severe headache, altered mental status, seizures, cranial nerve palsies, meningismus, cerebral edema, and ischemic or hemorrhagic stroke. Given the nonspecific nature of these symptoms, “it is imperative that a diagnostic evaluation for MIS-C include investigation for other possible causes, as deemed appropriate by the treating provider,” the authors emphasized. Other diagnostic considerations include the prevalence and chronology of COVID-19 in the community, which may change over time.
 

MIS-C and Kawasaki disease phenotypes

Earlier in the pandemic, when MIS-C first emerged, it was compared with Kawasaki disease (KD). “However, a closer examination of the literature shows that only about one-quarter to half of patients with a reported diagnosis of MIS-C meet the full diagnostic criteria for KD,” the authors wrote. Key features that separate MIS-C from KD include the greater incidence of KD among children in Japan and East Asia versus the higher incidence of MIS-C among non-Hispanic Black children. In addition, children with MIS-C have shown a wider age range, more prominent gastrointestinal and neurologic symptoms, and more frequent cardiac dysfunction, compared with those with KD.

Cardiac management

Close follow-up with cardiology is essential for children with MIS-C, according to the authors. The recommendations call for repeat echocardiograms for all children with MIS-C at a minimum of 7-14 days, then again at 4-6 weeks after the initial presentation. The authors also recommended additional echocardiograms for children with left ventricular dysfunction and cardiac aortic aneurysms. 

MIS-C treatment

Current treatment recommendations emphasize that patients under investigation for MIS-C with life-threatening manifestations may need immunomodulatory therapy before a full diagnostic evaluation is complete, the authors said. However, patients without life-threatening manifestations should be evaluated before starting immunomodulatory treatment to avoid potentially harmful therapies for pediatric patients who don’t need them.

When MIS-C is refractory to initial immunomodulatory treatment, a second dose of IVIg is not recommended, but intensification therapy is advised with either high-dose (10-30 mg/kg per day) glucocorticoids, anakinra, or infliximab. However, there is little evidence available for selecting a specific agent for intensification therapy.

The task force also advises giving low-dose aspirin (3-5 mg/kg per day, up to 81 mg once daily) to all MIS-C patients without active bleeding or significant bleeding risk until normalization of the platelet count and confirmed normal coronary arteries at least 4 weeks after diagnosis.
 

COVID-19 and hyperinflammation

The task force also noted a distinction between MIS-C and severe COVID-19 in children. Although many children with MIS-C are previously healthy, most children who develop severe COVID-19 during an initial infection have complex conditions or comorbidities such as developmental delay or genetic anomaly, or chronic conditions such as congenital heart disease, type 1 diabetes, or asthma, the authors said. They recommend that “hospitalized children with COVID-19 requiring supplemental oxygen or respiratory support should be considered for immunomodulatory therapy in addition to supportive care and antiviral medications.”

The authors acknowledged the limitations and evolving nature of the recommendations, which will continue to change and do not replace clinical judgment for the management of individual patients. In the meantime, the ACR will support the task force in reviewing new evidence and providing revised versions of the current document.

Many questions about MIS-C remain, Dr. Henderson said in an interview. “It can be very hard to diagnose children with MIS-C because many of the symptoms are similar to those seen in other febrile illness of childhood. We need to identify better biomarkers to help us make the diagnosis of MIS-C. In addition, we need studies to provide information about what treatments should be used if children fail to respond to IVIg and steroids. Finally, it appears that vaccination [against SARS-CoV-2] protects against severe forms of MIS-C, and studies are needed to see how vaccination protects children from MIS-C.”

The development of the guidance was supported by the American College of Rheumatology. Dr. Henderson disclosed relationships with companies including Sobi, Pfizer, and Adaptive Biotechnologies (less than $10,000) and research support from the Childhood Arthritis and Rheumatology Research Alliance and research grant support from Bristol-Myers Squibb.

A version of this article first appeared on Medscape.com.

Updated guidance for health care providers on multisystem inflammatory syndrome in children (MIS-C) recognizes the evolving nature of the disease and offers strategies for pediatric rheumatologists, who also may be asked to recommend treatment for hyperinflammation in children with acute COVID-19.

Guidance is needed for many reasons, including the variable case definitions for MIS-C, the presence of MIS-C features in other infections and childhood rheumatic diseases, the extrapolation of treatment strategies from other conditions with similar presentations, and the issue of myocardial dysfunction, wrote Lauren A. Henderson, MD, MMSC, of Boston Children’s Hospital, and members of the American College of Rheumatology MIS-C and COVID-19–Related Hyperinflammation Task Force.

However, “modifications to treatment plans, particularly in patients with complex conditions, are highly disease, patient, geography, and time specific, and therefore must be individualized as part of a shared decision-making process,” the authors said. The updated guidance was published in Arthritis & Rheumatology.
 

Update needed in wake of Omicron

“We continue to see cases of MIS-C across the United States due to the spike in SARS-CoV-2 infections from the Omicron variant,” and therefore updated guidance is important at this time, Dr. Henderson told this news organization.

“MIS-C remains a serious complication of COVID-19 in children and the ACR wanted to continue to provide pediatricians with up-to-date recommendations for the management of MIS-C,” she said.

“Children began to present with MIS-C in April 2020. At that time, little was known about this entity. Most of the recommendations in the first version of the MIS-C guidance were based on expert opinion,” she explained. However, “over the last 2 years, pediatricians have worked very hard to conduct high-quality research studies to better understand MIS-C, so we now have more scientific evidence to guide our recommendations.

“In version three of the MIS-C guidance, there are new recommendations on treatment. Previously, it was unclear what medications should be used for first-line treatment in patients with MIS-C. Some children were given intravenous immunoglobulin while others were given IVIg and steroids together. Several new studies show that children with MIS-C who are treated with a combination of IVIg and steroids have better outcomes. Accordingly, the MIS-C guidance now recommends dual therapy with IVIg and steroids in children with MIS-C.”

Diagnostic evaluation

The guidance calls for maintaining a broad differential diagnosis of MIS-C, given that the condition remains rare, and that most children with COVID-19 present with mild symptoms and have excellent outcomes, the authors noted. The range of clinical features associated with MIS-C include fever, mucocutaneous findings, myocardial dysfunction, cardiac conduction abnormalities, shock, gastrointestinal symptoms, and lymphadenopathy.

Some patients also experience neurologic involvement in the form of severe headache, altered mental status, seizures, cranial nerve palsies, meningismus, cerebral edema, and ischemic or hemorrhagic stroke. Given the nonspecific nature of these symptoms, “it is imperative that a diagnostic evaluation for MIS-C include investigation for other possible causes, as deemed appropriate by the treating provider,” the authors emphasized. Other diagnostic considerations include the prevalence and chronology of COVID-19 in the community, which may change over time.
 

MIS-C and Kawasaki disease phenotypes

Earlier in the pandemic, when MIS-C first emerged, it was compared with Kawasaki disease (KD). “However, a closer examination of the literature shows that only about one-quarter to half of patients with a reported diagnosis of MIS-C meet the full diagnostic criteria for KD,” the authors wrote. Key features that separate MIS-C from KD include the greater incidence of KD among children in Japan and East Asia versus the higher incidence of MIS-C among non-Hispanic Black children. In addition, children with MIS-C have shown a wider age range, more prominent gastrointestinal and neurologic symptoms, and more frequent cardiac dysfunction, compared with those with KD.

Cardiac management

Close follow-up with cardiology is essential for children with MIS-C, according to the authors. The recommendations call for repeat echocardiograms for all children with MIS-C at a minimum of 7-14 days, then again at 4-6 weeks after the initial presentation. The authors also recommended additional echocardiograms for children with left ventricular dysfunction and cardiac aortic aneurysms. 

MIS-C treatment

Current treatment recommendations emphasize that patients under investigation for MIS-C with life-threatening manifestations may need immunomodulatory therapy before a full diagnostic evaluation is complete, the authors said. However, patients without life-threatening manifestations should be evaluated before starting immunomodulatory treatment to avoid potentially harmful therapies for pediatric patients who don’t need them.

When MIS-C is refractory to initial immunomodulatory treatment, a second dose of IVIg is not recommended, but intensification therapy is advised with either high-dose (10-30 mg/kg per day) glucocorticoids, anakinra, or infliximab. However, there is little evidence available for selecting a specific agent for intensification therapy.

The task force also advises giving low-dose aspirin (3-5 mg/kg per day, up to 81 mg once daily) to all MIS-C patients without active bleeding or significant bleeding risk until normalization of the platelet count and confirmed normal coronary arteries at least 4 weeks after diagnosis.
 

COVID-19 and hyperinflammation

The task force also noted a distinction between MIS-C and severe COVID-19 in children. Although many children with MIS-C are previously healthy, most children who develop severe COVID-19 during an initial infection have complex conditions or comorbidities such as developmental delay or genetic anomaly, or chronic conditions such as congenital heart disease, type 1 diabetes, or asthma, the authors said. They recommend that “hospitalized children with COVID-19 requiring supplemental oxygen or respiratory support should be considered for immunomodulatory therapy in addition to supportive care and antiviral medications.”

The authors acknowledged the limitations and evolving nature of the recommendations, which will continue to change and do not replace clinical judgment for the management of individual patients. In the meantime, the ACR will support the task force in reviewing new evidence and providing revised versions of the current document.

Many questions about MIS-C remain, Dr. Henderson said in an interview. “It can be very hard to diagnose children with MIS-C because many of the symptoms are similar to those seen in other febrile illness of childhood. We need to identify better biomarkers to help us make the diagnosis of MIS-C. In addition, we need studies to provide information about what treatments should be used if children fail to respond to IVIg and steroids. Finally, it appears that vaccination [against SARS-CoV-2] protects against severe forms of MIS-C, and studies are needed to see how vaccination protects children from MIS-C.”

The development of the guidance was supported by the American College of Rheumatology. Dr. Henderson disclosed relationships with companies including Sobi, Pfizer, and Adaptive Biotechnologies (less than $10,000) and research support from the Childhood Arthritis and Rheumatology Research Alliance and research grant support from Bristol-Myers Squibb.

A version of this article first appeared on Medscape.com.

Updated guidance for health care providers on multisystem inflammatory syndrome in children (MIS-C) recognizes the evolving nature of the disease and offers strategies for pediatric rheumatologists, who also may be asked to recommend treatment for hyperinflammation in children with acute COVID-19.

Guidance is needed for many reasons, including the variable case definitions for MIS-C, the presence of MIS-C features in other infections and childhood rheumatic diseases, the extrapolation of treatment strategies from other conditions with similar presentations, and the issue of myocardial dysfunction, wrote Lauren A. Henderson, MD, MMSC, of Boston Children’s Hospital, and members of the American College of Rheumatology MIS-C and COVID-19–Related Hyperinflammation Task Force.

However, “modifications to treatment plans, particularly in patients with complex conditions, are highly disease, patient, geography, and time specific, and therefore must be individualized as part of a shared decision-making process,” the authors said. The updated guidance was published in Arthritis & Rheumatology.
 

Update needed in wake of Omicron

“We continue to see cases of MIS-C across the United States due to the spike in SARS-CoV-2 infections from the Omicron variant,” and therefore updated guidance is important at this time, Dr. Henderson told this news organization.

“MIS-C remains a serious complication of COVID-19 in children and the ACR wanted to continue to provide pediatricians with up-to-date recommendations for the management of MIS-C,” she said.

“Children began to present with MIS-C in April 2020. At that time, little was known about this entity. Most of the recommendations in the first version of the MIS-C guidance were based on expert opinion,” she explained. However, “over the last 2 years, pediatricians have worked very hard to conduct high-quality research studies to better understand MIS-C, so we now have more scientific evidence to guide our recommendations.

“In version three of the MIS-C guidance, there are new recommendations on treatment. Previously, it was unclear what medications should be used for first-line treatment in patients with MIS-C. Some children were given intravenous immunoglobulin while others were given IVIg and steroids together. Several new studies show that children with MIS-C who are treated with a combination of IVIg and steroids have better outcomes. Accordingly, the MIS-C guidance now recommends dual therapy with IVIg and steroids in children with MIS-C.”

Diagnostic evaluation

The guidance calls for maintaining a broad differential diagnosis of MIS-C, given that the condition remains rare, and that most children with COVID-19 present with mild symptoms and have excellent outcomes, the authors noted. The range of clinical features associated with MIS-C include fever, mucocutaneous findings, myocardial dysfunction, cardiac conduction abnormalities, shock, gastrointestinal symptoms, and lymphadenopathy.

Some patients also experience neurologic involvement in the form of severe headache, altered mental status, seizures, cranial nerve palsies, meningismus, cerebral edema, and ischemic or hemorrhagic stroke. Given the nonspecific nature of these symptoms, “it is imperative that a diagnostic evaluation for MIS-C include investigation for other possible causes, as deemed appropriate by the treating provider,” the authors emphasized. Other diagnostic considerations include the prevalence and chronology of COVID-19 in the community, which may change over time.
 

MIS-C and Kawasaki disease phenotypes

Earlier in the pandemic, when MIS-C first emerged, it was compared with Kawasaki disease (KD). “However, a closer examination of the literature shows that only about one-quarter to half of patients with a reported diagnosis of MIS-C meet the full diagnostic criteria for KD,” the authors wrote. Key features that separate MIS-C from KD include the greater incidence of KD among children in Japan and East Asia versus the higher incidence of MIS-C among non-Hispanic Black children. In addition, children with MIS-C have shown a wider age range, more prominent gastrointestinal and neurologic symptoms, and more frequent cardiac dysfunction, compared with those with KD.

Cardiac management

Close follow-up with cardiology is essential for children with MIS-C, according to the authors. The recommendations call for repeat echocardiograms for all children with MIS-C at a minimum of 7-14 days, then again at 4-6 weeks after the initial presentation. The authors also recommended additional echocardiograms for children with left ventricular dysfunction and cardiac aortic aneurysms. 

MIS-C treatment

Current treatment recommendations emphasize that patients under investigation for MIS-C with life-threatening manifestations may need immunomodulatory therapy before a full diagnostic evaluation is complete, the authors said. However, patients without life-threatening manifestations should be evaluated before starting immunomodulatory treatment to avoid potentially harmful therapies for pediatric patients who don’t need them.

When MIS-C is refractory to initial immunomodulatory treatment, a second dose of IVIg is not recommended, but intensification therapy is advised with either high-dose (10-30 mg/kg per day) glucocorticoids, anakinra, or infliximab. However, there is little evidence available for selecting a specific agent for intensification therapy.

The task force also advises giving low-dose aspirin (3-5 mg/kg per day, up to 81 mg once daily) to all MIS-C patients without active bleeding or significant bleeding risk until normalization of the platelet count and confirmed normal coronary arteries at least 4 weeks after diagnosis.
 

COVID-19 and hyperinflammation

The task force also noted a distinction between MIS-C and severe COVID-19 in children. Although many children with MIS-C are previously healthy, most children who develop severe COVID-19 during an initial infection have complex conditions or comorbidities such as developmental delay or genetic anomaly, or chronic conditions such as congenital heart disease, type 1 diabetes, or asthma, the authors said. They recommend that “hospitalized children with COVID-19 requiring supplemental oxygen or respiratory support should be considered for immunomodulatory therapy in addition to supportive care and antiviral medications.”

The authors acknowledged the limitations and evolving nature of the recommendations, which will continue to change and do not replace clinical judgment for the management of individual patients. In the meantime, the ACR will support the task force in reviewing new evidence and providing revised versions of the current document.

Many questions about MIS-C remain, Dr. Henderson said in an interview. “It can be very hard to diagnose children with MIS-C because many of the symptoms are similar to those seen in other febrile illness of childhood. We need to identify better biomarkers to help us make the diagnosis of MIS-C. In addition, we need studies to provide information about what treatments should be used if children fail to respond to IVIg and steroids. Finally, it appears that vaccination [against SARS-CoV-2] protects against severe forms of MIS-C, and studies are needed to see how vaccination protects children from MIS-C.”

The development of the guidance was supported by the American College of Rheumatology. Dr. Henderson disclosed relationships with companies including Sobi, Pfizer, and Adaptive Biotechnologies (less than $10,000) and research support from the Childhood Arthritis and Rheumatology Research Alliance and research grant support from Bristol-Myers Squibb.

A version of this article first appeared on Medscape.com.

The Omicron subvariant, BA.2, is not only more transmissible than the original Omicron strain, BA.1, but may cause more severe disease, a lab study from Japan says.

“Our multiscale investigations suggest that the risk of BA.2 for global health is potentially higher than that of BA.1,” the researchers said in the study published on the preprint server bioRxiv. The study has not been peer-reviewed.

The researchers infected hamsters with BA.1 and BA.2. The hamsters infected with BA.2 got sicker, with more lung damage and loss of body weight. Results were similar when mice were infected with BA.1 and BA.2.

“Infection experiments using hamsters show that BA.2 is more pathogenic than BA.1,” the study said.

BA.1 and BA.2 both appear to evade immunity created by COVID-19 vaccines, the study said. But a booster shot makes illness after infection 74% less likely, CNN said.

What’s more, therapeutic monoclonal antibodies used to treat people infected with COVID didn’t have much effect on BA.2. 

BA.2 was “almost completely resistant” to casirivimab and imdevimab and was 35 times more resistant to sotrovimab, compared to the original B.1.1 virus, the researchers wrote. 

“In summary, our data suggest the possibility that BA.2 would be the most concerned variant to global health,” the researchers wrote. “Currently, both BA.2 and BA.1 are recognised together as Omicron and these are almost undistinguishable. Based on our findings, we propose that BA.2 should be recognised as a unique variant of concern, and this SARS-CoV-2 variant should be monitored in depth.”

If the World Health Organization recognized BA.2 as a “unique variant of concern,” it would be given its own Greek letter.

But some scientists noted that findings in the lab don’t always reflect what’s happening in the real world of people.

“I think it’s always hard to translate differences in animal and cell culture models to what’s going on with regards to human disease,” Jeremy Kamil, PhD, an associate professor of microbiology and immunology at Louisiana State University Health Shreveport, told Newsweek. “That said, the differences do look real.”

“It might be, from a human’s perspective, a worse virus than BA.1 and might be able to transmit better and cause worse disease,” Daniel Rhoads, MD, section head of microbiology at the Cleveland Clinic in Ohio, told CNN. He reviewed the Japanese study but was not involved in it.

Another scientist who reviewed the study but was not involved in the research noted that human immune systems are evolving along with the COVID variants. 

“One of the caveats that we have to think about, as we get new variants that might seem more dangerous, is the fact that there’s two sides to the story,” Deborah Fuller, PhD, a virologist at the University of Washington School of Medicine, told CNN. “Our immune system is evolving as well. And so that’s pushing back on things.”

Scientists have already established that BA.2 is more transmissible than BA.1. The Omicron subvariant has been detected in 74 countries and 47 U.S. states, according to CNN. About 4% of Americans with COVID were infected with BA.2, the outlet reported, citing the CDC, but it’s now the dominant strain in other nations.

It’s not clear yet if BA.2 causes more severe illness in people. While BA.2 spreads faster than BA.1, there’s no evidence the subvariant makes people any sicker, an official with the World Health Organization said, according to CNBC.

A version of this article first appeared on WebMD.com.

The Omicron subvariant, BA.2, is not only more transmissible than the original Omicron strain, BA.1, but may cause more severe disease, a lab study from Japan says.

“Our multiscale investigations suggest that the risk of BA.2 for global health is potentially higher than that of BA.1,” the researchers said in the study published on the preprint server bioRxiv. The study has not been peer-reviewed.

The researchers infected hamsters with BA.1 and BA.2. The hamsters infected with BA.2 got sicker, with more lung damage and loss of body weight. Results were similar when mice were infected with BA.1 and BA.2.

“Infection experiments using hamsters show that BA.2 is more pathogenic than BA.1,” the study said.

BA.1 and BA.2 both appear to evade immunity created by COVID-19 vaccines, the study said. But a booster shot makes illness after infection 74% less likely, CNN said.

What’s more, therapeutic monoclonal antibodies used to treat people infected with COVID didn’t have much effect on BA.2. 

BA.2 was “almost completely resistant” to casirivimab and imdevimab and was 35 times more resistant to sotrovimab, compared to the original B.1.1 virus, the researchers wrote. 

“In summary, our data suggest the possibility that BA.2 would be the most concerned variant to global health,” the researchers wrote. “Currently, both BA.2 and BA.1 are recognised together as Omicron and these are almost undistinguishable. Based on our findings, we propose that BA.2 should be recognised as a unique variant of concern, and this SARS-CoV-2 variant should be monitored in depth.”

If the World Health Organization recognized BA.2 as a “unique variant of concern,” it would be given its own Greek letter.

But some scientists noted that findings in the lab don’t always reflect what’s happening in the real world of people.

“I think it’s always hard to translate differences in animal and cell culture models to what’s going on with regards to human disease,” Jeremy Kamil, PhD, an associate professor of microbiology and immunology at Louisiana State University Health Shreveport, told Newsweek. “That said, the differences do look real.”

“It might be, from a human’s perspective, a worse virus than BA.1 and might be able to transmit better and cause worse disease,” Daniel Rhoads, MD, section head of microbiology at the Cleveland Clinic in Ohio, told CNN. He reviewed the Japanese study but was not involved in it.

Another scientist who reviewed the study but was not involved in the research noted that human immune systems are evolving along with the COVID variants. 

“One of the caveats that we have to think about, as we get new variants that might seem more dangerous, is the fact that there’s two sides to the story,” Deborah Fuller, PhD, a virologist at the University of Washington School of Medicine, told CNN. “Our immune system is evolving as well. And so that’s pushing back on things.”

Scientists have already established that BA.2 is more transmissible than BA.1. The Omicron subvariant has been detected in 74 countries and 47 U.S. states, according to CNN. About 4% of Americans with COVID were infected with BA.2, the outlet reported, citing the CDC, but it’s now the dominant strain in other nations.

It’s not clear yet if BA.2 causes more severe illness in people. While BA.2 spreads faster than BA.1, there’s no evidence the subvariant makes people any sicker, an official with the World Health Organization said, according to CNBC.

A version of this article first appeared on WebMD.com.

The Omicron subvariant, BA.2, is not only more transmissible than the original Omicron strain, BA.1, but may cause more severe disease, a lab study from Japan says.

“Our multiscale investigations suggest that the risk of BA.2 for global health is potentially higher than that of BA.1,” the researchers said in the study published on the preprint server bioRxiv. The study has not been peer-reviewed.

The researchers infected hamsters with BA.1 and BA.2. The hamsters infected with BA.2 got sicker, with more lung damage and loss of body weight. Results were similar when mice were infected with BA.1 and BA.2.

“Infection experiments using hamsters show that BA.2 is more pathogenic than BA.1,” the study said.

BA.1 and BA.2 both appear to evade immunity created by COVID-19 vaccines, the study said. But a booster shot makes illness after infection 74% less likely, CNN said.

What’s more, therapeutic monoclonal antibodies used to treat people infected with COVID didn’t have much effect on BA.2. 

BA.2 was “almost completely resistant” to casirivimab and imdevimab and was 35 times more resistant to sotrovimab, compared to the original B.1.1 virus, the researchers wrote. 

“In summary, our data suggest the possibility that BA.2 would be the most concerned variant to global health,” the researchers wrote. “Currently, both BA.2 and BA.1 are recognised together as Omicron and these are almost undistinguishable. Based on our findings, we propose that BA.2 should be recognised as a unique variant of concern, and this SARS-CoV-2 variant should be monitored in depth.”

If the World Health Organization recognized BA.2 as a “unique variant of concern,” it would be given its own Greek letter.

But some scientists noted that findings in the lab don’t always reflect what’s happening in the real world of people.

“I think it’s always hard to translate differences in animal and cell culture models to what’s going on with regards to human disease,” Jeremy Kamil, PhD, an associate professor of microbiology and immunology at Louisiana State University Health Shreveport, told Newsweek. “That said, the differences do look real.”

“It might be, from a human’s perspective, a worse virus than BA.1 and might be able to transmit better and cause worse disease,” Daniel Rhoads, MD, section head of microbiology at the Cleveland Clinic in Ohio, told CNN. He reviewed the Japanese study but was not involved in it.

Another scientist who reviewed the study but was not involved in the research noted that human immune systems are evolving along with the COVID variants. 

“One of the caveats that we have to think about, as we get new variants that might seem more dangerous, is the fact that there’s two sides to the story,” Deborah Fuller, PhD, a virologist at the University of Washington School of Medicine, told CNN. “Our immune system is evolving as well. And so that’s pushing back on things.”

Scientists have already established that BA.2 is more transmissible than BA.1. The Omicron subvariant has been detected in 74 countries and 47 U.S. states, according to CNN. About 4% of Americans with COVID were infected with BA.2, the outlet reported, citing the CDC, but it’s now the dominant strain in other nations.

It’s not clear yet if BA.2 causes more severe illness in people. While BA.2 spreads faster than BA.1, there’s no evidence the subvariant makes people any sicker, an official with the World Health Organization said, according to CNBC.

A version of this article first appeared on WebMD.com.

Health authorities in Malawi have declared an outbreak of wild poliovirus type 1 after a case was confirmed in a 3-year-old girl in the capital, Lilongwe. It was the first case in Africa in 5 years, according to the World Health Organization.

Globally, there were only five cases of wild poliovirus in 2021, the WHO states.

“As long as wild polio exists anywhere in the world all countries remain at risk of importation of the virus,” Matshidiso Moeti, MBBS, WHO regional director for Africa, said in the statement.
 

Girl paralyzed in November

The Global Polio Eradication Initiative (GPEI) said in a statement that the 3-year-old girl  experienced paralysis in November, and stool specimens were collected. Sequencing of the virus was conducted in February, 2022, by the National Institute for Communicable Diseases in South Africa, and the Centers for Disease Control and Prevention confirmed the case as WPV1.

According to the WHO announcement, laboratory analysis shows that the strain identified in Malawi is linked to one circulating in Sindh Province in Pakistan. Polio remains endemic only in Afghanistan and Pakistan.

Kacey C. Ernst, PhD, MPH, professor and infectious disease epidemiologist at the University of Arizona’s Zuckerman College of Public Health in Tucson, pointed out that what is not clear from the press release is whether the girl had traveled to Pakistan or was infected in Malawi.

“This is a very significant detail that would indicate whether or not transmission was actively occurring in Malawi. Until that information is released, it is hard to judge the extent of the possible outbreak,” she said in an interview. “The good news is that this case was in fact detected. The surveillance systems are in place and they were able to identify wild-type cases.”

Dr. Ernst said that although there is cause for concern, it is “not a reason to panic. Malawi has very high polio vaccination rates and it is quite possible that this will be a very small defined outbreak that will be well contained.”

She added that the medical community should be alerted that this case has been identified so travelers who have been to affected areas who have any symptoms can be appropriately screened.

The WHO said it is helping Malawi health authorities in the response, including increasing immunizations.

However, a vaccination campaign comes at a time of health system upheaval in Malawi.

“Malawi, like countries all over the world, has seen an interruption in services due to COVID,” Joia S. Mukherjee, MD, MPH, chief medical officer with Partners in Health and associate professor with the division of global health equity at Brigham and Women’s Hospital and in the department of global health and social medicine at Harvard Medical School, Boston, said in an interview. “In addition, Malawi is currently dealing with the aftermath of a cyclone – where nearly a million people were displaced. Vaccination campaigns work best if there is solid infrastructure. Both COVID and the impact of climate change have shaken the health system.”

UN health agencies warned last year that millions of children who have not received immunizations during the pandemic, especially in Africa, “are now at risk from life-threatening diseases such as measles, polio, yellow fever, and diphtheria,” Reuters reported.

Africa was certified as wild poliovirus free on Aug. 25, 2020. The CDC had served as the lead partner over 3 decades in helping Africa reach the milestone. Africa will retain that status, the WHO stated, because the strain originated in Pakistan.

Five of six WHO regions have been certified polio free. The Americas received eradication certification in 1994.

There is no cure for polio, which can cause irreversible paralysis within hours, but the disease has been largely eradicated globally with an effective vaccine.
 

GPEI sending teams

The GPEI is sending a team to Malawi to support emergency operations, communications, and surveillance. Partner organizations will also send teams to support operations and innovative vaccination campaign solutions.

GPEI was launched in 1988 with the combined efforts of national governments, WHO, Rotary International, the CDC, and UNICEF. The GPEI partnership has included the Bill & Melinda Gates Foundation and, in recent years, Gavi, the Vaccine Alliance.

The CDC states, “[G]lobal incidence of polio has decreased by 99.9% since GPEI’s foundation. An estimated 16 million people today are walking who would otherwise have been paralyzed by the disease, and more than 1.5 million people are alive, whose lives would otherwise have been lost. Now the task remains to tackle polio in its last few strongholds and get rid of the final 0.1% of polio cases.”
 

Three wild poliovirus strains

There are three wild poliovirus strains: type 1 (WPV1), type 2 (WPV2), and type 3 (WPV3).

“Symptomatically, all three strains are identical, in that they cause irreversible paralysis or even death. But there are genetic and virologic differences which make these three strains three separate viruses that must each be eradicated individually,” according to WHO.

WPV3 is the second strain to be wiped out, following the certification of the eradication of WPV2 in 2015.

A version of this article first appeared on Medscape.com.

Health authorities in Malawi have declared an outbreak of wild poliovirus type 1 after a case was confirmed in a 3-year-old girl in the capital, Lilongwe. It was the first case in Africa in 5 years, according to the World Health Organization.

Globally, there were only five cases of wild poliovirus in 2021, the WHO states.

“As long as wild polio exists anywhere in the world all countries remain at risk of importation of the virus,” Matshidiso Moeti, MBBS, WHO regional director for Africa, said in the statement.
 

Girl paralyzed in November

The Global Polio Eradication Initiative (GPEI) said in a statement that the 3-year-old girl  experienced paralysis in November, and stool specimens were collected. Sequencing of the virus was conducted in February, 2022, by the National Institute for Communicable Diseases in South Africa, and the Centers for Disease Control and Prevention confirmed the case as WPV1.

According to the WHO announcement, laboratory analysis shows that the strain identified in Malawi is linked to one circulating in Sindh Province in Pakistan. Polio remains endemic only in Afghanistan and Pakistan.

Kacey C. Ernst, PhD, MPH, professor and infectious disease epidemiologist at the University of Arizona’s Zuckerman College of Public Health in Tucson, pointed out that what is not clear from the press release is whether the girl had traveled to Pakistan or was infected in Malawi.

“This is a very significant detail that would indicate whether or not transmission was actively occurring in Malawi. Until that information is released, it is hard to judge the extent of the possible outbreak,” she said in an interview. “The good news is that this case was in fact detected. The surveillance systems are in place and they were able to identify wild-type cases.”

Dr. Ernst said that although there is cause for concern, it is “not a reason to panic. Malawi has very high polio vaccination rates and it is quite possible that this will be a very small defined outbreak that will be well contained.”

She added that the medical community should be alerted that this case has been identified so travelers who have been to affected areas who have any symptoms can be appropriately screened.

The WHO said it is helping Malawi health authorities in the response, including increasing immunizations.

However, a vaccination campaign comes at a time of health system upheaval in Malawi.

“Malawi, like countries all over the world, has seen an interruption in services due to COVID,” Joia S. Mukherjee, MD, MPH, chief medical officer with Partners in Health and associate professor with the division of global health equity at Brigham and Women’s Hospital and in the department of global health and social medicine at Harvard Medical School, Boston, said in an interview. “In addition, Malawi is currently dealing with the aftermath of a cyclone – where nearly a million people were displaced. Vaccination campaigns work best if there is solid infrastructure. Both COVID and the impact of climate change have shaken the health system.”

UN health agencies warned last year that millions of children who have not received immunizations during the pandemic, especially in Africa, “are now at risk from life-threatening diseases such as measles, polio, yellow fever, and diphtheria,” Reuters reported.

Africa was certified as wild poliovirus free on Aug. 25, 2020. The CDC had served as the lead partner over 3 decades in helping Africa reach the milestone. Africa will retain that status, the WHO stated, because the strain originated in Pakistan.

Five of six WHO regions have been certified polio free. The Americas received eradication certification in 1994.

There is no cure for polio, which can cause irreversible paralysis within hours, but the disease has been largely eradicated globally with an effective vaccine.
 

GPEI sending teams

The GPEI is sending a team to Malawi to support emergency operations, communications, and surveillance. Partner organizations will also send teams to support operations and innovative vaccination campaign solutions.

GPEI was launched in 1988 with the combined efforts of national governments, WHO, Rotary International, the CDC, and UNICEF. The GPEI partnership has included the Bill & Melinda Gates Foundation and, in recent years, Gavi, the Vaccine Alliance.

The CDC states, “[G]lobal incidence of polio has decreased by 99.9% since GPEI’s foundation. An estimated 16 million people today are walking who would otherwise have been paralyzed by the disease, and more than 1.5 million people are alive, whose lives would otherwise have been lost. Now the task remains to tackle polio in its last few strongholds and get rid of the final 0.1% of polio cases.”
 

Three wild poliovirus strains

There are three wild poliovirus strains: type 1 (WPV1), type 2 (WPV2), and type 3 (WPV3).

“Symptomatically, all three strains are identical, in that they cause irreversible paralysis or even death. But there are genetic and virologic differences which make these three strains three separate viruses that must each be eradicated individually,” according to WHO.

WPV3 is the second strain to be wiped out, following the certification of the eradication of WPV2 in 2015.

A version of this article first appeared on Medscape.com.

Health authorities in Malawi have declared an outbreak of wild poliovirus type 1 after a case was confirmed in a 3-year-old girl in the capital, Lilongwe. It was the first case in Africa in 5 years, according to the World Health Organization.

Globally, there were only five cases of wild poliovirus in 2021, the WHO states.

“As long as wild polio exists anywhere in the world all countries remain at risk of importation of the virus,” Matshidiso Moeti, MBBS, WHO regional director for Africa, said in the statement.
 

Girl paralyzed in November

The Global Polio Eradication Initiative (GPEI) said in a statement that the 3-year-old girl  experienced paralysis in November, and stool specimens were collected. Sequencing of the virus was conducted in February, 2022, by the National Institute for Communicable Diseases in South Africa, and the Centers for Disease Control and Prevention confirmed the case as WPV1.

According to the WHO announcement, laboratory analysis shows that the strain identified in Malawi is linked to one circulating in Sindh Province in Pakistan. Polio remains endemic only in Afghanistan and Pakistan.

Kacey C. Ernst, PhD, MPH, professor and infectious disease epidemiologist at the University of Arizona’s Zuckerman College of Public Health in Tucson, pointed out that what is not clear from the press release is whether the girl had traveled to Pakistan or was infected in Malawi.

“This is a very significant detail that would indicate whether or not transmission was actively occurring in Malawi. Until that information is released, it is hard to judge the extent of the possible outbreak,” she said in an interview. “The good news is that this case was in fact detected. The surveillance systems are in place and they were able to identify wild-type cases.”

Dr. Ernst said that although there is cause for concern, it is “not a reason to panic. Malawi has very high polio vaccination rates and it is quite possible that this will be a very small defined outbreak that will be well contained.”

She added that the medical community should be alerted that this case has been identified so travelers who have been to affected areas who have any symptoms can be appropriately screened.

The WHO said it is helping Malawi health authorities in the response, including increasing immunizations.

However, a vaccination campaign comes at a time of health system upheaval in Malawi.

“Malawi, like countries all over the world, has seen an interruption in services due to COVID,” Joia S. Mukherjee, MD, MPH, chief medical officer with Partners in Health and associate professor with the division of global health equity at Brigham and Women’s Hospital and in the department of global health and social medicine at Harvard Medical School, Boston, said in an interview. “In addition, Malawi is currently dealing with the aftermath of a cyclone – where nearly a million people were displaced. Vaccination campaigns work best if there is solid infrastructure. Both COVID and the impact of climate change have shaken the health system.”

UN health agencies warned last year that millions of children who have not received immunizations during the pandemic, especially in Africa, “are now at risk from life-threatening diseases such as measles, polio, yellow fever, and diphtheria,” Reuters reported.

Africa was certified as wild poliovirus free on Aug. 25, 2020. The CDC had served as the lead partner over 3 decades in helping Africa reach the milestone. Africa will retain that status, the WHO stated, because the strain originated in Pakistan.

Five of six WHO regions have been certified polio free. The Americas received eradication certification in 1994.

There is no cure for polio, which can cause irreversible paralysis within hours, but the disease has been largely eradicated globally with an effective vaccine.
 

GPEI sending teams

The GPEI is sending a team to Malawi to support emergency operations, communications, and surveillance. Partner organizations will also send teams to support operations and innovative vaccination campaign solutions.

GPEI was launched in 1988 with the combined efforts of national governments, WHO, Rotary International, the CDC, and UNICEF. The GPEI partnership has included the Bill & Melinda Gates Foundation and, in recent years, Gavi, the Vaccine Alliance.

The CDC states, “[G]lobal incidence of polio has decreased by 99.9% since GPEI’s foundation. An estimated 16 million people today are walking who would otherwise have been paralyzed by the disease, and more than 1.5 million people are alive, whose lives would otherwise have been lost. Now the task remains to tackle polio in its last few strongholds and get rid of the final 0.1% of polio cases.”
 

Three wild poliovirus strains

There are three wild poliovirus strains: type 1 (WPV1), type 2 (WPV2), and type 3 (WPV3).

“Symptomatically, all three strains are identical, in that they cause irreversible paralysis or even death. But there are genetic and virologic differences which make these three strains three separate viruses that must each be eradicated individually,” according to WHO.

WPV3 is the second strain to be wiped out, following the certification of the eradication of WPV2 in 2015.

A version of this article first appeared on Medscape.com.

Two features are significantly associated with a higher risk for developing long COVID symptoms among people with inflammatory bowel disease (IBD), according to a large Danish population study.

People with Crohn’s disease (CD) who experienced adverse acute COVID-19, defined as requiring hospitalization, were nearly three times more likely to report persistent symptoms 12 weeks after acute infection.

“Long-term, persisting symptoms following COVID-19 is a frequently occurring problem, which is probably underappreciated. IBD specialists should therefore be aware of any of these symptoms and actively ask patients whether they have these problems,” lead author Mohamed Attauabi, MD, PhD, said in an interview.

Dr. Attauabi and colleagues also found that people with ulcerative colitis (UC) who discontinued immunosuppressive agents because of COVID-19 were 1.5 times more likely to experience long COVID symptoms, a result that surprised the researchers.

“This has not been shown before and remains to be confirmed,” said Dr. Attauabi, a fellow in the department of gastroenterology at Herlev Hospital at the University of Copenhagen.

Attauabi presented the results as a digital oral presentation at the 17th congress of the European Crohn’s and Colitis Organisation.
 

A closer look at IBD and COVID-19

Large, hospital-based studies of symptoms consistent with long COVID reveal a high prevalence of fatigue, sleep difficulties, and anxiety at 12 weeks or more post acute infection. However, these were not specific to people with CD or UC, Dr. Attauabi said.

“In patients with IBD, the risk of long-term sequelae of COVID-19 remains to be investigated,” he said.

Dr. Attauabi and colleagues studied 197 people with CD and 319 with UC, all of whom had polymerase chain reaction–confirmed COVID-19. Participants were prospectively enrolled in the population-based Danish IBD-COVID registry from January 28, 2020 to April 1, 2021. At a median of 5.1 months, a subset of 85 people with CD and 137 with UC agreed to report any post-COVID symptoms.

Older age, smoking, IBD disease activity, and presence of comorbidities were not associated with a significantly elevated risk of long COVID.

In a multivariate analysis, hospitalization for COVID-19 among people with CD was significantly associated with long COVID (odds ratio, 2.76; 95% confidence interval, 1.05-3.90; P = .04).

Furthermore, people with UC who stopped taking immunosuppressive agents also had a significantly higher risk (OR, 1.50; 95% CI, 1.07-10.22; P = .01).

“However, IBD medications such as systemic steroids were not associated with this outcome,” Dr. Attauabi said.
 

Fatigue most common long COVID symptom

Fatigue was the most common long COVID symptom, reported by 37% of patients with CD and 36% with UC.

Anosmia and ageusia were also common, reported by 29% and 28% of patients with CD, and 27% and 19% of those with UC, respectively.

“In our cohort of patients with UC or CD who developed COVID-19, the long-term health effects of COVID-19 did not appear to differ among patients with UC or CD nor according to IBD medications,” Dr. Attauabi said.

That is a “great study,” said session cochair Torsten Kucharzik, MD, PhD, head of internal medicine and gastroenterology at Lueneburg (Germany) Hospital.

When Dr. Kucharzik asked about smoking, Dr. Attauabi responded that they collected information on current and previous smoking, but they chose not to include the data because it was not statistically significant.

Dr. Attauabi has reported no relevant financial relationships. Dr. Kucharzik has reported receiving grants from Takeda and personal fees from companies including MSD/Essex, AbbVie, Falk Foundation, Biogen, Bristol-Myers Squibb, Arena, Celgene, Celltrion, Ferring, Janssen, Galapagos, Olympus, Mundipharma, Takeda, Amgen, Pfizer, Roche, and Vifor Pharma.

A version of this article first appeared on Medscape.com.

Two features are significantly associated with a higher risk for developing long COVID symptoms among people with inflammatory bowel disease (IBD), according to a large Danish population study.

People with Crohn’s disease (CD) who experienced adverse acute COVID-19, defined as requiring hospitalization, were nearly three times more likely to report persistent symptoms 12 weeks after acute infection.

“Long-term, persisting symptoms following COVID-19 is a frequently occurring problem, which is probably underappreciated. IBD specialists should therefore be aware of any of these symptoms and actively ask patients whether they have these problems,” lead author Mohamed Attauabi, MD, PhD, said in an interview.

Dr. Attauabi and colleagues also found that people with ulcerative colitis (UC) who discontinued immunosuppressive agents because of COVID-19 were 1.5 times more likely to experience long COVID symptoms, a result that surprised the researchers.

“This has not been shown before and remains to be confirmed,” said Dr. Attauabi, a fellow in the department of gastroenterology at Herlev Hospital at the University of Copenhagen.

Attauabi presented the results as a digital oral presentation at the 17th congress of the European Crohn’s and Colitis Organisation.
 

A closer look at IBD and COVID-19

Large, hospital-based studies of symptoms consistent with long COVID reveal a high prevalence of fatigue, sleep difficulties, and anxiety at 12 weeks or more post acute infection. However, these were not specific to people with CD or UC, Dr. Attauabi said.

“In patients with IBD, the risk of long-term sequelae of COVID-19 remains to be investigated,” he said.

Dr. Attauabi and colleagues studied 197 people with CD and 319 with UC, all of whom had polymerase chain reaction–confirmed COVID-19. Participants were prospectively enrolled in the population-based Danish IBD-COVID registry from January 28, 2020 to April 1, 2021. At a median of 5.1 months, a subset of 85 people with CD and 137 with UC agreed to report any post-COVID symptoms.

Older age, smoking, IBD disease activity, and presence of comorbidities were not associated with a significantly elevated risk of long COVID.

In a multivariate analysis, hospitalization for COVID-19 among people with CD was significantly associated with long COVID (odds ratio, 2.76; 95% confidence interval, 1.05-3.90; P = .04).

Furthermore, people with UC who stopped taking immunosuppressive agents also had a significantly higher risk (OR, 1.50; 95% CI, 1.07-10.22; P = .01).

“However, IBD medications such as systemic steroids were not associated with this outcome,” Dr. Attauabi said.
 

Fatigue most common long COVID symptom

Fatigue was the most common long COVID symptom, reported by 37% of patients with CD and 36% with UC.

Anosmia and ageusia were also common, reported by 29% and 28% of patients with CD, and 27% and 19% of those with UC, respectively.

“In our cohort of patients with UC or CD who developed COVID-19, the long-term health effects of COVID-19 did not appear to differ among patients with UC or CD nor according to IBD medications,” Dr. Attauabi said.

That is a “great study,” said session cochair Torsten Kucharzik, MD, PhD, head of internal medicine and gastroenterology at Lueneburg (Germany) Hospital.

When Dr. Kucharzik asked about smoking, Dr. Attauabi responded that they collected information on current and previous smoking, but they chose not to include the data because it was not statistically significant.

Dr. Attauabi has reported no relevant financial relationships. Dr. Kucharzik has reported receiving grants from Takeda and personal fees from companies including MSD/Essex, AbbVie, Falk Foundation, Biogen, Bristol-Myers Squibb, Arena, Celgene, Celltrion, Ferring, Janssen, Galapagos, Olympus, Mundipharma, Takeda, Amgen, Pfizer, Roche, and Vifor Pharma.

A version of this article first appeared on Medscape.com.

Two features are significantly associated with a higher risk for developing long COVID symptoms among people with inflammatory bowel disease (IBD), according to a large Danish population study.

People with Crohn’s disease (CD) who experienced adverse acute COVID-19, defined as requiring hospitalization, were nearly three times more likely to report persistent symptoms 12 weeks after acute infection.

“Long-term, persisting symptoms following COVID-19 is a frequently occurring problem, which is probably underappreciated. IBD specialists should therefore be aware of any of these symptoms and actively ask patients whether they have these problems,” lead author Mohamed Attauabi, MD, PhD, said in an interview.

Dr. Attauabi and colleagues also found that people with ulcerative colitis (UC) who discontinued immunosuppressive agents because of COVID-19 were 1.5 times more likely to experience long COVID symptoms, a result that surprised the researchers.

“This has not been shown before and remains to be confirmed,” said Dr. Attauabi, a fellow in the department of gastroenterology at Herlev Hospital at the University of Copenhagen.

Attauabi presented the results as a digital oral presentation at the 17th congress of the European Crohn’s and Colitis Organisation.
 

A closer look at IBD and COVID-19

Large, hospital-based studies of symptoms consistent with long COVID reveal a high prevalence of fatigue, sleep difficulties, and anxiety at 12 weeks or more post acute infection. However, these were not specific to people with CD or UC, Dr. Attauabi said.

“In patients with IBD, the risk of long-term sequelae of COVID-19 remains to be investigated,” he said.

Dr. Attauabi and colleagues studied 197 people with CD and 319 with UC, all of whom had polymerase chain reaction–confirmed COVID-19. Participants were prospectively enrolled in the population-based Danish IBD-COVID registry from January 28, 2020 to April 1, 2021. At a median of 5.1 months, a subset of 85 people with CD and 137 with UC agreed to report any post-COVID symptoms.

Older age, smoking, IBD disease activity, and presence of comorbidities were not associated with a significantly elevated risk of long COVID.

In a multivariate analysis, hospitalization for COVID-19 among people with CD was significantly associated with long COVID (odds ratio, 2.76; 95% confidence interval, 1.05-3.90; P = .04).

Furthermore, people with UC who stopped taking immunosuppressive agents also had a significantly higher risk (OR, 1.50; 95% CI, 1.07-10.22; P = .01).

“However, IBD medications such as systemic steroids were not associated with this outcome,” Dr. Attauabi said.
 

Fatigue most common long COVID symptom

Fatigue was the most common long COVID symptom, reported by 37% of patients with CD and 36% with UC.

Anosmia and ageusia were also common, reported by 29% and 28% of patients with CD, and 27% and 19% of those with UC, respectively.

“In our cohort of patients with UC or CD who developed COVID-19, the long-term health effects of COVID-19 did not appear to differ among patients with UC or CD nor according to IBD medications,” Dr. Attauabi said.

That is a “great study,” said session cochair Torsten Kucharzik, MD, PhD, head of internal medicine and gastroenterology at Lueneburg (Germany) Hospital.

When Dr. Kucharzik asked about smoking, Dr. Attauabi responded that they collected information on current and previous smoking, but they chose not to include the data because it was not statistically significant.

Dr. Attauabi has reported no relevant financial relationships. Dr. Kucharzik has reported receiving grants from Takeda and personal fees from companies including MSD/Essex, AbbVie, Falk Foundation, Biogen, Bristol-Myers Squibb, Arena, Celgene, Celltrion, Ferring, Janssen, Galapagos, Olympus, Mundipharma, Takeda, Amgen, Pfizer, Roche, and Vifor Pharma.

A version of this article first appeared on Medscape.com.

It’s January 1, 2022, as I write, and my CHEST presidency came to an end last night as the fireworks lit up the sky. With COVID-19 waxing and waning across the United States and around the world, I have been a wartime president. CHEST has not been able to do a number of the things that we would normally have done in person, including that there has not been an in-person CHEST annual meeting during my entire presidency. We have, nonetheless, achieved some important things that I will share with you.

If you’re a typical CHEST member, you probably don’t spend a lot of time wondering about CHEST’s finances, nor should you. Nevertheless, CHEST – your organization – does have to be fiscally responsible if we desire to continue our educational and research missions, and that is the job of your Board of Regents, your presidents, and your professional staff at the CHEST headquarters. I’m happy to tell you that your organization is in healthy financial condition, in spite of a challenging economic environment and, being forced into remote, online annual meetings and board reviews for 2 years. What that means to us and to you is that we get to maintain and improve our full array of educational activities, including our annual meeting, our journal, our board reviews, our hands-on courses at the CHEST headquarters, and our web content. And, we get to accelerate our advocacy activities for our patients and for the clinical folks who care for them (us!). CHEST is primed for emerging from this pandemic stronger, because we have had to make the most of every dollar we have, and more innovative, because that’s how we have done it. We are ready for new ways of interacting and for innovative new ways of delivering education, sponsoring research, fostering networking, and leading in the clinical arena of chest medicine.

During my time as CHEST President, many of us have become progressively more aware of the blatant inequities that continue in society – and, yes, even in medicine. Perhaps more than anything, it both saddens and angers me when anyone values or devalues someone else’s life because of the color of their skin, who they feel attracted to or love, the sex they were born with or their knowledge that nature gave them the wrong physical characteristics for their gender, what physical impairments they have, where they were born, where they were educated - or not, what language is their first language, or what opportunities they were presented with in their lives. Everyone deserves the opportunity to be who and what they are and to be respected for who they are, and everyone deserves the opportunity to excel. The strongest collaborations have diverse constituents with unified goals, and I want for CHEST to be among the strongest of professional collaborations. It has been deeply important to me during my presidency to champion these values, and we have worked hard to make CHEST an inclusive and diverse organization. Much remains to be done, but we did make some good progress this year.

We established a spirometry working group to look at the science around race-based adjustments for normal values, to call out if there are mistakes or omissions in that approach, and to propose the work that needs to be done to correct them. We invited the American Thoracic Society and the Canadian Thoracic Society to join us in this effort. Race is a social construct, not a physiologic principle, and some data suggest that apparent differences in physiology could actually reflect differences in socioeconomic status of study participants. In similar work, our nephrology colleagues demonstrated that apparent differences in normal glomerular filtration rate (GFR) are related to socio-economic and health care access issues; they called for labs to no longer report race-based norms for creatinine and GFR values. Our colleagues believe that race-based GFR norms have harmed patients by promoting delay in treatments aimed at preventing dialysis or by causing delays in the initiation of dialysis. In our world, asbestos companies have argued that African American and other populations of color should receive lower asbestosis settlements on the basis that they began with lower predicted lung function and, therefore, had been less damaged by exposure to asbestos. I am very interested to see our working group’s output. I think it could result in landmark changes in our evaluation and treatment of patients with lung diseases.

It’s January 1, 2022, as I write, and my CHEST presidency came to an end last night as the fireworks lit up the sky. With COVID-19 waxing and waning across the United States and around the world, I have been a wartime president. CHEST has not been able to do a number of the things that we would normally have done in person, including that there has not been an in-person CHEST annual meeting during my entire presidency. We have, nonetheless, achieved some important things that I will share with you.

If you’re a typical CHEST member, you probably don’t spend a lot of time wondering about CHEST’s finances, nor should you. Nevertheless, CHEST – your organization – does have to be fiscally responsible if we desire to continue our educational and research missions, and that is the job of your Board of Regents, your presidents, and your professional staff at the CHEST headquarters. I’m happy to tell you that your organization is in healthy financial condition, in spite of a challenging economic environment and, being forced into remote, online annual meetings and board reviews for 2 years. What that means to us and to you is that we get to maintain and improve our full array of educational activities, including our annual meeting, our journal, our board reviews, our hands-on courses at the CHEST headquarters, and our web content. And, we get to accelerate our advocacy activities for our patients and for the clinical folks who care for them (us!). CHEST is primed for emerging from this pandemic stronger, because we have had to make the most of every dollar we have, and more innovative, because that’s how we have done it. We are ready for new ways of interacting and for innovative new ways of delivering education, sponsoring research, fostering networking, and leading in the clinical arena of chest medicine.

During my time as CHEST President, many of us have become progressively more aware of the blatant inequities that continue in society – and, yes, even in medicine. Perhaps more than anything, it both saddens and angers me when anyone values or devalues someone else’s life because of the color of their skin, who they feel attracted to or love, the sex they were born with or their knowledge that nature gave them the wrong physical characteristics for their gender, what physical impairments they have, where they were born, where they were educated - or not, what language is their first language, or what opportunities they were presented with in their lives. Everyone deserves the opportunity to be who and what they are and to be respected for who they are, and everyone deserves the opportunity to excel. The strongest collaborations have diverse constituents with unified goals, and I want for CHEST to be among the strongest of professional collaborations. It has been deeply important to me during my presidency to champion these values, and we have worked hard to make CHEST an inclusive and diverse organization. Much remains to be done, but we did make some good progress this year.

We established a spirometry working group to look at the science around race-based adjustments for normal values, to call out if there are mistakes or omissions in that approach, and to propose the work that needs to be done to correct them. We invited the American Thoracic Society and the Canadian Thoracic Society to join us in this effort. Race is a social construct, not a physiologic principle, and some data suggest that apparent differences in physiology could actually reflect differences in socioeconomic status of study participants. In similar work, our nephrology colleagues demonstrated that apparent differences in normal glomerular filtration rate (GFR) are related to socio-economic and health care access issues; they called for labs to no longer report race-based norms for creatinine and GFR values. Our colleagues believe that race-based GFR norms have harmed patients by promoting delay in treatments aimed at preventing dialysis or by causing delays in the initiation of dialysis. In our world, asbestos companies have argued that African American and other populations of color should receive lower asbestosis settlements on the basis that they began with lower predicted lung function and, therefore, had been less damaged by exposure to asbestos. I am very interested to see our working group’s output. I think it could result in landmark changes in our evaluation and treatment of patients with lung diseases.

It’s January 1, 2022, as I write, and my CHEST presidency came to an end last night as the fireworks lit up the sky. With COVID-19 waxing and waning across the United States and around the world, I have been a wartime president. CHEST has not been able to do a number of the things that we would normally have done in person, including that there has not been an in-person CHEST annual meeting during my entire presidency. We have, nonetheless, achieved some important things that I will share with you.

If you’re a typical CHEST member, you probably don’t spend a lot of time wondering about CHEST’s finances, nor should you. Nevertheless, CHEST – your organization – does have to be fiscally responsible if we desire to continue our educational and research missions, and that is the job of your Board of Regents, your presidents, and your professional staff at the CHEST headquarters. I’m happy to tell you that your organization is in healthy financial condition, in spite of a challenging economic environment and, being forced into remote, online annual meetings and board reviews for 2 years. What that means to us and to you is that we get to maintain and improve our full array of educational activities, including our annual meeting, our journal, our board reviews, our hands-on courses at the CHEST headquarters, and our web content. And, we get to accelerate our advocacy activities for our patients and for the clinical folks who care for them (us!). CHEST is primed for emerging from this pandemic stronger, because we have had to make the most of every dollar we have, and more innovative, because that’s how we have done it. We are ready for new ways of interacting and for innovative new ways of delivering education, sponsoring research, fostering networking, and leading in the clinical arena of chest medicine.

During my time as CHEST President, many of us have become progressively more aware of the blatant inequities that continue in society – and, yes, even in medicine. Perhaps more than anything, it both saddens and angers me when anyone values or devalues someone else’s life because of the color of their skin, who they feel attracted to or love, the sex they were born with or their knowledge that nature gave them the wrong physical characteristics for their gender, what physical impairments they have, where they were born, where they were educated - or not, what language is their first language, or what opportunities they were presented with in their lives. Everyone deserves the opportunity to be who and what they are and to be respected for who they are, and everyone deserves the opportunity to excel. The strongest collaborations have diverse constituents with unified goals, and I want for CHEST to be among the strongest of professional collaborations. It has been deeply important to me during my presidency to champion these values, and we have worked hard to make CHEST an inclusive and diverse organization. Much remains to be done, but we did make some good progress this year.

We established a spirometry working group to look at the science around race-based adjustments for normal values, to call out if there are mistakes or omissions in that approach, and to propose the work that needs to be done to correct them. We invited the American Thoracic Society and the Canadian Thoracic Society to join us in this effort. Race is a social construct, not a physiologic principle, and some data suggest that apparent differences in physiology could actually reflect differences in socioeconomic status of study participants. In similar work, our nephrology colleagues demonstrated that apparent differences in normal glomerular filtration rate (GFR) are related to socio-economic and health care access issues; they called for labs to no longer report race-based norms for creatinine and GFR values. Our colleagues believe that race-based GFR norms have harmed patients by promoting delay in treatments aimed at preventing dialysis or by causing delays in the initiation of dialysis. In our world, asbestos companies have argued that African American and other populations of color should receive lower asbestosis settlements on the basis that they began with lower predicted lung function and, therefore, had been less damaged by exposure to asbestos. I am very interested to see our working group’s output. I think it could result in landmark changes in our evaluation and treatment of patients with lung diseases.