Prevention and management of hand-foot syndromes - ONA

Prevention and management of hand-foot syndromes - ONA: "COX-2 agents"

'Second-hand' danger in radiation therapy? - UPI.com

'Second-hand' danger in radiation therapy? - UPI.com

CancerCompass: New Drug Promising for Advanced Thyroid Cancer

New Drug Promising for Advanced Thyroid Cancer

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FRIDAY, Sept. 17 (HealthDay News) -- A targeted drug called pazopanib could prove effective against difficult-to-treat cases of thyroid cancer cases, researchers say.

Most thyroid cancers can be treated with surgery or radioiodine, but about 5 percent of patients will develop an aggressive, life-threatening form of the disease.

Pazopanib (Votrient), already approved by the U.S. Food and Drug Administration for treating advanced kidney cancer, works by inhibiting growth of blood vessels essential for tumor growth and survival.

"Thyroid cancers, when they grow, they need to form a lot of blood vessels," explained researcher Dr. Julian Molina, an assistant professor of oncology at the Mayo Clinic and co-author of the study. "For blood vessels to grow, the growth factor VEGF is required, and the drug targets this protein," he said.

Not only does the drug block production of new blood vessels, it also interferes with the tumor cells' ability to continue growing, Molina said.

Pazopanib, a pill that's taken daily, doesn't have the severe side effects of standard chemotherapy, Molina said. But it is expensive. According to the U.S. Department of Health and Human Services, the average wholesale price, which is used to set drug reimbursements, is $6,595 a month.

For this phase 2 study, published in the Sept. 17 online edition of The Lancet Oncology, Molina and colleagues tested the efficacy and safety of pazopanib in 37 patients with advanced, rapidly progressing thyroid cancer.

About half of the patients --18 -- had a partial response to the drug, meaning their tumor shrank 30 percent or more, Molina said. None had a complete response, in which the tumor disappears completely, he added.

Twelve patients are still responding to the drug about a year later. "Patients take the drug until the drug is no longer effective," Molina said, noting these patients still take pazopanib every day.

Side effects were commonplace but typically mild. The most usual were diarrhea, hypertension, and an increase in a liver enzyme called aminotransferase. However, 15 patients had to have their dose lowered because of side effects, the researchers note.

The U.S. National Cancer Institute funded the study.

Molina noted that larger phase 3 trials will start soon, and he hopes the drug, made by GlaxoSmithKline, will be approved for treating advanced thyroid cancer.

"One of the goals in cancer care is to make cancer a chronic disease," Molina said. "If we can make cancer something like that, where your pills keep your disease controlled, that's a good goal," he said.

One expert said that any effective therapy would be welcome.

"There are not a lot of treatment options available for people with advanced thyroid cancer," said Dr. Leonard Lichtenfeld, deputy chief medical officer at the American Cancer Society.

While the study results will need to be replicated and tested against other treatment options before pazopanib can be approved as a therapy for thyroid cancer, he agreed that the drug shows promise.

"Targeted therapies are providing some effective treatment options for patients with diseases that traditionally have been difficult to treat," he said. "I find that very helpful and very exciting."

More information

For more information on thyroid cancer, visit the American Cancer Society.

SOURCES: Julian Molina, M.D., Ph.D., assistant professor of oncology, Mayo Clinic, Rochester, Minn.; Leonard Lichtenfeld, M.D., M.A.C.P., deputy chief medical officer, American Cancer Society, Atlanta; Sept. 17, 2010, The Lancet Oncology, online

Copyright © 2010 HealthDay. All rights reserved.

CureToday.com: "The Good Cancer?" - by Charlotte Huff - From CureToday.com

The Good Cancer?

BY CHARLOTTE HUFF

Thyroid cancer's high survival rate masks the sometimes tricky tumor.

• The Low-Iodine Diet
• Web Exclusive: Types of Thyroid Cancer
• Web Exclusive: Find a Clinical Trial That's Right for You

• Illustration: The Radioactive Magic Bullet

The first biopsy on Julia McGuire’s thyroid came back negative, so the college student was regularly monitored for two years until, at one visit, the slight lump had swelled to the size of a walnut. Concerned about its recent surge in growth, her endocrinologist recommended removal, describing the surgery primarily as a precaution, although cancer was a possibility.

The 20-year-old wasn’t particularly worried until her phone rang one day with the biopsy results: stage 1 papillary thyroid cancer, the most common form of the disease.
“I think it was the most traumatic moment of my life,” says McGuire, now age 27. She underwent a second surgery to remove the remainder of her thyroid—a butterfly-shaped gland in the neck that regulates metabolism—and followed up with radioactive iodine to kill any lingering cancer cells. In the past seven years, she has largely moved on, with annual checkups as the only cancer reminder.
The treatment path for Rabbi Len Troupp unfolded much differently. In 1999, Troupp learned he had medullary thyroid cancer, a potentially more aggressive type, comprising fewer than 5 percent of all thyroid malignancies. Since then, Troupp has combated the cancer on several fronts, starting with the removal of his thyroid and lymph nodes in his neck and chest, followed by experimental drugs after the cancer spread to his liver and a lung, among other areas.
Nine years later, the 62-year-old appears to be benefiting from XL184, one in a cadre of investigational drug treatments for aggressive or difficult-to-treat thyroid malignancies.

At least a dozen drugs, possibly as many as two dozen, are now in the clinical development pipeline to potentially treat aggressive or difficult-to-treat thyroid malignancies, according to several specialists interviewed. These drugs build on emerging insights into the roles of blood vessel growth and genetic mutations that can influence the cancer’s development and progression, says David Pfister, MD, chief of the Head and Neck Medical Oncology Service at Memorial Sloan-Kettering Cancer Center in New York City.
“This is a rapidly evolving area where I think we will see a lot of research activity over the next five to 10 years,” he says.

The Big Picture

About 37,000 Americans are diagnosed annually with thyroid cancer, a malignancy that can seem relatively benign, at least where cancer is concerned.
Overall, the five-year relative survival rate for thyroid cancer is 96.9 percent or better, as long as the malignancy is diagnosed while still confined to the thyroid or nearby lymph nodes, according to the National Cancer Institute’s Surveillance, Epidemiology and End Results (SEER) data.
About 90 percent of people develop either the papillary or follicular types, frequently considered treatable with surgery and radioactive iodine. Even if the malignancy can’t be knocked out completely by treatment, the cancer can often be controlled for years, in part because it can be slow-growing. But cancer survivors and treating physicians frequently wince at thyroid malignancies being described as the “good” cancer because it can throw curveballs.
The two less common types—medullary and anaplastic—can be far more aggressive and rarely respond to radioactive iodine therapy. Seemingly treatable types, such as papillary, can become less responsive over time to repeated radioactive iodine treatments. And regular checkups are crucial as recurrences can appear sometimes decades later, physicians say. In all, nearly 1,600 people die each year of thyroid cancer, according to NCI data.
Although McGuire’s tumor measured about an inch, the cancer hadn’t spread to the nearby lymph nodes. She worked treatment around her college schedule, completing surgery before her junior year and then returning home for radioactive iodine treatment over holiday break.
In retrospect, the stressful ordeal served as a wakeup call, McGuire says. She now works as an IT consultant and has assisted several cancer-related groups, including the Thyroid Cancer Survivors’ Association. “I went back to school and I did better in school. I just took things more seriously.”
How much of the thyroid is removed and whether radioactive iodine is recommended depends upon a number of factors, including the tumor’s size and the extent to which it has spread beyond the thyroid itself.
Age also can play a significant role. Younger men and women—those diagnosed before age 45—are more likely to respond better to radioactive iodine treatment than older patients, says Stephanie Lee, MD, PhD, associate chief of endocrinology, diabetes, and nutrition at Boston Medical Center. The cancer is considered stage 1 in that age group, as long as it hasn’t spread to distant organs, such as the lung.
For follicular and papillary malignancies, radioactive iodine therapy can serve as a magic bullet. That’s because the thyroid naturally pulls iodine into the gland to produce hormones needed to regulate the body’s metabolism. Thus, the radioactive iodine, an isotope usually given in liquid or pill form, is easily absorbed into the thyroid, killing cancerous cells.

View Illustration: The Radioactive Magic Bullet

Patients are typically kept isolated for 24 hours and should avoid prolonged exposure to children and pregnant women for a week or two after treatment.
Once the individual’s thyroid has been removed, levothyroxine (Synthroid, Levoxyl) is prescribed to replace the body’s natural thyroid hormone. (Patients must temporarily stop thyroid hormone pills prior to radioactive iodine treatment.) The dose of the synthetic hormone may need to be adjusted based on any symptoms that develop. Too much thyroid hormone can cause a rapid heart beat and weight loss. If the levels drop too low, the result can be sluggishness, weight gain, and dry skin.

Beyond Radioactive Iodine

In some malignancies, radioactive iodine isn’t sufficient—or can’t be used at all. The treatment is no longer recommended for medullary or anaplastic thyroid cancer. (Anaplastic comprises 1 to 2 percent of all thyroid malignancies.) Neither does radioactive iodine fully protect against recurrence.
Until recently, options beyond radioactive iodine and surgery have been limited, Pfister says. Chemotherapy has been infrequently used, other than for the most aggressive malignancies. “When we do use available chemotherapy, the response rate is disappointing,” Pfister says. “That’s one of the reasons there is a keen interest in these new agents.”
The drugs that are emerging, nearly all in phase I or phase II clinical trials, frequently work on a variety of receptors. One common element involves inhibition of angiogenesis, or blood vessel growth to the tumor, which is believed to fuel cancer’s spread.
Vascular blood vessel growth is particularly intriguing in thyroid cancer, given the density of blood vessels in thyroid malignancies, says Ezra Cohen, MD, assistant professor of medicine at the University of Chicago. Last October, the Journal of Clinical Oncology published results from two phase II studies showing some patients responded to Nexavar (sorafenib)—an agent approved for liver and kidney cancer—and axitinib, which are believed to work at least in part by inhibiting blood vessel growth, specifically receptors for a protein called vascular endothelial growth factor, or VEGF.
In the Nexavar study, seven of the 30 patients with advanced disease had a partial response (tumor shrinkage of at least half) to the drug that lasted 18 to 84 weeks. The cancer stabilized in another 16 patients for 14 to at least 89 weeks.
The axitinib study, which involved 60 patients with advanced cancer, found that 18 patients experienced a partial response to the drug. In another 23 patients the cancer stabilized for at least 24 weeks.
“I think we can safely say from this study that this drug (axitinib) has activity,” says Cohen, the study’s lead author. “The question really is, does it ultimately improve [overall] survival in this disease?”
Other drugs for advanced or radioactive iodine-resistant malignancies also have garnered encouraging, albeit early, results. In July of 2008, a phase II study published in The New England Journal of Medicine reported that motesanib (AMG 706) achieved a partial response in 13 of 93 patients who took the drug. In 62 patients, the cancer stabilized, lasting at least 24 weeks in 33 of the 62 patients.
Steven I. Sherman, MD, chair of the department of endocrine neoplasia and hormonal disorders at M.D. Anderson Cancer Center in Houston and lead author of the NEJM study, is researching another drug that he describes as promising in medullary cancer. Called XL184, the drug targets VEGF and other receptors, including RET. (A mutation of the RET gene, which can run in families, is strongly associated with medullary cancer and other endocrine malignancies.)
The phase I trial of 84 patients, including 36 with medullary thyroid cancer, found XL184 to be generally well tolerated. In a subset of 22 medullary patients who took the drug for at least three months, 12 patients experienced a partial response, according to results presented at the Molecular Targets and Cancer Therapeutics conference last October. By year’s end, medullary cancer patients were being enrolled in a phase III trial with XL184.
Another investigational drug for medullary cancer, Zactima (vandetanib), may be closer to approval, Sherman says. A randomized phase III trial studying Zactima wrapped up in 2008.
As these and other promising drugs are identified, physicians will be able to transform difficult-to-treat thyroid malignancies into chronic conditions, rather than lethal ones, Sherman says. “This is clearly where we are headed,” he says. “This isn’t a conversation we could have had three years ago.”
In 2001, once the medullary cancer had spread to his organs, Troupp was given no treatment options until his physician learned of a clinical trial. That first drug, oral suberoylanilide hydroxamic acid (SAHA), now marketed under the brand name Zolinza (vorinostat) for a type of lymphoma, halted the cancer’s spread for more than five years, Troupp says. Last summer, Troupp switched to a phase I study of XL184 after scans showed cancer advancing in his liver and his bones. By year’s end, two sets of scans showed the cancer had stalled again.
Troupp has been retired since 2005, after cancer-related fatigue made it impossible to keep pace with his 750-family congregation in Commack, New York. But he credits these two experimental drugs with buying crucial years, time with his wife, and an occasional evening at the theater when his energy allows.
In the meantime, Troupp closely monitors the latest clinical trials. “I fully expect that I’ll ride this horse (XL184) for as long as I can, and then I’ll look for a new mount.”

Thyroid cancer is not the good cancer- from EmpowHER.com

No Such Thing As "Good Cancer"
By Some of ThyCa's Lifetime Members
We've all heard it at one time or another: "If you have to get cancer, then this is the one to get." "Thyroid cancer is good cancer," and similar statements. These comments fail to take into account just how serious and complex thyroid cancer can be.
Those of us who have been diagnosed with thyroid cancer know these statements aren't true. There is no "good cancer."
Telling someone diagnosed with papillary or follicular thyroid cancer that he or she has an excellent prognosis for a long life of living with thyroid cancer is reasonable. Telling the same person that he/she has "good cancer" diminishes both how dangerous the disease can be, and what the person diagnosed is going through.
Medical professionals need to speak to us in the same way they discuss any other cancer, so that we will realize how important lifetime monitoring is even when we have a good prognosis. Not clearly delivering this message can lead survivors to not understand how important lifetime monitoring and follow-up are to managing their thyroid cancer.
To put things in context, when someone feels poorly and goes to the doctor for a checkup, the doctor may say, "you have a bad cold." How can a person be told he or she has a "bad cold," but can have "good cancer"?

Dirty Dancing and Dancing With the Stars' Jennifer Grey is a Thyroid Cancer Survivor (From About.com)

Tuesday August 31, 2010

Until today, I didn't know that actress Jennifer Grey, beloved for her role as "Baby" alongside Patrick Swayze in the film "Dirty Dancing," was a thyroid cancer survivor. Her two recent thyroid cancer surgeries, however, are mentioned and discussed in a USA Today article today that announces the new celebrity cast of ABC's Dancing With the Stars this fall. According to USA Today, , the 50-year-old Grey is feeling well, and has a new exercise regimen and outlook on life, saying: "I began saying yes to everything scary that could be fun and joyful and not be controlled by fear....[Dancing With the Stars] could be a huge disaster for me, but I'm willing to take that chance. Life is short."
Learn more about other prominent and celebrity thyroid cancer patients in the arts, politics and sports.

Hand-foot Syndrome Overview - References, Advice, News, Videos, Coping & Support

Hand-foot Syndrome Overview - References, Advice, News, Videos, Coping & Support

Hand-Foot Syndrome (HFS) > OncUView > OncUView.tv - Symptom Management - Oncology News and Information for Healthcare Professionals

Current Articles | Archives | Search Hand-Foot Syndrome (HFS) blowes posted on August 13, 2010 01:00 Background Hand-foot syndrome (HFS; also known as palmar-plantar erythrodysesthesia [PPE]) is a cutaneous complication associated with continuous fluorouracil therapy and oral capecitabine (therapies used in the treatment of CRC) and is seen with several other agents used in the treatment of various cancers. First reported in 1974, this complication was noted in patients receiving antimetabolites and some chemotherapy antibiotics.1 The median time to onset of HFS with capecitabine is approximately 79 days, ranging from 11 to 360 days. In patients with CRC, HFS is the most frequently reported side effect of oral capecitabine (> 50% of patients) and is the dose-limiting side effect for this agent.2,3 Pathobiology Although the exact mechanism of action is not known, some researchers have theorized that HFS may be related to the crushing of deep capillaries in the soles of the feet and palms of the hands, which may cause drug extravasation into those same capillaries, causing the symptoms of this condition. Another report, by Lin et al,4 describes a different mechanism of action, in which HFS is a consequence of an inflammatory reaction that may result from overexpression of COX-2. These researchers note that COX-2 is upregulated with chemotherapy administration, possibly leading to a COX inflammatory-type reaction.3 Because the condition primarily affects the palms of the hands and the soles of the feet, researchers have also postulated a theory that HFS is caused by the accumulation of drug in the eccrine sweat or the eccrine sweat glands of the hands and feet, causing the damage characteristic of this toxicity.1 Histologically, changes in keratinocytes and vacuolar degeneration of the basal layer are seen, with scattered necrotic areas noted.5 Dilated blood vessels and papillary edema may also appear. However, more research is needed to determine the complete mechanism of action of this common cutaneous side effect. Physical Presentation Symptoms may include Numbness Tingling Swelling Dryness, cracking, edema Erythema Pain, blistering, or even desquamation (Figure 1) Skin reactions may not be noted until the second week of therapy. To control or relieve symptoms, dose reduction or temporary drug cessation may be required (Table 2). Figure 1. Toxicity Grading Scale*: HFS Images courtesy of Susan Moore, RN, MSN, ANP, AOCN. *Data from the National Cancer Institute Cancer Therapy Evaluation Program (page 15).6 Few randomized clinical trial data look at the prevention and management of HFS. Table 1 - Selected trials of treatments for HFS Study Author Study Design Results Recommendations Lauman et al7 Retrospective study in which patients were evaluated in 3 arms: capecitbine alone, pyridixoine prophylaxis with capecitabine, and pyridoxine to alleviate symptoms of HFS Patients who took pyridoxine > 200 mg/d had better symptom control of their HFS than patients who took less than that amount Patients may need higher doses of pyridoxine to ameliorate the symptoms of HFS Fabian et al8 Phase 2 trial of metastatic CRC patients receiving continuous 5-FU; 5 of 25 patients with HFS received pyridoxine 50 or 150 mg/d when moderate HFS noted 4 of 5 patients who received pyridoxine had reversal of HFS without interruption of the 5-FU, and no adverse effect on clinical response was noted Large, controlled trials are needed Karo et al9 Small trial of 5 patients with metastatic breast cancer treated with docetaxel and capecitabine; all patients developed grade 2-3 HFS. Vitamin E therapy 300 mg/d PO was given without dose reduction of therapy After 1 week, HFS symptoms began to disappear It could be of interest to consider vitamin E as a preventive drug with HFS-associated agents Yamamoto et al10 Patients on capecitabine were followed for HFS symptoms; 42 episodes of grade 2 toxicity were identified; all patients received oral vitamin E BID during chemotherapy Reduction in desquamation, pain, and comfort level of all the patients improved; neurologic symptoms improved as well. All patients were able to complete chemotherapy without interruption or delay; 38 of 42 did not develop cutaneous manifestation, and 4 had grade 1 toxicity Vitamin E minimized drug delays and schedule interruptions and maintained the dose density of therapy Cin et al11 13 patients with HFS used bag balm topically in a nonblinded study 12 of 13 reported improvement of symptoms after bag balm; 55% were able to continue chemotherapy without dose delay or reduction Large placebo-controlled trials are needed to determine the effectiveness of bag balm Lopez et al12 Topical DMSO was given to 2 patients undergoing chemotherapy with liposomal doxorubicin who developed grade 3 HFS With topical DMSO 4 times daily for 14 days, HFS resolved over a period of 1-3 weeks Small study; patients must be treated in a prospective trial to definitively document therapeutic efficacy In small case reports, treatment with oral corticosteroids (not topical), with COX-2 inhibitors, or sometimes with a nicotine patch has ameliorated HFS symptoms; however, large prospective trials are clearly needed to help refine the optimal therapy of this frequent side effect. Therefore, HFS treatment is largely symptomatic. Patients should be instructed to Avoid immersion in hot water, which could exacerbate symptoms Avoid activities that may increase pressure in affected areas, such as high-impact exercise Avoid tight clothing, vigorous skin rubbing, and sun exposure13 Apply cold compresses, which may help Use topical emollients or other preparations containing urea or lanolin2,3,14 (Table 3) Use protective gloves if needed15 Additional Clinical Information Several case reports have been published recently regarding another complication associated with HFS from capecitabine. In patients with metastatic breast cancer, 2 cases of acquired palmoplantar keratoderma were noted, thought to be a sequela of HFS.16 Another published report described HFS with scleroderma-like changes, also thought to be linked to oral capecitabine, with hyperpigmentation of the palms and soles.17 These cases should be noted as single reports, and more information is needed before these side effects can be conclusively linked to capecitabine. Nurses should continue to be vigilant and report to FDA MedWatch (http://www.fda.gov/medwatch/) all new effects and toxicities thought to be drug related. Drs Saif and Elfiky18 report on differentiating between the presentation of fluoropyrimidine-associated HFS in white and nonwhite patients. Three cases illustrating the disparities between white and nonwhite patients are discussed. The authors suggest a modified grading schema for nonwhite patients. An algorithm outlines pretreatment patient education and monitoring of skin changes during therapy. (See Reference 18 within the reference list for a link to the full-text article without charge.) Nursing Implications HFS can be painful and disruptive to patients’ quality of life. However, the current literature on HFS is limited to identification and treatment, with no existing reports on the effect of HFS on patients’ quality of life (QOL).19 More research on that effect is needed. Oncology nurses should instruct patients regarding the possibility of HFS and the need for early communication of symptoms. Because capecitabine is an oral therapy administered at home, symptom communication is crucial. Early reporting of HSF symptoms can assist nursing and physician staff in appropriate grading of HFS and sooner implementation of care interventions. In most patients, the syndrome is completely reversible.20 However, significant HFS usually requires dose interruption, and if the syndrome persists, dose adjustment becomes necessary.21 Although pyridoxine (50-150 mg/d) has been useful in some patient populations, others receive no benefit from adding this therapy.20 Additionally, because this an oral therapy, adherence may be a concern. Nurses may assess patients’ adherence by suggesting that they bring their medication bottles to clinic visits for pill counts. Table 2. Capecitabine Dose Modification Table Toxicity NCI CTCAE v3.0* During a Course of Therapy Dose Adjustment for Next Treatment Cycle, % of Starting Dose Grade 1 Maintain dose level Maintain dose level Grade 2 1st appearance Interrupt until resolved to grade 0-1 100% 2nd appearance Interrupt until resolved to grade 0-1 75% 3rd appearance Interrupt until resolved to grade 0-1 50% 4th appearance Discontinue treatment permanently Grade 3 1st appearance Interrupt until resolved to grade 0-1 75% 2nd appearance Interrupt until resolved to grade 0-1 50% 3rd appearance Interrupt until resolved to grade 0-1 Grade 4 1st appearance Discontinue permanently or If physician deems it to be in the patient's best interest to continue, interrupt until resolved to grade 0-1 50% Data from Xeloda prescribing information.22 Data from the National Cancer Institute Cancer Therapy Evaluation Program.6 Assessment Tools Polovich et al include a description of HFS under Cutaneous Toxicity in Side Effects of Cancer Therapy.23 Guidelines for coping with HFS skin problems are available here Clinical Practice Guidelines Evidence-based national guidelines do not currently exist. Table 3. Patient Management of Hand-Foot Syndrome: Capecitabine Related Grade Clinical Feature Functional Status Suggested Interventions 1 Numbness, paresthesia, dysesthesia, tingling, painless swelling or erythema of the hands and/or feet Activities of daily living generally unaffected Call nurse or doctor when symptoms first appear. Do not “wait and see.” Skin care: § Reduce friction and pressure: kneeling for long periods of time; leaning on elbows; power walking, jogging, or regular walking for long periods of time; using hand tools; gardening § Wear sunscreen; avoid exposure to heat § Use mild soap to bathe; pat (don’t rub) skin dry § Keep shower and bath water lukewarm to cool; avoid hot tubs and long exposure to hot water § Keep skin moist; gently apply moisturizing creams or topical emollients. Apply at night and wear loose-fitting cotton gloves; avoid rubber ones (dishwashing gloves), since they retain heat § Put hands and feet in cool water to relieve symptoms Clothing: § Wear comfortable, loose-fitting clothes, shoes, and gloves § Do not go barefoot; wear shoes or slippers when possible 2 Painful erythema and swelling of the hands and/or feet, skin remains intact Activities of daily living more difficult 3 Moist desquamation, ulceration, blistering, or severe pain of the hands and/or feet, tissue breakdown Activities of daily living interrupted: unable to work; difficulty walking and using hands Data from the National Cancer Institute Cancer Therapy Evaluation Program (page 18)6 and Wilkes and Doyle.24 References Clark AS, Vahdat LT. Chemotherapy-induced palmar-plantar erythrodysesthesia syndrome: etiology and emerging therapies. Support Cancer Ther. 2004;1: 213-218. Viale PH, Fung A, Zitella L. Advanced colorectal cancer: current treatment and nursing management with economic considerations. Clin J Oncol Nurs. 2005;9:541-552. Berg D. Capecitabine: a new adjuvant option for colorectal cancer. Clin J Oncol Nurs. 2006;10:479-486. Lin E, Morris JS, Ayers GD. Effect of celecoxib on capectabine-induced hand-foot syndrome and antitumor activity. Oncology (Williston Park). 2002;16 (suppl): 31-37. Nagore E, Insa A, Sanmartin O. Antineoplastic therapy-induced palmar plantar erythrodysesthesia (“hand-foot”) syndrome. Incidence, recognition and management. Am J Clin Dermatol. 2000;1:225-234. National Cancer Institute Cancer Therapy Evaluation Program. Common Terminology Criteria for Adverse Events v3.0. http://ctep.cancer.gov/protocolDevelopment/electronic_applications/docs/ctcaev3.pdf. Page 15. Accessed March 19, 2010. Lauman MK, Mortimer J. Effect of pyridoxine on the incidence of palmar plantar erythrodysesthesia (PPE) in patients receiving capecitabine. Proc Am Soc Clin Oncol. 2001;20:392a. Abstract 1565. Fabian CJ, Molina R, Slavik M, et al. Pyridoxine therapy for palmar-plantar erythrodysesthesia associated with continuous 5-fluorouracil infusion. Invest New Drugs. 1990;8:57-63. Karo IO, Sahin B, Erkisi M. Palmar-plantar erythrodysesthesia due to docetaxel-capecitabine therapy is treated with vitamin E without dose reduction. Breast. 2006;5:414-424. Yamamoto D, Yamamoto C, Tanaka K. Novel and effective management of capecitabine induced hand foot syndrome. J Clin Oncol. 2008;26(suppl):734s. Abstract 20615. Cin SF, Tchen N, Oza AM, et al. Use of “bag balm” as topical treatment of palmar-plantar erythrodysesthesia syndrome (PPES) in patients receiving selected chemotherapeutic agents. Proc Am Soc Clin Oncol. 2001;20:409a. Abstract 1632. Lopez A, Wallace L, Dorr R, et al. Topical DMSO treatment for pegylated liposomal doxorubicin-induced palmar-plantar erythrodysesthesia. Cancer Chemother Pharmacol. 1999;44:303-306. Morse MA. Supportive care in the management of colon cancer. Support Cancer Ther. 2006;3:158-170. Wilkes GM. Therapeutic options in the management of colon cancer: 2005 update. Clin J Oncol Nurs. 2005;9:31-44. Viale PH. Chemotherapy and cutaneous toxicities: implications for oncology nurses. Semin Oncol Nurs. 2006;22:144-151. Do JE, Kim YC. Capecitabine-induced diffuse palmoplantar keratoderma: is it a sequential event of hand-foot syndrome? Clin Exp Dermatol. 2007;32:519-521. Lee SD, Kim HJ, Hwang SJ, et al. Hand-foot syndrome with scleroderma-like change induced by the oral capecitabine: a case report. Korean J Intern Med. 2007;22:109-112. Saif MW, Elfiky AA. Identifying and treating fluoropyrimidine-associated hand-and-foot syndrome in whites and non-white patients. J Support Oncol. 2007;5:337-343. http://www.supportiveoncology.net/journal/articles/0507337.pdf Keating KN, Anderson RT, O’Leary JJ. Hand-foot syndrome: symptom assessment and the impact on quality of life—a review of the peer-reviewed literature. J Clin Oncol. 2008;26(suppl):739s. Abstract 20685. Janusch M, Fischer M, Marsch WCH. et al. The hand-foot syndrome: a frequent secondary manifestation in antineoplastic chemotherapy. Eur J Dermatol. 2006; 16:494-499. Gressett SM, Stanford BL, Hardwicke F. Management of hand-foot syndrome induced by capecitabine. J Oncol Pharm Pract. 2006;12:131-141. Xeloda prescribing information. Genentech USA, Inc. 2009. Available here. Accessed March 19, 2010. Polovich M, White JM, Kelleher LO, eds. Chemotherapy and Biotherapy Guidelines and Recommendations for Practice. Pittsburgh, PA: ONS Publishing Division; 2005:208. Wilkes GM, Doyle D. Palmar-plantar erythrodysesthesia. Clin J Oncol Nurs. 2005;9:103-106. Key Definitions cyclo-oxygenase (COX)—an enzyme that catalyzes the conversion of arachidonic acid to prostaglandins and is inactivated by aspirin and other NSAIDs desquamation—peeling off in the form of scales; scaling off, particularly of skin dysesthesia—impairment of sensitivity, especially to touch emollient—agent that softens or soothes the skin erythema—abnormal redness of the skin due to capillary congestion (as in inflammation) erythrodysesthesia—condition caused by continuous infusion therapy or certain oral chemotherapies resulting in a tingling sensation of the palms and soles, progressing to severe pain and tenderness with erythema and edema paresthesia—skin sensation such as burning, prickling, itching, or tingling pyridoxine—vitamin B6, found especially in cereals vacuolar degeneration—formation of nonlipid vacuoles in cytoplasm, most frequently due to accumulation of water by cloudy swelling