Commentary

The TPA ambulance, armed with its own CT scanner, has arrived in the United States after several successful years in Germany.

Now what?

Like all new advances, it’s a difficult balance between costs and benefits. The money, in the end, is what it really comes down to. Will the cost of a CT ambulance, the equipment needed to send images to a radiologist, the extra training for EMTs, the price of stocking TPA on board, and maybe even having a neurologist on the ride (or telemedicine for one to see the patient) be offset by money saved on rehabilitation costs, better recoveries, fewer complications, even returning a patient to work?

I have no idea. I’m not sure anyone else does, either.

Certainly, I support the idea of improved stroke care. Although far from ideal, TPA is the only thing we have right now, and the sooner it’s given, the better. Most neurologists will agree. But who’s going to pay for this?

The insurance companies, obviously. But money is finite. What if we upgrade all these ambulances, only to find that there’s no significant cost savings on rehab and recovery when TPA is used in the field? Then the money comes out of doctors’ and nurses’ salaries, higher premiums for everyone, and a cutback in treatment for some other disorder. I’m pretty sure it won’t be taken out of an insurance executive’s year-end bonus.

And just try explaining that to the family of a stroke victim.

It’s not practical to put a CT scanner in every ambulance, so where do we put those so equipped? Again, there’s no easy answer. In areas with large retirement communities? Seems like a safe bet, but young people have strokes, too. Only in cities? More people live in cities, but those in rural areas may be too far from a hospital to receive TPA early. Shouldn’t they have one, too?

Who’s going to make the decision to send the TPA ambulance vs. the regular ambulance? That’s another tough question. The layman who calls in usually isn’t sure what’s going on, only that an ambulance is needed. The dispatcher often can’t tell over the phone if the patient has had a stroke, seizure, or psychogenic event. Should a neurologist or emergency medicine physician make the decision? Maybe, but how much extra time will it take to get one on the line? And, even then, they’ll be making a critical decision with sparse, secondhand information. What if the special ambulance is mistakenly sent to deal with a conversion disorder, only to have a legitimate stroke occur elsewhere when it’s no longer immediately available? That, inevitably, will lead to a lawsuit because the wrong ambulance was sent.

I’m not against the stroke ambulance – far from it – but there are still a lot questions to be answered. Putting a CT scanner and TPA in an ambulance is, comparatively, the easiest part.

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

The TPA ambulance, armed with its own CT scanner, has arrived in the United States after several successful years in Germany.

Now what?

Like all new advances, it’s a difficult balance between costs and benefits. The money, in the end, is what it really comes down to. Will the cost of a CT ambulance, the equipment needed to send images to a radiologist, the extra training for EMTs, the price of stocking TPA on board, and maybe even having a neurologist on the ride (or telemedicine for one to see the patient) be offset by money saved on rehabilitation costs, better recoveries, fewer complications, even returning a patient to work?

I have no idea. I’m not sure anyone else does, either.

Certainly, I support the idea of improved stroke care. Although far from ideal, TPA is the only thing we have right now, and the sooner it’s given, the better. Most neurologists will agree. But who’s going to pay for this?

The insurance companies, obviously. But money is finite. What if we upgrade all these ambulances, only to find that there’s no significant cost savings on rehab and recovery when TPA is used in the field? Then the money comes out of doctors’ and nurses’ salaries, higher premiums for everyone, and a cutback in treatment for some other disorder. I’m pretty sure it won’t be taken out of an insurance executive’s year-end bonus.

And just try explaining that to the family of a stroke victim.

It’s not practical to put a CT scanner in every ambulance, so where do we put those so equipped? Again, there’s no easy answer. In areas with large retirement communities? Seems like a safe bet, but young people have strokes, too. Only in cities? More people live in cities, but those in rural areas may be too far from a hospital to receive TPA early. Shouldn’t they have one, too?

Who’s going to make the decision to send the TPA ambulance vs. the regular ambulance? That’s another tough question. The layman who calls in usually isn’t sure what’s going on, only that an ambulance is needed. The dispatcher often can’t tell over the phone if the patient has had a stroke, seizure, or psychogenic event. Should a neurologist or emergency medicine physician make the decision? Maybe, but how much extra time will it take to get one on the line? And, even then, they’ll be making a critical decision with sparse, secondhand information. What if the special ambulance is mistakenly sent to deal with a conversion disorder, only to have a legitimate stroke occur elsewhere when it’s no longer immediately available? That, inevitably, will lead to a lawsuit because the wrong ambulance was sent.

I’m not against the stroke ambulance – far from it – but there are still a lot questions to be answered. Putting a CT scanner and TPA in an ambulance is, comparatively, the easiest part.

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

The TPA ambulance, armed with its own CT scanner, has arrived in the United States after several successful years in Germany.

Now what?

Like all new advances, it’s a difficult balance between costs and benefits. The money, in the end, is what it really comes down to. Will the cost of a CT ambulance, the equipment needed to send images to a radiologist, the extra training for EMTs, the price of stocking TPA on board, and maybe even having a neurologist on the ride (or telemedicine for one to see the patient) be offset by money saved on rehabilitation costs, better recoveries, fewer complications, even returning a patient to work?

I have no idea. I’m not sure anyone else does, either.

Certainly, I support the idea of improved stroke care. Although far from ideal, TPA is the only thing we have right now, and the sooner it’s given, the better. Most neurologists will agree. But who’s going to pay for this?

The insurance companies, obviously. But money is finite. What if we upgrade all these ambulances, only to find that there’s no significant cost savings on rehab and recovery when TPA is used in the field? Then the money comes out of doctors’ and nurses’ salaries, higher premiums for everyone, and a cutback in treatment for some other disorder. I’m pretty sure it won’t be taken out of an insurance executive’s year-end bonus.

And just try explaining that to the family of a stroke victim.

It’s not practical to put a CT scanner in every ambulance, so where do we put those so equipped? Again, there’s no easy answer. In areas with large retirement communities? Seems like a safe bet, but young people have strokes, too. Only in cities? More people live in cities, but those in rural areas may be too far from a hospital to receive TPA early. Shouldn’t they have one, too?

Who’s going to make the decision to send the TPA ambulance vs. the regular ambulance? That’s another tough question. The layman who calls in usually isn’t sure what’s going on, only that an ambulance is needed. The dispatcher often can’t tell over the phone if the patient has had a stroke, seizure, or psychogenic event. Should a neurologist or emergency medicine physician make the decision? Maybe, but how much extra time will it take to get one on the line? And, even then, they’ll be making a critical decision with sparse, secondhand information. What if the special ambulance is mistakenly sent to deal with a conversion disorder, only to have a legitimate stroke occur elsewhere when it’s no longer immediately available? That, inevitably, will lead to a lawsuit because the wrong ambulance was sent.

I’m not against the stroke ambulance – far from it – but there are still a lot questions to be answered. Putting a CT scanner and TPA in an ambulance is, comparatively, the easiest part.

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

Kinetin (N6-furfuryladenine or 6-furfurylaminopurine) is a plant cytokinin or phytohormone that promotes cell division, delays senescence in plants, and is reputed to aid in the restoration of skin barrier function and, possibly, in reducing the signs and symptoms of rosacea (Clin. Exp. Dermatol. 2007;32:693-5; Plant Sci. 1999;148:37-45).

Kinetin is believed to develop in cellular DNA as a product of the oxidative, secondary modification of DNA (Plant Sci. 1999;148:37-45). In 1955, it became the first cytokinin isolated from DNA (from herring sperm) as an artifactual rearrangement product of the autoclaving process (J. Cosmet. Dermatol. 2007;6:243-9; Int. J. Biol. Macromol. 2007;40:182-92).

It has since been found to be present in human urine as well as DNA freshly extracted from human cells (Int. J. Biol. Macromol. 2007;40:182-92). The preponderance of amassed experimental evidence suggests that endogenous kinetin acts in vitro and in vivo as a potent antioxidant (Plant Sci. 1999;148:37-45). Currently, it is used as an anti-aging agent in various cosmetic products (J. Cosmet. Dermatol. 2007;6:243-9; J. Cosmet. Dermatol. 2010;9:218-25). Synthetic kinetin is thought to have the capacity to neutralize free radicals as well as limit the damage to DNA and fibroblasts (Photochem. Photobiol. 2012;88:748-52).

In vitro results

Olsen et al. demonstrated in vitro in 1999 that kinetin dose-dependently protected DNA against oxidative damage mediated by the Fenton reaction, and noted that kinetin had previously been linked to anti-aging activity in plants, fruit flies, and human cells in culture (Biochem. Biophys. Res. Commun. 1999;265:499-502). The following year, Verbeke et al. showed in vitro that kinetin potently inhibited damage caused by oxidation and glycoxidation (Biochem. Biophys. Res. Commun. 2000;276:1265-70).

In 2006, Vicanova et al. analyzed the effects of active ingredients from topical and systemic skin care formulations in vitro, finding that kinetin affected the upper dermis by enhancing deposits of fibrillin-1 and elastin fibers as well as their organization perpendicular to the dermal-epidermal junction. In the epidermis, kinetin stimulated keratinocyte production. Further, the investigators noted that the combination of topically applied kinetin with Imedeen Time Perfection ingredients (i.e., BioMarine Complex, grape seed extract, tomato extract, and vitamin C) supplemented systemically into culture medium yielded complementary benefits to dermal and epidermal development (Ann. N.Y. Acad. Sci. 2006;1067:337-42).

It is worth noting that in a study by Tournas et al. published the same month, investigators found that the topical application of a combination of vitamins C and E and ferulic acid yielded photoprotection to pig skin at 5 times the minimal erythema dose (MED) while individual antioxidants to which it was compared (i.e., coenzyme Q10, idebenone, and kinetin) delivered no photoprotective effects (J. Invest. Dermatol. 2006;126:1185-7). Nevertheless, Barciszewski et al. have observed that kinetin is the first stable secondary DNA damage product characterized by well defined cytokinin and anti-aging activity, with data showing that it has delayed human cellular aging in culture (Int. J. Biol. Macromol. 2007;40:182-92).

Rosacea

In 2007, Wu et al. performed a 12-week open-label study in 15 women and 3 men (aged 30-67 years) to ascertain the tolerability and efficacy of kinetin 0.1% lotion in the treatment of mild to moderate facial rosacea. Patients (17 of whom completed the study) applied the lotion twice daily, also daily applying an SPF 30 sunscreen. By week 4, significant improvements were observed in the reduction of skin roughness and mottled hyperpigmentation. Subject assessments at each 4-week interval after baseline and after 12 weeks revealed that kinetin 0.1% was well tolerated and effective for mild to moderate inflammatory rosacea (Clin. Exp. Dermatol. 2007;32:693-5).

Anti-aging

A 2002 study by J.L. McCullough and G.D. Weinstein represented the first evidence of the efficacy of topical kinetin in human beings, with twice-daily application for 24 weeks found to ameliorate skin texture, color, and blotchiness while diminishing rhytides and transepidermal water loss (J. Cosmet. Dermatol. 2002;15:29-32).

Two years later, T. Kimura and K. Doi showed that topical administration of kinetin improved the texture, wrinkling, and pigmentation of aged skin of hairless descendants of Mexican hairless dogs, resulting in notable depigmentation and rejuvenation after 100 days of treatment (Rejuvenation Res. 2004;7:32-9).In 2007, Chiu et al. conducted a randomized, double-blind, placebo-controlled, split-face comparative study in 52 Taiwanese subjects aged 30-60 years (90% of whom were female, all of whom had Fitzpatrick skin types II, III, or IV) to evaluate the clinical anti-aging effects and efficacy differences between kinetin plus niacinamide (kinetin 0.03%, niacinamide 4%) and niacinamide 4% alone versus vehicle placebo.

In the combination group, significant and sustained decreases were observed in counts of spots, pores, wrinkles, and evenness as well as persistent reductions in erythema index at weeks 8 and 12. At week 12, stratum corneum hydration status also was significantly enhanced in this group. In the niacinamide-only group, pore and evenness counts were significantly decreased at week 8, with declines in wrinkle counts emerging at week 12. The investigators concluded that kinetin and niacinamide display synergistic and dynamic anti-aging effects, showing substantial potential as topical anti-aging cosmeceutical agents (J. Cosmet. Dermatol. 2007;6:243-9).

However, Levin et al. noted in 2010 that while the effects of kinetin have been established in plants and its antioxidant properties have been displayed in vitro, the anti-aging effects and clinical efficacy ascribed to kinetin have been based on limited evidence, with no studies extant on the percutaneous absorption of kinetin. They added that research elucidating the mechanisms through which kinetin appears to improve skin barrier function, texture, and pigmentation also are lacking (J. Clin. Aesthet. Dermatol. 2010;3:22-41).

In 2012, Campos et al. assessed the effects on hydration, viscoelastic characteristics, and photoprotection of cosmetic preparations containing a dispersion of liposome with magnesium ascorbyl phosphate, alpha-lipoic acid, and kinetin. They observed that the formulation protected hairless mouse skin barrier function against UV harm. After 4 weeks of application on human skin, the combination product was found to have improved moisturization of the stratum corneum, also delivering hydration effects to deeper skin layers. The researchers concluded that the cosmetic formulation containing kinetin shows promise as a cutaneous anti-aging product (Photochem. Photobiol. 2012;88:748-52).

Conclusion

While some experimental and clinical results appear to suggest an anti-aging effect exerted by topically applied kinetin, much more research – particularly randomized controlled and comparison studies – are needed to provide a clearer picture as to the mechanisms and appropriate role of kinetin in the dermatologic armamentarium.

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 Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy,Topix Pharmaceuticals, and Unilever.

Kinetin (N6-furfuryladenine or 6-furfurylaminopurine) is a plant cytokinin or phytohormone that promotes cell division, delays senescence in plants, and is reputed to aid in the restoration of skin barrier function and, possibly, in reducing the signs and symptoms of rosacea (Clin. Exp. Dermatol. 2007;32:693-5; Plant Sci. 1999;148:37-45).

Kinetin is believed to develop in cellular DNA as a product of the oxidative, secondary modification of DNA (Plant Sci. 1999;148:37-45). In 1955, it became the first cytokinin isolated from DNA (from herring sperm) as an artifactual rearrangement product of the autoclaving process (J. Cosmet. Dermatol. 2007;6:243-9; Int. J. Biol. Macromol. 2007;40:182-92).

It has since been found to be present in human urine as well as DNA freshly extracted from human cells (Int. J. Biol. Macromol. 2007;40:182-92). The preponderance of amassed experimental evidence suggests that endogenous kinetin acts in vitro and in vivo as a potent antioxidant (Plant Sci. 1999;148:37-45). Currently, it is used as an anti-aging agent in various cosmetic products (J. Cosmet. Dermatol. 2007;6:243-9; J. Cosmet. Dermatol. 2010;9:218-25). Synthetic kinetin is thought to have the capacity to neutralize free radicals as well as limit the damage to DNA and fibroblasts (Photochem. Photobiol. 2012;88:748-52).

In vitro results

Olsen et al. demonstrated in vitro in 1999 that kinetin dose-dependently protected DNA against oxidative damage mediated by the Fenton reaction, and noted that kinetin had previously been linked to anti-aging activity in plants, fruit flies, and human cells in culture (Biochem. Biophys. Res. Commun. 1999;265:499-502). The following year, Verbeke et al. showed in vitro that kinetin potently inhibited damage caused by oxidation and glycoxidation (Biochem. Biophys. Res. Commun. 2000;276:1265-70).

In 2006, Vicanova et al. analyzed the effects of active ingredients from topical and systemic skin care formulations in vitro, finding that kinetin affected the upper dermis by enhancing deposits of fibrillin-1 and elastin fibers as well as their organization perpendicular to the dermal-epidermal junction. In the epidermis, kinetin stimulated keratinocyte production. Further, the investigators noted that the combination of topically applied kinetin with Imedeen Time Perfection ingredients (i.e., BioMarine Complex, grape seed extract, tomato extract, and vitamin C) supplemented systemically into culture medium yielded complementary benefits to dermal and epidermal development (Ann. N.Y. Acad. Sci. 2006;1067:337-42).

It is worth noting that in a study by Tournas et al. published the same month, investigators found that the topical application of a combination of vitamins C and E and ferulic acid yielded photoprotection to pig skin at 5 times the minimal erythema dose (MED) while individual antioxidants to which it was compared (i.e., coenzyme Q10, idebenone, and kinetin) delivered no photoprotective effects (J. Invest. Dermatol. 2006;126:1185-7). Nevertheless, Barciszewski et al. have observed that kinetin is the first stable secondary DNA damage product characterized by well defined cytokinin and anti-aging activity, with data showing that it has delayed human cellular aging in culture (Int. J. Biol. Macromol. 2007;40:182-92).

Rosacea

In 2007, Wu et al. performed a 12-week open-label study in 15 women and 3 men (aged 30-67 years) to ascertain the tolerability and efficacy of kinetin 0.1% lotion in the treatment of mild to moderate facial rosacea. Patients (17 of whom completed the study) applied the lotion twice daily, also daily applying an SPF 30 sunscreen. By week 4, significant improvements were observed in the reduction of skin roughness and mottled hyperpigmentation. Subject assessments at each 4-week interval after baseline and after 12 weeks revealed that kinetin 0.1% was well tolerated and effective for mild to moderate inflammatory rosacea (Clin. Exp. Dermatol. 2007;32:693-5).

Anti-aging

A 2002 study by J.L. McCullough and G.D. Weinstein represented the first evidence of the efficacy of topical kinetin in human beings, with twice-daily application for 24 weeks found to ameliorate skin texture, color, and blotchiness while diminishing rhytides and transepidermal water loss (J. Cosmet. Dermatol. 2002;15:29-32).

Two years later, T. Kimura and K. Doi showed that topical administration of kinetin improved the texture, wrinkling, and pigmentation of aged skin of hairless descendants of Mexican hairless dogs, resulting in notable depigmentation and rejuvenation after 100 days of treatment (Rejuvenation Res. 2004;7:32-9).In 2007, Chiu et al. conducted a randomized, double-blind, placebo-controlled, split-face comparative study in 52 Taiwanese subjects aged 30-60 years (90% of whom were female, all of whom had Fitzpatrick skin types II, III, or IV) to evaluate the clinical anti-aging effects and efficacy differences between kinetin plus niacinamide (kinetin 0.03%, niacinamide 4%) and niacinamide 4% alone versus vehicle placebo.

In the combination group, significant and sustained decreases were observed in counts of spots, pores, wrinkles, and evenness as well as persistent reductions in erythema index at weeks 8 and 12. At week 12, stratum corneum hydration status also was significantly enhanced in this group. In the niacinamide-only group, pore and evenness counts were significantly decreased at week 8, with declines in wrinkle counts emerging at week 12. The investigators concluded that kinetin and niacinamide display synergistic and dynamic anti-aging effects, showing substantial potential as topical anti-aging cosmeceutical agents (J. Cosmet. Dermatol. 2007;6:243-9).

However, Levin et al. noted in 2010 that while the effects of kinetin have been established in plants and its antioxidant properties have been displayed in vitro, the anti-aging effects and clinical efficacy ascribed to kinetin have been based on limited evidence, with no studies extant on the percutaneous absorption of kinetin. They added that research elucidating the mechanisms through which kinetin appears to improve skin barrier function, texture, and pigmentation also are lacking (J. Clin. Aesthet. Dermatol. 2010;3:22-41).

In 2012, Campos et al. assessed the effects on hydration, viscoelastic characteristics, and photoprotection of cosmetic preparations containing a dispersion of liposome with magnesium ascorbyl phosphate, alpha-lipoic acid, and kinetin. They observed that the formulation protected hairless mouse skin barrier function against UV harm. After 4 weeks of application on human skin, the combination product was found to have improved moisturization of the stratum corneum, also delivering hydration effects to deeper skin layers. The researchers concluded that the cosmetic formulation containing kinetin shows promise as a cutaneous anti-aging product (Photochem. Photobiol. 2012;88:748-52).

Conclusion

While some experimental and clinical results appear to suggest an anti-aging effect exerted by topically applied kinetin, much more research – particularly randomized controlled and comparison studies – are needed to provide a clearer picture as to the mechanisms and appropriate role of kinetin in the dermatologic armamentarium.

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 Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy,Topix Pharmaceuticals, and Unilever.

Kinetin (N6-furfuryladenine or 6-furfurylaminopurine) is a plant cytokinin or phytohormone that promotes cell division, delays senescence in plants, and is reputed to aid in the restoration of skin barrier function and, possibly, in reducing the signs and symptoms of rosacea (Clin. Exp. Dermatol. 2007;32:693-5; Plant Sci. 1999;148:37-45).

Kinetin is believed to develop in cellular DNA as a product of the oxidative, secondary modification of DNA (Plant Sci. 1999;148:37-45). In 1955, it became the first cytokinin isolated from DNA (from herring sperm) as an artifactual rearrangement product of the autoclaving process (J. Cosmet. Dermatol. 2007;6:243-9; Int. J. Biol. Macromol. 2007;40:182-92).

It has since been found to be present in human urine as well as DNA freshly extracted from human cells (Int. J. Biol. Macromol. 2007;40:182-92). The preponderance of amassed experimental evidence suggests that endogenous kinetin acts in vitro and in vivo as a potent antioxidant (Plant Sci. 1999;148:37-45). Currently, it is used as an anti-aging agent in various cosmetic products (J. Cosmet. Dermatol. 2007;6:243-9; J. Cosmet. Dermatol. 2010;9:218-25). Synthetic kinetin is thought to have the capacity to neutralize free radicals as well as limit the damage to DNA and fibroblasts (Photochem. Photobiol. 2012;88:748-52).

In vitro results

Olsen et al. demonstrated in vitro in 1999 that kinetin dose-dependently protected DNA against oxidative damage mediated by the Fenton reaction, and noted that kinetin had previously been linked to anti-aging activity in plants, fruit flies, and human cells in culture (Biochem. Biophys. Res. Commun. 1999;265:499-502). The following year, Verbeke et al. showed in vitro that kinetin potently inhibited damage caused by oxidation and glycoxidation (Biochem. Biophys. Res. Commun. 2000;276:1265-70).

In 2006, Vicanova et al. analyzed the effects of active ingredients from topical and systemic skin care formulations in vitro, finding that kinetin affected the upper dermis by enhancing deposits of fibrillin-1 and elastin fibers as well as their organization perpendicular to the dermal-epidermal junction. In the epidermis, kinetin stimulated keratinocyte production. Further, the investigators noted that the combination of topically applied kinetin with Imedeen Time Perfection ingredients (i.e., BioMarine Complex, grape seed extract, tomato extract, and vitamin C) supplemented systemically into culture medium yielded complementary benefits to dermal and epidermal development (Ann. N.Y. Acad. Sci. 2006;1067:337-42).

It is worth noting that in a study by Tournas et al. published the same month, investigators found that the topical application of a combination of vitamins C and E and ferulic acid yielded photoprotection to pig skin at 5 times the minimal erythema dose (MED) while individual antioxidants to which it was compared (i.e., coenzyme Q10, idebenone, and kinetin) delivered no photoprotective effects (J. Invest. Dermatol. 2006;126:1185-7). Nevertheless, Barciszewski et al. have observed that kinetin is the first stable secondary DNA damage product characterized by well defined cytokinin and anti-aging activity, with data showing that it has delayed human cellular aging in culture (Int. J. Biol. Macromol. 2007;40:182-92).

Rosacea

In 2007, Wu et al. performed a 12-week open-label study in 15 women and 3 men (aged 30-67 years) to ascertain the tolerability and efficacy of kinetin 0.1% lotion in the treatment of mild to moderate facial rosacea. Patients (17 of whom completed the study) applied the lotion twice daily, also daily applying an SPF 30 sunscreen. By week 4, significant improvements were observed in the reduction of skin roughness and mottled hyperpigmentation. Subject assessments at each 4-week interval after baseline and after 12 weeks revealed that kinetin 0.1% was well tolerated and effective for mild to moderate inflammatory rosacea (Clin. Exp. Dermatol. 2007;32:693-5).

Anti-aging

A 2002 study by J.L. McCullough and G.D. Weinstein represented the first evidence of the efficacy of topical kinetin in human beings, with twice-daily application for 24 weeks found to ameliorate skin texture, color, and blotchiness while diminishing rhytides and transepidermal water loss (J. Cosmet. Dermatol. 2002;15:29-32).

Two years later, T. Kimura and K. Doi showed that topical administration of kinetin improved the texture, wrinkling, and pigmentation of aged skin of hairless descendants of Mexican hairless dogs, resulting in notable depigmentation and rejuvenation after 100 days of treatment (Rejuvenation Res. 2004;7:32-9).In 2007, Chiu et al. conducted a randomized, double-blind, placebo-controlled, split-face comparative study in 52 Taiwanese subjects aged 30-60 years (90% of whom were female, all of whom had Fitzpatrick skin types II, III, or IV) to evaluate the clinical anti-aging effects and efficacy differences between kinetin plus niacinamide (kinetin 0.03%, niacinamide 4%) and niacinamide 4% alone versus vehicle placebo.

In the combination group, significant and sustained decreases were observed in counts of spots, pores, wrinkles, and evenness as well as persistent reductions in erythema index at weeks 8 and 12. At week 12, stratum corneum hydration status also was significantly enhanced in this group. In the niacinamide-only group, pore and evenness counts were significantly decreased at week 8, with declines in wrinkle counts emerging at week 12. The investigators concluded that kinetin and niacinamide display synergistic and dynamic anti-aging effects, showing substantial potential as topical anti-aging cosmeceutical agents (J. Cosmet. Dermatol. 2007;6:243-9).

However, Levin et al. noted in 2010 that while the effects of kinetin have been established in plants and its antioxidant properties have been displayed in vitro, the anti-aging effects and clinical efficacy ascribed to kinetin have been based on limited evidence, with no studies extant on the percutaneous absorption of kinetin. They added that research elucidating the mechanisms through which kinetin appears to improve skin barrier function, texture, and pigmentation also are lacking (J. Clin. Aesthet. Dermatol. 2010;3:22-41).

In 2012, Campos et al. assessed the effects on hydration, viscoelastic characteristics, and photoprotection of cosmetic preparations containing a dispersion of liposome with magnesium ascorbyl phosphate, alpha-lipoic acid, and kinetin. They observed that the formulation protected hairless mouse skin barrier function against UV harm. After 4 weeks of application on human skin, the combination product was found to have improved moisturization of the stratum corneum, also delivering hydration effects to deeper skin layers. The researchers concluded that the cosmetic formulation containing kinetin shows promise as a cutaneous anti-aging product (Photochem. Photobiol. 2012;88:748-52).

Conclusion

While some experimental and clinical results appear to suggest an anti-aging effect exerted by topically applied kinetin, much more research – particularly randomized controlled and comparison studies – are needed to provide a clearer picture as to the mechanisms and appropriate role of kinetin in the dermatologic armamentarium.

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 Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy,Topix Pharmaceuticals, and Unilever.

They say you can’t have it all, and they’re right. But you can have most of it. By that I mean you can achieve a work-life balance that will enable you to thrive in your career while you raise your dream family. While this goal may never be easy, and you may always feel like you want to do more, give more, and reach more, that’s just the nature of the beast. We are all overachievers. That’s how we’re programmed; it’s in our DNA. Why else would we have taken on so much debt and sacrificed so many years for a career? And while many of us specifically chose hospital medicine so we could offset our stressful, hectic work life with plenty of time off for self and family, our reality is still replete with everyday challenges and, frequently, burnout.

We eagerly seek out best practices to optimize patient care, but how often do we seek advice from trusted colleagues on their “best practices” for balancing work and home? While talking with some of my female colleagues recently, I expressed my dismay that my dishwasher had broken and I frequently found myself washing dinner dishes as I juggled homework for my two 6-year-olds and responded to a seemingly incessant pager. One laughed as she recalled the pains she went through to have not one, but two dishwashers installed in her kitchen during her remodel. Washing dishes by hand simply wasn’t realistic for her. Her two little boys demanded whatever physical and emotional energy she had left after a stressful day at the hospital.

It is okay to admit that you don’t have all the answers, and it is cathartic to accept that you may never be the homemaker your mother was and forget about matching your grandmothers’ skillsets. At some Alcoholics Anonymous meetings, new members stand up and introduce themselves by saying, “Hello, my name is ___, and I am an alcoholic.” I personally felt like a huge weight had been lifted from my shoulders when one day, I finally acknowledged I didn’t have all the answers and I could never follow all of the parenting experts’ advice. After all, experts come and go, and with it, their expert recommendations. I don’t even want to abide by the “no more than 30 minutes of screen time per day” mantra. My parents raised five children on rerun after rerun of “The Andy Griffith Show,” “The Brady Bunch,” and other sitcoms, not to mention movies and musicals, and every one of us has a terminal degree, and still remember how much fun we had as children. My parents set high expectations, and they taught us how to reach them, plain and simple. We worked hard and we got to play hard, too.

The bottom line is that different techniques work for different people. Find out which ones work for you and your family and pursue them, regardless of what others may think. And above all, don’t let guilt get the best of you, because it will eat away at you and potentially destroy all you want to accomplish. You know, the guilt of missing a soccer game or a school play, or even the guilt of stopping for fast food when you are just too tired to cook a nutritious meal. Give yourself a break. The realistic goal is to optimize your work-life balance; the elusive one is to perfect it.

Dr. Hester is a hospitalist at Baltimore-Washington Medical Center in Glen Burnie, Md. She is the creator of the Patient Whiz, a patient-engagement app for iOS. Reach her at [email protected].

They say you can’t have it all, and they’re right. But you can have most of it. By that I mean you can achieve a work-life balance that will enable you to thrive in your career while you raise your dream family. While this goal may never be easy, and you may always feel like you want to do more, give more, and reach more, that’s just the nature of the beast. We are all overachievers. That’s how we’re programmed; it’s in our DNA. Why else would we have taken on so much debt and sacrificed so many years for a career? And while many of us specifically chose hospital medicine so we could offset our stressful, hectic work life with plenty of time off for self and family, our reality is still replete with everyday challenges and, frequently, burnout.

We eagerly seek out best practices to optimize patient care, but how often do we seek advice from trusted colleagues on their “best practices” for balancing work and home? While talking with some of my female colleagues recently, I expressed my dismay that my dishwasher had broken and I frequently found myself washing dinner dishes as I juggled homework for my two 6-year-olds and responded to a seemingly incessant pager. One laughed as she recalled the pains she went through to have not one, but two dishwashers installed in her kitchen during her remodel. Washing dishes by hand simply wasn’t realistic for her. Her two little boys demanded whatever physical and emotional energy she had left after a stressful day at the hospital.

It is okay to admit that you don’t have all the answers, and it is cathartic to accept that you may never be the homemaker your mother was and forget about matching your grandmothers’ skillsets. At some Alcoholics Anonymous meetings, new members stand up and introduce themselves by saying, “Hello, my name is ___, and I am an alcoholic.” I personally felt like a huge weight had been lifted from my shoulders when one day, I finally acknowledged I didn’t have all the answers and I could never follow all of the parenting experts’ advice. After all, experts come and go, and with it, their expert recommendations. I don’t even want to abide by the “no more than 30 minutes of screen time per day” mantra. My parents raised five children on rerun after rerun of “The Andy Griffith Show,” “The Brady Bunch,” and other sitcoms, not to mention movies and musicals, and every one of us has a terminal degree, and still remember how much fun we had as children. My parents set high expectations, and they taught us how to reach them, plain and simple. We worked hard and we got to play hard, too.

The bottom line is that different techniques work for different people. Find out which ones work for you and your family and pursue them, regardless of what others may think. And above all, don’t let guilt get the best of you, because it will eat away at you and potentially destroy all you want to accomplish. You know, the guilt of missing a soccer game or a school play, or even the guilt of stopping for fast food when you are just too tired to cook a nutritious meal. Give yourself a break. The realistic goal is to optimize your work-life balance; the elusive one is to perfect it.

Dr. Hester is a hospitalist at Baltimore-Washington Medical Center in Glen Burnie, Md. She is the creator of the Patient Whiz, a patient-engagement app for iOS. Reach her at [email protected].

They say you can’t have it all, and they’re right. But you can have most of it. By that I mean you can achieve a work-life balance that will enable you to thrive in your career while you raise your dream family. While this goal may never be easy, and you may always feel like you want to do more, give more, and reach more, that’s just the nature of the beast. We are all overachievers. That’s how we’re programmed; it’s in our DNA. Why else would we have taken on so much debt and sacrificed so many years for a career? And while many of us specifically chose hospital medicine so we could offset our stressful, hectic work life with plenty of time off for self and family, our reality is still replete with everyday challenges and, frequently, burnout.

We eagerly seek out best practices to optimize patient care, but how often do we seek advice from trusted colleagues on their “best practices” for balancing work and home? While talking with some of my female colleagues recently, I expressed my dismay that my dishwasher had broken and I frequently found myself washing dinner dishes as I juggled homework for my two 6-year-olds and responded to a seemingly incessant pager. One laughed as she recalled the pains she went through to have not one, but two dishwashers installed in her kitchen during her remodel. Washing dishes by hand simply wasn’t realistic for her. Her two little boys demanded whatever physical and emotional energy she had left after a stressful day at the hospital.

It is okay to admit that you don’t have all the answers, and it is cathartic to accept that you may never be the homemaker your mother was and forget about matching your grandmothers’ skillsets. At some Alcoholics Anonymous meetings, new members stand up and introduce themselves by saying, “Hello, my name is ___, and I am an alcoholic.” I personally felt like a huge weight had been lifted from my shoulders when one day, I finally acknowledged I didn’t have all the answers and I could never follow all of the parenting experts’ advice. After all, experts come and go, and with it, their expert recommendations. I don’t even want to abide by the “no more than 30 minutes of screen time per day” mantra. My parents raised five children on rerun after rerun of “The Andy Griffith Show,” “The Brady Bunch,” and other sitcoms, not to mention movies and musicals, and every one of us has a terminal degree, and still remember how much fun we had as children. My parents set high expectations, and they taught us how to reach them, plain and simple. We worked hard and we got to play hard, too.

The bottom line is that different techniques work for different people. Find out which ones work for you and your family and pursue them, regardless of what others may think. And above all, don’t let guilt get the best of you, because it will eat away at you and potentially destroy all you want to accomplish. You know, the guilt of missing a soccer game or a school play, or even the guilt of stopping for fast food when you are just too tired to cook a nutritious meal. Give yourself a break. The realistic goal is to optimize your work-life balance; the elusive one is to perfect it.

Dr. Hester is a hospitalist at Baltimore-Washington Medical Center in Glen Burnie, Md. She is the creator of the Patient Whiz, a patient-engagement app for iOS. Reach her at [email protected].

The pathogenesis of respiratory infections such as acute otitis media (AOM), sinusitis, and pneumonia involves complex interactions among bacteria, respiratory viruses, and host immune responses.

My clinical and laboratory group and others have described respiratory infections as resulting from the growth of a single otopathogen, such as Streptococcus pneumoniae (Spn), nontypeable Haemophilus influenzae (NTHi), or Moraxella catarrhalis (Mcat) in the nasopharynx (NP) followed by ascension to the middle ear, sinuses, or descent to the lungs. Recent research from my group and others has resulted in a shift from a single pathogen focus toward consideration of respiratory infections as a polymicrobial disease. Bacterial and viral interactions are critical in respiratory infection pathogenesis. Commensal bacteria can alter virulence of bacterial pathogens and interfere with antibiotic treatment.

The traditional view of the immune system is that it is an assembly of human tissues, cells, and molecules that work to eliminate pathogens. Recent discoveries indicate that commensals play a central role in regulating human immune responses. Thus, the key questions in the field are:

1) How do members of the NP microbiome and innate immune responses maintain health in young children over time?

2) Do specific deleterious members of the NP microbiome alter host innate immune responses in a manner that predisposes to respiratory infections?

3) How does the microbiome and innate response in the NP differ when recovery, relapse of infection, or persistent infection occurs?

Virtually all young children are colonized by Spn, NTHi, or Mcat during the first 3 years of life. My group and others have shown that competitive interactions among bacteria influence whether these potential pathogens successfully colonize and cause respiratory infections. Recent studies have demonstrated that hundreds of different bacterial species colonize the upper respiratory tract. Diverse communities have been shown to be more stable and resistant to invasion by foreign species. Data from cross-sectional studies demonstrate that specific commensals, including Dolosigranulum, Corynebacterium, and Lactococcus, are associated with decreased risk of respiratory infections. Prior studies have been limited by the use of culture-based methods or have been cross sectional in design. Therefore, the optimal levels of diversity and NP commensals critical for maintaining health in the upper respiratory tract of children are currently unknown and under study by my group and others. Studies that utilize high-throughput culture-independent molecular detection methods are now used to identify optimal levels of diversity and commensal members of the microbiome critical for maintaining health homeostasis.

The innate immune system constitutes the first line of defense against respiratory pathogen colonization and respiratory virus infection. It relies on pattern recognition receptors on innate immune cells to detect evolutionarily conserved pathogen-associated molecular patterns expressed on pathogen surfaces. Toll-like receptors (TLRs) are crucial in the innate immune response; TLR 3, 7, and 8 recognize respiratory infection-associated viral pathogens. TLR2, 4, and 5 recognize respiratory infection-associated bacterial pathogens, and TLR9 and TLR13 recognize both viral and bacterial pathogens. The activation of TLRs triggers signaling cascades and regulates the expression of a wide range of cytokines leading to antimicrobial and inflammatory responses. Cytokines (there are dozens) associated with the pathogenesis, development, severity, and clinical outcomes of respiratory infections identify hypotheses that our group is exploring to expand our understanding of how innate responses might be manipulated to favor the child host. Importantly, it has already been shown that cytokine profiles differ in the NP depending on the number and type of bacteria and viruses involved.

My group recently has shown that serum IL-10 levels are significantly higher in AOM from Spn than are the levels associated with NTHi and Mcat, suggesting use of detection of this cytokine as a serum biomarker. Others have shown that the levels of IL-1-beta, TNF-alpha, IL-6, IL-8, IL-10, and IL-17a in middle ear fluids from children with recurrent AOM correlate significantly with higher bacterial load (and worse disease). Previous studies on cytokine responses associated with AOM have focused on limited numbers of cytokines and have not examined any relationship with commensals of the NP microbiome. Moreover, the subset of children who experience excessively frequent respiratory infections likely have disturbances in their microbiome (made worse with antibiotics) and innate immune response. Because of our growing knowledge about the microbiome and innate immune response, I see a compelling need to assess interactions of the NP microbiome and innate immune responses in children that are associated with sustained health and control of respiratory infections.

Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute, Rochester (N.Y.) General Hospital. He is also a pediatrician at Legacy Pediatrics in Rochester. Dr. Pichichero said the work was supported by a National Institutes of Health grant, and he had no relevant conflicts of interest. E-mail him at [email protected].

The pathogenesis of respiratory infections such as acute otitis media (AOM), sinusitis, and pneumonia involves complex interactions among bacteria, respiratory viruses, and host immune responses.

My clinical and laboratory group and others have described respiratory infections as resulting from the growth of a single otopathogen, such as Streptococcus pneumoniae (Spn), nontypeable Haemophilus influenzae (NTHi), or Moraxella catarrhalis (Mcat) in the nasopharynx (NP) followed by ascension to the middle ear, sinuses, or descent to the lungs. Recent research from my group and others has resulted in a shift from a single pathogen focus toward consideration of respiratory infections as a polymicrobial disease. Bacterial and viral interactions are critical in respiratory infection pathogenesis. Commensal bacteria can alter virulence of bacterial pathogens and interfere with antibiotic treatment.

The traditional view of the immune system is that it is an assembly of human tissues, cells, and molecules that work to eliminate pathogens. Recent discoveries indicate that commensals play a central role in regulating human immune responses. Thus, the key questions in the field are:

1) How do members of the NP microbiome and innate immune responses maintain health in young children over time?

2) Do specific deleterious members of the NP microbiome alter host innate immune responses in a manner that predisposes to respiratory infections?

3) How does the microbiome and innate response in the NP differ when recovery, relapse of infection, or persistent infection occurs?

Virtually all young children are colonized by Spn, NTHi, or Mcat during the first 3 years of life. My group and others have shown that competitive interactions among bacteria influence whether these potential pathogens successfully colonize and cause respiratory infections. Recent studies have demonstrated that hundreds of different bacterial species colonize the upper respiratory tract. Diverse communities have been shown to be more stable and resistant to invasion by foreign species. Data from cross-sectional studies demonstrate that specific commensals, including Dolosigranulum, Corynebacterium, and Lactococcus, are associated with decreased risk of respiratory infections. Prior studies have been limited by the use of culture-based methods or have been cross sectional in design. Therefore, the optimal levels of diversity and NP commensals critical for maintaining health in the upper respiratory tract of children are currently unknown and under study by my group and others. Studies that utilize high-throughput culture-independent molecular detection methods are now used to identify optimal levels of diversity and commensal members of the microbiome critical for maintaining health homeostasis.

The innate immune system constitutes the first line of defense against respiratory pathogen colonization and respiratory virus infection. It relies on pattern recognition receptors on innate immune cells to detect evolutionarily conserved pathogen-associated molecular patterns expressed on pathogen surfaces. Toll-like receptors (TLRs) are crucial in the innate immune response; TLR 3, 7, and 8 recognize respiratory infection-associated viral pathogens. TLR2, 4, and 5 recognize respiratory infection-associated bacterial pathogens, and TLR9 and TLR13 recognize both viral and bacterial pathogens. The activation of TLRs triggers signaling cascades and regulates the expression of a wide range of cytokines leading to antimicrobial and inflammatory responses. Cytokines (there are dozens) associated with the pathogenesis, development, severity, and clinical outcomes of respiratory infections identify hypotheses that our group is exploring to expand our understanding of how innate responses might be manipulated to favor the child host. Importantly, it has already been shown that cytokine profiles differ in the NP depending on the number and type of bacteria and viruses involved.

My group recently has shown that serum IL-10 levels are significantly higher in AOM from Spn than are the levels associated with NTHi and Mcat, suggesting use of detection of this cytokine as a serum biomarker. Others have shown that the levels of IL-1-beta, TNF-alpha, IL-6, IL-8, IL-10, and IL-17a in middle ear fluids from children with recurrent AOM correlate significantly with higher bacterial load (and worse disease). Previous studies on cytokine responses associated with AOM have focused on limited numbers of cytokines and have not examined any relationship with commensals of the NP microbiome. Moreover, the subset of children who experience excessively frequent respiratory infections likely have disturbances in their microbiome (made worse with antibiotics) and innate immune response. Because of our growing knowledge about the microbiome and innate immune response, I see a compelling need to assess interactions of the NP microbiome and innate immune responses in children that are associated with sustained health and control of respiratory infections.

Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute, Rochester (N.Y.) General Hospital. He is also a pediatrician at Legacy Pediatrics in Rochester. Dr. Pichichero said the work was supported by a National Institutes of Health grant, and he had no relevant conflicts of interest. E-mail him at [email protected].

The pathogenesis of respiratory infections such as acute otitis media (AOM), sinusitis, and pneumonia involves complex interactions among bacteria, respiratory viruses, and host immune responses.

My clinical and laboratory group and others have described respiratory infections as resulting from the growth of a single otopathogen, such as Streptococcus pneumoniae (Spn), nontypeable Haemophilus influenzae (NTHi), or Moraxella catarrhalis (Mcat) in the nasopharynx (NP) followed by ascension to the middle ear, sinuses, or descent to the lungs. Recent research from my group and others has resulted in a shift from a single pathogen focus toward consideration of respiratory infections as a polymicrobial disease. Bacterial and viral interactions are critical in respiratory infection pathogenesis. Commensal bacteria can alter virulence of bacterial pathogens and interfere with antibiotic treatment.

The traditional view of the immune system is that it is an assembly of human tissues, cells, and molecules that work to eliminate pathogens. Recent discoveries indicate that commensals play a central role in regulating human immune responses. Thus, the key questions in the field are:

1) How do members of the NP microbiome and innate immune responses maintain health in young children over time?

2) Do specific deleterious members of the NP microbiome alter host innate immune responses in a manner that predisposes to respiratory infections?

3) How does the microbiome and innate response in the NP differ when recovery, relapse of infection, or persistent infection occurs?

Virtually all young children are colonized by Spn, NTHi, or Mcat during the first 3 years of life. My group and others have shown that competitive interactions among bacteria influence whether these potential pathogens successfully colonize and cause respiratory infections. Recent studies have demonstrated that hundreds of different bacterial species colonize the upper respiratory tract. Diverse communities have been shown to be more stable and resistant to invasion by foreign species. Data from cross-sectional studies demonstrate that specific commensals, including Dolosigranulum, Corynebacterium, and Lactococcus, are associated with decreased risk of respiratory infections. Prior studies have been limited by the use of culture-based methods or have been cross sectional in design. Therefore, the optimal levels of diversity and NP commensals critical for maintaining health in the upper respiratory tract of children are currently unknown and under study by my group and others. Studies that utilize high-throughput culture-independent molecular detection methods are now used to identify optimal levels of diversity and commensal members of the microbiome critical for maintaining health homeostasis.

The innate immune system constitutes the first line of defense against respiratory pathogen colonization and respiratory virus infection. It relies on pattern recognition receptors on innate immune cells to detect evolutionarily conserved pathogen-associated molecular patterns expressed on pathogen surfaces. Toll-like receptors (TLRs) are crucial in the innate immune response; TLR 3, 7, and 8 recognize respiratory infection-associated viral pathogens. TLR2, 4, and 5 recognize respiratory infection-associated bacterial pathogens, and TLR9 and TLR13 recognize both viral and bacterial pathogens. The activation of TLRs triggers signaling cascades and regulates the expression of a wide range of cytokines leading to antimicrobial and inflammatory responses. Cytokines (there are dozens) associated with the pathogenesis, development, severity, and clinical outcomes of respiratory infections identify hypotheses that our group is exploring to expand our understanding of how innate responses might be manipulated to favor the child host. Importantly, it has already been shown that cytokine profiles differ in the NP depending on the number and type of bacteria and viruses involved.

My group recently has shown that serum IL-10 levels are significantly higher in AOM from Spn than are the levels associated with NTHi and Mcat, suggesting use of detection of this cytokine as a serum biomarker. Others have shown that the levels of IL-1-beta, TNF-alpha, IL-6, IL-8, IL-10, and IL-17a in middle ear fluids from children with recurrent AOM correlate significantly with higher bacterial load (and worse disease). Previous studies on cytokine responses associated with AOM have focused on limited numbers of cytokines and have not examined any relationship with commensals of the NP microbiome. Moreover, the subset of children who experience excessively frequent respiratory infections likely have disturbances in their microbiome (made worse with antibiotics) and innate immune response. Because of our growing knowledge about the microbiome and innate immune response, I see a compelling need to assess interactions of the NP microbiome and innate immune responses in children that are associated with sustained health and control of respiratory infections.

Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute, Rochester (N.Y.) General Hospital. He is also a pediatrician at Legacy Pediatrics in Rochester. Dr. Pichichero said the work was supported by a National Institutes of Health grant, and he had no relevant conflicts of interest. E-mail him at [email protected].

Perhaps one of the biggest ways in which I’ve evolved as a doctor over the 4.5 years I’ve been in private practice is that I am not so shy about ordering tests anymore.

My point is illustrated by the case of a lovely lady I met when I was starting out in practice who complained of being in pain all the time. She was referred to me for a very low titer antinuclear antibody and a barely positive rheumatoid factor. She’d had a very long history of severe depression and anxiety. She clearly connected her symptoms to having stopped her antidepressants. She attributed her dry mouth to her benzodiazepine. I told her that I thought she had fibromyalgia and that, as she herself pointed out, it was probably related to her emotional health. We talked about the lack of any real pharmacologic treatment for the illness. We addressed self-care: that she needed to sleep better, exercise more, and treat her depression.

Three years later she came back to me with hand swelling, hypergammaglobulinemia, renal tubular acidosis, this time with significantly higher ANA and RF titers, and hypocomplementemia. You guessed it; she has Sjögren’s syndrome.

Seeing patients 40 hours a week has been incredibly challenging but also incredibly rewarding. While the large number of cases that I’ve seen has sharpened my clinical eye, it has also broadened my differential diagnoses and improved my knowledge of when it will be helpful to order more tests.

It used to be that I was extremely conservative about ordering tests. This comes from having gone to med school in the Philippines, where each test was paid for by the patient out of pocket and GDP per capita is $2,765 (compared with $53,041 for the United States) and minimum wage is less than 2 dollars a day. Every CBC has to count. If a professor asked you why you were ordering a test, “to establish a baseline” was an unacceptable reason. When I started residency here, I was incredulous that the admitted patients got a CBC and chem-7 daily. This seemed like a huge and unjustifiable waste to me.

Today, I am not so uptight. Of course, I am still extremely thoughtful about ordering tests. I do not order tests without knowing what I am looking for, or how the result will affect management. But I also recognize that there is a non-zero probability that what I suspect is fibromyalgia is something else, something with a different prognosis, better or worse, something that needs to be managed and monitored differently.

After all, “clinical judgment” does not mean relying on the history and physical exam alone. Good clinical judgment requires medical knowledge, informed by experience, supplemented by test results, and complemented by an open, inquisitive mind.

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

Perhaps one of the biggest ways in which I’ve evolved as a doctor over the 4.5 years I’ve been in private practice is that I am not so shy about ordering tests anymore.

My point is illustrated by the case of a lovely lady I met when I was starting out in practice who complained of being in pain all the time. She was referred to me for a very low titer antinuclear antibody and a barely positive rheumatoid factor. She’d had a very long history of severe depression and anxiety. She clearly connected her symptoms to having stopped her antidepressants. She attributed her dry mouth to her benzodiazepine. I told her that I thought she had fibromyalgia and that, as she herself pointed out, it was probably related to her emotional health. We talked about the lack of any real pharmacologic treatment for the illness. We addressed self-care: that she needed to sleep better, exercise more, and treat her depression.

Three years later she came back to me with hand swelling, hypergammaglobulinemia, renal tubular acidosis, this time with significantly higher ANA and RF titers, and hypocomplementemia. You guessed it; she has Sjögren’s syndrome.

Seeing patients 40 hours a week has been incredibly challenging but also incredibly rewarding. While the large number of cases that I’ve seen has sharpened my clinical eye, it has also broadened my differential diagnoses and improved my knowledge of when it will be helpful to order more tests.

It used to be that I was extremely conservative about ordering tests. This comes from having gone to med school in the Philippines, where each test was paid for by the patient out of pocket and GDP per capita is $2,765 (compared with $53,041 for the United States) and minimum wage is less than 2 dollars a day. Every CBC has to count. If a professor asked you why you were ordering a test, “to establish a baseline” was an unacceptable reason. When I started residency here, I was incredulous that the admitted patients got a CBC and chem-7 daily. This seemed like a huge and unjustifiable waste to me.

Today, I am not so uptight. Of course, I am still extremely thoughtful about ordering tests. I do not order tests without knowing what I am looking for, or how the result will affect management. But I also recognize that there is a non-zero probability that what I suspect is fibromyalgia is something else, something with a different prognosis, better or worse, something that needs to be managed and monitored differently.

After all, “clinical judgment” does not mean relying on the history and physical exam alone. Good clinical judgment requires medical knowledge, informed by experience, supplemented by test results, and complemented by an open, inquisitive mind.

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

Perhaps one of the biggest ways in which I’ve evolved as a doctor over the 4.5 years I’ve been in private practice is that I am not so shy about ordering tests anymore.

My point is illustrated by the case of a lovely lady I met when I was starting out in practice who complained of being in pain all the time. She was referred to me for a very low titer antinuclear antibody and a barely positive rheumatoid factor. She’d had a very long history of severe depression and anxiety. She clearly connected her symptoms to having stopped her antidepressants. She attributed her dry mouth to her benzodiazepine. I told her that I thought she had fibromyalgia and that, as she herself pointed out, it was probably related to her emotional health. We talked about the lack of any real pharmacologic treatment for the illness. We addressed self-care: that she needed to sleep better, exercise more, and treat her depression.

Three years later she came back to me with hand swelling, hypergammaglobulinemia, renal tubular acidosis, this time with significantly higher ANA and RF titers, and hypocomplementemia. You guessed it; she has Sjögren’s syndrome.

Seeing patients 40 hours a week has been incredibly challenging but also incredibly rewarding. While the large number of cases that I’ve seen has sharpened my clinical eye, it has also broadened my differential diagnoses and improved my knowledge of when it will be helpful to order more tests.

It used to be that I was extremely conservative about ordering tests. This comes from having gone to med school in the Philippines, where each test was paid for by the patient out of pocket and GDP per capita is $2,765 (compared with $53,041 for the United States) and minimum wage is less than 2 dollars a day. Every CBC has to count. If a professor asked you why you were ordering a test, “to establish a baseline” was an unacceptable reason. When I started residency here, I was incredulous that the admitted patients got a CBC and chem-7 daily. This seemed like a huge and unjustifiable waste to me.

Today, I am not so uptight. Of course, I am still extremely thoughtful about ordering tests. I do not order tests without knowing what I am looking for, or how the result will affect management. But I also recognize that there is a non-zero probability that what I suspect is fibromyalgia is something else, something with a different prognosis, better or worse, something that needs to be managed and monitored differently.

After all, “clinical judgment” does not mean relying on the history and physical exam alone. Good clinical judgment requires medical knowledge, informed by experience, supplemented by test results, and complemented by an open, inquisitive mind.

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

Editors note: The following are a selection of responses from the SVS membership sent to Dr. Peter Lawrence based upon his article in a recent issue of Vascular Specialist on the topic of the abuse of peripheral artery disease stenting in Medicare patients.

Despite the unfortunate press, we as a more global medical vascular community are unable to police our own. I have been involved in two specific instances in which inappropriate and overuse of endovascular therapy has been addressed. Unfortunately, these practitioners continue to perform unindicated procedures while hospitals and state medical boards refuse to act.

What is Medicare to do when our own medical regulatory bodies fail to act on behalf of patients and the payor? The two routes of targeting practitioners through Medicare high outliers and legal recourse for poor outcome in unindicated procedures will remain until our societies (this includes SVIR and ACC) decide to collaborate and ensure appropriate practice. Simply stating that SVS has guidelines in place will not solve the problem.

Jason M. Johanning, M.D., Omaha, Neb.

My office of five vascular surgeons actually has an in-office procedure suite. We have converted about 30%-40% of our minimally invasive patient care to this setting. In review of what we have done, we have actually decreased the cost of patient care as there is no facility or hospital add-on charge. Our cost per patient is actually about one-third of what is typically charged by the hospital, and our quality based on our independent QA is the same in our office setting as it is in the hospital. These types of settings can significantly reduce health care costs if done in the proper fashion.

Dennis Fry, M.D., West Des Moines, Iowa

The comments in the article that hospitals confer a greater degree of oversight seems to come right from the AHA. The problem is not office-based procedures but the ethics of fraudulent practices, something that occurs in and among hospitals as well. Hospitals can be as much driven by case volume, even at academic centers, as are the practices of private outpatient procedures.

Paul Gagne, M.D., Darien, Conn.

I cannot help but wonder how our specialty’s lack of identity – and thus lack of appreciation of its responsibility and role in public awareness – has contributed to this scenario. Our inclusion under the umbrella of the American Heart Association, again without any designation of our separate identity, leads only to more confusion about our specialty in the eyes of the public.

The SVS must address its lack of a public identity in a more forceful manner. Unfortunately, it’s biggest hurdle in this may well be the hospital-employed vascular surgeons who cannot fight the administrators marketing theme of “Heart and Vascular,” implying to the public that we are all one, “like the cardiologists do” as many patients state. This is not to fault anyone, but it is to awaken our leadership to the need to establish a separate, independent “awareness” vehicle to better craft our identity as a separate specialty to the entire nation.

It will take time but will be a project which, when done properly, we will never regret. It calls for a board heavily weighted toward the independent vascular surgeons, who try daily, with limited resources, to accomplish this.

Carlo Dall’Olmo, M.D., Flint, Mich.

What the article misrepresents is that this happens only in outpatient labs. The same thing occurs, albeit to a lesser degree, in our hospitals. I am glad to see no vascular surgeons were named. I am also glad they are starting to shine a light on the massive ongoing fraud in EVLT and RF ablation procedures. This is particularly bad in Florida. I wonder if SVS can come up with some response to suggest ways to police this behavior. None of us want more government oversight, but it seems like something needs to be done at the state board level to better regulate these procedures.

Geoffrey L. Risley, M.D., Jacksonville, Fla.

I think most members of SVS have intimate knowledge of a handful of physicians in their communities whose practices would be considered abusive, if not overtly fraudulent. We have struggled locally with the belief that we, as ethical and well-reasoned providers, should have some obligation to report these providers to someone. However, there are no acceptable mechanisms with which to do so, and there is a sense that this would not be accepted well by our colleagues.

We also do not want to be written off as disgruntled competitors. Physicians have never done a good job of policing themselves. Maybe articles like this can be a springboard to discuss ways to reign in the outlier providers in our communities.

Steven Merrell, M.D., Murray, Utah

I agree with Dr. Lawrence 100%. We need the SVS to be a major speaker in this debate. We have to give patients the confidence that they are being cared for by physicians who are not only capable to diagnose the problem but are also able to care for it in the most appropriate fashion. We need to silence the naysayers and the media hogs by developing a method so that surgeons who care for vascular patients in an office-based vascular suite are certified by the Society in the form a Center of Excellence designation. Initial certification would be followed by ongoing proactive reviews on a serial basis. I would ask that the leaders of our society take a step toward developing the concept of this certification body as soon as possible. We need to police ourselves and this may be the way to do it.

Thank you in advance for your attention and ongoing vigilance for the vascular surgical community.

Khash Salartash, M.D., Galloway, N.J.

Editors note: The following are a selection of responses from the SVS membership sent to Dr. Peter Lawrence based upon his article in a recent issue of Vascular Specialist on the topic of the abuse of peripheral artery disease stenting in Medicare patients.

Despite the unfortunate press, we as a more global medical vascular community are unable to police our own. I have been involved in two specific instances in which inappropriate and overuse of endovascular therapy has been addressed. Unfortunately, these practitioners continue to perform unindicated procedures while hospitals and state medical boards refuse to act.

What is Medicare to do when our own medical regulatory bodies fail to act on behalf of patients and the payor? The two routes of targeting practitioners through Medicare high outliers and legal recourse for poor outcome in unindicated procedures will remain until our societies (this includes SVIR and ACC) decide to collaborate and ensure appropriate practice. Simply stating that SVS has guidelines in place will not solve the problem.

Jason M. Johanning, M.D., Omaha, Neb.

My office of five vascular surgeons actually has an in-office procedure suite. We have converted about 30%-40% of our minimally invasive patient care to this setting. In review of what we have done, we have actually decreased the cost of patient care as there is no facility or hospital add-on charge. Our cost per patient is actually about one-third of what is typically charged by the hospital, and our quality based on our independent QA is the same in our office setting as it is in the hospital. These types of settings can significantly reduce health care costs if done in the proper fashion.

Dennis Fry, M.D., West Des Moines, Iowa

The comments in the article that hospitals confer a greater degree of oversight seems to come right from the AHA. The problem is not office-based procedures but the ethics of fraudulent practices, something that occurs in and among hospitals as well. Hospitals can be as much driven by case volume, even at academic centers, as are the practices of private outpatient procedures.

Paul Gagne, M.D., Darien, Conn.

I cannot help but wonder how our specialty’s lack of identity – and thus lack of appreciation of its responsibility and role in public awareness – has contributed to this scenario. Our inclusion under the umbrella of the American Heart Association, again without any designation of our separate identity, leads only to more confusion about our specialty in the eyes of the public.

The SVS must address its lack of a public identity in a more forceful manner. Unfortunately, it’s biggest hurdle in this may well be the hospital-employed vascular surgeons who cannot fight the administrators marketing theme of “Heart and Vascular,” implying to the public that we are all one, “like the cardiologists do” as many patients state. This is not to fault anyone, but it is to awaken our leadership to the need to establish a separate, independent “awareness” vehicle to better craft our identity as a separate specialty to the entire nation.

It will take time but will be a project which, when done properly, we will never regret. It calls for a board heavily weighted toward the independent vascular surgeons, who try daily, with limited resources, to accomplish this.

Carlo Dall’Olmo, M.D., Flint, Mich.

What the article misrepresents is that this happens only in outpatient labs. The same thing occurs, albeit to a lesser degree, in our hospitals. I am glad to see no vascular surgeons were named. I am also glad they are starting to shine a light on the massive ongoing fraud in EVLT and RF ablation procedures. This is particularly bad in Florida. I wonder if SVS can come up with some response to suggest ways to police this behavior. None of us want more government oversight, but it seems like something needs to be done at the state board level to better regulate these procedures.

Geoffrey L. Risley, M.D., Jacksonville, Fla.

I think most members of SVS have intimate knowledge of a handful of physicians in their communities whose practices would be considered abusive, if not overtly fraudulent. We have struggled locally with the belief that we, as ethical and well-reasoned providers, should have some obligation to report these providers to someone. However, there are no acceptable mechanisms with which to do so, and there is a sense that this would not be accepted well by our colleagues.

We also do not want to be written off as disgruntled competitors. Physicians have never done a good job of policing themselves. Maybe articles like this can be a springboard to discuss ways to reign in the outlier providers in our communities.

Steven Merrell, M.D., Murray, Utah

I agree with Dr. Lawrence 100%. We need the SVS to be a major speaker in this debate. We have to give patients the confidence that they are being cared for by physicians who are not only capable to diagnose the problem but are also able to care for it in the most appropriate fashion. We need to silence the naysayers and the media hogs by developing a method so that surgeons who care for vascular patients in an office-based vascular suite are certified by the Society in the form a Center of Excellence designation. Initial certification would be followed by ongoing proactive reviews on a serial basis. I would ask that the leaders of our society take a step toward developing the concept of this certification body as soon as possible. We need to police ourselves and this may be the way to do it.

Thank you in advance for your attention and ongoing vigilance for the vascular surgical community.

Khash Salartash, M.D., Galloway, N.J.

Editors note: The following are a selection of responses from the SVS membership sent to Dr. Peter Lawrence based upon his article in a recent issue of Vascular Specialist on the topic of the abuse of peripheral artery disease stenting in Medicare patients.

Despite the unfortunate press, we as a more global medical vascular community are unable to police our own. I have been involved in two specific instances in which inappropriate and overuse of endovascular therapy has been addressed. Unfortunately, these practitioners continue to perform unindicated procedures while hospitals and state medical boards refuse to act.

What is Medicare to do when our own medical regulatory bodies fail to act on behalf of patients and the payor? The two routes of targeting practitioners through Medicare high outliers and legal recourse for poor outcome in unindicated procedures will remain until our societies (this includes SVIR and ACC) decide to collaborate and ensure appropriate practice. Simply stating that SVS has guidelines in place will not solve the problem.

Jason M. Johanning, M.D., Omaha, Neb.

My office of five vascular surgeons actually has an in-office procedure suite. We have converted about 30%-40% of our minimally invasive patient care to this setting. In review of what we have done, we have actually decreased the cost of patient care as there is no facility or hospital add-on charge. Our cost per patient is actually about one-third of what is typically charged by the hospital, and our quality based on our independent QA is the same in our office setting as it is in the hospital. These types of settings can significantly reduce health care costs if done in the proper fashion.

Dennis Fry, M.D., West Des Moines, Iowa

The comments in the article that hospitals confer a greater degree of oversight seems to come right from the AHA. The problem is not office-based procedures but the ethics of fraudulent practices, something that occurs in and among hospitals as well. Hospitals can be as much driven by case volume, even at academic centers, as are the practices of private outpatient procedures.

Paul Gagne, M.D., Darien, Conn.

I cannot help but wonder how our specialty’s lack of identity – and thus lack of appreciation of its responsibility and role in public awareness – has contributed to this scenario. Our inclusion under the umbrella of the American Heart Association, again without any designation of our separate identity, leads only to more confusion about our specialty in the eyes of the public.

The SVS must address its lack of a public identity in a more forceful manner. Unfortunately, it’s biggest hurdle in this may well be the hospital-employed vascular surgeons who cannot fight the administrators marketing theme of “Heart and Vascular,” implying to the public that we are all one, “like the cardiologists do” as many patients state. This is not to fault anyone, but it is to awaken our leadership to the need to establish a separate, independent “awareness” vehicle to better craft our identity as a separate specialty to the entire nation.

It will take time but will be a project which, when done properly, we will never regret. It calls for a board heavily weighted toward the independent vascular surgeons, who try daily, with limited resources, to accomplish this.

Carlo Dall’Olmo, M.D., Flint, Mich.

What the article misrepresents is that this happens only in outpatient labs. The same thing occurs, albeit to a lesser degree, in our hospitals. I am glad to see no vascular surgeons were named. I am also glad they are starting to shine a light on the massive ongoing fraud in EVLT and RF ablation procedures. This is particularly bad in Florida. I wonder if SVS can come up with some response to suggest ways to police this behavior. None of us want more government oversight, but it seems like something needs to be done at the state board level to better regulate these procedures.

Geoffrey L. Risley, M.D., Jacksonville, Fla.

I think most members of SVS have intimate knowledge of a handful of physicians in their communities whose practices would be considered abusive, if not overtly fraudulent. We have struggled locally with the belief that we, as ethical and well-reasoned providers, should have some obligation to report these providers to someone. However, there are no acceptable mechanisms with which to do so, and there is a sense that this would not be accepted well by our colleagues.

We also do not want to be written off as disgruntled competitors. Physicians have never done a good job of policing themselves. Maybe articles like this can be a springboard to discuss ways to reign in the outlier providers in our communities.

Steven Merrell, M.D., Murray, Utah

I agree with Dr. Lawrence 100%. We need the SVS to be a major speaker in this debate. We have to give patients the confidence that they are being cared for by physicians who are not only capable to diagnose the problem but are also able to care for it in the most appropriate fashion. We need to silence the naysayers and the media hogs by developing a method so that surgeons who care for vascular patients in an office-based vascular suite are certified by the Society in the form a Center of Excellence designation. Initial certification would be followed by ongoing proactive reviews on a serial basis. I would ask that the leaders of our society take a step toward developing the concept of this certification body as soon as possible. We need to police ourselves and this may be the way to do it.

Thank you in advance for your attention and ongoing vigilance for the vascular surgical community.

Khash Salartash, M.D., Galloway, N.J.

Neurology, like any other field, has its share of tragic and incurable diseases. We do our best to shepherd patients and their families through a disorder by offering advice, symptomatic treatment, Family and Medical Leave Act signatures, and a shoulder.

But, inevitably, we come down to one of the most difficult discussions: the end game.

Hospice is never an easy subject to raise. I try to initiate the discussion in advance, so that the decisions and paperwork are in place.

One of the hardest parts is the misconception that hospice means you’re giving up: giving up on caring, giving up on hoping, giving up on treating. I work to try and overcome this.

Hospice may be a change in the treatment plan, but it’s still part of treatment. Finding a way to relieve suffering and provide comfortable surroundings in the final days, while often overlooked, is very important. Peace at a difficult time is sorely needed, more so than another round of tests or invasive procedures.

Yet, it’s not seen that way. Maybe this is cultural. Here, medicine is seen as a cutting-edge field, where there’s always something else that can be done: more scans, another hi-tech bioengineered drug, or some sort of amazing interventional procedure. Although we usually think of all the things we can do, it’s equally important to focus on what we should do. They aren’t always the same – a point that’s often lost.

Sometimes the best thing to do is … everything you can to just make someone comfortable. That’s not giving up. It’s recognizing when it becomes the right decision for the patient and not their family, friends, or anyone else. The patient is the one who really matters.

In an age when newer and flashier facilities and treatments are promoted, keeping the patient’s best interests in mind is critical. Sometimes we get blindsided by the amazing breakthroughs we didn’t have 20, 10, even 5 years ago. So we need to recognize when the best treatment is … to stop.

Quality of life extends all the way up to the moment of death. Part of our job is to keep the Grim Reaper away, but we inevitably lose. It is equally important, though, and sometimes forgotten, to keep the patient as comfortable as possible on the journey. And that isn’t giving up.

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

Neurology, like any other field, has its share of tragic and incurable diseases. We do our best to shepherd patients and their families through a disorder by offering advice, symptomatic treatment, Family and Medical Leave Act signatures, and a shoulder.

But, inevitably, we come down to one of the most difficult discussions: the end game.

Hospice is never an easy subject to raise. I try to initiate the discussion in advance, so that the decisions and paperwork are in place.

One of the hardest parts is the misconception that hospice means you’re giving up: giving up on caring, giving up on hoping, giving up on treating. I work to try and overcome this.

Hospice may be a change in the treatment plan, but it’s still part of treatment. Finding a way to relieve suffering and provide comfortable surroundings in the final days, while often overlooked, is very important. Peace at a difficult time is sorely needed, more so than another round of tests or invasive procedures.

Yet, it’s not seen that way. Maybe this is cultural. Here, medicine is seen as a cutting-edge field, where there’s always something else that can be done: more scans, another hi-tech bioengineered drug, or some sort of amazing interventional procedure. Although we usually think of all the things we can do, it’s equally important to focus on what we should do. They aren’t always the same – a point that’s often lost.

Sometimes the best thing to do is … everything you can to just make someone comfortable. That’s not giving up. It’s recognizing when it becomes the right decision for the patient and not their family, friends, or anyone else. The patient is the one who really matters.

In an age when newer and flashier facilities and treatments are promoted, keeping the patient’s best interests in mind is critical. Sometimes we get blindsided by the amazing breakthroughs we didn’t have 20, 10, even 5 years ago. So we need to recognize when the best treatment is … to stop.

Quality of life extends all the way up to the moment of death. Part of our job is to keep the Grim Reaper away, but we inevitably lose. It is equally important, though, and sometimes forgotten, to keep the patient as comfortable as possible on the journey. And that isn’t giving up.

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

Neurology, like any other field, has its share of tragic and incurable diseases. We do our best to shepherd patients and their families through a disorder by offering advice, symptomatic treatment, Family and Medical Leave Act signatures, and a shoulder.

But, inevitably, we come down to one of the most difficult discussions: the end game.

Hospice is never an easy subject to raise. I try to initiate the discussion in advance, so that the decisions and paperwork are in place.

One of the hardest parts is the misconception that hospice means you’re giving up: giving up on caring, giving up on hoping, giving up on treating. I work to try and overcome this.

Hospice may be a change in the treatment plan, but it’s still part of treatment. Finding a way to relieve suffering and provide comfortable surroundings in the final days, while often overlooked, is very important. Peace at a difficult time is sorely needed, more so than another round of tests or invasive procedures.

Yet, it’s not seen that way. Maybe this is cultural. Here, medicine is seen as a cutting-edge field, where there’s always something else that can be done: more scans, another hi-tech bioengineered drug, or some sort of amazing interventional procedure. Although we usually think of all the things we can do, it’s equally important to focus on what we should do. They aren’t always the same – a point that’s often lost.

Sometimes the best thing to do is … everything you can to just make someone comfortable. That’s not giving up. It’s recognizing when it becomes the right decision for the patient and not their family, friends, or anyone else. The patient is the one who really matters.

In an age when newer and flashier facilities and treatments are promoted, keeping the patient’s best interests in mind is critical. Sometimes we get blindsided by the amazing breakthroughs we didn’t have 20, 10, even 5 years ago. So we need to recognize when the best treatment is … to stop.

Quality of life extends all the way up to the moment of death. Part of our job is to keep the Grim Reaper away, but we inevitably lose. It is equally important, though, and sometimes forgotten, to keep the patient as comfortable as possible on the journey. And that isn’t giving up.

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