Honeybees, Apis mellifera, play an important role in the web of life. We rely on bees for pollinating approximately one-third of our crops, including multiple fruits, vegetables, nuts, and seeds.^1,2 Bees are also instrumental in the propagation of other plants, flower nectar, and flower pollen. A. mellifera, the European honeybee, is the main pollinator in Europe and North America, but other species, including A. cerana, A. dorsata, A. floria, A. andreniformis, A. koschevnikov, and A. laboriosa, yield honey.³ Honey, propolis, and royal jelly, along with beeswax and bee pollen, are among some of the celebrated bee products that have been found to confer health benefits to human beings.^4,5 Bee venom, a toxin bees use for protection, is a convoluted combination of peptides and toxic proteins such as phospholipase A2 (PLA2) and melittin that has garnered significant scientific attention of late and is used to treat various inflammatory conditions.^6-8 This column will focus on the investigation of the use of bee venom to treat atopic dermatitis (AD) and acne.

temmuzcan/Getty Images

Atopic dermatitis

In 2013, Kim et al. assessed the impact of bee venom on AD-related symptoms in mice, finding that it attenuated the effects of AD-simulating compounds in 48 of 80 patients injected subcutaneously. They concluded that bee venom acted by suppressing mast cell degranulation and proinflammatory cytokine expression.⁹ Three years later, You et al. conducted a double-blind, randomized, base-controlled multicenter study of 136 patients with AD to ascertain the effects of a bee venom emollient. For 4 weeks, patients applied an emollient with bee venom and silk protein or a vehicle lacking bee venom twice daily. Eczema area and severity index (EASI) scores were significantly lower in the bee venom group, as were the visual analogue scale (VAS) scores. The investigators concluded that bee venom is an effective and safe therapeutic choice for treating patients with AD.¹⁰ Further, in 2018, Shin et al. demonstrated that PLA2 derived from bee venom mitigates atopic skin inflammation via the CD206 mannose receptor. They had previously shown in a mouse model that PLA2 from bee venom exerts such activity against AD-like lesions induced by 2,4-dinitrochlorobenzene (DNCB) and house dust mite (Dermatophagoides farinae) extract.¹¹ Gu et al. observed later that year that intraperitoneal administration of bee venom eased the symptoms of ovalbumin-induced AD-like skin lesions in an experimental mouse model. Bee venom also lowered serum immunoglobulin E levels and suppressed infiltration of eosinophils and mast cells. They concluded that bee venom is a viable alternative for attenuating the allergic skin inflammation characteristic of AD.¹² At the end of 2018, An et al. reported on the use of an in vivo female Balb/c mouse AD model in which 1-chloro-DNCB acted as inducer in cultures of human keratinocytes, stimulated by TNF-alpha/IFN-gamma. The investigators found that bee venom and melittin displayed robust antiatopic effects as evidenced by reduced lesions. The bee products were also found to have hindered elevated expression of various chemokines and proinflammatory cytokines. The authors suggested that bee venom and melittin appear to warrant consideration as a topical treatment for AD.¹³ In 2019, Kim et al. demonstrated in mice that bee venom eases the symptoms of AD by inactivating the complement system, particularly through CD55 induction, which might account for its effectiveness in AD treatment in humans, they suggested.⁶ Early in 2020, Lee et al. demonstrated in a Balb/c mouse model that bee venom appears to be a possible therapeutic macromolecule for treating phthalic anhydride-induced AD.⁷
 

Acne

In 2013, in vitro experiments by Han et al. showed that purified bee venom exhibited antimicrobial activity, in a concentration-dependent manner, against Cutibacterium acnes (or Propionibacterium acnes). They followed up with a small randomized, double-blind, controlled trial with 12 subjects who were treated with cosmetics with pure bee venom or cosmetics without it for two weeks. The group receiving bee venom experienced significantly fewer inflammatory and noninflammatory lesions, and a significant decline in adenosine triphosphate levels (a 57.5% reduction) was noted in subjects in the bee venom group, with a nonsignificant decrease of 4.7% observed in the control group. The investigators concluded the purified bee venom may be suitable as an antiacne agent.¹⁴ Using a mouse model, An et al. studied the therapeutic effects of bee venom against C. acnes–induced skin inflammation. They found that bee venom significantly diminished the volume of infiltrated inflammatory cells in the treated mice, compared with untreated mice. Bee venom also decreased expression levels of tumor necrosis factor (TNF)-α, and interleukin (IL)-1beta and suppressed Toll-like receptor (TLR)2 and CD14 expression in C. acnes–injected tissue. The investigators concluded that bee venom imparts notable anti-inflammatory activity and has potential for use in treating acne and as an anti-inflammatory agent in skin care.¹⁵

In 2015, Kim et al. studied the influence of bee venom against C. acnes–induced inflammation in human keratinocytes (HaCaT) and monocytes (THP-1). They found that bee venom successfully suppressed the secretion of interferon-gamma, IL-1beta, IL-8, and TNF-alpha. It also galvanized the expression of IL-8 and TLR2 in HaCaT cells but hampered their expression in heat-killed C. acnes. The researchers concluded that bee venom displays considerable anti-inflammatory activity against C. acnes and warrants consideration as an alternative to antibiotic acne treatment.¹⁶ It is worth noting that early that year, in a comprehensive database review to evaluate the effects and safety of a wide range of complementary treatments for acne, Cao et al. found, among 35 studies including parallel-group randomized controlled trials, that one trial indicated bee venom was superior to control in lowering the number of acne lesions.¹⁷
 

Conclusion

More research, in the form of randomized, controlled trials, is required before bee venom can be incorporated into the dermatologic armamentarium as a first-line therapy for common and vexing cutaneous conditions. Nevertheless, the current evidence provides reasons for optimism that bee venom can play a role among the various treatments for AD and acne.
 

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann has written two textbooks and a New York Times Best Sellers book for consumers. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Revance, Evolus, and Burt’s Bees. She is the CEO of Skin Type Solutions Inc., a company that independently tests skin care products and makes recommendations to physicians on which skin care technologies are best. Write to her at dermnews@mdedge.com.

References

1. Walsh B. The plight of the honeybee: Mass deaths in bee colonies may mean disaster for farmers – and your favorite Foods. Time Magazine, 2013 Aug 19.

2. Klein AM et al. Proc Biol Sci. 2007 Feb 7;274(1608):303-13. doi: 10.1098/rspb.2006.3721.

3. Ediriweera ER and Premarathna NY. AYU. 2012 Apr;33(2):178-82. doi: 10.4103/0974-8520.105233.

4. Baumann, L. Honey/Propolis/Royal Jelly. In Cosmeceuticals and Cosmetic Ingredients. New York:McGraw-Hill; 2014:203-212.

5. Cornara L et al. Front Pharmacol. 2017 Jun 28;8:412. doi: 10.3389/fphar.2017.00412.

6. Kim Y et al. Toxins (Basel). 2019 Apr 26;11(5):239. doi: 10.3390/toxins11050239.

7. Lee YJ et al. Inflammopharmacology. 2020 Feb;28(1):253-63. doi: 10.1007/s10787-019-00646-w.

8. Lee G and Bae H. Molecules. 2016 May 11;21(5):616. doi: 10.3390/molecules21050616.

9. Kim KH et al. Int J Clin Exp Pathol. 2013 Nov 15;6(12):2896-903.

10. You CE et al. Ann Dermatol. 2016 Oct;28(5):593-9. doi: 10.5021/ad.2016.28.5.593.

11. Shin D et al. Toxins (Basel). 2018 Apr 2;10(4):146. doi: 10.3390/toxins10040146.

12. Gu H et al. Mol Med Rep. 2018 Oct;18(4):3711-8. doi: 10.3892/mmr.2018.9398.

13. An HJ et al. Br J Pharmacol. 2018 Dec;175(23):4310-24. doi: 10.1111/bph.14487.

14. Han SM et al. J Integr Med. 2013 Sep;11(5):320-6. doi: 10.3736/jintegrmed2013043.

15. An HJ et al. Int J Mol Med. 2014 Nov;34(5):1341-8. doi: 10.3892/ijmm.2014.1933.

16. Kim JY et al. Int J Mol Med. 2015 Jun;35(6):1651-6. doi: 10.3892/ijmm.2015.2180.

17. Cao H et al. Cochrane Database Syst Rev. 2015 Jan 19;1:CD009436. doi: 10.1002/14651858.CD009436.pub2.

Honeybees, Apis mellifera, play an important role in the web of life. We rely on bees for pollinating approximately one-third of our crops, including multiple fruits, vegetables, nuts, and seeds.^1,2 Bees are also instrumental in the propagation of other plants, flower nectar, and flower pollen. A. mellifera, the European honeybee, is the main pollinator in Europe and North America, but other species, including A. cerana, A. dorsata, A. floria, A. andreniformis, A. koschevnikov, and A. laboriosa, yield honey.³ Honey, propolis, and royal jelly, along with beeswax and bee pollen, are among some of the celebrated bee products that have been found to confer health benefits to human beings.^4,5 Bee venom, a toxin bees use for protection, is a convoluted combination of peptides and toxic proteins such as phospholipase A2 (PLA2) and melittin that has garnered significant scientific attention of late and is used to treat various inflammatory conditions.^6-8 This column will focus on the investigation of the use of bee venom to treat atopic dermatitis (AD) and acne.

temmuzcan/Getty Images

Atopic dermatitis

In 2013, Kim et al. assessed the impact of bee venom on AD-related symptoms in mice, finding that it attenuated the effects of AD-simulating compounds in 48 of 80 patients injected subcutaneously. They concluded that bee venom acted by suppressing mast cell degranulation and proinflammatory cytokine expression.⁹ Three years later, You et al. conducted a double-blind, randomized, base-controlled multicenter study of 136 patients with AD to ascertain the effects of a bee venom emollient. For 4 weeks, patients applied an emollient with bee venom and silk protein or a vehicle lacking bee venom twice daily. Eczema area and severity index (EASI) scores were significantly lower in the bee venom group, as were the visual analogue scale (VAS) scores. The investigators concluded that bee venom is an effective and safe therapeutic choice for treating patients with AD.¹⁰ Further, in 2018, Shin et al. demonstrated that PLA2 derived from bee venom mitigates atopic skin inflammation via the CD206 mannose receptor. They had previously shown in a mouse model that PLA2 from bee venom exerts such activity against AD-like lesions induced by 2,4-dinitrochlorobenzene (DNCB) and house dust mite (Dermatophagoides farinae) extract.¹¹ Gu et al. observed later that year that intraperitoneal administration of bee venom eased the symptoms of ovalbumin-induced AD-like skin lesions in an experimental mouse model. Bee venom also lowered serum immunoglobulin E levels and suppressed infiltration of eosinophils and mast cells. They concluded that bee venom is a viable alternative for attenuating the allergic skin inflammation characteristic of AD.¹² At the end of 2018, An et al. reported on the use of an in vivo female Balb/c mouse AD model in which 1-chloro-DNCB acted as inducer in cultures of human keratinocytes, stimulated by TNF-alpha/IFN-gamma. The investigators found that bee venom and melittin displayed robust antiatopic effects as evidenced by reduced lesions. The bee products were also found to have hindered elevated expression of various chemokines and proinflammatory cytokines. The authors suggested that bee venom and melittin appear to warrant consideration as a topical treatment for AD.¹³ In 2019, Kim et al. demonstrated in mice that bee venom eases the symptoms of AD by inactivating the complement system, particularly through CD55 induction, which might account for its effectiveness in AD treatment in humans, they suggested.⁶ Early in 2020, Lee et al. demonstrated in a Balb/c mouse model that bee venom appears to be a possible therapeutic macromolecule for treating phthalic anhydride-induced AD.⁷
 

Acne

In 2013, in vitro experiments by Han et al. showed that purified bee venom exhibited antimicrobial activity, in a concentration-dependent manner, against Cutibacterium acnes (or Propionibacterium acnes). They followed up with a small randomized, double-blind, controlled trial with 12 subjects who were treated with cosmetics with pure bee venom or cosmetics without it for two weeks. The group receiving bee venom experienced significantly fewer inflammatory and noninflammatory lesions, and a significant decline in adenosine triphosphate levels (a 57.5% reduction) was noted in subjects in the bee venom group, with a nonsignificant decrease of 4.7% observed in the control group. The investigators concluded the purified bee venom may be suitable as an antiacne agent.¹⁴ Using a mouse model, An et al. studied the therapeutic effects of bee venom against C. acnes–induced skin inflammation. They found that bee venom significantly diminished the volume of infiltrated inflammatory cells in the treated mice, compared with untreated mice. Bee venom also decreased expression levels of tumor necrosis factor (TNF)-α, and interleukin (IL)-1beta and suppressed Toll-like receptor (TLR)2 and CD14 expression in C. acnes–injected tissue. The investigators concluded that bee venom imparts notable anti-inflammatory activity and has potential for use in treating acne and as an anti-inflammatory agent in skin care.¹⁵

In 2015, Kim et al. studied the influence of bee venom against C. acnes–induced inflammation in human keratinocytes (HaCaT) and monocytes (THP-1). They found that bee venom successfully suppressed the secretion of interferon-gamma, IL-1beta, IL-8, and TNF-alpha. It also galvanized the expression of IL-8 and TLR2 in HaCaT cells but hampered their expression in heat-killed C. acnes. The researchers concluded that bee venom displays considerable anti-inflammatory activity against C. acnes and warrants consideration as an alternative to antibiotic acne treatment.¹⁶ It is worth noting that early that year, in a comprehensive database review to evaluate the effects and safety of a wide range of complementary treatments for acne, Cao et al. found, among 35 studies including parallel-group randomized controlled trials, that one trial indicated bee venom was superior to control in lowering the number of acne lesions.¹⁷
 

Conclusion

More research, in the form of randomized, controlled trials, is required before bee venom can be incorporated into the dermatologic armamentarium as a first-line therapy for common and vexing cutaneous conditions. Nevertheless, the current evidence provides reasons for optimism that bee venom can play a role among the various treatments for AD and acne.
 

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann has written two textbooks and a New York Times Best Sellers book for consumers. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Revance, Evolus, and Burt’s Bees. She is the CEO of Skin Type Solutions Inc., a company that independently tests skin care products and makes recommendations to physicians on which skin care technologies are best. Write to her at dermnews@mdedge.com.

References

1. Walsh B. The plight of the honeybee: Mass deaths in bee colonies may mean disaster for farmers – and your favorite Foods. Time Magazine, 2013 Aug 19.

2. Klein AM et al. Proc Biol Sci. 2007 Feb 7;274(1608):303-13. doi: 10.1098/rspb.2006.3721.

3. Ediriweera ER and Premarathna NY. AYU. 2012 Apr;33(2):178-82. doi: 10.4103/0974-8520.105233.

4. Baumann, L. Honey/Propolis/Royal Jelly. In Cosmeceuticals and Cosmetic Ingredients. New York:McGraw-Hill; 2014:203-212.

5. Cornara L et al. Front Pharmacol. 2017 Jun 28;8:412. doi: 10.3389/fphar.2017.00412.

6. Kim Y et al. Toxins (Basel). 2019 Apr 26;11(5):239. doi: 10.3390/toxins11050239.

7. Lee YJ et al. Inflammopharmacology. 2020 Feb;28(1):253-63. doi: 10.1007/s10787-019-00646-w.

8. Lee G and Bae H. Molecules. 2016 May 11;21(5):616. doi: 10.3390/molecules21050616.

9. Kim KH et al. Int J Clin Exp Pathol. 2013 Nov 15;6(12):2896-903.

10. You CE et al. Ann Dermatol. 2016 Oct;28(5):593-9. doi: 10.5021/ad.2016.28.5.593.

11. Shin D et al. Toxins (Basel). 2018 Apr 2;10(4):146. doi: 10.3390/toxins10040146.

12. Gu H et al. Mol Med Rep. 2018 Oct;18(4):3711-8. doi: 10.3892/mmr.2018.9398.

13. An HJ et al. Br J Pharmacol. 2018 Dec;175(23):4310-24. doi: 10.1111/bph.14487.

14. Han SM et al. J Integr Med. 2013 Sep;11(5):320-6. doi: 10.3736/jintegrmed2013043.

15. An HJ et al. Int J Mol Med. 2014 Nov;34(5):1341-8. doi: 10.3892/ijmm.2014.1933.

16. Kim JY et al. Int J Mol Med. 2015 Jun;35(6):1651-6. doi: 10.3892/ijmm.2015.2180.

17. Cao H et al. Cochrane Database Syst Rev. 2015 Jan 19;1:CD009436. doi: 10.1002/14651858.CD009436.pub2.

Honeybees, Apis mellifera, play an important role in the web of life. We rely on bees for pollinating approximately one-third of our crops, including multiple fruits, vegetables, nuts, and seeds.^1,2 Bees are also instrumental in the propagation of other plants, flower nectar, and flower pollen. A. mellifera, the European honeybee, is the main pollinator in Europe and North America, but other species, including A. cerana, A. dorsata, A. floria, A. andreniformis, A. koschevnikov, and A. laboriosa, yield honey.³ Honey, propolis, and royal jelly, along with beeswax and bee pollen, are among some of the celebrated bee products that have been found to confer health benefits to human beings.^4,5 Bee venom, a toxin bees use for protection, is a convoluted combination of peptides and toxic proteins such as phospholipase A2 (PLA2) and melittin that has garnered significant scientific attention of late and is used to treat various inflammatory conditions.^6-8 This column will focus on the investigation of the use of bee venom to treat atopic dermatitis (AD) and acne.

temmuzcan/Getty Images

Atopic dermatitis

In 2013, Kim et al. assessed the impact of bee venom on AD-related symptoms in mice, finding that it attenuated the effects of AD-simulating compounds in 48 of 80 patients injected subcutaneously. They concluded that bee venom acted by suppressing mast cell degranulation and proinflammatory cytokine expression.⁹ Three years later, You et al. conducted a double-blind, randomized, base-controlled multicenter study of 136 patients with AD to ascertain the effects of a bee venom emollient. For 4 weeks, patients applied an emollient with bee venom and silk protein or a vehicle lacking bee venom twice daily. Eczema area and severity index (EASI) scores were significantly lower in the bee venom group, as were the visual analogue scale (VAS) scores. The investigators concluded that bee venom is an effective and safe therapeutic choice for treating patients with AD.¹⁰ Further, in 2018, Shin et al. demonstrated that PLA2 derived from bee venom mitigates atopic skin inflammation via the CD206 mannose receptor. They had previously shown in a mouse model that PLA2 from bee venom exerts such activity against AD-like lesions induced by 2,4-dinitrochlorobenzene (DNCB) and house dust mite (Dermatophagoides farinae) extract.¹¹ Gu et al. observed later that year that intraperitoneal administration of bee venom eased the symptoms of ovalbumin-induced AD-like skin lesions in an experimental mouse model. Bee venom also lowered serum immunoglobulin E levels and suppressed infiltration of eosinophils and mast cells. They concluded that bee venom is a viable alternative for attenuating the allergic skin inflammation characteristic of AD.¹² At the end of 2018, An et al. reported on the use of an in vivo female Balb/c mouse AD model in which 1-chloro-DNCB acted as inducer in cultures of human keratinocytes, stimulated by TNF-alpha/IFN-gamma. The investigators found that bee venom and melittin displayed robust antiatopic effects as evidenced by reduced lesions. The bee products were also found to have hindered elevated expression of various chemokines and proinflammatory cytokines. The authors suggested that bee venom and melittin appear to warrant consideration as a topical treatment for AD.¹³ In 2019, Kim et al. demonstrated in mice that bee venom eases the symptoms of AD by inactivating the complement system, particularly through CD55 induction, which might account for its effectiveness in AD treatment in humans, they suggested.⁶ Early in 2020, Lee et al. demonstrated in a Balb/c mouse model that bee venom appears to be a possible therapeutic macromolecule for treating phthalic anhydride-induced AD.⁷
 

Acne

In 2013, in vitro experiments by Han et al. showed that purified bee venom exhibited antimicrobial activity, in a concentration-dependent manner, against Cutibacterium acnes (or Propionibacterium acnes). They followed up with a small randomized, double-blind, controlled trial with 12 subjects who were treated with cosmetics with pure bee venom or cosmetics without it for two weeks. The group receiving bee venom experienced significantly fewer inflammatory and noninflammatory lesions, and a significant decline in adenosine triphosphate levels (a 57.5% reduction) was noted in subjects in the bee venom group, with a nonsignificant decrease of 4.7% observed in the control group. The investigators concluded the purified bee venom may be suitable as an antiacne agent.¹⁴ Using a mouse model, An et al. studied the therapeutic effects of bee venom against C. acnes–induced skin inflammation. They found that bee venom significantly diminished the volume of infiltrated inflammatory cells in the treated mice, compared with untreated mice. Bee venom also decreased expression levels of tumor necrosis factor (TNF)-α, and interleukin (IL)-1beta and suppressed Toll-like receptor (TLR)2 and CD14 expression in C. acnes–injected tissue. The investigators concluded that bee venom imparts notable anti-inflammatory activity and has potential for use in treating acne and as an anti-inflammatory agent in skin care.¹⁵

In 2015, Kim et al. studied the influence of bee venom against C. acnes–induced inflammation in human keratinocytes (HaCaT) and monocytes (THP-1). They found that bee venom successfully suppressed the secretion of interferon-gamma, IL-1beta, IL-8, and TNF-alpha. It also galvanized the expression of IL-8 and TLR2 in HaCaT cells but hampered their expression in heat-killed C. acnes. The researchers concluded that bee venom displays considerable anti-inflammatory activity against C. acnes and warrants consideration as an alternative to antibiotic acne treatment.¹⁶ It is worth noting that early that year, in a comprehensive database review to evaluate the effects and safety of a wide range of complementary treatments for acne, Cao et al. found, among 35 studies including parallel-group randomized controlled trials, that one trial indicated bee venom was superior to control in lowering the number of acne lesions.¹⁷
 

Conclusion

More research, in the form of randomized, controlled trials, is required before bee venom can be incorporated into the dermatologic armamentarium as a first-line therapy for common and vexing cutaneous conditions. Nevertheless, the current evidence provides reasons for optimism that bee venom can play a role among the various treatments for AD and acne.
 

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann has written two textbooks and a New York Times Best Sellers book for consumers. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Revance, Evolus, and Burt’s Bees. She is the CEO of Skin Type Solutions Inc., a company that independently tests skin care products and makes recommendations to physicians on which skin care technologies are best. Write to her at dermnews@mdedge.com.

References

1. Walsh B. The plight of the honeybee: Mass deaths in bee colonies may mean disaster for farmers – and your favorite Foods. Time Magazine, 2013 Aug 19.

2. Klein AM et al. Proc Biol Sci. 2007 Feb 7;274(1608):303-13. doi: 10.1098/rspb.2006.3721.

3. Ediriweera ER and Premarathna NY. AYU. 2012 Apr;33(2):178-82. doi: 10.4103/0974-8520.105233.

4. Baumann, L. Honey/Propolis/Royal Jelly. In Cosmeceuticals and Cosmetic Ingredients. New York:McGraw-Hill; 2014:203-212.

5. Cornara L et al. Front Pharmacol. 2017 Jun 28;8:412. doi: 10.3389/fphar.2017.00412.

6. Kim Y et al. Toxins (Basel). 2019 Apr 26;11(5):239. doi: 10.3390/toxins11050239.

7. Lee YJ et al. Inflammopharmacology. 2020 Feb;28(1):253-63. doi: 10.1007/s10787-019-00646-w.

8. Lee G and Bae H. Molecules. 2016 May 11;21(5):616. doi: 10.3390/molecules21050616.

9. Kim KH et al. Int J Clin Exp Pathol. 2013 Nov 15;6(12):2896-903.

10. You CE et al. Ann Dermatol. 2016 Oct;28(5):593-9. doi: 10.5021/ad.2016.28.5.593.

11. Shin D et al. Toxins (Basel). 2018 Apr 2;10(4):146. doi: 10.3390/toxins10040146.

12. Gu H et al. Mol Med Rep. 2018 Oct;18(4):3711-8. doi: 10.3892/mmr.2018.9398.

13. An HJ et al. Br J Pharmacol. 2018 Dec;175(23):4310-24. doi: 10.1111/bph.14487.

14. Han SM et al. J Integr Med. 2013 Sep;11(5):320-6. doi: 10.3736/jintegrmed2013043.

15. An HJ et al. Int J Mol Med. 2014 Nov;34(5):1341-8. doi: 10.3892/ijmm.2014.1933.

16. Kim JY et al. Int J Mol Med. 2015 Jun;35(6):1651-6. doi: 10.3892/ijmm.2015.2180.

17. Cao H et al. Cochrane Database Syst Rev. 2015 Jan 19;1:CD009436. doi: 10.1002/14651858.CD009436.pub2.

Key clinical point: In 10-year follow-up of ENESTnd trial, nilotinib demonstrated benefits over imatinib for various clinical outcomes in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP).

Major finding: Cumulative 10-year rates of treatment-free remission eligibility and molecular response rate with nilotinib 300 mg and 400 mg vs. imatinib was 48.6% and 47.3% vs. 29.7% and 77.7% and 79.7% vs. 62.5%, respectively. Progression to accelerated (6 and 4 vs. 11) or blast (6 and 6 vs. 14) phase was lower with nilotinib 300 mg and 400 mg vs. imatinib, respectively. Overall, the frequency of adverse events was similar, but rates of cardiovascular events were higher with nilotinib.

Study details: ENESTnd, a phase 3 study, randomly allocated patients with newly diagnosed CML-CP to receive nilotinib 300 mg twice daily (n=282), nilotinib 400 mg twice daily (n=281), or imatinib 400 mg once daily (n=283).

Disclosures: The study was funded by Novartis Pharmaceuticals Corporation. The presenting author reported ties with Pharmaceuticals companies including Novartis. Some of the study investigators reported being an employee of, receiving grants, honoraria, support, and/or consulting for Novartis and other pharmaceutical companies.

Source: Kantarjian HM et al. Leukemia. 2021 Jan 7. doi: 10.1038/s41375-020-01111-2.

Key clinical point: In 10-year follow-up of ENESTnd trial, nilotinib demonstrated benefits over imatinib for various clinical outcomes in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP).

Major finding: Cumulative 10-year rates of treatment-free remission eligibility and molecular response rate with nilotinib 300 mg and 400 mg vs. imatinib was 48.6% and 47.3% vs. 29.7% and 77.7% and 79.7% vs. 62.5%, respectively. Progression to accelerated (6 and 4 vs. 11) or blast (6 and 6 vs. 14) phase was lower with nilotinib 300 mg and 400 mg vs. imatinib, respectively. Overall, the frequency of adverse events was similar, but rates of cardiovascular events were higher with nilotinib.

Study details: ENESTnd, a phase 3 study, randomly allocated patients with newly diagnosed CML-CP to receive nilotinib 300 mg twice daily (n=282), nilotinib 400 mg twice daily (n=281), or imatinib 400 mg once daily (n=283).

Disclosures: The study was funded by Novartis Pharmaceuticals Corporation. The presenting author reported ties with Pharmaceuticals companies including Novartis. Some of the study investigators reported being an employee of, receiving grants, honoraria, support, and/or consulting for Novartis and other pharmaceutical companies.

Source: Kantarjian HM et al. Leukemia. 2021 Jan 7. doi: 10.1038/s41375-020-01111-2.

Key clinical point: In 10-year follow-up of ENESTnd trial, nilotinib demonstrated benefits over imatinib for various clinical outcomes in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP).

Major finding: Cumulative 10-year rates of treatment-free remission eligibility and molecular response rate with nilotinib 300 mg and 400 mg vs. imatinib was 48.6% and 47.3% vs. 29.7% and 77.7% and 79.7% vs. 62.5%, respectively. Progression to accelerated (6 and 4 vs. 11) or blast (6 and 6 vs. 14) phase was lower with nilotinib 300 mg and 400 mg vs. imatinib, respectively. Overall, the frequency of adverse events was similar, but rates of cardiovascular events were higher with nilotinib.

Study details: ENESTnd, a phase 3 study, randomly allocated patients with newly diagnosed CML-CP to receive nilotinib 300 mg twice daily (n=282), nilotinib 400 mg twice daily (n=281), or imatinib 400 mg once daily (n=283).

Disclosures: The study was funded by Novartis Pharmaceuticals Corporation. The presenting author reported ties with Pharmaceuticals companies including Novartis. Some of the study investigators reported being an employee of, receiving grants, honoraria, support, and/or consulting for Novartis and other pharmaceutical companies.

Source: Kantarjian HM et al. Leukemia. 2021 Jan 7. doi: 10.1038/s41375-020-01111-2.

Key clinical point: Patients with chronic myeloid leukemia (CML) in the era of tyrosine kinase inhibitors (TKIs) are at a greater risk for adverse cardiovascular events (ACEs) compared with the general population.

Major finding: From 2001 onwards, the risk for major ACEs (subdistribution hazard ratio [SHR], 1.27; 95% confidence interval [CI], 0.96-1.43) and cardiovascular death (SHR, 0.99; 95% CI, 0.84-1.18) was similar between patients with vs. without CML. However, before 2001, the risk for major ACE (SHR, 0.59; 95% CI, 0.46-0.76) and cardiovascular death (SHR, 0.43; 95% CI, 0.36-0.52) was lower in patients with vs. without CML.

Study details: A population-based retrospective study of 4,238 patients with CML who were age- and sex-matched with 42,380 controls without CML.

Disclosures: The study was funded by the Population Health Research Institute, McMaster University, and Institute of Clinical and Evaluative Sciences. The authors reported no conflicts of interest.

Source: Leong D et al. Heart. 2021 Jan 8. doi: 10.1136/heartjnl-2020-318251.

Key clinical point: Patients with chronic myeloid leukemia (CML) in the era of tyrosine kinase inhibitors (TKIs) are at a greater risk for adverse cardiovascular events (ACEs) compared with the general population.

Major finding: From 2001 onwards, the risk for major ACEs (subdistribution hazard ratio [SHR], 1.27; 95% confidence interval [CI], 0.96-1.43) and cardiovascular death (SHR, 0.99; 95% CI, 0.84-1.18) was similar between patients with vs. without CML. However, before 2001, the risk for major ACE (SHR, 0.59; 95% CI, 0.46-0.76) and cardiovascular death (SHR, 0.43; 95% CI, 0.36-0.52) was lower in patients with vs. without CML.

Study details: A population-based retrospective study of 4,238 patients with CML who were age- and sex-matched with 42,380 controls without CML.

Disclosures: The study was funded by the Population Health Research Institute, McMaster University, and Institute of Clinical and Evaluative Sciences. The authors reported no conflicts of interest.

Source: Leong D et al. Heart. 2021 Jan 8. doi: 10.1136/heartjnl-2020-318251.

Key clinical point: Patients with chronic myeloid leukemia (CML) in the era of tyrosine kinase inhibitors (TKIs) are at a greater risk for adverse cardiovascular events (ACEs) compared with the general population.

Major finding: From 2001 onwards, the risk for major ACEs (subdistribution hazard ratio [SHR], 1.27; 95% confidence interval [CI], 0.96-1.43) and cardiovascular death (SHR, 0.99; 95% CI, 0.84-1.18) was similar between patients with vs. without CML. However, before 2001, the risk for major ACE (SHR, 0.59; 95% CI, 0.46-0.76) and cardiovascular death (SHR, 0.43; 95% CI, 0.36-0.52) was lower in patients with vs. without CML.

Study details: A population-based retrospective study of 4,238 patients with CML who were age- and sex-matched with 42,380 controls without CML.

Disclosures: The study was funded by the Population Health Research Institute, McMaster University, and Institute of Clinical and Evaluative Sciences. The authors reported no conflicts of interest.

Source: Leong D et al. Heart. 2021 Jan 8. doi: 10.1136/heartjnl-2020-318251.

Key clinical point: High levels of cholesterol plasma and low-density lipoprotein (LDL) after 3 months of nilotinib initiation were associated with a higher risk for arterial occlusive events (AOEs) in patients with chronic myeloid leukemia (CML).

Major finding: Cholesterol plasma level greater than 200 mg/dL and LDL greater than 70 mg/dL after 3 months since nilotinib initiation was associated with a significantly higher risk of AOEs (hazard ratio, 3.5; P = .008).

Study details: Findings are from a retrospective study of 369 patients with CML treated with nilotinib.

Disclosures: The study was performed within the framework of the research project funded by P.O.R. SARDEGNA F.S.E. 2014-2020 - Asse III. The authors declared no conflicts of interest.

Source: Caocci G et al. Ann Hematol. 2021 Jan 3. doi: 10.1007/s00277-020-04392-w.

Key clinical point: High levels of cholesterol plasma and low-density lipoprotein (LDL) after 3 months of nilotinib initiation were associated with a higher risk for arterial occlusive events (AOEs) in patients with chronic myeloid leukemia (CML).

Major finding: Cholesterol plasma level greater than 200 mg/dL and LDL greater than 70 mg/dL after 3 months since nilotinib initiation was associated with a significantly higher risk of AOEs (hazard ratio, 3.5; P = .008).

Study details: Findings are from a retrospective study of 369 patients with CML treated with nilotinib.

Disclosures: The study was performed within the framework of the research project funded by P.O.R. SARDEGNA F.S.E. 2014-2020 - Asse III. The authors declared no conflicts of interest.

Source: Caocci G et al. Ann Hematol. 2021 Jan 3. doi: 10.1007/s00277-020-04392-w.

Key clinical point: High levels of cholesterol plasma and low-density lipoprotein (LDL) after 3 months of nilotinib initiation were associated with a higher risk for arterial occlusive events (AOEs) in patients with chronic myeloid leukemia (CML).

Major finding: Cholesterol plasma level greater than 200 mg/dL and LDL greater than 70 mg/dL after 3 months since nilotinib initiation was associated with a significantly higher risk of AOEs (hazard ratio, 3.5; P = .008).

Study details: Findings are from a retrospective study of 369 patients with CML treated with nilotinib.

Disclosures: The study was performed within the framework of the research project funded by P.O.R. SARDEGNA F.S.E. 2014-2020 - Asse III. The authors declared no conflicts of interest.

Source: Caocci G et al. Ann Hematol. 2021 Jan 3. doi: 10.1007/s00277-020-04392-w.

An analysis of data from the U.S. military suggests that the maternal morbidity disparities between Black and White women cannot be attributed solely to differences in access to care and socioeconomics.

Even in the U.S. military health care system, where all service members have universal access to the same facilities and providers, researchers found substantial racial disparities in cesarean deliveries, maternal ICU admission, and overall severe maternal morbidity and mortality between Black patients and White patients, according to findings from a new study presented Jan. 28, 2021, at a meeting sponsored by the Society for Maternal-Fetal Medicine.

“This was surprising given some of the driving theories behind maternal race disparities encountered in this country, such as access to care and socioeconomic status, are controlled for in this health care system,” Capt. Jameaka Hamilton, MD, who presented the research, said in an interview. “Our findings indicate that there are likely additional factors at play which impact the obstetrical outcomes of women based upon their race, including systems-based barriers to accessing the military health care system which contribute to health care disparities, or in systemic or implicit biases which occur within our health care delivery.”

Plenty of recent research has documented the rise in maternal morbidity and mortality in the United States and the considerable racial disparities within those statistics. Black women are twice as likely to suffer morbidity and three to four times more likely to die in childbirth, compared with White women, Dr. Hamilton, an ob.gyn. from the San Antonio Uniformed Services Health Education Consortium at Ft. Sam Houston in San Antonio, Texas, reminded attendees. So far, much of this disparity has been attributed to social determinants of health.

Military retirees, active-duty personnel, and dependents, however, have equal access to federal health insurance and care at military health care facilities, or at covered civilian facilities where needed. Hence the researchers’ hypothesis that the military medical system would not show the same disparities by race that are seen in civilian populations.

The researchers analyzed maternal morbidity data from the Neonatal Perinatal Information Center from April 2018 to March 2019. The retrospective study included data from 13 military treatment facilities that had more than 1,000 deliveries per year. In addition to statistics on cesarean delivery and adult ICU admission, the researchers compared numbers on overall severe maternal morbidity based on the indicators defined by the Centers for Disease Control and Prevention.

The 15,305 deliveries included 23% Black patients and 77% White patients from the Air Force, Army, and Navy branches.

The cesarean delivery rate ranged from 19.4% to 35.5%. ICU admissions totaled 38 women, 190 women had postpartum hemorrhage, and 282 women experienced severe maternal morbidity. All three measures revealed racial disparities:

• Overall severe maternal morbidity occurred in 2.66% of Black women and 1.66% of White women (P =.0001).
• ICU admission occurred in 0.49% of Black women and 0.18% of White women (P =.0026).
• 31.68% of Black women had a cesarean delivery, compared with 23.58% of White women (P <.0001).

After excluding cases with blood transfusions, Black women were twice as likely to have severe maternal morbidity (0.64% vs. 0.32%). There were no significant differences in postpartum hemorrhage rates between Black and White women, but this analysis was limited by the small overall numbers of postpartum hemorrhage.

Among the study’s limitations were the inability to stratify patients by retiree, active duty, or dependent status, and the lack of data on preeclampsia rates, maternal age, obesity, or other preexisting conditions. In addition, the initial dataset included 61% of patients who reported their race as “other” than Black or White, limiting the number of patients whose data could be analyzed. Since low-volume hospitals were excluded, the outcomes could be skewed if lower-volume facilities are more likely to care for more complex cases, Dr. Hamilton added.

Allison Bryant Mantha, MD, MPH, vice chair for quality, equity, and safety in the ob.gyn. department at Massachusetts General Hospital, Boston, praised Dr. Hamilton’s work for revealing that differential access – though still problematic – cannot fully explain inequities between Black women and other women.

“The findings are not shocking given that what underlies some of these inequities – namely structural and institutional racism, and differential treatment within the system – are not exclusive to civilian health care settings,” Dr. Bryant Mantha, who moderated the session, said in an interview. “That said, doing the work to demonstrate this is extremely valuable.”

Although the causes of these disparities are systemic, Dr. Hamilton said individual providers can play a role in addressing them.

“There can certainly be more done to address this dangerous trend at the provider, hospital/institution, and national level,” she said. I think we as providers should continue to self-reflect and address our own biases. Hospitals and institutions should continue to develop policies that draw attention health care disparities.”

Completely removing these inequalities, however, will require confronting the racism embedded in U.S. health care at all levels, Dr. Bryant Mantha suggested.

“Ultimately, moving to an antiracist health care system – and criminal justice system, educational system, political system, etc. – and dismantling the existing structural racism in policies and practices will be needed to drive this change,” Dr. Bryant Mantha said. “Individual clinicians can use their voices to advocate for these changes in their health systems, communities, and states. Awareness of these inequities is critical, as is a sense of collective efficacy that we can, indeed, change the status quo.”

Dr. Hamilton and Dr. Bryant Mantha reported no disclosures.

An analysis of data from the U.S. military suggests that the maternal morbidity disparities between Black and White women cannot be attributed solely to differences in access to care and socioeconomics.

Even in the U.S. military health care system, where all service members have universal access to the same facilities and providers, researchers found substantial racial disparities in cesarean deliveries, maternal ICU admission, and overall severe maternal morbidity and mortality between Black patients and White patients, according to findings from a new study presented Jan. 28, 2021, at a meeting sponsored by the Society for Maternal-Fetal Medicine.

“This was surprising given some of the driving theories behind maternal race disparities encountered in this country, such as access to care and socioeconomic status, are controlled for in this health care system,” Capt. Jameaka Hamilton, MD, who presented the research, said in an interview. “Our findings indicate that there are likely additional factors at play which impact the obstetrical outcomes of women based upon their race, including systems-based barriers to accessing the military health care system which contribute to health care disparities, or in systemic or implicit biases which occur within our health care delivery.”

Plenty of recent research has documented the rise in maternal morbidity and mortality in the United States and the considerable racial disparities within those statistics. Black women are twice as likely to suffer morbidity and three to four times more likely to die in childbirth, compared with White women, Dr. Hamilton, an ob.gyn. from the San Antonio Uniformed Services Health Education Consortium at Ft. Sam Houston in San Antonio, Texas, reminded attendees. So far, much of this disparity has been attributed to social determinants of health.

Military retirees, active-duty personnel, and dependents, however, have equal access to federal health insurance and care at military health care facilities, or at covered civilian facilities where needed. Hence the researchers’ hypothesis that the military medical system would not show the same disparities by race that are seen in civilian populations.

The researchers analyzed maternal morbidity data from the Neonatal Perinatal Information Center from April 2018 to March 2019. The retrospective study included data from 13 military treatment facilities that had more than 1,000 deliveries per year. In addition to statistics on cesarean delivery and adult ICU admission, the researchers compared numbers on overall severe maternal morbidity based on the indicators defined by the Centers for Disease Control and Prevention.

The 15,305 deliveries included 23% Black patients and 77% White patients from the Air Force, Army, and Navy branches.

The cesarean delivery rate ranged from 19.4% to 35.5%. ICU admissions totaled 38 women, 190 women had postpartum hemorrhage, and 282 women experienced severe maternal morbidity. All three measures revealed racial disparities:

• Overall severe maternal morbidity occurred in 2.66% of Black women and 1.66% of White women (P =.0001).
• ICU admission occurred in 0.49% of Black women and 0.18% of White women (P =.0026).
• 31.68% of Black women had a cesarean delivery, compared with 23.58% of White women (P <.0001).

After excluding cases with blood transfusions, Black women were twice as likely to have severe maternal morbidity (0.64% vs. 0.32%). There were no significant differences in postpartum hemorrhage rates between Black and White women, but this analysis was limited by the small overall numbers of postpartum hemorrhage.

Among the study’s limitations were the inability to stratify patients by retiree, active duty, or dependent status, and the lack of data on preeclampsia rates, maternal age, obesity, or other preexisting conditions. In addition, the initial dataset included 61% of patients who reported their race as “other” than Black or White, limiting the number of patients whose data could be analyzed. Since low-volume hospitals were excluded, the outcomes could be skewed if lower-volume facilities are more likely to care for more complex cases, Dr. Hamilton added.

Allison Bryant Mantha, MD, MPH, vice chair for quality, equity, and safety in the ob.gyn. department at Massachusetts General Hospital, Boston, praised Dr. Hamilton’s work for revealing that differential access – though still problematic – cannot fully explain inequities between Black women and other women.

“The findings are not shocking given that what underlies some of these inequities – namely structural and institutional racism, and differential treatment within the system – are not exclusive to civilian health care settings,” Dr. Bryant Mantha, who moderated the session, said in an interview. “That said, doing the work to demonstrate this is extremely valuable.”

Although the causes of these disparities are systemic, Dr. Hamilton said individual providers can play a role in addressing them.

“There can certainly be more done to address this dangerous trend at the provider, hospital/institution, and national level,” she said. I think we as providers should continue to self-reflect and address our own biases. Hospitals and institutions should continue to develop policies that draw attention health care disparities.”

Completely removing these inequalities, however, will require confronting the racism embedded in U.S. health care at all levels, Dr. Bryant Mantha suggested.

“Ultimately, moving to an antiracist health care system – and criminal justice system, educational system, political system, etc. – and dismantling the existing structural racism in policies and practices will be needed to drive this change,” Dr. Bryant Mantha said. “Individual clinicians can use their voices to advocate for these changes in their health systems, communities, and states. Awareness of these inequities is critical, as is a sense of collective efficacy that we can, indeed, change the status quo.”

Dr. Hamilton and Dr. Bryant Mantha reported no disclosures.

An analysis of data from the U.S. military suggests that the maternal morbidity disparities between Black and White women cannot be attributed solely to differences in access to care and socioeconomics.

Even in the U.S. military health care system, where all service members have universal access to the same facilities and providers, researchers found substantial racial disparities in cesarean deliveries, maternal ICU admission, and overall severe maternal morbidity and mortality between Black patients and White patients, according to findings from a new study presented Jan. 28, 2021, at a meeting sponsored by the Society for Maternal-Fetal Medicine.

“This was surprising given some of the driving theories behind maternal race disparities encountered in this country, such as access to care and socioeconomic status, are controlled for in this health care system,” Capt. Jameaka Hamilton, MD, who presented the research, said in an interview. “Our findings indicate that there are likely additional factors at play which impact the obstetrical outcomes of women based upon their race, including systems-based barriers to accessing the military health care system which contribute to health care disparities, or in systemic or implicit biases which occur within our health care delivery.”

Plenty of recent research has documented the rise in maternal morbidity and mortality in the United States and the considerable racial disparities within those statistics. Black women are twice as likely to suffer morbidity and three to four times more likely to die in childbirth, compared with White women, Dr. Hamilton, an ob.gyn. from the San Antonio Uniformed Services Health Education Consortium at Ft. Sam Houston in San Antonio, Texas, reminded attendees. So far, much of this disparity has been attributed to social determinants of health.

Military retirees, active-duty personnel, and dependents, however, have equal access to federal health insurance and care at military health care facilities, or at covered civilian facilities where needed. Hence the researchers’ hypothesis that the military medical system would not show the same disparities by race that are seen in civilian populations.

The researchers analyzed maternal morbidity data from the Neonatal Perinatal Information Center from April 2018 to March 2019. The retrospective study included data from 13 military treatment facilities that had more than 1,000 deliveries per year. In addition to statistics on cesarean delivery and adult ICU admission, the researchers compared numbers on overall severe maternal morbidity based on the indicators defined by the Centers for Disease Control and Prevention.

The 15,305 deliveries included 23% Black patients and 77% White patients from the Air Force, Army, and Navy branches.

The cesarean delivery rate ranged from 19.4% to 35.5%. ICU admissions totaled 38 women, 190 women had postpartum hemorrhage, and 282 women experienced severe maternal morbidity. All three measures revealed racial disparities:

• Overall severe maternal morbidity occurred in 2.66% of Black women and 1.66% of White women (P =.0001).
• ICU admission occurred in 0.49% of Black women and 0.18% of White women (P =.0026).
• 31.68% of Black women had a cesarean delivery, compared with 23.58% of White women (P <.0001).

After excluding cases with blood transfusions, Black women were twice as likely to have severe maternal morbidity (0.64% vs. 0.32%). There were no significant differences in postpartum hemorrhage rates between Black and White women, but this analysis was limited by the small overall numbers of postpartum hemorrhage.

Among the study’s limitations were the inability to stratify patients by retiree, active duty, or dependent status, and the lack of data on preeclampsia rates, maternal age, obesity, or other preexisting conditions. In addition, the initial dataset included 61% of patients who reported their race as “other” than Black or White, limiting the number of patients whose data could be analyzed. Since low-volume hospitals were excluded, the outcomes could be skewed if lower-volume facilities are more likely to care for more complex cases, Dr. Hamilton added.

Allison Bryant Mantha, MD, MPH, vice chair for quality, equity, and safety in the ob.gyn. department at Massachusetts General Hospital, Boston, praised Dr. Hamilton’s work for revealing that differential access – though still problematic – cannot fully explain inequities between Black women and other women.

“The findings are not shocking given that what underlies some of these inequities – namely structural and institutional racism, and differential treatment within the system – are not exclusive to civilian health care settings,” Dr. Bryant Mantha, who moderated the session, said in an interview. “That said, doing the work to demonstrate this is extremely valuable.”

Although the causes of these disparities are systemic, Dr. Hamilton said individual providers can play a role in addressing them.

“There can certainly be more done to address this dangerous trend at the provider, hospital/institution, and national level,” she said. I think we as providers should continue to self-reflect and address our own biases. Hospitals and institutions should continue to develop policies that draw attention health care disparities.”

Completely removing these inequalities, however, will require confronting the racism embedded in U.S. health care at all levels, Dr. Bryant Mantha suggested.

“Ultimately, moving to an antiracist health care system – and criminal justice system, educational system, political system, etc. – and dismantling the existing structural racism in policies and practices will be needed to drive this change,” Dr. Bryant Mantha said. “Individual clinicians can use their voices to advocate for these changes in their health systems, communities, and states. Awareness of these inequities is critical, as is a sense of collective efficacy that we can, indeed, change the status quo.”

Dr. Hamilton and Dr. Bryant Mantha reported no disclosures.

Key clinical point: Patients with chronic myeloid leukemia (CML) resistant or intolerant to imatinib showed superior 2-year adherence with second-line therapy dasatinib vs. nilotinib. Efficacy outcomes between both drugs were similar.

Major finding: Mean adherence calculated over 2 years was superior for dasatinib vs. nilotinib (0.91 vs. 0.82; P = .0043). Persistence for both drugs was 77%. At 2 years, 92% of patients were not in progression for both drugs (P = .02163).

Study details: This retrospective observational study evaluated 117 patients with CML treated with dasatinib (n = 70) or nilotinib (n = 47). Included patients showed resistance/intolerance to first-line treatment with imatinib.

Disclosures: The study did not receive any funding. The authors declared no conflicts of interest.

Source: Santoleri F et al. Curr Med Res Opin. 2021 Jan 16. doi: 10.1080/03007995.2021.1876006.

Key clinical point: Patients with chronic myeloid leukemia (CML) resistant or intolerant to imatinib showed superior 2-year adherence with second-line therapy dasatinib vs. nilotinib. Efficacy outcomes between both drugs were similar.

Major finding: Mean adherence calculated over 2 years was superior for dasatinib vs. nilotinib (0.91 vs. 0.82; P = .0043). Persistence for both drugs was 77%. At 2 years, 92% of patients were not in progression for both drugs (P = .02163).

Study details: This retrospective observational study evaluated 117 patients with CML treated with dasatinib (n = 70) or nilotinib (n = 47). Included patients showed resistance/intolerance to first-line treatment with imatinib.

Disclosures: The study did not receive any funding. The authors declared no conflicts of interest.

Source: Santoleri F et al. Curr Med Res Opin. 2021 Jan 16. doi: 10.1080/03007995.2021.1876006.

Key clinical point: Patients with chronic myeloid leukemia (CML) resistant or intolerant to imatinib showed superior 2-year adherence with second-line therapy dasatinib vs. nilotinib. Efficacy outcomes between both drugs were similar.

Major finding: Mean adherence calculated over 2 years was superior for dasatinib vs. nilotinib (0.91 vs. 0.82; P = .0043). Persistence for both drugs was 77%. At 2 years, 92% of patients were not in progression for both drugs (P = .02163).

Study details: This retrospective observational study evaluated 117 patients with CML treated with dasatinib (n = 70) or nilotinib (n = 47). Included patients showed resistance/intolerance to first-line treatment with imatinib.

Disclosures: The study did not receive any funding. The authors declared no conflicts of interest.

Source: Santoleri F et al. Curr Med Res Opin. 2021 Jan 16. doi: 10.1080/03007995.2021.1876006.

Key clinical point: Comparison of mortality rates highlights benefits of second-generation tyrosine kinase inhibitors (TKIs) in elderly patients aged 75 years or more with chronic myeloid leukemia in chronic phase (CML-CP). However, data need further confirmation in long-term studies.

Major finding: Mortality rates reduced in patients with CML-CP aged 75 years and more vs. the general population (−0.65%). The increased rate of mortality in patients with CP-CML in the age groups 0-29, 30-44, 45-59, and 60-74 years was 0.60%, 1.94%, 1.77%, and 1.43%, respectively.

Study details: A retrospective study of 2,315 patients with CP-CML treated with frontline second-generation TKIs.

Disclosures: No information on funding was available. The presenting author M Breccia reported honoraria from Novartis, Incyte, Pfizer, and Celgene. All other authors declared no conflicts of interest.

Source: Breccia M et al. Ann Hematol. 2021 Jan 7. doi: 10.1007/s00277-021-04406-1.

Key clinical point: Comparison of mortality rates highlights benefits of second-generation tyrosine kinase inhibitors (TKIs) in elderly patients aged 75 years or more with chronic myeloid leukemia in chronic phase (CML-CP). However, data need further confirmation in long-term studies.

Major finding: Mortality rates reduced in patients with CML-CP aged 75 years and more vs. the general population (−0.65%). The increased rate of mortality in patients with CP-CML in the age groups 0-29, 30-44, 45-59, and 60-74 years was 0.60%, 1.94%, 1.77%, and 1.43%, respectively.

Study details: A retrospective study of 2,315 patients with CP-CML treated with frontline second-generation TKIs.

Disclosures: No information on funding was available. The presenting author M Breccia reported honoraria from Novartis, Incyte, Pfizer, and Celgene. All other authors declared no conflicts of interest.

Source: Breccia M et al. Ann Hematol. 2021 Jan 7. doi: 10.1007/s00277-021-04406-1.

Key clinical point: Comparison of mortality rates highlights benefits of second-generation tyrosine kinase inhibitors (TKIs) in elderly patients aged 75 years or more with chronic myeloid leukemia in chronic phase (CML-CP). However, data need further confirmation in long-term studies.

Major finding: Mortality rates reduced in patients with CML-CP aged 75 years and more vs. the general population (−0.65%). The increased rate of mortality in patients with CP-CML in the age groups 0-29, 30-44, 45-59, and 60-74 years was 0.60%, 1.94%, 1.77%, and 1.43%, respectively.

Study details: A retrospective study of 2,315 patients with CP-CML treated with frontline second-generation TKIs.

Disclosures: No information on funding was available. The presenting author M Breccia reported honoraria from Novartis, Incyte, Pfizer, and Celgene. All other authors declared no conflicts of interest.

Source: Breccia M et al. Ann Hematol. 2021 Jan 7. doi: 10.1007/s00277-021-04406-1.

New research suggests that proposed lung cancer screening guidelines could inadvertently increase racial and ethnic disparities, but adding in a risk prediction model could reduce some of these disparities by identifying people with high predicted benefit, regardless of race or ethnicity.

The draft United States Preventive Services Task Force (USPSTF) 2020 guidelines recommend annual lung cancer screening for individuals aged 50-80 who currently smoke or quit in the last 15 years, and who have a smoking history equivalent to at least one pack of cigarettes per day for 20 years or more.

This expands the age range and smoking history requirement compared to the 2013 USPSTF recommendations in an attempt to partially ameliorate racial disparities in screening eligibility. The 2013 guidelines recommend screening ever-smokers aged 55-80 with 30 or more pack-years and 15 or fewer quit-years.

However, neither the 2013 nor the 2020 USPSTF recommendations consider the higher risk of lung cancer and younger ages at diagnosis among African Americans, despite their smoking less than Whites, according to Rebecca Landy, PhD, of the National Cancer Institute in Bethesda, Md.

“For the same age and smoking history as Whites, minorities have substantially different lung cancer risk,” Dr. Landy said. “Incorporating individualized prediction models into USPSTF guidelines may reduce racial/ethnic disparities in lung cancer screening eligibility.”

Dr. Landy and colleagues set out to test that theory, and she presented the results at the 2020 World Congress on Lung Cancer (Abstract 3564), which was rescheduled for January 2021. The results were published in the Journal of the National Cancer Institute.
 

Study details

Dr. Landy and colleagues modeled the performance of National Lung Screening Trial–like screening (three annual CT screens, 5 years of follow-up) among three cohorts of ever-smokers aged 50-80 using the 2015 National Health Interview Survey.

One group was eligible by USPSTF 2013 guidelines, another by draft USPSTF 2020 guidelines, and yet another by augmenting the USPSTF 2020 guidelines using risk prediction to include individuals with 12 or more days of life gained according to the Life-Years From Screening–CT (LYFS-CT) model.

“Among each race/ethnicity, we calculated the number eligible for screening, proportion of preventable lung cancer deaths prevented, proportion of gainable life-years gained, and screening effectiveness, as well as the relative disparities in lung cancer deaths prevented and life-years gained,” Dr. Landy said.
 

Results

Under the 2013 guidelines, 8 million ever-smokers were eligible. The disparities in lung cancer death sensitivity, compared to Whites, were 15% for African Americans, 15% for Asian Americans, and 24% for Hispanic Americans. Disparities for life-year gained sensitivity were 15%, 13%, and 24%, respectively.

Under the 2020 draft guidelines, 14.5 million ever-smokers were eligible, but racial/ethnic disparities persisted. Disparities in lung cancer death sensitivity were 13% for African Americans, 19% for Asian Americans, and 27% for Hispanic Americans. Disparities for life-year gained sensitivity were 16%, 19%, and 27%, respectively.

Using the LYFS-CT predictive-risk model added an additional 3.5 million people and “nearly eliminated” disparities for African Americans, Dr. Landy noted. However, disparities persisted for Asian Americans and Hispanic Americans.

Disparities in lung cancer death sensitivity were 0% for African Americans, 19% for Asian Americans, and 23% for Hispanic Americans. Disparities for life-year gained sensitivity were 1%, 19%, and 24%, respectively.
 

More and widening disparity

The results showed that augmenting USPSTF criteria to include high-benefit people selected significantly more African Americans than Whites and could therefore reduce or even eliminate disparities between Whites and African Americans.

“The 2020 USPSTF draft recommendations would make 6.5 million more people eligible to be screened, in addition to the 8 million from the 2013 criteria,” said Gerard Silvestri, MD, of the Medical University of South Carolina, Charleston, who was not involved in this study.

“But there will be more White people than African American people added, and the disparity between them may widen. Using the risk prediction model outlined in this well-researched study could close the gap in disparity. It’s important to identify individual risk and life expectancy.”

Dr. Silvestri pointed out that, compared to Whites, African Americans develop lung cancer at an earlier age with fewer pack-years history of smoking and have worse outcomes.

“We can’t just focus on one aspect of disparity,” he said. “African Americans are much less likely to be insured or to identify a primary care provider for integrated care. We know that screening works. The 2020 USPSTF draft recommendations will enlarge the pool of eligible African Americans and reduce disparities if the other part of the equation holds; that is, they get access to care and screening.”

This study was funded by the National Institutes of Health/National Cancer Institute. Dr. Landy and Dr. Silvestri have no disclosures.

New research suggests that proposed lung cancer screening guidelines could inadvertently increase racial and ethnic disparities, but adding in a risk prediction model could reduce some of these disparities by identifying people with high predicted benefit, regardless of race or ethnicity.

The draft United States Preventive Services Task Force (USPSTF) 2020 guidelines recommend annual lung cancer screening for individuals aged 50-80 who currently smoke or quit in the last 15 years, and who have a smoking history equivalent to at least one pack of cigarettes per day for 20 years or more.

This expands the age range and smoking history requirement compared to the 2013 USPSTF recommendations in an attempt to partially ameliorate racial disparities in screening eligibility. The 2013 guidelines recommend screening ever-smokers aged 55-80 with 30 or more pack-years and 15 or fewer quit-years.

However, neither the 2013 nor the 2020 USPSTF recommendations consider the higher risk of lung cancer and younger ages at diagnosis among African Americans, despite their smoking less than Whites, according to Rebecca Landy, PhD, of the National Cancer Institute in Bethesda, Md.

“For the same age and smoking history as Whites, minorities have substantially different lung cancer risk,” Dr. Landy said. “Incorporating individualized prediction models into USPSTF guidelines may reduce racial/ethnic disparities in lung cancer screening eligibility.”

Dr. Landy and colleagues set out to test that theory, and she presented the results at the 2020 World Congress on Lung Cancer (Abstract 3564), which was rescheduled for January 2021. The results were published in the Journal of the National Cancer Institute.
 

Study details

Dr. Landy and colleagues modeled the performance of National Lung Screening Trial–like screening (three annual CT screens, 5 years of follow-up) among three cohorts of ever-smokers aged 50-80 using the 2015 National Health Interview Survey.

One group was eligible by USPSTF 2013 guidelines, another by draft USPSTF 2020 guidelines, and yet another by augmenting the USPSTF 2020 guidelines using risk prediction to include individuals with 12 or more days of life gained according to the Life-Years From Screening–CT (LYFS-CT) model.

“Among each race/ethnicity, we calculated the number eligible for screening, proportion of preventable lung cancer deaths prevented, proportion of gainable life-years gained, and screening effectiveness, as well as the relative disparities in lung cancer deaths prevented and life-years gained,” Dr. Landy said.
 

Results

Under the 2013 guidelines, 8 million ever-smokers were eligible. The disparities in lung cancer death sensitivity, compared to Whites, were 15% for African Americans, 15% for Asian Americans, and 24% for Hispanic Americans. Disparities for life-year gained sensitivity were 15%, 13%, and 24%, respectively.

Under the 2020 draft guidelines, 14.5 million ever-smokers were eligible, but racial/ethnic disparities persisted. Disparities in lung cancer death sensitivity were 13% for African Americans, 19% for Asian Americans, and 27% for Hispanic Americans. Disparities for life-year gained sensitivity were 16%, 19%, and 27%, respectively.

Using the LYFS-CT predictive-risk model added an additional 3.5 million people and “nearly eliminated” disparities for African Americans, Dr. Landy noted. However, disparities persisted for Asian Americans and Hispanic Americans.

Disparities in lung cancer death sensitivity were 0% for African Americans, 19% for Asian Americans, and 23% for Hispanic Americans. Disparities for life-year gained sensitivity were 1%, 19%, and 24%, respectively.
 

More and widening disparity

The results showed that augmenting USPSTF criteria to include high-benefit people selected significantly more African Americans than Whites and could therefore reduce or even eliminate disparities between Whites and African Americans.

“The 2020 USPSTF draft recommendations would make 6.5 million more people eligible to be screened, in addition to the 8 million from the 2013 criteria,” said Gerard Silvestri, MD, of the Medical University of South Carolina, Charleston, who was not involved in this study.

“But there will be more White people than African American people added, and the disparity between them may widen. Using the risk prediction model outlined in this well-researched study could close the gap in disparity. It’s important to identify individual risk and life expectancy.”

Dr. Silvestri pointed out that, compared to Whites, African Americans develop lung cancer at an earlier age with fewer pack-years history of smoking and have worse outcomes.

“We can’t just focus on one aspect of disparity,” he said. “African Americans are much less likely to be insured or to identify a primary care provider for integrated care. We know that screening works. The 2020 USPSTF draft recommendations will enlarge the pool of eligible African Americans and reduce disparities if the other part of the equation holds; that is, they get access to care and screening.”

This study was funded by the National Institutes of Health/National Cancer Institute. Dr. Landy and Dr. Silvestri have no disclosures.

New research suggests that proposed lung cancer screening guidelines could inadvertently increase racial and ethnic disparities, but adding in a risk prediction model could reduce some of these disparities by identifying people with high predicted benefit, regardless of race or ethnicity.

The draft United States Preventive Services Task Force (USPSTF) 2020 guidelines recommend annual lung cancer screening for individuals aged 50-80 who currently smoke or quit in the last 15 years, and who have a smoking history equivalent to at least one pack of cigarettes per day for 20 years or more.

This expands the age range and smoking history requirement compared to the 2013 USPSTF recommendations in an attempt to partially ameliorate racial disparities in screening eligibility. The 2013 guidelines recommend screening ever-smokers aged 55-80 with 30 or more pack-years and 15 or fewer quit-years.

However, neither the 2013 nor the 2020 USPSTF recommendations consider the higher risk of lung cancer and younger ages at diagnosis among African Americans, despite their smoking less than Whites, according to Rebecca Landy, PhD, of the National Cancer Institute in Bethesda, Md.

“For the same age and smoking history as Whites, minorities have substantially different lung cancer risk,” Dr. Landy said. “Incorporating individualized prediction models into USPSTF guidelines may reduce racial/ethnic disparities in lung cancer screening eligibility.”

Dr. Landy and colleagues set out to test that theory, and she presented the results at the 2020 World Congress on Lung Cancer (Abstract 3564), which was rescheduled for January 2021. The results were published in the Journal of the National Cancer Institute.
 

Study details

Dr. Landy and colleagues modeled the performance of National Lung Screening Trial–like screening (three annual CT screens, 5 years of follow-up) among three cohorts of ever-smokers aged 50-80 using the 2015 National Health Interview Survey.

One group was eligible by USPSTF 2013 guidelines, another by draft USPSTF 2020 guidelines, and yet another by augmenting the USPSTF 2020 guidelines using risk prediction to include individuals with 12 or more days of life gained according to the Life-Years From Screening–CT (LYFS-CT) model.

“Among each race/ethnicity, we calculated the number eligible for screening, proportion of preventable lung cancer deaths prevented, proportion of gainable life-years gained, and screening effectiveness, as well as the relative disparities in lung cancer deaths prevented and life-years gained,” Dr. Landy said.
 

Results

Under the 2013 guidelines, 8 million ever-smokers were eligible. The disparities in lung cancer death sensitivity, compared to Whites, were 15% for African Americans, 15% for Asian Americans, and 24% for Hispanic Americans. Disparities for life-year gained sensitivity were 15%, 13%, and 24%, respectively.

Under the 2020 draft guidelines, 14.5 million ever-smokers were eligible, but racial/ethnic disparities persisted. Disparities in lung cancer death sensitivity were 13% for African Americans, 19% for Asian Americans, and 27% for Hispanic Americans. Disparities for life-year gained sensitivity were 16%, 19%, and 27%, respectively.

Using the LYFS-CT predictive-risk model added an additional 3.5 million people and “nearly eliminated” disparities for African Americans, Dr. Landy noted. However, disparities persisted for Asian Americans and Hispanic Americans.

Disparities in lung cancer death sensitivity were 0% for African Americans, 19% for Asian Americans, and 23% for Hispanic Americans. Disparities for life-year gained sensitivity were 1%, 19%, and 24%, respectively.
 

More and widening disparity

The results showed that augmenting USPSTF criteria to include high-benefit people selected significantly more African Americans than Whites and could therefore reduce or even eliminate disparities between Whites and African Americans.

“The 2020 USPSTF draft recommendations would make 6.5 million more people eligible to be screened, in addition to the 8 million from the 2013 criteria,” said Gerard Silvestri, MD, of the Medical University of South Carolina, Charleston, who was not involved in this study.

“But there will be more White people than African American people added, and the disparity between them may widen. Using the risk prediction model outlined in this well-researched study could close the gap in disparity. It’s important to identify individual risk and life expectancy.”

Dr. Silvestri pointed out that, compared to Whites, African Americans develop lung cancer at an earlier age with fewer pack-years history of smoking and have worse outcomes.

“We can’t just focus on one aspect of disparity,” he said. “African Americans are much less likely to be insured or to identify a primary care provider for integrated care. We know that screening works. The 2020 USPSTF draft recommendations will enlarge the pool of eligible African Americans and reduce disparities if the other part of the equation holds; that is, they get access to care and screening.”

This study was funded by the National Institutes of Health/National Cancer Institute. Dr. Landy and Dr. Silvestri have no disclosures.

Key clinical point: Biomarkers can predict relapse in patients with chronic myeloid leukemia (CML) who are eligible for a controlled treatment interruption.

Major finding: Predictors of CML relapse after treatment interruptions were low levels of cytotoxic cells such as CD56+ with low expression of CD16 and CD94/NKG2 receptors and CD8± T cells expressing TCRγβ+; low expression of activating receptors on the surface of natural killer (NK) and NK T cells; impaired synthesis of proinflammatory cytokines or proteases from NK cells; and HLA-E*0103 homozygosis and KIR haplotype BX.

Study details: The data come from an observational, cross-sectional study of 93 patients with chronic phase CML and 20 age- and gender-matched controls. Among patients with CML, 45 were on treatment with tyrosine kinase inhibitors (TKIs), 27 on sustained treatment-free remission (off TKIs), 15 had a relapse, and 6 had newly diagnosed CML.

Disclosures: The study was funded by the Foundation for Biomedical Research of the Hospital Universitario Ramón y Cajal, the Spanish Ministry of Economy and Competitiveness, and the Spanish AIDS Research Network. The authors declared no conflicts of interest.

Source: Vigón L et al. J Clin Med. 2020 Dec 25. doi: 10.3390/jcm10010042.

Key clinical point: Biomarkers can predict relapse in patients with chronic myeloid leukemia (CML) who are eligible for a controlled treatment interruption.

Major finding: Predictors of CML relapse after treatment interruptions were low levels of cytotoxic cells such as CD56+ with low expression of CD16 and CD94/NKG2 receptors and CD8± T cells expressing TCRγβ+; low expression of activating receptors on the surface of natural killer (NK) and NK T cells; impaired synthesis of proinflammatory cytokines or proteases from NK cells; and HLA-E*0103 homozygosis and KIR haplotype BX.

Study details: The data come from an observational, cross-sectional study of 93 patients with chronic phase CML and 20 age- and gender-matched controls. Among patients with CML, 45 were on treatment with tyrosine kinase inhibitors (TKIs), 27 on sustained treatment-free remission (off TKIs), 15 had a relapse, and 6 had newly diagnosed CML.

Disclosures: The study was funded by the Foundation for Biomedical Research of the Hospital Universitario Ramón y Cajal, the Spanish Ministry of Economy and Competitiveness, and the Spanish AIDS Research Network. The authors declared no conflicts of interest.

Source: Vigón L et al. J Clin Med. 2020 Dec 25. doi: 10.3390/jcm10010042.

Key clinical point: Biomarkers can predict relapse in patients with chronic myeloid leukemia (CML) who are eligible for a controlled treatment interruption.

Major finding: Predictors of CML relapse after treatment interruptions were low levels of cytotoxic cells such as CD56+ with low expression of CD16 and CD94/NKG2 receptors and CD8± T cells expressing TCRγβ+; low expression of activating receptors on the surface of natural killer (NK) and NK T cells; impaired synthesis of proinflammatory cytokines or proteases from NK cells; and HLA-E*0103 homozygosis and KIR haplotype BX.

Study details: The data come from an observational, cross-sectional study of 93 patients with chronic phase CML and 20 age- and gender-matched controls. Among patients with CML, 45 were on treatment with tyrosine kinase inhibitors (TKIs), 27 on sustained treatment-free remission (off TKIs), 15 had a relapse, and 6 had newly diagnosed CML.

Disclosures: The study was funded by the Foundation for Biomedical Research of the Hospital Universitario Ramón y Cajal, the Spanish Ministry of Economy and Competitiveness, and the Spanish AIDS Research Network. The authors declared no conflicts of interest.

Source: Vigón L et al. J Clin Med. 2020 Dec 25. doi: 10.3390/jcm10010042.

Key clinical point: Older age and imatinib therapy were associated with a higher mortality rate in patients with chronic myeloid leukemia (CML) who contracted COVID-19. However, imatinib could be a confounding factor.

Major finding: Outcome was favorable and fatal in 86% and 14% of patients, respectively. COVID-19 mortality rate was higher in patients aged 75 years vs. less than 75 years (60% vs. 7%; P less than .001) and in those on imatinib vs. second-generation tyrosine kinase inhibitors (TKIs) vs. no TKIs (25% vs. 3% vs. 0%; P = .003). However, 25% vs. 0% of patients treated with imatinib vs. second-generation TKIs were more than 75 years old.

Study details: The CANDID study evaluated 110 cases of COVID-19 in patients with CML reported by physicians to the International CML Foundation until July 1, 2020 across 20 countries.

Disclosures: No study sponsor was identified. The lead author reported ties with BMS, Incyte, Novartis, and Pfizer. Some co-authors also reported ties with various pharmaceutical companies.

Source: Rea D et al. ASH 2020. 2020 Dec 7.  Abstract 649.

Key clinical point: Older age and imatinib therapy were associated with a higher mortality rate in patients with chronic myeloid leukemia (CML) who contracted COVID-19. However, imatinib could be a confounding factor.

Major finding: Outcome was favorable and fatal in 86% and 14% of patients, respectively. COVID-19 mortality rate was higher in patients aged 75 years vs. less than 75 years (60% vs. 7%; P less than .001) and in those on imatinib vs. second-generation tyrosine kinase inhibitors (TKIs) vs. no TKIs (25% vs. 3% vs. 0%; P = .003). However, 25% vs. 0% of patients treated with imatinib vs. second-generation TKIs were more than 75 years old.

Study details: The CANDID study evaluated 110 cases of COVID-19 in patients with CML reported by physicians to the International CML Foundation until July 1, 2020 across 20 countries.

Disclosures: No study sponsor was identified. The lead author reported ties with BMS, Incyte, Novartis, and Pfizer. Some co-authors also reported ties with various pharmaceutical companies.

Source: Rea D et al. ASH 2020. 2020 Dec 7.  Abstract 649.

Key clinical point: Older age and imatinib therapy were associated with a higher mortality rate in patients with chronic myeloid leukemia (CML) who contracted COVID-19. However, imatinib could be a confounding factor.

Major finding: Outcome was favorable and fatal in 86% and 14% of patients, respectively. COVID-19 mortality rate was higher in patients aged 75 years vs. less than 75 years (60% vs. 7%; P less than .001) and in those on imatinib vs. second-generation tyrosine kinase inhibitors (TKIs) vs. no TKIs (25% vs. 3% vs. 0%; P = .003). However, 25% vs. 0% of patients treated with imatinib vs. second-generation TKIs were more than 75 years old.

Study details: The CANDID study evaluated 110 cases of COVID-19 in patients with CML reported by physicians to the International CML Foundation until July 1, 2020 across 20 countries.

Disclosures: No study sponsor was identified. The lead author reported ties with BMS, Incyte, Novartis, and Pfizer. Some co-authors also reported ties with various pharmaceutical companies.

Source: Rea D et al. ASH 2020. 2020 Dec 7.  Abstract 649.