Commentary

The three most exposed areas of the body that give away a person’s age are the face, neck, and hands. Rejuvenation of the hands is an often simple and nice addition to facial and neck aesthetic rejuvenation.

When examining aging hands, the three most prominent features are decreased volume in the interosseous spaces (leading to increased crepiness of the skin and increased show of extensor tendons), lentigines, and prominent veins. Therefore, the treatment for hands is quite simple: Restore volume, treat the pigmented lesions, and if needed, treat the prominent veins.

The anatomy of the dorsal hand can be divided into three major compartments. First, the skin, which on the dorsal hand is quite pliable. Second, the subcutaneous tissue, which consists of a loose areolar tissue where the lymphatics and veins lie. Third, beneath the subcutaneous tissue is the dorsal fascia of the hand, which is contiguous with extensor tendons and underlying compartments. It is in the subcutaneous layer (or loose areolar tissue) where fillers or fat are placed to treat volume loss.

While several fillers are currently used off label for hand rejuvenation, the Food and Drug Administration is meeting in February to consider officially approving Radiesse for this indication. Currently, hyaluronic acid (HA) fillers, calcium- hydroxylapatite (Radiesse), poly-L-lactic acid, and autologous fat are all utilized. I tend to use HAs in this location because of the reversibility, if needed, and decreased risk of nodule formation. Several techniques exist, including injecting between each tendon space vs. a bolus technique. I tend to use a bolus technique, where one or two boluses are injected while tenting the skin up to ensure injection into the correct plane and to avoid the vessels. Subsequently, the boluses are massaged into place while the patient makes a fist.

Once the interosseous spaces have been treated, the veins often appear less prominent and often don’t require direct treatment. I typically do not treat the dorsal hand veins, but sclerotherapy can be performed. Lentigines may be treated with a variety of devices including intense pulse light, Q-switched lasers, and fractionated nonablative lasers. Chemical peels and topical antipigment agents also may help to a lesser degree or also may be used for maintenance to keep the lentigines away.

Dr. Talakoub and Dr. Wesley are co-contributors to a monthly Aesthetic Dermatology column in Dermatology News. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Wesley.

The three most exposed areas of the body that give away a person’s age are the face, neck, and hands. Rejuvenation of the hands is an often simple and nice addition to facial and neck aesthetic rejuvenation.

When examining aging hands, the three most prominent features are decreased volume in the interosseous spaces (leading to increased crepiness of the skin and increased show of extensor tendons), lentigines, and prominent veins. Therefore, the treatment for hands is quite simple: Restore volume, treat the pigmented lesions, and if needed, treat the prominent veins.

The anatomy of the dorsal hand can be divided into three major compartments. First, the skin, which on the dorsal hand is quite pliable. Second, the subcutaneous tissue, which consists of a loose areolar tissue where the lymphatics and veins lie. Third, beneath the subcutaneous tissue is the dorsal fascia of the hand, which is contiguous with extensor tendons and underlying compartments. It is in the subcutaneous layer (or loose areolar tissue) where fillers or fat are placed to treat volume loss.

While several fillers are currently used off label for hand rejuvenation, the Food and Drug Administration is meeting in February to consider officially approving Radiesse for this indication. Currently, hyaluronic acid (HA) fillers, calcium- hydroxylapatite (Radiesse), poly-L-lactic acid, and autologous fat are all utilized. I tend to use HAs in this location because of the reversibility, if needed, and decreased risk of nodule formation. Several techniques exist, including injecting between each tendon space vs. a bolus technique. I tend to use a bolus technique, where one or two boluses are injected while tenting the skin up to ensure injection into the correct plane and to avoid the vessels. Subsequently, the boluses are massaged into place while the patient makes a fist.

Once the interosseous spaces have been treated, the veins often appear less prominent and often don’t require direct treatment. I typically do not treat the dorsal hand veins, but sclerotherapy can be performed. Lentigines may be treated with a variety of devices including intense pulse light, Q-switched lasers, and fractionated nonablative lasers. Chemical peels and topical antipigment agents also may help to a lesser degree or also may be used for maintenance to keep the lentigines away.

Dr. Talakoub and Dr. Wesley are co-contributors to a monthly Aesthetic Dermatology column in Dermatology News. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Wesley.

The three most exposed areas of the body that give away a person’s age are the face, neck, and hands. Rejuvenation of the hands is an often simple and nice addition to facial and neck aesthetic rejuvenation.

When examining aging hands, the three most prominent features are decreased volume in the interosseous spaces (leading to increased crepiness of the skin and increased show of extensor tendons), lentigines, and prominent veins. Therefore, the treatment for hands is quite simple: Restore volume, treat the pigmented lesions, and if needed, treat the prominent veins.

The anatomy of the dorsal hand can be divided into three major compartments. First, the skin, which on the dorsal hand is quite pliable. Second, the subcutaneous tissue, which consists of a loose areolar tissue where the lymphatics and veins lie. Third, beneath the subcutaneous tissue is the dorsal fascia of the hand, which is contiguous with extensor tendons and underlying compartments. It is in the subcutaneous layer (or loose areolar tissue) where fillers or fat are placed to treat volume loss.

While several fillers are currently used off label for hand rejuvenation, the Food and Drug Administration is meeting in February to consider officially approving Radiesse for this indication. Currently, hyaluronic acid (HA) fillers, calcium- hydroxylapatite (Radiesse), poly-L-lactic acid, and autologous fat are all utilized. I tend to use HAs in this location because of the reversibility, if needed, and decreased risk of nodule formation. Several techniques exist, including injecting between each tendon space vs. a bolus technique. I tend to use a bolus technique, where one or two boluses are injected while tenting the skin up to ensure injection into the correct plane and to avoid the vessels. Subsequently, the boluses are massaged into place while the patient makes a fist.

Once the interosseous spaces have been treated, the veins often appear less prominent and often don’t require direct treatment. I typically do not treat the dorsal hand veins, but sclerotherapy can be performed. Lentigines may be treated with a variety of devices including intense pulse light, Q-switched lasers, and fractionated nonablative lasers. Chemical peels and topical antipigment agents also may help to a lesser degree or also may be used for maintenance to keep the lentigines away.

Dr. Talakoub and Dr. Wesley are co-contributors to a monthly Aesthetic Dermatology column in Dermatology News. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Wesley.

Rudolph Virchow clearly demonstrated the association between malignancy and venous thromboembolic events. VTE – deep vein thrombosis and pulmonary embolism – affect between 15% and 38% of patients with gynecologic malignancies after surgery.

The rate of pulmonary embolism (PE) in this patient population can be as high as 6.8%, with the case fatality rate being 11%-12% (Obstet. Gynecol. 2012;119:155-67). Other factors associated with the development of VTE include prior VTE, older age, African American race, prolonged operative time, obesity, and prior radiation therapy (Obstet. Gynecol. 1987;69:146-50). The risk of VTE in women undergoing gynecologic surgery is quadrupled in the presence of malignancy(Obstet. Gynecol. 2006;107:666-71) and these patients are twice as likely to die from a VTE compared to matched controls (Gynecol. Oncol. 2007;106:439-45).

Additionally, cancer patients are typically older, have longer and more complex surgeries, and the presence of a pelvic mass further contributes to venous stasis (Obstet. Gynecol. 2012;119:155-67).

Although the treatment of VTE is fairly similar between patients with malignancy and those without cancer, treatment of a VTE in patients with cancer can be further complicated by higher VTE recurrence rates and increased risk of bleeding. Furthermore, issues related to the malignant disease process such as prognosis, presence and location of metastasis, and life expectancy should be taken into consideration when managing VTE in this patient population.

Generally, in the setting of an acute or recurrent VTE, initial therapy with a parenteral anticoagulant (heparin or low-molecular-weight heparins [LMWH]) should be immediately instituted in patients with a gynecologic malignancy, unless there is evidence of active bleeding or any other contraindication for the use of an anticoagulant.

Other factors associated with cancer such as immobilization, the presence of metastases, and impaired renal function with a creatinine clearance less than 30 mL/min, may increase the risk of bleeding complications but are not absolute contraindications to anticoagulation (Thromb. Haemost. 2008;100:435-9). The initial treatment phase, which last for 5-10 days, is then followed by a longer treatment phase lasting 3-6 months.

In the majority of cases, LMWH is the preferred agent for both the initial and prolonged treatment phase assuming adequate renal function. Based on evidence from a meta-analysis of 16 randomized controlled trials in cancer patients receiving initial anticoagulation for VTE, LMWH is associated with a 30% reduction in mortality without an increased risk of bleeding in comparison to unfractionated heparin (Cochrane Database. Syst. Rev. 2014;6:CD006649).

When compared with the vitamin K antagonist warfarin, LMWH appears to be associated with a significantly reduced rate of recurrent VTE (hazard ratio, 0.47; 95% confidence interval 0.32-0.71). However, this was not associated with a survival advantage (N. Engl. J. Med. 2003;349:146-53).

There are no trials comparing the different formulations of LMWH. In our practice, we routinely use the LMWH enoxaparin dosed at 1 mg/kg subcutaneously twice daily. Other well-studied LMWHs include dalteparin and tinzaparin.

LMWHs are primarily renally excreted, thus, in patients with compromised renal function, the biological half-life of the medication may be prolonged, leading to potential bleeding complications. The majority of LMWH trials excluded patients with creatinine clearance less than 30 mL/min, therefore, in patients with compromised renal function, one option would be to decrease the daily dose by as much as 50% and closely monitor antifactor XA levels. Alternatively, the use of unfractionated heparin in the acute setting followed by warfarin with close monitoring of the patient’s international normalized ratio could prove less cumbersome and ultimately safer for these patients. However, given the limitations of the currently available data we would not recommend the routine use of newer oral anticoagulation agents.

Patients with a malignancy are at increased risk for the development of a recurrent VTE even in the setting of anticoagulation. Some of the risks factors for this phenomenon include presence of central venous catheters, interruption of therapy for procedures, and immobilization. In cases of recurrent VTE, consideration should be given to extending the duration of treatment beyond the initial planned 3-6 months. Other patients that may benefit from extended therapy include those with continued immobility or active cancer burden.

LMWH is also the preferred agent for extended therapy based on very limited evidence from experimental studies suggesting that LMWH may have antineoplastic effects and thus a survival advantage. However, in the setting of a recurrent VTE, there is very limited data on which to base the choice of extended treatment. Options include switching the therapeutic agent, increasing the dose or frequency of administration, or placement of an inferior vena cava filter. Consultation with a hematologist may also be warranted in this and more complicated scenarios.

Ultimately, LMWH appears to be the best available therapy for patients with a gynecologic malignancy. However, the decision to anticoagulate should be carefully planned out, taking into consideration the individual patient’s disease burden and associated comorbidities in order to select the most appropriate treatment option.

Dr. Roque is a fellow in the gynecologic oncology program at the University of North Carolina at Chapel Hill. Dr. Clarke-Pearson is the chair and the Robert A. Ross Distinguished Professor of Obstetrics and Gynecology and a professor in the division of gynecologic oncology at the university. Dr. Roque and Dr. Clarke-Pearson said they had no relevant financial disclosures.

Rudolph Virchow clearly demonstrated the association between malignancy and venous thromboembolic events. VTE – deep vein thrombosis and pulmonary embolism – affect between 15% and 38% of patients with gynecologic malignancies after surgery.

The rate of pulmonary embolism (PE) in this patient population can be as high as 6.8%, with the case fatality rate being 11%-12% (Obstet. Gynecol. 2012;119:155-67). Other factors associated with the development of VTE include prior VTE, older age, African American race, prolonged operative time, obesity, and prior radiation therapy (Obstet. Gynecol. 1987;69:146-50). The risk of VTE in women undergoing gynecologic surgery is quadrupled in the presence of malignancy(Obstet. Gynecol. 2006;107:666-71) and these patients are twice as likely to die from a VTE compared to matched controls (Gynecol. Oncol. 2007;106:439-45).

Additionally, cancer patients are typically older, have longer and more complex surgeries, and the presence of a pelvic mass further contributes to venous stasis (Obstet. Gynecol. 2012;119:155-67).

Although the treatment of VTE is fairly similar between patients with malignancy and those without cancer, treatment of a VTE in patients with cancer can be further complicated by higher VTE recurrence rates and increased risk of bleeding. Furthermore, issues related to the malignant disease process such as prognosis, presence and location of metastasis, and life expectancy should be taken into consideration when managing VTE in this patient population.

Generally, in the setting of an acute or recurrent VTE, initial therapy with a parenteral anticoagulant (heparin or low-molecular-weight heparins [LMWH]) should be immediately instituted in patients with a gynecologic malignancy, unless there is evidence of active bleeding or any other contraindication for the use of an anticoagulant.

Other factors associated with cancer such as immobilization, the presence of metastases, and impaired renal function with a creatinine clearance less than 30 mL/min, may increase the risk of bleeding complications but are not absolute contraindications to anticoagulation (Thromb. Haemost. 2008;100:435-9). The initial treatment phase, which last for 5-10 days, is then followed by a longer treatment phase lasting 3-6 months.

In the majority of cases, LMWH is the preferred agent for both the initial and prolonged treatment phase assuming adequate renal function. Based on evidence from a meta-analysis of 16 randomized controlled trials in cancer patients receiving initial anticoagulation for VTE, LMWH is associated with a 30% reduction in mortality without an increased risk of bleeding in comparison to unfractionated heparin (Cochrane Database. Syst. Rev. 2014;6:CD006649).

When compared with the vitamin K antagonist warfarin, LMWH appears to be associated with a significantly reduced rate of recurrent VTE (hazard ratio, 0.47; 95% confidence interval 0.32-0.71). However, this was not associated with a survival advantage (N. Engl. J. Med. 2003;349:146-53).

There are no trials comparing the different formulations of LMWH. In our practice, we routinely use the LMWH enoxaparin dosed at 1 mg/kg subcutaneously twice daily. Other well-studied LMWHs include dalteparin and tinzaparin.

LMWHs are primarily renally excreted, thus, in patients with compromised renal function, the biological half-life of the medication may be prolonged, leading to potential bleeding complications. The majority of LMWH trials excluded patients with creatinine clearance less than 30 mL/min, therefore, in patients with compromised renal function, one option would be to decrease the daily dose by as much as 50% and closely monitor antifactor XA levels. Alternatively, the use of unfractionated heparin in the acute setting followed by warfarin with close monitoring of the patient’s international normalized ratio could prove less cumbersome and ultimately safer for these patients. However, given the limitations of the currently available data we would not recommend the routine use of newer oral anticoagulation agents.

Patients with a malignancy are at increased risk for the development of a recurrent VTE even in the setting of anticoagulation. Some of the risks factors for this phenomenon include presence of central venous catheters, interruption of therapy for procedures, and immobilization. In cases of recurrent VTE, consideration should be given to extending the duration of treatment beyond the initial planned 3-6 months. Other patients that may benefit from extended therapy include those with continued immobility or active cancer burden.

LMWH is also the preferred agent for extended therapy based on very limited evidence from experimental studies suggesting that LMWH may have antineoplastic effects and thus a survival advantage. However, in the setting of a recurrent VTE, there is very limited data on which to base the choice of extended treatment. Options include switching the therapeutic agent, increasing the dose or frequency of administration, or placement of an inferior vena cava filter. Consultation with a hematologist may also be warranted in this and more complicated scenarios.

Ultimately, LMWH appears to be the best available therapy for patients with a gynecologic malignancy. However, the decision to anticoagulate should be carefully planned out, taking into consideration the individual patient’s disease burden and associated comorbidities in order to select the most appropriate treatment option.

Dr. Roque is a fellow in the gynecologic oncology program at the University of North Carolina at Chapel Hill. Dr. Clarke-Pearson is the chair and the Robert A. Ross Distinguished Professor of Obstetrics and Gynecology and a professor in the division of gynecologic oncology at the university. Dr. Roque and Dr. Clarke-Pearson said they had no relevant financial disclosures.

Rudolph Virchow clearly demonstrated the association between malignancy and venous thromboembolic events. VTE – deep vein thrombosis and pulmonary embolism – affect between 15% and 38% of patients with gynecologic malignancies after surgery.

The rate of pulmonary embolism (PE) in this patient population can be as high as 6.8%, with the case fatality rate being 11%-12% (Obstet. Gynecol. 2012;119:155-67). Other factors associated with the development of VTE include prior VTE, older age, African American race, prolonged operative time, obesity, and prior radiation therapy (Obstet. Gynecol. 1987;69:146-50). The risk of VTE in women undergoing gynecologic surgery is quadrupled in the presence of malignancy(Obstet. Gynecol. 2006;107:666-71) and these patients are twice as likely to die from a VTE compared to matched controls (Gynecol. Oncol. 2007;106:439-45).

Additionally, cancer patients are typically older, have longer and more complex surgeries, and the presence of a pelvic mass further contributes to venous stasis (Obstet. Gynecol. 2012;119:155-67).

Although the treatment of VTE is fairly similar between patients with malignancy and those without cancer, treatment of a VTE in patients with cancer can be further complicated by higher VTE recurrence rates and increased risk of bleeding. Furthermore, issues related to the malignant disease process such as prognosis, presence and location of metastasis, and life expectancy should be taken into consideration when managing VTE in this patient population.

Generally, in the setting of an acute or recurrent VTE, initial therapy with a parenteral anticoagulant (heparin or low-molecular-weight heparins [LMWH]) should be immediately instituted in patients with a gynecologic malignancy, unless there is evidence of active bleeding or any other contraindication for the use of an anticoagulant.

Other factors associated with cancer such as immobilization, the presence of metastases, and impaired renal function with a creatinine clearance less than 30 mL/min, may increase the risk of bleeding complications but are not absolute contraindications to anticoagulation (Thromb. Haemost. 2008;100:435-9). The initial treatment phase, which last for 5-10 days, is then followed by a longer treatment phase lasting 3-6 months.

In the majority of cases, LMWH is the preferred agent for both the initial and prolonged treatment phase assuming adequate renal function. Based on evidence from a meta-analysis of 16 randomized controlled trials in cancer patients receiving initial anticoagulation for VTE, LMWH is associated with a 30% reduction in mortality without an increased risk of bleeding in comparison to unfractionated heparin (Cochrane Database. Syst. Rev. 2014;6:CD006649).

When compared with the vitamin K antagonist warfarin, LMWH appears to be associated with a significantly reduced rate of recurrent VTE (hazard ratio, 0.47; 95% confidence interval 0.32-0.71). However, this was not associated with a survival advantage (N. Engl. J. Med. 2003;349:146-53).

There are no trials comparing the different formulations of LMWH. In our practice, we routinely use the LMWH enoxaparin dosed at 1 mg/kg subcutaneously twice daily. Other well-studied LMWHs include dalteparin and tinzaparin.

LMWHs are primarily renally excreted, thus, in patients with compromised renal function, the biological half-life of the medication may be prolonged, leading to potential bleeding complications. The majority of LMWH trials excluded patients with creatinine clearance less than 30 mL/min, therefore, in patients with compromised renal function, one option would be to decrease the daily dose by as much as 50% and closely monitor antifactor XA levels. Alternatively, the use of unfractionated heparin in the acute setting followed by warfarin with close monitoring of the patient’s international normalized ratio could prove less cumbersome and ultimately safer for these patients. However, given the limitations of the currently available data we would not recommend the routine use of newer oral anticoagulation agents.

Patients with a malignancy are at increased risk for the development of a recurrent VTE even in the setting of anticoagulation. Some of the risks factors for this phenomenon include presence of central venous catheters, interruption of therapy for procedures, and immobilization. In cases of recurrent VTE, consideration should be given to extending the duration of treatment beyond the initial planned 3-6 months. Other patients that may benefit from extended therapy include those with continued immobility or active cancer burden.

LMWH is also the preferred agent for extended therapy based on very limited evidence from experimental studies suggesting that LMWH may have antineoplastic effects and thus a survival advantage. However, in the setting of a recurrent VTE, there is very limited data on which to base the choice of extended treatment. Options include switching the therapeutic agent, increasing the dose or frequency of administration, or placement of an inferior vena cava filter. Consultation with a hematologist may also be warranted in this and more complicated scenarios.

Ultimately, LMWH appears to be the best available therapy for patients with a gynecologic malignancy. However, the decision to anticoagulate should be carefully planned out, taking into consideration the individual patient’s disease burden and associated comorbidities in order to select the most appropriate treatment option.

Dr. Roque is a fellow in the gynecologic oncology program at the University of North Carolina at Chapel Hill. Dr. Clarke-Pearson is the chair and the Robert A. Ross Distinguished Professor of Obstetrics and Gynecology and a professor in the division of gynecologic oncology at the university. Dr. Roque and Dr. Clarke-Pearson said they had no relevant financial disclosures.

Kaempferol (3,5,7,4’-tetrahydroxyflavone; C₁₅H₁₀O₆) is among the natural flavonols found in green tea, broccoli, cabbage, kale, endive, beans, leeks, tomatoes, grapes, apples, grapefruit, berries, and propolis, as well as myriad other plant sources, including Brassica and species (J. Agric. Food Chem. 2006;54:2951-6; Cancer Prev. Res. (Phila) 2014;7:958-67; Biochem. Pharmacol. 2010;80:2042-9; Chem. Pharm. Bull. (Tokyo) 2012;60:1171-5; J. Eur. Acad. Dermatol. Venereol. 2013 June 27 [doi:10.1111/jdv.12204]).

It is one of the most commonly found dietary flavonoids and is also present in beer, particularly hops (Carcinogenesis 2010;31:1338-43; J. Eur. Acad. Dermatol. Venereol. 2013 June 27 [doi:10.1111/jdv.12204]). Significantly, kaempferol is known to exhibit anticancer, anti-inflammatory, antioxidant, cytoprotective, and antiapoptotic activity (Cancer Prev. Res. (Phila) 2014;7:958-67; Biochem. Pharmacol. 2010;80:2042-9; Exp. Mol. Med. 2008;40:208-19), and is believed to play a role in protecting plants from ultraviolet (UV)-induced damage (J. Agric. Food Chem. 2012;60:6966-76).

Skin protection: antioxidant and anti-inflammatory activity

Among 35 flavonoids tested by Cos et al. in 2001 for lipid peroxidation-inhibiting activity, kaempferol was identified as having the highest antioxidant selectivity index (Planta Med. 2001;67:515-9).

Work by Kim et al. in 2002 revealed that four kaempferol glycosides are key active ingredients in the flowers of Prunus persica, which has long been used in traditional Chinese medicine to treat skin disorders (J. Cosmet. Sci. 2002;53:27-34). Kim and colleagues have also shown in animal studies that the topical application of P. persica may be effective at thwarting UVB-induced skin damage (J. Cosmet. Sci. 2002;53:27-34).

In addition, kaempferol is a key component in Punica granatum, which has been found to act as an effective protector against UVB-induced photodamage and aging in cultured skin fibroblasts (Int. J. Dermatol. 2010;49:276-82).

In various tests on the effects of natural flavonoids on matrix metalloproteinase (MMP)-1 activity and expression, Lim et al. reported in 2007 that kaempferol and quercetin potently inhibited recombinant human MMP-1, and both flavonols along with apigenin and wogonin were found to be strong inhibitors of MMP-1 induction in 12-O-tetradecanoylphorbol-13-acetate–treated human dermal fibroblasts. All four flavonoids also suppressed the activation of activator protein (AP)-1. Kaempferol also hindered p38 mitogen-activated protein kinase c-Jun N-terminal kinase (JNK) activation. The investigators concluded that kaempferol is among the flavonoids or plant extracts containing them that may be useful as an agent to protect against photoaging and to treat some cutaneous inflammatory conditions (Planta Med. 2007;73:1267-74).

In 2010, Park et al. demonstrated that kaempferol alleviated burn injuries in mice and that expression of tumor necrosis factor–alpha (TNF-alpha) induced by burn injuries was reduced by kaempferol. They concluded that their findings suggest the possible application of kaempferol to treat thermal burn–induced skin injuries (BMB Rep. 2010;43:46-51).

Anti-inflammatory as well as depigmenting activity was found by Rho et al. in 2011 to be associated with kaempferol and kaempferol rhamnosides isolated from Hibiscus cannabinus (Molecules 2011;16:3338-44).

In 2014, Kim et al. found that extracts of Aceriphyllum rossii (native to Korea and China) and its active constituents, quercetin and kaempferol, blocked secretion of beta-hexosaminidase and histamine; lowered the production and mRNA expression of interleukin-4 and TNF-alpha; and reduced prostaglandin E₂ and leukotriene B₄ synthesis as well as the expression of cyclooxygenase-2 (COX-2) and 5-lipoxygenase. These and other findings led the investigators to conclude that A. rossii and its active ingredients kaempferol and quercetin may be effective agents for the treatment of immediate-type hypersensitivity (J. Agric. Food Chem. 2014;62:3750-8).

Anticancer activity

Lee et al. reported in 2010 that the inhibition by kaempferol of phosphatidylinositol 3-kinase (PI3K) activity, a key factor in carcinogenesis, and its concomitant effects may account for the chemopreventive activity of the flavonol (Carcinogenesis 2010;31:1338-43).

At the end of that year, Lee et al. found that kaempferol inhibited UVB-induced COX-2 protein expression in mouse skin epidermal JB6 P+ cells, by blocking Src kinase activity and attenuated the UVB-induced transcriptional activities of COX-2 gene and the transcription factor AP-1. They concluded that kaempferol exerts robust chemopreventive activity against skin cancer by suppressing Src (Biochem. Pharmacol. 2010;80:2042-9).

In 2014, Yao et al. found that kaempferol acted as a safe and potent inhibitor of solar ultraviolet-induced mouse skin carcinogenesis that acted by targeting RSK2 and MSK1 (Cancer Prev. Res. (Phila) 2014;7:958-67).

Significantly, in terms of topical delivery, Chao et al. recently showed that submicron emulsions are effective carriers for the transdermal delivery of kaempferol (Chem. Pharm. Bull. (Tokyo) 2012;60:1171-5).

Conclusion

Kaempferol is one among the many natural flavonols found to exert significant salutary effects. Evidence suggests reasons for confidence that kaempferol can play a role in skin health. More research is necessary to determine the effectiveness of topical products intended to harness the benefits of this flavonoid as proper formulation is challenging.

Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook, “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Dermatology News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy, Topix Pharmaceuticals, and Unilever.

Kaempferol (3,5,7,4’-tetrahydroxyflavone; C₁₅H₁₀O₆) is among the natural flavonols found in green tea, broccoli, cabbage, kale, endive, beans, leeks, tomatoes, grapes, apples, grapefruit, berries, and propolis, as well as myriad other plant sources, including Brassica and species (J. Agric. Food Chem. 2006;54:2951-6; Cancer Prev. Res. (Phila) 2014;7:958-67; Biochem. Pharmacol. 2010;80:2042-9; Chem. Pharm. Bull. (Tokyo) 2012;60:1171-5; J. Eur. Acad. Dermatol. Venereol. 2013 June 27 [doi:10.1111/jdv.12204]).

It is one of the most commonly found dietary flavonoids and is also present in beer, particularly hops (Carcinogenesis 2010;31:1338-43; J. Eur. Acad. Dermatol. Venereol. 2013 June 27 [doi:10.1111/jdv.12204]). Significantly, kaempferol is known to exhibit anticancer, anti-inflammatory, antioxidant, cytoprotective, and antiapoptotic activity (Cancer Prev. Res. (Phila) 2014;7:958-67; Biochem. Pharmacol. 2010;80:2042-9; Exp. Mol. Med. 2008;40:208-19), and is believed to play a role in protecting plants from ultraviolet (UV)-induced damage (J. Agric. Food Chem. 2012;60:6966-76).

Skin protection: antioxidant and anti-inflammatory activity

Among 35 flavonoids tested by Cos et al. in 2001 for lipid peroxidation-inhibiting activity, kaempferol was identified as having the highest antioxidant selectivity index (Planta Med. 2001;67:515-9).

Work by Kim et al. in 2002 revealed that four kaempferol glycosides are key active ingredients in the flowers of Prunus persica, which has long been used in traditional Chinese medicine to treat skin disorders (J. Cosmet. Sci. 2002;53:27-34). Kim and colleagues have also shown in animal studies that the topical application of P. persica may be effective at thwarting UVB-induced skin damage (J. Cosmet. Sci. 2002;53:27-34).

In addition, kaempferol is a key component in Punica granatum, which has been found to act as an effective protector against UVB-induced photodamage and aging in cultured skin fibroblasts (Int. J. Dermatol. 2010;49:276-82).

In various tests on the effects of natural flavonoids on matrix metalloproteinase (MMP)-1 activity and expression, Lim et al. reported in 2007 that kaempferol and quercetin potently inhibited recombinant human MMP-1, and both flavonols along with apigenin and wogonin were found to be strong inhibitors of MMP-1 induction in 12-O-tetradecanoylphorbol-13-acetate–treated human dermal fibroblasts. All four flavonoids also suppressed the activation of activator protein (AP)-1. Kaempferol also hindered p38 mitogen-activated protein kinase c-Jun N-terminal kinase (JNK) activation. The investigators concluded that kaempferol is among the flavonoids or plant extracts containing them that may be useful as an agent to protect against photoaging and to treat some cutaneous inflammatory conditions (Planta Med. 2007;73:1267-74).

In 2010, Park et al. demonstrated that kaempferol alleviated burn injuries in mice and that expression of tumor necrosis factor–alpha (TNF-alpha) induced by burn injuries was reduced by kaempferol. They concluded that their findings suggest the possible application of kaempferol to treat thermal burn–induced skin injuries (BMB Rep. 2010;43:46-51).

Anti-inflammatory as well as depigmenting activity was found by Rho et al. in 2011 to be associated with kaempferol and kaempferol rhamnosides isolated from Hibiscus cannabinus (Molecules 2011;16:3338-44).

In 2014, Kim et al. found that extracts of Aceriphyllum rossii (native to Korea and China) and its active constituents, quercetin and kaempferol, blocked secretion of beta-hexosaminidase and histamine; lowered the production and mRNA expression of interleukin-4 and TNF-alpha; and reduced prostaglandin E₂ and leukotriene B₄ synthesis as well as the expression of cyclooxygenase-2 (COX-2) and 5-lipoxygenase. These and other findings led the investigators to conclude that A. rossii and its active ingredients kaempferol and quercetin may be effective agents for the treatment of immediate-type hypersensitivity (J. Agric. Food Chem. 2014;62:3750-8).

Anticancer activity

Lee et al. reported in 2010 that the inhibition by kaempferol of phosphatidylinositol 3-kinase (PI3K) activity, a key factor in carcinogenesis, and its concomitant effects may account for the chemopreventive activity of the flavonol (Carcinogenesis 2010;31:1338-43).

At the end of that year, Lee et al. found that kaempferol inhibited UVB-induced COX-2 protein expression in mouse skin epidermal JB6 P+ cells, by blocking Src kinase activity and attenuated the UVB-induced transcriptional activities of COX-2 gene and the transcription factor AP-1. They concluded that kaempferol exerts robust chemopreventive activity against skin cancer by suppressing Src (Biochem. Pharmacol. 2010;80:2042-9).

In 2014, Yao et al. found that kaempferol acted as a safe and potent inhibitor of solar ultraviolet-induced mouse skin carcinogenesis that acted by targeting RSK2 and MSK1 (Cancer Prev. Res. (Phila) 2014;7:958-67).

Significantly, in terms of topical delivery, Chao et al. recently showed that submicron emulsions are effective carriers for the transdermal delivery of kaempferol (Chem. Pharm. Bull. (Tokyo) 2012;60:1171-5).

Conclusion

Kaempferol is one among the many natural flavonols found to exert significant salutary effects. Evidence suggests reasons for confidence that kaempferol can play a role in skin health. More research is necessary to determine the effectiveness of topical products intended to harness the benefits of this flavonoid as proper formulation is challenging.

Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook, “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Dermatology News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy, Topix Pharmaceuticals, and Unilever.

Kaempferol (3,5,7,4’-tetrahydroxyflavone; C₁₅H₁₀O₆) is among the natural flavonols found in green tea, broccoli, cabbage, kale, endive, beans, leeks, tomatoes, grapes, apples, grapefruit, berries, and propolis, as well as myriad other plant sources, including Brassica and species (J. Agric. Food Chem. 2006;54:2951-6; Cancer Prev. Res. (Phila) 2014;7:958-67; Biochem. Pharmacol. 2010;80:2042-9; Chem. Pharm. Bull. (Tokyo) 2012;60:1171-5; J. Eur. Acad. Dermatol. Venereol. 2013 June 27 [doi:10.1111/jdv.12204]).

It is one of the most commonly found dietary flavonoids and is also present in beer, particularly hops (Carcinogenesis 2010;31:1338-43; J. Eur. Acad. Dermatol. Venereol. 2013 June 27 [doi:10.1111/jdv.12204]). Significantly, kaempferol is known to exhibit anticancer, anti-inflammatory, antioxidant, cytoprotective, and antiapoptotic activity (Cancer Prev. Res. (Phila) 2014;7:958-67; Biochem. Pharmacol. 2010;80:2042-9; Exp. Mol. Med. 2008;40:208-19), and is believed to play a role in protecting plants from ultraviolet (UV)-induced damage (J. Agric. Food Chem. 2012;60:6966-76).

Skin protection: antioxidant and anti-inflammatory activity

Among 35 flavonoids tested by Cos et al. in 2001 for lipid peroxidation-inhibiting activity, kaempferol was identified as having the highest antioxidant selectivity index (Planta Med. 2001;67:515-9).

Work by Kim et al. in 2002 revealed that four kaempferol glycosides are key active ingredients in the flowers of Prunus persica, which has long been used in traditional Chinese medicine to treat skin disorders (J. Cosmet. Sci. 2002;53:27-34). Kim and colleagues have also shown in animal studies that the topical application of P. persica may be effective at thwarting UVB-induced skin damage (J. Cosmet. Sci. 2002;53:27-34).

In addition, kaempferol is a key component in Punica granatum, which has been found to act as an effective protector against UVB-induced photodamage and aging in cultured skin fibroblasts (Int. J. Dermatol. 2010;49:276-82).

In various tests on the effects of natural flavonoids on matrix metalloproteinase (MMP)-1 activity and expression, Lim et al. reported in 2007 that kaempferol and quercetin potently inhibited recombinant human MMP-1, and both flavonols along with apigenin and wogonin were found to be strong inhibitors of MMP-1 induction in 12-O-tetradecanoylphorbol-13-acetate–treated human dermal fibroblasts. All four flavonoids also suppressed the activation of activator protein (AP)-1. Kaempferol also hindered p38 mitogen-activated protein kinase c-Jun N-terminal kinase (JNK) activation. The investigators concluded that kaempferol is among the flavonoids or plant extracts containing them that may be useful as an agent to protect against photoaging and to treat some cutaneous inflammatory conditions (Planta Med. 2007;73:1267-74).

In 2010, Park et al. demonstrated that kaempferol alleviated burn injuries in mice and that expression of tumor necrosis factor–alpha (TNF-alpha) induced by burn injuries was reduced by kaempferol. They concluded that their findings suggest the possible application of kaempferol to treat thermal burn–induced skin injuries (BMB Rep. 2010;43:46-51).

Anti-inflammatory as well as depigmenting activity was found by Rho et al. in 2011 to be associated with kaempferol and kaempferol rhamnosides isolated from Hibiscus cannabinus (Molecules 2011;16:3338-44).

In 2014, Kim et al. found that extracts of Aceriphyllum rossii (native to Korea and China) and its active constituents, quercetin and kaempferol, blocked secretion of beta-hexosaminidase and histamine; lowered the production and mRNA expression of interleukin-4 and TNF-alpha; and reduced prostaglandin E₂ and leukotriene B₄ synthesis as well as the expression of cyclooxygenase-2 (COX-2) and 5-lipoxygenase. These and other findings led the investigators to conclude that A. rossii and its active ingredients kaempferol and quercetin may be effective agents for the treatment of immediate-type hypersensitivity (J. Agric. Food Chem. 2014;62:3750-8).

Anticancer activity

Lee et al. reported in 2010 that the inhibition by kaempferol of phosphatidylinositol 3-kinase (PI3K) activity, a key factor in carcinogenesis, and its concomitant effects may account for the chemopreventive activity of the flavonol (Carcinogenesis 2010;31:1338-43).

At the end of that year, Lee et al. found that kaempferol inhibited UVB-induced COX-2 protein expression in mouse skin epidermal JB6 P+ cells, by blocking Src kinase activity and attenuated the UVB-induced transcriptional activities of COX-2 gene and the transcription factor AP-1. They concluded that kaempferol exerts robust chemopreventive activity against skin cancer by suppressing Src (Biochem. Pharmacol. 2010;80:2042-9).

In 2014, Yao et al. found that kaempferol acted as a safe and potent inhibitor of solar ultraviolet-induced mouse skin carcinogenesis that acted by targeting RSK2 and MSK1 (Cancer Prev. Res. (Phila) 2014;7:958-67).

Significantly, in terms of topical delivery, Chao et al. recently showed that submicron emulsions are effective carriers for the transdermal delivery of kaempferol (Chem. Pharm. Bull. (Tokyo) 2012;60:1171-5).

Conclusion

Kaempferol is one among the many natural flavonols found to exert significant salutary effects. Evidence suggests reasons for confidence that kaempferol can play a role in skin health. More research is necessary to determine the effectiveness of topical products intended to harness the benefits of this flavonoid as proper formulation is challenging.

Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook, “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Dermatology News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy, Topix Pharmaceuticals, and Unilever.

As we all know, professional life gets more complicated every passing year. Meaningful use regulations grow more burdensome, even as the medical records we get fill up with electronic medical records boilerplate. To renew my medical license, my state board has me take a course in opioid management and end-of-life issues. Fill in your own examples.

But recently I’ve become aware of a new wrinkle that complicates daily practice life for both doctors and patients in a significant way. I can’t make any sense if it.

I mean the high price of desonide.

When I was student many years ago, my teachers told me that I should prescribe generic drugs whenever possible. This would help hold down medical costs. It was the right thing to do.

Because I am a good person who tries to do the right thing, I prescribe generics because it’s the right thing to do. I also do it for Pavlovian reasons: prescribing brand-name drugs means more prior authorization forms – we have enough of those anyway – and more calls from patients unhappy with high copays or other out-of-pocket costs. Also, fewer threats of sanctions from insurers or hospital purchasing groups over my pricey prescribing habits.

Besides, most patients I prescribe generics for do just fine.

Of course, some of the anomalous realities of generic prescribing filter through at times. Generic terbinafine and finasteride, for instance, may have higher profit margins, but don’t save patients much money.

But lately I’ve been getting complaints from patients about the high cost of desonide. My first reaction to these was, “How on earth is that possible?”

One patient a few months ago insisted that I contact his mail order pharmacy in Nevada to find a cheaper alternative. I considered this an unreasonable demand – I obviously can’t do a cost comparison for every patient, but this time I went along. The pharmacist came up with another nonfluorinated steroid that was much less expensive under that patient’s particular contract.

Then this week it happened again. I prescribed hydrocortisone valerate 0.2% for a groin rash. The patient left a message asking me for an over-the-counter suggestion, since the prescription was going to cost him $52.70 out of pocket.

I asked my secretary to call the pharmacy to get a price for other generic steroid creams. Triamcinolone would cost $14.70. Alclometasone would cost $35.20.

And desonide – generic desonide – would cost $111.70. For a 15-g tube. $111.70 for 15 g of a generic cream that’s been on the market forever! Does that make any sense?

I’ve gotten similar calls, by the way, from patients unhappy with the cost of generic doxycycline.

There are no doubt economic reasons for such pricing anomalies. Maybe generic manufacturers have dropped out of making certain drugs because they don’t make enough money on them, leaving the ones who remain in a position to charge whatever they can get away with. Maybe insurers or pharmacies cut deals with the makers of some drugs at the expense of others.

I don’t know. And that’s the point.

Because I have no way of knowing any more which of the plain-vanilla generic drugs I’ve prescribed forever are going to be fine, and which are going to cost my patients an arm and a leg and encourage them to call back and yell at me – or else not bother to pick up the medication at all – I don’t even know half the time what to recommend anymore. I certainly don’t have the time to go shopping for every prescription I order. There are just too many drugs, too many prescriptions, too many patients, too many pharmacies, too many insurance contracts, each with its own formulary quirks.

If anyone out there has any explanations or suggestions, I’m all ears.

In the meantime, I may try to simplify my life by sending all my patients to the local Russian deli and prescribing topical caviar. It’s likely to be cheaper than desonide. 

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years.

As we all know, professional life gets more complicated every passing year. Meaningful use regulations grow more burdensome, even as the medical records we get fill up with electronic medical records boilerplate. To renew my medical license, my state board has me take a course in opioid management and end-of-life issues. Fill in your own examples.

But recently I’ve become aware of a new wrinkle that complicates daily practice life for both doctors and patients in a significant way. I can’t make any sense if it.

I mean the high price of desonide.

When I was student many years ago, my teachers told me that I should prescribe generic drugs whenever possible. This would help hold down medical costs. It was the right thing to do.

Because I am a good person who tries to do the right thing, I prescribe generics because it’s the right thing to do. I also do it for Pavlovian reasons: prescribing brand-name drugs means more prior authorization forms – we have enough of those anyway – and more calls from patients unhappy with high copays or other out-of-pocket costs. Also, fewer threats of sanctions from insurers or hospital purchasing groups over my pricey prescribing habits.

Besides, most patients I prescribe generics for do just fine.

Of course, some of the anomalous realities of generic prescribing filter through at times. Generic terbinafine and finasteride, for instance, may have higher profit margins, but don’t save patients much money.

But lately I’ve been getting complaints from patients about the high cost of desonide. My first reaction to these was, “How on earth is that possible?”

One patient a few months ago insisted that I contact his mail order pharmacy in Nevada to find a cheaper alternative. I considered this an unreasonable demand – I obviously can’t do a cost comparison for every patient, but this time I went along. The pharmacist came up with another nonfluorinated steroid that was much less expensive under that patient’s particular contract.

Then this week it happened again. I prescribed hydrocortisone valerate 0.2% for a groin rash. The patient left a message asking me for an over-the-counter suggestion, since the prescription was going to cost him $52.70 out of pocket.

I asked my secretary to call the pharmacy to get a price for other generic steroid creams. Triamcinolone would cost $14.70. Alclometasone would cost $35.20.

And desonide – generic desonide – would cost $111.70. For a 15-g tube. $111.70 for 15 g of a generic cream that’s been on the market forever! Does that make any sense?

I’ve gotten similar calls, by the way, from patients unhappy with the cost of generic doxycycline.

There are no doubt economic reasons for such pricing anomalies. Maybe generic manufacturers have dropped out of making certain drugs because they don’t make enough money on them, leaving the ones who remain in a position to charge whatever they can get away with. Maybe insurers or pharmacies cut deals with the makers of some drugs at the expense of others.

I don’t know. And that’s the point.

Because I have no way of knowing any more which of the plain-vanilla generic drugs I’ve prescribed forever are going to be fine, and which are going to cost my patients an arm and a leg and encourage them to call back and yell at me – or else not bother to pick up the medication at all – I don’t even know half the time what to recommend anymore. I certainly don’t have the time to go shopping for every prescription I order. There are just too many drugs, too many prescriptions, too many patients, too many pharmacies, too many insurance contracts, each with its own formulary quirks.

If anyone out there has any explanations or suggestions, I’m all ears.

In the meantime, I may try to simplify my life by sending all my patients to the local Russian deli and prescribing topical caviar. It’s likely to be cheaper than desonide. 

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years.

As we all know, professional life gets more complicated every passing year. Meaningful use regulations grow more burdensome, even as the medical records we get fill up with electronic medical records boilerplate. To renew my medical license, my state board has me take a course in opioid management and end-of-life issues. Fill in your own examples.

But recently I’ve become aware of a new wrinkle that complicates daily practice life for both doctors and patients in a significant way. I can’t make any sense if it.

I mean the high price of desonide.

When I was student many years ago, my teachers told me that I should prescribe generic drugs whenever possible. This would help hold down medical costs. It was the right thing to do.

Because I am a good person who tries to do the right thing, I prescribe generics because it’s the right thing to do. I also do it for Pavlovian reasons: prescribing brand-name drugs means more prior authorization forms – we have enough of those anyway – and more calls from patients unhappy with high copays or other out-of-pocket costs. Also, fewer threats of sanctions from insurers or hospital purchasing groups over my pricey prescribing habits.

Besides, most patients I prescribe generics for do just fine.

Of course, some of the anomalous realities of generic prescribing filter through at times. Generic terbinafine and finasteride, for instance, may have higher profit margins, but don’t save patients much money.

But lately I’ve been getting complaints from patients about the high cost of desonide. My first reaction to these was, “How on earth is that possible?”

One patient a few months ago insisted that I contact his mail order pharmacy in Nevada to find a cheaper alternative. I considered this an unreasonable demand – I obviously can’t do a cost comparison for every patient, but this time I went along. The pharmacist came up with another nonfluorinated steroid that was much less expensive under that patient’s particular contract.

Then this week it happened again. I prescribed hydrocortisone valerate 0.2% for a groin rash. The patient left a message asking me for an over-the-counter suggestion, since the prescription was going to cost him $52.70 out of pocket.

I asked my secretary to call the pharmacy to get a price for other generic steroid creams. Triamcinolone would cost $14.70. Alclometasone would cost $35.20.

And desonide – generic desonide – would cost $111.70. For a 15-g tube. $111.70 for 15 g of a generic cream that’s been on the market forever! Does that make any sense?

I’ve gotten similar calls, by the way, from patients unhappy with the cost of generic doxycycline.

There are no doubt economic reasons for such pricing anomalies. Maybe generic manufacturers have dropped out of making certain drugs because they don’t make enough money on them, leaving the ones who remain in a position to charge whatever they can get away with. Maybe insurers or pharmacies cut deals with the makers of some drugs at the expense of others.

I don’t know. And that’s the point.

Because I have no way of knowing any more which of the plain-vanilla generic drugs I’ve prescribed forever are going to be fine, and which are going to cost my patients an arm and a leg and encourage them to call back and yell at me – or else not bother to pick up the medication at all – I don’t even know half the time what to recommend anymore. I certainly don’t have the time to go shopping for every prescription I order. There are just too many drugs, too many prescriptions, too many patients, too many pharmacies, too many insurance contracts, each with its own formulary quirks.

If anyone out there has any explanations or suggestions, I’m all ears.

In the meantime, I may try to simplify my life by sending all my patients to the local Russian deli and prescribing topical caviar. It’s likely to be cheaper than desonide. 

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years.

Question: C, age 17 years, was diagnosed with Hodgkin’s lymphoma. According to her oncologists, chemotherapy would offer an 80% chance of cure, whereas death within 2 years was almost a certainty without treatment. C refused treatment, a decision supported by her mother. Under these facts, which of the following is best?

A. C has a constitutional right to forgo medical treatment.

B. C is a minor and needs parental consent regarding all medical intervention.

C. The mother’s refusal to give consent means the doctors have no recourse but to accept the joint decision of mother and daughter.

D. If C can show she is a mature minor or an emancipated minor, she can then decide for herself.

E. In life-and-death matters, the state has the authority to compel lifesaving beneficial treatment without prior judicial approval.

Answer: D. The above scenario raises the issue of doing what’s best when a minor refuses clearly beneficial medical treatment. It is taken from a very recent case wherein the Connecticut Supreme Court held that the state could force treatment in a minor with Hodgkin’s lymphoma. The patient, a 17-year-old teenager, knowingly and with full information, objected to receiving treatment, a decision supported by her mother. There was no finding of mental incompetence or deficiency in either mother or daughter. Can the daughter, against her will, be forced to receive treatment?

The teenager, known as Cassandra, was diagnosed with Hodgkin’s lymphoma, which her oncologists believed had an 80% chance of remission if treated with chemotherapy. Cassandra refused, a decision supported by her mother with whom she lives. Placed under the jurisdiction of Connecticut’s Department of Children and Families (DCF), she initially agreed to a trial of medication if the state allowed her to stay at home with her mother, but she ran away. The case is reminiscent of Billy Best, a 16-year-old diagnosed with Hodgkin’s disease in August 1994, who ran away from his Massachusetts home after 2½ months of chemotherapy because he felt the medicine was killing him instead of helping him.¹

In order to compel treatment, DCF had to obtain judicial approval, which the lower court granted notwithstanding arguments that forcing Cassandra to undergo unwanted medical treatment against her will violated her constitutional substantive due process rights. Also, as there was no competency hearing, so the litigants asserted that this was also a violation of her procedural due process rights. On appeal, the Supreme Court of Connecticut found that Cassandra was not a mature minor, and thus had no constitutional claim to the right of medical decision-making autonomy.² The Court unanimously ruled that the state could compel treatment. Its final opinion is yet to be published, but in its preliminary order, the Court wrote: “… Cassandra is suffering from Hodgkin’s lymphoma, a cancer that has a high rate of cure if treated and that will certainly kill Cassandra if not treated … Cassandra represented, under oath … that she would undergo treatment for her cancer if she were allowed to return home, and then was allowed to do so, she ran away from home and stopped treatment. Thus, … Cassandra either intentionally misrepresented her intentions to the trial court or she changed her mind on this issue of life and death. In either case, her conduct amply supports Judge Quinn’s finding that the respondents have failed to prove that Cassandra was a mature minor under any standard.”

Whereas all adults of sound mind are presumed to be competent to give informed consent, the doctor typically needs permission from the parents or guardian for a minor unless emancipated, i.e., conducting himself or herself as an adult and is no longer under the support or control of the parents. Another exception is the “mature minor,” a term used to describe the minor who is able to understand the nature and consequences of treatment. In 1987, the Tennessee Supreme Court was the first to recognize a mature minor exception to the common law rule that requires a physician to obtain parental consent.³ The issue there was whether Sandra, an alleged malpractice victim 5 months shy of her 18th birthday, was capable of giving consent for an osteopathic treatment. The court acknowledged that for well over a century, the common law recognized that minors achieved varying degrees of maturity and responsibility, and referenced the common law rule of capacity, known as “The Rule of Sevens.” The Rule presumes differing levels of capacity depending on whether the individual is less than 7 years old, between the ages of 7 and 14, or older than 14 years. The youngest group lacks capacity, but a rebuttable presumption of lack of capacity exists for children between the ages of 7 and 14, and one presuming capacity exists for children between the ages of 14 and 21. In Commonwealth jurisdictions, the term “Gillick competence” is used to describe a minor under the age of 16 years who is deemed to have legal capacity to consent to medical treatment if there is sufficient intelligence and maturity to understand the nature, implications, and consequences of treatment.

Two years later in a landmark case,⁴ the Illinois Supreme Court specifically recognized the right of some minors to refuse medical treatment. The litigant was a 17-year-old girl with leukemia who needed life-sustaining blood transfusions. Both the minor and her mother were Jehovah’s Witnesses, and withheld consent to the blood transfusion because of their religious beliefs. The Court opined that the age of majority, “is not an impenetrable barrier that magically precludes a minor from possessing and exercising certain rights normally associated with adulthood,” and that if clear and convincing evidence was presented regarding maturity, then the “mature minor doctrine affords [the minor] the common law right to consent to or refuse medical treatment.” The following year, the Maine Supreme Judicial Court held that a minor’s clear and convincing decision not to be maintained by life-sustaining procedures must be respected.⁵ In that instance, Chad, a minor just under 18, had lapsed into a persistent vegetative state following an auto accident.

Other court decisions favoring the minor abound.⁶ For example, a court held that a 14-year-old boy could decide whether he wanted his cleft palate and harelip repaired, regardless of his father’s objections to the operation. In another case, the court ordered treatment for a 12-year-old arthritis victim whose parents relied on faith healing, where there was uncontested medical testimony in favor of treatment. In yet another, a 13-year-old boy was placed under state supervision for purposes of receiving chemotherapy and surgery that was estimated to have a 65% of curing his cancer. The court ruled that the information given by his father regarding the preference for and effectiveness of herbal therapy was wrong, and the minor’s refusal of consent was not an informed one. On the other hand, even a mature minor does not have an unfettered right to refuse treatment, especially where such refusal is against medical advice. For example, a 16-year-old was forced, against her will, to accept tube feedings to treat her condition of anorexia nervosa.

In addressing the right of mature minors to refuse life-sustaining treatment, the 1985 New York Task Force on Life and the Law acknowledged the need to balance “the developing rights of the minor and parental rights,” and society’s interest “in promoting the autonomy and well-being of minors.” The Task Force recognized that some minors have the maturity and capacity to participate in medical decisions, and recommended that the treating physician assess the minor’s maturity, conceptual ability and life’s experience in order for the minor to assume a substantial, though not exclusive, role in decisions to refuse life-sustaining treatment.

Notes

1. Joan-Margaret Kun, Rejecting the Adage Children Should Be Seen and Not Heard – The Mature Minor Doctrine, 16 Pace L. Rev. 423 (1996). Available at http://digitalcommons.pace.edu/plr/vol16/iss2/13.

2. In re Cassandra C., Supreme Court, State of Connecticut, No. 19426, Jan. 8, 2015.

3. Cardwell v. Bechtol, 724 S.W. 2d 739 (Tenn. 1987)

4. In re E.G., 549 N.E. 2d 322 (Ill. 1990).

5. In re Swan, 569 A. 2d 1202 (Me. 1990).

6. Weir RF and Peters C. Affirming the Decisions Adolescents Make about Life and Death. Hastings Center Report 1997; 27:29-40.

Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, Honolulu, and currently directs the St. Francis International Center for Healthcare Ethics, also in Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. Some of the articles in this series are adapted from the author’s 2006 book, “Medical Malpractice: Understanding the Law, Managing the Risk,” and his 2012 Halsbury treatise, “Medical Negligence and Professional Misconduct.” For additional information, readers may contact the author at [email protected].

Question: C, age 17 years, was diagnosed with Hodgkin’s lymphoma. According to her oncologists, chemotherapy would offer an 80% chance of cure, whereas death within 2 years was almost a certainty without treatment. C refused treatment, a decision supported by her mother. Under these facts, which of the following is best?

A. C has a constitutional right to forgo medical treatment.

B. C is a minor and needs parental consent regarding all medical intervention.

C. The mother’s refusal to give consent means the doctors have no recourse but to accept the joint decision of mother and daughter.

D. If C can show she is a mature minor or an emancipated minor, she can then decide for herself.

E. In life-and-death matters, the state has the authority to compel lifesaving beneficial treatment without prior judicial approval.

Answer: D. The above scenario raises the issue of doing what’s best when a minor refuses clearly beneficial medical treatment. It is taken from a very recent case wherein the Connecticut Supreme Court held that the state could force treatment in a minor with Hodgkin’s lymphoma. The patient, a 17-year-old teenager, knowingly and with full information, objected to receiving treatment, a decision supported by her mother. There was no finding of mental incompetence or deficiency in either mother or daughter. Can the daughter, against her will, be forced to receive treatment?

The teenager, known as Cassandra, was diagnosed with Hodgkin’s lymphoma, which her oncologists believed had an 80% chance of remission if treated with chemotherapy. Cassandra refused, a decision supported by her mother with whom she lives. Placed under the jurisdiction of Connecticut’s Department of Children and Families (DCF), she initially agreed to a trial of medication if the state allowed her to stay at home with her mother, but she ran away. The case is reminiscent of Billy Best, a 16-year-old diagnosed with Hodgkin’s disease in August 1994, who ran away from his Massachusetts home after 2½ months of chemotherapy because he felt the medicine was killing him instead of helping him.¹

In order to compel treatment, DCF had to obtain judicial approval, which the lower court granted notwithstanding arguments that forcing Cassandra to undergo unwanted medical treatment against her will violated her constitutional substantive due process rights. Also, as there was no competency hearing, so the litigants asserted that this was also a violation of her procedural due process rights. On appeal, the Supreme Court of Connecticut found that Cassandra was not a mature minor, and thus had no constitutional claim to the right of medical decision-making autonomy.² The Court unanimously ruled that the state could compel treatment. Its final opinion is yet to be published, but in its preliminary order, the Court wrote: “… Cassandra is suffering from Hodgkin’s lymphoma, a cancer that has a high rate of cure if treated and that will certainly kill Cassandra if not treated … Cassandra represented, under oath … that she would undergo treatment for her cancer if she were allowed to return home, and then was allowed to do so, she ran away from home and stopped treatment. Thus, … Cassandra either intentionally misrepresented her intentions to the trial court or she changed her mind on this issue of life and death. In either case, her conduct amply supports Judge Quinn’s finding that the respondents have failed to prove that Cassandra was a mature minor under any standard.”

Whereas all adults of sound mind are presumed to be competent to give informed consent, the doctor typically needs permission from the parents or guardian for a minor unless emancipated, i.e., conducting himself or herself as an adult and is no longer under the support or control of the parents. Another exception is the “mature minor,” a term used to describe the minor who is able to understand the nature and consequences of treatment. In 1987, the Tennessee Supreme Court was the first to recognize a mature minor exception to the common law rule that requires a physician to obtain parental consent.³ The issue there was whether Sandra, an alleged malpractice victim 5 months shy of her 18th birthday, was capable of giving consent for an osteopathic treatment. The court acknowledged that for well over a century, the common law recognized that minors achieved varying degrees of maturity and responsibility, and referenced the common law rule of capacity, known as “The Rule of Sevens.” The Rule presumes differing levels of capacity depending on whether the individual is less than 7 years old, between the ages of 7 and 14, or older than 14 years. The youngest group lacks capacity, but a rebuttable presumption of lack of capacity exists for children between the ages of 7 and 14, and one presuming capacity exists for children between the ages of 14 and 21. In Commonwealth jurisdictions, the term “Gillick competence” is used to describe a minor under the age of 16 years who is deemed to have legal capacity to consent to medical treatment if there is sufficient intelligence and maturity to understand the nature, implications, and consequences of treatment.

Two years later in a landmark case,⁴ the Illinois Supreme Court specifically recognized the right of some minors to refuse medical treatment. The litigant was a 17-year-old girl with leukemia who needed life-sustaining blood transfusions. Both the minor and her mother were Jehovah’s Witnesses, and withheld consent to the blood transfusion because of their religious beliefs. The Court opined that the age of majority, “is not an impenetrable barrier that magically precludes a minor from possessing and exercising certain rights normally associated with adulthood,” and that if clear and convincing evidence was presented regarding maturity, then the “mature minor doctrine affords [the minor] the common law right to consent to or refuse medical treatment.” The following year, the Maine Supreme Judicial Court held that a minor’s clear and convincing decision not to be maintained by life-sustaining procedures must be respected.⁵ In that instance, Chad, a minor just under 18, had lapsed into a persistent vegetative state following an auto accident.

Other court decisions favoring the minor abound.⁶ For example, a court held that a 14-year-old boy could decide whether he wanted his cleft palate and harelip repaired, regardless of his father’s objections to the operation. In another case, the court ordered treatment for a 12-year-old arthritis victim whose parents relied on faith healing, where there was uncontested medical testimony in favor of treatment. In yet another, a 13-year-old boy was placed under state supervision for purposes of receiving chemotherapy and surgery that was estimated to have a 65% of curing his cancer. The court ruled that the information given by his father regarding the preference for and effectiveness of herbal therapy was wrong, and the minor’s refusal of consent was not an informed one. On the other hand, even a mature minor does not have an unfettered right to refuse treatment, especially where such refusal is against medical advice. For example, a 16-year-old was forced, against her will, to accept tube feedings to treat her condition of anorexia nervosa.

In addressing the right of mature minors to refuse life-sustaining treatment, the 1985 New York Task Force on Life and the Law acknowledged the need to balance “the developing rights of the minor and parental rights,” and society’s interest “in promoting the autonomy and well-being of minors.” The Task Force recognized that some minors have the maturity and capacity to participate in medical decisions, and recommended that the treating physician assess the minor’s maturity, conceptual ability and life’s experience in order for the minor to assume a substantial, though not exclusive, role in decisions to refuse life-sustaining treatment.

Notes

1. Joan-Margaret Kun, Rejecting the Adage Children Should Be Seen and Not Heard – The Mature Minor Doctrine, 16 Pace L. Rev. 423 (1996). Available at http://digitalcommons.pace.edu/plr/vol16/iss2/13.

2. In re Cassandra C., Supreme Court, State of Connecticut, No. 19426, Jan. 8, 2015.

3. Cardwell v. Bechtol, 724 S.W. 2d 739 (Tenn. 1987)

4. In re E.G., 549 N.E. 2d 322 (Ill. 1990).

5. In re Swan, 569 A. 2d 1202 (Me. 1990).

6. Weir RF and Peters C. Affirming the Decisions Adolescents Make about Life and Death. Hastings Center Report 1997; 27:29-40.

Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, Honolulu, and currently directs the St. Francis International Center for Healthcare Ethics, also in Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. Some of the articles in this series are adapted from the author’s 2006 book, “Medical Malpractice: Understanding the Law, Managing the Risk,” and his 2012 Halsbury treatise, “Medical Negligence and Professional Misconduct.” For additional information, readers may contact the author at [email protected].

Question: C, age 17 years, was diagnosed with Hodgkin’s lymphoma. According to her oncologists, chemotherapy would offer an 80% chance of cure, whereas death within 2 years was almost a certainty without treatment. C refused treatment, a decision supported by her mother. Under these facts, which of the following is best?

A. C has a constitutional right to forgo medical treatment.

B. C is a minor and needs parental consent regarding all medical intervention.

C. The mother’s refusal to give consent means the doctors have no recourse but to accept the joint decision of mother and daughter.

D. If C can show she is a mature minor or an emancipated minor, she can then decide for herself.

E. In life-and-death matters, the state has the authority to compel lifesaving beneficial treatment without prior judicial approval.

Answer: D. The above scenario raises the issue of doing what’s best when a minor refuses clearly beneficial medical treatment. It is taken from a very recent case wherein the Connecticut Supreme Court held that the state could force treatment in a minor with Hodgkin’s lymphoma. The patient, a 17-year-old teenager, knowingly and with full information, objected to receiving treatment, a decision supported by her mother. There was no finding of mental incompetence or deficiency in either mother or daughter. Can the daughter, against her will, be forced to receive treatment?

The teenager, known as Cassandra, was diagnosed with Hodgkin’s lymphoma, which her oncologists believed had an 80% chance of remission if treated with chemotherapy. Cassandra refused, a decision supported by her mother with whom she lives. Placed under the jurisdiction of Connecticut’s Department of Children and Families (DCF), she initially agreed to a trial of medication if the state allowed her to stay at home with her mother, but she ran away. The case is reminiscent of Billy Best, a 16-year-old diagnosed with Hodgkin’s disease in August 1994, who ran away from his Massachusetts home after 2½ months of chemotherapy because he felt the medicine was killing him instead of helping him.¹

In order to compel treatment, DCF had to obtain judicial approval, which the lower court granted notwithstanding arguments that forcing Cassandra to undergo unwanted medical treatment against her will violated her constitutional substantive due process rights. Also, as there was no competency hearing, so the litigants asserted that this was also a violation of her procedural due process rights. On appeal, the Supreme Court of Connecticut found that Cassandra was not a mature minor, and thus had no constitutional claim to the right of medical decision-making autonomy.² The Court unanimously ruled that the state could compel treatment. Its final opinion is yet to be published, but in its preliminary order, the Court wrote: “… Cassandra is suffering from Hodgkin’s lymphoma, a cancer that has a high rate of cure if treated and that will certainly kill Cassandra if not treated … Cassandra represented, under oath … that she would undergo treatment for her cancer if she were allowed to return home, and then was allowed to do so, she ran away from home and stopped treatment. Thus, … Cassandra either intentionally misrepresented her intentions to the trial court or she changed her mind on this issue of life and death. In either case, her conduct amply supports Judge Quinn’s finding that the respondents have failed to prove that Cassandra was a mature minor under any standard.”

Whereas all adults of sound mind are presumed to be competent to give informed consent, the doctor typically needs permission from the parents or guardian for a minor unless emancipated, i.e., conducting himself or herself as an adult and is no longer under the support or control of the parents. Another exception is the “mature minor,” a term used to describe the minor who is able to understand the nature and consequences of treatment. In 1987, the Tennessee Supreme Court was the first to recognize a mature minor exception to the common law rule that requires a physician to obtain parental consent.³ The issue there was whether Sandra, an alleged malpractice victim 5 months shy of her 18th birthday, was capable of giving consent for an osteopathic treatment. The court acknowledged that for well over a century, the common law recognized that minors achieved varying degrees of maturity and responsibility, and referenced the common law rule of capacity, known as “The Rule of Sevens.” The Rule presumes differing levels of capacity depending on whether the individual is less than 7 years old, between the ages of 7 and 14, or older than 14 years. The youngest group lacks capacity, but a rebuttable presumption of lack of capacity exists for children between the ages of 7 and 14, and one presuming capacity exists for children between the ages of 14 and 21. In Commonwealth jurisdictions, the term “Gillick competence” is used to describe a minor under the age of 16 years who is deemed to have legal capacity to consent to medical treatment if there is sufficient intelligence and maturity to understand the nature, implications, and consequences of treatment.

Two years later in a landmark case,⁴ the Illinois Supreme Court specifically recognized the right of some minors to refuse medical treatment. The litigant was a 17-year-old girl with leukemia who needed life-sustaining blood transfusions. Both the minor and her mother were Jehovah’s Witnesses, and withheld consent to the blood transfusion because of their religious beliefs. The Court opined that the age of majority, “is not an impenetrable barrier that magically precludes a minor from possessing and exercising certain rights normally associated with adulthood,” and that if clear and convincing evidence was presented regarding maturity, then the “mature minor doctrine affords [the minor] the common law right to consent to or refuse medical treatment.” The following year, the Maine Supreme Judicial Court held that a minor’s clear and convincing decision not to be maintained by life-sustaining procedures must be respected.⁵ In that instance, Chad, a minor just under 18, had lapsed into a persistent vegetative state following an auto accident.

Other court decisions favoring the minor abound.⁶ For example, a court held that a 14-year-old boy could decide whether he wanted his cleft palate and harelip repaired, regardless of his father’s objections to the operation. In another case, the court ordered treatment for a 12-year-old arthritis victim whose parents relied on faith healing, where there was uncontested medical testimony in favor of treatment. In yet another, a 13-year-old boy was placed under state supervision for purposes of receiving chemotherapy and surgery that was estimated to have a 65% of curing his cancer. The court ruled that the information given by his father regarding the preference for and effectiveness of herbal therapy was wrong, and the minor’s refusal of consent was not an informed one. On the other hand, even a mature minor does not have an unfettered right to refuse treatment, especially where such refusal is against medical advice. For example, a 16-year-old was forced, against her will, to accept tube feedings to treat her condition of anorexia nervosa.

In addressing the right of mature minors to refuse life-sustaining treatment, the 1985 New York Task Force on Life and the Law acknowledged the need to balance “the developing rights of the minor and parental rights,” and society’s interest “in promoting the autonomy and well-being of minors.” The Task Force recognized that some minors have the maturity and capacity to participate in medical decisions, and recommended that the treating physician assess the minor’s maturity, conceptual ability and life’s experience in order for the minor to assume a substantial, though not exclusive, role in decisions to refuse life-sustaining treatment.

Notes

1. Joan-Margaret Kun, Rejecting the Adage Children Should Be Seen and Not Heard – The Mature Minor Doctrine, 16 Pace L. Rev. 423 (1996). Available at http://digitalcommons.pace.edu/plr/vol16/iss2/13.

2. In re Cassandra C., Supreme Court, State of Connecticut, No. 19426, Jan. 8, 2015.

3. Cardwell v. Bechtol, 724 S.W. 2d 739 (Tenn. 1987)

4. In re E.G., 549 N.E. 2d 322 (Ill. 1990).

5. In re Swan, 569 A. 2d 1202 (Me. 1990).

6. Weir RF and Peters C. Affirming the Decisions Adolescents Make about Life and Death. Hastings Center Report 1997; 27:29-40.

Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, Honolulu, and currently directs the St. Francis International Center for Healthcare Ethics, also in Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. Some of the articles in this series are adapted from the author’s 2006 book, “Medical Malpractice: Understanding the Law, Managing the Risk,” and his 2012 Halsbury treatise, “Medical Negligence and Professional Misconduct.” For additional information, readers may contact the author at [email protected].

Some things make my job much harder than it should be. One of them is prior authorizations.

At the start of every year, insurers release a new formulary, so prior authorizations are often required, even drugs that patients have been on for a long time. Everyday I spend anywhere from 10 to 30 minutes filling out prior authorization paperwork.

Sometimes, it’s not too difficult. If someone is getting a biologic for the first time, it usually means they’ve had an inadequate response to methotrexate. The form makes sure we’ve checked the patient’s TB status. Sometimes, it asks about a history of heart failure. These are reasonable questions designed to protect the patient.

Frequently, though, the questionnaires are more onerous, and for less altruistic motives. A prior authorization for celecoxib (Celebrex) requires that I list at least two other prescription NSAIDs that the patient has been on. I can guarantee that I do not know that information off the top of my head, so this requires some digging into the chart. If it’s a patient whose care I’ve assumed from someone else, or whose chart is several volumes thick, I won’t even know where to begin. Even worse is the pregabalin (Lyrica) prior authorization that asks about previous use of tricyclic antidepressants, cyclobenzaprine, SSRIs, gabapentin. When were they on these agents and for how long? What was the outcome of each failed medication?

These two examples do not ensure patient safety. They simply go directly to what the insurer’s bottom line is. They benefit no one but the insurer, and create lots of problems for everyone who has to abide by the insurer’s rules.

The worst of it, this year, has to be prior authorization for injectable methotrexate. I have recently run into a lot of problems with this one. For one patient who had been on weekly adalimumab (Humira) and subcutaneous methotrexate, I was asked to justify the combination with a journal article or two, because mechanistically the insurers reject methotrexate as having any role in therapy for patients already on weekly adalimumab, antidrug antibodies notwithstanding. I had inherited this patient from another rheumatologist, and she’d been on this regimen for over a decade; it was infuriating and frustrating to be asked to justify a regimen that the patient had not had problems with for the previous 10 years and that was working fine for her.

For another patient, I was asked to fax a letter to the pharmacy stating why the drug was necessary. Then I was asked to fax another letter to the insurer’s benefits manager. A day later, I was informed that there was no process of appeal for medications that were not on formulary. None whatsoever. The letters that they had asked me to write had no bearing and meant nothing to them. This was the very definition of a complete waste of time.

If I wanted the patient to be on subcutaneous methotrexate, the patient would have to pay out of pocket for the drug. I got on the phone with someone whose job was to repeatedly tell me that I had no options. She couldn’t direct me to anyone higher up than her. I understand that this automaton would have no intelligent answers for me, but I asked rhetorically if etanercept would be covered. She said yes. I then asked rhetorically if she knew how much more the biologic agent would cost the insurance company. I cut her off as she was about to look up the price of the drug.

I can think of hundreds of ways in which I could make better use of my time instead of playing a game I am forced to play against my will, a game that is shrouded in layers of bureaucracy over which I have very little control and has no benefit to my patients. There are days when the game is enough to make me want to throw in the towel.

Dr. Chan practices rheumatology in Pawtucket, R.I.

Some things make my job much harder than it should be. One of them is prior authorizations.

At the start of every year, insurers release a new formulary, so prior authorizations are often required, even drugs that patients have been on for a long time. Everyday I spend anywhere from 10 to 30 minutes filling out prior authorization paperwork.

Sometimes, it’s not too difficult. If someone is getting a biologic for the first time, it usually means they’ve had an inadequate response to methotrexate. The form makes sure we’ve checked the patient’s TB status. Sometimes, it asks about a history of heart failure. These are reasonable questions designed to protect the patient.

Frequently, though, the questionnaires are more onerous, and for less altruistic motives. A prior authorization for celecoxib (Celebrex) requires that I list at least two other prescription NSAIDs that the patient has been on. I can guarantee that I do not know that information off the top of my head, so this requires some digging into the chart. If it’s a patient whose care I’ve assumed from someone else, or whose chart is several volumes thick, I won’t even know where to begin. Even worse is the pregabalin (Lyrica) prior authorization that asks about previous use of tricyclic antidepressants, cyclobenzaprine, SSRIs, gabapentin. When were they on these agents and for how long? What was the outcome of each failed medication?

These two examples do not ensure patient safety. They simply go directly to what the insurer’s bottom line is. They benefit no one but the insurer, and create lots of problems for everyone who has to abide by the insurer’s rules.

The worst of it, this year, has to be prior authorization for injectable methotrexate. I have recently run into a lot of problems with this one. For one patient who had been on weekly adalimumab (Humira) and subcutaneous methotrexate, I was asked to justify the combination with a journal article or two, because mechanistically the insurers reject methotrexate as having any role in therapy for patients already on weekly adalimumab, antidrug antibodies notwithstanding. I had inherited this patient from another rheumatologist, and she’d been on this regimen for over a decade; it was infuriating and frustrating to be asked to justify a regimen that the patient had not had problems with for the previous 10 years and that was working fine for her.

For another patient, I was asked to fax a letter to the pharmacy stating why the drug was necessary. Then I was asked to fax another letter to the insurer’s benefits manager. A day later, I was informed that there was no process of appeal for medications that were not on formulary. None whatsoever. The letters that they had asked me to write had no bearing and meant nothing to them. This was the very definition of a complete waste of time.

If I wanted the patient to be on subcutaneous methotrexate, the patient would have to pay out of pocket for the drug. I got on the phone with someone whose job was to repeatedly tell me that I had no options. She couldn’t direct me to anyone higher up than her. I understand that this automaton would have no intelligent answers for me, but I asked rhetorically if etanercept would be covered. She said yes. I then asked rhetorically if she knew how much more the biologic agent would cost the insurance company. I cut her off as she was about to look up the price of the drug.

I can think of hundreds of ways in which I could make better use of my time instead of playing a game I am forced to play against my will, a game that is shrouded in layers of bureaucracy over which I have very little control and has no benefit to my patients. There are days when the game is enough to make me want to throw in the towel.

Dr. Chan practices rheumatology in Pawtucket, R.I.

Some things make my job much harder than it should be. One of them is prior authorizations.

At the start of every year, insurers release a new formulary, so prior authorizations are often required, even drugs that patients have been on for a long time. Everyday I spend anywhere from 10 to 30 minutes filling out prior authorization paperwork.

Sometimes, it’s not too difficult. If someone is getting a biologic for the first time, it usually means they’ve had an inadequate response to methotrexate. The form makes sure we’ve checked the patient’s TB status. Sometimes, it asks about a history of heart failure. These are reasonable questions designed to protect the patient.

Frequently, though, the questionnaires are more onerous, and for less altruistic motives. A prior authorization for celecoxib (Celebrex) requires that I list at least two other prescription NSAIDs that the patient has been on. I can guarantee that I do not know that information off the top of my head, so this requires some digging into the chart. If it’s a patient whose care I’ve assumed from someone else, or whose chart is several volumes thick, I won’t even know where to begin. Even worse is the pregabalin (Lyrica) prior authorization that asks about previous use of tricyclic antidepressants, cyclobenzaprine, SSRIs, gabapentin. When were they on these agents and for how long? What was the outcome of each failed medication?

These two examples do not ensure patient safety. They simply go directly to what the insurer’s bottom line is. They benefit no one but the insurer, and create lots of problems for everyone who has to abide by the insurer’s rules.

The worst of it, this year, has to be prior authorization for injectable methotrexate. I have recently run into a lot of problems with this one. For one patient who had been on weekly adalimumab (Humira) and subcutaneous methotrexate, I was asked to justify the combination with a journal article or two, because mechanistically the insurers reject methotrexate as having any role in therapy for patients already on weekly adalimumab, antidrug antibodies notwithstanding. I had inherited this patient from another rheumatologist, and she’d been on this regimen for over a decade; it was infuriating and frustrating to be asked to justify a regimen that the patient had not had problems with for the previous 10 years and that was working fine for her.

For another patient, I was asked to fax a letter to the pharmacy stating why the drug was necessary. Then I was asked to fax another letter to the insurer’s benefits manager. A day later, I was informed that there was no process of appeal for medications that were not on formulary. None whatsoever. The letters that they had asked me to write had no bearing and meant nothing to them. This was the very definition of a complete waste of time.

If I wanted the patient to be on subcutaneous methotrexate, the patient would have to pay out of pocket for the drug. I got on the phone with someone whose job was to repeatedly tell me that I had no options. She couldn’t direct me to anyone higher up than her. I understand that this automaton would have no intelligent answers for me, but I asked rhetorically if etanercept would be covered. She said yes. I then asked rhetorically if she knew how much more the biologic agent would cost the insurance company. I cut her off as she was about to look up the price of the drug.

I can think of hundreds of ways in which I could make better use of my time instead of playing a game I am forced to play against my will, a game that is shrouded in layers of bureaucracy over which I have very little control and has no benefit to my patients. There are days when the game is enough to make me want to throw in the towel.

Dr. Chan practices rheumatology in Pawtucket, R.I.

One out of every 10 adults in the United States has diabetes, and the percentage of Americans aged 65 years or older who have diabetes continues to increase. The treatment of diabetes consumes an enormous amount of health care and personal resources. This would palatable if such expenditures did nothing but improve outcomes and reduce morbidity and mortality.

But they don’t.

Compared with young healthy patients with diabetes, older patients with diabetes and complex medical conditions may derive little benefit from intensive management but may incur harm. Hypoglycemia is associated with significant medical costs and adverse health consequences among older patients. Hypoglycemic agents (oral and injectable) are implicated in one-fourth of emergency hospitalizations for adverse drugs events in this population.

Dr. Kasia J. Lipska of Yale University, New Haven, Conn., and her colleagues evaluated the potential overtreatment of diabetes in older patients (at least 65 years) by examining participants in the National Health and Nutrition Examination Survey from 2001 through 2010 who had an HbA_1c measurement. Participants were grouped into different health status categories using available data: very complex/poor, complex/intermediate, and relatively healthy (JAMA Intern. Med. 2015 [doi:10.1001/jamainternmed.2014.7345]).

The investigators found that almost two-thirds of this population had an HbA_1c less than 7% (i.e., tight control), which did not differ across health status categories. Of the adults with an HbA_1c less than 7%, more than one-half were treated with insulin or sulfonylureas, and this was similar across health status categories. During the 10 study years, no changes were observed in the proportion with an HbA_1c less than 7% or the proportion of patients with an HbA_1c less than 7% who were treated with insulin or a sulfonylurea.

These data tell us we are not racheting our care back when patients reach an age when aggressive care does more harm than good. We may feel hamstrung by quality metrics, a limited ability to manage large populations using health management approach, algorithmic approaches to facilitate appropriate de-escalations in medication management, and lack of time to engage in these discussions with our patients. What we tend to do is decrease these medications after patients have an office or emergency department visit for a hypoglycemic event or complication.

Moving forward, we need to embrace more liberal HbA_1c goals for our patients at least 65 years of age. Most important, yet most challenging, we need to have ongoing goals of care discussions with our patients, and comorbidities need to be considered when setting such goals. Decision aids would be helpful tools in this space.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

One out of every 10 adults in the United States has diabetes, and the percentage of Americans aged 65 years or older who have diabetes continues to increase. The treatment of diabetes consumes an enormous amount of health care and personal resources. This would palatable if such expenditures did nothing but improve outcomes and reduce morbidity and mortality.

But they don’t.

Compared with young healthy patients with diabetes, older patients with diabetes and complex medical conditions may derive little benefit from intensive management but may incur harm. Hypoglycemia is associated with significant medical costs and adverse health consequences among older patients. Hypoglycemic agents (oral and injectable) are implicated in one-fourth of emergency hospitalizations for adverse drugs events in this population.

Dr. Kasia J. Lipska of Yale University, New Haven, Conn., and her colleagues evaluated the potential overtreatment of diabetes in older patients (at least 65 years) by examining participants in the National Health and Nutrition Examination Survey from 2001 through 2010 who had an HbA_1c measurement. Participants were grouped into different health status categories using available data: very complex/poor, complex/intermediate, and relatively healthy (JAMA Intern. Med. 2015 [doi:10.1001/jamainternmed.2014.7345]).

The investigators found that almost two-thirds of this population had an HbA_1c less than 7% (i.e., tight control), which did not differ across health status categories. Of the adults with an HbA_1c less than 7%, more than one-half were treated with insulin or sulfonylureas, and this was similar across health status categories. During the 10 study years, no changes were observed in the proportion with an HbA_1c less than 7% or the proportion of patients with an HbA_1c less than 7% who were treated with insulin or a sulfonylurea.

These data tell us we are not racheting our care back when patients reach an age when aggressive care does more harm than good. We may feel hamstrung by quality metrics, a limited ability to manage large populations using health management approach, algorithmic approaches to facilitate appropriate de-escalations in medication management, and lack of time to engage in these discussions with our patients. What we tend to do is decrease these medications after patients have an office or emergency department visit for a hypoglycemic event or complication.

Moving forward, we need to embrace more liberal HbA_1c goals for our patients at least 65 years of age. Most important, yet most challenging, we need to have ongoing goals of care discussions with our patients, and comorbidities need to be considered when setting such goals. Decision aids would be helpful tools in this space.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

One out of every 10 adults in the United States has diabetes, and the percentage of Americans aged 65 years or older who have diabetes continues to increase. The treatment of diabetes consumes an enormous amount of health care and personal resources. This would palatable if such expenditures did nothing but improve outcomes and reduce morbidity and mortality.

But they don’t.

Compared with young healthy patients with diabetes, older patients with diabetes and complex medical conditions may derive little benefit from intensive management but may incur harm. Hypoglycemia is associated with significant medical costs and adverse health consequences among older patients. Hypoglycemic agents (oral and injectable) are implicated in one-fourth of emergency hospitalizations for adverse drugs events in this population.

Dr. Kasia J. Lipska of Yale University, New Haven, Conn., and her colleagues evaluated the potential overtreatment of diabetes in older patients (at least 65 years) by examining participants in the National Health and Nutrition Examination Survey from 2001 through 2010 who had an HbA_1c measurement. Participants were grouped into different health status categories using available data: very complex/poor, complex/intermediate, and relatively healthy (JAMA Intern. Med. 2015 [doi:10.1001/jamainternmed.2014.7345]).

The investigators found that almost two-thirds of this population had an HbA_1c less than 7% (i.e., tight control), which did not differ across health status categories. Of the adults with an HbA_1c less than 7%, more than one-half were treated with insulin or sulfonylureas, and this was similar across health status categories. During the 10 study years, no changes were observed in the proportion with an HbA_1c less than 7% or the proportion of patients with an HbA_1c less than 7% who were treated with insulin or a sulfonylurea.

These data tell us we are not racheting our care back when patients reach an age when aggressive care does more harm than good. We may feel hamstrung by quality metrics, a limited ability to manage large populations using health management approach, algorithmic approaches to facilitate appropriate de-escalations in medication management, and lack of time to engage in these discussions with our patients. What we tend to do is decrease these medications after patients have an office or emergency department visit for a hypoglycemic event or complication.

Moving forward, we need to embrace more liberal HbA_1c goals for our patients at least 65 years of age. Most important, yet most challenging, we need to have ongoing goals of care discussions with our patients, and comorbidities need to be considered when setting such goals. Decision aids would be helpful tools in this space.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.