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On second thought, lenalidomide does improve DLBCL outcomes
LUGANO, Switzerland – Hot on the heels of the phase 3 ROBUST study showing that adding lenalidomide to standard chemotherapy did not improve outcomes for patients with untreated diffuse large B-cell lymphoma come results of a different study showing a significant benefit with the therapy.
Although, as previously reported, adding lenalidomide (Revlimid) to standard chemotherapy for patients with newly diagnosed ABC-type diffuse large B-cell lymphoma (DLBCL) – the so-called R2-CHOP regimen – did not significantly improve either progression-free or overall survival, compared with R-CHOP alone in ROBUST, results from the randomized phase 2 ECOG-ACRIN 1412 study showed that R2-CHOP was associated with a 34% reduction in the risk of disease progression or death, compared with R-CHOP alone.
“The efficacy endpoints are consistent, with trends toward higher PET complete response rate and improved overall survival with R-squared CHOP,” Grzegorz S. Nowakowski, MD, of the Mayo Clinic, Rochester, Minn., said at the International Conference on Malignant Lymphoma.
So what’s behind the conflicting findings?
The differences between the results of the two studies may be accounted for by the higher lenalidomide dose used in ECOG-ACRIN 1412, the patient populations – all comers in ECOG-ACRIN versus only patients with activated B-cell (ABC) type DLBCL in ROBUST – and by a 10-day shorter median time to treatment in ECOG-ACRIN 1412, said invited discussant Margaret A. Shipp, MD, of the Dana-Farber Cancer Institute in Boston.
The rationale for adding lenalidomide to R-CHOP came from in vitro studies showing antiproliferative and immunomodulatory action of lenalidomide against DLBCL, as well as two proof-of-concept clinical studies (REAL07 and MC078E) indicating efficacy against non-germinal center-like B (GCB) type DLBCL.
In a subanalysis of patients enrolled in MC078E, Dr. Nowakowski and colleagues found that using classification of patients by cell of origin with the NanoString Lymphoma Subtype assay, the addition of lenalidomide to R-CHOP “appears to mitigate the negative impact of an ABC molecular subtype on the outcome.”
ECOG-ACRIN 1412 details
Goals of the ECOG-ACRIN 1412 study were to evaluate the effect of lenalidomide both in all DLBCL subtypes and in the ABC subtype, maximize the synergy of the immunomodulator with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) while maintaining R-CHOP dose intensity, and facilitate the enrollment of patients with rapidly progressive disease.
To accomplish the last goal, the study was designed to allow enrollment based on local laboratory findings, scans, and diagnostic pathology, without required identification of the cell of origin. Built in to the design was the plan for final eligibility to be based on central pathology review. In other words, the trial design took into account the likelihood that some enrolled patients would not qualify for eligibility based on later pathology review.
The investigators enrolled 349 adults aged 18 years or older with pathologically confirmed DLBCL (regardless of the cell of origin), stage II bulky to stage IV disease, International Prognostic Index (IPI) scores of 2 or greater, and Eastern Cooperative Oncology Group performance status scores of 2 or less.
The patients were stratified by age (younger than 60 years vs. 60 years and older) and by IPI score (2/3 vs. 4/5), and then randomized to receive either six cycles of R-CHOP or R2-CHOP. Lenalidomide was given in a dose of 25 mg on days 1-10 of each cycle. In contrast, the dose used in ROBUST was 15 mg given on days 1-14 of each cycle.
In ECOG-ACRIN 1412, patients assigned to lenalidomide received mandatory neutropenia prophylaxis with granulocyte-colony stimulating factor.
The time from diagnosis to treatment was a median of 21 days, with only 61 of 280 evaluable patients starting treatment more than 31 days after diagnosis. In ROBUST, the median time to start therapy was 31 days.
Dr. Nowakowski and his colleagues had previously shown that time to treatment is an important prognostic factor in DLBCL.
The efficacy evaluation included 145 patients assigned to R2-CHOP, and 135 assigned to R-CHOP. Primary reasons for exclusion were ineligibity following central pathology review or lack of diagnostic material for review.
After a median follow-up of 2.5 years, R2-CHOP was associated with a 34% improvement in progression-free survival, the primary endpoint (hazard ratio [HR] 0.66, P = .03). The 1-year progression-free survival rates were 83% with R2-CHOP and 73% with R-CHOP. Respective 2-year progression-free survival rates were 76% and 70%.
There was no significant difference, however, in the secondary overall survival endpoints with 1-year and 2-year overall survival of 93% vs. 87% and 86% vs. 80%, respectively.
Similarly, there was no difference in rates of PET-ascertained complete response, at 72% with R2-CHOP and 67% with R-CHOP.
R2-CHOP showed greater benefit across most subgroups, including patients with lower IPI score, patients with bulky disease, patients younger than 60 years, women, and patients with shorter time to treatment. There were also nonsignificant trends hinting at better outcomes with R2-CHOP, regardless of cell of origin.
Toxicities were typical for R-CHOP, although patients on R2-CHOP had significantly higher rates of grade 3 or 4 diarrhea, febrile neutropenia, and thrombocytopenia.
In addition to the trial differences mentioned previously, the differences in outcomes might be explained by the possibility that lenalidomide activity is not restricted to ABC DLBCL, Dr. Shipp said.
“One of the things that’s important to remember about lenalidomide is that it’s an immunomodulating agent and it has also has effects on tumor-infiltrating T cells,” she said.
Differences in response to therapy may also be explained by recent findings showing genetic heterogeneity in transcription-defined ABC DLBCLs, she said.
ECOG-ACRIN 1412 was supported by the National Cancer Institute and by Celgene. Dr. Nowakowski reported consulting/advising for and research funding from Celgene and others. Dr. Shipp reported consulting/advising for Bristol-Myers Squibb, honoraria from BMS and AstraZeneca, and institutional research funding from BMS and Bayer.
SOURCE: Nowakowski GS et al. 15-ICML, Abstract 006.
LUGANO, Switzerland – Hot on the heels of the phase 3 ROBUST study showing that adding lenalidomide to standard chemotherapy did not improve outcomes for patients with untreated diffuse large B-cell lymphoma come results of a different study showing a significant benefit with the therapy.
Although, as previously reported, adding lenalidomide (Revlimid) to standard chemotherapy for patients with newly diagnosed ABC-type diffuse large B-cell lymphoma (DLBCL) – the so-called R2-CHOP regimen – did not significantly improve either progression-free or overall survival, compared with R-CHOP alone in ROBUST, results from the randomized phase 2 ECOG-ACRIN 1412 study showed that R2-CHOP was associated with a 34% reduction in the risk of disease progression or death, compared with R-CHOP alone.
“The efficacy endpoints are consistent, with trends toward higher PET complete response rate and improved overall survival with R-squared CHOP,” Grzegorz S. Nowakowski, MD, of the Mayo Clinic, Rochester, Minn., said at the International Conference on Malignant Lymphoma.
So what’s behind the conflicting findings?
The differences between the results of the two studies may be accounted for by the higher lenalidomide dose used in ECOG-ACRIN 1412, the patient populations – all comers in ECOG-ACRIN versus only patients with activated B-cell (ABC) type DLBCL in ROBUST – and by a 10-day shorter median time to treatment in ECOG-ACRIN 1412, said invited discussant Margaret A. Shipp, MD, of the Dana-Farber Cancer Institute in Boston.
The rationale for adding lenalidomide to R-CHOP came from in vitro studies showing antiproliferative and immunomodulatory action of lenalidomide against DLBCL, as well as two proof-of-concept clinical studies (REAL07 and MC078E) indicating efficacy against non-germinal center-like B (GCB) type DLBCL.
In a subanalysis of patients enrolled in MC078E, Dr. Nowakowski and colleagues found that using classification of patients by cell of origin with the NanoString Lymphoma Subtype assay, the addition of lenalidomide to R-CHOP “appears to mitigate the negative impact of an ABC molecular subtype on the outcome.”
ECOG-ACRIN 1412 details
Goals of the ECOG-ACRIN 1412 study were to evaluate the effect of lenalidomide both in all DLBCL subtypes and in the ABC subtype, maximize the synergy of the immunomodulator with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) while maintaining R-CHOP dose intensity, and facilitate the enrollment of patients with rapidly progressive disease.
To accomplish the last goal, the study was designed to allow enrollment based on local laboratory findings, scans, and diagnostic pathology, without required identification of the cell of origin. Built in to the design was the plan for final eligibility to be based on central pathology review. In other words, the trial design took into account the likelihood that some enrolled patients would not qualify for eligibility based on later pathology review.
The investigators enrolled 349 adults aged 18 years or older with pathologically confirmed DLBCL (regardless of the cell of origin), stage II bulky to stage IV disease, International Prognostic Index (IPI) scores of 2 or greater, and Eastern Cooperative Oncology Group performance status scores of 2 or less.
The patients were stratified by age (younger than 60 years vs. 60 years and older) and by IPI score (2/3 vs. 4/5), and then randomized to receive either six cycles of R-CHOP or R2-CHOP. Lenalidomide was given in a dose of 25 mg on days 1-10 of each cycle. In contrast, the dose used in ROBUST was 15 mg given on days 1-14 of each cycle.
In ECOG-ACRIN 1412, patients assigned to lenalidomide received mandatory neutropenia prophylaxis with granulocyte-colony stimulating factor.
The time from diagnosis to treatment was a median of 21 days, with only 61 of 280 evaluable patients starting treatment more than 31 days after diagnosis. In ROBUST, the median time to start therapy was 31 days.
Dr. Nowakowski and his colleagues had previously shown that time to treatment is an important prognostic factor in DLBCL.
The efficacy evaluation included 145 patients assigned to R2-CHOP, and 135 assigned to R-CHOP. Primary reasons for exclusion were ineligibity following central pathology review or lack of diagnostic material for review.
After a median follow-up of 2.5 years, R2-CHOP was associated with a 34% improvement in progression-free survival, the primary endpoint (hazard ratio [HR] 0.66, P = .03). The 1-year progression-free survival rates were 83% with R2-CHOP and 73% with R-CHOP. Respective 2-year progression-free survival rates were 76% and 70%.
There was no significant difference, however, in the secondary overall survival endpoints with 1-year and 2-year overall survival of 93% vs. 87% and 86% vs. 80%, respectively.
Similarly, there was no difference in rates of PET-ascertained complete response, at 72% with R2-CHOP and 67% with R-CHOP.
R2-CHOP showed greater benefit across most subgroups, including patients with lower IPI score, patients with bulky disease, patients younger than 60 years, women, and patients with shorter time to treatment. There were also nonsignificant trends hinting at better outcomes with R2-CHOP, regardless of cell of origin.
Toxicities were typical for R-CHOP, although patients on R2-CHOP had significantly higher rates of grade 3 or 4 diarrhea, febrile neutropenia, and thrombocytopenia.
In addition to the trial differences mentioned previously, the differences in outcomes might be explained by the possibility that lenalidomide activity is not restricted to ABC DLBCL, Dr. Shipp said.
“One of the things that’s important to remember about lenalidomide is that it’s an immunomodulating agent and it has also has effects on tumor-infiltrating T cells,” she said.
Differences in response to therapy may also be explained by recent findings showing genetic heterogeneity in transcription-defined ABC DLBCLs, she said.
ECOG-ACRIN 1412 was supported by the National Cancer Institute and by Celgene. Dr. Nowakowski reported consulting/advising for and research funding from Celgene and others. Dr. Shipp reported consulting/advising for Bristol-Myers Squibb, honoraria from BMS and AstraZeneca, and institutional research funding from BMS and Bayer.
SOURCE: Nowakowski GS et al. 15-ICML, Abstract 006.
LUGANO, Switzerland – Hot on the heels of the phase 3 ROBUST study showing that adding lenalidomide to standard chemotherapy did not improve outcomes for patients with untreated diffuse large B-cell lymphoma come results of a different study showing a significant benefit with the therapy.
Although, as previously reported, adding lenalidomide (Revlimid) to standard chemotherapy for patients with newly diagnosed ABC-type diffuse large B-cell lymphoma (DLBCL) – the so-called R2-CHOP regimen – did not significantly improve either progression-free or overall survival, compared with R-CHOP alone in ROBUST, results from the randomized phase 2 ECOG-ACRIN 1412 study showed that R2-CHOP was associated with a 34% reduction in the risk of disease progression or death, compared with R-CHOP alone.
“The efficacy endpoints are consistent, with trends toward higher PET complete response rate and improved overall survival with R-squared CHOP,” Grzegorz S. Nowakowski, MD, of the Mayo Clinic, Rochester, Minn., said at the International Conference on Malignant Lymphoma.
So what’s behind the conflicting findings?
The differences between the results of the two studies may be accounted for by the higher lenalidomide dose used in ECOG-ACRIN 1412, the patient populations – all comers in ECOG-ACRIN versus only patients with activated B-cell (ABC) type DLBCL in ROBUST – and by a 10-day shorter median time to treatment in ECOG-ACRIN 1412, said invited discussant Margaret A. Shipp, MD, of the Dana-Farber Cancer Institute in Boston.
The rationale for adding lenalidomide to R-CHOP came from in vitro studies showing antiproliferative and immunomodulatory action of lenalidomide against DLBCL, as well as two proof-of-concept clinical studies (REAL07 and MC078E) indicating efficacy against non-germinal center-like B (GCB) type DLBCL.
In a subanalysis of patients enrolled in MC078E, Dr. Nowakowski and colleagues found that using classification of patients by cell of origin with the NanoString Lymphoma Subtype assay, the addition of lenalidomide to R-CHOP “appears to mitigate the negative impact of an ABC molecular subtype on the outcome.”
ECOG-ACRIN 1412 details
Goals of the ECOG-ACRIN 1412 study were to evaluate the effect of lenalidomide both in all DLBCL subtypes and in the ABC subtype, maximize the synergy of the immunomodulator with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) while maintaining R-CHOP dose intensity, and facilitate the enrollment of patients with rapidly progressive disease.
To accomplish the last goal, the study was designed to allow enrollment based on local laboratory findings, scans, and diagnostic pathology, without required identification of the cell of origin. Built in to the design was the plan for final eligibility to be based on central pathology review. In other words, the trial design took into account the likelihood that some enrolled patients would not qualify for eligibility based on later pathology review.
The investigators enrolled 349 adults aged 18 years or older with pathologically confirmed DLBCL (regardless of the cell of origin), stage II bulky to stage IV disease, International Prognostic Index (IPI) scores of 2 or greater, and Eastern Cooperative Oncology Group performance status scores of 2 or less.
The patients were stratified by age (younger than 60 years vs. 60 years and older) and by IPI score (2/3 vs. 4/5), and then randomized to receive either six cycles of R-CHOP or R2-CHOP. Lenalidomide was given in a dose of 25 mg on days 1-10 of each cycle. In contrast, the dose used in ROBUST was 15 mg given on days 1-14 of each cycle.
In ECOG-ACRIN 1412, patients assigned to lenalidomide received mandatory neutropenia prophylaxis with granulocyte-colony stimulating factor.
The time from diagnosis to treatment was a median of 21 days, with only 61 of 280 evaluable patients starting treatment more than 31 days after diagnosis. In ROBUST, the median time to start therapy was 31 days.
Dr. Nowakowski and his colleagues had previously shown that time to treatment is an important prognostic factor in DLBCL.
The efficacy evaluation included 145 patients assigned to R2-CHOP, and 135 assigned to R-CHOP. Primary reasons for exclusion were ineligibity following central pathology review or lack of diagnostic material for review.
After a median follow-up of 2.5 years, R2-CHOP was associated with a 34% improvement in progression-free survival, the primary endpoint (hazard ratio [HR] 0.66, P = .03). The 1-year progression-free survival rates were 83% with R2-CHOP and 73% with R-CHOP. Respective 2-year progression-free survival rates were 76% and 70%.
There was no significant difference, however, in the secondary overall survival endpoints with 1-year and 2-year overall survival of 93% vs. 87% and 86% vs. 80%, respectively.
Similarly, there was no difference in rates of PET-ascertained complete response, at 72% with R2-CHOP and 67% with R-CHOP.
R2-CHOP showed greater benefit across most subgroups, including patients with lower IPI score, patients with bulky disease, patients younger than 60 years, women, and patients with shorter time to treatment. There were also nonsignificant trends hinting at better outcomes with R2-CHOP, regardless of cell of origin.
Toxicities were typical for R-CHOP, although patients on R2-CHOP had significantly higher rates of grade 3 or 4 diarrhea, febrile neutropenia, and thrombocytopenia.
In addition to the trial differences mentioned previously, the differences in outcomes might be explained by the possibility that lenalidomide activity is not restricted to ABC DLBCL, Dr. Shipp said.
“One of the things that’s important to remember about lenalidomide is that it’s an immunomodulating agent and it has also has effects on tumor-infiltrating T cells,” she said.
Differences in response to therapy may also be explained by recent findings showing genetic heterogeneity in transcription-defined ABC DLBCLs, she said.
ECOG-ACRIN 1412 was supported by the National Cancer Institute and by Celgene. Dr. Nowakowski reported consulting/advising for and research funding from Celgene and others. Dr. Shipp reported consulting/advising for Bristol-Myers Squibb, honoraria from BMS and AstraZeneca, and institutional research funding from BMS and Bayer.
SOURCE: Nowakowski GS et al. 15-ICML, Abstract 006.
REPORTING FROM 15-ICML
The changing epidemiology of hepatocellular carcinoma
Three main changes characterize the secular trends in the incidence of hepatocellular carcinoma (HCC) in the United States. First, the overall incidence and mortality rates of HCC have been rising for the past 3 decades. Second, Hispanics are disproportionately affected by the HCC increase and have recently surpassed Asian Americans as the racial/ethnic group at highest HCC risk. Third, Southern and Western states have registered higher incidence rates of HCC than did the rest of the country, with Texas having the highest rates.
There are significant racial/ethnic differences in the population distribution of HCC risk factors, notably the disproportionately high prevalence of metabolic syndrome (e.g., obesity, abdominal obesity, and diabetes) and nonalcoholic fatty liver disease (NAFLD) in Hispanics. This observation may explain some of the findings in the secular trends of HCC described above. Most, but not all, studies have reported modest increases in relative risk of HCC in persons with obesity as measured by body mass index. However, studies investigating more specific obesity measures such as obesity in early adulthood or abdominal obesity reported higher and more consistent HCC risk than did those using body mass index. Hispanics have been shown to have a higher proportion of abdominal, especially visceral fat, than African Americans. The prevalence of NAFLD in the United States has doubled over the last 2 decades, and is estimated to affect 15%-20% of adults overall, but up to 30% in adult Texas Hispanics. Recently, a large cohort study including 296,707 patients with NAFLD and an equal number of matched controls without NAFLD from 130 facilities of the Department of Veterans Affairs found that patients with NAFLD had several-fold higher HCC risk than controls. The study also reported that HCC incidence rates for patients with NAFLD ranged from 1.6 to 23.7 per 1000 person-years, with the highest risk among older Hispanic patients with cirrhosis. Approximately 20% of patients with NAFLD and HCC had no evidence of cirrhosis. Lastly, type 2 diabetes, a condition that also is disproportionately higher in Hispanics than in other racial/ethnic groups in the United States has been consistently associated with an approximately twofold increase in the risk of HCC.
Risk factors for cirrhosis and HCC in contemporary clinical practice, and to a lesser extent, in the general population have shifted from active viral hepatitis to resolved hepatitis C infection or adequately suppressed hepatitis B infection as well as alcoholic liver disease and NAFLD. The shift from uncommon risk factors that carry a considerable increased risk of cirrhosis and HCC (active hepatitis C virus, hepatitis B virus) to more common but weaker risk factors (alcohol, NAFLD) is likely to result in a larger pool of chronic liver disease patients at risk for developing cirrhosis and HCC. However, given that the relative risk of HCC is lower with these emerging risk factors, it also will become increasingly difficult to define the highest-risk groups in need of interventions or monitoring. Therefore, there is a clear need for risk-stratification tools for cirrhosis and HCC in patients with HCV and a sustained virologic response, adequate HBV suppression, alcoholic liver disease, and NAFLD.
Dr. El-Serag is with the section of gastroenterology and hepatology, department of medicine, Baylor College of Medicine, Houston. Dr. El-Serag made these comments during the AGA Institute Presidential Plenary at the annual Digestive Disease Week®.
Three main changes characterize the secular trends in the incidence of hepatocellular carcinoma (HCC) in the United States. First, the overall incidence and mortality rates of HCC have been rising for the past 3 decades. Second, Hispanics are disproportionately affected by the HCC increase and have recently surpassed Asian Americans as the racial/ethnic group at highest HCC risk. Third, Southern and Western states have registered higher incidence rates of HCC than did the rest of the country, with Texas having the highest rates.
There are significant racial/ethnic differences in the population distribution of HCC risk factors, notably the disproportionately high prevalence of metabolic syndrome (e.g., obesity, abdominal obesity, and diabetes) and nonalcoholic fatty liver disease (NAFLD) in Hispanics. This observation may explain some of the findings in the secular trends of HCC described above. Most, but not all, studies have reported modest increases in relative risk of HCC in persons with obesity as measured by body mass index. However, studies investigating more specific obesity measures such as obesity in early adulthood or abdominal obesity reported higher and more consistent HCC risk than did those using body mass index. Hispanics have been shown to have a higher proportion of abdominal, especially visceral fat, than African Americans. The prevalence of NAFLD in the United States has doubled over the last 2 decades, and is estimated to affect 15%-20% of adults overall, but up to 30% in adult Texas Hispanics. Recently, a large cohort study including 296,707 patients with NAFLD and an equal number of matched controls without NAFLD from 130 facilities of the Department of Veterans Affairs found that patients with NAFLD had several-fold higher HCC risk than controls. The study also reported that HCC incidence rates for patients with NAFLD ranged from 1.6 to 23.7 per 1000 person-years, with the highest risk among older Hispanic patients with cirrhosis. Approximately 20% of patients with NAFLD and HCC had no evidence of cirrhosis. Lastly, type 2 diabetes, a condition that also is disproportionately higher in Hispanics than in other racial/ethnic groups in the United States has been consistently associated with an approximately twofold increase in the risk of HCC.
Risk factors for cirrhosis and HCC in contemporary clinical practice, and to a lesser extent, in the general population have shifted from active viral hepatitis to resolved hepatitis C infection or adequately suppressed hepatitis B infection as well as alcoholic liver disease and NAFLD. The shift from uncommon risk factors that carry a considerable increased risk of cirrhosis and HCC (active hepatitis C virus, hepatitis B virus) to more common but weaker risk factors (alcohol, NAFLD) is likely to result in a larger pool of chronic liver disease patients at risk for developing cirrhosis and HCC. However, given that the relative risk of HCC is lower with these emerging risk factors, it also will become increasingly difficult to define the highest-risk groups in need of interventions or monitoring. Therefore, there is a clear need for risk-stratification tools for cirrhosis and HCC in patients with HCV and a sustained virologic response, adequate HBV suppression, alcoholic liver disease, and NAFLD.
Dr. El-Serag is with the section of gastroenterology and hepatology, department of medicine, Baylor College of Medicine, Houston. Dr. El-Serag made these comments during the AGA Institute Presidential Plenary at the annual Digestive Disease Week®.
Three main changes characterize the secular trends in the incidence of hepatocellular carcinoma (HCC) in the United States. First, the overall incidence and mortality rates of HCC have been rising for the past 3 decades. Second, Hispanics are disproportionately affected by the HCC increase and have recently surpassed Asian Americans as the racial/ethnic group at highest HCC risk. Third, Southern and Western states have registered higher incidence rates of HCC than did the rest of the country, with Texas having the highest rates.
There are significant racial/ethnic differences in the population distribution of HCC risk factors, notably the disproportionately high prevalence of metabolic syndrome (e.g., obesity, abdominal obesity, and diabetes) and nonalcoholic fatty liver disease (NAFLD) in Hispanics. This observation may explain some of the findings in the secular trends of HCC described above. Most, but not all, studies have reported modest increases in relative risk of HCC in persons with obesity as measured by body mass index. However, studies investigating more specific obesity measures such as obesity in early adulthood or abdominal obesity reported higher and more consistent HCC risk than did those using body mass index. Hispanics have been shown to have a higher proportion of abdominal, especially visceral fat, than African Americans. The prevalence of NAFLD in the United States has doubled over the last 2 decades, and is estimated to affect 15%-20% of adults overall, but up to 30% in adult Texas Hispanics. Recently, a large cohort study including 296,707 patients with NAFLD and an equal number of matched controls without NAFLD from 130 facilities of the Department of Veterans Affairs found that patients with NAFLD had several-fold higher HCC risk than controls. The study also reported that HCC incidence rates for patients with NAFLD ranged from 1.6 to 23.7 per 1000 person-years, with the highest risk among older Hispanic patients with cirrhosis. Approximately 20% of patients with NAFLD and HCC had no evidence of cirrhosis. Lastly, type 2 diabetes, a condition that also is disproportionately higher in Hispanics than in other racial/ethnic groups in the United States has been consistently associated with an approximately twofold increase in the risk of HCC.
Risk factors for cirrhosis and HCC in contemporary clinical practice, and to a lesser extent, in the general population have shifted from active viral hepatitis to resolved hepatitis C infection or adequately suppressed hepatitis B infection as well as alcoholic liver disease and NAFLD. The shift from uncommon risk factors that carry a considerable increased risk of cirrhosis and HCC (active hepatitis C virus, hepatitis B virus) to more common but weaker risk factors (alcohol, NAFLD) is likely to result in a larger pool of chronic liver disease patients at risk for developing cirrhosis and HCC. However, given that the relative risk of HCC is lower with these emerging risk factors, it also will become increasingly difficult to define the highest-risk groups in need of interventions or monitoring. Therefore, there is a clear need for risk-stratification tools for cirrhosis and HCC in patients with HCV and a sustained virologic response, adequate HBV suppression, alcoholic liver disease, and NAFLD.
Dr. El-Serag is with the section of gastroenterology and hepatology, department of medicine, Baylor College of Medicine, Houston. Dr. El-Serag made these comments during the AGA Institute Presidential Plenary at the annual Digestive Disease Week®.
New COPD subtypes help refine risk
Chronic obstructive pulmonary disease (COPD) is often heterogeneous in its presentation and prognosis, and neither pulmonary function tests nor CT alone are always adequate to characterize a patient’s disease. a study has found.
In a paper published in CHEST, Jinkyeong Park, MD, PhD, of Dongguk University Ilsan Hospital in Goyang, South Korea, and colleagues looked at data from 9,080 subjects enrolled in the COPDGene study, an observational cohort of longtime smokers with and without COPD. By assessing visually defined patterns of emphysema with quantitative imaging features and spirometry data, the researchers identified 10 distinct subtypes of COPD (including no disease) and noted significant differences in mortality and progression among them.
Dr. Park and colleagues found that patients in the subgroups with quantitative but no visual emphysema and those with visual but not quantitative emphysema represented unique groups with mild COPD that were both at risk for progression – but with likely different underlying mechanisms. Current smokers, women, and whites were more common among subjects showing visually defined emphysema without quantitative evidence. “Many of the subjects in the visual-only emphysema subtype have areas of low lung density due to emphysema masked by smoking-induced lung inflammation,” the researchers wrote.
Overall 5-year mortality differed significantly among the groups (P less than .01) and was highest in the three groups with moderate to severe centrilobular emphysema. Patients with paraseptal and moderate to severe centrilobular emphysema showed substantial progression of emphysema over 5 years, compared with individuals with no CT abnormality (P less than .05).
“These results suggest that the combination of visual and quantitative CT features, which may reflect different underlying pathobiological processes in COPD, may provide a superior approach to classify individuals with COPD, compared to the use of visual or quantitative CT features alone,” the researchers wrote.
The study received funding from the National Heart, Lung and Blood Institute. Three of the study’s coauthors reported conflicts of interest in the form of patent applications or financial support from pharmaceutical firms. The COPDGene Project receives pharmaceutical industry and U.S. government support.
SOURCE: Park J et al. CHEST. 2019 Jul 5. doi:10:1016/j.chest.2019.06.15.
Chronic obstructive pulmonary disease (COPD) is often heterogeneous in its presentation and prognosis, and neither pulmonary function tests nor CT alone are always adequate to characterize a patient’s disease. a study has found.
In a paper published in CHEST, Jinkyeong Park, MD, PhD, of Dongguk University Ilsan Hospital in Goyang, South Korea, and colleagues looked at data from 9,080 subjects enrolled in the COPDGene study, an observational cohort of longtime smokers with and without COPD. By assessing visually defined patterns of emphysema with quantitative imaging features and spirometry data, the researchers identified 10 distinct subtypes of COPD (including no disease) and noted significant differences in mortality and progression among them.
Dr. Park and colleagues found that patients in the subgroups with quantitative but no visual emphysema and those with visual but not quantitative emphysema represented unique groups with mild COPD that were both at risk for progression – but with likely different underlying mechanisms. Current smokers, women, and whites were more common among subjects showing visually defined emphysema without quantitative evidence. “Many of the subjects in the visual-only emphysema subtype have areas of low lung density due to emphysema masked by smoking-induced lung inflammation,” the researchers wrote.
Overall 5-year mortality differed significantly among the groups (P less than .01) and was highest in the three groups with moderate to severe centrilobular emphysema. Patients with paraseptal and moderate to severe centrilobular emphysema showed substantial progression of emphysema over 5 years, compared with individuals with no CT abnormality (P less than .05).
“These results suggest that the combination of visual and quantitative CT features, which may reflect different underlying pathobiological processes in COPD, may provide a superior approach to classify individuals with COPD, compared to the use of visual or quantitative CT features alone,” the researchers wrote.
The study received funding from the National Heart, Lung and Blood Institute. Three of the study’s coauthors reported conflicts of interest in the form of patent applications or financial support from pharmaceutical firms. The COPDGene Project receives pharmaceutical industry and U.S. government support.
SOURCE: Park J et al. CHEST. 2019 Jul 5. doi:10:1016/j.chest.2019.06.15.
Chronic obstructive pulmonary disease (COPD) is often heterogeneous in its presentation and prognosis, and neither pulmonary function tests nor CT alone are always adequate to characterize a patient’s disease. a study has found.
In a paper published in CHEST, Jinkyeong Park, MD, PhD, of Dongguk University Ilsan Hospital in Goyang, South Korea, and colleagues looked at data from 9,080 subjects enrolled in the COPDGene study, an observational cohort of longtime smokers with and without COPD. By assessing visually defined patterns of emphysema with quantitative imaging features and spirometry data, the researchers identified 10 distinct subtypes of COPD (including no disease) and noted significant differences in mortality and progression among them.
Dr. Park and colleagues found that patients in the subgroups with quantitative but no visual emphysema and those with visual but not quantitative emphysema represented unique groups with mild COPD that were both at risk for progression – but with likely different underlying mechanisms. Current smokers, women, and whites were more common among subjects showing visually defined emphysema without quantitative evidence. “Many of the subjects in the visual-only emphysema subtype have areas of low lung density due to emphysema masked by smoking-induced lung inflammation,” the researchers wrote.
Overall 5-year mortality differed significantly among the groups (P less than .01) and was highest in the three groups with moderate to severe centrilobular emphysema. Patients with paraseptal and moderate to severe centrilobular emphysema showed substantial progression of emphysema over 5 years, compared with individuals with no CT abnormality (P less than .05).
“These results suggest that the combination of visual and quantitative CT features, which may reflect different underlying pathobiological processes in COPD, may provide a superior approach to classify individuals with COPD, compared to the use of visual or quantitative CT features alone,” the researchers wrote.
The study received funding from the National Heart, Lung and Blood Institute. Three of the study’s coauthors reported conflicts of interest in the form of patent applications or financial support from pharmaceutical firms. The COPDGene Project receives pharmaceutical industry and U.S. government support.
SOURCE: Park J et al. CHEST. 2019 Jul 5. doi:10:1016/j.chest.2019.06.15.
FROM CHEST
Endoscopic treatment effective in T1b esophageal cancer
Findings from a systematic review may help guide treatment of patients with T1b esophageal cancer.
The review suggests that endoscopic submucosal dissection and endoscopic mucosal resection are appropriate for T1b esophageal cancers with a low risk of metastasis. The authors identified several factors associated with a higher risk of lymph node metastasis and said patients with these risk factors may benefit from adjuvant chemotherapy and radiation.
Mohamed O. Othman, MD, of Baylor College of Medicine, Houston, and colleagues conducted the review. Their report is in Clinical Gastroenterology and Hepatology.
The authors cited studies suggesting that survival rates would not be significantly different among early-stage esophageal cancer patients who undergo esophagectomy and those who receive endoscopic treatment, in the absence of lymph node metastasis. The risk of lymph node metastasis is higher in esophageal squamous cell carcinoma (ESCC) than in esophageal adenocarcinoma (EAC), and in those with deeper submucosal invasion (greater than 200 microm for ESCC or greater than 500 microm for EAC). Patients also have a higher risk of lymph node metastasis if they have poorly differentiated tumors, tumors larger than 2 cm, or lymphovascular invasion.
In the studies cited in the review, overall 5-year survival for esophageal squamous cell CA (ESCC) ranged from 68.6% (chemoradiation therapy alone) to 75% (endoscopic resection followed by chemoradiation), compared with 77.7% for surgery. For esophageal adenocarcinoma (EAC), there is less data but greater efficacy, with one study demonstrating 5-year overall survival of 93.9% in the ESD group compared with 97.3% in the surgery group. However, only approximately 15 patients in this study were diagnosed T1b.
The authors concluded that “ESD or EMR can be successfully applied to submucosal invasive cancers that have a low risk of metastatic potential....Future research should focus on novel biological and immunohistochemistry markers which can aid in the prediction of tumor behavior and lymph node metastasis status in T1b esophageal cancer.”
The authors disclosed relationships with Olympus, Boston Scientific, Lumendi, Aries Pharmaceutical, and Fujinon.
SOURCE: Othman MO et al. Clin Gastroenterol Hepatol 2019. doi: 10.1016/j.cgh.2019.05.045.
Findings from a systematic review may help guide treatment of patients with T1b esophageal cancer.
The review suggests that endoscopic submucosal dissection and endoscopic mucosal resection are appropriate for T1b esophageal cancers with a low risk of metastasis. The authors identified several factors associated with a higher risk of lymph node metastasis and said patients with these risk factors may benefit from adjuvant chemotherapy and radiation.
Mohamed O. Othman, MD, of Baylor College of Medicine, Houston, and colleagues conducted the review. Their report is in Clinical Gastroenterology and Hepatology.
The authors cited studies suggesting that survival rates would not be significantly different among early-stage esophageal cancer patients who undergo esophagectomy and those who receive endoscopic treatment, in the absence of lymph node metastasis. The risk of lymph node metastasis is higher in esophageal squamous cell carcinoma (ESCC) than in esophageal adenocarcinoma (EAC), and in those with deeper submucosal invasion (greater than 200 microm for ESCC or greater than 500 microm for EAC). Patients also have a higher risk of lymph node metastasis if they have poorly differentiated tumors, tumors larger than 2 cm, or lymphovascular invasion.
In the studies cited in the review, overall 5-year survival for esophageal squamous cell CA (ESCC) ranged from 68.6% (chemoradiation therapy alone) to 75% (endoscopic resection followed by chemoradiation), compared with 77.7% for surgery. For esophageal adenocarcinoma (EAC), there is less data but greater efficacy, with one study demonstrating 5-year overall survival of 93.9% in the ESD group compared with 97.3% in the surgery group. However, only approximately 15 patients in this study were diagnosed T1b.
The authors concluded that “ESD or EMR can be successfully applied to submucosal invasive cancers that have a low risk of metastatic potential....Future research should focus on novel biological and immunohistochemistry markers which can aid in the prediction of tumor behavior and lymph node metastasis status in T1b esophageal cancer.”
The authors disclosed relationships with Olympus, Boston Scientific, Lumendi, Aries Pharmaceutical, and Fujinon.
SOURCE: Othman MO et al. Clin Gastroenterol Hepatol 2019. doi: 10.1016/j.cgh.2019.05.045.
Findings from a systematic review may help guide treatment of patients with T1b esophageal cancer.
The review suggests that endoscopic submucosal dissection and endoscopic mucosal resection are appropriate for T1b esophageal cancers with a low risk of metastasis. The authors identified several factors associated with a higher risk of lymph node metastasis and said patients with these risk factors may benefit from adjuvant chemotherapy and radiation.
Mohamed O. Othman, MD, of Baylor College of Medicine, Houston, and colleagues conducted the review. Their report is in Clinical Gastroenterology and Hepatology.
The authors cited studies suggesting that survival rates would not be significantly different among early-stage esophageal cancer patients who undergo esophagectomy and those who receive endoscopic treatment, in the absence of lymph node metastasis. The risk of lymph node metastasis is higher in esophageal squamous cell carcinoma (ESCC) than in esophageal adenocarcinoma (EAC), and in those with deeper submucosal invasion (greater than 200 microm for ESCC or greater than 500 microm for EAC). Patients also have a higher risk of lymph node metastasis if they have poorly differentiated tumors, tumors larger than 2 cm, or lymphovascular invasion.
In the studies cited in the review, overall 5-year survival for esophageal squamous cell CA (ESCC) ranged from 68.6% (chemoradiation therapy alone) to 75% (endoscopic resection followed by chemoradiation), compared with 77.7% for surgery. For esophageal adenocarcinoma (EAC), there is less data but greater efficacy, with one study demonstrating 5-year overall survival of 93.9% in the ESD group compared with 97.3% in the surgery group. However, only approximately 15 patients in this study were diagnosed T1b.
The authors concluded that “ESD or EMR can be successfully applied to submucosal invasive cancers that have a low risk of metastatic potential....Future research should focus on novel biological and immunohistochemistry markers which can aid in the prediction of tumor behavior and lymph node metastasis status in T1b esophageal cancer.”
The authors disclosed relationships with Olympus, Boston Scientific, Lumendi, Aries Pharmaceutical, and Fujinon.
SOURCE: Othman MO et al. Clin Gastroenterol Hepatol 2019. doi: 10.1016/j.cgh.2019.05.045.
FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
Caution is key when pregnancy and psoriasis mix
NEWPORT BEACH, CALIF. – Psoriasis often clears in pregnant women, giving them a rare break from the skin disease. But
Data from 2011 found 45% of pregnancies in U.S. women aged 15-44 years were unintended (N Engl J Med. 2016 Mar 3;374[9]:843-52), cautioned Jashin J. Wu, MD, of Dermatology Research and Education Foundation, Irvine, Calif.
In a presentation at the Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar, Dr. Wu offered these tips about pregnancy and psoriasis:
Counsel patients before pregnancy
There’s conflicting data about the risks of psoriasis in pregnancy, Dr. Wu said. One 23-year-old study suggests a link to adverse outcomes such as preterm and low-birth-weight babies. But another more recent study found no sign of increased risk (Int J Dermatol. 1996;35:169-72; J Am Acad Dermatol. 2011;64:71-7).
Counseling can include information about risks such as hospitalization during pregnancy because of undertreatment of psoriasis, he said. Discuss lowering medication doses to the lowest effective dose, he recommended, and talk about alternatives to systemic medications.
Make adjustments to timing as needed
In patients with severe cases, it may be appropriate to recommend that they postpone pregnancy until their psoriasis is under better control. As for treatment of psoriasis, “you may want to consider timing medication to end around the first trimester to get the medication out of them during the greatest risk period for the baby,” Dr. Wu said.
Adjust steroids as necessary
There are no “good” studies about the use of steroids in pregnant women with psoriasis, Dr. Wu said. “We can probably assume they are safe overall. Weaker steroids may have less risk,” and some of the stronger steroids may raise concerns.
Dr. Wu made these recommendations: Limit mild-potency topical corticosteroids to less than 100 g/week, potent topical corticosteroids to less than 50 g/week, and superpotent topical corticosteroids to less than 30 g/week.
Some topical drugs appear to be OK
Vitamin D analogues have not been well-studied in pregnancy, he said, but “we consider topical use to be fairly safe.”
There’s no data on calcineurin inhibitors in pregnancy, he said, but topical use is considered to be safe because there’s limited systemic absorption.
Beware of certain drugs in pregnancyTazarotene is considered to be dangerous in pregnancy, Dr. Wu said, and females of childbearing age who take it should use effective contraception, and have a recent negative pregnancy test (within 2 weeks before treatment begins). “In general, I’d probably not use this,” he said. “We have so many other options.”
Data about pregnancy safety for three topical drugs – coal tar, anthralin, and salicylic acid – is limited or nonexistent, Dr. Wu said, and he recommends against their use in pregnancy.
Phototherapy is OK in pregnancy
Phototherapy is considered safe because UVB doesn’t penetrate the superficial layer of the skin, he said. But phototherapy brings a potential risk of lowered folic acid levels, and he urges folic acid supplementation in women undergoing the treatment who are considering pregnancy or who are in the first trimester.
Avoid certain systemic drugs
Dr. Wu offered these recommendations:
- Methotrexate: Do not take during pregnancy, or 3 months prior to conception.
- Acitretin (Soriatane): Avoid all use in women who may become pregnant.
- Cyclosporine: Be aware of reports of prematurity and low birth weight linked to the drug.
- Apremilast (Otezla): Animal studies have shown a risk in pregnancy. Stop the drug at least 2 days before conception.
Avoid monoclonal antibodies
These drugs “result in therapeutic levels in the fetus, which is not a good thing,” Dr. Wu said. “You obviously don’t want to have monoclonal antibodies in the baby.”
Nix the PUVA
While one study found no link between psoralen plus UVA (PUVA) and birth defects (Arch Dermatol. 1993 Mar;129[3]:320-3), there’s still a theoretical risk, Dr. Wu said. He recommended that the treatment be avoided during pregnancy.
Watch for waxing and waning
Dr. Wu pointed to a small 2005 study that suggested that psoriasis activity declines during pregnancy. The study used different measures, finding that psoriasis improved by 30% (based on at least a 3% change in body surface area) or 55% (based on patient self-reporting). But it flares after pregnancy as reported by 65% of women surveyed; a body surface area analysis found that psoriasis worsened in 41% (Arch Dermatol. 2005 May;141[5]:601-6).
Dr. Wu reports various relationships (research, consultation and speaking) with 15 pharmaceutical companies. SDEF and this news organization are owned by the same parent company.
NEWPORT BEACH, CALIF. – Psoriasis often clears in pregnant women, giving them a rare break from the skin disease. But
Data from 2011 found 45% of pregnancies in U.S. women aged 15-44 years were unintended (N Engl J Med. 2016 Mar 3;374[9]:843-52), cautioned Jashin J. Wu, MD, of Dermatology Research and Education Foundation, Irvine, Calif.
In a presentation at the Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar, Dr. Wu offered these tips about pregnancy and psoriasis:
Counsel patients before pregnancy
There’s conflicting data about the risks of psoriasis in pregnancy, Dr. Wu said. One 23-year-old study suggests a link to adverse outcomes such as preterm and low-birth-weight babies. But another more recent study found no sign of increased risk (Int J Dermatol. 1996;35:169-72; J Am Acad Dermatol. 2011;64:71-7).
Counseling can include information about risks such as hospitalization during pregnancy because of undertreatment of psoriasis, he said. Discuss lowering medication doses to the lowest effective dose, he recommended, and talk about alternatives to systemic medications.
Make adjustments to timing as needed
In patients with severe cases, it may be appropriate to recommend that they postpone pregnancy until their psoriasis is under better control. As for treatment of psoriasis, “you may want to consider timing medication to end around the first trimester to get the medication out of them during the greatest risk period for the baby,” Dr. Wu said.
Adjust steroids as necessary
There are no “good” studies about the use of steroids in pregnant women with psoriasis, Dr. Wu said. “We can probably assume they are safe overall. Weaker steroids may have less risk,” and some of the stronger steroids may raise concerns.
Dr. Wu made these recommendations: Limit mild-potency topical corticosteroids to less than 100 g/week, potent topical corticosteroids to less than 50 g/week, and superpotent topical corticosteroids to less than 30 g/week.
Some topical drugs appear to be OK
Vitamin D analogues have not been well-studied in pregnancy, he said, but “we consider topical use to be fairly safe.”
There’s no data on calcineurin inhibitors in pregnancy, he said, but topical use is considered to be safe because there’s limited systemic absorption.
Beware of certain drugs in pregnancyTazarotene is considered to be dangerous in pregnancy, Dr. Wu said, and females of childbearing age who take it should use effective contraception, and have a recent negative pregnancy test (within 2 weeks before treatment begins). “In general, I’d probably not use this,” he said. “We have so many other options.”
Data about pregnancy safety for three topical drugs – coal tar, anthralin, and salicylic acid – is limited or nonexistent, Dr. Wu said, and he recommends against their use in pregnancy.
Phototherapy is OK in pregnancy
Phototherapy is considered safe because UVB doesn’t penetrate the superficial layer of the skin, he said. But phototherapy brings a potential risk of lowered folic acid levels, and he urges folic acid supplementation in women undergoing the treatment who are considering pregnancy or who are in the first trimester.
Avoid certain systemic drugs
Dr. Wu offered these recommendations:
- Methotrexate: Do not take during pregnancy, or 3 months prior to conception.
- Acitretin (Soriatane): Avoid all use in women who may become pregnant.
- Cyclosporine: Be aware of reports of prematurity and low birth weight linked to the drug.
- Apremilast (Otezla): Animal studies have shown a risk in pregnancy. Stop the drug at least 2 days before conception.
Avoid monoclonal antibodies
These drugs “result in therapeutic levels in the fetus, which is not a good thing,” Dr. Wu said. “You obviously don’t want to have monoclonal antibodies in the baby.”
Nix the PUVA
While one study found no link between psoralen plus UVA (PUVA) and birth defects (Arch Dermatol. 1993 Mar;129[3]:320-3), there’s still a theoretical risk, Dr. Wu said. He recommended that the treatment be avoided during pregnancy.
Watch for waxing and waning
Dr. Wu pointed to a small 2005 study that suggested that psoriasis activity declines during pregnancy. The study used different measures, finding that psoriasis improved by 30% (based on at least a 3% change in body surface area) or 55% (based on patient self-reporting). But it flares after pregnancy as reported by 65% of women surveyed; a body surface area analysis found that psoriasis worsened in 41% (Arch Dermatol. 2005 May;141[5]:601-6).
Dr. Wu reports various relationships (research, consultation and speaking) with 15 pharmaceutical companies. SDEF and this news organization are owned by the same parent company.
NEWPORT BEACH, CALIF. – Psoriasis often clears in pregnant women, giving them a rare break from the skin disease. But
Data from 2011 found 45% of pregnancies in U.S. women aged 15-44 years were unintended (N Engl J Med. 2016 Mar 3;374[9]:843-52), cautioned Jashin J. Wu, MD, of Dermatology Research and Education Foundation, Irvine, Calif.
In a presentation at the Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar, Dr. Wu offered these tips about pregnancy and psoriasis:
Counsel patients before pregnancy
There’s conflicting data about the risks of psoriasis in pregnancy, Dr. Wu said. One 23-year-old study suggests a link to adverse outcomes such as preterm and low-birth-weight babies. But another more recent study found no sign of increased risk (Int J Dermatol. 1996;35:169-72; J Am Acad Dermatol. 2011;64:71-7).
Counseling can include information about risks such as hospitalization during pregnancy because of undertreatment of psoriasis, he said. Discuss lowering medication doses to the lowest effective dose, he recommended, and talk about alternatives to systemic medications.
Make adjustments to timing as needed
In patients with severe cases, it may be appropriate to recommend that they postpone pregnancy until their psoriasis is under better control. As for treatment of psoriasis, “you may want to consider timing medication to end around the first trimester to get the medication out of them during the greatest risk period for the baby,” Dr. Wu said.
Adjust steroids as necessary
There are no “good” studies about the use of steroids in pregnant women with psoriasis, Dr. Wu said. “We can probably assume they are safe overall. Weaker steroids may have less risk,” and some of the stronger steroids may raise concerns.
Dr. Wu made these recommendations: Limit mild-potency topical corticosteroids to less than 100 g/week, potent topical corticosteroids to less than 50 g/week, and superpotent topical corticosteroids to less than 30 g/week.
Some topical drugs appear to be OK
Vitamin D analogues have not been well-studied in pregnancy, he said, but “we consider topical use to be fairly safe.”
There’s no data on calcineurin inhibitors in pregnancy, he said, but topical use is considered to be safe because there’s limited systemic absorption.
Beware of certain drugs in pregnancyTazarotene is considered to be dangerous in pregnancy, Dr. Wu said, and females of childbearing age who take it should use effective contraception, and have a recent negative pregnancy test (within 2 weeks before treatment begins). “In general, I’d probably not use this,” he said. “We have so many other options.”
Data about pregnancy safety for three topical drugs – coal tar, anthralin, and salicylic acid – is limited or nonexistent, Dr. Wu said, and he recommends against their use in pregnancy.
Phototherapy is OK in pregnancy
Phototherapy is considered safe because UVB doesn’t penetrate the superficial layer of the skin, he said. But phototherapy brings a potential risk of lowered folic acid levels, and he urges folic acid supplementation in women undergoing the treatment who are considering pregnancy or who are in the first trimester.
Avoid certain systemic drugs
Dr. Wu offered these recommendations:
- Methotrexate: Do not take during pregnancy, or 3 months prior to conception.
- Acitretin (Soriatane): Avoid all use in women who may become pregnant.
- Cyclosporine: Be aware of reports of prematurity and low birth weight linked to the drug.
- Apremilast (Otezla): Animal studies have shown a risk in pregnancy. Stop the drug at least 2 days before conception.
Avoid monoclonal antibodies
These drugs “result in therapeutic levels in the fetus, which is not a good thing,” Dr. Wu said. “You obviously don’t want to have monoclonal antibodies in the baby.”
Nix the PUVA
While one study found no link between psoralen plus UVA (PUVA) and birth defects (Arch Dermatol. 1993 Mar;129[3]:320-3), there’s still a theoretical risk, Dr. Wu said. He recommended that the treatment be avoided during pregnancy.
Watch for waxing and waning
Dr. Wu pointed to a small 2005 study that suggested that psoriasis activity declines during pregnancy. The study used different measures, finding that psoriasis improved by 30% (based on at least a 3% change in body surface area) or 55% (based on patient self-reporting). But it flares after pregnancy as reported by 65% of women surveyed; a body surface area analysis found that psoriasis worsened in 41% (Arch Dermatol. 2005 May;141[5]:601-6).
Dr. Wu reports various relationships (research, consultation and speaking) with 15 pharmaceutical companies. SDEF and this news organization are owned by the same parent company.
EXPERT ANALYSIS FROM SDEF WOMEN’S & PEDIATRIC DERMATOLOGY SEMINAR
White light exposure is associated with acute risk of headache in migraine
PHILADELPHIA – , according to research presented at the annual meeting of the American Headache Society. The data raise the question of whether modifying light exposure could reduce headache frequency in this population, said Suzanne M. Bertisch, MD, MPH, a physician and clinical investigator in the division of sleep and circadian disorders at Brigham and Women’s Hospital in Boston.
About 40% of patients with migraine identify light as a trigger. Most studies that have examined the association between light and migraine onset have been retrospective and have relied on subjective measures of light exposure.
From March 2016 to August 2017, Dr. Bertisch and colleagues enrolled 101 adults with episodic migraine into a prospective cohort study. For 79 of these participants, light exposure was measured continuously for 6 weeks by actigraph. In the morning and evening, participants recorded data such as headache onset, duration, and intensity in electronic headache diaries. They also recorded data about covariates such as caffeine intake, alcohol intake, sleep, and stress.
Dr. Bertisch and colleagues divided the day into four 6-hour periods and calculated mean light exposure within each period. After researchers adjusted for covariates, they found that higher mean photopic illuminance was associated with a 12% higher risk of headache during the same period. Mean photopic illuminance was not associated with headache onset in the next period, however.
Dr. Bertisch had no disclosures relevant to this study.
PHILADELPHIA – , according to research presented at the annual meeting of the American Headache Society. The data raise the question of whether modifying light exposure could reduce headache frequency in this population, said Suzanne M. Bertisch, MD, MPH, a physician and clinical investigator in the division of sleep and circadian disorders at Brigham and Women’s Hospital in Boston.
About 40% of patients with migraine identify light as a trigger. Most studies that have examined the association between light and migraine onset have been retrospective and have relied on subjective measures of light exposure.
From March 2016 to August 2017, Dr. Bertisch and colleagues enrolled 101 adults with episodic migraine into a prospective cohort study. For 79 of these participants, light exposure was measured continuously for 6 weeks by actigraph. In the morning and evening, participants recorded data such as headache onset, duration, and intensity in electronic headache diaries. They also recorded data about covariates such as caffeine intake, alcohol intake, sleep, and stress.
Dr. Bertisch and colleagues divided the day into four 6-hour periods and calculated mean light exposure within each period. After researchers adjusted for covariates, they found that higher mean photopic illuminance was associated with a 12% higher risk of headache during the same period. Mean photopic illuminance was not associated with headache onset in the next period, however.
Dr. Bertisch had no disclosures relevant to this study.
PHILADELPHIA – , according to research presented at the annual meeting of the American Headache Society. The data raise the question of whether modifying light exposure could reduce headache frequency in this population, said Suzanne M. Bertisch, MD, MPH, a physician and clinical investigator in the division of sleep and circadian disorders at Brigham and Women’s Hospital in Boston.
About 40% of patients with migraine identify light as a trigger. Most studies that have examined the association between light and migraine onset have been retrospective and have relied on subjective measures of light exposure.
From March 2016 to August 2017, Dr. Bertisch and colleagues enrolled 101 adults with episodic migraine into a prospective cohort study. For 79 of these participants, light exposure was measured continuously for 6 weeks by actigraph. In the morning and evening, participants recorded data such as headache onset, duration, and intensity in electronic headache diaries. They also recorded data about covariates such as caffeine intake, alcohol intake, sleep, and stress.
Dr. Bertisch and colleagues divided the day into four 6-hour periods and calculated mean light exposure within each period. After researchers adjusted for covariates, they found that higher mean photopic illuminance was associated with a 12% higher risk of headache during the same period. Mean photopic illuminance was not associated with headache onset in the next period, however.
Dr. Bertisch had no disclosures relevant to this study.
EXPERT ANALYSIS FROM AHS 2019
Almost half of sudden cardiac deaths linked to prior silent MI
Almost half of individuals who died of sudden cardiac death (SCD) had a myocardial scar at autopsy, indicating a prior silent myocardial infarction (SMI), in a case-controlled study.
The research team led by Juha H. Vähätalo, MD, from the University of Oulu (Finland), compared autopsy findings, clinical characteristics, and ECG markers associated with SMI in 5,869 people in Northern Finland who had sudden cardiac deaths during 1998-2017.
Overall, 75% of the deaths were caused by coronary artery disease (CAD), and of them, 71% had no previous diagnosis of CAD. Of these latter individuals, 42% had a myocardial scar at autopsy (detected by macroscopic and microscopic evaluation of myocardium), a finding that the authors said indicated a previous, unrecognized MI.
The analysis showed that individuals with SMI were slightly older, at 69.9 years, than were those with no SMI, at 65.5 years, and were more likely to be male (83.4% vs. 75.5%).
The group with prior SMI also died during physical activity at a greater rate than did those without (18.2% vs. 12.4%), the study authors reported in their paper published in JAMA Cardiology.
The research team obtained 438 ECGs prior to SCD; 187 in individuals with SMI and 251 in the group previously diagnosed with CAD.
Of the premortem ECGs in the individuals who had had an SCD after an SMI, 67% were abnormal, the researchers reported.
The SMI group had more frequently inverted T waves (16.6% vs. 8.4%) and pathologic Q waves (12.8% vs. 6.8%), compared with the non-SMI group. Both differences were statistically significant.
Fragmented QRS was the most common marker of a scar in the SMI group, however the authors noted that the fQRS complex was “probably a sensitive marker of myocardial scarring, but its specificity is not very high”.
Overall, having at least one of the following ECG abnormalities – fQRS, Q wave, T-wave inversion, or QRS of at least 110 msec – was more common in the SMI group (66.8%) compared with the non-SMI group (55.4%).
“Among patients in whom SCD without a prior MI is the first sign of cardiac disease, a previous ECG result is likely to be normal. ... ECGs were available only in 187 individuals with SMI, so the data are not sufficient to draw definite conclusions. Rather, they support motivation for further studies on this question,” the study authors noted.
“In the future, other, more efficient methods might be useful for diagnosing SMI, in addition to standard ECGs,” such as cardiac magnetic resonance imaging, but the cost-effectiveness “is likely to be unreasonable. Therefore, screening high-risk populations with ECG to identify individuals for further examinations would probably be reasonable,” they wrote.
The research team noted some limitations of the study such as the autopsy data not revealing the size of the scar detected in the myocardium and not all individuals had an ECG recorded prior to death.
SOURCE: JAMA Cardiol. 2019 Jul 10; doi: 10.1001/jamacardio.2019.2210
Almost half of individuals who died of sudden cardiac death (SCD) had a myocardial scar at autopsy, indicating a prior silent myocardial infarction (SMI), in a case-controlled study.
The research team led by Juha H. Vähätalo, MD, from the University of Oulu (Finland), compared autopsy findings, clinical characteristics, and ECG markers associated with SMI in 5,869 people in Northern Finland who had sudden cardiac deaths during 1998-2017.
Overall, 75% of the deaths were caused by coronary artery disease (CAD), and of them, 71% had no previous diagnosis of CAD. Of these latter individuals, 42% had a myocardial scar at autopsy (detected by macroscopic and microscopic evaluation of myocardium), a finding that the authors said indicated a previous, unrecognized MI.
The analysis showed that individuals with SMI were slightly older, at 69.9 years, than were those with no SMI, at 65.5 years, and were more likely to be male (83.4% vs. 75.5%).
The group with prior SMI also died during physical activity at a greater rate than did those without (18.2% vs. 12.4%), the study authors reported in their paper published in JAMA Cardiology.
The research team obtained 438 ECGs prior to SCD; 187 in individuals with SMI and 251 in the group previously diagnosed with CAD.
Of the premortem ECGs in the individuals who had had an SCD after an SMI, 67% were abnormal, the researchers reported.
The SMI group had more frequently inverted T waves (16.6% vs. 8.4%) and pathologic Q waves (12.8% vs. 6.8%), compared with the non-SMI group. Both differences were statistically significant.
Fragmented QRS was the most common marker of a scar in the SMI group, however the authors noted that the fQRS complex was “probably a sensitive marker of myocardial scarring, but its specificity is not very high”.
Overall, having at least one of the following ECG abnormalities – fQRS, Q wave, T-wave inversion, or QRS of at least 110 msec – was more common in the SMI group (66.8%) compared with the non-SMI group (55.4%).
“Among patients in whom SCD without a prior MI is the first sign of cardiac disease, a previous ECG result is likely to be normal. ... ECGs were available only in 187 individuals with SMI, so the data are not sufficient to draw definite conclusions. Rather, they support motivation for further studies on this question,” the study authors noted.
“In the future, other, more efficient methods might be useful for diagnosing SMI, in addition to standard ECGs,” such as cardiac magnetic resonance imaging, but the cost-effectiveness “is likely to be unreasonable. Therefore, screening high-risk populations with ECG to identify individuals for further examinations would probably be reasonable,” they wrote.
The research team noted some limitations of the study such as the autopsy data not revealing the size of the scar detected in the myocardium and not all individuals had an ECG recorded prior to death.
SOURCE: JAMA Cardiol. 2019 Jul 10; doi: 10.1001/jamacardio.2019.2210
Almost half of individuals who died of sudden cardiac death (SCD) had a myocardial scar at autopsy, indicating a prior silent myocardial infarction (SMI), in a case-controlled study.
The research team led by Juha H. Vähätalo, MD, from the University of Oulu (Finland), compared autopsy findings, clinical characteristics, and ECG markers associated with SMI in 5,869 people in Northern Finland who had sudden cardiac deaths during 1998-2017.
Overall, 75% of the deaths were caused by coronary artery disease (CAD), and of them, 71% had no previous diagnosis of CAD. Of these latter individuals, 42% had a myocardial scar at autopsy (detected by macroscopic and microscopic evaluation of myocardium), a finding that the authors said indicated a previous, unrecognized MI.
The analysis showed that individuals with SMI were slightly older, at 69.9 years, than were those with no SMI, at 65.5 years, and were more likely to be male (83.4% vs. 75.5%).
The group with prior SMI also died during physical activity at a greater rate than did those without (18.2% vs. 12.4%), the study authors reported in their paper published in JAMA Cardiology.
The research team obtained 438 ECGs prior to SCD; 187 in individuals with SMI and 251 in the group previously diagnosed with CAD.
Of the premortem ECGs in the individuals who had had an SCD after an SMI, 67% were abnormal, the researchers reported.
The SMI group had more frequently inverted T waves (16.6% vs. 8.4%) and pathologic Q waves (12.8% vs. 6.8%), compared with the non-SMI group. Both differences were statistically significant.
Fragmented QRS was the most common marker of a scar in the SMI group, however the authors noted that the fQRS complex was “probably a sensitive marker of myocardial scarring, but its specificity is not very high”.
Overall, having at least one of the following ECG abnormalities – fQRS, Q wave, T-wave inversion, or QRS of at least 110 msec – was more common in the SMI group (66.8%) compared with the non-SMI group (55.4%).
“Among patients in whom SCD without a prior MI is the first sign of cardiac disease, a previous ECG result is likely to be normal. ... ECGs were available only in 187 individuals with SMI, so the data are not sufficient to draw definite conclusions. Rather, they support motivation for further studies on this question,” the study authors noted.
“In the future, other, more efficient methods might be useful for diagnosing SMI, in addition to standard ECGs,” such as cardiac magnetic resonance imaging, but the cost-effectiveness “is likely to be unreasonable. Therefore, screening high-risk populations with ECG to identify individuals for further examinations would probably be reasonable,” they wrote.
The research team noted some limitations of the study such as the autopsy data not revealing the size of the scar detected in the myocardium and not all individuals had an ECG recorded prior to death.
SOURCE: JAMA Cardiol. 2019 Jul 10; doi: 10.1001/jamacardio.2019.2210
FROM JAMA CARDIOLOGY
Recertification: The FPHM option
ABIM now offers increased flexibility
Everyone always told me that my time in residency would fly by, and the 3 years of internal medicine training really did seem to pass in just a few moments. Before I knew it, I had passed my internal medicine boards and practiced hospital medicine at an academic medical center.
One day last fall, I received notice from the American Board of Internal Medicine that it was time to recertify. I was surprised – had it already been 10 years? What did I have to do to maintain my certification?
As I investigated what it would take to maintain certification, I discovered that the recertification process provided more flexibility, compared with original board certification. I now had the option to recertify in internal medicine with a Focused Practice in Hospital Medicine (FPHM). Beginning in 2014, ABIM offered hospitalists, or internists whose clinical practice is mainly in the inpatient setting, the option to recertify in internal medicine, but with the designation that highlighted their clinical practice in the inpatient setting.
The first step in recertification for me was deciding to recertify with the focus in hospital medicine or maintain the traditional internal medicine certification. I talked with several colleagues who are also practicing hospitalists and weighed their reasons for opting for FPHM. Ultimately, my decision to pursue a recertification with a focus in hospital medicine relied on three factors: First, my clinical practice since completing residency was exclusively in the inpatient setting. Day in and day out, I care for patients who are acutely ill and require inpatient medical care. Second, I wanted my board certification to reflect what I consider to be my area of clinical expertise, which is inpatient adult medicine. Pursuing the FPHM would provide that recognition. Finally, I wanted to study and be tested on topics that I could utilize in my day-to-day practice. Because I exclusively practiced hospital medicine since graduation, areas of clinical internal medicine that I did not frequently encounter in my daily practice became less accessible in my knowledge base.
The next step then was to enter the FPHM Maintenance of Certification (MOC) program.
The ABIM requires two attestations to verify that I met the requirements to be a hospitalist. First was a self-attestation confirming at least 3 years of unsupervised inpatient care practice experience, and meeting patient encounter thresholds in the inpatient setting. The second attestation was from a “Senior Hospital Officer” confirming the information in the self-attestation was accurate.
Once entered into the program and having an unrestricted medical license to practice, I had to complete the remaining requirements of earning MOC points and then passing a knowledge-based assessment. I had to accumulate a total of 100 MOC points in the past 5 years, which I succeeded in doing through participating in quality improvement projects, recording CME credits, studying for the exam, and even taking the exam. I could track my point totals through the ABIM Physician Portal, which updated my point tally automatically for activities that counted toward MOC, such as attending SHM’s annual conference.
The final component was to pass the knowledge assessment, the dreaded exam. In 2018, I had the option to take the 10-year FPHM exam or do a general internal medicine Knowledge Check-In. Beginning in 2020, candidates will be able to sit for either the 10-year Focused Practice in Hospital Medicine exam or begin the Hospital Medicine Knowledge Check-In pathway. I had already decided to pursue FPHM and began to prepare to sit for an exam. I scheduled my exam through the ABIM portal at a local testing center.
The exam was scheduled for a full day, consisting of four sections broken up by a lunch break and section breaks. Specifically, the 220 single best answer, multiple-choice exam covered diagnosis, testing, treatment decisions, epidemiology, and basic science content through patient scenarios that reflected the scope of practice of a hospitalist. The ABIM provided an exam blueprint that detailed the specific clinical topics and the likelihood that a question pertaining to that topic would show up on the exam. Content was described as high, medium, or low importance and the number of questions related to the content was 75% for high importance, no more than 25% for medium importance, and no questions for low-importance content. In addition, content was distributed in a way that was reflective of my clinical practice as a hospitalist: 63.5% inpatient and traditional care; 6.5% palliative care; 15% consultative comanagement; and 15% quality, safety, and clinical reasoning.
Beginning 6 months prior to my scheduled exam, I purchased two critical resources to guide my studying efforts: the SHM Spark Self-Assessment Tool and the American College of Physicians Medical Knowledge Self-Assessment Program to review subject matter content and also do practice questions.
The latest version of SHM’s program, Spark Edition 2, provides updated questions and resources tailored to the hospital medicine exams. I appreciated the ability to answer questions online, as well as on my phone so I could do questions on the go. Moreover, I was able to track which content areas were stronger or weaker for me, and focus attention on areas that needed more work. Importantly, the questions I answered using the Spark self-assessment tool closely aligned with the subject matter I encountered in the exam, as well as the clinical cases I encounter every day in my practice.
While the day-long exam was challenging, I was gratified to receive notice from the ABIM that I had successfully recertified in internal medicine with a Focused Practice in Hospital Medicine!
Dr. Tad-y is a hospitalist at the University of Colorado at Denver, Aurora, and associate vice chair of quality in the department of medicine at the University of Colorado.
ABIM now offers increased flexibility
ABIM now offers increased flexibility
Everyone always told me that my time in residency would fly by, and the 3 years of internal medicine training really did seem to pass in just a few moments. Before I knew it, I had passed my internal medicine boards and practiced hospital medicine at an academic medical center.
One day last fall, I received notice from the American Board of Internal Medicine that it was time to recertify. I was surprised – had it already been 10 years? What did I have to do to maintain my certification?
As I investigated what it would take to maintain certification, I discovered that the recertification process provided more flexibility, compared with original board certification. I now had the option to recertify in internal medicine with a Focused Practice in Hospital Medicine (FPHM). Beginning in 2014, ABIM offered hospitalists, or internists whose clinical practice is mainly in the inpatient setting, the option to recertify in internal medicine, but with the designation that highlighted their clinical practice in the inpatient setting.
The first step in recertification for me was deciding to recertify with the focus in hospital medicine or maintain the traditional internal medicine certification. I talked with several colleagues who are also practicing hospitalists and weighed their reasons for opting for FPHM. Ultimately, my decision to pursue a recertification with a focus in hospital medicine relied on three factors: First, my clinical practice since completing residency was exclusively in the inpatient setting. Day in and day out, I care for patients who are acutely ill and require inpatient medical care. Second, I wanted my board certification to reflect what I consider to be my area of clinical expertise, which is inpatient adult medicine. Pursuing the FPHM would provide that recognition. Finally, I wanted to study and be tested on topics that I could utilize in my day-to-day practice. Because I exclusively practiced hospital medicine since graduation, areas of clinical internal medicine that I did not frequently encounter in my daily practice became less accessible in my knowledge base.
The next step then was to enter the FPHM Maintenance of Certification (MOC) program.
The ABIM requires two attestations to verify that I met the requirements to be a hospitalist. First was a self-attestation confirming at least 3 years of unsupervised inpatient care practice experience, and meeting patient encounter thresholds in the inpatient setting. The second attestation was from a “Senior Hospital Officer” confirming the information in the self-attestation was accurate.
Once entered into the program and having an unrestricted medical license to practice, I had to complete the remaining requirements of earning MOC points and then passing a knowledge-based assessment. I had to accumulate a total of 100 MOC points in the past 5 years, which I succeeded in doing through participating in quality improvement projects, recording CME credits, studying for the exam, and even taking the exam. I could track my point totals through the ABIM Physician Portal, which updated my point tally automatically for activities that counted toward MOC, such as attending SHM’s annual conference.
The final component was to pass the knowledge assessment, the dreaded exam. In 2018, I had the option to take the 10-year FPHM exam or do a general internal medicine Knowledge Check-In. Beginning in 2020, candidates will be able to sit for either the 10-year Focused Practice in Hospital Medicine exam or begin the Hospital Medicine Knowledge Check-In pathway. I had already decided to pursue FPHM and began to prepare to sit for an exam. I scheduled my exam through the ABIM portal at a local testing center.
The exam was scheduled for a full day, consisting of four sections broken up by a lunch break and section breaks. Specifically, the 220 single best answer, multiple-choice exam covered diagnosis, testing, treatment decisions, epidemiology, and basic science content through patient scenarios that reflected the scope of practice of a hospitalist. The ABIM provided an exam blueprint that detailed the specific clinical topics and the likelihood that a question pertaining to that topic would show up on the exam. Content was described as high, medium, or low importance and the number of questions related to the content was 75% for high importance, no more than 25% for medium importance, and no questions for low-importance content. In addition, content was distributed in a way that was reflective of my clinical practice as a hospitalist: 63.5% inpatient and traditional care; 6.5% palliative care; 15% consultative comanagement; and 15% quality, safety, and clinical reasoning.
Beginning 6 months prior to my scheduled exam, I purchased two critical resources to guide my studying efforts: the SHM Spark Self-Assessment Tool and the American College of Physicians Medical Knowledge Self-Assessment Program to review subject matter content and also do practice questions.
The latest version of SHM’s program, Spark Edition 2, provides updated questions and resources tailored to the hospital medicine exams. I appreciated the ability to answer questions online, as well as on my phone so I could do questions on the go. Moreover, I was able to track which content areas were stronger or weaker for me, and focus attention on areas that needed more work. Importantly, the questions I answered using the Spark self-assessment tool closely aligned with the subject matter I encountered in the exam, as well as the clinical cases I encounter every day in my practice.
While the day-long exam was challenging, I was gratified to receive notice from the ABIM that I had successfully recertified in internal medicine with a Focused Practice in Hospital Medicine!
Dr. Tad-y is a hospitalist at the University of Colorado at Denver, Aurora, and associate vice chair of quality in the department of medicine at the University of Colorado.
Everyone always told me that my time in residency would fly by, and the 3 years of internal medicine training really did seem to pass in just a few moments. Before I knew it, I had passed my internal medicine boards and practiced hospital medicine at an academic medical center.
One day last fall, I received notice from the American Board of Internal Medicine that it was time to recertify. I was surprised – had it already been 10 years? What did I have to do to maintain my certification?
As I investigated what it would take to maintain certification, I discovered that the recertification process provided more flexibility, compared with original board certification. I now had the option to recertify in internal medicine with a Focused Practice in Hospital Medicine (FPHM). Beginning in 2014, ABIM offered hospitalists, or internists whose clinical practice is mainly in the inpatient setting, the option to recertify in internal medicine, but with the designation that highlighted their clinical practice in the inpatient setting.
The first step in recertification for me was deciding to recertify with the focus in hospital medicine or maintain the traditional internal medicine certification. I talked with several colleagues who are also practicing hospitalists and weighed their reasons for opting for FPHM. Ultimately, my decision to pursue a recertification with a focus in hospital medicine relied on three factors: First, my clinical practice since completing residency was exclusively in the inpatient setting. Day in and day out, I care for patients who are acutely ill and require inpatient medical care. Second, I wanted my board certification to reflect what I consider to be my area of clinical expertise, which is inpatient adult medicine. Pursuing the FPHM would provide that recognition. Finally, I wanted to study and be tested on topics that I could utilize in my day-to-day practice. Because I exclusively practiced hospital medicine since graduation, areas of clinical internal medicine that I did not frequently encounter in my daily practice became less accessible in my knowledge base.
The next step then was to enter the FPHM Maintenance of Certification (MOC) program.
The ABIM requires two attestations to verify that I met the requirements to be a hospitalist. First was a self-attestation confirming at least 3 years of unsupervised inpatient care practice experience, and meeting patient encounter thresholds in the inpatient setting. The second attestation was from a “Senior Hospital Officer” confirming the information in the self-attestation was accurate.
Once entered into the program and having an unrestricted medical license to practice, I had to complete the remaining requirements of earning MOC points and then passing a knowledge-based assessment. I had to accumulate a total of 100 MOC points in the past 5 years, which I succeeded in doing through participating in quality improvement projects, recording CME credits, studying for the exam, and even taking the exam. I could track my point totals through the ABIM Physician Portal, which updated my point tally automatically for activities that counted toward MOC, such as attending SHM’s annual conference.
The final component was to pass the knowledge assessment, the dreaded exam. In 2018, I had the option to take the 10-year FPHM exam or do a general internal medicine Knowledge Check-In. Beginning in 2020, candidates will be able to sit for either the 10-year Focused Practice in Hospital Medicine exam or begin the Hospital Medicine Knowledge Check-In pathway. I had already decided to pursue FPHM and began to prepare to sit for an exam. I scheduled my exam through the ABIM portal at a local testing center.
The exam was scheduled for a full day, consisting of four sections broken up by a lunch break and section breaks. Specifically, the 220 single best answer, multiple-choice exam covered diagnosis, testing, treatment decisions, epidemiology, and basic science content through patient scenarios that reflected the scope of practice of a hospitalist. The ABIM provided an exam blueprint that detailed the specific clinical topics and the likelihood that a question pertaining to that topic would show up on the exam. Content was described as high, medium, or low importance and the number of questions related to the content was 75% for high importance, no more than 25% for medium importance, and no questions for low-importance content. In addition, content was distributed in a way that was reflective of my clinical practice as a hospitalist: 63.5% inpatient and traditional care; 6.5% palliative care; 15% consultative comanagement; and 15% quality, safety, and clinical reasoning.
Beginning 6 months prior to my scheduled exam, I purchased two critical resources to guide my studying efforts: the SHM Spark Self-Assessment Tool and the American College of Physicians Medical Knowledge Self-Assessment Program to review subject matter content and also do practice questions.
The latest version of SHM’s program, Spark Edition 2, provides updated questions and resources tailored to the hospital medicine exams. I appreciated the ability to answer questions online, as well as on my phone so I could do questions on the go. Moreover, I was able to track which content areas were stronger or weaker for me, and focus attention on areas that needed more work. Importantly, the questions I answered using the Spark self-assessment tool closely aligned with the subject matter I encountered in the exam, as well as the clinical cases I encounter every day in my practice.
While the day-long exam was challenging, I was gratified to receive notice from the ABIM that I had successfully recertified in internal medicine with a Focused Practice in Hospital Medicine!
Dr. Tad-y is a hospitalist at the University of Colorado at Denver, Aurora, and associate vice chair of quality in the department of medicine at the University of Colorado.
Extended-Release Arbaclofen Reduces MS-related Spasticity
Key clinical point: Twice-daily, extended-release arbaclofen effectively reduces MS-related spasticity.
Major finding: Mean change in TNmAS-MAL was −2.90 with arbaclofen and −1.95 with placebo.
Study details: A multicenter, double-blind, parallel-group study of 341 adults with MS and spasticity.
Disclosures: The study did not have funding support. Dr. Kantor reported having received consulting fees from AbbVie, Actelion, Bayer, Biogen, Celgene, EMD Serono, Genentech/Roche, Mylan, Novartis, Osmotica, and Sanofi Genzyme.
Citation: Kantor D et al. CMSC 2019, Abstract SXM07.
Key clinical point: Twice-daily, extended-release arbaclofen effectively reduces MS-related spasticity.
Major finding: Mean change in TNmAS-MAL was −2.90 with arbaclofen and −1.95 with placebo.
Study details: A multicenter, double-blind, parallel-group study of 341 adults with MS and spasticity.
Disclosures: The study did not have funding support. Dr. Kantor reported having received consulting fees from AbbVie, Actelion, Bayer, Biogen, Celgene, EMD Serono, Genentech/Roche, Mylan, Novartis, Osmotica, and Sanofi Genzyme.
Citation: Kantor D et al. CMSC 2019, Abstract SXM07.
Key clinical point: Twice-daily, extended-release arbaclofen effectively reduces MS-related spasticity.
Major finding: Mean change in TNmAS-MAL was −2.90 with arbaclofen and −1.95 with placebo.
Study details: A multicenter, double-blind, parallel-group study of 341 adults with MS and spasticity.
Disclosures: The study did not have funding support. Dr. Kantor reported having received consulting fees from AbbVie, Actelion, Bayer, Biogen, Celgene, EMD Serono, Genentech/Roche, Mylan, Novartis, Osmotica, and Sanofi Genzyme.
Citation: Kantor D et al. CMSC 2019, Abstract SXM07.
Three-Step Algorithm for the Management of MS Relapse
Key clinical point: Management of multiple sclerosis relapse consists of three main steps: timely and careful evaluation; treatment, if necessary; and assessment of treatment response, according to an algorithm developed by MS clinicians.
Major finding: Between 3 and 5 weeks after the initial evaluation, the group recommends clinical reassessment using a tool such as the Assessing Relapse in Multiple Sclerosis (ARMS) Questionnaire.
Study details: A consensus statement developed by a work group of MS clinicians based on a literature review and clinical experience.
Disclosures: The work group did not receive funding. The authors disclosed financial ties with various pharmaceutical companies.
Citation: REPORTING FROM CMSC 2019
Key clinical point: Management of multiple sclerosis relapse consists of three main steps: timely and careful evaluation; treatment, if necessary; and assessment of treatment response, according to an algorithm developed by MS clinicians.
Major finding: Between 3 and 5 weeks after the initial evaluation, the group recommends clinical reassessment using a tool such as the Assessing Relapse in Multiple Sclerosis (ARMS) Questionnaire.
Study details: A consensus statement developed by a work group of MS clinicians based on a literature review and clinical experience.
Disclosures: The work group did not receive funding. The authors disclosed financial ties with various pharmaceutical companies.
Citation: REPORTING FROM CMSC 2019
Key clinical point: Management of multiple sclerosis relapse consists of three main steps: timely and careful evaluation; treatment, if necessary; and assessment of treatment response, according to an algorithm developed by MS clinicians.
Major finding: Between 3 and 5 weeks after the initial evaluation, the group recommends clinical reassessment using a tool such as the Assessing Relapse in Multiple Sclerosis (ARMS) Questionnaire.
Study details: A consensus statement developed by a work group of MS clinicians based on a literature review and clinical experience.
Disclosures: The work group did not receive funding. The authors disclosed financial ties with various pharmaceutical companies.
Citation: REPORTING FROM CMSC 2019