TOPLINE:

An impaired central sensitivity to thyroid hormone may be associated with an increased risk for death in patients with chronic kidney disease (CKD) and normal thyroid function.

METHODOLOGY:

• Previous studies have shown that abnormal levels of thyroid-stimulating hormone (TSH) are associated with a higher mortality risk in patients with CKD, but whether the risk extends to those with normal thyroid function remains controversial.
• Researchers investigated the association between central sensitivity to thyroid hormone and the risk for all-cause mortality in 1303 euthyroid patients with CKD (mean age, 60 years; 59% women) from the National Health and Nutrition Examination Survey database (2007-2012).
• All participants had CKD stages I-IV, defined as an estimated glomerular filtration rate < 60 mL/min/1.73 m² and/or a urinary albumin to urinary creatinine ratio ≥ 30 mg/g.
• The central sensitivity to thyroid hormone was primarily evaluated using a new central thyroid hormone resistance index, the Thyroid Feedback Quantile–based Index (TFQI), using free thyroxine and TSH concentrations.
• The participants were followed for a median duration of 115 months, during which 503 died.

TAKEAWAY:

• Patients with CKD who died during the follow-up period had a significantly higher TFQI (P < .001) than those who survived.
• The rates of all-cause mortality increased from 26.61% in the lowest TFQI tertile to 40.89% in the highest tertile (P = .001).
• A per unit increase in the TFQI was associated with a 40% increased risk for all-cause mortality (hazard ratio, 1.40; 95% CI, 1.10-1.79).
• This association between TFQI level and all-cause mortality persisted in all subgroups stratified by age, gender, race, body mass index, hypertension, diabetes, cardiovascular diseases, and CKD stages.

IN PRACTICE:

“Our study demonstrates that impaired sensitivity to thyroid hormone might be associated with all-cause mortality in CKD patients with normal thyroid function, independent of other traditional risk factors and comorbidities,” the authors wrote.

SOURCE:

This study was led by Qichao Yang and Ru Dong, Department of Endocrinology, Affiliated Wujin Hospital of Jiangsu University, Changzhou, China, and was published online on August 6, 2024, in BMC Public Health.

LIMITATIONS:

Thyroid function was measured only at baseline, and the changes in thyroid function over time were not measured. The study excluded people on thyroid hormone replacement therapy but did not consider other medication use that might have affected thyroid function, such as beta-blockers, steroids, and amiodarone. Thyroid-related antibodies, metabolic syndrome, and nonalcoholic fatty liver disease were not included in the analysis as possible confounding factors. The US-based sample requires further validation.

DISCLOSURES:

The study was supported by the Changzhou Health Commission. The authors declared no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

An impaired central sensitivity to thyroid hormone may be associated with an increased risk for death in patients with chronic kidney disease (CKD) and normal thyroid function.

METHODOLOGY:

• Previous studies have shown that abnormal levels of thyroid-stimulating hormone (TSH) are associated with a higher mortality risk in patients with CKD, but whether the risk extends to those with normal thyroid function remains controversial.
• Researchers investigated the association between central sensitivity to thyroid hormone and the risk for all-cause mortality in 1303 euthyroid patients with CKD (mean age, 60 years; 59% women) from the National Health and Nutrition Examination Survey database (2007-2012).
• All participants had CKD stages I-IV, defined as an estimated glomerular filtration rate < 60 mL/min/1.73 m² and/or a urinary albumin to urinary creatinine ratio ≥ 30 mg/g.
• The central sensitivity to thyroid hormone was primarily evaluated using a new central thyroid hormone resistance index, the Thyroid Feedback Quantile–based Index (TFQI), using free thyroxine and TSH concentrations.
• The participants were followed for a median duration of 115 months, during which 503 died.

TAKEAWAY:

• Patients with CKD who died during the follow-up period had a significantly higher TFQI (P < .001) than those who survived.
• The rates of all-cause mortality increased from 26.61% in the lowest TFQI tertile to 40.89% in the highest tertile (P = .001).
• A per unit increase in the TFQI was associated with a 40% increased risk for all-cause mortality (hazard ratio, 1.40; 95% CI, 1.10-1.79).
• This association between TFQI level and all-cause mortality persisted in all subgroups stratified by age, gender, race, body mass index, hypertension, diabetes, cardiovascular diseases, and CKD stages.

IN PRACTICE:

“Our study demonstrates that impaired sensitivity to thyroid hormone might be associated with all-cause mortality in CKD patients with normal thyroid function, independent of other traditional risk factors and comorbidities,” the authors wrote.

SOURCE:

This study was led by Qichao Yang and Ru Dong, Department of Endocrinology, Affiliated Wujin Hospital of Jiangsu University, Changzhou, China, and was published online on August 6, 2024, in BMC Public Health.

LIMITATIONS:

Thyroid function was measured only at baseline, and the changes in thyroid function over time were not measured. The study excluded people on thyroid hormone replacement therapy but did not consider other medication use that might have affected thyroid function, such as beta-blockers, steroids, and amiodarone. Thyroid-related antibodies, metabolic syndrome, and nonalcoholic fatty liver disease were not included in the analysis as possible confounding factors. The US-based sample requires further validation.

DISCLOSURES:

The study was supported by the Changzhou Health Commission. The authors declared no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

An impaired central sensitivity to thyroid hormone may be associated with an increased risk for death in patients with chronic kidney disease (CKD) and normal thyroid function.

METHODOLOGY:

• Previous studies have shown that abnormal levels of thyroid-stimulating hormone (TSH) are associated with a higher mortality risk in patients with CKD, but whether the risk extends to those with normal thyroid function remains controversial.
• Researchers investigated the association between central sensitivity to thyroid hormone and the risk for all-cause mortality in 1303 euthyroid patients with CKD (mean age, 60 years; 59% women) from the National Health and Nutrition Examination Survey database (2007-2012).
• All participants had CKD stages I-IV, defined as an estimated glomerular filtration rate < 60 mL/min/1.73 m² and/or a urinary albumin to urinary creatinine ratio ≥ 30 mg/g.
• The central sensitivity to thyroid hormone was primarily evaluated using a new central thyroid hormone resistance index, the Thyroid Feedback Quantile–based Index (TFQI), using free thyroxine and TSH concentrations.
• The participants were followed for a median duration of 115 months, during which 503 died.

TAKEAWAY:

• Patients with CKD who died during the follow-up period had a significantly higher TFQI (P < .001) than those who survived.
• The rates of all-cause mortality increased from 26.61% in the lowest TFQI tertile to 40.89% in the highest tertile (P = .001).
• A per unit increase in the TFQI was associated with a 40% increased risk for all-cause mortality (hazard ratio, 1.40; 95% CI, 1.10-1.79).
• This association between TFQI level and all-cause mortality persisted in all subgroups stratified by age, gender, race, body mass index, hypertension, diabetes, cardiovascular diseases, and CKD stages.

IN PRACTICE:

“Our study demonstrates that impaired sensitivity to thyroid hormone might be associated with all-cause mortality in CKD patients with normal thyroid function, independent of other traditional risk factors and comorbidities,” the authors wrote.

SOURCE:

This study was led by Qichao Yang and Ru Dong, Department of Endocrinology, Affiliated Wujin Hospital of Jiangsu University, Changzhou, China, and was published online on August 6, 2024, in BMC Public Health.

LIMITATIONS:

Thyroid function was measured only at baseline, and the changes in thyroid function over time were not measured. The study excluded people on thyroid hormone replacement therapy but did not consider other medication use that might have affected thyroid function, such as beta-blockers, steroids, and amiodarone. Thyroid-related antibodies, metabolic syndrome, and nonalcoholic fatty liver disease were not included in the analysis as possible confounding factors. The US-based sample requires further validation.

DISCLOSURES:

The study was supported by the Changzhou Health Commission. The authors declared no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

Information readily available on a newborn screening, combined with clinical risk factors, may eventually be able to help identify infants at increased risk for sudden infant death syndrome (SIDS), new data suggest.

Findings of the study by Scott P. Oltman, MS, of the Department of Epidemiology & Biostatistics, University of California, San Francisco, and colleagues were published in JAMA Pediatrics.

The case-controlled study showed a link between aberrant metabolic analytes at birth and SIDS. Researchers used data from the California Office of Statewide Health Planning and Development and the California Department of Public Health and included 2.3 million infants born between 2005 and 2011 in the dataset.

Of the 2.3 million infants, 354 had SIDS. The researchers found that 14 newborn screening metabolites were significantly associated with SIDS. After the screens, the babies who had elevated metabolite markers, compared with the control babies had 14.4 times higher odds of having SIDS, the researchers reported.

“It’s really promising research,” Joanna J. Parga-Belinkie, MD, an attending neonatologist who was not involved in the study, said in an interview. She practices in the Division of Neonatology at Children’s Hospital of Philadelphia in Pennsylvania. “It doesn’t really give us the answer to what causes SIDS, but I think in the long term it’s going to inform a lot of research that will help us understand whether there are biomarkers that can predict SIDS.”

Other studies have looked at different metabolic markers to see if they can help predict SIDS, she said, but the innovation in this study is that it uses newborn screens, which are collected on all babies born in a hospital. Dr. Parga-Belinkie added that another strength of the study is its large sample size and matched controls to compare the SIDS cases with healthy babies.

“That said, newborn screens are a screening test, they are not diagnostic,” Dr. Parga-Belinkie said. “We definitely need further testing to see if (the metabolic biomarkers) really make that link to SIDS.”

It will be important to test this in a prospective study over time and in real time, she said, which is something the authors acknowledge. They list the retrospective design of the study as a major limitation.

These study results won’t change the counseling for families on decreasing risk, Dr. Parga-Belinkie said, “because there’s not a clear biomarker that has emerged and we don’t have a clear link yet.” Safe sleep hygiene will continue to be the primary focus of counseling parents, such as placing the baby on its back on a firm, flat surface with no loose bedding or stuffed animals.

The study authors said several things will need to be clarified with future research, noting that a majority of the infants in the California database were of Hispanic ethnicity. Testing other populations will help determine generalizability.

Also, there has been ambiguity in the definition of SIDS, which has led to inconsistencies in classifying a death as SIDS or death from an unknown cause of suffocation or asphyxiation.

They added: “It may also be the case that these markers are predictive and reliable but not causal in nature and distinguishing between the two is a crucial topic for future investigation.”

This work was supported in part by the California Preterm Birth Initiative within the University of California, San Francisco, and by the National Institutes of Health. Mr. Oltman reported having a patent pending for a newborn metabolic vulnerability model for identifying preterm infants at risk of adverse outcomes and uses thereof. One coauthor reported having a patent pending and a patent issued; another reported having a patent pending for a newborn metabolic vulnerability model for identifying preterm infants at risk of adverse outcomes and uses thereof. Dr. Parga-Belinkie declared no relevant financial disclosures.

Information readily available on a newborn screening, combined with clinical risk factors, may eventually be able to help identify infants at increased risk for sudden infant death syndrome (SIDS), new data suggest.

Findings of the study by Scott P. Oltman, MS, of the Department of Epidemiology & Biostatistics, University of California, San Francisco, and colleagues were published in JAMA Pediatrics.

The case-controlled study showed a link between aberrant metabolic analytes at birth and SIDS. Researchers used data from the California Office of Statewide Health Planning and Development and the California Department of Public Health and included 2.3 million infants born between 2005 and 2011 in the dataset.

Of the 2.3 million infants, 354 had SIDS. The researchers found that 14 newborn screening metabolites were significantly associated with SIDS. After the screens, the babies who had elevated metabolite markers, compared with the control babies had 14.4 times higher odds of having SIDS, the researchers reported.

“It’s really promising research,” Joanna J. Parga-Belinkie, MD, an attending neonatologist who was not involved in the study, said in an interview. She practices in the Division of Neonatology at Children’s Hospital of Philadelphia in Pennsylvania. “It doesn’t really give us the answer to what causes SIDS, but I think in the long term it’s going to inform a lot of research that will help us understand whether there are biomarkers that can predict SIDS.”

Other studies have looked at different metabolic markers to see if they can help predict SIDS, she said, but the innovation in this study is that it uses newborn screens, which are collected on all babies born in a hospital. Dr. Parga-Belinkie added that another strength of the study is its large sample size and matched controls to compare the SIDS cases with healthy babies.

“That said, newborn screens are a screening test, they are not diagnostic,” Dr. Parga-Belinkie said. “We definitely need further testing to see if (the metabolic biomarkers) really make that link to SIDS.”

It will be important to test this in a prospective study over time and in real time, she said, which is something the authors acknowledge. They list the retrospective design of the study as a major limitation.

These study results won’t change the counseling for families on decreasing risk, Dr. Parga-Belinkie said, “because there’s not a clear biomarker that has emerged and we don’t have a clear link yet.” Safe sleep hygiene will continue to be the primary focus of counseling parents, such as placing the baby on its back on a firm, flat surface with no loose bedding or stuffed animals.

The study authors said several things will need to be clarified with future research, noting that a majority of the infants in the California database were of Hispanic ethnicity. Testing other populations will help determine generalizability.

Also, there has been ambiguity in the definition of SIDS, which has led to inconsistencies in classifying a death as SIDS or death from an unknown cause of suffocation or asphyxiation.

They added: “It may also be the case that these markers are predictive and reliable but not causal in nature and distinguishing between the two is a crucial topic for future investigation.”

This work was supported in part by the California Preterm Birth Initiative within the University of California, San Francisco, and by the National Institutes of Health. Mr. Oltman reported having a patent pending for a newborn metabolic vulnerability model for identifying preterm infants at risk of adverse outcomes and uses thereof. One coauthor reported having a patent pending and a patent issued; another reported having a patent pending for a newborn metabolic vulnerability model for identifying preterm infants at risk of adverse outcomes and uses thereof. Dr. Parga-Belinkie declared no relevant financial disclosures.

Information readily available on a newborn screening, combined with clinical risk factors, may eventually be able to help identify infants at increased risk for sudden infant death syndrome (SIDS), new data suggest.

Findings of the study by Scott P. Oltman, MS, of the Department of Epidemiology & Biostatistics, University of California, San Francisco, and colleagues were published in JAMA Pediatrics.

The case-controlled study showed a link between aberrant metabolic analytes at birth and SIDS. Researchers used data from the California Office of Statewide Health Planning and Development and the California Department of Public Health and included 2.3 million infants born between 2005 and 2011 in the dataset.

Of the 2.3 million infants, 354 had SIDS. The researchers found that 14 newborn screening metabolites were significantly associated with SIDS. After the screens, the babies who had elevated metabolite markers, compared with the control babies had 14.4 times higher odds of having SIDS, the researchers reported.

“It’s really promising research,” Joanna J. Parga-Belinkie, MD, an attending neonatologist who was not involved in the study, said in an interview. She practices in the Division of Neonatology at Children’s Hospital of Philadelphia in Pennsylvania. “It doesn’t really give us the answer to what causes SIDS, but I think in the long term it’s going to inform a lot of research that will help us understand whether there are biomarkers that can predict SIDS.”

Other studies have looked at different metabolic markers to see if they can help predict SIDS, she said, but the innovation in this study is that it uses newborn screens, which are collected on all babies born in a hospital. Dr. Parga-Belinkie added that another strength of the study is its large sample size and matched controls to compare the SIDS cases with healthy babies.

“That said, newborn screens are a screening test, they are not diagnostic,” Dr. Parga-Belinkie said. “We definitely need further testing to see if (the metabolic biomarkers) really make that link to SIDS.”

It will be important to test this in a prospective study over time and in real time, she said, which is something the authors acknowledge. They list the retrospective design of the study as a major limitation.

These study results won’t change the counseling for families on decreasing risk, Dr. Parga-Belinkie said, “because there’s not a clear biomarker that has emerged and we don’t have a clear link yet.” Safe sleep hygiene will continue to be the primary focus of counseling parents, such as placing the baby on its back on a firm, flat surface with no loose bedding or stuffed animals.

The study authors said several things will need to be clarified with future research, noting that a majority of the infants in the California database were of Hispanic ethnicity. Testing other populations will help determine generalizability.

Also, there has been ambiguity in the definition of SIDS, which has led to inconsistencies in classifying a death as SIDS or death from an unknown cause of suffocation or asphyxiation.

They added: “It may also be the case that these markers are predictive and reliable but not causal in nature and distinguishing between the two is a crucial topic for future investigation.”

This work was supported in part by the California Preterm Birth Initiative within the University of California, San Francisco, and by the National Institutes of Health. Mr. Oltman reported having a patent pending for a newborn metabolic vulnerability model for identifying preterm infants at risk of adverse outcomes and uses thereof. One coauthor reported having a patent pending and a patent issued; another reported having a patent pending for a newborn metabolic vulnerability model for identifying preterm infants at risk of adverse outcomes and uses thereof. Dr. Parga-Belinkie declared no relevant financial disclosures.

Background

IDH1 mutations are detected in 3-4% of MDS, nearly always with one or more co-mutations. Treatment with IDH1 inhibitor ivosidenib typically resulted in regression of the abnormal clone in 15 reported responders. However, in a few cases differentiation was restored from the abnormal clone. Here we report a durable MDS remission despite sustained proliferation of a clone with IDH1 and ZRSR2 mutations.

Case Presentation

A 49-year-old man developed severe neutropenia and macrocytic anemia in January 2019. Mild marrow dysplasia developed by March 2020 with IDH1 (31.1%) and splicing gene ZRSR2 (55.7%) mutations. In October 2022 biopsy showed MDS with 4% blasts, megakaryocytic/granulocytic hypoplasia, normal cytogenetics and 43% IDH1/89% ZRSR2. After azacytidine failure, ivosidenib was started in November 2023 following FDA approval. Within weeks ANCs increased from 170 to 1580 and hemoglobin from 7.9 to 11.6 with MCV 115, reticulocytes 1.72%. At 3 months a CBC was normal except for MCV 111. IDH1 and ZRSR2 were 36.4% and 71%. After 6 months, ANC was 2380, hemoglobin 14.7, MCV 108.6, reticulo-cytes 1.77%. IDH1 PCR showed a 33.1% allele frequency consistent with a clonal remission.

Discussion

IDH1 mutations in MDS/AML frequently co-occur with mutations in RNA splicing genes SRSF2 or ZRSR2. For ZRSR2, we previously reported that isolated mutations of this gene cause refractory macrocytic anemias without dysplasia, thus presenting as clonal cytopenias of undetermined significance (Fleischman et al., Leuk Res, 2017). In this MDS case, after ivosidenib treatment the ZRSR2 splicing defect sustained clonal dominance over polyclonal hematopoiesis while accounting for macrocytosis. Longitudinal data for two ivosidenib-treated IDH1/SRSF2 MDS cases are incomplete, but one case of IDH2/SRSF2 MDS treated with the inhibitor enasidenib similarly achieved complete remission without regression of the mutated clone for 12 months.

Conclusions

Following the FDA approval of ivosidenib, all cases of MDS should have DNA sequencing performed at diagnosis to identify IDH1 mutations. Treatment induces high rates of remission even when polyclonal hematopoiesis does not recover. Moreover, the restoration of hematopoietic differentiation by the abnormal clone provides unique insights into the clinical phenotype and fitness advantage conferred by the co-existing driver mutations.

Background

IDH1 mutations are detected in 3-4% of MDS, nearly always with one or more co-mutations. Treatment with IDH1 inhibitor ivosidenib typically resulted in regression of the abnormal clone in 15 reported responders. However, in a few cases differentiation was restored from the abnormal clone. Here we report a durable MDS remission despite sustained proliferation of a clone with IDH1 and ZRSR2 mutations.

Case Presentation

A 49-year-old man developed severe neutropenia and macrocytic anemia in January 2019. Mild marrow dysplasia developed by March 2020 with IDH1 (31.1%) and splicing gene ZRSR2 (55.7%) mutations. In October 2022 biopsy showed MDS with 4% blasts, megakaryocytic/granulocytic hypoplasia, normal cytogenetics and 43% IDH1/89% ZRSR2. After azacytidine failure, ivosidenib was started in November 2023 following FDA approval. Within weeks ANCs increased from 170 to 1580 and hemoglobin from 7.9 to 11.6 with MCV 115, reticulocytes 1.72%. At 3 months a CBC was normal except for MCV 111. IDH1 and ZRSR2 were 36.4% and 71%. After 6 months, ANC was 2380, hemoglobin 14.7, MCV 108.6, reticulo-cytes 1.77%. IDH1 PCR showed a 33.1% allele frequency consistent with a clonal remission.

Discussion

IDH1 mutations in MDS/AML frequently co-occur with mutations in RNA splicing genes SRSF2 or ZRSR2. For ZRSR2, we previously reported that isolated mutations of this gene cause refractory macrocytic anemias without dysplasia, thus presenting as clonal cytopenias of undetermined significance (Fleischman et al., Leuk Res, 2017). In this MDS case, after ivosidenib treatment the ZRSR2 splicing defect sustained clonal dominance over polyclonal hematopoiesis while accounting for macrocytosis. Longitudinal data for two ivosidenib-treated IDH1/SRSF2 MDS cases are incomplete, but one case of IDH2/SRSF2 MDS treated with the inhibitor enasidenib similarly achieved complete remission without regression of the mutated clone for 12 months.

Conclusions

Following the FDA approval of ivosidenib, all cases of MDS should have DNA sequencing performed at diagnosis to identify IDH1 mutations. Treatment induces high rates of remission even when polyclonal hematopoiesis does not recover. Moreover, the restoration of hematopoietic differentiation by the abnormal clone provides unique insights into the clinical phenotype and fitness advantage conferred by the co-existing driver mutations.

Background

IDH1 mutations are detected in 3-4% of MDS, nearly always with one or more co-mutations. Treatment with IDH1 inhibitor ivosidenib typically resulted in regression of the abnormal clone in 15 reported responders. However, in a few cases differentiation was restored from the abnormal clone. Here we report a durable MDS remission despite sustained proliferation of a clone with IDH1 and ZRSR2 mutations.

Case Presentation

A 49-year-old man developed severe neutropenia and macrocytic anemia in January 2019. Mild marrow dysplasia developed by March 2020 with IDH1 (31.1%) and splicing gene ZRSR2 (55.7%) mutations. In October 2022 biopsy showed MDS with 4% blasts, megakaryocytic/granulocytic hypoplasia, normal cytogenetics and 43% IDH1/89% ZRSR2. After azacytidine failure, ivosidenib was started in November 2023 following FDA approval. Within weeks ANCs increased from 170 to 1580 and hemoglobin from 7.9 to 11.6 with MCV 115, reticulocytes 1.72%. At 3 months a CBC was normal except for MCV 111. IDH1 and ZRSR2 were 36.4% and 71%. After 6 months, ANC was 2380, hemoglobin 14.7, MCV 108.6, reticulo-cytes 1.77%. IDH1 PCR showed a 33.1% allele frequency consistent with a clonal remission.

Discussion

IDH1 mutations in MDS/AML frequently co-occur with mutations in RNA splicing genes SRSF2 or ZRSR2. For ZRSR2, we previously reported that isolated mutations of this gene cause refractory macrocytic anemias without dysplasia, thus presenting as clonal cytopenias of undetermined significance (Fleischman et al., Leuk Res, 2017). In this MDS case, after ivosidenib treatment the ZRSR2 splicing defect sustained clonal dominance over polyclonal hematopoiesis while accounting for macrocytosis. Longitudinal data for two ivosidenib-treated IDH1/SRSF2 MDS cases are incomplete, but one case of IDH2/SRSF2 MDS treated with the inhibitor enasidenib similarly achieved complete remission without regression of the mutated clone for 12 months.

Conclusions

Following the FDA approval of ivosidenib, all cases of MDS should have DNA sequencing performed at diagnosis to identify IDH1 mutations. Treatment induces high rates of remission even when polyclonal hematopoiesis does not recover. Moreover, the restoration of hematopoietic differentiation by the abnormal clone provides unique insights into the clinical phenotype and fitness advantage conferred by the co-existing driver mutations.

Background

Over one-third of newly diagnosed Diffuse Large B-Cell Lymphoma (DLBCL) cases are in people age ≥75. Although a potentially curable malignancy, older adults have a comparatively lower survival rate. This may be due to multiple factors including suboptimal management. In one study, up to 23% of patients age ≥80 did not receive any therapy for DLBCL. This age-related survival disparity is potentially magnified in patients who reside in rural areas. As there is no standard of care for this population, we speculate that there is wide variation in treatment practices which may influence outcomes. The purpose of this study is to describe treatment patterns and outcomes in in veterans age ≥80 with DLBCL by area of residence.

Methods

We conducted a retrospective study of veterans age ≥80 newly diagnosed with Stage II-IV DLBCL between 2006-2023 using the Veterans Affairs (VA) Cancer Registry System (VACRS). Patient, disease, and treatment variables were extracted from the VA Corporate Data Warehouse (CDW) and via chart review. Variables were compared amongst Veterans residing at urban vs. rural addresses.

Results

We evaluated a total of 181 Veterans. Most veterans resided in an urban area (60.2%). At least 18.8% of veterans failed to start lymphoma-directed therapy, but only 6.6% of veterans were not explicitly offered treatment per documentation. In total, 68.5% of veterans were offered a curative treatment regimen by their provider; curative treatment was more likely to be offered to urban patients (68.8% vs 61.5%, p=0.86). Pre-phase steroids and geriatric assessments prior to treatment were severely underutilized (2.8% and 0.6%). More urban veterans started treatment (75.2% vs 65.4%, p=0.38) and 40.9% started an anthracyclinecontaining regimen. Only 27.6% of veterans completed 6 total cycles of treatment. Only 37.6% of veterans achieved a complete response at end of treatment, although response was not reported in 46.4% of patients.

Conclusions

Most elderly veterans with DLBCL are being offered and started on a curative treatment regimen; however, most do not complete a full course of treatment. Although not statistically significant, more urban veterans were offered a curative regimen and received treatment. Wider adoption of pre-phase steroids and geriatric assessments could improve response outcomes.

Background

Over one-third of newly diagnosed Diffuse Large B-Cell Lymphoma (DLBCL) cases are in people age ≥75. Although a potentially curable malignancy, older adults have a comparatively lower survival rate. This may be due to multiple factors including suboptimal management. In one study, up to 23% of patients age ≥80 did not receive any therapy for DLBCL. This age-related survival disparity is potentially magnified in patients who reside in rural areas. As there is no standard of care for this population, we speculate that there is wide variation in treatment practices which may influence outcomes. The purpose of this study is to describe treatment patterns and outcomes in in veterans age ≥80 with DLBCL by area of residence.

Methods

We conducted a retrospective study of veterans age ≥80 newly diagnosed with Stage II-IV DLBCL between 2006-2023 using the Veterans Affairs (VA) Cancer Registry System (VACRS). Patient, disease, and treatment variables were extracted from the VA Corporate Data Warehouse (CDW) and via chart review. Variables were compared amongst Veterans residing at urban vs. rural addresses.

Results

We evaluated a total of 181 Veterans. Most veterans resided in an urban area (60.2%). At least 18.8% of veterans failed to start lymphoma-directed therapy, but only 6.6% of veterans were not explicitly offered treatment per documentation. In total, 68.5% of veterans were offered a curative treatment regimen by their provider; curative treatment was more likely to be offered to urban patients (68.8% vs 61.5%, p=0.86). Pre-phase steroids and geriatric assessments prior to treatment were severely underutilized (2.8% and 0.6%). More urban veterans started treatment (75.2% vs 65.4%, p=0.38) and 40.9% started an anthracyclinecontaining regimen. Only 27.6% of veterans completed 6 total cycles of treatment. Only 37.6% of veterans achieved a complete response at end of treatment, although response was not reported in 46.4% of patients.

Conclusions

Most elderly veterans with DLBCL are being offered and started on a curative treatment regimen; however, most do not complete a full course of treatment. Although not statistically significant, more urban veterans were offered a curative regimen and received treatment. Wider adoption of pre-phase steroids and geriatric assessments could improve response outcomes.

Background

Over one-third of newly diagnosed Diffuse Large B-Cell Lymphoma (DLBCL) cases are in people age ≥75. Although a potentially curable malignancy, older adults have a comparatively lower survival rate. This may be due to multiple factors including suboptimal management. In one study, up to 23% of patients age ≥80 did not receive any therapy for DLBCL. This age-related survival disparity is potentially magnified in patients who reside in rural areas. As there is no standard of care for this population, we speculate that there is wide variation in treatment practices which may influence outcomes. The purpose of this study is to describe treatment patterns and outcomes in in veterans age ≥80 with DLBCL by area of residence.

Methods

We conducted a retrospective study of veterans age ≥80 newly diagnosed with Stage II-IV DLBCL between 2006-2023 using the Veterans Affairs (VA) Cancer Registry System (VACRS). Patient, disease, and treatment variables were extracted from the VA Corporate Data Warehouse (CDW) and via chart review. Variables were compared amongst Veterans residing at urban vs. rural addresses.

Results

We evaluated a total of 181 Veterans. Most veterans resided in an urban area (60.2%). At least 18.8% of veterans failed to start lymphoma-directed therapy, but only 6.6% of veterans were not explicitly offered treatment per documentation. In total, 68.5% of veterans were offered a curative treatment regimen by their provider; curative treatment was more likely to be offered to urban patients (68.8% vs 61.5%, p=0.86). Pre-phase steroids and geriatric assessments prior to treatment were severely underutilized (2.8% and 0.6%). More urban veterans started treatment (75.2% vs 65.4%, p=0.38) and 40.9% started an anthracyclinecontaining regimen. Only 27.6% of veterans completed 6 total cycles of treatment. Only 37.6% of veterans achieved a complete response at end of treatment, although response was not reported in 46.4% of patients.

Conclusions

Most elderly veterans with DLBCL are being offered and started on a curative treatment regimen; however, most do not complete a full course of treatment. Although not statistically significant, more urban veterans were offered a curative regimen and received treatment. Wider adoption of pre-phase steroids and geriatric assessments could improve response outcomes.

Background

Melanoma is a malignant type of skin cancer and is the fifth most common type of cancer in the United States. The purpose of this study is to determine how demographic information such as race and gender may influence mortality rates in melanoma patients. To date, no previous studies have analyzed epidemiological trends in melanoma mortality using the CDC Wonder database. However, previous literature has suggested that non-Hispanic Whites have the highest mortality rate.

Methods

CDC Wonder is a database that contains mortality and demographic information for various pathologies. Melanoma cases were specified using the ICD-10 code C43. Patients over the age of 35 were considered for this study. Mortality rates were generated based on gender, race, and a combination of both variables. Data analysis involved finding the rates and 95% confidence intervals for the crude and age-adjusted mortality rate (AAMR) per 100,000. Joinpoint regression analysis was also used.

Results

Several differences in the age-adjusted mortality rate were observed. In every year from 1999 to 2022, the non-Hispanic White group (NH White) had the highest mortality rate, whereas all other races had similar rates. Meanwhile, when stratifying by both race and gender, it appears that NH White males have the highest rate in mortality. In 2022, the mortality rate for NH White males was 8.8 per 100,000, whereas the second highest rate belonged to the NH White female group (4 per 100,000). All other racial and gender combinations had similar mortality rates. The trends in mortality rates did not fluctuate much from the years 1999-2022. No significant deviation in mortality trends were seen after the start of the COVID-19 pandemic.

Conclusions

This data corroborates with the results from previous studies. It also indicates that certain demographics that may be at greater risk for mortality, and that the mortality rates have remained relatively stable. The mortality rate for melanoma may vary by race and gender. More specifically, NH White males may be susceptible to higher mortality rates compared to other demographic groups. Future research on cancer staging and treatment modality received could help explain these differences.

Background

Melanoma is a malignant type of skin cancer and is the fifth most common type of cancer in the United States. The purpose of this study is to determine how demographic information such as race and gender may influence mortality rates in melanoma patients. To date, no previous studies have analyzed epidemiological trends in melanoma mortality using the CDC Wonder database. However, previous literature has suggested that non-Hispanic Whites have the highest mortality rate.

Methods

CDC Wonder is a database that contains mortality and demographic information for various pathologies. Melanoma cases were specified using the ICD-10 code C43. Patients over the age of 35 were considered for this study. Mortality rates were generated based on gender, race, and a combination of both variables. Data analysis involved finding the rates and 95% confidence intervals for the crude and age-adjusted mortality rate (AAMR) per 100,000. Joinpoint regression analysis was also used.

Results

Several differences in the age-adjusted mortality rate were observed. In every year from 1999 to 2022, the non-Hispanic White group (NH White) had the highest mortality rate, whereas all other races had similar rates. Meanwhile, when stratifying by both race and gender, it appears that NH White males have the highest rate in mortality. In 2022, the mortality rate for NH White males was 8.8 per 100,000, whereas the second highest rate belonged to the NH White female group (4 per 100,000). All other racial and gender combinations had similar mortality rates. The trends in mortality rates did not fluctuate much from the years 1999-2022. No significant deviation in mortality trends were seen after the start of the COVID-19 pandemic.

Conclusions

This data corroborates with the results from previous studies. It also indicates that certain demographics that may be at greater risk for mortality, and that the mortality rates have remained relatively stable. The mortality rate for melanoma may vary by race and gender. More specifically, NH White males may be susceptible to higher mortality rates compared to other demographic groups. Future research on cancer staging and treatment modality received could help explain these differences.

Background

Melanoma is a malignant type of skin cancer and is the fifth most common type of cancer in the United States. The purpose of this study is to determine how demographic information such as race and gender may influence mortality rates in melanoma patients. To date, no previous studies have analyzed epidemiological trends in melanoma mortality using the CDC Wonder database. However, previous literature has suggested that non-Hispanic Whites have the highest mortality rate.

Methods

CDC Wonder is a database that contains mortality and demographic information for various pathologies. Melanoma cases were specified using the ICD-10 code C43. Patients over the age of 35 were considered for this study. Mortality rates were generated based on gender, race, and a combination of both variables. Data analysis involved finding the rates and 95% confidence intervals for the crude and age-adjusted mortality rate (AAMR) per 100,000. Joinpoint regression analysis was also used.

Results

Several differences in the age-adjusted mortality rate were observed. In every year from 1999 to 2022, the non-Hispanic White group (NH White) had the highest mortality rate, whereas all other races had similar rates. Meanwhile, when stratifying by both race and gender, it appears that NH White males have the highest rate in mortality. In 2022, the mortality rate for NH White males was 8.8 per 100,000, whereas the second highest rate belonged to the NH White female group (4 per 100,000). All other racial and gender combinations had similar mortality rates. The trends in mortality rates did not fluctuate much from the years 1999-2022. No significant deviation in mortality trends were seen after the start of the COVID-19 pandemic.

Conclusions

This data corroborates with the results from previous studies. It also indicates that certain demographics that may be at greater risk for mortality, and that the mortality rates have remained relatively stable. The mortality rate for melanoma may vary by race and gender. More specifically, NH White males may be susceptible to higher mortality rates compared to other demographic groups. Future research on cancer staging and treatment modality received could help explain these differences.

Black Friday is coming up. Although it seems (fortunately) to have lost some of its insanity since the pandemic, it’s still a huge shopping day for those who want to spend their day off in hand-to-hand combat at a Walmart. For me it’s a good day not to leave my house at all.

Following Black Friday we have Cyber Monday, where people go online to start buying stuff, presumably using business WiFi when they’re back at work. In spite of the apparent contradiction of having an online shopping day when people are at their jobs, it’s shamelessly promoted by the online retail giants.

Sandwiched between them is the quieter Small Business Saturday, started in 2010 by American Express and since gradually taking hold here and across the pond. The idea is to support the smaller local, perhaps family-owned, stores of varying kinds. Politicians love to talk about small businesses, calling them the backbone of the economy, promising to support them, etc.

I have no issue with that. I agree with it. I try to support my smaller, local places whenever I can. I’m glad AMEX started it, and that it’s taken off.

So why don’t we have a campaign to support small medical practices? Aren’t we small businesses, too? I’m the only doctor at my place, that’s about as small as you can get.

Like other small businesses, I don’t have the resources to advertise, aside from a simple website. At the same time I can’t drive too far without seeing a billboard, or hearing a radio ad, for one of the large local healthcare systems promising better convenience and care than that of their competitors.

I’m certainly not in a position to offer extended or weekend hours — I mean, I could, but I also have my own sanity to keep. But at the same time small practices may know their patients better than Huge Medicine Inc. We don’t have as many patients, and the staff turnover at small places is usually lower.

No one, though, is going to stand up for us, AMEX included (outside of cosmetic services, doctor visit charges are probably a tiny fraction of credit card company charges). Even our own organizations, like the AMA and others, won’t (at least not too much). They might pay lip service to us, but the reality is that most of their members work for large healthcare systems. Those groups probably make some big donations to them, too. So the last thing they want to do is tick them off.

I’m not against large groups. They have capabilities I don’t, like the ability to run research trials and have subspecialists. Even the best of us in solo practice needs someone better to refer to, such as an epileptologist, Parkinsonologist, neuromuscular disease-ologist, When I can’t help a patient any further those are the doctors I turn to, and, believe me, I appreciate them.

But it sometimes seems odd that, in a world where financial companies and public figures often stress their support for small business, those of us in the small medical practice are forgotten.
 

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

Black Friday is coming up. Although it seems (fortunately) to have lost some of its insanity since the pandemic, it’s still a huge shopping day for those who want to spend their day off in hand-to-hand combat at a Walmart. For me it’s a good day not to leave my house at all.

Following Black Friday we have Cyber Monday, where people go online to start buying stuff, presumably using business WiFi when they’re back at work. In spite of the apparent contradiction of having an online shopping day when people are at their jobs, it’s shamelessly promoted by the online retail giants.

Sandwiched between them is the quieter Small Business Saturday, started in 2010 by American Express and since gradually taking hold here and across the pond. The idea is to support the smaller local, perhaps family-owned, stores of varying kinds. Politicians love to talk about small businesses, calling them the backbone of the economy, promising to support them, etc.

I have no issue with that. I agree with it. I try to support my smaller, local places whenever I can. I’m glad AMEX started it, and that it’s taken off.

So why don’t we have a campaign to support small medical practices? Aren’t we small businesses, too? I’m the only doctor at my place, that’s about as small as you can get.

Like other small businesses, I don’t have the resources to advertise, aside from a simple website. At the same time I can’t drive too far without seeing a billboard, or hearing a radio ad, for one of the large local healthcare systems promising better convenience and care than that of their competitors.

I’m certainly not in a position to offer extended or weekend hours — I mean, I could, but I also have my own sanity to keep. But at the same time small practices may know their patients better than Huge Medicine Inc. We don’t have as many patients, and the staff turnover at small places is usually lower.

No one, though, is going to stand up for us, AMEX included (outside of cosmetic services, doctor visit charges are probably a tiny fraction of credit card company charges). Even our own organizations, like the AMA and others, won’t (at least not too much). They might pay lip service to us, but the reality is that most of their members work for large healthcare systems. Those groups probably make some big donations to them, too. So the last thing they want to do is tick them off.

I’m not against large groups. They have capabilities I don’t, like the ability to run research trials and have subspecialists. Even the best of us in solo practice needs someone better to refer to, such as an epileptologist, Parkinsonologist, neuromuscular disease-ologist, When I can’t help a patient any further those are the doctors I turn to, and, believe me, I appreciate them.

But it sometimes seems odd that, in a world where financial companies and public figures often stress their support for small business, those of us in the small medical practice are forgotten.
 

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

Black Friday is coming up. Although it seems (fortunately) to have lost some of its insanity since the pandemic, it’s still a huge shopping day for those who want to spend their day off in hand-to-hand combat at a Walmart. For me it’s a good day not to leave my house at all.

Following Black Friday we have Cyber Monday, where people go online to start buying stuff, presumably using business WiFi when they’re back at work. In spite of the apparent contradiction of having an online shopping day when people are at their jobs, it’s shamelessly promoted by the online retail giants.

Sandwiched between them is the quieter Small Business Saturday, started in 2010 by American Express and since gradually taking hold here and across the pond. The idea is to support the smaller local, perhaps family-owned, stores of varying kinds. Politicians love to talk about small businesses, calling them the backbone of the economy, promising to support them, etc.

I have no issue with that. I agree with it. I try to support my smaller, local places whenever I can. I’m glad AMEX started it, and that it’s taken off.

So why don’t we have a campaign to support small medical practices? Aren’t we small businesses, too? I’m the only doctor at my place, that’s about as small as you can get.

Like other small businesses, I don’t have the resources to advertise, aside from a simple website. At the same time I can’t drive too far without seeing a billboard, or hearing a radio ad, for one of the large local healthcare systems promising better convenience and care than that of their competitors.

I’m certainly not in a position to offer extended or weekend hours — I mean, I could, but I also have my own sanity to keep. But at the same time small practices may know their patients better than Huge Medicine Inc. We don’t have as many patients, and the staff turnover at small places is usually lower.

No one, though, is going to stand up for us, AMEX included (outside of cosmetic services, doctor visit charges are probably a tiny fraction of credit card company charges). Even our own organizations, like the AMA and others, won’t (at least not too much). They might pay lip service to us, but the reality is that most of their members work for large healthcare systems. Those groups probably make some big donations to them, too. So the last thing they want to do is tick them off.

I’m not against large groups. They have capabilities I don’t, like the ability to run research trials and have subspecialists. Even the best of us in solo practice needs someone better to refer to, such as an epileptologist, Parkinsonologist, neuromuscular disease-ologist, When I can’t help a patient any further those are the doctors I turn to, and, believe me, I appreciate them.

But it sometimes seems odd that, in a world where financial companies and public figures often stress their support for small business, those of us in the small medical practice are forgotten.
 

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

This transcript has been edited for clarity. 

New updated COVID vaccines are now available, but who can get them, who should get them, and when? Two updated mRNA COVID vaccines, one by Moderna and the other by Pfizer, have been authorized or approved by the US Food and Drug Administration (FDA) for those aged 6 months or older.

Both vaccines target Omicron’s KP.2 strain of the JN.1 lineage. An updated protein-based version by Novavax, also directed at JN.1, has been authorized, but only for those aged 12 years or older. 

The Centers for Disease Control and Prevention’s (CDC’s) Advisory Committee on Immunization Practices recommends a dose of the 2024-2025 updated COVID vaccine for everyone aged 6 months or older. This includes people who have never been vaccinated against COVID, those who have been vaccinated, as well as people with previous COVID infection. 

The big question is when, and FDA and CDC have set some parameters. For mRNA updated vaccines, patients should wait at least 2 months after their last dose of any COVID vaccine before getting a dose of the updated vaccine.

If the patient has recently had COVID, the wait time is even longer: Patients can wait 3 months after a COVID infection to be vaccinated, but they don’t have to. FDA’s instructions for the Novavax version are not as straightforward. People can get an updated Novavax dose at least 2 months after their last mRNA COVID vaccine dose, or at least 2 months after completing a Novavax two-dose primary series. Those two Novavax doses should be given at least 3 weeks apart. 

Patients can personalize their vaccine plan. They will have the greatest protection in the first few weeks to months after a vaccine, after which antibodies tend to wane. It is a good idea to time vaccination so that protection peaks at big events like weddings and major meetings.

If patients decide to wait, they run the risk of getting a COVID infection. Also keep in mind which variants are circulating and the amount of local activity. Right now, there is a lot of COVID going around, and most of it is related to JN.1, the target of this year’s updated vaccine. If patients decide to wait, they should avoid crowded indoor settings or wear a high-quality mask for some protection. 

Here’s the bottom line: Most people (more than 95%) have some degree of COVID protection from previous infection, vaccination, or both. But if they haven’t recently had COVID infection and didn’t get a dose of last year’s vaccine, they are sitting ducks for getting sick without updated protection. The best way to stay well is to get a dose of the updated vaccine as soon as possible. This is especially true for those in high-risk groups or who are near someone who is high risk. 

Two thirds of COVID hospitalizations are in those aged 65 or older. Hospitalization rates are highest for those aged 75 or older and among infants under 6 months of age. These babies are too young to be vaccinated, but maternal vaccination during pregnancy and breastfeeding can help protect them. 

We’re still seeing racial and ethnic disparities in COVID-related hospitalizations, which are highest among American Indians, Alaska Natives, and Black populations. People with immunocompromising conditions, those with chronic medical conditions, and people living in long-term care facilities are also at greater risk. Unlike last year, additional mRNA doses are not recommended for those aged 65 or older at this time, but that could change.

Since 2020, we’ve come a long way in our fight against COVID, but the battle is still on. In 2023, nearly a million people were hospitalized from COVID. More than 75,000 died. COVID vaccines help protect us from severe disease, hospitalization, and death. 

Let’s face it — we all have booster fatigue, but COVID is now endemic. It’s here to stay, and it’s much safer to update antibody protection with vaccination than with infection. Another benefit of getting vaccinated is that it decreases the chance of getting long COVID. The uptake of last year’s COVID vaccine was abysmal; only about 23% of adults and 14% of children received it.

But this is a new year and a new vaccine. Please make sure your patients understand that the virus has changed a lot. Antibodies we built from previous infection and previous vaccination don’t work as well against these new variants. Antibody levels wane over time, so even if they missed the last few vaccine doses without getting sick, they really should consider getting a dose of this new vaccine. The 2024-2025 updated COVID vaccine is the best way to catch up, update their immunity, and keep them protected. 

Furthermore, we are now entering respiratory virus season, which means we need to think about, recommend, and administer three shots if indicated: COVID, flu, and RSV. Now is the time. Patients can get all three at the same time, in the same visit, if they choose to do so. 

Your recommendation as a physician is powerful. Adults and children who receive a healthcare provider recommendation are more likely to get vaccinated.

Dr. Fryhofer is an adjunct clinical associate professor of medicine, Emory University School of Medicine, Atlanta, Georgia. She reported conflicts of interest with the American Medical Association, the Medical Association of Atlanta, the American College of Physicians, and Medscape.

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

This transcript has been edited for clarity. 

New updated COVID vaccines are now available, but who can get them, who should get them, and when? Two updated mRNA COVID vaccines, one by Moderna and the other by Pfizer, have been authorized or approved by the US Food and Drug Administration (FDA) for those aged 6 months or older.

Both vaccines target Omicron’s KP.2 strain of the JN.1 lineage. An updated protein-based version by Novavax, also directed at JN.1, has been authorized, but only for those aged 12 years or older. 

The Centers for Disease Control and Prevention’s (CDC’s) Advisory Committee on Immunization Practices recommends a dose of the 2024-2025 updated COVID vaccine for everyone aged 6 months or older. This includes people who have never been vaccinated against COVID, those who have been vaccinated, as well as people with previous COVID infection. 

The big question is when, and FDA and CDC have set some parameters. For mRNA updated vaccines, patients should wait at least 2 months after their last dose of any COVID vaccine before getting a dose of the updated vaccine.

If the patient has recently had COVID, the wait time is even longer: Patients can wait 3 months after a COVID infection to be vaccinated, but they don’t have to. FDA’s instructions for the Novavax version are not as straightforward. People can get an updated Novavax dose at least 2 months after their last mRNA COVID vaccine dose, or at least 2 months after completing a Novavax two-dose primary series. Those two Novavax doses should be given at least 3 weeks apart. 

Patients can personalize their vaccine plan. They will have the greatest protection in the first few weeks to months after a vaccine, after which antibodies tend to wane. It is a good idea to time vaccination so that protection peaks at big events like weddings and major meetings.

If patients decide to wait, they run the risk of getting a COVID infection. Also keep in mind which variants are circulating and the amount of local activity. Right now, there is a lot of COVID going around, and most of it is related to JN.1, the target of this year’s updated vaccine. If patients decide to wait, they should avoid crowded indoor settings or wear a high-quality mask for some protection. 

Here’s the bottom line: Most people (more than 95%) have some degree of COVID protection from previous infection, vaccination, or both. But if they haven’t recently had COVID infection and didn’t get a dose of last year’s vaccine, they are sitting ducks for getting sick without updated protection. The best way to stay well is to get a dose of the updated vaccine as soon as possible. This is especially true for those in high-risk groups or who are near someone who is high risk. 

Two thirds of COVID hospitalizations are in those aged 65 or older. Hospitalization rates are highest for those aged 75 or older and among infants under 6 months of age. These babies are too young to be vaccinated, but maternal vaccination during pregnancy and breastfeeding can help protect them. 

We’re still seeing racial and ethnic disparities in COVID-related hospitalizations, which are highest among American Indians, Alaska Natives, and Black populations. People with immunocompromising conditions, those with chronic medical conditions, and people living in long-term care facilities are also at greater risk. Unlike last year, additional mRNA doses are not recommended for those aged 65 or older at this time, but that could change.

Since 2020, we’ve come a long way in our fight against COVID, but the battle is still on. In 2023, nearly a million people were hospitalized from COVID. More than 75,000 died. COVID vaccines help protect us from severe disease, hospitalization, and death. 

Let’s face it — we all have booster fatigue, but COVID is now endemic. It’s here to stay, and it’s much safer to update antibody protection with vaccination than with infection. Another benefit of getting vaccinated is that it decreases the chance of getting long COVID. The uptake of last year’s COVID vaccine was abysmal; only about 23% of adults and 14% of children received it.

But this is a new year and a new vaccine. Please make sure your patients understand that the virus has changed a lot. Antibodies we built from previous infection and previous vaccination don’t work as well against these new variants. Antibody levels wane over time, so even if they missed the last few vaccine doses without getting sick, they really should consider getting a dose of this new vaccine. The 2024-2025 updated COVID vaccine is the best way to catch up, update their immunity, and keep them protected. 

Furthermore, we are now entering respiratory virus season, which means we need to think about, recommend, and administer three shots if indicated: COVID, flu, and RSV. Now is the time. Patients can get all three at the same time, in the same visit, if they choose to do so. 

Your recommendation as a physician is powerful. Adults and children who receive a healthcare provider recommendation are more likely to get vaccinated.

Dr. Fryhofer is an adjunct clinical associate professor of medicine, Emory University School of Medicine, Atlanta, Georgia. She reported conflicts of interest with the American Medical Association, the Medical Association of Atlanta, the American College of Physicians, and Medscape.

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

This transcript has been edited for clarity. 

New updated COVID vaccines are now available, but who can get them, who should get them, and when? Two updated mRNA COVID vaccines, one by Moderna and the other by Pfizer, have been authorized or approved by the US Food and Drug Administration (FDA) for those aged 6 months or older.

Both vaccines target Omicron’s KP.2 strain of the JN.1 lineage. An updated protein-based version by Novavax, also directed at JN.1, has been authorized, but only for those aged 12 years or older. 

The Centers for Disease Control and Prevention’s (CDC’s) Advisory Committee on Immunization Practices recommends a dose of the 2024-2025 updated COVID vaccine for everyone aged 6 months or older. This includes people who have never been vaccinated against COVID, those who have been vaccinated, as well as people with previous COVID infection. 

The big question is when, and FDA and CDC have set some parameters. For mRNA updated vaccines, patients should wait at least 2 months after their last dose of any COVID vaccine before getting a dose of the updated vaccine.

If the patient has recently had COVID, the wait time is even longer: Patients can wait 3 months after a COVID infection to be vaccinated, but they don’t have to. FDA’s instructions for the Novavax version are not as straightforward. People can get an updated Novavax dose at least 2 months after their last mRNA COVID vaccine dose, or at least 2 months after completing a Novavax two-dose primary series. Those two Novavax doses should be given at least 3 weeks apart. 

Patients can personalize their vaccine plan. They will have the greatest protection in the first few weeks to months after a vaccine, after which antibodies tend to wane. It is a good idea to time vaccination so that protection peaks at big events like weddings and major meetings.

If patients decide to wait, they run the risk of getting a COVID infection. Also keep in mind which variants are circulating and the amount of local activity. Right now, there is a lot of COVID going around, and most of it is related to JN.1, the target of this year’s updated vaccine. If patients decide to wait, they should avoid crowded indoor settings or wear a high-quality mask for some protection. 

Here’s the bottom line: Most people (more than 95%) have some degree of COVID protection from previous infection, vaccination, or both. But if they haven’t recently had COVID infection and didn’t get a dose of last year’s vaccine, they are sitting ducks for getting sick without updated protection. The best way to stay well is to get a dose of the updated vaccine as soon as possible. This is especially true for those in high-risk groups or who are near someone who is high risk. 

Two thirds of COVID hospitalizations are in those aged 65 or older. Hospitalization rates are highest for those aged 75 or older and among infants under 6 months of age. These babies are too young to be vaccinated, but maternal vaccination during pregnancy and breastfeeding can help protect them. 

We’re still seeing racial and ethnic disparities in COVID-related hospitalizations, which are highest among American Indians, Alaska Natives, and Black populations. People with immunocompromising conditions, those with chronic medical conditions, and people living in long-term care facilities are also at greater risk. Unlike last year, additional mRNA doses are not recommended for those aged 65 or older at this time, but that could change.

Since 2020, we’ve come a long way in our fight against COVID, but the battle is still on. In 2023, nearly a million people were hospitalized from COVID. More than 75,000 died. COVID vaccines help protect us from severe disease, hospitalization, and death. 

Let’s face it — we all have booster fatigue, but COVID is now endemic. It’s here to stay, and it’s much safer to update antibody protection with vaccination than with infection. Another benefit of getting vaccinated is that it decreases the chance of getting long COVID. The uptake of last year’s COVID vaccine was abysmal; only about 23% of adults and 14% of children received it.

But this is a new year and a new vaccine. Please make sure your patients understand that the virus has changed a lot. Antibodies we built from previous infection and previous vaccination don’t work as well against these new variants. Antibody levels wane over time, so even if they missed the last few vaccine doses without getting sick, they really should consider getting a dose of this new vaccine. The 2024-2025 updated COVID vaccine is the best way to catch up, update their immunity, and keep them protected. 

Furthermore, we are now entering respiratory virus season, which means we need to think about, recommend, and administer three shots if indicated: COVID, flu, and RSV. Now is the time. Patients can get all three at the same time, in the same visit, if they choose to do so. 

Your recommendation as a physician is powerful. Adults and children who receive a healthcare provider recommendation are more likely to get vaccinated.

Dr. Fryhofer is an adjunct clinical associate professor of medicine, Emory University School of Medicine, Atlanta, Georgia. She reported conflicts of interest with the American Medical Association, the Medical Association of Atlanta, the American College of Physicians, and Medscape.

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

TOPLINE:

The presence of an operational classification of drug interactions (ORCA) class 3 or 4 drug-drug interactions (DDIs) did not increase the risk for colchicine-related gastrointestinal adverse events or modify the effect of colchicine on death or hospitalization caused by COVID-19 infection in ambulatory patients.

METHODOLOGY:

• This secondary analysis of the COLCORONA trial aimed to evaluate if a potential DDI of colchicine was associated with changes in its pharmacokinetics or modified its clinical safety and efficacy in patients with COVID-19.
• Overall, 4432 ambulatory patients with COVID-19 (median age, 54 years; 54% women) were randomly assigned to receive colchicine 0.5 mg twice daily for 3 days and then 0.5 mg once daily for 27 days (n = 2205) or a placebo (n = 2227).
• All the participants had at least one high-risk criterion such as age ≥ 70 years, diabetes, heart failure, systolic blood pressure ≥ 150 mm Hg, respiratory disease, coronary disease, body temperature ≥ 38.4 °C within the last 48 hours, dyspnea, bicytopenia, pancytopenia, or high neutrophil count with low lymphocyte count.
• The medications that could interact with colchicine were determined and categorized under ORCA classes 1 (contraindicated), 2 (provisionally contraindicated), 3 (conditional use), or 4 (minimal risk).
• The primary outcome was any gastrointestinal adverse event assessed over a 30-day follow-up period.

TAKEAWAY:

• Among all the participants, 1% received medications with an ORCA class 2 interaction, 14% with a class 3 interaction, and 13% with a class 4 interaction; rosuvastatin (12%) and atorvastatin (10%) were the most common interacting medications.
• The odds of any gastrointestinal adverse event were 1.80 times and 1.68 times higher in the colchicine arm than in the placebo arm among those without and with a DDI, respectively, with the effect of colchicine being consistent regardless of the presence of drug interactions (P = .69 for interaction).
• Similarly, DDIs did not influence the effect of colchicine on combined risk for COVID-19 hospitalization or mortality (P = .80 for interaction).

IN PRACTICE:

“Once potential DDIs have been identified through screening, they must be tested,” Hemalkumar B. Mehta, PhD, and G. Caleb Alexander, MD, of the Johns Hopkins Bloomberg School of Public Health, Baltimore, wrote in an invited commentary published online in JAMA Network Open. “Theoretical DDIs may not translate into real-world harms,” they added.

SOURCE:

The study was led by Lama S. Alfehaid, PharmD, of Brigham and Women’s Hospital, Boston. It was published online in JAMA Network Open.

LIMITATIONS:

This study focused on the medications used by participants at baseline, which may not have captured all potential DDIs. The findings did not provide information on rare adverse events, such as rhabdomyolysis, which usually occur months after initiating drug therapy. Furthermore, all the study participants had confirmed SARS-CoV-2 infection, which may have increased their susceptibility to adverse reactions associated with the use of colchicine.

DISCLOSURES:

Some authors were supported by grants from the National Institutes of Health/National Heart, Lung, and Blood Institute, American Heart Association, and other sources. The authors also declared serving on advisory boards or on the board of directors; receiving personal fees, grants, research support, or speaking fees; or having other ties with many pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

The presence of an operational classification of drug interactions (ORCA) class 3 or 4 drug-drug interactions (DDIs) did not increase the risk for colchicine-related gastrointestinal adverse events or modify the effect of colchicine on death or hospitalization caused by COVID-19 infection in ambulatory patients.

METHODOLOGY:

• This secondary analysis of the COLCORONA trial aimed to evaluate if a potential DDI of colchicine was associated with changes in its pharmacokinetics or modified its clinical safety and efficacy in patients with COVID-19.
• Overall, 4432 ambulatory patients with COVID-19 (median age, 54 years; 54% women) were randomly assigned to receive colchicine 0.5 mg twice daily for 3 days and then 0.5 mg once daily for 27 days (n = 2205) or a placebo (n = 2227).
• All the participants had at least one high-risk criterion such as age ≥ 70 years, diabetes, heart failure, systolic blood pressure ≥ 150 mm Hg, respiratory disease, coronary disease, body temperature ≥ 38.4 °C within the last 48 hours, dyspnea, bicytopenia, pancytopenia, or high neutrophil count with low lymphocyte count.
• The medications that could interact with colchicine were determined and categorized under ORCA classes 1 (contraindicated), 2 (provisionally contraindicated), 3 (conditional use), or 4 (minimal risk).
• The primary outcome was any gastrointestinal adverse event assessed over a 30-day follow-up period.

TAKEAWAY:

• Among all the participants, 1% received medications with an ORCA class 2 interaction, 14% with a class 3 interaction, and 13% with a class 4 interaction; rosuvastatin (12%) and atorvastatin (10%) were the most common interacting medications.
• The odds of any gastrointestinal adverse event were 1.80 times and 1.68 times higher in the colchicine arm than in the placebo arm among those without and with a DDI, respectively, with the effect of colchicine being consistent regardless of the presence of drug interactions (P = .69 for interaction).
• Similarly, DDIs did not influence the effect of colchicine on combined risk for COVID-19 hospitalization or mortality (P = .80 for interaction).

IN PRACTICE:

“Once potential DDIs have been identified through screening, they must be tested,” Hemalkumar B. Mehta, PhD, and G. Caleb Alexander, MD, of the Johns Hopkins Bloomberg School of Public Health, Baltimore, wrote in an invited commentary published online in JAMA Network Open. “Theoretical DDIs may not translate into real-world harms,” they added.

SOURCE:

The study was led by Lama S. Alfehaid, PharmD, of Brigham and Women’s Hospital, Boston. It was published online in JAMA Network Open.

LIMITATIONS:

This study focused on the medications used by participants at baseline, which may not have captured all potential DDIs. The findings did not provide information on rare adverse events, such as rhabdomyolysis, which usually occur months after initiating drug therapy. Furthermore, all the study participants had confirmed SARS-CoV-2 infection, which may have increased their susceptibility to adverse reactions associated with the use of colchicine.

DISCLOSURES:

Some authors were supported by grants from the National Institutes of Health/National Heart, Lung, and Blood Institute, American Heart Association, and other sources. The authors also declared serving on advisory boards or on the board of directors; receiving personal fees, grants, research support, or speaking fees; or having other ties with many pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

The presence of an operational classification of drug interactions (ORCA) class 3 or 4 drug-drug interactions (DDIs) did not increase the risk for colchicine-related gastrointestinal adverse events or modify the effect of colchicine on death or hospitalization caused by COVID-19 infection in ambulatory patients.

METHODOLOGY:

• This secondary analysis of the COLCORONA trial aimed to evaluate if a potential DDI of colchicine was associated with changes in its pharmacokinetics or modified its clinical safety and efficacy in patients with COVID-19.
• Overall, 4432 ambulatory patients with COVID-19 (median age, 54 years; 54% women) were randomly assigned to receive colchicine 0.5 mg twice daily for 3 days and then 0.5 mg once daily for 27 days (n = 2205) or a placebo (n = 2227).
• All the participants had at least one high-risk criterion such as age ≥ 70 years, diabetes, heart failure, systolic blood pressure ≥ 150 mm Hg, respiratory disease, coronary disease, body temperature ≥ 38.4 °C within the last 48 hours, dyspnea, bicytopenia, pancytopenia, or high neutrophil count with low lymphocyte count.
• The medications that could interact with colchicine were determined and categorized under ORCA classes 1 (contraindicated), 2 (provisionally contraindicated), 3 (conditional use), or 4 (minimal risk).
• The primary outcome was any gastrointestinal adverse event assessed over a 30-day follow-up period.

TAKEAWAY:

• Among all the participants, 1% received medications with an ORCA class 2 interaction, 14% with a class 3 interaction, and 13% with a class 4 interaction; rosuvastatin (12%) and atorvastatin (10%) were the most common interacting medications.
• The odds of any gastrointestinal adverse event were 1.80 times and 1.68 times higher in the colchicine arm than in the placebo arm among those without and with a DDI, respectively, with the effect of colchicine being consistent regardless of the presence of drug interactions (P = .69 for interaction).
• Similarly, DDIs did not influence the effect of colchicine on combined risk for COVID-19 hospitalization or mortality (P = .80 for interaction).

IN PRACTICE:

“Once potential DDIs have been identified through screening, they must be tested,” Hemalkumar B. Mehta, PhD, and G. Caleb Alexander, MD, of the Johns Hopkins Bloomberg School of Public Health, Baltimore, wrote in an invited commentary published online in JAMA Network Open. “Theoretical DDIs may not translate into real-world harms,” they added.

SOURCE:

The study was led by Lama S. Alfehaid, PharmD, of Brigham and Women’s Hospital, Boston. It was published online in JAMA Network Open.

LIMITATIONS:

This study focused on the medications used by participants at baseline, which may not have captured all potential DDIs. The findings did not provide information on rare adverse events, such as rhabdomyolysis, which usually occur months after initiating drug therapy. Furthermore, all the study participants had confirmed SARS-CoV-2 infection, which may have increased their susceptibility to adverse reactions associated with the use of colchicine.

DISCLOSURES:

Some authors were supported by grants from the National Institutes of Health/National Heart, Lung, and Blood Institute, American Heart Association, and other sources. The authors also declared serving on advisory boards or on the board of directors; receiving personal fees, grants, research support, or speaking fees; or having other ties with many pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.