Tools for identifying, treating, monitoring, and preventing skin toxicities

As therapies improve cancer survival, oncologists will have to better manage the associated skin toxicities, according to Mario E. Lacouture, MD, a dermatologist and associate attending at the Memorial Sloan-Kettering Cancer Center in New York.

“These conditions will become even more important when the drugs you are using already in the metastatic setting enter the adjuvant setting and with dose escalation and combination studies,” he said. “And, of course, these patients are living so long with your therapies right now that there is more emphasis on survivorship issues.”

Skin issues are hardly superficial in the oncology population, Dr. Lacouture asserted. They often trigger a reduction or discontinuation of lifesaving treatment, markedly impair quality of life, threaten physical health and activities of daily living, and can be costly to treat.

With the introduction of novel targeted agents that spare normal tissues better than conventional cytotoxic chemotherapy, it was expected that skin toxicity would become less problematic, he said. However, “it turns out that blocking these proteins or pathways leads to a constellation of dermatologic adverse events that will be specific for a type of drug, depending on the target that they are blocking.”

Dr. Lacouture discussed features of some of the skin toxicities that oncologists are increasingly seeing and gave pointers for their prevention and management.

Although it is unlikely, oncologists may encounter any of the three main classes of sporadic, life-threatening cutaneous adverse events, Dr. Lacouture said. They are the type 1 hypersensitivity reactions, mainly to platinum-based regimens and taxanes; drug rash with eosinophilia and systemic symptoms (DRESS); and the Stevens-Johnson syndrome and toxic epidermal necrolysis, which are milder and more severe forms, respectively, of the same condition, characterized by tender, erythematous skin lesions with necrosis and desquamation.

“These are unpredictable; there is no test to predict any severe reaction to any chemotherapeutic agent,” he commented. “But [they] are very rare in reviews we have conducted,” occurring in about one patient in a million each year. Unfortunately, he added, in contrast to the case with many other types of skin toxicities, with these severe forms, the drug is usually permanently discontinued.

The rash triggered by epidermal growth factor receptor (EGFR) inhibitors manifests as red papules and pustules on the face and upper body and is often tender or pruritic. “Patients usually can be treated through it, if the rash is treated appropriately,” Dr. Lacouture said.

Findings in the randomized STEPP trial showed that preemptive skin treatment (moisturizer, sunscreen, a topical corticosteroid, and doxycycline) was superior to reactive skin treatment (investigator’s choice) for reducing the rate of grade 2 or higher rash and other skin toxicity in patients receiving panitumumab (Vectibix; 29% vs 62%; J Clin Oncol 2010;28:1351–1357). Another randomized trial similarly found that prophylactic oral minocycline reduced the number of skin lesions and itch when compared with placebo in patients receiving cetuximab (Erbitux; J Clin Oncol 2007;25:5390–5396).

Long-term treatment with EGFR inhibitors universally causes dry skin, which can lead to painful, paper-cut–like fissures on the fingertips and is associated with very painful paronychia or periungual inflammation in about half of patients. “The sad part about this is that patients on long-term therapy are probably those who are responding to therapy,” Dr. Lacouture commented. “And the paronychia and side effects are sometimes hindering the consistent administration of the EGFR inhibitor.”

The dry skin can be treated with ammonium lactate- or urea-containing preparations as moisturizers, he said. Zinc oxide preparations, such as Desitin, can be used for finger fissures.

The paronychia is treated with antiseptic soaks and chemical cauterization. For the former, patients simply soak their fingers and toes nightly in a solution of white vinegar, which has antibacterial and astringent properties. Chemical cauterization is performed with inexpensive silver nitrate sticks; the sticks are activated in water and some of the liquid is applied to the lateral nail fold and allowed to dry (for a demonstration, visit www.youtube.com/watch?v=HF5oopqheJY). Patients will need to do this about once a week, and usually only two to three applications are needed. The treatment is so simple that patients can be taught to do it themselves at home and so effective that it has almost abolished the need to perform nail avulsions.

EGFR inhibitors can also cause thinning of scalp hair and, paradoxically, facial hirsutism. It is important that women be advised not to use chemical depilatories to remove the facial hair because they may experience severe burns related to drug-induced skin atrophy. “Of all the side effects, perhaps the only one that your patients will be thankful for is trichomegaly of the eyelashes,” he commented. But these long, curly eyelashes sometimes grow into the eye, causing corneal erosions and ulcerations. “So I ask all patients on EGFR inhibitors if they are having any eye complaints,” he said.

Some 38% of patients treated with EGFR inhibitors develop secondary skin infections as a result of skin toxicity (J Natl Cancer Inst 2010;102:47–53). “In other words, they have a complication of a complication,” Dr. Lacouture observed. These infections can be odd ones, too, such as fungal infections of the face or gram-negative cellulitis. “I highly recommend [you have culture swabs in your office] because I have been surprised by the kinds of organisms I recover from patients that are pathogens,” he said.

Patients treated with inhibitors of the mammalian target of rapamycin (mTOR), such as everolimus (Afinitor) and temsirolimus (Torisel), may develop a nonspecific erythematous rash that is intensely pruritic. “I feel it’s very difficult to treat, very different [from] the rash you see with EGFR inhibitors,” Dr. Lacouture said. “It is so pruritic in these patients that you have to treat them with oral steroids, high-potency topical steroids, antihistamines, GABA agonists such as pregabalin (Lyrica) or gabapentin, or even doxepin.”

In addition, the mTOR inhibitors can produce a painful mucositis with ulcer-like lesions that is distinctly different from that seen with cytotoxic chemotherapy (Cancer 2010;116:210–215). It is “a completely new type of entity…more like canker sores or aphthous stomatitis,” he explained. This mucositis responds well to high-potency topical steroids.

The multitargeted tyrosine kinase inhibitors (TKIs) sorafenib (Nexavar), sunitinib (Sutent), and pazopanib (Votrient) can all cause a hand-foot syndrome characterized by painful blisters on the palms and soles. It differs from that seen with fluoropyrimidines or anthracyclines in that it produces diffuse swelling, Dr. Lacouture said.

“Sorafenib appears to be the [biggest] culprit here,” he commented. The rate of high-grade hand-foot syndrome is about 9% with sorafenib, compared with roughly 6% with sunitinib and 1% with pazopanib. Management consists of high-potency topical steroids and analgesics.

When it comes to reducing the hand-foot syndrome associated with cytotoxic chemotherapy, randomized trials have found vitamin B6 (pyridoxine) to be ineffective, Dr. Lacouture noted. But dexamethasone started the day before infusion is effective in patients receiving pegylated doxorubicin (Doxil). And the nonste¬roidal anti-inflammatory drug celecoxib (Celebrex) is effective in patients receiving capecitabine (Xeloda).

Taxanes, especially docetaxel (Taxotere), produce some type of nail alteration in most patients, including subungual hemorrhage followed by onycholysis in some cases. “They are grade 2 and associated with pain in about a third of all treated patients,” Dr. Lacouture noted. 

A quarter of patients develop a secondary infection with pathogens such as Pseudomonas, which gives their nails a green tinge due to the pyocyanin it produces.  This complication can be treated with antibiotics and vinegar soaks. But better yet, nail toxicity can largely be prevented from the get-go with use of cooling gloves during the taxane infusion. In one study, for example, the rate of grade 2 nail toxicity was 22% in patients’ unprotected control hands, but 0% in their frozen glove-protected hands (J Clin Oncol 2005;23:4424–4429).

“So this is something that we have instituted,” he commented. “In the absence of these cold gloves, we just have the patients hold ice packs during the infusion to try to minimize the blood flow, [thereby limiting] the delivery of docetaxel to the nails.”

A persistent misconception is that radiation dermatitis is a drying of the skin, Dr. Lacouture said. “It is not really a drying, as you have apoptosis and death of skin cells, and that’s why you see the desquamation.” In fact, six trials in patients with head and neck or breast cancer have shown that trolamine (Biafine), a topical emulsion, does not prevent or reduce the severity of radiation dermatitis (Curr Oncol 2010;17:94–112). “Biafine is not effective; it hasn’t been shown to be effective in any of these studies,” he stressed. “However, it is still widely used for some reason.”

On the other hand, four trials have shown that high-potency topical corticosteroids, such as mometasone cream, used prophylactically are effective for reducing symptoms of radiation dermatitis. When patients develop severe radiation dermatitis and moist desquamation, “Staphylococcus aureus is uniformly present, so consider culturing that area,” he recommended.

Dr. Lacouture reported being a consultant to Genentech, Hana Biosciences, OSI Pharmaceuticals, Amgen, GlaxoSmithKline, ImClone Systems, Bristol Myers-Squibb, Onyx Pharmaceuticals, Lindi Skin, and Bayer Pharmaceuticals.

As therapies improve cancer survival, oncologists will have to better manage the associated skin toxicities, according to Mario E. Lacouture, MD, a dermatologist and associate attending at the Memorial Sloan-Kettering Cancer Center in New York.

“These conditions will become even more important when the drugs you are using already in the metastatic setting enter the adjuvant setting and with dose escalation and combination studies,” he said. “And, of course, these patients are living so long with your therapies right now that there is more emphasis on survivorship issues.”

Skin issues are hardly superficial in the oncology population, Dr. Lacouture asserted. They often trigger a reduction or discontinuation of lifesaving treatment, markedly impair quality of life, threaten physical health and activities of daily living, and can be costly to treat.

With the introduction of novel targeted agents that spare normal tissues better than conventional cytotoxic chemotherapy, it was expected that skin toxicity would become less problematic, he said. However, “it turns out that blocking these proteins or pathways leads to a constellation of dermatologic adverse events that will be specific for a type of drug, depending on the target that they are blocking.”

Dr. Lacouture discussed features of some of the skin toxicities that oncologists are increasingly seeing and gave pointers for their prevention and management.

Although it is unlikely, oncologists may encounter any of the three main classes of sporadic, life-threatening cutaneous adverse events, Dr. Lacouture said. They are the type 1 hypersensitivity reactions, mainly to platinum-based regimens and taxanes; drug rash with eosinophilia and systemic symptoms (DRESS); and the Stevens-Johnson syndrome and toxic epidermal necrolysis, which are milder and more severe forms, respectively, of the same condition, characterized by tender, erythematous skin lesions with necrosis and desquamation.

“These are unpredictable; there is no test to predict any severe reaction to any chemotherapeutic agent,” he commented. “But [they] are very rare in reviews we have conducted,” occurring in about one patient in a million each year. Unfortunately, he added, in contrast to the case with many other types of skin toxicities, with these severe forms, the drug is usually permanently discontinued.

The rash triggered by epidermal growth factor receptor (EGFR) inhibitors manifests as red papules and pustules on the face and upper body and is often tender or pruritic. “Patients usually can be treated through it, if the rash is treated appropriately,” Dr. Lacouture said.

Findings in the randomized STEPP trial showed that preemptive skin treatment (moisturizer, sunscreen, a topical corticosteroid, and doxycycline) was superior to reactive skin treatment (investigator’s choice) for reducing the rate of grade 2 or higher rash and other skin toxicity in patients receiving panitumumab (Vectibix; 29% vs 62%; J Clin Oncol 2010;28:1351–1357). Another randomized trial similarly found that prophylactic oral minocycline reduced the number of skin lesions and itch when compared with placebo in patients receiving cetuximab (Erbitux; J Clin Oncol 2007;25:5390–5396).

Long-term treatment with EGFR inhibitors universally causes dry skin, which can lead to painful, paper-cut–like fissures on the fingertips and is associated with very painful paronychia or periungual inflammation in about half of patients. “The sad part about this is that patients on long-term therapy are probably those who are responding to therapy,” Dr. Lacouture commented. “And the paronychia and side effects are sometimes hindering the consistent administration of the EGFR inhibitor.”

The dry skin can be treated with ammonium lactate- or urea-containing preparations as moisturizers, he said. Zinc oxide preparations, such as Desitin, can be used for finger fissures.

The paronychia is treated with antiseptic soaks and chemical cauterization. For the former, patients simply soak their fingers and toes nightly in a solution of white vinegar, which has antibacterial and astringent properties. Chemical cauterization is performed with inexpensive silver nitrate sticks; the sticks are activated in water and some of the liquid is applied to the lateral nail fold and allowed to dry (for a demonstration, visit www.youtube.com/watch?v=HF5oopqheJY). Patients will need to do this about once a week, and usually only two to three applications are needed. The treatment is so simple that patients can be taught to do it themselves at home and so effective that it has almost abolished the need to perform nail avulsions.

EGFR inhibitors can also cause thinning of scalp hair and, paradoxically, facial hirsutism. It is important that women be advised not to use chemical depilatories to remove the facial hair because they may experience severe burns related to drug-induced skin atrophy. “Of all the side effects, perhaps the only one that your patients will be thankful for is trichomegaly of the eyelashes,” he commented. But these long, curly eyelashes sometimes grow into the eye, causing corneal erosions and ulcerations. “So I ask all patients on EGFR inhibitors if they are having any eye complaints,” he said.

Some 38% of patients treated with EGFR inhibitors develop secondary skin infections as a result of skin toxicity (J Natl Cancer Inst 2010;102:47–53). “In other words, they have a complication of a complication,” Dr. Lacouture observed. These infections can be odd ones, too, such as fungal infections of the face or gram-negative cellulitis. “I highly recommend [you have culture swabs in your office] because I have been surprised by the kinds of organisms I recover from patients that are pathogens,” he said.

Patients treated with inhibitors of the mammalian target of rapamycin (mTOR), such as everolimus (Afinitor) and temsirolimus (Torisel), may develop a nonspecific erythematous rash that is intensely pruritic. “I feel it’s very difficult to treat, very different [from] the rash you see with EGFR inhibitors,” Dr. Lacouture said. “It is so pruritic in these patients that you have to treat them with oral steroids, high-potency topical steroids, antihistamines, GABA agonists such as pregabalin (Lyrica) or gabapentin, or even doxepin.”

In addition, the mTOR inhibitors can produce a painful mucositis with ulcer-like lesions that is distinctly different from that seen with cytotoxic chemotherapy (Cancer 2010;116:210–215). It is “a completely new type of entity…more like canker sores or aphthous stomatitis,” he explained. This mucositis responds well to high-potency topical steroids.

The multitargeted tyrosine kinase inhibitors (TKIs) sorafenib (Nexavar), sunitinib (Sutent), and pazopanib (Votrient) can all cause a hand-foot syndrome characterized by painful blisters on the palms and soles. It differs from that seen with fluoropyrimidines or anthracyclines in that it produces diffuse swelling, Dr. Lacouture said.

“Sorafenib appears to be the [biggest] culprit here,” he commented. The rate of high-grade hand-foot syndrome is about 9% with sorafenib, compared with roughly 6% with sunitinib and 1% with pazopanib. Management consists of high-potency topical steroids and analgesics.

When it comes to reducing the hand-foot syndrome associated with cytotoxic chemotherapy, randomized trials have found vitamin B6 (pyridoxine) to be ineffective, Dr. Lacouture noted. But dexamethasone started the day before infusion is effective in patients receiving pegylated doxorubicin (Doxil). And the nonste¬roidal anti-inflammatory drug celecoxib (Celebrex) is effective in patients receiving capecitabine (Xeloda).

Taxanes, especially docetaxel (Taxotere), produce some type of nail alteration in most patients, including subungual hemorrhage followed by onycholysis in some cases. “They are grade 2 and associated with pain in about a third of all treated patients,” Dr. Lacouture noted. 

A quarter of patients develop a secondary infection with pathogens such as Pseudomonas, which gives their nails a green tinge due to the pyocyanin it produces.  This complication can be treated with antibiotics and vinegar soaks. But better yet, nail toxicity can largely be prevented from the get-go with use of cooling gloves during the taxane infusion. In one study, for example, the rate of grade 2 nail toxicity was 22% in patients’ unprotected control hands, but 0% in their frozen glove-protected hands (J Clin Oncol 2005;23:4424–4429).

“So this is something that we have instituted,” he commented. “In the absence of these cold gloves, we just have the patients hold ice packs during the infusion to try to minimize the blood flow, [thereby limiting] the delivery of docetaxel to the nails.”

A persistent misconception is that radiation dermatitis is a drying of the skin, Dr. Lacouture said. “It is not really a drying, as you have apoptosis and death of skin cells, and that’s why you see the desquamation.” In fact, six trials in patients with head and neck or breast cancer have shown that trolamine (Biafine), a topical emulsion, does not prevent or reduce the severity of radiation dermatitis (Curr Oncol 2010;17:94–112). “Biafine is not effective; it hasn’t been shown to be effective in any of these studies,” he stressed. “However, it is still widely used for some reason.”

On the other hand, four trials have shown that high-potency topical corticosteroids, such as mometasone cream, used prophylactically are effective for reducing symptoms of radiation dermatitis. When patients develop severe radiation dermatitis and moist desquamation, “Staphylococcus aureus is uniformly present, so consider culturing that area,” he recommended.

Dr. Lacouture reported being a consultant to Genentech, Hana Biosciences, OSI Pharmaceuticals, Amgen, GlaxoSmithKline, ImClone Systems, Bristol Myers-Squibb, Onyx Pharmaceuticals, Lindi Skin, and Bayer Pharmaceuticals.

As therapies improve cancer survival, oncologists will have to better manage the associated skin toxicities, according to Mario E. Lacouture, MD, a dermatologist and associate attending at the Memorial Sloan-Kettering Cancer Center in New York.

“These conditions will become even more important when the drugs you are using already in the metastatic setting enter the adjuvant setting and with dose escalation and combination studies,” he said. “And, of course, these patients are living so long with your therapies right now that there is more emphasis on survivorship issues.”

Skin issues are hardly superficial in the oncology population, Dr. Lacouture asserted. They often trigger a reduction or discontinuation of lifesaving treatment, markedly impair quality of life, threaten physical health and activities of daily living, and can be costly to treat.

With the introduction of novel targeted agents that spare normal tissues better than conventional cytotoxic chemotherapy, it was expected that skin toxicity would become less problematic, he said. However, “it turns out that blocking these proteins or pathways leads to a constellation of dermatologic adverse events that will be specific for a type of drug, depending on the target that they are blocking.”

Dr. Lacouture discussed features of some of the skin toxicities that oncologists are increasingly seeing and gave pointers for their prevention and management.

Although it is unlikely, oncologists may encounter any of the three main classes of sporadic, life-threatening cutaneous adverse events, Dr. Lacouture said. They are the type 1 hypersensitivity reactions, mainly to platinum-based regimens and taxanes; drug rash with eosinophilia and systemic symptoms (DRESS); and the Stevens-Johnson syndrome and toxic epidermal necrolysis, which are milder and more severe forms, respectively, of the same condition, characterized by tender, erythematous skin lesions with necrosis and desquamation.

“These are unpredictable; there is no test to predict any severe reaction to any chemotherapeutic agent,” he commented. “But [they] are very rare in reviews we have conducted,” occurring in about one patient in a million each year. Unfortunately, he added, in contrast to the case with many other types of skin toxicities, with these severe forms, the drug is usually permanently discontinued.

The rash triggered by epidermal growth factor receptor (EGFR) inhibitors manifests as red papules and pustules on the face and upper body and is often tender or pruritic. “Patients usually can be treated through it, if the rash is treated appropriately,” Dr. Lacouture said.

Findings in the randomized STEPP trial showed that preemptive skin treatment (moisturizer, sunscreen, a topical corticosteroid, and doxycycline) was superior to reactive skin treatment (investigator’s choice) for reducing the rate of grade 2 or higher rash and other skin toxicity in patients receiving panitumumab (Vectibix; 29% vs 62%; J Clin Oncol 2010;28:1351–1357). Another randomized trial similarly found that prophylactic oral minocycline reduced the number of skin lesions and itch when compared with placebo in patients receiving cetuximab (Erbitux; J Clin Oncol 2007;25:5390–5396).

Long-term treatment with EGFR inhibitors universally causes dry skin, which can lead to painful, paper-cut–like fissures on the fingertips and is associated with very painful paronychia or periungual inflammation in about half of patients. “The sad part about this is that patients on long-term therapy are probably those who are responding to therapy,” Dr. Lacouture commented. “And the paronychia and side effects are sometimes hindering the consistent administration of the EGFR inhibitor.”

The dry skin can be treated with ammonium lactate- or urea-containing preparations as moisturizers, he said. Zinc oxide preparations, such as Desitin, can be used for finger fissures.

The paronychia is treated with antiseptic soaks and chemical cauterization. For the former, patients simply soak their fingers and toes nightly in a solution of white vinegar, which has antibacterial and astringent properties. Chemical cauterization is performed with inexpensive silver nitrate sticks; the sticks are activated in water and some of the liquid is applied to the lateral nail fold and allowed to dry (for a demonstration, visit www.youtube.com/watch?v=HF5oopqheJY). Patients will need to do this about once a week, and usually only two to three applications are needed. The treatment is so simple that patients can be taught to do it themselves at home and so effective that it has almost abolished the need to perform nail avulsions.

EGFR inhibitors can also cause thinning of scalp hair and, paradoxically, facial hirsutism. It is important that women be advised not to use chemical depilatories to remove the facial hair because they may experience severe burns related to drug-induced skin atrophy. “Of all the side effects, perhaps the only one that your patients will be thankful for is trichomegaly of the eyelashes,” he commented. But these long, curly eyelashes sometimes grow into the eye, causing corneal erosions and ulcerations. “So I ask all patients on EGFR inhibitors if they are having any eye complaints,” he said.

Some 38% of patients treated with EGFR inhibitors develop secondary skin infections as a result of skin toxicity (J Natl Cancer Inst 2010;102:47–53). “In other words, they have a complication of a complication,” Dr. Lacouture observed. These infections can be odd ones, too, such as fungal infections of the face or gram-negative cellulitis. “I highly recommend [you have culture swabs in your office] because I have been surprised by the kinds of organisms I recover from patients that are pathogens,” he said.

Patients treated with inhibitors of the mammalian target of rapamycin (mTOR), such as everolimus (Afinitor) and temsirolimus (Torisel), may develop a nonspecific erythematous rash that is intensely pruritic. “I feel it’s very difficult to treat, very different [from] the rash you see with EGFR inhibitors,” Dr. Lacouture said. “It is so pruritic in these patients that you have to treat them with oral steroids, high-potency topical steroids, antihistamines, GABA agonists such as pregabalin (Lyrica) or gabapentin, or even doxepin.”

In addition, the mTOR inhibitors can produce a painful mucositis with ulcer-like lesions that is distinctly different from that seen with cytotoxic chemotherapy (Cancer 2010;116:210–215). It is “a completely new type of entity…more like canker sores or aphthous stomatitis,” he explained. This mucositis responds well to high-potency topical steroids.

The multitargeted tyrosine kinase inhibitors (TKIs) sorafenib (Nexavar), sunitinib (Sutent), and pazopanib (Votrient) can all cause a hand-foot syndrome characterized by painful blisters on the palms and soles. It differs from that seen with fluoropyrimidines or anthracyclines in that it produces diffuse swelling, Dr. Lacouture said.

“Sorafenib appears to be the [biggest] culprit here,” he commented. The rate of high-grade hand-foot syndrome is about 9% with sorafenib, compared with roughly 6% with sunitinib and 1% with pazopanib. Management consists of high-potency topical steroids and analgesics.

When it comes to reducing the hand-foot syndrome associated with cytotoxic chemotherapy, randomized trials have found vitamin B6 (pyridoxine) to be ineffective, Dr. Lacouture noted. But dexamethasone started the day before infusion is effective in patients receiving pegylated doxorubicin (Doxil). And the nonste¬roidal anti-inflammatory drug celecoxib (Celebrex) is effective in patients receiving capecitabine (Xeloda).

Taxanes, especially docetaxel (Taxotere), produce some type of nail alteration in most patients, including subungual hemorrhage followed by onycholysis in some cases. “They are grade 2 and associated with pain in about a third of all treated patients,” Dr. Lacouture noted. 

A quarter of patients develop a secondary infection with pathogens such as Pseudomonas, which gives their nails a green tinge due to the pyocyanin it produces.  This complication can be treated with antibiotics and vinegar soaks. But better yet, nail toxicity can largely be prevented from the get-go with use of cooling gloves during the taxane infusion. In one study, for example, the rate of grade 2 nail toxicity was 22% in patients’ unprotected control hands, but 0% in their frozen glove-protected hands (J Clin Oncol 2005;23:4424–4429).

“So this is something that we have instituted,” he commented. “In the absence of these cold gloves, we just have the patients hold ice packs during the infusion to try to minimize the blood flow, [thereby limiting] the delivery of docetaxel to the nails.”

A persistent misconception is that radiation dermatitis is a drying of the skin, Dr. Lacouture said. “It is not really a drying, as you have apoptosis and death of skin cells, and that’s why you see the desquamation.” In fact, six trials in patients with head and neck or breast cancer have shown that trolamine (Biafine), a topical emulsion, does not prevent or reduce the severity of radiation dermatitis (Curr Oncol 2010;17:94–112). “Biafine is not effective; it hasn’t been shown to be effective in any of these studies,” he stressed. “However, it is still widely used for some reason.”

On the other hand, four trials have shown that high-potency topical corticosteroids, such as mometasone cream, used prophylactically are effective for reducing symptoms of radiation dermatitis. When patients develop severe radiation dermatitis and moist desquamation, “Staphylococcus aureus is uniformly present, so consider culturing that area,” he recommended.

Dr. Lacouture reported being a consultant to Genentech, Hana Biosciences, OSI Pharmaceuticals, Amgen, GlaxoSmithKline, ImClone Systems, Bristol Myers-Squibb, Onyx Pharmaceuticals, Lindi Skin, and Bayer Pharmaceuticals.